OSHA: Proposed Standard For Indoor Air Quality: ETS Hearings, September 22, 1994

OSHA: Proposed Standard For Indoor Air Quality: ETS Hearings, September 22, 1994


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UNITED STATES DEPARTMENT OF LABOR
OCCUPATIONAL SAFETY AND HEALTH ADMINISTRATION

PUBLIC HEARING
PROPOSED STANDARD FOR INDOOR AIR QUALITY

Thursday, September 22, 1994

U. S. Department of Interior

Washington, D.C.

The above-entitled matter came on for hearing, pursuant to notice, at 9:36 a.m.

BEFORE: HONORABLE JOHN VITTONE

Administrative Law Judge

AGENDA

PAGE

Discussion 637

Hal Levin
Hal Levin & Associates 649

Questions:

Jim Dinegar 682
Rex Tingle 694
John Rupp 698
Jim Dinegar 713

Joseph Lstiburek 716

Questions:

Rex Tingle 753
Cathy Sarri 758
Lee Hathan 768
Ms. Sherman 771

Dr. Jonathan Michael Samet 775

Questions:

Rex Tingle 793
Jim Denigar 794
Ted Grossman 803
Pat Sirridge 872
John Rupp 902
Steven Bayard 929
Ms. Sherman 933

EXHIBITS

EXHIBIT NO. IDENTIFIED RECEIVED

23 681 681

24 740 741

P R O C E E D I N G S
(9:03 p.m.)

JUDGE VITTONE: We recessed yesterday evening, and we'll resume this morning. We are on the record.

We have three witnesses scheduled for today. Before proceeding with the witnesses, though, I would like to go back to a matter that we raised yesterday at the hearing, the request from Mr. Tyson that was supported by other participants in this proceeding.

Mr. Tyson requested yesterday that there be an adjustment made in the schedule. In particular, his request was that the schedule be adjusted in the following manner: that we hold two weeks worth of hearings and then have a week off, and then hold two weeks and then have a week off, so we complete all of the witnesses.

The people have already been scheduled, but to adjust the schedule will be somewhat difficult, but I have been looking at the schedule in light of statements made yesterday. I must say, I do have somewhat of a concern with respect to process here.

I'm not so much concerned with the inconvenience or disruption from the parties who are participating, but I am somewhat concerned with respect to the orderly procedure so that this record is developed in a complete way as possible, and in a manner that we proceed so that all parties have a fair opportunity to participate to get their positions on the record and to develop whatever questions in an adequate manner that they believe should be raised in this proceeding, in support or in opposition to the proposed rule.

As I looked through the schedule yesterday, I see that we are scheduled to go through the week of October 14th. There will be a break for the week of October 17th. Resume again on October the 24th. Recess on November 22nd for the Thanksgiving holiday, then resume on the next week, the week of the 28th, and go until Friday, December 2nd.

I have a proposal that I would like that parties to consider. I'm just going to ask that you consider it now and think about it, because I think you have to look at who might be involved. I think that a possible way of not extending the proceeding for any great length of time but a way of developing some breaks in between the schedule that we presently have, so that there will be some time for the more orderly development, I believe, of this record.

My proposal would be this, and I ask that you think about it.

The third week of the schedule that we have scheduled here has a number of witnesses, and we would go that entire -- we're supposedly going to be scheduled to go that entire week, from October the 3rd through October the 7th.

The week of November 7th, which is a short week in that there is a holiday there -- we're only scheduled to be in hearing for four days, I was wondering if it would be possible to move as a group, en masse, that entire week of witnesses, for the week of December the 5th, and then move the week of November 7th, that group of witnesses, until the week of December the 19th, since there are four days scheduled there.

That way, we would only be extending the entire time of the hearings by another two to three weeks, but it would be at a pace that might benefit all of us in the course of our proceedings.

Also, it would provide some flexibility, in that if there are some witnesses -- and we are already falling a little behind here -- if there are some witnesses whose schedule we cannot meet under the schedule as it is right now, whose appearance we cannot meet under the schedule, we might be able to come back, say, during the week of October 3rd and hold a day's worth of hearings and get those people in or at some other point.

It might give us a little bit more flexibility as far as making sure that the people that we have not been able to get to, according to this schedule, might be able to come in and we can work them in on a day that we might be off.

I throw that out for you all to consider, and I'm going to depend on you because I'm not familiar with the people who are listed, and I'm not sure how much of an imposition this would be by changing the schedule that we have here.

It seems to me, if we can do that, as I said, we are only extending this hearing by another couple of weeks, for the scheduled witnesses, and we would be able to complete all of them before the end of the year. Now, I realize there probably will be some adjustments where people will be moved around anyway, and I certainly don't have a problem with that.

There is another question that I would like to raise, through. There is a Week 11 scheduled, or tentatively scheduled, I guess, and the only description I have is 510 participants whose notices of intention to appear were filed as a group.

In some of our discussions, I guess there is some question whether these people actually will appear or will not appear to testify.

If they do appear, or any number of them appear, then we have to have an additional period of time for those people to appear.

I would like for you to think about that proposal, take a look at the schedule, the people who are listed for those weeks, October 3rd and November 7th, and maybe we could bring it up right after lunch, and you can tell me how you feel about it, but that's my proposal.

It seems to me it builds a little more flexibility, but it's still a very reasonable pace. It's still a very intense pace for all of us and one that, if we can't adhere to, we will still be done with the public hearings by the end of December.

MR. GORDON: Could I ask for clarification, Your Honor?

JUDGE VITTONE: Sure.

MR. GORDON: You suggested moving the week of October 3rd through 7, through the week of December 5th.

JUDGE VITTONE: My proposal is that we take the week of October 3rd and move that whole week until December the 5th.

MR. GORDON: Right. Now what I was confused about was the week of November 7 to 10. Are you moving that to the week of December 12 or the week of December 19th?

JUDGE VITTONE: I would propose to move it until the week of December the 19th.

MR. GORDON: That would cause a lot of problems, because that is the pre-Christmas week.

JUDGE VITTONE: I don't have children anymore, so I don't really think about it.

[Laughter]

JUDGE VITTONE: I'm sorry. Okay. I appreciate that. I'm open for anything that's reasonable. If we do that December 5th, if you wanted to start, say, the 14th through the 15th and then finish the 19th or whatever, it would give you a week before Christmas.

MR. GORDON: And I'd like clarification on another matter, for which some of the tobacco people might wish to comment.

JUDGE VITTONE: Sure.

MR. GORDON: We don't know how many of the 510 will show up. This will require moving them into January, I think, because of the uncertainties of how many would show up, unless we had a commitment from the tobacco people, to letting us know how many are actually going to show up.

The other thing is, since it's crucial to the department to keep this on schedule, would the post-hearing comment periods commence running from, say, December 19th as opposed to whatever day in January these 510 would run to, those would be important considerations for the Department.

JUDGE VITTONE: If you're able to comment now or if you would rather wait and take it up after lunch,
but -- Mr. Tyson, I think maybe you better come up to the podium so we can hear you.

MR. GORDON: Excuse me, Your Honor. I'm Charles Gordon. I'm counsel for Health Standards of the Solicitor's of Labor Office.

JUDGE VITTONE: I'm sorry, Mr. Gordon. That was my fault. Thank you.

MR. TYSON: Pat Tyson representing Philip Morris. We are attempting to contact a number of the people that are in the 500-and-whatever the number is, and we anticipate that some of them are going to want to testify. At this point, I can't give you a feel for the number of those, but clearly some will come and intend to testify.

MR. GORDON: Your Honor, could --

JUDGE VITTONE: Just a second. For the record, who are these people? Is there a way to describe them?

MR. TYSON: There are a number of people who have been contacted by representatives of the industry and in the industry has indicated their willingness and desire to come testify at this hearing.

JUDGE VITTONE: So, essentially, they're private citizens?

MR. TYSON: Yes. They're employers.

JUDGE VITTONE: They're what?

MR. TYSON: They will be employers, in most cases, but they are not large organizations.

JUDGE VITTONE: Okay. Small businessmen?

MR. TYSON: Typically.

JUDGE VITTONE: Typically small businessman. Okay. I'm sorry. Mr. Gordon?

MR. GORDON: If you could ask counsel for the tobacco people for clarification. Putting that group into January, with uncertainty of the numbers is less of a problem if we begin the post-hearing comment period from December 9th, or whatever date we finish the testimony of all the witnesses. Would that be agreeable?

MR. TYSON: Well, I mean the whole purpose of the post-hearing comment period is to allow all parties the opportunity to review in detail the hearings themselves. That requirement doesn't change, and therefore I think the time originally set is a reasonable time, and it should begin at the end of the hearing.

JUDGE VITTONE: What is the time now set for post-hearing comments? How many days, 60?

MR. TYSON: 60, and then 30 for brief.

MR. GORDON: But, you know, that was a suggestion in your guidelines.

JUDGE VITTONE: Is it possible that some of these people would be willing, or a number of them would be willing, to submit their comments in writing? That is possible. It is also possible that some of these individuals may wish to schedule time, if time is available in the earlier part of the schedule, assuming we may have some breaks in there where we don't take full days. I don't anticipate that these witnesses will wish to testify for a long period of time.

JUDGE VITTONE: I think I probably know what the answer is going to be, but I assume these people are not just local people from the Washington, D.C. area, but
from --

MR. TYSON: You are correct, Your Honor.

JUDGE VITTONE: -- from across the country?

MR. TYSON: Yes, Your Honor.

JUDGE VITTONE: Certainly, if during the schedule of the people we have scheduled now, if there is some free time and you are able, let's say something happens and half of our witnesses drop out on a particular day and we only have a half a day, would the Department have any objection to bringing some of these people in for that afternoon, or something like that?

MR. GORDON: So long as it's orderly, we would have no objection.

MR. TYSON: Our problem with that, of course, is we would need to know with some degree of advanced notice when those dates might be.

JUDGE VITTONE: All right.

Do you have any other questions, Mr. Gordon?

MR. GORDON: No, Your Honor.

JUDGE VITTONE: Anyway, that's my proposal. I would like for you all to think about it. Take a look at the witnesses. As I said, I think you probably know them a heck of a lot better -- I know you know them better than I do, but give me your thoughts after the lunch break, and we'll talk about it, and one way or the other, I'll bite the bullet.

MR. GORDON: Thank you.

MR. TYSON: Thank you, Your Honor.

JUDGE VITTONE: Ms. Ward.

MS. WARD: May I just get a clarification of what Mr. Gordon was saying?

JUDGE VITTONE: Sure.

MS. WARD: Your proposal was to begin the post-hearing comment period at the end of the last of the calendar witnesses.

MR. GORDON: Yes. Started running. Not ended, of course, just started running from that period.

MS. WARD: Right. It would start the 60-day period running from then, but not to include the nameless 510?

MR. GORDON: Well, obviously, they can make post-hearing comments too as long as they make it within the period.

MS. WARD: Right. But I'm just talking about the period that it would run. You're not proposing that if we continue with, say, the October 3 witnesses into December 5, you're not proposing that the post-hearing comment period begin running on December 5 or until those witnesses and the witnesses of November 7, to whenever they've moved have testified?

MR. GORDON: Yes. Wait until they have testified, until all of the calendar witnesses, as you called them, have testified.

MS. WARD: Okay. That's all I wanted to know. Thank you.

MR. GORDON: I have to clarify, it's not my proposal, it's my clarification.

[Laughter]

JUDGE VITTONE: Okay. Thank you very much.

Our first witness for this morning -- let me ask the Department. Ms. Sherman, who is the first witness?

MS. SHERMAN: I would like to introduce Mr. Hal Levin.

JUDGE VITTONE: Mr. Levin, would you come forward, please?

Are you going to ask him some questions, or are you going to let him --

MS. SHERMAN: I'm going to let him speak.

JUDGE VITTONE: All right. Mr. Levin, would you state your name and your affiliation and present whatever testimony you have?

MR. LEVIN: All right.

JUDGE VITTONE: Am I in your way here, by the way?

MR. LEVIN: No, I don't think so.

HAL LEVIN
HAL LEVIN & ASSOCIATES

MR. LEVIN: My name is Hal Levin, and I'm self-employed as a consultant and researcher on indoor air quality. My work focuses primarily on consultation to building owners; designers, primarily architects and engineers, and, in some cases, employers and occasionally employees, with regard to indoor air quality issues, in new buildings and in remodeled, renovated buildings.

My work on indoor air quality began in 1978, when I was appointed as a research specialist in the College of Environmental Design at the University of California at Berkeley, and I've been involved with the subject almost exclusively since 1983.

My consultation has included state and federal government agencies, local government agencies, and even foreign government agencies.

I've also taught courses at the University of California at Berkeley and Santa Cruz on the subject and lectured extensively on symposia and seminars and taught continuing education courses for Harvard University Graduate School Design, the International Facility Management Association and others.

I've published more than 70 articles and over 2000 total pages on the subject of indoor air quality, both as editor of the newsletter, Indoor Air Quality Update, published by Cutter Information Service, from its founding until 1988, until February of '91 and, since that time, Indoor Air Bulletin, which I edit and publish myself.

My public service includes, since 1985, at its founding, the chairmanship of ASTM Subcommittee D22.05 on indoor air, a Committee which develops standards for sampling an analysis of indoor air;

Since 1992, chairman of ASHRAE's Guideline Project Committee GPC10P;

Criteria for achieving acceptable indoor environments;

And I'm currently a member of ASHRAE SSPC62, Ventilation for Acceptable Indoor Air Quality, as well as a member of several other ASHRAE Committees.

I'm here to testify in support of the OSHA proposal.

(Slide Presentation.)

Reasons for my support include my experience in the field, where I've also conducted investigations of indoor air quality problems, primarily in office buildings, but also in other types of facilities, including retail and educational facilities.

It's been my observation that, in many cases, building ventilation systems simply fail to deliver the necessary outside air due either to insufficient capacity or improper operation of those systems, either the timing and scheduling of the operations or the management of the controls for them.

It's been my observation that building ventilation systems are inadequately designed or not operated according to the need to handle the pollutant or thermal loads that are present. I apologize for the misspellings.

Published literature on indoor air quality consistently points to the higher prevalence of health and comfort problems in buildings with low ventilation rates.

Filtration is often inadequate in these buildings, due to filters not being properly sized and specified;

Filters not being tightly fitted into their frames or, in some cases, completely missing from the system;

Insufficient circulation of air through the air handling system in order to provide an opportunity for the filters to remove, according to their rated capacity, or filters being poorly maintained, resulting in odors and microbial contaminants.

Problems are often found in the air distribution system. In other systems, ductwork is not properly connected, or it's not even connected at all, to the diffusers.

Outside air used for ventilation is often contaminated; becomes a source of exposure that may result in material harm to the occupants.

This can result from entrainment of exhaust, from idling trucks at loading docks, from building exhausts, or from vehicles entering garages, odors from garbage dumpsters, entrainment of exhaust fumes from vehicles entering parking garages located at the lower portion of the building, and many other sources.

Very often indoor air quality problems result from the use of spaces for purposes for which they were not intended and for which the ventilation system was inadequate or totally inappropriate. Very frequently, we find space, air distribution problems.

As a result, I see a need for better operation and maintenance in order to achieve good air quality. Adequate training of housekeeping staff is often totally lacking or minimal, at best, and often this lack of training and improper techniques or inappropriately applied materials result in significant air quality deterioration.

There is a need for the employees themselves, especially in the private sector, to have access to information about their work place environment, including the quality of the indoor air and the operations of the building operators that affect it.

There is a need for employers to be able to request and obtain assistance, including indoor air quality investigation, if necessary, when air quality-related problems persist.

There's a need for clear records of building design, intent, operation, and maintenance.

The California Occupational Safety & Health Administration rule regarding building ventilation requires documentation of HVAC system maintenance and inspection, required by the rule, and retention of such records for at least five years. This rule was adopted in 1987 and has been in force and has done much to enable the California OSHA as well as the protected employees to obtain better indoor air quality.

There is a need for improved and widely useful and effective assessment tool to investigate cases of poor IAQ, and there's a need for implementation of source control to limit people's exposure.

MS. SHERMAN: Excuse me. Could you label the slide that you just spoke with, both on the hard copy and for the transcript, so we'll be able, in reviewing the transcript, tell what you just spoke about.

MR. LEVIN: Okay. That was labeled The Need.

MS. SHERMAN: Thank you. And if you could do it on all succeeding slides.

MR. LEVIN: This slide is labeled Reasons for Support of the OSHA Proposal.

First and foremost, in my mind, it makes good economic sense, it's likely to produce improvements and productivity and building operating efficiency that will far outweigh the costs of implementing the rule.

The reasons for this are employer costs for office workers in salaries and benefits is approximately 10 times the employer costs for the buildings themselves.

Small increases in productivity easily offset any additional expenses required to improve the environment that enables the productivity increases.

Improving IAQ is cost effective.

Avoided costs of resolving problems of poor IAQ are much greater than the costs of improving the indoor air quality.

Preventive maintenance, plus good ventilation system, operating procedures, will increase productivity and create more income for building owners.

This is labeled for Reasons for the Support of the OSHA Proposal, Continued:

No. 6: Energy costs of building ventilation are much less than 1 percent of the salaried costs of office workers. So small savings and energy costs by low ventilation significantly affects indoor air quality.

Resulting economic losses can be 10 to 100 times the energy cost savings.

Conversely, small incremental increases in energy costs for building ventilation can dramatically reduce contaminant concentrations, including infectious microorganisms, volatile organic chemicals, and particulate matter.

Increases in outdoor air ventilation rates through the use of outside air economizer cycles can be obtained in most parts of the United States for many parts of the year at no additional energy costs and, in many instances, at substantial energy cost savings.

This slide shows two graphs, labeled Figure 3 and Figure 4, and they illustrate the point I just made with respect to the costs of energy for 8 different locations -- 12 different locations of the
United States -- and they show that even in the most expensive areas, such as Miami, energy costs for going from 2.5 liters per second, or 5 cubic feet per minute outside air, to 20 cubic feet per minute outside air, increase less than 5 percent.

The dollar costs, therefore, are very small from such increases, even in the most adverse climates. We see lower increases for the cold weather locations, such an Minneapolis.

This slide, entitled General Comments: Good IAQ is like preventive medicine, daily exercise or good dietary habits; an ounce of prevention is worth a pound of cure.

Experience from numerous lawsuits, and I've been involved in over a dozen involving indoor air quality problems, suggests that prudent avoidance is generally wise, although allocation of resources is always an issue in the reality of limited resources.

Public health perspectives suggest that material harm that occurs from exposure to poor air quality is not only directly observable in terms of absenteeism, illness, and reduced worker productivity, but that there are large personal and societal costs associated with the direct effects, as well as the exacerbation or potentiation of other risk factors.

This slide has no title. The first line: Employers are more concerned generally than the building managers or developers.

Even in owner-employer occupied or operated facilities, there may be a division of management responsibilities for worker productivity and/or health care cost containment and/or responsibilities for facility development, management, and operation.

In my experience, this division of responsibility means that people responsible for production don't necessarily consider the implications of poor indoor air quality and the need for attention to this in the design and operation of facilities due to the effects of poor air quality on worker health and productivity.

Meanwhile, decisions by facilities managers to reduce costs of construction or operational costs are usually made with little to no concern for the impact on worker health and productivity since these people are not working from the same budgets and are not evaluated on the basis of the impact on health and productivity.

Slide entitled Table 3: Types of predominant environmental stressors, from Dr. Jim Woods; a presentation at a congressional hearing in 1987, where he identifies from over 30 investigations conducted by him and his colleagues while at Honeywell's indoor air diagnostics program, the prevalence in problem buildings in percent.

That is, all of the buildings investigated were problem buildings.

By type of environmental stressor would be:

Chemical and particulate contaminants, 75 percent;

With 70 percent of the total with odor discomfort.

55 percent with thermal discomfort;

45 percent with microbiological contaminants; and,

30 percent non-thermal humidity problems, with eye irritation and mold growth, from low and high relative humidities, respectively.

Slide titled Table 4: Frequencies of occurrence of physical causes of problem buildings, from Dr. Woods, again the same presentation, and the same data set.

He found problems from design in terms of the physical cause in the HVAC systems, inadequate outdoor air, 75 percent of the investigations.

Inadequate supplier distribution to occupied space is 65 percent.

Inadequate return air and exhaust air 75 percent.

Equipment problems; inadequate filtration of supplier 65 percent.

Inadequate drain lines and drain pens 60 percent.

Contaminated ductwork or duct linings 45 percent.

Malfunctioning humidifiers, 20 percent.

Inadequate access panels to equipment, 60 percent; and,

Operational problems, including inappropriate control strategies, 90 percent.

In addition maintenance, 75 percent.

Thermal contaminant load changes 60 percent.

I think most of these problems are addressed by the Rule and represent one of the major reasons for my support of the Rule.

With respect to productivity and indoor air quality, it is clear that worker costs dwarf building costs. Small increases in productivity produce economic returns that far outweigh the investment in the environment required to achieve them.

Employer costs per employee -- that is, salaries, plus benefits, insurance, et cetera -- for office workers range from an estimated low of around $125 to around $500 per square foot per year, depending on salary level and square footage allocated.

Typical values, considering the usual matches of salary levels and space allocations range from $150 to $250 per square foot per year. Using $40,000 as the employer's annual office worker cost and $200 gross square feet per worker, an annual building cost of $20 per square foot, the annual building cost is about 10 percent of the total cost of worker and building.

This does not include training and other investments and costs prior to actual productive period for the worker.

Of this 10 percent, building ventilation and building cleaning repairs and maintenance, account for less than 2 percent. These are the factors that most affect indoor air quality.

An increase in productivity of 3 percent, as estimated by OSHA, could pay for more than a doubling in the expenses for the factors that most effect indoor air quality.

Slide entitled: Potential impacts of OSHA's Proposed Rule. The 3 percent estimate of productivity improvements achievable through the Proposed Rule is a reasonable one; however, it is difficult to obtain reliable data to precisely estimate the actual improvements that are possible.

I believe it is plausible that the improvements in productivity could be considerably larger if the real costs of poor indoor air quality were actually taken into account.

This is titled Components of Costs, and represents a series of slides showing the assumptions underlying my conclusions about productivity.

Approximately 4 percent of office building debt services for the mechanical equipment. The debt service represents only about half of building costs. These are very rough numbers but I think representative.

So the actual annual costs for building mechanical equipment is less than 2 percent of the total building costs. Again, the 3 percent increase in productivity estimated by OSHA, as a result of the Rule, would easily pay for a doubling of this investment and leave enough to double the energy expenses to operate it.

I'm not necessarily suggesting that we do this, nor am I suggesting that these investments would be required by the Rule. I simply make these statements to illustrate how I view the return from this Rule as being an economic gain for everyone concerned.

Very much smaller investments in expenditures will actually be required to achieve the improvements in the indoor air quality that OSHA has estimated to produce the three percent increase in productivity.

Components of Costs, Slide 2: Building operating costs. Typical building costs, including cleaning, repairs, security, roads, grounds, utilities, taxes and maintenance are about $3 to $10 per square foot per year.

In 1989 to 1990, total operating expenses, operating and fixed, averaged $8.23 per square foot and $8.47 per square foot, according to the 1991 BOMA Experience Exchanging Report, Income/Expense Analysis for Office Buildings, by the building owners and Managers Association International. BOMA International.

Median values for total operating expenses were $4.55 per square foot and $4.66 per square foot in 1989 and 1990, respectively.

Components of Costs, Slide 3: Energy Costs.

Building energy costs for office buildings are about $1 to $2 per square foot per year. This varies greatly from region to region. Typically, about 35 percent to 65 percent of this energy cost will be heating, cooling, and ventilating buildings with mechanical HVAC systems.

Ventilating costs vary by building, region, season, and local costs of energy. Energy costs alone vary from less than 4 cents per kilowatt hour to more than 16 cents per kilowatt hour in different parts of the
United States.

I might add that per square foot energy consumption varies from a low of around 25,000 to 30,000 BTUs per square foot per year to something on the order of 200,000 BTUs per square foot per year or more, a very large range, depending on the condition of the building and the degree to which energy concerns have been addressed.

During much of the day, for much of the year, in many locations in the United States, economizer cycle operations allow the introduction of increased outside air fractions at no additional energy costs.

In fact, in many locations increasing the outside air fraction during much of the fall, winter and spring will actually reduce building energy costs.

Components of Cost, No. 4: Outdoor air amounts and HVAC system economizers; assumptions commonly used for offices with economizer, and office worker with 140 square of office space would receive as much as 70 to 140 cfm per person outside air ventilation.

Based on the usual range of total supply air volume of one-half to 1 cubic foot per minute per square foot of floor area, and based on using a more conservative figure of 200 square feet per worker, the outside air delivered would be as much as 200 cfm per person.

Economizer Cycle, is the title of this slide. Economizer Cycle design is common in temperate climates. All outdoor supply is a common economical and energy efficient operating mode when outdoor air temperatures are between 10 and 30 degrees Fahrenheit less than indoor air temperatures.

This provides so-called free cooling because the natural temperature differential is used to provide the cooler air needed to provide thermal comfort in the office.

Obviously, it is not free since fan energy is expended to move the air, and fan energy can be as much as half the energy consumed by the HVAC system in temperate climates.

Nevertheless, it is economical to use outside air for cooling when the temperature warrants it.

I should add the most office buildings in the United States for most of the day, for most of the year, are in the cooling mode.

Salaries Versus Energy Costs: Office workers' salaries and benefits are much greater than 100 times the cost of the energy used for all purposes in such buildings. Costs for ventilating, heating and cooling buildings at 35 to 65 percent of the total energy costs, and the employee costs may then be roughly 200 times the energy cost for heating, cooling and ventilating the buildings.

Thus, an increase in productivity of only a half a percent would offset a doubling in the cost of energy to operate the building. Alternatively, energy conservation measures, including but not limited to adequate maintenance of HVAC systems, use of economizer cycles, and more effective operating schedules, could reduce the energy costs and improve indoor air quality at the same time.

Debt Service Costs. Debt Service Costs for office buildings, I've estimated for office buildings, I've estimated it at $8.00 to $20.00 a square foot per year based on acquisition costs from $50 to $250 per square foot and interest rates at 9 percent.

Using an intermediate estimate of $125 a square foot, the debt service would be in the $10 - $12 1/2 per square foot per year range with typical amortization periods.

Adding debt service to operating costs brings total billing cost to a low of approximately of $13, with an upper end estimate of around $30 per square foot per year.

Actual square footage per occupant. There's a wide range of values in the literature, from lows well below 100 square feet per person on up to 450 square feet per person in the Department of Energy, Department of Commerce Survey published every two or three years.

The typical area per occupant values available cover that range depending upon the source. GESA's standard for new space is about 120 occupiable square feet per occupant for new facilities.

ASHRAE design values use 140 square feet per office worker as net square foot values and do not consider associated office storage space, printing, computer and other office related spaces. Circulation space, including corridors, stairs, elevators and escalators, service areas including mechanical equipment areas, communication equipment closets, janitorial areas and building storage areas.

Department of Commerce data indicates that the median gross area provided for office workers is about 400 square feet in the United States. But this figure includes square footage that is not related to the office work activities and organizations as well. Therefore I've used the square foot value of 200 square feet per occupant to estimate the cost that I show in the following.

Furnishings/equipment costs. These are often neglected from analyses of this type. Costs for typical office workstation furnishings, equipment and other support, the per employee costs range from an estimated $2,500 for low-end clerical workers to as much as $25,000 or more for high-level professionals and managers. Using $7,500 per employee in a well-equipped office, amortized over a five year period -- a conservative estimate -- the annual cost per employee would be $1,500 per year plus financing costs.

In many organizations and for many employees the investment will be considerably smaller and/or the amortization period considerably larger.

Assuming a 10 percent interest rate for this equipment, then the average annualized cost would be approximately $1,875 per employee. Using 200 square feet per occupant, annual costs of furnishings and equipment would be $9.38 a square foot.

Using ASHRAE design value of 140 square foot per occupant, the annual cost goes up to $13.40 a square foot for furnishings and equipment. Using the 450 square foot per occupant range from the Department of Commerce, we get a value of $4.17 a square foot per year for furnishings and equipment.

I then concluded a reasonable value is about $9 per square foot per year.

This is titled "Total Facility Costs." If we add the values calculated above for debt service, building operating costs and equipment and furnishings we obtain a best estimate of approximately $20 to $30 per square foot per year. With respect to the costs of the proposed rule, the portions of the building costs affected by the rule are primarily the cost of design, construction, operation and maintenance of the ventilation system, as well as certain management costs.

Table 5 contains our estimates of the cost related to the ventilation system of the proposed rule. And I've listed those items design, construction, operation -- including energy -- and maintenance. Looking at the increased costs of the rule with low, high and typical estimates, for design a low of nothing, a high of 10 cents a square foot and typical, five cents a square foot. For construction, a low of nothing, a high of $1, and typical of 20 cents a square foot. Operation, including energy, a low of three cents a square foot, a high of 20 cents square foot, and a typical of 10 cents a square foot. And for maintenance, a low of two cents a square foot, a high of ten cents, and a typical of five cents.

Obviously, there is a wide range out in real practice and those increments to existing buildings or to new buildings will be a function of the base from which they start.

For salary costs -- this is "Table 6. Annual Employer Costs for White Collar Workers." From the Bureau of Labor Statistics, "Employer Costs for Employee Compensation," published in March of 1993. Professionals, an hourly cost of $29.33 an hour, or $61,000 a year. Executive, administrative and managerial, $30.48 an hour, $63,400 annual cost, and administrative support $14,000.36, or an annual cost of $29,868. Thus, my figure of $40,000 I consider to be a reasonable figure.

With respect to the areas allocated to each employee -- this is "Table 7. Annual Employer Costs for Employees Per Square Foot of Office Space." Using those figures, you can see I've simply done the multiplication. If we look in the $40,000 column under Annual Employee Cost Per Employee, and we look at $200 per square foot, we end up with our figure of $200 per square foot per employee.

This is titled, "Direct Measures of Productivity Based on Absence and Poor Performance." This is a very difficult subject. There is a lot of evidence from indirect measures, including death, job injury, hypersensitivity pneumonitis, asthma, illness and doctors visits and days absent. It becomes more difficult when we look at task performance, attention span, concentration and so on, but these are the sources of information that support estimates of increased productivity as a result of a better environment.

I've chosen to focus on one of the most serious problems from poor indoor air quality, especially related to ventilation. That is, the slight impact of respiratory illness on worker productivity. There are serious threats from microbial agents in buildings covered by the proposed rule. These include bacterial, viral and fungal agents, and among them are Legionella, pneumophilla, tuberculosis bacteria, and viruses for flu and the common cold. The effect here of increased ventilation is similar to the effect of ventilation on any environmental contaminant generally. Increased ventilation can reduce significantly the rate of infection, especially respiratory infection that may account for two to four days of lost work time per year. This is especially true at the lower end of the ventilation rates found in most workplaces. These infections are distributed evenly across the building population. We believe they are more likely to be in the higher density, poorly ventilated spaces based on the limited evidence available from reports in the literature by Brundage, Nardell and from theoretical analyses. Then if we can reduce the risk of infection by 50 percent by a doubling of the ventilation in the 30 percent of office buildings with the lowest ventilation rates, we can decrease the numbers of days of illness by half of the 16.2 to 32.4 million respiratory illness days per year among office workers. Thus, at least 9 to 18 million additional workdays could be available with the hypothesized reduction in respiratory illness.

"The Nardell TB Study." What makes us think that this reduction is achievable? A study by Nardell and colleagues in Massachusetts of a tuberculosis case in a study of infection rates in an office building found that had the ventilation been reduced from 15 to 5 cubic feet per minute per person, the infection rate would have nearly doubled to 78 percent. An increase in the ventilation rate from 15 to 15 cubic feet per minute per person would have reduced the infection rate by only a third to 25 percent, and a further increase to 35 cfm per person would have reduced the theoretical infection rate an additional 7 to 19 percent, just under half the actual rate.

So we see from this that in the critical ventilation rate range, below 15 cfm, we get tremendous returns for relatively small increases in outside air ventilation.

This is entitled "Ventilation's Impact on Contaminant Concentrations and Risk of Infection." Ventilation reduces contaminant concentrations and thereby reduces risk of infection. An increase from 5 to 15, or from 2 to 5 cfm per person are going to have a significant impact on exposure. We control exposure by ventilation where source control has either been utilized to the extent possible or where it is not possible, such as the case very often with respiratory infectious agents. The relationships between ventilation, source strength and resulting concentration demonstrated that increasing ventilation is most critical at the low end of the range. In the presence of strong sources it can be overwhelmingly beneficial to increase ventilation rates slightly. Thus, the OSHA proposal has tremendous potential to address the buildings most likely to cause serious illness or disease by exposure to toxic chemicals and infectious agents where ventilation is currently below the levels designed for in those buildings. Thus, at the low end of the ventilation range found in the buildings covered by the proposed rule, improvements to ventilation where it is currently insufficient will be effective in reducing risk. Strong support for this is contained in the following two sections of my written testimony related to a study of febrile respiratory disease in Army barracks -- that's the Brundage study -- and in the investigation of tuberculosis in an office building -- that's the Nardell study.

To further make my point, I'd like to list what I consider to be the most important general categories of ways to control indoor air problems. Certainly source control in the case of the infectious agents would be the most effective. If we can keep the Legionella and pneumofilla out of he cooling tower then we don't have to worry about the dilution in the building. If we can keep the infected person out of the building or if we can keep the chemical contaminant source out. Once having done that, then ventilation with dilution with outside air or with local direct exhaust for strong point sources, air cleaning and space air distribution.

This is a slide of "Figure 1. The Prevalence of General Symptoms in 24 Buildings With 15 or More Males and 27 Buildings With 15 or More Female Occupants As Function of Outdoor Air Flow Rate." The correlation coefficients for women, -.38 with a P of .001 and for men .35 with a P of less than .001. This is from the study of Sunberg and Stendler, two doctoral theses recently published in Sweden of a very large study of a wide variety of office buildings and a wide variety of individuals. And you can see clearly in this slide that as the outside air flow rate decreases the prevalence of general symptoms studied as SDS also decreases. And what you see in particular is at below 20 liters per second per person, and especially lower than 10, we see significant increases relative to the higher ventilation rate. This, the authors conclude, is evidence that ventilation -- low ventilation -- does have an adverse impact on indoor air quality and that it is the indoor air quality that is responsible, at least in part, for many of the reported symptoms

We can see the effect of ventilation on sources such as housekeeping activities, wet products such as caulking compounds or paint, and so on, in this slide titled "Emission Factor vs. Time Caulking Compound." At two different air exchange rates, .36 air changes per hour, the solid line, and 1.84 air changes per hour, the dotted line -- this study by Bruce Tischner and others at the U.S. Environmental Protection Agency -- and what we see is that the emission factor for these sources goes down much more rapidly and is practically zero by the time of 6 hours when we use the higher ventilation rate, but at the lower ventilation rate it goes down more slowly and continues for a much longer period of time. Further evidence of the effectiveness of ventilation.

In a study by Lawrence Berkeley Laboratory -- and this slide is not titled, but it is a graph with a vertical axis labeled "Concentration" and the horizontal axis "Ventilation Rate in Air Changes Per Hour," we see measured and predicted values for solvents from photocopy machines. And what we find out is that there is a direct relationship and that the concentration increases much more rapidly when we get below eight-tenths of six-tenths of an air change per hour. And this is the critical area addressed by the rule for buildings whose ventilation systems are not being operated to the levels for which they were designed or required by code at the time of their construction.

A study by Andy Persily at the National Institute of Standards and Technology titled "Figure 20. Unbiased Frequency Distribution of Air Exchange Rates for All Buildings (Except for A and C)" shows -- and you're looking here at the vertical axis, the number of measurements, a very large number of measurements, in a range of buildings that the bulk of the measurements are below one and half air changes per hour and in fact most of them below one air change per hour. This is the region where small decreases in ventilation result in significant increases in contaminant concentration. This is the region addressed by the rule. Since ASHRAE Standard 62, 1989, the 15 cubic feet per minute per person results in a typical office building in about nine-tenths of an air change per hour.

These are measurements from a single building of the daily maximum CO-2 concentration with occupants being the primary source but outside air setting a base level of around 350 or 400 and the daily average air exchange rate varying from around .4 up to about .9. And what you see again is a direct relationship between the concentration of the contaminant and the ventilation rate. And in this range, approximately a doubling of the concentration attributable to the indoor source.

"The U.S. EPA Base Program Pilot Studies." Nine buildings, generally believed to be good buildings when offered for study. These are preliminary findings not yet published but discussed by John Girman of the Indoor Air Division at the Institute for Environmental Quality, University of Wisconsin - Milwaukee on September 10th of this year. In one building the ventilation system simply wasn't running. The ventilation contractor visited but did not correct or inform of the problem. In another building air was being exhausted through the intakes. The drip pans contained microbial slime and a national ventilation contractor firm representative visited but did not remedy the problem. In the third building, intake and exhaust dampers on the air handling unit were chasing each other all day; that is, opening and closing and not coming to a stable position. And in other buildings there were additional operational problems.

This is an EPA-based study program, randomly selected sample field studies, 13 buildings to date. The full scale randomly selected studies are now ongoing, and the buildings have been selected by statistical techniques as random representative buildings. You should note that permission has been granted to the EPA contractor to study the buildings which in my mind, at least means that the owners and operators of these buildings believe that they are reasonably good buildings. There's a wider range of problems found in the random survey than was found in the pilot study. People are not getting what they are paying for in the way of ventilation system design and operation, in effect, performance. And national ventilation contractor site visits are not always effective in fixing the problems.

Indoor air quality is basically a function of the source strength and the air exchange rate. This is a graph with the vertical axis showing the concentration in milligrams per meters cubed for any pollutant, and the air exchange rate going from zero up to six air changes per hour. It's a theoretical analysis, assuming no syncs, for emission factors ranging from one to 50 milligrams per square meter per hour. And I would like to point out that down in the range where most of the buildings measured by Persily were found, very small decreases in ventilation result in significant increases in contaminant concentration for all of these source strengths. Clearly, the most effective strategy is to reduce the source strength at any ventilation rate, and to be sure that the ventilation is sufficient to get us into the point where the curves start going flat. I believe the OSHA rule does this.

This is titled "Reasons for support of OSHA's IAQ rule." In summary, the real indoor air quality problems in many U.S. non-industrial workplaces do exist and are being confirmed by a number of sources, as well as my own experience. IAQ problems can create significant harm to the occupants. The Proposed Rule simply requires buildings be operated according to the standard to which they were designed. The proposal will not only provide healthier work environments, it will also make money for those who follow it. It will provide a level playing field for the real estate industry -- not just developers, but building managers and operators. It is not different from what is being proposed by every responsible body working on IAQ guidelines and standards. These include the current version of the draft revision of ASRAE Standard 62-1989R, ventilation for acceptable indoor air quality; the EPA NIOSH publication, "Building air quality for building owners and facility managers"; the United States General Services Administration federal property management regulations as well as their model lease; the California Occupational Safety and Health Administration rules for ventilation; the information being provided in the EPA-BOMA joint training courses and other courses supported by EPA; the training courses of IFMA which I myself have been teaching for four years; guidance recently published by Public Works Canada; and most responsible IAQ researchers and consultants throughout the world.

I think in the interest of time I'll conclude my remarks and be available for questions.

JUDGE VITTONE: Thank you, Mr. Levin.

MS. SHERMAN: Mr. Levin, do you want to submit a copy of your slides for the record?

MR. LEVIN: I can do that.

MR. SHERMAN: Do you have them with you now?

MR. LEVIN: I have all the verbal slides. I don't have all the charts and graphs.

MS. SHERMAN: Your Honor, can we reserve an exhibit number?

JUDGE VITTONE: What number are we up to, Ms. Reporter?

(Pause)

COURT REPORTER: No. 22.

MS. SHERMAN: MR. Levin, would you like to submit your written testimony for the record and your slides will be an addendum to that. Exhibit No. 23.

JUDGE VITTONE: Exhibit No. 23, his testimony and slides which will be submitted, can you do that within a week?

MR. LEVIN: Certainly.

JUDGE VITTONE: Will be received into the record of this proceeding.

(The document referred to was marked for identification as Exhibit No. 23, and was received in evidence.)

JUDGE VITTONE: Let me get an estimate of how many people have questions for Mr. Levin. Will the people who have questions for Mr. Levin, please stand.

(Pause)

JUDGE VITTONE: Thank you very much. We'll have a five minute break. It's now 14 minutes until 10:00.

JUDGE VITTONE: Will the three individuals who have indicated they would like to ask some questions of Mr. Levin come up. I'm first going to call on the representative for BOMA to come forward, please.

MR. DINEGAR: Good morning.

JUDGE VITTONE: Good morning. Sir, would
you --

MR. DINEGAR: Jim Dinegar, Building Owners and Managers Association; 1 on the hearing docket.

Mr. Levin, I have a number of questions regarding your statement, and if I could refer to a couple of pages and submit it to the record.

You call for support on page two, actually, saying you support OSHA's proposal for regulations of indoor air quality and non-industrial work places.

You recommend adoption of the proposed rule, albeit with some improvements described later, and you go on to describe a number of those.

Can we talk about the non-industrial work places. The ones you've had experience with really run the gamut from office buildings to educational facilities. I assume hospitals, hospitality industry, the full range of buildings.

Can you briefly describe the different types of buildings you've worked with?

MR. LEVIN: Actually, I did in my oral comments identify office facilities, schools, and retail. I haven't worked on hospital facilities nor hospitality.

MR. DINEGAR: State, local government and federal government buildings?

MR. LEVIN: And many private sector buildings.

MR. DINEGAR: In terms of the reasons --

JUDGE VITTONE: Excuse me a second. Your answer is you have worked on state, local government buildings?

MR. DINEGAR: Yes, I have.

JUDGE VITTONE: Okay.

MR. DINEGAR: The reasons for support of the OSHA proposal, and you list out five, with a number of bullet points, two come to mind in terms of avoiding cost, and I wanted to raise a distinction and also ask for some commentary on it.

MR. LEVIN: I'm sorry, where are you?

MR. DINEGAR: On page 3.

MR. LEVIN: Okay.

MR. DINEGAR: The OSHA proposal, your first bullet point, right above 1: The OSHA proposal makes good economic sense because it is likely to produce improvements in productivity in building operating efficiency that will far outweigh the costs of implementing the rule or the reasons for this, or as listed below.

Then you go to list the number regarding the costs associated with salaries and benefits, improving indoor air and the rest.

The distinction and the work that you've done with IFMA -- the International Facilities Management Association -- that represents typically corporate owned facilities, and then also government facilities, where all the employees in the building are employees of the person who own that building, or manage that building;

Whereas you've got the private sector, and you've got 30 different tenants in an office building, the owner owns the building, rents out the space, but the productivity, except for the janitorial and maintenance crew doesn't really matter to that person.

It matters in terms of economic health or the health and safety and productivity of the workers to the employer as well.

But the distinction would be in terms of the cost associated with this proposal as it stands now, $8 billion, you say, that would far outweigh the fact 10 times as much. We're saying here, for sake of argument, that there's a $15 billion cost savings in worker productivity improvements, the argument would have us believe that it's upwards of $80 billion in worker productivity improvements.

Do you have any statistics that bear that out in terms of how many times over worker productivity would be outweighed by the costs associated with improving indoor air quality?

MR. LEVIN: If I understand your question, I think you're using OSHA's figure for cost, and my comparison of the cost for the facility and the cost for the employees, that was the 10:1 or greater ratio, was the worker cost versus the facility cost.

I wasn't saying the productivity would be 10 times greater than the cost of the implementation. I think, in my oral testimony, I said that I believed that the three percent was a reasonable figure and that the cost savings or the economic benefits would far outweigh the costs, but I didn't say by a factor of 10, and I didn't apply my -- well, I didn't say by a factor of 10 in that regard.

MR. DINEGAR: On Point 3, you say that avoided costs of resolving problems related to poor indoor air are far greater than the costs of improving indoor air quality to reduce dramatically the number and severity of such problems. Problem resolution can involve building evacuation, either short- or long-term, and significant costs for investigating and remediating the causes of poor indoor air quality.

Are you familiar, besides the county courthouse in DePage County, with the number of buildings that have had to be either evacuated or short- or long-term evacuations?

MR. LEVIN: Yes, I am.

MR. DINEGAR: Can you give us a couple of examples of different types of buildings that you're talking about?

MR. LEVIN: There is a -- I don't know how far to go in identifying the building, but let's say a very large office building in a major U.S. city, where an asbestos abatement took place, and the installations following the abatement resulted in some contaminant emissions.

One-fifth was evacuated, and they were about to evacuate two more floors when the cause of the problem was discovered and the source removed.

MR. DINEGAR: And it was asbestos related?

MR. LEVIN: No, no, no. This is after the asbestos abatement, a problem related to new materials installed.

MR. DINEGAR: Okay.

MR. LEVIN: Another example is a low rise but fairly large office building in the San Francisco Bay area, where there were a number of individuals reporting severe health problems, and the initial investigations were unable to identify the cause or the source of the contaminants, and the building was evacuated until the problem could be identified and remediated.

MR. DINEGAR: How long did that evacuation last, approximately?

MR. LEVIN: My recollection, and it's about 7 years ago, is that it was for a week.

Another instance was a school in the
San Francisco Bay area, where following a roofing project, the staff and the students became ill, and it was evacuated, presumably remediated. They went back in, they became ill again; it was evacuated again. Each of those evacuations was at least a week, possibly two, and actually the parents went to court to try to get an order to close the school.

MR. DINEGAR: The office building in
San Francisco, was that a private building, was it a government building?

MR. LEVIN: That was a private building.

MR. DINEGAR: Do you have any examples for different buildings that have been evacuated in the past, let's say, three to five years?

MR. LEVIN: I don't try to track these things, and so I think probably reports in the press and other sources might be able to better answer your question.

MR. DINEGAR: You also state that, on Point 5, conversely, small incremental increases in energy costs for building ventilation can dramatically reduce contaminant concentrations, including to, but not limited to, infectious microorganisms, volatile organic chemicals and particulate matter that caused occupant illness and disease, resulting in less absenteeism and improved performance at work.

Are you aware that the OSHA proposal, at this point, does not address ventilation in terms of any increases in the ventilation rate, except for operating your system as designed?

MR. LEVIN: In my mind, that would result in an increase in ventilation in those buildings which most need it, and that's where I feel this rule is exactly on target; that, at the low end, the concentrations rise so rapidly, that any building that isn't meeting at least the design standard, is likely containing concentrations that are significantly elevated over what they would be were it meeting the design standards.

MR. DINEGAR: Why, then, if the amounts increased, or ventilation in the costs assumed for increasing that ventilation would be far outweighed by the increase in productivity and the less cause of occupant illness and disease, resulting in less absenteeism and improved performance at work, why would you argue that you would need regulations for that as opposed to what's offered within the marketplace?

There would appear to be plenty of incentive associated with it, in terms of making those changes, and you need an $8 billion government regulation to come up with that kind of change within an office building?

MR. LEVIN: Well, you have at least two different questions I'd like to address.

I would agree with you, it would appear that there would be a market incentive, but my experience doesn't bear that out. The experience of EPA now and the base study doesn't bear that out.

In favor of that argument, I have, in fact, consulted to high-end private sector, speculative building owners and operators, with providing rental space, and they believe that.

They have taken advantage of that market opportunity, and I've consulted to them and found their staffs to be extremely well-educated, well-trained, and knowledgeable and on top of the problem, so obviously there seemed a market advantage to pursuing adequate ventilation.

It's the buildings where the owners haven't had that enlightened view, and those are not limited to rental buildings. Those include private sector, owner-occupied buildings, as well as -- I hesitate to say it, but many government buildings, both at the federal and state and local level.

MR. DINEGAR: Just in terms of point of clarification on the EPA base study, I was aware of the information that was, in fact, discussed at a meeting in Milwaukee recently.

But I was under the impression that that was information that was not yet released to the company nor with this record. Do you know if that information is going to be provided to OSHA as part of this record for the hearing docket?

MR. LEVIN: I contacted Mr. Girman before including those slides and that content in my oral presentation. It was not part of my written submittal since it occurred since the day.

He told me that they are currently analyzing the data from those studies and hoped to make a presentation of it as soon as possible. He didn't discuss whether or not they planned to submit it to these proceedings.

MR. DINEGAR: Okay. I have one more question, Your Honor.

JUDGE VITTONE: Yes.

MR. DINEGAR: On Point 6, page 4, I'd like to just read a paragraph, if I could:

"In my experience, investigating problems in dozens of office buildings and schools, primarily in California, I have found spaces used for purposes for which they were not intended, and for which the ventilation system was inadequate or totally inappropriate.

"Examples of classrooms were art activities, such as ceramic studios are located that generate particulate matter that clogs the ventilation system in that space and often in other spaces. I've seen photographic darkrooms set up without proper ventilation. I have seen clogged filters virtually preventing the entry of outdoor air. I have seen outdoor dampers closed completely, thus leaving the system to rely on leakage alone for outside air supply.

"I have seen operating schedules that were simply inefficient to remove the contaminants that were released from the new building materials and furnishings, or from chemicals emitted from janitorial activities.

"I have seen positively pressurized bathrooms where odors emitted from the bathrooms could be detected through a wide area on the same floor. I have seen painting, carpeting, and other floor installation and a host of other construction or renovation activities taking place immediately around the building occupants without any special ventilation provided.

"These are just a few of the many examples of poor design, maintenance, operation, or combinations of these that I have personally witnessed."

The last sentence I would like to reiterate.

"These are just a few of the many examples of poor design maintenance operation or combination of these that I have personally witnessed."

OSHA's proposal, as it stands now, goes to manage the problem of indoor air quality; ventilation, for the operation as designed, record keeping, tenant logs, and a number of other steps to check the equipment but not, beyond that, a whole lot of guidance, if any, on how to operate the system, except to point that it should be operated as originally designed, which may or may not be good.

It's been our argument all our along, and it continues to be our argument, and I would be interested in your concerns and views on that, as you talk about simply inefficient to remove the contaminants that were released from the new building materials and furnishings or from chemicals emitted from janitorial activities, wouldn't it be far more effective to remove the contaminants at the source, whether it's by paints and chemicals, solvents, the new furnishings, so that if the chemicals that are causing indoor air quality problems or removed from those different furnishings, from those paints, from those building materials and from those solvents, wouldn't we, in effect, solve the majority of the indoor air quality-related problems addressed under OSHA's proposal?

MR. LEVIN: I was ready to say yes, until the last phrase. We won't necessarily solve the majority of problems addressed under the proposal. There are many problems from operation, where source control isn't an alternative or isn't as viable an alternative with present technology, although I look forward to the day when that will be the case.

But, in general, as I think you know, I strongly support emphasis on source control as the first order for maintaining good indoor air quality. My recommendations with respect to ventilation are that it be applied as necessary after source control has been implemented.

I believe that the OSHA rule will instigate attention to sources that may not otherwise be present, and will, in effect, in many cases, result in source control rather than ventilation as an effective way to remediate.

MR. DINEGAR: Do you see the provisions regarding the tobacco smoke issue as one of the areas that they've addressed source control?

MR. LEVIN: That's certainly one example, yes.

MR. DINEGAR: Thank you, Mr. Levin.

Thank you.

JUDGE VITTONE: Thank you, sir.

The gentleman from AFL-CIO.

MR. TINGLE: Good morning. My name is
Rex Tingle of the AFL-CIO. Today, I will also be representing the UAW and AFSCME.

Mr. Levin, I would like to start off with the question: From your experience, is the inclusion of Sick Buildings syndrome signs or symptoms warranted as a trigger in the implementation of any good IAQ program?

MR. LEVIN: Yes. If you look at my written statement, you'll see that I have included a recommendation that SBS be included in the proposed rule, for precisely the reason implied in your question.

MR. TINGLE: So, basically, can you answer this question for me, even though it's redundant?

Should OSHA include Sick Buildings syndrome signs or symptoms into their final standard?

MR. LEVIN: Yes, they should.

MR. TINGLE: Okay. The second question I have for you: From your experience, what percentage of buildings affected by this proposed standard are covered by city or state building codes which affect the HVAC system?

MR. LEVIN: I would have to do some research to respond to that. I know there are still jurisdictions where codes are not enforced, but the majority of the states had adopted codes, and so I could only, at this time, say the majority.

MR. TINGLE: All right. Also, could you elaborate on how these codes mirror or require more regulations in the proposed standard?

MR. LEVIN: How the building codes --

MR. TINGLE: Correct.

MR. LEVIN: -- require more regulation than the people?

MR. TINGLE: Or mirror what's required by this proposed standard?

MR. LEVIN: The codes apply to the application for a permit, the planned check and approval and inspection of the construction. In most cases, they don't regulate the operation and use of the building.

In California, until the adoption of the Cal-OSHA rule on ventilation, there was no legal rkim that ventilation systems be operated, and the only protection workers had was under general health and safety kinds of provisions, but those agencies regulating ambient air quality were hesitant; in most cases, did not deal with indoor air problems under those general provisions, and it would only be in regard to a contaminant regulated by EPA, such as asbestos, that regulatory relief or remedy would be available, where regulations would apply.

MR. TINGLE: So, basically, building owners and managers can operate systems at this point, unchecked, excluding those local and state governments that require some type of building inspections?

MR. LEVIN: Right. And my understanding is that Massachusetts and New Jersey and perhaps Connecticut, maybe some other states, have such regulations, besides California, but that, in most jurisdictions, such regulations do not exist.

MR. TINGLE: So, in your opinion, this is a very important factor in developing an IAQ standard that does look at building system functions?

MR. LEVIN: It is extremely important.

MR. TINGLE: Okay. From your experience, what kind of problems have you found in the field, in general, with IAQ problems across the board? You can just be very, very general about that.

MR. LEVIN: The paragraph that Jim Dinegar read is a listing of the many types of problems that I've found.

MR. TINGLE: Okay.

MR. LEVIN: I would add to that that, even in buildings where considerable attention is spent to operate the buildings properly, I have had experience that a computer printout will say that the system is on when, in fact, it's not, but the computer has given or sent a signal for the system to turn on and records, therefore, that the system is on.

This is from a study I was conducting in a state office building where this occurred.

I was monitoring the electrical flow to various parts of the building, including the fans and the ventilation system, and there was no flow. In spite of that, the computer printout said the system was on.

Since that time, I've become more aware of the commonness of this occurrence, and I think the EPA base study is supporting that nation.

MR. TINGLE: So another important factor of why we should have a standard in looking at building system functions?

MR. LEVIN: Yes.

MR. TYSON: On page 18, Table 5 are your cost estimates of implementation of the IAQ Rule.

Are the costs which you estimate designed for buildings starting with no operation and maintenance program or for buildings that have some type of operation and maintenance program?

MR. LEVIN: I'm assuming that there is some program in place. A building, like a car, will not run forever without attention to its operation and maintenance.

I should indicate here that these are simply estimates. I'm not aware of any hard data to support these numbers. I was attempting, from my experience, to place some values on these costs.

MR. TINGLE: The last question I have for you: On pages 3, 19, 20, and 21, you talked extensively about increased worker productivity and increased building efficiency by improving indoor air quality.

From your countless years of experience as an expert in the field, do you think that OSHA's proposed standard is feasible?

MR. LEVIN: Certainly.

MR. TINGLE: Thank you.

JUDGE VITTONE: Thank you, sir.

Mr. Rupp.

MR. RUPP: Thank you, Your Honor.

Mr. Levin, good morning. My name is John Rupp. I'm with Covington & Burling, and I will be asking you a few questions this morning on behalf of a number of scientists and others who have submitted comments to the docket of this proceeding, on behalf of the Tobacco Institute.

I notice in your printed statement that you state that, and I quote: "IAQ improvements are cost-effective in that the results would avoid the cost
attrib -- excuse me. Let me re-read that. I can read.

JUDGE VITTONE: What page, Mr. Rupp?

MR. RUPP: This is on page --

JUDGE VITTONE: The numbers are in the bottom right corner.

MR. RUPP: Mr. Levin, the quote that I want to read to you is from page three, and it is as follows:

"Improving IAQ is cost-effective in that it results in avoiding the costs attributable to poor IAQ."

I'm not having any problem with that proposition as a general proposition, but I'm wondering whether the value of the proposition is -- the devil is in the details, that this is not a proposition; in an application, one has to exercise some judgment and common sense, and I'd like to pursue with you, if I may, a couple of hypothetical examples and try to elicit your reaction.

We know, for example, that human beings are sources of pollution because of body odors, respiration, which results in CO2 being emitted.

One measure to improve IAQ indoors, I take it, would be to issue a rule that required all people to work outside, no people to work inside, but that would be quite ridiculous, would it not?

MR. LEVIN: Yes.

MR. RUPP: I take it you would also agree that if OSHA issued a rule that said people should work outside at least two hours per day and that that would result in IAQ problems, they would be correct about the possible reduction in IAQ problems, but it would also be fairly imprudent and not very feasible?

MR. LEVIN: I believe that's correct. I'm not sure I follow the question.

MR. RUPP: Let me shorten the time somewhat.

What if we were talking about a rule here that required a substantial number of people to leave the building for a half an hour a day or 45 hours a day as a measure to improve IAQ? I take it you would agree with me that that might improve IAQ because it would reduce the number of people in the building over the course of a day, but that there would be a number of costs and other trade-offs that one would have to take into account in determining whether that was a reasonable and appropriate measure?

MR. LEVIN: I need to go back to some of the premises here, first of all. You may have misspoke when you said either a half hour a day or 45 hours a day.

MR. RUPP: Excuse me. 45 minutes a day. I appreciate the correction. Choose any time you want, really.

MR. LEVIN: I was trained as an architect, and you said the devil is in the details. Architects like to believe that God is in the details.

[Laughter]

MR. RUPP: Ahh, but God is everywhere, as we know, so that goes without saying.

MR. LEVIN: With respect to your question, I'm not sure whether this is responsive, but I think it addresses some of the assumptions that you're making or attributing to me, perhaps, and that is, while people are sources of contaminants, I don't regard people as the primary source of contaminants, and I don't personally view the approach that ASHRAE has taken in the past, which is to require outside air ventilation solely on the basis of a number of occupants in the space, as an adequate approach to controlling indoor air quality.

MR. RUPP: Yes. That may be so. I think I'm asking a slightly different question, and I'm not really implying anything by it or attributing anything to you by the questions that I'm asking.

The premises of the questions -- the line of questions -- that I'm pursuing with you now are really quite simple.

One is that the people are a source of pollution, if we simply focus on human respiration. If our only goal -- our only goal -- is to reduce pollution levels indoor, to improve IAQ, if you will, any measure that reduced the number of people in buildings, other things being equal, would be a plus.

MR. LEVIN: I still find that there's a built-in assumption that people as a source are so important and there's something somewhat, if you'll permit me with all due respects, absurd about the question.

If the purpose is to improve people's productivity while they work in the building, removing them from the building doesn't really address the concern here.

MR. RUPP: It doesn't make much sense. So that measures that required people to leave a building, in order to improve the air quality of the building, which is for their benefit, is something that has a built in conflict, a built in nonsensical quality, if you will. Would you agree with that?

MR. LEVIN: Well, I think I know where you're going.

MR. RUPP: Well, answer the question, then, and then we'll see where we're going.

MR. LEVIN: With respect to the contaminants emitted by people, to the extent that the concern with respect to indoor air quality is to control those contaminants, the density of occupants in a building is a critical issue, and especially the relationship of that density to the ventilation available to dilute the contaminants they emit.

MR. RUPP: Okay. Fair enough, and I have no problem with that, certainly.

When we are talking about improvements in IAQ, the impact of the measures taken to improve IAQ on worker productivity are important, are they not?

MR. LEVIN: I think that's why we're here.

MR. RUPP: Okay. I would have thought so as well.

Let me try another example, and I think you'll find this perhaps equally as ridiculous, but I think it conveys a point that I think is valuable, and let's see if it is valuable.

Another way to improve IAQ would be to require that all carpets and drapes, perhaps wallboard, desks, and furnishings, be removed from buildings and they be replaced by low-emitting or no-emitting tiles, and metal desks, that would improve IAQ, other things being equal, would it not?

MR. LEVIN: I believe so.

MR. RUPP: But that, would you agree, is another circumstance in which one has to take into account the larger series of tradeoffs that are involved in a measure of that sort? That is, that is a measure that has potentially quite large consequences, and one needs to consider those in a careful and prudent manner?

MR. LEVIN: Absolutely.

MR. RUPP: On page 4 of your statement, you refer to, and I quote, the material harm, and that's the phrase I'm quoting.

"It may be done to building occupants if poor quality outside air is brought into buildings."

Do you see the quotation to which I'm referring on page 4? I think it's about in the middle of the page. In fact, it's No. 4 on page 4 -- point 4 on page 4.

MR. LEVIN: Yes.

MR. RUPP: Among the items you refer to there as a cause of possible concern is, quote, "Entrainment of cigarette smoke from individuals who have gone outside to smoke."

Do you know of any study that has sought to determine what effects smoking outdoors has, whether at the entrance to buildings or elsewhere, might have on indoor air constituent levels? Is there such a study?

MR. LEVIN: I know of no published study. The reason I included this was I training some professionals to deal with indoor air quality in buildings and the building that was being used as the model to walk through and look at was a hospital in a major U.S. city, which did not permit smoking indoors, and placed a bench right outside the air intakes at ground level, where the smokers congregated.

So that, in effect, the cigarette smoke was being drawn directly into the building, but there's been not study, to my knowledge, of the impact of that on air quality.

MR. RUPP: But it certainly is true that when one travels around cities where there have been restrictions on smoking, one does see lots of people near the entrance of buildings smoking. Would you agree?

MR. LEVIN: That's correct. It is important when such restrictions are adopted, that provisions be made for the locations for the smoking.

MR. RUPP: Do you know of any health effects studies that have looked at the issue of whether smoke from outside -- cigarette smoke from outside -- that may be entrained in a system because people are smoking in proximity to the building -- has any health effects?

MR. LEVIN: No.

MR. RUPP: Or has any culpable irritation?

MR. LEVIN: I know of no study of smoke entrained from outside.

MR. RUPP: Okay.

Were you involved in the study of the Environmental Protection Agency's headquarter buildings at Waterside Mall?

MR. LEVIN: I want to answer accurately. I have been retained by the EPA's Division of Administration to do some consulting in the past and, as part of one of the projects I worked on, I was asked to look at some spaces in the headquarters building. I was not involved in the formal published study of Waterside Mall.

MR. RUPP: You mentioned that study in your statement, and I would be interested in knowing some more of the details of what went wrong in that building.

I take it, what we had there was a building in which there were persistent complaints over a long period of time, yet it was a building in which smoking had been prohibited for a great long time. What were the problems that were documented in that building?

To the extent they were documented, do we know what went wrong in that building?

MR. LEVIN: As I said, I was not involved in the study itself, and the work I did do was very limited in scope, so the only answers I can give are my visits to the building; my discussions with people who conducted the studies, my discussions with the Division of Administration staff, and a national public radio program, which I think referenced in my submitted text.

The problems ranged from what are characterized as typical symptoms of Sick Buildings syndrome to exacerbation of asthma, and some people believe the onset of hypersensitivity to chemicals or multiple chemical sensitivity.

MR. RUPP: Were there some people in that building reporting respiratory distress at one degree or another?

MR. LEVIN: Asthma was, of course, one.

MR. RUPP: Any other types of respiratory distress? Wheezing, coughing?

MR. LEVIN: I could look into the studies, but I'm not an authority on what was going on in that study.

MR. RUPP: All right. Let me leave the issue of symptoms that were reported and ask you what you know, if you do know, about any conclusions that may have been reached concerning the causes of the symptoms that were reported.

MR. LEVIN: My reading of the studies and my discussion with individuals involved in them, suggest that the studies themselves were not able to relate environmental measurements to reported symptoms. However, the questionnaire studies did identify some risk factors, including dust, or perceived dustiness, of an area.

Recent -- I believe either recent installation of carpet or simply the presence of carpet.

I'm sorry. I'm going from memory. Again, I could refer to the studies.

Apart from that, I did hear from many people among those I identified a couple minutes ago, that there was such a large number of ventilation systems in the building that many of them were undocumented;

That they were discovered in the course of the investigating the building;

That little was known about them until the investigation. Some existed that were simply unknown to many people involved.

That it was very difficult to get a handle on the ventilation systems design, layout, operation, and so on.

There were dirty ducts liners found and removed in some systems.

JUDGE VITTONE: I think -- do you have a question?

MR. RUPP: No. The explanation that Mr. Levin has given me is quite satisfactory. I appreciate that.

Let me move to one final issue, if I may.

MR. LEVIN: If I may --

MR. RUPP: Yes.

MR. LEVIN: -- I wanted to observe that the lack of correlation between ventilation of the environmental measurements and the symptoms found in the studies, for me, may have been a result of the supply of far more outside air during the study measurement week than is normally found at that building.

The temperatures began at about 29 degrees at the beginning of the week, and I think reached about 45, and that suggests that free cooling, as I discussed in my oral comments here today and is in my submitted comments, could have been used, and some of the measurements indicate that, in fact, considerable ventilation was present, and occupants of the building reported that they noticed a significant difference in the ventilation during that week.

MR. RUPP: Thank you. Let me move to a final issue. That is, the question of productivity and what kind of gains or losses in productivity one might anticipate in the event of various kinds of requirements that might be imposed.

Let me begin by asking whether you, personally, have undertaken any survey or study attempting to document improvements or decrements in productivity that might flow from various alternative measurements designed to improve indoor air quality?

MR. LEVIN: My studies have been of the paper sort that I went through in my oral presentation, and that is contained in my submitted testimony, which is based on the numbers one can reasonably develop related to.

In terms of actually measuring the productivity itself, the basis for my estimates are experiential and anecdotal in nature.

MR. RUPP: To reach any kind of firm conclusions, I take it, on an issue of that sort would require a quite careful, probably quite complicated sort of study?

MR. LEVIN: Well, as I indicated in one slide I showed, there are indirect measures of productivity such as absenteeism, that can be used, so that, at the most simple level, either being present or absent at work, as a result of illness, is a fairly clear indicator.

One can become involved in very complicated and sophisticated studies as well. Productivity in office environments is difficult to get a handle on.

I was involved in a retail establishment where sales records are used to indicate productivity, and where environmental features were credited with a significant difference in productivity as measured by sales, compared to a baseline of one of the major, if not the major, U.S. retailer.

MR. RUPP: One would expect productivity to vary along a whole range of factors, I take it, including the baseline situation, the type of establishment, the number of employees, climactic conditions.

One could probably list another 10 or 15, but all of those kind of things would be factors in any such evaluation, would they not?

MR. LEVIN: Certainly.

MR. RUPP: I understand that you're not a medical doctor or scientist, or a health scientist. Let me ask you if you have any view, nonetheless.

If one were to force a significant number of employees outside, regardless of climactic conditions -- rain, snow, sleet, hail, you name it -- for a significant portion of the day, in addition to productivity losses that we have discussed, would one reasonably expect, even as a layman, to see some additional losses attributable to such things as additional sickness, flu, colds, that sort of thing?

MR. LEVIN: Well, as you said, I'm not a health scientist, and I can't say whether or not exposure to those climactic conditions would increase the illness rate. Certainly, as I assume concern the 100 questions would have, with regard to forcing people outside in order to smoke, whatever other risk factors might be present, it's my understanding that smoking would enhance or exacerbate those risk factors.

MR. RUPP: Colds?

MR. LEVIN: I say risk factors being the conditions that you made up as adverse conditions.

MR. RUPP: Yes. Thank you very much.

JUDGE VITTONE: Are you finished, Mr. Rupp?

MR. RUPP: I have no further questions, Your Honor.

JUDGE VITTONE: Thank you. Any redirect?

Ms. Sherman?

MS. SHERMAN: I believe the gentleman from BOMA has his hand up, sir.

MR. DINEGAR: I wanted to find out if we could readdress the witness, two additional questions.

JUDGE VITTONE: Two additional questions? Okay. Two additional questions.

MR. DINEGAR: Jim Dinegar again, with Building Owners and Managers Association.

Mr. Levin, I was calling to mind before a couple of different statements that you had raised and I heard the follow up for, and would like to follow up a couple of questions that you have since been asked. This is simply regarding going outside, whether it's to do a variety of activities or to undertake smoking.

I'm glad to hear that you don't think we should allow everybody to work outside a number of hours. Plenty of people like to work outside and it's a great place, but our vacancy rates are pretty high, so it makes it difficult.

When you start to talk about smoking, for instance, and going outside, is it better, in your mind, to allow the involuntary inhalation of secondhand smoke of Group A carcinogens classified by the EPA, or should those people who choose to smoke be sent outside where the air is able to dilute and not cause as much of a significant health risk as has been described by the Environmental Protection Agency?

MR. LEVIN: I can only answer not as a scientist who understands the risks but as a person who consults to building owners and to architects and engineers, that my recommendations are to protect nonsmokers from smoke by the most clear and simple means of source control, which is to not recirculate air from smoking permitted areas.

If there are no designated smoking areas with direct exhaust to the outside, then I recommend that smoking take place outside the building.

MR. DINEGAR: In the different surveys that you've undertaken of builds across the country, whether educational facilities or office buildings, or any other facilities that you work on, is it your experience in the number of complaints that have been received, that some of those complaints, many of those complaints, relate to exposure to secondhand tobacco smoke as one source of contaminants?

MR. LEVIN: When I first got involved in indoor air quality, since there weren't many people in the field, a lot of my work did concern investigations. I heard from occupants and owners and operators of buildings much more. Now, when I receive calls, I refer them to people who specialize in investigations, so I have less contact.

In that same time frame, the rate of smoking has declined. Mind you, I live in California where the per capita cigarette consumption annually is half the national average, so I tend to not hear very much about complaints in general and, specifically, tobacco smoke or any other source anymore.

When I was receiving calls more frequently, cigarette smoke was frequently named as one, if not the, contaminant of concern.

MR. DINEGAR: Thank you very much.

Thank you, Your Honor.

JUDGE VITTONE: All right. Thank you, sir.

Ms. Sherman.

MS. SHERMAN: Yes. I believe Mr. Hathon has a question.

MR. HATHON: I don't have any questions.

JUDGE VITTONE: Ms. Sherman.

MS. SHERMAN: I don't have any questions either.

JUDGE VITTONE: Thank you, Mr. Levin.

MR. LEVIN: Thank you.

JUDGE VITTONE: Who's your next witness?

MS. SHERMAN: Mr. Lstiburek.

JUDGE VITTONE: Okay. Would he come forward, please? Would you come up here, sir?

We're going to take a few minutes to get you re-fixed here.

[Off the record.]

JUDGE VITTONE: Back on the record.

JOSEPH W. LSTIBUREK

JUDGE VITTONE: Sir, would you identify your name and your affiliation, for the record, please?

MR. LSTIBUREK: My name is Joseph Lstiburek. I'm with Building Science Corporation, a Boston-based architectural and engineering firm.

JUDGE VITTONE: Okay. Are you prepared to go forward with your testimony?

MR. LSTIBUREK: Yes, I am.

JUDGE VITTONE: You've already submitted your written testimony; is that right, sir?

MR. LSTIBUREK: Yes, sir, I have.

JUDGE VITTONE: You're going to be using the slide machine, so I'm going to get out of your way. You may begin.

MR. LSTIBUREK: Thank you.

I'd like to start with a little bit of my background. I'm a building scientist. I specialize in investigating building-related problems. My discipline is in forensic engineering. I specifically look at the interrelationship of building envelopes and mechanical systems.

I'm a professional engineer. My educational background is an undergraduate degree in mechanical engineering, a Master's Degree in Civil, and I hope to receive very shortly a Doctorate in Civil Engineering.

I first became involved in 1982 in the investigation of indoor air quality-related issues when I was involved in numerous coroner's inquests and to a rash of deaths from carbon monoxide poisoning during several heating seasonings.

I've been actively involved indoor air quality and indoor environmental issues since then. I've conducted several hundred investigations over the years, problems that have run the full gamut of annoyance to disease to sickness and, in some cases, to death.

I'm also a member of the Board of Directors to the Energy Efficient Building Association. A fair amount of time and effort has been involved in promoting energy conservation in the nation's building stock.

I'm a member of ASHRAE and ASTM, specifically E6, performance of buildings.

I'm perhaps best known for my work on microbial contamination in southern buildings.

I've written numerous technical papers over the years. I have several books that are in print. I'm here in support of the OSHA Proposed Rules.

I'd like to start off with I guess perhaps an obvious statement: Nobody wants bad air. Occupants want a safe work place, and owners and managers certainly recognize that it's bad for business to annoy their tenants or clients. It's bad for business to make them sick, and it's certainly bad for business if they die on them.

The problem that we follow from that premise is a very simple one. It's based on the concentration of stuff or pollutants in the air. Concentration of pollutants is a well understand relationship.

MS. SHERMAN: Mr. Lstiburek, would you please identify your slides as you go through them.

[Slide Presentation.]

MR. LSTIBUREK: This slide is identified Indoor Environment. Pollutant concentrations are based on source strength, compared to the rate of removal or dilution. If the rate of entry generation and off-gassing increases the rate, or is greater than the rate of removal, then concentrations go up, and we get ourselves typically into difficulty.

If the rate of removal is greater than the rate of entry generation and off-gassing, then concentrations fall, and we don't generally have a problem.

The whole concept of controlling the indoor environment appears to be a very straightforward one, one of matching source strength to the rate of removal.

The difficulty is is that if we look at the dilution side of things, dilution typically involves air change.

If I throw up another overhead, if I can find it, we look at this map of the United States. For those of you who don't recognize it, it's pretty hot and miserable down here all of the time, and it's pretty cold and miserable up here most of the time, and in the middle of the country, it's cold and miserable half of the time and hot and miserable the other half of the time.

What that implies is that the greater the air change in North American or American buildings, the greater the amount of energy that has to be expanded into conditioning that air. Wherever we are in this country, we have to spend money on either heating that air or cooling that air, or humidifying that air, or dehumidifying that air. So the greater the rate of air change, typically, the greater the operating costs, the greater the size of the capital equipment.

The tendency is to not to want to increase the ventilation rates because of operating costs problems.

The other part of the problem is that as we increase, or we look at the effect of dilution rates or air change on source strengths, we know that any powerful pollutant source completely overpowers your ability to ventilate it or dilate it out of the building.

So not only is air change or ventilation an expensive proposition, it also doesn't work very well, so why are we promoting it? Well, the obvious answer is that we, therefore, must control source strength, right?

If we prevent any of the pollutants from coming into the building, we don't allow any to be generated inside, and nothing is given off, then we really don't need any ventilation whatsoever.

The problem is is one of the pollutants of major concern in the building are the people themselves. People can be considered as evaporatively cooled, unvented combustion appliances. Most people tend to burn a rather sophisticated form of propane.

When we generate products of combustion, carbon dioxide and moisture, we vent right into the space. Well, I think it's pretty impractical to apply source control to people. Otherwise, we won't have anybody able to work in our particular buildings, so we have this awful thing that we have to do as a nation here. We have to do something very un-American. We have to compromise, we have to use judgment. We have to understand that we can't apply source control to the nth degree, and plus we can't rely on dilution or ventilation in its entirety either.

We have to look at what is probably the best approach, which is source strength control, wherever practical and wherever possible, coupled with some form of dilution.

Now, when we talked about source strength, it's real important to understand or appreciate that source strength implies more than just preventing nasty pollutants from being outgas from particular building materials and furnishings.

I would like to put on a second overhead called Source Control Strategies. There are two specific or general source control strategies. One is called exclusion, and the second is called capture at source.

When we think of exclusion, most people think in terms of material selection and furnishings and the way that we choose our housekeeping strategy, and people don't really appreciate, typically, that exclusion involves air pressure control in the way the buildings and mechanical system is operating.

For example, if the mechanical system is extracting more air out of the building than is supplied to the building by the mechanical system, we create a negative pressure in the building. The building basically sucks from the exterior.

If we have pollutant sources on the exterior of the building, those pollutant sources will be drawn inwards. So air pressure control that can occur as a result of the operation of the mechanical system is a significant factor in providing source control for a building. I don't believe that it's possible to provide source control without having a functioning mechanical system. Hopefully, one that functions according to the original design intent.

In terms of capture at source, some of the most effective strategies for capture at source involve creating a zone of negative pressure and the location in the facility where something particularly nasty or unpleasant is happening.

Special use areas such as swimming pool or a xerox facility or a print shop or a delicatessen, or a lunch room or a bathroom or a smoking room, should be maintained or typically attempted to be maintained under a slight negative pressure.

The object of the game is that we're capturing those pollutant activities that are occurring in that spot as a result of this negative pressure field and extracting or expelling those pollutants to the exterior.

That is a method of source control, but yet that source control cannot occur without a fully functioning mechanical system.

In an ideal situation, the theoretically perfect approach to providing indoor environmental control for a typical building would be provide ventilation only for the pollutants generated by occupants and provide source control for everything else.

It's a very nice ideal. I think that a lot of us can agree to that, but it's very difficult to achieve.

We have to decide how much air an individual happens to need. We also have to understand that it's not practical to completely exclude all of the pollutant sources within a building, so we have to use this judgment and this compromise.

I'm very much in favor of ventilating buildings when occupants are present. The principal function of a building is to have people in it, and it's kind of difficult to justify not providing a healthful space for those occupants when they're present.

The rule requirement D-1 that states: Maintain and operate the HVAC system to assure that it operates up to original design specifications and continues to provide at least the minimum outdoor air ventilation rate, based on actual occupancy required by the building code, mechanical code, or ventilation code, at the time the facility was reconstructed, renovated, or remodelled, whichever is recent, I don't believe is an onerous requirement and constitutes my experience, a significant factor in providing for acceptable indoor air quality.

When this requirement is coupled with basic source control, in my experience, acceptable indoor air quality, typical results.

It's very important to recognize that if a building's mechanical system is not operating, random air change, leakage through openings within the building that have been accidentally left there as a result of the construction process are not capable of providing air change in a controlled manner.

So maintaining an acceptable indoor environment by relying on leaky buildings and the effect of temperature differences and the wind, is just inappropriate. It's incredibly energy-wasteful to do.

Providing controlled ventilation in an intelligent manner is actually the most energy-efficient and cost-effective way to provide an acceptable indoor environment.

A requirement that asks that the HVAC system is operating during work shifts, except during emergency HVAC repairs and during scheduled HVAC maintenance, I believe is a reasonable requirement and it's the only reliable way of providing for adequate dilution or air change,and therefore acceptable indoor air quality.

During non-work shift periods, such as weekends and late evenings, when minimal occupancy is occurring, and the HVAC system is not operating, the occupancy to volume ratio is typically small. I think this factor, coupled with uncontrolled random air change is typically sufficient to provide dilution.

I think we are all aware that there are going to be situations where the ventilation system can be turned down and shut down, and the guidelines that we can rely on making those decisions, I think you can look towards the new requirements for intermittent occupancy on ASHRAE Standard 62.

The requirement in the proposed standards, D-6, which states, "Monitor carbon dioxide levels when routine maintenance stuff is done, and when carbon dioxide levels exceed 800 parts per million, employer shall check to make sure the HVAC system is operating as it should. If not, the employer shall take the necessary step to create the deficiencies if they exist."

I don't believe there's an onerous requirement, and I believe it provides a very good Surrogate basis for assessing building ventilation during routine inspection and maintenance.

It's very important to note in this requirement that it's not a statutory requirement. It's not a requirement that says, Thou shalt maintain 800 parts per million.

I look at it as when I do a building investigation, one of the first things that I do is, I try to assess how much outside air is coming into the building. I routinely take a carbon dioxide reading.

I compare it with the exterior carbon dioxide measurement, and I ask myself, is it low, is it high. If it is particularly high, it's an indication that perhaps, maybe, something may be amiss with the building ventilation system, and it's one of those signs that I look at to try to take a closer look at the mechanical system.

Now, I'm less concerned about what the actual number is, just that it is used as an indication for me to ask additional questions. I recommend this to almost all of my builder clients and my manager-operating clients and say, look, you ought to routinely sample for carbon dioxide measurements just to give yourself an indication of how effectively your ventilation system is operating.

Remember, it's just a first Surrogate step to ask yourself whether we need to look any further.

The requirement in the Standard D-5, which states: Maintain relative humidity below 60 percent in buildings with mechanical cooling systems, I believe is a fundamental requirement in controlling unwanted and unhealthy biological activity on building envelope surfaces.

I also believe that such a requirement is also readily achievable within the existing capabilities of the current building community.

There has been a lot of debate over the past several years about what are the critical relative humidities that are required to sustain microbial growth in buildings.

The community is coming to a consensus agreement that the critical relative humidity for growth to occur on hygroscopic surfaces or surfaces which have an affinity to water, is approximately 70 percent. So if you allow the relative humidity at a surface to go above 70 percent, chances are there's an extremely good likelihood that you're going to have some form of microbial growth.

So the object of the game is to control the relative humidities at surfaces, such that they are below 70 percent.

My experience over the past 10 years has shown me that if we can maintain the relative humidity within the conditioned space no higher than 60 percent, that's a very, very good way of preventing the critical 70 percent from occurring at a particular surface.

It's very important to appreciate that the relative humidity that is measured in the middle of a space is different from the relative humidity that is measured on the surface.

So if we're trying to talk about specific requirements and regulations, we have to understand that the 70 is a threshold limit on the surface, but we will have to control the conditions in the middle of the building differently, to avoid that 70 percent on the surface.

In my experience, when we have found that the mechanical system in the building is unable to be maintained below 60 percent during air conditioning periods, I found that the problem has not been due to the capacity of the dehumidification capabilities of the air conditioning system. I found that the problem has been typically due to design issues with respect to the building envelope.

For instance, the inability to keep the rain out of the building. If you can't keep rain out of your building, you can't expect your mechanical system to be able to control the humidity in the building. If your roof is leaking, you can't expect your mechanical system to maintain that.

We found that there have been operational issues. When the building has been maintained at too low of a temperature and, as a result, the cool temperatures, overcooling of the space, in fact, serves to draw even more moisture from the exterior into the particular building.

We found problems with maintenance and serviceability, such as sprinkler systems that are wetting the exterior walls and that exterior water is being driven through the wall as a result of sunlight.

We found problems with improperly balanced air handling systems that maintain significant negative pressures in the building that serve to draw exterior humid air into the space and that exceed the ability of the air handling, air conditioning system, to dehumidify.

The irony in a lot of these cases is that when we've gone in and altered the pressure relationships, that it not only has resulted in a healthier indoor environment, but it's resulted in dramatic and significant savings to the operating cost of the facility.

In fact, in the residential arena, an example may be illustrative to what is likely to happen in the commercial area.

Several of the major southern utilities -- Florida Power and Light and others -- are offering incentive payments of 500 to 700 dollars a homeowner to correct and balance their homes or residence's mechanical system to prevent excessive negative pressures, resulting as a result of duct leakage.

These pressure relationships, after they've been altered, have saved so much energy, that it's estimated that several nuclear power plants of energy is not going to have to be built in the State of Florida. I believe that we have similar opportunities in commercial and institutional buildings in the south as well.

One of the important factors in the requirement to maintain relative humidity below 60 percent in buildings with mechanical cooling systems is to recognize that excursions from the 60 percent are typically going to happen.

Meaning that, when I said earlier that a critical 70 percent surface relative humidity leads to microbial growth and hygroscopic surfaces, this is very much a time-dependent requirement.

Meaning, I look at that as about a one-week average, so I'm not concerned during two or three days or on a weekend, the humidity in the building rises. I'm concerned when we have a persistent relative humidity of above 60 percent for one week or more.

For example, a very high relative humidity for a very short period of time is very different from a slightly elevated relative humidity for a longer period of time.

The 60 percent should be interpreted as persistent elevated levels, not for something that occurs within a day or two days, because there are always going to be times during the day, and hours or portions of the day, when that 60 percent will be exceeded.

The issue here is for how long, and my experience has been for one week or more that's enough to lead us to difficulties, and it warrants typical intervention or further investigation.

Most microbial problems -- in fact, I'm going to say all microbial problems -- are an issue of moisture control. If we can control moisture at surfaces, microbials will not occur.

Controlling moisture at surfaces is a combination of both the operation of the building's mechanical system as well as the construction and operation of the building envelope.

I believe that we have to look at both factors, and one of the most significant factors is relying on the mechanical system to maintain interior humidities at 60 percent during cooling periods.

What I would like to do now is I'd like to show or share with you several case studies.

This is Slide #1. The facility in question is a single-story building in Trenton, New Jersey, constructed over a crawl space foundation. There's significant evidence of moisture damaged materials and microbial growth is found within this particular building.

JUDGE VITTONE: Would you identify the slides by number?

MR. LSTIBUREK: Yes. Slide No. 2 illustrates microbial growth and deteriorated and wet moisture damaged materials within this particular building.

Slide No. 3 illustrates a return air drop ceiling that is connected to the interior wall. What is happening on this slide is that the drop ceiling is operating under a negative pressure because it's the return air portion of the air-handling system in the building.

Because that space is operating at a negative pressure, it's drawing air out of the walls, and the walls are connected -- with this overhead, which is identified, I believe, as Figure 13 in the handouts -- shows that air from the crawl space is being drawn up through that wall by the air handling system into the school.

As that air out of the crawl space, which is now saturated with moisture enters the wall, it is cooled, and as it is cooled, it deposits the moisture in the wall, leading to the deterioration of the materials and the microbial growth.

Slide No. 3 illustrates source control utilized as part of the remediation or remedial measure in this particular school. In terms of how the proposed regulation would have impacted this particular case study, the following rules would have impacted the remediation and diagnosis of a problem.

Proposed Rule C-5: The employer shall establish a written record of complaints and signs or symptoms that may be related to building-related illness, to include at least information on the nature of the illness reported, number of employees affected, the date of employee complaint, or remedial action, if any, is taken to correct the source of the problem -- would have had an impact in this case because it was several heating seasons and air conditioning seasons that went by before sufficient complaints had occurred to attract the attention of somebody to instigate remedial work.

It was far more difficult for us to investigate and deal with this problem without having a sound information base to work from. We could have saved a great deal of time had we known how long the problems have occurred and when they first started.

The second point: Section E-2, Item 1: The employer shall implement measures, such as the relocation of air intakes and other pathways of building entry where necessary to restrict the entry of outdoor air contaminants, such as vehicle exhaust fumes into the building.

This is a matter of controlling pathways, and I am interpreting this to say if we had had a proper ground cover in this particular building, we would have employed source control, and we've eliminated the pathway of pollutant entry into this particular building.

Finally, E-3, double item: The employer shall control microbial contamination in the building by promptly drying, replacing, or removing or the clean-up of wet materials.

What we did was we asked that these wet and damaged materials be removed after the ground cover had been in place.

These proposed rules, if implemented, would have avoided or mitigated the problem. For example, we talked about E-2 item, would have addressed the issue of entry of the primary pollutant, which is moisture from the crawl space and would have also resulted in the rehabilitation approach actually implemented, which is the ground cover.

Applying E-3, double item, would have resulted in the removal of the damaged materials and the cleaning that was also implemented. Since the proposed rules would have resulted in the same recommended rehabilitation measures, and since these rehabilitation measures were successful, the proposed rules would have successfully addressed this particular problem or complaint.

Look at Slide No. 4. This is a facility constructed in 1973.

Slide No. 5 illustrates a dumpster, loading dock, automobiles, parked under an overhanging portion of the building. There's also a sewer grate and a steam grate located in close proximity to this overhanging portion of the building.

Slide No. 6 shows all of the building's fresh air intakes located directly over the sewer grate, the steam grate, the dumpster, the loading dock, the automobiles in the particular building.

Slide No. 7 is illustrating the release of a tracer, indicating that whatever is coming out of the sewer is eventually appearing in the return side of the system from the fresh air intake portion of the facility.

Slide No. 8 takes us to the roof, where the other half of the building's mechanical systems are located, and shows that the fresh air intakes are immediately in close proximity to the exhaust from the bathrooms, the exhaust from the toilet vents, and that the air handling system is located in the lowest part of the roof where we have ponding of water.

MS. SHERMAN: Would you label that slide, please?

MR. LSTIBUREK: That's slide No. 10.

I point out that the theory is that life evolved on this planet in warm ponds, and I believe we are breeding new life forms in this pond-like activity, and that the building's air intakes are located directly above this new life source.

In terms of the remediation methods and in terms how the proposed rules would have impacted this particular facility, during our investigation, since the very day the facility was opened in 1973, complaints and problems were issued, and it took almost 23 years to get around to dealing with the problem.

Section C-5, "employer shall establish a written record of employee complaints of signs or symptoms that may be related to building related illness to include at least information on the nature of the illness reported, the number of employees affected, the date of employee complaint, and remedial action, if any, taken to correct the source of the problem" would have assisted greatly in, number one, dealing with the problem in the first case, and two, assisting our initial investigation.

Section E-2, item the employer shall implement measures such as the relocation of air intakes and other pathways of building entry where necessary to restrict the entry of outdoor air contaminants such as the equal exhaust into the building, I believe would have addressed all of the issues in this particular example.

Slide number 11 shows a facility in the southern states recently constructed. Slide number 12 illustrates an air handling system built into the corner of the exterior portion of this wall, and slide number 12 is a slide that we can't see. Let me describe it for you.

(Laughter.)

What you are not looking at is a supply diffuser that has significant microbial contamination around it as a result of growth occurring in cellulose ceiling tiles. Slide number 14 illustrates the removal of these damaged ceiling tiles as part of the regular maintenance program in this particular building.

Slide number 15 illustrates pink blotches that are occurring on the vinyl wall covering that is located to the interior surfaces of this particular building. Slide number 16 shows what happens when the vinyl wall covering is removed.

The problem in this particular facility was that we had a mechanical system that was not operating according to the way that it was originally intended to operate or designed. It was extracting air from both the wall cavities and from the actual building facility itself to a much greater extent than was originally designed.

This led to a negative pressure within the building. The negative pressure resulted in hot, humid air being drawn into the building and the building cavities. As this hot, humid air was brought in, it was cooled as a result of the operation of the air conditioning system. The cooling led to the creation of elevated levels of relative humidity on the surface which led to the microbial growth and the pink blotches.

The recommended rehabilitation measures that were implemented were impacted by the proposed rules. D-1 which is maintain and operate the HVAC system to ensure that it operates up to the original design specifications would have greatly impacted this particular problem. In fact, the problem would not have occurred had the system been operating according to the original design intent.

Item E-2, item "the employer shall input measures such as the relocation of air intakes and other pathways of building entry where necessary to restrict the entry of outdoor air contaminants such as the equal exhaust in the building."

The moisture in the south as an exterior contaminant and had the mechanical system been balanced correctly, we would have eliminated that pathway of entry, and then "the employer shall control", E-3 double item, "the employer shall control microbial contamination in the building by promptly drying, replacing, removing or cleaning damp or wet materials" was obviously implemented after the mechanical system was brought into operating condition which was originally intended. That resulted in the removal of the damaged and moisture saturated materials.

What I'd like to do is I'd like to close as follows: Over the past 12 or 13 years, my involvement has been principally in dealing with problem buildings for the private sector. I occasionally get involved dealing with public buildings, but most of my work has been involved on the mitigation and investigation side in private buildings and I believe that the proposed OSHA rule is a good one.

I don't believe it's unreasonable to ask building owners and managers and operators to operated a ventilation system if they have one. My finding is that if they have one, they ought to operate it especially when there are people in the darn building, and it ought to operate according to the original design intent. It would be nice to know what the heck that original design intent is or was.

A lot of the time the owners themselves have no idea what they bought, what they have, and a requirement to provide at least minimal documentation as to what the system is and what it's supposed to do is going to be of enormous assistance to the owners and managers themselves in operating the facility and also in ensuring that down the road when problems do occur, we can very quickly get to the bottom of the concerns.

Thank you very much.

JUDGE VITTONE: Thank you, Mr. Lstiburek.

Mr. Lstiburek's testimony will be 24?

(The document referred to was marked for identification as Exhibit No. 24.)

MS. SHERMAN: I believe so, Your Honor.

JUDGE VITTONE: Plus slides.

You want to offer his slides as well?

MS. SHERMAN: Do you have your slides with you?

MR. LSTIBUREK: I have prints being made, and I will supply the prints within the week.

JUDGE VITTONE: Within a week?

MR. LSTIBUREK: Within a week. They will be numbered according to the numbers that you give me. I'm not sure, but I think we may have dropped a number there around 11 or 12.

MS. SHERMAN: Okay. Would you like to admit your written testimony to the record and the slides will be appended to that when they come in?

MR. LSTIBUREK: Yes.

MS. SHERMAN: So that will be Exhibit 24 I believe.

JUDGE VITTONE: They will be received into evidence as Exhibit 24.

(The document referred to, having been previously marked for identification as Exhibit No. 24 was received in evidence.)

JUDGE VITTONE: Let me ask for a sign of how many people intend to question Mr. Lstiburek? Would the people who intend to question him please stand?

(The question was complied with.)

I see three individuals: AFL-CIO.

Who are you, ma'am?

THE SPEAKER: (Inaudible answer.)

JUDGE VITTONE: Are any of you going to need these slides or any of these things for the questioning?

No, okay. We will remove it during the lunch break and then proceed with your examination. We will recess right now. It is approximately 12:30. Let's return at 1:30 and resume again. Thank you.

AFTERNOON SESSION
1:35 p.m.

JUDGE VITTONE: When we began this morning, I threw out a proposal for possible readjustment of the schedule of this hearing and let me just add a few comments at this time before I hear from everyone.

Let me make very clear that this is my proposal even though it prompted by a motion by one of the parties and joined in by several others. The proposal to adjust the schedule in the manner that I suggested really is mine, and I did this for several reasons.

Primarily based on what is over ten years of experience as an administrative law judge in presiding at cases involving an hour up to several months, and it's been my experience presiding at cases involving mergers, and international writ proceedings, and being a special master for a couple of Courts of Appeals and a special judge for the D.C. Circuit Court of Appeals, and operating under some very rigid and strict guidelines, it's my belief based on all of that experience that sometimes it's better for the record, it is often better for the record if there is some flexibility in the schedule.

I do not believe that if we continue for much longer of holding hearings until 7:00, 6:00 o'clock every night that it would be good for the development of this record. It may have an adverse impact on the quality of the record when you finally look at it.

Therefore, I thought without unduly extending the length of time it takes for this process, for this Rule which is admittedly probably the most controversial proposed Rule ever proposed by the Occupational Safety and Health Administration, that the addition of several weeks may do us more good in the long run than do any harm. That was why I proposed that those two weeks be rescheduled.

Somebody reminded me this morning that some of the rules for formaldehyde has taken 15 or so years. I'm not even sure if that's a final rule yet. Anyway, that is primarily the reason that I proposed the adjustment that I suggested and that particular schedule is not offered by anyone, but it is one that I thought about yesterday afternoon and yesterday evening and that's why I came to his point. Let me call on the parties.

Mr. Tyson.

MR. TYSON: Mr. Gordon.

JUDGE VITTONE: Okay. Mr. Gordon.

MR. GORDON: Yes, Your Honor.

As understand your proposal with certain clarifications, the week of October 3rd through 7th would be put off, and many of those witnesses would be scheduled in the week of December 5th through December 9th. Many of the week of November 7th through 10th, which is a short week, many of those witnesses would be scheduled the week of December 12th through December 16th although we might not need one of those days if that's not possible for you.

We will not go into the week of December 19th which is very difficult for OSHA. In addition, OSHA will have some flexibility in moving the witnesses around to meet the new schedule and will come up with this new schedule early next week.

To consolidate their testimony, the tobacco companies have agreed that the Philip Morris testimony scheduled for September 30, Number 51, and the Constangy and Brooks testimony scheduled for October 5th, Number 74, will be consolidated on December 7th and will be sufficiently short so that we would have another witness on that day at least.

Then the post-hearing comment period would start running on December 16th. That's within your discretion to set the exact number of dates of guidelines. Say 60 days for comments, 30 days for post-hearing briefs thereafter.

This leaves out the group of 510 people whose notice of intention to appear was filed by a marketing firm and who were otherwise scheduled for the week of December 5th and these people will be scheduled at some convenient time at the agreement of everybody in January.

In addition, we were hoping, Your Honor, that you could give us one day either in the week of October 3rd through 7th or November 7th through 10th or will be freeing up the Friday, September 30th so that we can bring back the two witnesses who we were not able to get in. We could talk about that afterwards what exact day.

This is the proposal as you have clarified it. The Department of Labor believes that its proposal is very crucial in order to protect the health of workers exposed to poor indoor air quality and nonsmokers to protect them from environmental tobacco smoke. It believes that the schedule that we were on was an appropriate schedule, and that if some of the representatives of the tobacco groups had not engaged in unduly lengthy cross examination, perhaps we wouldn't have had this problem.

But, nonetheless, Your Honor, there is some merit to the points which you have expressed at length and, therefore, your proposal as clarified, would be acceptable to the Department of Labor.

JUDGE VITTONE: Mr. Tyson.

MR. TYSON: Thank you, Your Honor.

I'm Pat Tyson representing Philip Morris. Let me first note for the record that the proposal that Your Honor has put forward is significantly less than what we asked for initially, but in the interest of cooperating as fully as possible with this process and with one clarification, we are prepared to agree to this.

The clarification I would seek is of the 510 notices that were filed as a group that, time permitting, if it's possible for some of those individuals and employers to be heard during the course of these scheduled hearing prior to the 16th of December, would that be permitted to occur?

JUDGE VITTONE: You have no objection?

MR. GORDON: I have no objection so long as we can find a time.

MS. SHERMAN: We have no objection, but we would like to know in advance.

MR. TYSON: Of course.

JUDGE VITTONE: Okay. As long as there is time, we might as well fill in the days as best as possible.

Anyone else wish to comment?

Sir?

MR. DINEGAR: I'm Jim Dinegar with the Building Owners and Managers.

I understand the reason for the changes in the schedule and certainly with the variety of witnesses we've got coming up, this could drag out for a long time. Our concern speaks to the specifics to the proposal including Friday, September 30th that Philip Morris organization's representatives would be moved to the later date in December and then the entire next week, Monday October 3rd through October 7th also incorporates RJ Reynolds, Constangy, Brooks & Smith, and I'm not sure if there are other tobacco company representatives included within that week.

Our concern would be that virtually all of the tobacco company representatives or the majority of the main proponents are moved to the end or very near the end in December. We would ask that either their representatives be included in the beginning to give us an opportunity and other interested parties an opportunity to spread out the interests and cross examine at different times rather than saving it all up until the end.

JUDGE VITTONE: I'm not sure I understand what you're saying, sir.

MR. DINEGAR: As I understand it the proposal right now, the proposal would be to move Philip Morris which is scheduled for September 30th and the entire next week which includes RJ Reynolds, Constangy, Brooks & Smith and I'm not sure if there are other interested tobacco parties involved within that week, towards the end if not at the very end of the hearing process.

JUDGE VITTONE: And?

MR. DINEGAR: And we would ask that they either be included in the beginning or that it's split or that perhaps Philip Morris remains where they are scheduled for Friday, September 30th.

MR. GORDON: We will not concentrate it too much to give people adequate time to prepare. We will be doing the schedule over the weekend and we'll take into account your concerns.

MR. DINEGAR: Well, with all due respect, I understood it to be that those groups were going to be moved toward the end of the schedule sometime in December of perhaps even January. If that's not the case, if we're talking about September or October, I'd be more than comfortable with that, but the indication is that it was going to moved to December or January.

MR. GORDON: It's true. It would be early December, but there will be time afterwards, and there will be time to prepare. Not January.

JUDGE VITTONE: December.

MR. DINEGAR: There is plenty of time to prepare. I'm requesting that they be moved towards the further part of the program as it's scheduled no.

MR. GORDON: Do you mean you want them moved up earlier than the 30th?

MR. DINEGAR: Yes, I would recommend that Philip Morris on the 30th of September stays where Philip Morris is scheduled to be on the 30th of September.

JUDGE VITTONE: Why?

MR. DINEGAR: In order to give us an opportunity to cross examine and other interested parties. There are no tobacco interests being represented up until the end of the program really December or January.

JUDGE VITTONE: I'm not sure I understand what difference it makes whether it's September 30th or December 7th or whatever the date was.

MR. DINEGAR: In terms of preparing the testimony; in terms of cross examining and evolving the body of knowledge in front of OSHA representatives. We would be concerned about the advantage given to the tobacco companies.

JUDGE VITTONE: The advantage of the tobacco companies; is that what you're saying?

MR. DINEGAR: The advantage.

JUDGE VITTONE: I'm not sure I see an advantage.

MR. DINEGAR: I guess it's more of a perceived advantage, but it would cause us discomfort because we are not in support of the tobacco provisions, but to have them spaced out the way they are, we were fine with. We had no objections at all. We'd have some concerns about putting them towards the end of the program, in essence, sitting back, listening to all of the witnesses right up until the get to the tobacco companies at the end.

JUDGE VITTONE: But their testimony or their positions are already stated on the record.

MR. DINEGAR: Yes, but not with the benefit of cross examining each of the witnesses as they come up before December of January when they have an opportunity to testify at the end of the entire process.

JUDGE VITTONE: Mr. Rupp, you wanted to respond?

MR. RUPP: I don't know whether this properly called a response or not. John Rupp.

Again, I don't know understand what the perceived advantage is either, but as far as I'm concerned for the scientists whom I've been representing thus far, we are more than happy to work with the OSHA staff and the General Counsel's office to try to spread them out if that's of any value to others in the proceeding and perhaps we could make and effort at that early next week if that's acceptable to everyone.

MR. GORDON: Yes, I would like to agree then on these days, and then we will work on the schedule to meet the concerns of the gentlemen from BOMA.

JUDGE VITTONE: Is that acceptable, sir?

MR. DINEGAR: Okay.

JUDGE VITTONE: Let me throw out something else as I looked at the schedule. If we need an extra day, October 17th, which is a Monday, if you need that to bring in somebody who may fall on the wayside here as we proceed along, it's a Monday. I am scheduled to be out-of-town that entire week, but I can be here on Monday and leave Monday night, and then I will be out-of-town for the rest of the week. October 17th is a day that you can use as a fill-in or something like that. Okay.

MR. GORDON: Thank you, Your Honor.

MR. TYSON: Could I be heard on the issue earlier?

JUDGE VITTONE: Sure.

MR. TYSON: I want to note for the record that BOMA requested the time in which they would be permitted to testify. They asked to be the first and that request was granted. I see no difference in acceding to their request and our own.

At the same time, I concur with Mr. Rudd. There doesn't seem to be any advantage in the timing of the cross examination. They're going to have an ample opportunity to do so. They will have the opportunity to review our testimony in great detail prior to that time. In fact, they'll have more.

We would like for the schedule to hold as indicated earlier. There are a number of conflicts that govern that and that's just background for our request.

JUDGE VITTONE: Generally, as I understand it, though you are in agreement with what Mr. Gordon stated with respect to the time?

MR. TYSON: Yes, sir, we are.

JUDGE VITTONE: And you all are going to get together and try to work out some kind of a schedule according to the adjustment?

MR. TYSON: Within that adjustment. A couple of days one way or the other perhaps.

MS. SHERMAN: We can do that at the beginning of the week.

MR. TYSON: Okay. Thank you.

JUDGE VITTONE: Yes, sir.

MR. DINEGAR: Jim Dinegar with BOMA.

Just a point of clarification. We did not request to testify first. We were the first to request to testify. It was not our intention to lead off the docket. We just wanted to get our request on the first floor as soon as we could.

JUDGE VITTONE: Sometimes it's an advantage to be first, and sometimes it's an advantage to be last I guess. It depends on the proceeding I guess, but in my mind you're all equal whether you come first or last.

MR. GORDON: Your Honor, you'll issue that order?

JUDGE VITTONE: Yes, I adopt it based upon clarification which you have requested and it has been agreed to by the representatives who originally asked for the adjustment. I assume this will not be the first time. We'll have to adjust the schedule over the next several months, but I hope we can keep it to a minimum, and I hope we can proceed as rapidly as possible.

Very good. Thank you very much. I appreciate your cooperation in this.

MR. GORDON: Thank you, Your Honor.

JUDGE VITTONE: We finished with Mr. Lstiburek's direct testimony, and three individuals that they would prefer to question him.

Does anybody have a preference?

AFL-CIO, would you like to go first, please?

MR. TINGLE: Good afternoon. My name is Rex Tingle. I'm representing the AFL-CIO. My docket number is 123.

MS. SHERMAN: Would you speak a little bit louder, please?

MR. TINGLE: How's that?

MS. SHERMAN: That's better.

MR. TINGLE: Good afternoon, and my first question I would like to ask you is in your experience in the field over several years, who generally has control over the HVAC systems in most of the buildings that you've done research at?

MR. LSTIBUREK: The owner of the building.

MR. TINGLE: Also looking back in your experience, is this individual, in your opinion, the best individual to correct an IAQ problem?

MR. LSTIBUREK: I believe that the owner is responsible, but the owner will probably by training or disposition may not have all of the information in that individual personally.

JUDGE VITTONE: Excuse me.

Mr. Lstiburek, could you pull that microphone closer?

MR. LSTIBUREK: I believe that the owner is responsible. The owner will probably designate suitable representatives or individuals to operate that facility or that building. Those individuals should have the knowledge and experience necessary to operate the building.

MR. TINGLE: Could you just elaborate for me a little bit on do you think the best individual, maybe I didn't clarify myself correctly, that has control over the HVAC system, would be the best person to correct that problem if they did have a designated individual in their capacity?

MR. LSTIBUREK: I'm lost. Could you repeat the question, please?

MR. TINGLE: Okay. Basically what I'm asking you is if an individual, an employee, or building owner has control over the HVAC system, would that individual be the proper individual or designated person according to the OSHA proposed standard be the best person to help resolve the IAQ problems?

MR. LSTIBUREK: Yes, I believe that somebody should be designated by the owner to be responsible for the operation of that facility and be responsible to make sure that it's operated appropriately.

MR. TINGLE: Do you feel that there is any level of training or education that this designated person that the owner or employer should have on his staff?

MR. LSTIBUREK: I believe that they should have knowledge sufficient to understand the operation of their particular building or facility and depending on the nature or the complexity of the building or facility that knowledge will vary.

MR. TINGLE: Okay. Thank you. Second question: There are some individuals who are opposed to the standard would have to believe that there is sufficient lack of data to develop an IAQ standard. From your experience, case studies or current information, is there sufficient data to support that poor indoor air quality poses a significant risk to workers' health?

MR. LSTIBUREK: I can only answer as from my area of expertise as a professional engineer. I'm not fully versed in health affects, but I have been involved in building-related problems that have had health affects, and my feeling is that appropriate standards would have avoided those particular health affects.

So my indirect answer, I guess, is yes I believe there is sufficient knowledge and information to be able to create a standard or requirement or regulation.

MR. TINGLE: Thank you. The third question I have for you: In your opinion and from general practices that you've observed in the field, does this proposed standard have the level of control criteria that allow the standard to meet its goal to provide improved indoor air quality?

MR. LSTIBUREK: I believe it's going to go in the right direction. I don't believe that just regulation by itself will ensure this. It will help significantly.

MR. TINGLE: Okay. Two more questions, please. From your experience, what percentage of IAQ problems are directly related to environmental tobacco smoke?

MR. LSTIBUREK: I don't believe I'm able to answer that question because I've only been involved in my career in one case over the last I guess 12 years that was directly related to environmental tobacco smoke, and the nature of my work is more microbial and other issues. So I see a lot of them. I can't tell you in general. I can only tell you specifically.

MR. TINGLE: So what you're basically saying is that a large percentage of environmental tobacco smoke complaints aren't there?

MR. LSTIBUREK: Yes, I don't normally get involved in environmental tobacco smoke complaints. I believe that there are a few. I've heard rumors that some people are upset about them, but I don't get involved in them.

MR. TINGLE: But the majority of the complaints are non-ETS related complaints that you're dealing with?

MR. LSTIBUREK: The majority of the complaints that I deal with are not ETS complaints.

MR. TINGLE: Do you feel that the percentage is large enough to warrant an OSHA standard for this?

MR. LSTIBUREK: Of what? A percentage of what?

MR. TINGLE: Do you feel that the percentage of non-ETS complaints or other microbial and other contaminants, is that high enough number of cases out there that would warrant OSHA to proceed with the standard?

MR. LSTIBUREK: Yes, maybe I'd like to clarify. If there were no environmental tobacco smoke in existence, I believe that this standard would still be necessary and would still be a good idea.

MR. TINGLE: Thank you very much.

JUDGE VITTONE: Thank you, sir.

Who would like to go next?

Would you state your name and the organization you're representing?

MS. SARRI: Sure.\par My name is Cathy Sarri. I'm with the Service Employees International Union, and we're docket number 172.

The Service Employees International Union represents over a million service workers who a number of which we've received complaints from on indoor air quality issues and a number of those complaints have to do with the ventilation system.

One group of workers that we represent are building service and maintenance workers, and they've had... I'd just like to give you a little context and then I want to talk about how the standard might protect their health.

They typically work after the normal work hours, yet they do have a regular scheduled work shift. That is, they tend to work after 6:00 o'clock for example. In many situations, the ventilation system is completely shut off and there is often no local exhaust ventilation. These janitors use very toxic chemicals, a number of which are carcinogenic with acute or chronic affects.

I'm happy that the standard proposes, I guess it's under paragraph D-4, to keep the system on or proposes that there be general or local exhaust ventilation during all regularly scheduled work shifts. I wonder if you could just explain or clarify how you think that applied to these building service workers; is that sufficient protection for them as they use chemicals on a daily basis?

MR. LSTIBUREK: If you're asking me whether I feel the building's ventilation system should be operating when they are cleaning the building, the answer is yes or at least the portion of the ventilation system should be operating in the portion of the building that they're active in.

Do I feel that they're sufficiently protected, I believe that the answer to our problems are both source control and dilution and the ventilation system offers some help on the dilution side, but I feel that more intelligent use or choice and selection of cleaning agents and cleaning products is also warranted.

MS. SARRI: When you say the ventilation system should be kept on, are you talking about the ventilation or are you talking specifically about local exhaust ventilation?

MR. LSTIBUREK: It's very difficult to be general. Each building has a particular characteristic. Some buildings can be ventilated on a floor-by-floor basis. Other buildings do not have that capability. It would depend on the individual building.

A plan should be adopted, and I make recommendations to my clients. I recommend that they deal with building maintenance housekeeping activities and coordinate that with the operation of ventilation systems. In some buildings, it's very straightforward. In other buildings, it becomes more complicated.

MS. SARRI: Is there some minimal level that it needs to be kept under or do you think that it should be kept fully operational even though it's somewhat less occupied; should it still be kept operational at the level it was previously early in the day?

MR. LSTIBUREK: I believe it should be in the portion of the building that cleaning activities are occurring, the system should be fully operational in that portion, but that doesn't mean that the whole facility needs to be operating.

MS. SARRI: Thank you. That's all I had to ask.

JUDGE VITTONE: Thank you very much.

BOMA?

MR. DINEGAR: I'm Jim Dinegar with Building Owners and Managers Association docket number 1.

Mr. Lstiburek, why do you get called into buildings to do investigations?

MR. LSTIBUREK: I get called in for a number of reasons. Sometimes there is a problem with the building envelope or the building fabric meaning we have a roof leak, we have a wall leak, we smell an odor or a mold problem, and I have to distinguish those type of complaints from an indoor air quality complaint meaning I have a problem with the building itself.

The second category of calls we get are I have a problem with a building. We have people complaining about bad air. We seem to have an air quality problem, and the third category of calls we get, we've been named in a law suit, and we would like you to offer an expert opinion as to what has occurred, and in that type of a situation, the problem is usually long over. It's a matter of looking at what has happened afterwards. Those are the three categories that my firm gets calls from.

MR. DINEGAR: Who typically calls you into those buildings?

MR. LSTIBUREK: In our particular experience, it's been almost always the building owner.

MR. DINEGAR: In response to complaints?

MR. LSTIBUREK: Yes.

MR. DINEGAR: How many complaints are typically filed with an office building and let's talk about office buildings for a minute. That's what I represent. How many does it take in an office building; how many complaints would it take usually to trigger an investigation that calls for a firm like yours?

MR. LSTIBUREK: That's a very, very difficult question to answer. I'll do my best. Sometimes it's taken only one and at other times complaints may have been persistent for years, and then suddenly for some reason somebody decides that okay, we need to go to somebody external.

It's very much also a function of the level of the quality of the management firm or the owner, the size of the building, and also the influence and importance of the particular tenant. Sometimes a tenant is very highly priced and valued, is a very substantial one and then sometimes even one call or even the suggestion of a call is enough to warrant a call to us.

So it varies all over the map. Usually it's one or two that I call fairly serious complaints before we get involved.

MR. DINEGAR: Do you, this is no reflection on your firm, do you always find the cause of the problem?

MR. LSTIBUREK: No, I hope that's no reflection.

MR. DINEGAR: I don't say that it is.

MR. LSTIBUREK: But we tend to solve the problem sometimes meaning it's possible to go into a facility and change something in a facility and get the ventilation system in operation, and the problem disappears, but we don't necessarily know exactly or specifically what that causal relationship happened to be.

So I say that we often don't know what the problem was. That's correct, but we have resolved the problem in that it's disappeared, but we don't often know why.

MR. DINEGAR: Are there times when you've changed ventilation systems and yet the problem persists, unidentified sources of the problem?

MR. LSTIBUREK: I personally have not ... I've been fortunate enough personally not to nor my firm, get involved in a situation like that, but I've heard that that does occur. There are situations where the problem has not been solved by the investigators involved.

MR. DINEGAR: Tenants are sometimes frustrated in getting immediate solutions to their complaints. What about this issue of indoor air quality would you say frustrates building owners and managers most?

MR. LSTIBUREK: Sometimes there is no readily identifiable cause, and it's very frustrating.

MR. DINEGAR: Readily identifiable?

MR. LSTIBUREK: Readily identifiable or easily or quickly identifiable cause for the complaints or the problem. I can be very frustrated for the building owner or manager to try to manage a building and try to deal with a complaint or problem and not have an immediate or quick answer within a day or couple of days. It's very frustrating at times, but sometimes the investigation may take several weeks.

MR. DINEGAR: What would help you both as an investigator and a member of that community as well as the building owners and managers in identifying the sources of contamination?

MR. LSTIBUREK: A number of things. My answer here is not intended by any means comprehensive or complete, but a few things would be very, very nice to know the original design intent of the building's mechanical system was. How is this building supposed to have been operating, and what was the original intent?

It would also be nice to know what is in the products in the building. I believe that the current information that manufacturers of building products and materials provide is woefully inadequate. The MSDS sheets are very much a joke.

MR. DINEGAR: By building products and materials, what are you referring to, the curtain wall?

MR. LSTIBUREK: All of the components that make up the building fabric as well as all of the furnishings within the building as well as the nature of the cleaning compounds and agents that are used in housekeeping as well as the products used in renovation, basically, everything that goes in that building. I would be really nice to know what the heck is in these products, and the information is not there.

MR. DINEGAR: You spoke before about ventilation and source control. Let's talk a little bit about source control. Let's assume money is no object, and ventilation rates can operate at 20 cfm, 30 cfm in that ball park right now. Rather than imagine a cure all for indoor air quality related problems, what other part of the component in terms of source control need to be addressed; would you like to find out beyond the information associated with those building products, the furnishings, the carpets, the solvents used, the cause and effect, what level is safe, would you recommend that OSHA and/or another agency sets a permissible exposure level for different contaminants either comprising those products?

MR. LSTIBUREK: Well, your question is getting into areas I don't believe I have the knowledge or experience to answer.

MR. DINEGAR: You focus on humidity for the most part; is that right?

MR. LSTIBUREK: I focus on air pressure relationships and pathways. I focus on moisture control. I can tell you why a pollutant moves from place to place. I'm not necessarily involved in identifying specifically what that pollutant happens to be nor what it's health effect is nor specifically what its concentration is. But we're very much involved in how it gets from place to place. So I don't think I can answer that.

MR. DINEGAR: OSHA calls for employers to be responsible on the record keeping on the complaint logs and complaints and things of that nature that employers identified as building owner, but also the employer within the building perhaps in the tenant's suites wherever employs a group of people working on the 4th floor for example.

In your experience, do the tenants contribute to indoor air quality problems, and could you give us a couple of different examples whether it's by impeding the circulation of the air as produced from outside or introducing contaminants through a course besides what we had established before as components of the human body and the off gassing that they have?

MR. LSTIBUREK: Well, I'd agree with you that tenants and occupants are sometimes very much the cause of indoor air quality problems. They obviously are by no means the only cause of indoor air quality problems, but they do impact in many cases adversely in a situation.

For example, a number of buildings I've seen supplied with users and registers disconnected or sealed or closed, and it's fairly, it's not unlikely to be in a building where a return grill has been taped shut or a fan system has been disabled or occupants have sometimes brought in their own portable humidifier for a particular portion of the building. Or they've brought in furnishings or some kind of printing setup or whatever that the building owner may have no knowledge of.

In those situations the building system may -- either the original design intent has been now thwarted, or the original design was not intended to be able to deal with the new activity that's happening in that particular space.

Thank you very much.

JUDGE VITTONE: Thank you, sir. Ms. Sherman, do you have any redirect?

MS. SHERMAN: Just a couple of questions. Has everybody else?

JUDGE VITTONE: Let me make sure. Is there anyone else who has any questions for Mr. Lstiburek? I don't see so.

MS. SHERMAN: Mr. Hathan had some questions, and I have one or two.

JUDGE VITTONE: Okay. Lee Hathan, OSHA.

MR. HATHAN (Lee): A couple of questions for you Mr. Lstiburek. Regarding the example you gave in the slides, I believe, with the space pressurization problem and the building was under negative pressure, bringing in the warm, humid air, and you enumerated in detail how two or three sections of our standard possibly would have prevented that from happening.

I was wondering, in our standard in Section C, we ask for a compliance program and listing performance criteria. Sometimes in our industry it's called a building operating plan. And we list, we require them under the proposal to list any space pressurization scenarios that are going on in their building. Buildings under positive pressure compared to outside.

Would this compliance plan, would that have possibly prevented any of these problems you saw there? In other words, the compliance plan itself, or had the owners thought ahead proactively about what the building was supposed to do?

MR. LSTIBUREK: I think it would have gone a long way. I'm a real supporter, a real fan of taking a floor plan and taking out a nice colored pen. Architects like colors, so you give them colors and say, "This part of the building is pink and it's going to be at a positive pressure compared to this part of the building which is green," and do it in a floor plan as well as an elevation.

And it would be very nice if that information was transmitted to the owner saying, "This is the way your facility was designed and built and this is the way your facility's mechanical system is supposed to operate, and here's the information you need in order to operate the system." Then with that information the owner should be able to train his own personnel sufficiently to be able to ensure that that happens. And to check, periodically, during a typical maintenance to see whether or not these pressure relationships are in fact being maintained.

And if a problem does occur, it's certainly a tremendous benefit to a firm like mine to know what it was that this building was supposed to be doing in the first place.

MR. HATHAN (Lee): Based on that answer, let me expand that into a second question from that. Do you find that owners understand, that building operators understand, design pressure relationships. You know, that certain parts of the building are supposed to be positive or negative compared to other parts or to outdoors?

MR. LSTIBUREK: It very much depends on the nature of the building manager, the building engineer, the degree of knowledge that that person is operating under. I've run across individuals that are extremely knowledgeable and are able to maintain the building appropriately, and I of course have run across other individuals who are completely in the dark about this.

MR. HATHAN (Lee): Okay. A last question. We had a question earlier about maintenance, housekeeping people during off shifts and running ventilation to accommodate the contaminants at that time and you mentioned a localized approach of the HVAC system for handling that. On page 16,028 of our Summary and Explanation in our proposal we talk about an example of where the HVAC system, the outside air function of the HVAC system could be used, for example when painting or laying carpeting or things like that during the off shift, and a liberal dosage of outside air for dilution removal at that time. Do you see that happening in the industry?

MR. LSTIBUREK: Some facilities, yes. But in general, no.

MR. HATHAN (Lee): Would that be an approach for handling it, for those contaminants?

MR. LSTIBUREK: Well, it's certainly an approach that we recommend to any owners that ask our opinion.

MR. HATHAN (Lee): Okay. Thank you.

MS. SHERMAN: I have just a couple of questions. I believe you testified about having, when you investigate problem buildings it would be useful to know how the building was designed to operate. Would it also be useful to you to have a list of employee complaints which such other information as when they occurred, what department they were in, etcetera?

MR. LSTIBUREK: Yes. It would be very useful. We typically have to reconstruct that, anyway. In other words, as part of our investigation we try to determine that and sometimes that can be very, very difficult. It's always been of use to us if that information has been available from the very start. It means that we are able to proceed much faster, much quicker to resolving a particular problem.

MS. SHERMAN: In your experience, do you find that there are more indoor air quality problems occurring in small buildings or large buildings?

MR. LSTIBUREK: I think they are found in all buildings. Size doesn't necessarily determine the thing. The problems in smaller buildings tend to be different from the problems in larger buildings, just as the problems in the southern, humid states are different from the problems in the northern states. So, I mean, there are problems everywhere. Size is not a requirement, but the problems tend to be different. As well as age. There are different problems in newer buildings than there are in older buildings. Small buildings, tall buildings as well.

MS. SHERMAN: I didn't quite understand your position on age.

MR. LSTIBUREK: Well, there are problems in new buildings; there are problems in old buildings; but the problems are all different. There are problems.

MS. SHERMAN: Could you elaborate a little bit more on a point that you made in answer to another question? I believe the point was that sometimes you can't figure out quite what the cause of the problem is but you can fix it.

MR. LSTIBUREK: Yes. I know that may sound absolutely, totally bizarre and strange, but we may not specifically be able to identify, for instance, a particular pollutant source. But by increasing the ventilation or dilution rate, the removal rate, the concentration of whatever that particular pollutant happens to be drops sufficiently that the problems or the complaints go away. And although we've increased the ventilation and the complaint has disappeared, we may have never known which specific source was responsible.

So here we have a solution, but without a specific identifiable cause.

MS. SHERMAN: And I take it that that would be for more things than just for indoor air contaminants.

MR. LSTIBUREK: Well, a lot of times...

MS. SHERMAN: Being able to fix a problem without knowing quite what it is.

MR. LSTIBUREK: Well, sometimes... Well, many times, in my experience, it has been very, very difficult to differentiate comfort issues from source strength issues in a particular building, and sometimes changing the ventilation rate also alters and improves the comfort in the building. And we understand and appreciate that comfort factors also affect people's perception of the indoor air as well. So sometimes changing, we might be dealing with a comfort issue and not necessarily know or identify it as such, and changing the ventilation rate affects both the comfort and the source strength.

So, yes, we go into buildings and change things and the problem goes away and we're not quite sure why. But our clients are happy.

MS. SHERMAN: Thank you. That's all I have now.

MR. LSTIBUREK: Thank you.

JUDGE VITTONE: Thank you Mr. Lstiburek. You may step down. The next scheduled witness is Jonathan Michael Samet. Dr. Samet, isn't it?

(Off the record.)

JUDGE VITTONE: Dr. Samet, would you state your full name and the organization you represent and just generally identify yourself for the record, please?

MR. SAMET: Yes. My name is Jonathan Michael Samet. I'm currently Professor and Chairman of the Department of Epidemiology at Johns Hopkins University.

JUDGE VITTONE: And you are testifying here today at the request of OSHA?

MR. SAMET: That is correct.

JUDGE VITTONE: Are you going to be using the slide machine?

MR. SAMET: Yes.

JUDGE VITTONE: Let me move out of your way. Then you may begin your testimony.

MS. SHERMAN: Could we have that light off if Dr. Samet is going to use the overhead projector? All right. What about the one directly in front of me?

(Pause)

JONATHAN MICHAEL SAMET, M.D.

MR. SAMET: My name is Jonathan M. Samet. I'm a medical doctor trained in internal medicine and the subspeciality of pulmonary medicine. I received a Bachelor's Degree from Harvard College, a Medical Degree from the University of Rochester School of Medicine and Dentistry, and a Master of Science in Epidemiology from the Harvard School of Public Health.

Most of my professional career has been spent at the University of New Mexico School of Medicine, where I most recently had the title of Professor of Medicine and Chief of the Pulmonary and Critical Care Division of the Department of Medicine. I recently assumed my present position as Professor and Chair of the Department of Epidemiology of the Johns Hopkins University's School of Hygiene and Public Health.

I first became interested in the health effects of indoor air pollution in the late 1970's. At that time I was involved in epidemiologic research studies on the health effects of outdoor air pollution. In these studies we also looked at the effects of indoor exposures and quickly learned that indoor air pollution, along with outdoor air pollution, was also significant for respiratory health.

In my position at the University of New Mexico my time was divided between the practice of pulmonary medicine and the conduct of epidemiologic research. My clinical practice has covered the full range of pulmonary diseases, but more recently it has increasingly focused on the diagnosis and management of patients with occupational environmental lung diseases. I have provided clinical care for patients with problems stemming from indoor air pollution exposures and for patients with the clinical syndromes often referred to as "sick building syndrome" and multiple chemical sensitivity.

In New Mexico my research emphasized the effects of inhaled agents on health, and particularly outdoor and indoor air pollutants, including radon, nitrogen dioxide and environmental tobacco smoke. This research has addressed the non-malignant and malignant effects of ETS, nitrogen dioxide and respiratory illnesses, and radon and lung cancer.

I've also conducted studies directed at time activity patterns. That is, how do people spend their time and what are the characteristics of those environments and activates and assess personal exposures to pollutants.

I've also studied the effects of active smoking. I've authored or co-authored many scientific papers on these topics and with a colleague at the Harvard School of Public Health, Dr. John Spengler, I edited a book, "Indoor Air Pollution: A Health Perspective," published by Johns Hopkins University Press in 1991. More recently I edited a book entitled "Epidemiology of Lung Cancer" published by Marcel Dekker, Inc. in 1994.

I've served on a number of committees and advisory groups concerned directly or indirectly with indoor air quality and health. These include the Indoor Air Quality and Total Human Exposure committee of the Science Advisory Board of the EPA, the National Air Conservation Commission of the American Lung Association, and SSPC-62 of the American Society of Heating, Refrigerating and Air Conditioning Engineers.

I also served on the Working Group on Tobacco Smoking of the International Agency for Research on Cancer and was a consulting scientific editor for the 1986 Report of the Surgeon General on Involuntary Smoking. I was subsequently the Senior Scientific Editor for the 1990 Report of the Surgeon General on Smoking Cessation.

I'm here today to testify in support of the proposed rule by the Occupational Safety and Health Administration. In my testimony I will provide a clinical and epidemiological perspective on the adverse effects of indoor air pollution -- in my view, a problem of significant public health import and one meriting the proposed rule. I will also address environmental tobacco smoke, or ETS, one of the pollutants given specific consideration in the proposed rule.

I'd like to begin first by describing a few patients representative of some of the patients I've seen in recent years in my direct clinical practice with problems related to indoor air pollution. My point is that patients come to doctors with complaints, symptoms and illnesses related to indoor air exposures.

For example, two women with acute onset of dizziness, difficulty thinking and shortness of breath, in an office at a time that this office area was undergoing renovation. An office worker with symptoms of upper airway irritation from smoking in an adjacent office. And a performing arts worker with mold exposure and probably hypersensitivity pneumonitis.

MS. SHERMAN: Let the record show that that was Slide No. 1.

MR. SAMET: That was Slide 1, and I will identify them.

MS. SHERMAN: Okay. Thank you.

MR. SAMET: My experience would not appear to be unique and, as is shown on Slide 2, the kinds of questions that have come to me from my colleagues have often also dealt with indoor air issues. I've been asked often, "What is sick building syndrome?" Often about the health effects of environmental tobacco smoke exposure. And, again, often about the risks of indoor asbestos. A representative series of the kinds of questions that have been directed at me by my clinical colleagues.

Why is indoor air quality in the workplace significant for the public's health? I've listed some of these reasons on Slide 3. Of course we spend most of our time indoors, as has been well documented by time activity studies in developed countries. For people who work, about 20 to 25 percent of the time is spent in the workplace. And importantly, in contrast to the home, the worker may have no control over ventilation nor the sources of indoor air pollution in the workplace.

Indoor air quality has some unique features, particularly as the Occupational Safety and Health Administration considers rulemaking to provide protection for workers against the problem of inadequate indoor air quality.

I'm going to take you through a listing of these special issues. Part of my intent in doing so is to provide some justification for the broad approach that the proposed rule takes to providing better indoor air quality in the workplace. These issues are listed on Slide 4, and I'll be going through each one in turn and amplifying on it.

First, indoor air contains a mixture of pollutants. When we talk about problems of poor indoor air quality we're not talking, usually, necessarily about simply one pollutant but often a more general problem. So we're dealing in fact with a complex exposure with indoor air contaminated often by multiple pollutants of concern for health.

The next two slides are simply a listing of sources of common indoor contaminants, taken from a table in a paper published within the book that Dr. Spengler and I edited.

Slide 5, some of the common sources of indoor air pollutants. Contaminants and source. Asbestos, used in insulation, sprayed on material, a variety of other uses in buildings. Combustion by-products. Carbon monoxide, nitrogen dioxide, sulfer dioxide particles, various nitrogenated compounds. Again, with multiple combustion sources within indoor environments.

Tobacco smoking with a partial listing of some of the contaminants generated by smoking of cigarettes, pipes and cigars. Formaldehyde, again with a number of the sources listed.

Slide 6 simply finishes the table. Biological Organisms. Again, a variety of types of organisms of concern for health. Fungi, bacteria, viruses, pollens, insects, protozoans. All associated with disease in indoor environments. Multiple sources, some related to water damage and too much humidity, others related to poor hygiene, the presence of insects and rodents.

And volatile organic compounds. Again, a group of agents united simply by the physical property of being present in gaseous form at room temperature, including a variety of compounds with many different sources in buildings, some related to processes that may be used in offices, others to cleaning materials, and still others to furnishings and other materials within the indoor environment.

So, I'd simply elaborate on some of the sources of volatile organic compounds in indoor air. Again, a table taken from this chapter authorized by Dr. Spengler, 1991, "General Categories of Sources, Examples and Important Emissions." Important sources, general categories, construction materials, structural components, furnishings, cleansers and solvents, personal care products, insects and pesticides, electrical equipment and combustion, all sources of volatile organic compounds.

A study by EPA in a single building in North Carolina exemplifies, as shown on Slide 8, the numbers of organics that may be found in buildings. In this study, measurements of volatile organic compounds were made in a new office building. The levels were shown for some to decline as presumably offgassing of these compounds from materials occurred. Levels of others rose, presumably reflecting use of materials and processes within this office building that were releasing these agents.

As those who consider the problem of workplace indoor air quality, it's also important to note that, as on Slide 9, that indoor air pollution causes disease through multiple mechanisms. So I pointed out already that a mixture of pollutants is of concern. These agents may cause disease in humans though a variety of mechanisms. And there are a variety of diseases, then, of concern, as I will move to later.

Some of these mechanisms, the principal ones, are listed on Slide 10. By immunologic mechanisms, I'm referring to diseases where the underlying process is a response of the immune system. For example, hypersensitivity pneumonitis, a scarring disease of the lung, reflects an immune response of the lung to the inhaled biological agent. Asthma also is immunologically mediated, at least to an extent.

Infection. Again, we begin with multiple infectious agents present with indoor environment. Carcinogenesis. Indoor air contains a number of carcinogens, including, for example, environmental tobacco smoke and radon.

Irritation. Again, triggering of irritant receptors to cause symptoms, with such receptors located in the mucous membranes of the airways and eyes, as well as the skin.

Inflammatory mechanisms. As, for example, may cause lung injury. By inflammation I'm referring to the production of a tissue response in which cells enter the injured area. The cells themselves may release various products that are damaging to the tissues and in some cases scarring may result as, for example, in hypersensitivity pneumonitis.

And, finally, a variety of neurophysiological mechanisms may underlie effects of indoor air pollution, including, perhaps, some of the components of what is referred to as the "sick building syndrome."

Now, these multiple mechanisms of disease production have diverse adverse health consequences. Slide 11, "Diverse Adverse Health Consequences" are of concern. They range in severity, and I think it's important to recognize that there is a range in severity from chronic symptoms and irritation to acute, even fatal exposures such as may occur with some combustion products, carbon monoxide or high levels of nitrogen dioxide for example.

I think it's important to view these health consequences within some framework so that we don't get lost with the multiple agents and adverse health effects of concern. In 1993 at the plenary session of Indoor Air 93, and international meeting on indoor air and health, I gave a plenary lecture in which I offered a classification of the adverse effects of indoor air pollution. Portions of that classification are listed on Slide 12, and I'd like to take you through this classification because it is a framework in which the problem that OSHA is addressing can be viewed and in which the benefits can be interpreted.

Now, the next slide, 12A, I've simply blown this up so that you can see it better and I'll follow with Slide 12B which finishes out this classification.

First, indoor air pollution is associated with clinically evident disease. Hypersensitivity pneumonitis, Legionnaire's Disease, other infections. It is clear that exposures within indoor environments produce disease that is clinically diagnosed, fits into specific diagnostic categories and patients with such disease come to physicians and other health care providers for treatment.

Indoor air pollution may also exacerbate a variety of chronic diseases, likely including asthma, chronic obstructive pulmonary disease, coronary artery disease, among others. It is also clear that indoor air pollution exposures increase risk for some diseases. And there are a number of diseases for which epidemiologic and other types of evidence establish increased risk.

As, for example, with indoor carcinogens. Here, the usual clinical methods indicative of injury typically cannot establish a causal link in an individual. In an individual. But we turn to evidence from populations studies with epidemiological tools and to toxicology to establish the basis for this category.

Turning to Slide 12B, the completion of the original Slide 12, we also know that indoor air pollution exposure may cause physiologic impairment. That is, there may be transient or persistent effects on some measure of physiological functioning, perhaps lung function, which are not of sufficient magnitude to cause clinical disease but, again, when populations or groups are studied we can detect such impairment.

And, finally, indoor air pollution is associated with symptom responses. And, again, we can have a variety of lines of evidence, including both epidemiological studies and clinical exposure studies in which volunteer subjects have been exposed to pollutants, showing that indoor air pollution exposures produce symptoms.

Still elaborating on this issue and relationship to indoor air quality, on Slide 13 I've listed some of the examples of clinically evident disease often referred to as building related illness linked to indoor air pollution. For example, carbon monoxide poisoning, hypersensitivity pneumonitis and humidifier fever, Legionella and pneumonia, and mite-induced asthma.

Slide 14 lists some examples of exposure disease associations. Again, associations established on the basis of epidemiological and other toxicological considerations. Radon and lung cancer. Environmental tobacco smoke and lung cancer. Benzene and leukemia. Asbestos, lung cancer and mesothelioma. Formaldehyde and nasal cancer.

Now, turning to the last of these issues on Slide 15, I would like to point out -- and, again, as one of these special issues -- that some of these adverse effects are nonspecific and they have causes other than indoor air pollution. Nevertheless, that does not mean that poor indoor quality, indoor air pollution, is not contributing to the public health burden for these diseases. It simply means that in a particular individual it may be difficult to isolate the contribution of indoor air pollution.

Slide 16 simply amplifies and exemplifies the difference between such specific effects and nonspecific effects. Asbestos, for example, is the cause of most cases of mesothelioma. Here there is a almost unique exposure disease relationship. Similarly, in a patient with diagnosed and confirmed Legionella pneumonia, there is a specific association, and such specific associations may also be identified in hypersensitivity pneumonitis, for example, finding in a patient with an appropriate clinical picture an elevation of precipitating antibody titre to thermophylic actinomycetes.

On the other hand, nonspecific associations. For example, environmental tobacco smoke and lung cancer, where a case of lung cancer caused by environmental tobacco smoke could not be distinguished from one with another cause.

Now, I'd like to turn, at the end of my testimony, to environmental tobacco smoke and its respiratory effects. Environmental tobacco smoke is one of the pollutants for which the proposed rule offers a specific handling.

With regard to environmental smoke and lung cancer, Slide 17, a number of expert groups have reviewed the evidence and reached the conclusion that environmental tobacco smoke causes lung cancer. In 1986, three reports were released, each with this shared conclusion.

The International Agency for Research on Cancer -- and I've listed what that report says. Knowledge of the nature of sidestream and mainstream smoke of the materials absorbed during passive smoking and of the quantitative relationships between dose and effect that are commonly observed from exposure to carcinogens, however, leads to the conclusion that passive smoking gives rise to some risk of cancer.

The Surgeon General's Report in 1986, involuntary smoking is a cause of disease, including lung cancer in health nonsmokers, and the 1986 report of the National Research Council. Considering the evidence as a whole, exposure to environmental tobacco smoke increases the incidence of lung cancer in non-smokers.

More recently, on Slide 18, the Environmental Protection Agency in its 1992 risk assessment stated "ETS is a human lung carcinogen responsible for approximately 3,000 lung cancer deaths annually in U.S. non-smokers."

Now, as shown on Slide 19, the Environmental Protection Agency report also reached some conclusions in its review of the evidence on nonmalignant respiratory diseases and health effects in children. And, again, to only quickly review these, the Agency's report found that ETS exposure was causally associated with increased risk of lower respiratory infections in infants and young children. The agency found that ETS exposure is causally associated with middle ear disease, symptoms of upper respiratory tract irritation and small but significant reduction of lung function.

The agency further concluded that ETS exposure is casually associated with additional episodes and increased severity of symptoms in children with asthma.

And finally, the agency said that ETS exposure is a risk factor for new cases of asthma in children who have not previously displayed symptoms.

In offering its proposed rule for indoor air quality, I think it is also important that OSHA acknowledge the heterogeneity of workers with regard to susceptibility to indoor air pollution.

There is likely a range of susceptibility within the general population and some workers may have chronic conditions that place them at increased risk for indoor air pollution.

These individuals need to be considered and protection needs to be extended to all workers.

Examples of such susceptible populations include persons with asthma, perhaps 3 to 5 percent of adults; those who are allergic or atopic, in the technical word, perhaps 25 to 35 percent of adults; those with underlying chronic obstructive pulmonary disease; the crippling loss of lung function that typically occurs in persons who have smoked.

Again, such persons have compromised their ventilatory reserve of their lungs and are at risk for pollutant exposures.

Possibly persons with underlying coronary artery disease, at risk for angina pectoris and myocardial infarction, and the persons in the workforce with immunologic impairment, perhaps because they have an underlying chronic condition associated with an immune --deficiency of immune responses.

Where are we, then, with indoor air pollution and our understanding of health effects in 1994? It's clear if we look, as in Slide 21, in a risk assessment framework, that a hazard has been identified.

We have evidence from clinicians, we have epidemiological evidence, and we have evidence from toxicologic investigations of multiple hazards.

Our information on exposure shows a variety of exposures of concern. For some agents, dose response relationships have been characterized, and for some agents we are now able to characterize the risks fully.

In summary, then, on Slide 22, indoor air pollutants are ubiquitous in the work place. Adverse health effects of indoor air pollution in the work place are documented, well documented, and there are clinically significant effects of indoor air pollutants that could be considered as material impairment.

To reiterate, then, on Slide 23, indoor air pollution in the work place is a significant public health problem. The Proposed Rule should reduce morbidity and mortality from indoor air pollution among the nation's workers.

I'm finished with my remarks.

JUDGE VITTONE: Thank you, Dr. Samet.

Dr. Samet and his slides would be No. 25.

MS. SHERMAN: Dr. Samet, would you like to put hard copies of your slides into the record?

DR. SAMET: Yes, I will.

MS. SHERMAN: Okay. That will be Exhibit 25 with attachments -- your written testimony and the slides.

JUDGE VITTONE: They will be received into the record of this proceeding.

(The document previously marked as Exhibit No. 25 was received in evidence.)

JUDGE VITTONE: Could I have a show of who would like to question Dr. Samet? Would you all stand, please?

Three, four, five.

Mr. Sirridge, how long?

MR. SIRRIDGE: Half an hour, 40 minutes.

JUDGE VITTONE: Mr. Rupp.

MR. RUPP: About a half an hour.

JUDGE VITTONE: Mr. Grossman?

MR. GROSSMAN: About an hour and a half.

JUDGE VITTONE: And you, gentlemen?

MR. TINGLE: Five minutes.

JUDGE VITTONE: Okay. Let's take the two shorter ones first, and then we will proceed with the others.

Did I get everybody? I don't think I missed anybody.

Let me ask quickly. Is anybody going to need these slides?

MR. TINGLE: Just three questions for you,
Dr. Samet.

The first one is, from you experience, is there significant data and scientific evidence for the inclusion of Sick Buildings syndrome into OSHA's final standard as a trigger into the standard?

DR. SAMET: Can you help me what you mean by "as a trigger"? I don't understand.

MR. TINGLE: Okay. In the current proposed standard, OSHA has building related illnesses and other like symptoms that trigger you into the compliance portion of the standard.

With the evidence that you've shown us today and the evidence that I'm sure you've read about it, is there sufficient evidence and medical data that would supply Sick Buildings syndrome to be a trigger, just like building-related illnesses into the compliance portion of the standard?

DR. SAMET: The patients whom I have seen who have symptoms compatible with Sick Buildings syndrome who received that diagnosis, have been impaired in the performance of their duties and of their well being, and I think, in that sense, the Sick Buildings syndrome represents an adverse health effect and produces a material impairment.

MR. TINGLE: Okay. So you would say that it should be included

DR. SAMET: It would be an appropriate trigger, yes.

MR. TINGLE: Okay. Someone else who imposed the standard has suggested that OSHA use permissible exposure limits and the single source risk assessments used so regularly in industrial settings and developing exposure risks for workers were looking at IAQ problems.

In your experience and research, is this the correct approach to take when looking at IAQ risk for workers?

DR. SAMET: No.

MR. TINGLE: Why is that?

DR. SAMET: We lack a quantitative definition of healthy indoor air quality that would allow us to apply a PEL approach.

MR. TINGLE: Thank you. The last question is: from your experience and research, is there significant evidence in the scientific data, research, and medical evidence which warrants that poor IAQ poses a significant risk to workers?

DR. SAMET: Yes.

MR. TINGLE: Thank you.

DR. SAMET: Thank you, sir.

JUDGE VITTONE: Mr. Deniger.

MR. DENIGER: Jim Deniger with Building Owners and Managers Association, Hearing Docket No. 1.

Dr. Samet, I read in your statement that on page three, you call the proposed rules timely. It would also suggest they're interesting, they're voluminous, they're well written. Do you find them appropriate? Do you find them to be the solution to the indoor air quality problems?

DR. SAMET: You're asking a complex question that lies outside my field of expertise as a physician and epidemiologist.

MR. DENIGER: But you've reviewed the rules and in response to OSHA's requests for people to be testifying, even though you were invited as an expert witness, in your estimation, do you find the rules appropriate as written now, to improve indoor air quality or do other steps need to be taken to improve indoor air quality?

In your previous response to Mr. Tingle from AFL-CIO, you had noted that more does need to be done.

Could you elaborate?

DR. SAMET: I guess I'm not sure I understand your interpretation of my prior response, that more needs to be done. Can you help me out on that?

MR. DENIGER: Okay. You talked about the sources of contaminants, or you talked about the health effects of indoor air quality, that not enough is known. Could you elaborate on your response from Mr. Tingle?

Maybe I'm misquoting.

DR. SAMET: I think you're misquoting me. I think I said that we had ample evidence that we have a public health problem, and I did respond affirmatively as to his question as to whether poor indoor air quality posed a problem for the health of workers.

MR. DENIGER: That was a later part of his questions, but I didn't write it down, so I don't have it accurately.

You go on to state on page 3 of your written remarks, "Adverse effects from indoor air quality exposure may be increasing," and I wanted to find out a little bit more about that.

I'm interested to find out how that could be. Is it because there has been longer-term exposure to different contaminants or is it because building management is paying less attention to indoor air quality contamination, or is it because there are more contaminant sources, or a mixture of those three?

What would be your assessment and reason for saying that adverse effects regarding indoor air quality, from indoor air quality problems, seem to be or may be increasing?

DR. SAMET: Let me answer that question.

The evidence would come from both the medical literature, where a term such as Sick Buildings syndrome were virtually absent 20 years ago, building reports, publications, building investigations, problem buildings identified, of reports of the health hazard evaluations done by the National Institute for Occupational Safety & Health, so within the medical literature, a problem that was essentially not known before has emerged as a problem that now merits case reports and epidemiological research.

I think within the medical literature that clinicians like myself read, we see evidence that we are seeing a problem that apparently we did not see before or else we simply did not recognize before.

When I began my career in medicine, I was not told about a problem such as Sick Buildings syndrome, and now I have patients coming to me with such problems.

My contacts with others who work in the indoor air quality field but in other disciplines, would also, again, suggest that there is something new going on. Again, I have many professional colleagues whose profession is building investigation and trying to solve problems.

When I receive telephone calls about problems, because I'm not such a person myself, I often make referrals. Again, in my career, previously, I was not doing that, and now, perhaps, in part, because of my known interest in this area, I get frequent calls.

MR. DENIGER: Okay. But you're saying that the literature has increased, the reports have increased in terms of the available body of information, but that does not suggest or state clearly that adverse effects associated with indoor air quality may be increasing. There may have been exposures to indoor air quality problems all along, but they may not be increasing; in fact, they may be decreasing? Wouldn't that be so?

DR. SAMET: I can only report that the medical literature on this area is mounting. I have no basis for speculating what may have been unreported in the past.

MR. DENIGER: On page 4, you explain that pollutants existing complex mixtures and the presence of one pollutant in the mixture may augment or diminish the effects of another pollutant. Could you give us a couple of examples of how one pollutant in the mixture may diminish the effect of another pollutant?

DR. SAMET: Yes. I'll give you a complex example.

Tobacco smoke in air essentially becomes a source of particulate material onto which the progeny of radon may stick, and the dose of radioactive delivered to the respiratory track to the target cells for lung cancer, depends on how much of the radon progeny is bound to the particle.

So, in this example, the presence of particulate matter in the air, whether from tobacco smoking or some other source, actually alters the dose of alpha energy delivered to target cells in the lung.

MR. DENIGER: Thank you.

On page 7, you state that in the work place, environmental tobacco smoke is a principal concern; and, before that, you state that respiratory carcinogens in indoor air include environmental tobacco smoke, radon, and asbestos. There are a number of rules regarding asbestos, I'm sure you're aware of.

There are also a number of rules coming out and already in place regarding radon.

Are you saying that environmental tobacco smoke in the work place is more of a concern than asbestos presently or more of a concern than asbestos as it was?

DR. SAMET: I'm sorry. Which page are you reading from?

MR. DENIGER: Page 7, top line.

[Pause.]

DR. SAMET: I'm sorry. The question again?

MR. DENIGER: You're mentioning three different contaminant sources: environmental tobacco smoke, radon and asbestos, and then you go on to state that, in the work place, environmental tobacco smoke is a principal concern.

I was wondering, is that moe of a concern than asbestos?

DR. SAMET: I have not done a quantitative comparison here. Such comparisons could be made. I'm not prepared to do it while sitting on this stand.

MR. DENIGER: But in terms of it being a principal concern, are you placing any value associated with debris or are just saying that they're a principal concern and go with the other two?

DR. SAMET: Radon levels in most work places tend to be lower in homes, and the home is the principal long cuts of the radon exposure that is likely to contribute to -- that contributes to the lung cancer risk associated with that particular carcinogen.

We have relatively limited information on asbestos levels in the non-industrial work place. Available information would suggest rather low exposures.

If I were to place these in an order, which apparently is what you're asking me to do, I would place environmental tobacco smoke ahead of the other two as a carcinogen.

MR. DENIGER: The reason I had asked that, Doctor, is really because we have not been dealing with radon in the work place a great deal. We dealt extensively with asbestos, much to our chagrin in many instances and certainly to our expense, and now we're wondering what we get to face with environmental tobacco smoke and, in large part, what OSHA is doing is of great concern in the work place.

The bottom of page 7: Increased risk for disease. Many pollutants in indoor air are associated with increased risk for a variety of malignant and non-malignant diseases. Then I would refer you to Table 3.

The evidence supporting the relationships between exposures to these agents and increased risk comes from epidemiological studies, short-term exposures of volunteer subjects, animal studies, and in vitro toxicological studies.

Table 3, which is in the back, you list five: Radon, a selected example of exposure to disease is associated for indoor air pollutants, radon, lung cancer, environmental tobacco smoke, lung cancer, increased lower respiratory illness and infants.

Benzene leukemia, asbestos lung cancer, and mesothelioma, formaldehyde nasal cancer. You've established that radon is not as prevalent in office buildings.

Environmental tobacco smoke; you shared your comments there.

You briefly discuss benzene and formaldehyde and what you're aware of as the sources within the -- perhaps in the work place for those two pollutants, for those two indoor air pollutants, that you listed out as selected examples of exposure disease associations?

DR. SAMET: To only briefly discuss this, and again there are extensive source listings, and I have not either brought that kind of information with me nor do I routinely remember such source listings.

Benzene exposures, for one, tobacco smoking is a source of benzene and indoor environments.

Combustion, fumes brought in from other sources might also contain benzene.

Formaldehyde again; furnishings, wood products, and other sources. Again, I think there are extensive listings of such sources.

MR. DENIGER: Okay. To wrap up, pass the note that explained I was on the wrong question, but you had said to Mr. Tingle from AFL-CIO that we don't know enough about healthy buildings. What more would you -- still misquoted?

DR. SAMET: I think so.

MR. DENIGER: I'm going to pass on this line of questioning completely until I get back to the transcript.

Thank you very much.

JUDGE VITTONE: Thank you, Mr. Deniger.

We're going to take a short break here of 10 minutes. It's 15 after.

[Recess]

JUDGE VITTONE: Dr. Samet is back up to the table and the witness stand.

Our first questioner is Mr. Grossman.

MR. GROSSMAN: Thank you very much, Your Honor.

We met in the hallway, Dr. Samet. I'm
Ted Grossman. I'm here on behalf of 12 different people who appear in the docket. I gave all of the names yesterday.

I understand that you're an author of many articles, and you have indicated in your testimony that you're and editor of the recently published Epidemiology of Lung Cancer.

You appear in some of the articles as a co-writer and in some articles as the first-named author. Is that correct?

DR. SAMET: Some of the articles, yes.

MR. GROSSMAN: Regardless of whether you appear as the first name in an article or as the last name or anything in between, you, nonetheless, feel you are, in part, responsible for the article, don't you?

DR. SAMET: Correct.

MR. GROSSMAN: And you stand by the article?

DR. SAMET: Correct.

MR. GROSSMAN: And, similarly, where you have edited textbooks, you have written some chapters and other people have written other chapters?

DR. SAMET: [No response.]

MR. GROSSMAN: Let me rephrase the question.

You wrote some chapters of the Epidemiology of Lung Cancer, published this year. Is that correct?

DR. SAMET: Correct.

MR. GROSSMAN: And you also edited the entire volume. Is that correct?

DR. SAMET: That is correct.

MR. GROSSMAN: And, as editor, you stand behind the entire volume?

DR. SAMET: What do you mean by "stand behind"?

MR. GROSSMAN: You reviewed the work of the others who contributed sections to the volume and you believed in what the others said in the volume that you edited?

DR. SAMET: I'm not sure editing is a matter of belief.

MR. GROSSMAN: You had no reason to disagree with the statements made in the volume that you edited? Is that correct?

DR. SAMET: Is the question, do I agree with every statement made in the volume?

MR. GROSSMAN: Did you have any substantial disagreements with any of the findings or conclusions that were drawn in the volume?

DR. SAMET: As an editor, my concern is that the contributions are prepared by experts in the field; that they have comprehensively reviewed the literature; that they have presented the materials in an appropriate and suitable manner, and, in an edited volume, as an editor, I would allow some latitude on matters of particular statements or assertions, provided the author was balanced in their view and had reviewed the literature appropriately.

MR. GROSSMAN: All right. You wouldn't allow a statement that you felt was unsupported by the literature?

DR. SAMET: I'm sorry?

MR. GROSSMAN: You would not allow a statement to be published in a volume that you edited if you believed the statement was unsupported by the underlying literature?

DR. SAMET: That's correct.

MR. GROSSMAN: Okay. Now, is it fair to say that you have never undertaken, personally, a cohort or case control, or other study of ETS in the work place?

DR. SAMET: Correct, in terms of looking at health effects.

MR. GROSSMAN: So you have never personally conducted a case control or cohort or other study of the health effects of ETS in the work place?

DR. SAMET: Correct.

MR. GROSSMAN: Is it also fair to say that you have not personally undertaken a quantitative review or another separate and intensive analysis of the literature regarding the health effects of ETS in the work place, per se?

DR. SAMET: Correct.

MR. GROSSMAN: Okay. As a predicate for discussing ETS in the work place, I would like to turn briefly to the question of primary smoking.

It was established through a number of case control studies in the 1950s that -- well, let me rephrase the question.

In the 1950s and since, there have been a number of case control and other studies, attempting to draw a statistical link between smoking and various kinds of lung cancer. Is that correct?

DR. SAMET: A number of case control and cohort studies have been conducted on the association of active smoking with lung cancer and other diseases.

MR. GROSSMAN: Yes. Famous early studies were the U.S. veteran study and the Dalin-Peto study, and several others? I'm sure you're familiar with those?

DR. SAMET: Correct.

MR. GROSSMAN: And those studies tended to show a significantly increased prevalence of certain kinds of lung cancer among people who had a history of active smoking; is that correct?

DR. SAMET: I think I need a little more guidance with regard to what you mean.

MR. GROSSMAN: Okay. Most of the studies that have been conducted in the field have shown that squamous cell carcinoma of the lung and small cell carcinoma of the lung, in particular, are much more common in people who have a history of active smoking than in people who don't?

DR. SAMET: That is correct.

MR. GROSSMAN: Many of the early studies did not show a correlation between cigarette smoking an later development of adenocarcinoma in the lungs, such as the Dalin-Peto study and the veterans study?

DR. SAMET: I think that you might be misquoting the literature, and I can't be certain without it in front of me. I think you said the -- the Dalin-Peto, you mean the British cohort?

MR. GROSSMAN: Yes.

DR. SAMET: Actually, Peto was not involved early on. You said the U.S. Veterans?

MR. GROSSMAN: Yes. The Doran study.

DR. SAMET: I'm not certain that the Doran study had information on histology. If I recall correctly, it was mortality studies, so you perhaps are not quoting that study correctly.

MR. GROSSMAN: Are you familiar with the Criberg definitions of histological types of lung cancer?

DR. SAMET: Certainly.

MR. GROSSMAN: Criberg I, Criberg II?

And those distinctions were based upon lung cancer that was believed at the time to be attributable to smoking and lung cancer that was not? Is that correct?

DR. SAMET: It was a histological classification developed by Criberg that was applied to this
particular -- to lung cancer, in general.

MR. GROSSMAN: Were small cell and squamous cell carcinoma were lumped together as Criberg Cell Type I?

DR. SAMET: Correct.

MR. GROSSMAN: Adenocarcinoma was Criberg Cell Type II?

DR. SAMET: Correct.

MR. GROSSMAN: Criberg believed that adenocarcinoma -- that is, Cell Type II -- was not related to smoking?

DR. SAMET: That was his belief.

MR. GROSSMAN: All right. Now other researchers have disagreed with that and believe there is a statistical relationship between smoking and adenocarcinoma?

DR. SAMET: A number of studies show that the risk of adenocarcinoma rises with the level of smoking.

MR. GROSSMAN: Even those studies, though, show a significantly smaller statistical correlation between adenocarcinoma and active smoking than squamous cell or small cell carcinoma and active smoking? Is that correct?

DR. SAMET: I don't use the term statistical correlation. You'll have to explain it to me.

MR. GROSSMAN: Okay. Risk ratio for squamous cell and small cell carcinoma from active smoking is higher than the reported risk ratio for adenocarcinoma from active smoking; is that correct?

DR. SAMET: In some studies, that has been observed.

MR. GROSSMAN: In most studies, that's been observed?

DR. SAMET: Not all studies have stratified the data histologically.

MR. GROSSMAN: An attempt to draw an inference of causality or risk factor from the observed statistical correlation between active smoking and later lung cancer, one of the critical factors considered was the dose. Is that correct -- the dose relationship?

DR. SAMET: One of the factors considered was the relationship between the reported about smoked or some other dimension of the smoking history and the risk of lung cancer.

MR. GROSSMAN: All things being equal, it was important to the researchers involved that a greater number of cigarettes smoked indicated a greater likelihood or greater incidence of lung cancer?

DR. SAMET: Such exposure responses were considered as the information on active smoking and lung cancer was interpreted.

MR. GROSSMAN: Dose response relationships are important to epidemiology, generally?

DR. SAMET: Examining the relationship between level of exposure and risk is often a component of data analysis.

MR. GROSSMAN: In the Surgeon General's works on active smoking and lung cancer, dose response relationships are reported?

DR. SAMET: There are tables summarizing dose response relationships.

MR. GROSSMAN: According to the Surgeon General, the relationship is more than linear? That is, all other things being equal, 50 pack years of cigarette smoking is more than twice as likely to produce lung cancer as 25 pack-years of cigarette smoke?

DR. SAMET: I'm not aware of the Surgeon General's report that reaches that conclusion.

MR. GROSSMAN: Are you aware of the Surgeon General's report reaching a different conclusion?

DR. SAMET: I'm not aware of the Surgeon General's report that has a quantitative description of dose response relationships as one of its conclusions.

MR. GROSSMAN: Are you aware of any reported literature on active smoking that does not report a dose response relationship between active smoking and lung cancer, at least squamous cell and small cell varieties?

DR. SAMET: Could you repeat the question, please?

MR. GROSSMAN: Sure. Are you aware of any literature that does not report -- well, let me rephrase the question again.

Are you aware of any literature that reports the lack of a dose response relationship between active smoking and the incidence of small cell or squamous cell carcinoma?

DR. SAMET: I'm aware of reports that do not provide such information. Of course, I'm also aware of reports that do provide such information.

MR. GROSSMAN: To the extent that reports provide information on dose response relationships, are you familiar with any reports that show the lack of a dose response curve between active smoking and the incidence of small cell or squamous cell lung carcinoma?

DR. SAMET: Most such reports show evidence of increasing risk with increasing smoking.

MR. GROSSMAN: The evidence of a dose response relationship in epidemiology is one of the steps that is generally reviewed as important in attempting to establish a cause and effect relationship?

DR. SAMET: I would regard that as an oversimplification.

MR. GROSSMAN: What is the use of the dose response relationship in epidemiology?

DR. SAMET: Well, the dose response relationship is, one of the ways of looking at data to provide evidence on how risk varies with dose.

A dose response relationship, I think, as you are using it, you are referring to an increasing risk. With increasing exposure, there are a variety of dose response relationships available, but typically we examine the relationship between risk and degree of exposure.

MR. GROSSMAN: And that's a common study in epidemiology?

DR. SAMET: It's a common approach to data analysis, yes.

MR. GROSSMAN: And the reason for that common approach is because it's believed to strengthen any epidemiological link between observed incidence of disease and exposure to the study component or phenomenon?

DR. SAMET: Could you repeat?

MR. GROSSMAN: Yes. The reason for studying a dose response relationship is because the presence of the dose response relationship is one aspect to support the presence of a -- let me rephrase the question again.

The reason for studying a dose response relationship is that, in the absence of dose response relationship, any observed increase in the incidence of a disease is less likely to arise from an associated exposure?

DR. SAMET: I cannot give a simple answer to that. Interpretation of dose response relationships depends on, one, the underlying biology; and, two, its interpretation must consider the way in which exposure is measured and the way in which response is measured.

MR. GROSSMAN: Or let's look at the way the dose is measured. In the case of active cigarette smoking, it's fairly easy to measure dose, isn't it?

DR. SAMET: I think, just to clarify some terms, in the epidemiological studies of active smoking, we've largely used an exposure measure, number of cigarettes smoked or duration of smoking; dose, to me, means amount of relevant agents delivered to target sites. I think the National Academy of Sciences reports clarifying terminology in this area would make clear.

So when I refer to number of cigarettes smoked per day or duration of smoking as examples, I'm referring to exposure measures.

MR. GROSSMAN: And those are exposure measures?

DR. SAMET: In my terminology.

MR. GROSSMAN: You said that there is a dose response curve that has been reported in most of the literature regarding the relationship between cigarette smoking and small cell and squamous cell carcinoma. Do you recall that a few moments ago?

DR. SAMET: Yes.

MR. GROSSMAN: You would expect a similar dose response curve to apply to ETS if human reaction to ETS were analogous of that of active cigarette smoking, wouldn't you?

DR. SAMET: I'm sorry, could you?

MR. GROSSMAN: If the human reaction to ETS were analogous to the human reaction to active smoking, you would expect the dose response relationship established in the literature regarding active smoking to apply, more or less, to human reaction to ETS, wouldn't you?

DR. SAMET: Well, I don't agree with your premise, which is that a dose response relationship has been demonstrated only for squamous cell and small cell.

There's abundant evidence in the literature showing dose response relationships for adenocarcinoma. So if that is the --

MR. GROSSMAN: I'm not drawing a distinction between --

DR. SAMET: -- premise of your question, I can't accept that.

MR. GROSSMAN: Okay. Add adeno to it. The same question; we'll just call it lung cancer.

You would expect to find the same or similar dose response relationship between the development of lung cancer and active smoking on one hand, and the development of lung cancer and exposure to ETS on the other, assuming that human reaction to ETS were similar to the human reaction to active smoking?

DR. SAMET: You gave a number of assumptions.

MR. GROSSMAN: Yes.

DR. SAMET: I think the additional assumption is, and I already mentioned, is assuming I can measure the relevant exposure with sufficient accuracy based on the current understanding of how lung cancer occurs, it would be reasonable to postulate a dose response relationship.

MR. GROSSMAN: To measure a dose of ETS in the work place, dose, as you understand it, would be a function of several parameters, wouldn't it? That is, it would be a function of the duration of exposure, the longevity of exposure, and the concentration of exposure?

DR. SAMET: The determinants of exposure would include, among others, duration and concentration. Determinants of dose would be -- there would be additional factors.

MR. GROSSMAN: What other factors would there be?

DR. SAMET: Factors of inhalation, level of activity, other factors that determine how much material gets into the lung.

MR. GROSSMAN: In the work place, that dose could vary with the proximity of the individual involved to smokers as one factor?

DR. SAMET: Proximity to smokers would likely determine the concentration.

MR. GROSSMAN: It would also vary with the number of smokers in the given room or area?

DR. SAMET: Again, these are factors that would determine the concentration.

MR. GROSSMAN: The concentration would also be determined in part by the size of the space involved?

DR. SAMET: Correct.

MR. GROSSMAN: The concentration, which is one of the aspects of dose, would be determined, in part, by the type of ventilation and the adequacy of ventilation in the building?

DR. SAMET: Correct.

MR. GROSSMAN: And the concentration would also be affected by other factors as well?

DR. SAMET: I don't know what other factors you refer.

MR. GROSSMAN: Well, the concentration could also be determined by the temperature of the room, the height of the ceiling, various other factors, that could bear upon the exact concentration received by the individual?

DR. SAMET: We mentioned a number of factors that would determine dilution. The height of the ceiling would be there. I can't comment on temperature.

MR. GROSSMAN: Okay. To a large extent, concentration of ETS is capable of measurement, isn't it?

DR. SAMET: Components of ETS can be measured.

MR. GROSSMAN: Personal monitoring would be the best evidence of concentrations of ETS delivered to any individual.

DR. SAMET: Well, there are a variety of approaches that could be used to assess exposure to agents. One of them is personal monitoring.

MR. GROSSMAN: Can you think of a better method than that?

DR. SAMET: I can think of additional methods, such as biomarkers, that can be useful.

MR. GROSSMAN: Biomarkers of individuals?

DR. SAMET: Correct.

MR. GROSSMAN: Certainly, personal monitoring would be a preferable form of measuring concentration than simply asking people were you exposed to ETS, wouldn't it?

DR. SAMET: I think that would depend on the circumstances and the purpose of asking or trying to determine the concentration. I cannot give a general answer to that question.

MR. GROSSMAN: The better the measurement of dose, the more reliable of results of any attempt to link dose with ultimate disease. Is that correct? That would be true of any epidemiological study?

DR. SAMET: I'm sorry. Can you repeat?

MR. GROSSMAN: Sure. The better the measurement of the dose, the better the measurement of a dose response.

DR. SAMET: If you replace "better" with "accurate," I would agree.

MR. GROSSMAN: Okay. That's a good amendment of my language. The more accurate the measurement of dose, the more accurate the drawing of any dose response curve.

DR. SAMET: Again, I won't play words with you, but I think we can learn more about does response relationships as we improve the accuracy of the exposure measurements.

MR. GROSSMAN: Okay. As the accuracy of the exposure measurement goes down, the quality of the results attempted to be drawn also goes down. Isn't that correct?

DR. SAMET: I don't know what you mean by "quality".

MR. GROSSMAN: Well, if the accuracy of the measurement of dose is suspect, then the inferences drawn from the size of the dose in relationship to disease are also suspect.

DR. SAMET: No. Inferences need to be made, with the understanding of the accuracy of the exposure measures that are available, that were used.

MR. GROSSMAN: The degree to which you can rely upon the inferences that we are referring to, depends, in part, on the accuracy of the measurement of the dose?

DR. SAMET: Can you repeat that again?

MR. GROSSMAN: Yes. The degree to which you can rely upon the inferences that are drawn by a study, depends, in part, on the accuracy of the measurement of the dose that's referred to in the study.

DR. SAMET: Correct.

MR. GROSSMAN: Okay. You were a member of the Scientific Advisory Board of the EPA --

DR. SAMET: Correct.

MR. GROSSMAN: -- in its study of ETS in
spousal -- I'm sorry. Let me start that again.

You were a member of the Scientific Advisory Board of the EPA with regard to its ETS study?

DR. SAMET: I was a member of the Science Advisory Board of the EPA.

MR. GROSSMAN: Okay. You were a member of the Science Advisory Board in 1992?

DR. SAMET: Correct.

MR. GROSSMAN: In 1992, the EPA issued a report on ETS and lung cancer. You're familiar with that study?

DR. SAMET: Yes.

MR. GROSSMAN: One aspect of that report was a meta analysis of various case control studies involving spouses of smokers and lung cancer. Are you familiar with that meta analysis?

DR. SAMET: Yes.

MR. GROSSMAN: Did you review that meta analysis?

DR. SAMET: I reviewed the entire report.

MR. GROSSMAN: Did you perform any of the quantifications of the meta analysis?

DR. SAMET: No.

MR. GROSSMAN: Did you review the quantifications of the meta analysis?

You didn't perform the quantifications yourself. Did you review the actual quantifications yourself? Did you re-do the math?

DR. SAMET: I'm sorry?

MR. GROSSMAN: Did you re-do the math?

DR. SAMET: Did I re-do the math, myself?

MR. GROSSMAN: Yes.

DR. SAMET: No.

MR. GROSSMAN: You didn't check the math, and you didn't check the data of the underlying studies themselves?

DR. SAMET: Meaning?

MR. GROSSMAN: You didn't seek to obtain the underlying data, the studies that were part of the meta analysis, that were combined in the meta analysis, did you?

DR. SAMET: In the sense of something beyond the published literature?

MR. GROSSMAN: Yes.

DR. SAMET: No.

MR. GROSSMAN: Okay. How is the meta analysis constructed?

DR. SAMET: Are you asking, did I review the details of the EPA meta analysis?
y MR. GROSSMAN: I'm asking you, in general, how is the EPA meta analysis constructed?

DR. SAMET: Well, I have the EPA report here. This meta analysis is rather long, and I wonder if this is something we want to go into the details of.

MR. GROSSMAN: I'm just asking in general.

DR. SAMET: I --

MR. GROSSMAN: Let me put it a different way. You're an epidemiologist. What is a meta analysis?

DR. SAMET: A meta analysis is a technique for data summarization.

MR. GROSSMAN: What's the purpose of a meta analysis?

DR. SAMET: The purpose of a meta analysis is to draw together evidence from multiple studies, typically, and to obtain a summary estimate of effect from those studies.

MR. GROSSMAN: Why would one undertake a meta-analysis?

DR. SAMET: Well, if you want a tutorial at this point, I mean, there are multiple reasons that a meta-analysis might be performed.

MR. GROSSMAN: Well, could you just list the most important of them?

DR. SAMET: A meta-analysis would be performed when there were multiple investigations contributing data and a summary of those data was being sought. It's a technique applied to observational and experimental data.

MR. GROSSMAN: Okay. Now, as used in epidemiology, a risk ratio of one means that an exposed group and unexposed group exhibit the same incidence of disease?

DR. SAMET: Have the same risk of disease.

MR. GROSSMAN: And a risk ratio of two would mean that an exposed group shows twice the risk of disease as the unexposed group?

DR. SAMET: Correct.

MR. GROSSMAN: Similarly, a risk ratio of ten would show that an exposed group has ten times the risk ratio of an unexposed group?

DR. SAMET: Correct.

MR. GROSSMAN: Now, if the EPA's meta-analysis had shown a risk ratio of one, you could not conclude on the basis of the epidemiological literature taken as a whole that exposure to ETS at the level that spouses of smokers are exposed to ETS could be shown to have a relationship to lung cancer, is that correct?

DR. SAMET: Could you repeat that?

MR. GROSSMAN: Yes. It's a long question.

The EPA's meta-analysis did not reach a risk ratio of one. It reached a higher risk ratio, is that correct?

DR. SAMET: Correct.

MR. GROSSMAN: Okay. But if the EPA's meta-analysis -- or let me ask another preparatory question.

All of the studies involving the EPA's meta-analysis were of spouses of smokers, non-smoking spouses of smokers. Is that correct?

DR. SAMET: That's not correct.

MR. GROSSMAN: What other studies were included?

DR. SAMET: Could you repeat your question?

MR. GROSSMAN: Yes.

The studies that were summarized and consolidated in the EPA's meta-analysis were exclusively the incidence of cancer in spouses, non-smoking spouses, of smoking husbands or wives. Is that correct?

DR. SAMET: It's not correct.

MR. GROSSMAN: What other kinds of studies were included, to your understanding?

DR. SAMET: The subjects in these studies included non-smokers, whether married to smokers or never smokers.

I'm sorry. You said that they were...

MR. GROSSMAN: The case controls, are you referring to the case controls as well as the case...

DR. SAMET: No. I'm sorry. In your characterization of the studies, you said that they were studies of non-smokers married to smokers. That is not a correct description of the studies. They were studies of non-smokers who had lung cancers as cases and they were married to smokers or to non-smokers.

MR. GROSSMAN: Okay. The cases -- the various case reports that were consolidated in the EPA's meta-analysis dealt exclusively with attempting to draw a distinction between the lung cancer rates of spouses of smokers, non-smoking spouses of smokers, and non-smoking spouses of non-smokers. Is that correct?

DR. SAMET: They're not case reports, as you characterized them, they were case controlled studies.

MR. GROSSMAN: Case studies. Yes.

DR. SAMET: Case controlled studies.

MR. GROSSMAN: Case controlled studies.

DR. SAMET: The exposure that was addressed was marriage to the smoker.

MR. GROSSMAN: The only exposure addressed was marriage to a smoker, is that correct?

DR. SAMET: Well, a number of the studies addressed other exposures.

MR. GROSSMAN: But the only exposure addressed by the meta-analysis was marriage to a smoker.

DR. SAMET: Correct.

MR. GROSSMAN: Now, if the risk ratio determined by that meta-analysis had been 1.0, it could not be concluded that there was an increased risk of lung cancer as a result of being married to a smoker, is that correct?

DR. SAMET: No, I don't think that's correct. I think that the interpretation of that risk ratio would have to consider, as I already mentioned, the validity of the exposure variable. If, for example, everyone were completely misclassified, I would anticipate a relative risk of one.

MR. GROSSMAN: Okay. We'll come to misclassification and other biases in a moment. But assuming that the EPA's own meta-analysis had shown a risk ratio of one, no conclusion could be drawn from that and from the epidemiological studies upon which it was based that the level of exposure that one suffers by being married to a smoker was sufficient to create lung cancer, is that correct?

DR. SAMET: That's such a long question that you're just going to have to repeat it.

MR. GROSSMAN: Could you repeat it, please?

DR. SAMET: I guess again I would find it very difficult to answer that absent information about the problem of exposure misclassification. So, again, you know, I recognize you said that...

MR. GROSSMAN: Okay. Let me rephrase the question.

If the EPA had properly adjusted for all biases, in its meta-analysis, a resulting risk ratio of 1.0 would show no increased risk of lung cancer for spouses of smoking husbands in relation to spouses of non-smoking husbands.

DR. SAMET: Well, I guess I really have two responses. One is that you're making an assumption about bias adjustment and I'm not sure what biases you're referring to so we might have to discuss those. And then I think the other important point here is that interpreting the evidence in the EPA report the risk assessment was -- the meta-analysis was only one of the lines of evidence considered in determining whether the agent, ETS, was or was not a class A carcinogen.

MR. GROSSMAN: The ETS relied heavily on its meta-analysis, didn't it?

DR. SAMET: I think there's actually a statement in this document that says that even absent the epidemiological information the agency's criteria for classifying carcinogenicity would have led to the class A designation. I can find the words in the report but...

MR. GROSSMAN: Well, you were an epidemiologist, is that correct?

DR. SAMET: I was and still am.

MR. GROSSMAN: You are an epidemiologist?

DR. SAMET: Yes.

MR. GROSSMAN: And I am referring to your expertise as an epidemiologist, Doctor. As an epidemiologist, a risk ratio of one means there is no increased risk in the exposed group versus the unexposed group, correct?

DR. SAMET: Correct.

MR. GROSSMAN: At the level of exposure, is that correct?

DR. SAMET: And subject to whatever biases may exist.

MR. GROSSMAN: Yes. And as an epidemiologist, a risk ratio of one from a meta-analysis of spousal studies would show no increased risk at the level of exposure that spouses have to ETS, is that correct?

DR. SAMET: Again, subject to my -- subject to the assumptions that we've already discussed about whatever biases may have affected that risk.

MR. GROSSMAN: Okay. And similarly subject to the assumptions about adjustments for biases, if a meta-analysis of exposure in the workplace showed a risk ratio of exactly one, it would mean that there would be no increased risk for people exposed in the workplace to ETS compared to people unexposed in the workplace to ETS at the level of exposure that arises in the workplace. Is that correct?

DR. SAMET: Again, you would have to -- one would have to assume that exposure can be measured with sufficient accuracy that the level of misclassification would not fully cloud interpretation of the risk ratio.

MR. GROSSMAN: All of those things are true but as an epidemiologist, a risk ratio of one in a meta-analysis of that kind would indicate that at that level of exposure there was no increased risk of lung cancer. Is that correct?

DR. SAMET: Presumably such a point estimate from a meta-analysis would come with confidence limits and other uncertainties associated with it that would describe the range of possible effects. You're describing central estimate of no effect. Correct.

MR. GROSSMAN: Okay. Now, let's turn for a moment to some general principles of epidemiology. In general, you said before, I believe, that epidemiology attempts to correlate the incidence of disease with exposure or levels of exposure and to draw inferences from that?

DR. SAMET: I said that in my written statement or...

MR. GROSSMAN: I believe you said that or something along those -- why don't you just describe what the field of epidemiology is? We'll shorten it. In general.

DR. SAMET: Epidemiology is a scientific method used to describe the occurrence of disease, the causes of disease, to evaluate innovations designed to reduce the burden of disease and to increasingly assess the use of health services and other quantitative aspects of health.

MR. GROSSMAN: One of the types of studies conducted in typical epidemiological literature is a double-blind prospective study? A cohort study?

DR. SAMET: I'm not familiar with a double-blind cohort study.

MR. GROSSMAN: Are you familiar with cohort studies?

DR. SAMET: Yes, I am.

MR. GROSSMAN: What is a cohort study?

DR. SAMET: A cohort study is a study in which subjects are selected on the basis of exposure status and followed through the development of disease.

MR. GROSSMAN: And a cohort study can be prospective or retrospective?

DR. SAMET: In timing, correct.

MR. GROSSMAN: Generally, a prospective cohort study is thought to be the gold standard of epidemiological studies?

DR. SAMET: That's the kind of generalization I would not make.

MR. GROSSMAN: All right. In epidemiology, you also use case studies?

DR. SAMET: A case study?

MR. GROSSMAN: Case control studies?

DR. SAMET: We do case control studies. Correct.

MR. GROSSMAN: What is a case control study?

DR. SAMET: In a case control study, subjects are selected on the basis of disease status, diseased or non-diseased, and their exposures are assessed.

MR. GROSSMAN: Now, you were referring a moment ago to elements of bias that are studied in epidemiology?

DR. SAMET: I mentioned bias.

MR. GROSSMAN: And bias is an important factor to be considered in any case control study?

DR. SAMET: Correct.

MR. GROSSMAN: There are generally three categories of bias: information bias, selection bias and confounding?

DR. SAMET: Correct.

MR. GROSSMAN: Briefly, what is information bias?

DR. SAMET: Information bias refers to information that has differential error based on any number of factors.

MR. GROSSMAN: What is selection bias?

DR. SAMET: Selection bias refers to subject selection procedures that alter the true relationship between exposure and disease.

MR. GROSSMAN: That is if you were to pick subjects for the test who were predisposed to a disease and you knew it or did not know it, that could confound the results of the test? Bias the results of the test?

DR. SAMET: What disease? What test?

MR. GROSSMAN: Okay. We'll get back to that type in a moment. What is confounding?

DR. SAMET: Confounding refers to the mingling of the effect of one causal factor with another factor under investigation.

MR. GROSSMAN: And it's a bias that's produced into the calculation by that other effect? By that other exposure?

DR. SAMET: I'm sorry...

MR. GROSSMAN: What is the effect of confounding?

DR. SAMET: The effect of confounding? The effect of confounding may be to increase or to decrease the effect of the agent of interest.

MR. GROSSMAN: Let's turn to the question of classification bias in the context of ETS studies. Clearly if non-smokers are classified as smokers or if smokers are classified as non-smokers, that could greatly skew the results of any ETS study. Is that correct?

DR. SAMET: I can't answer that without knowing what you mean by "greatly skew".

MR. GROSSMAN: Well, active smoking is a very substantial risk factor for lung cancer, is that correct?

DR. SAMET: Active smoking is a cause of lung cancer.

MR. GROSSMAN: And the risk ratio for active smoking for lung cancer is quite high, is that correct?

DR. SAMET: Quite high meaning?

MR. GROSSMAN: Well, you define it. What is the risk ratio for active smoking for lung cancer?

DR. SAMET: Depends on the amount smoked but in smokers that are two packs a day or more, the risks may rise as much as 40 times those of a never smoker.

MR. GROSSMAN: Over a period of how long?

DR. SAMET: A typical history that would bring somebody into late middle ages.

MR. GROSSMAN: Now, Doctor, assuming that your number is right, and that is the risk ratio that you have defined is correct, the classification of a smoker as a non-smoker would greatly affect the results of any attempt to compare the incidence of lung cancer in people who never smoked and were exposed to ETS and who never smoked and were not exposed to ETS, would it not?

DR. SAMET: I'm sorry. I'm just going to have to ask you to repeat that.

MR. GROSSMAN: Well, Doctor, if 10 percent, let's say, of the people in an ETS study who were classified as non-smokers and who had come down with lung cancer were in fact active smokers during their lives, that would significantly affect the results of the study, would it not?

DR. SAMET: It would affect the results of the study. I mean, since neither you nor I have defined the basis on which we're going to judge significance, I'm not sure what your use of the term means. It would be of concern, yes.

MR. GROSSMAN: And it would be a bias in the study, is that correct?

DR. SAMET: Presumably. You haven't described all the dimensions of disassociation but presumably.

MR. GROSSMAN: The EPA adjusted for smoker misclassification in its meta-analysis, did it not?

DR. SAMET: Correct.

MR. GROSSMAN: And it is commonly found that non-smokers -- I'm sorry. I'll start that again.

It is commonly found in studies that smokers, people with a history of active smoking, identify themselves in answers to questionnaires or to interviewers as lifetime never smokers. Is that correct?

DR. SAMET: I'm sorry. Some smokers may misclassify themselves. You said smokers.

MR. GROSSMAN: It is commonly found that some people who had a history of active smoking classify themselves as non-smokers in epidemiological studies.

DR. SAMET: And commonly found is how often?

MR. GROSSMAN: The literature reports ranges of three, five, 10 percent depending on the study involved.

DR. SAMET: I think it's important to interpret any such numbers in the context in which the question is asked and how it's asked. Such numbers are in the literature, yes.

MR. GROSSMAN: All right. Now, Doctor, where risk ratios are low, bias can play a greater role in skewing the results of a study than where risk ratios are high, is that correct?

DR. SAMET: I don't think you can make such simple, sweeping generalizations. I think that really depends on the agent of concern and what factors might introduce bias.

MR. GROSSMAN: Well, in the face of small and conflicting studies unidentified sources of bias should not be readily dismissed as an explanation for significant but modest elevations of risk. Is that correct?

DR. SAMET: Again, it would depend on the context and which exposure was being addressed.

MR. GROSSMAN: All right. Now, Doctor, you said earlier that the EPA adjusted for misclassification bias in its meta-analysis. Is that correct?

DR. SAMET: Correct.

MR. GROSSMAN: Are you aware of whether OSHA has adjusted for misclassification bias in its review of the literature on ETS in the workplace?

DR. SAMET: Well, I've read the OSHA review. I don't see a specific adjustment for misclassification there, if that's your question.

MR. GROSSMAN: Do you presume that they made such an adjustment, though?

DR. SAMET: I've made no such presumption.

MR. GROSSMAN: Okay. You're aware of the literature indicating that there is a range of typical misclassification of smokers as non-smokers in the epidemiological literature. You referred to that earlier.

DR. SAMET: Correct.

MR. GROSSMAN: And given the low risk ratios referred to in the ETS literature, unidentified sources of bias such as misclassification of smokers as non-smokers could account for significant elevations of risk, is that correct?

DR. SAMET: Is that -- one more time on that.

MR. GROSSMAN: Well, given the smaller risk ratios involved in ETS case control studies that report any risk ratios at all, sources of bias such as misclassification bias of smokers as non-smokers could account for significant elevations of risk, is that correct?

DR. SAMET: Well, I can't answer the question in your terms of significant elevation because I don't know what you mean quantitatively. Are such biases a concern? Yes.

MR. GROSSMAN: Do you recall writing an article entitled "Relationship Between Passive Exposure to Cigarette Smoke and Cancer" in 1985 published in Indoor Air and Human Health?

DR. SAMET: Yes, I do.

MR. GROSSMAN: At pages 236 to 237, you wrote, "These values," referring to values found in ETS studies, "are much lower than those associated with active smoking and could more readily be the consequence of bias. In the face of small and conflicting studies, unidentified sources of bias should not be readily dismissed as an explanation for significant but modest elevations of risk." You don't disagree with that statement that you made, do you?

DR. SAMET: Well, I cannot -- again, that statement as said there provides no quantitative dimensions on what I meant by significant and perhaps I had no particular quantitative definition in mind when that was written in 1984.

MR. GROSSMAN: But you don't disagree with it, do you? With what you wrote there, do you?

DR. SAMET: Well, again, I would only interpret that statement in the context of some bounds on what significant may be. Do I agree that bias always needs to be considered in interpreting data? Of course.

MR. GROSSMAN: Now, Doctor, let's turn for a moment to interview bias. Let's turn first to a work that was published this year. You said earlier that you were editor of Epidemiology of Lung Cancer published this year?

DR. SAMET: Correct.

MR. GROSSMAN: And one of the chapters of that is called "Passive Smoking and Lung Cancer"?

DR. SAMET: Correct.

MR. GROSSMAN: It was written by Glorian Pershagan, I hope I've pronounced that correctly

DR. SAMET: Well, you didn't but I know who you mean.

MR. GROSSMAN: And you edited that section?

DR. SAMET: Correct.

MR. GROSSMAN: And you reviewed it carefully, I'm sure?

DR. SAMET: Correct.

MR. GROSSMAN: Now, do you recall in the process of editing and publishing that volume the following passage: "Probably the most important potential source of bias in the epidemiological studies on ETS and lung cancer is confounding by unreported active smoking." Do you recall that?

DR. SAMET: Do I recall that sentence today? No.

MR. GROSSMAN: Do you disagree with it?

DR. SAMET: Well, I would disagree with using the word confounding in that sense in the true epidemiological sense.

MR. GROSSMAN: Pure bias rather than confounding?

DR. SAMET: Misclassification bias.

MR. GROSSMAN: It's misclassification bias. But apart from that you agree with it. So it is certainly a very important...

DR. SAMET: It's an important source. Sure.

MR. GROSSMAN: And further, in your edited work, it says, "There is a tendency for smokers to marry smokers and in conjunction with some misclassification of smokers as non-smokers, this would tend to produce a spurious association between spouse smoking and lung cancer." You agree with that, too, don't you?

DR. SAMET: That would depend on patterns of misclassification.

MR. GROSSMAN: It says further that "Using biological markers of nicotine exposure it has been indicated that up to 3 percent of subjects classifying themselves as non-smokers have levels consistent with regular smoking." Do you agree with that?

DR. SAMET: Such data have been reported in contexts other than the case control setting.

MR. GROSSMAN: All right. Let's turn for a moment to another kind of bias that you referred to which is interview bias. Do you recall that? Could you define for the record a little more precisely what you mean by interview bias?

DR. SAMET: Interview bias would refer to a bias introduced by the responses, patterns of response, to questions being differential, for example, in a case control study on case and control status.

MR. GROSSMAN: Now, if you were putting together a case control study on passive smoking and your interviewers -- and you were basing dose upon personal interviews, would you tell the interviewers whether the people they were interviewing had suffered from lung cancer or not?

DR. SAMET: I would not tell them directly. It's unfortunate that when you see people dying of lung cancer they are quite obvious.

MR. GROSSMAN: In certain cases but sometimes the controls may be people with other forms of cancer.

DR. SAMET: In some studies, that has been done.

MR. GROSSMAN: And let's refer to cases where the controls have other forms of cancer so the people being interviewed are suffering nonetheless. Would you tell the interviewers whether the people who are being interviewed had been diagnosed with primary lung cancer?

DR. SAMET: I would probably try to tell them simply that they were doing an interview.

MR. GROSSMAN: Because telling the interviewers that the individuals who they were interviewing suffered from lung cancer as opposed to another form of lung cancer could inject interview bias into the study, is that correct?

DR. SAMET: Yes and no. Possibly.

MR. GROSSMAN: It possibly could.

DR. SAMET: Possibly.

MR. GROSSMAN: And a better designed study would not tell the interviewers what disease the person being interviewed suffered from.

DR. SAMET: To minimize the potential for information bias, depending on what hypothesis are being addressed, that might be desirable.

MR. GROSSMAN: Also, there's a tendency both with people who have been diagnosed with lung cancer and with their next of kin to over-report exposure to ETS, isn't that correct?

DR. SAMET: I'm not aware that that's been demonstrated.

MR. GROSSMAN: Well, let me point you to an article that you wrote again called "Relationship Between Passive Exposure to Cigarette Smoke and Cancer" and I will quote from page 237. "Further validation of the questionnaire approach is needed with comparisons against biological markers and measured concentrations of tobacco smoke components. The reliability of questionnaire assessment of passive smoke exposure has not been established nor have sources of bias been evaluated. Further, interviews with next of kin may be particularly prone to information bias, almost certainly in the direction of over-reporting. In fact, as the public becomes increasingly aware of and sensitized to potential effects of passive smoking, the results of case control studies will become increasingly difficult to interpret." Do you recall writing that, Doctor?

DR. SAMET: I recall writing that but I did not, as I indicated earlier, provide data that supported what I offered as a concern for bias.

MR. GROSSMAN: So you're saying that you just write things off the top of your head and publish them in peer reviewed literature?

DR. SAMET: I didn't say that.

MR. GROSSMAN: Okay. I wanted to clarify that for you.

DR. SAMET: I said that I did not have data that showed the existence of such a bias and I expressed concern that such bias could arise.

MR. GROSSMAN: And that remains a concern, doesn't it?

DR. SAMET: I'm sorry?

MR. GROSSMAN: That remains a concern, doesn't it?

DR. SAMET: Bias is always a concern in epidemiology.

MR. GROSSMAN: And that particular form of bias remains a concern for ETS epidemiology, isn't it?

DR. SAMET: Information bias, again, is a concern.

MR. GROSSMAN: That particular form of information bias that you referred to in your article remains a concern.

DR. SAMET: It's one of several forms of bias that could affect information on ETS exposure.

MR. GROSSMAN: And thereby affect the validity of any results of any ETS case control study.

DR. SAMET: Such bias would need to be considered in interpreting the data.

MR. GROSSMAN: Now, Doctor, a third form of bias that you referred to was confounders when we were speaking a few moments ago. Do you recall that?

DR. SAMET: Yes.

MR. GROSSMAN: All right. And in confounders, one factor being studied may actually only be a surrogate for another factor or exposure that is related in incidence to the fact being studied. For example, active smokers, and we've gone over this earlier in these hearings, active smokers are far more likely to suffer from cirrhosis of the liver and there is in fact a dose response relationship that's been demonstrated in the literature, it's also been demonstrated in the literature that that's a spurious association because in fact active smokers are also often -- heavy smokers are often heavy drinkers as well. You're familiar with that kind of confounder and that's what you're referring to when you refer to confounders, is that correct?

DR. SAMET: Well, I gave a definition of confounding.

MR. GROSSMAN: All right. Now, in a well designed case control study, confounders are controlled for to the extent possible, is that correct?

DR. SAMET: Correct.

MR. GROSSMAN: There's a need to design the study so that it doesn't include an excess number of people who are at risk from sources other than those being studied. Is that correct?

DR. SAMET: You're getting into subtleties of design that simple generalizations are not possible.

MR. GROSSMAN: Let's talk for a moment about some of the established confounders, and that is established things that according to the literature have been shown to have an association with lung cancer apart from cigarette exposure. There is a significant body of literature indicating that dietary vitamins may have a protective effect for lung cancer, is that correct?

DR. SAMET: There is a substantial body of experimental and other investigation that suggests that some vitamins may have a role in determining lung cancer risk. Correct.

MR. GROSSMAN: In fact, people who have diets high in beta carotene and certain other vitamins and who are never smokers or former smokers may have half or less the risk of lung cancer of people who do not have a diet rich in beta carotene and certain other vitamins. Is that correct?

DR. SAMET: We have relatively limited information on diet and lung cancer risk for never smokers and relatively little on former smokers. There are, again, some studies indicating -- I've had to sort out some for former smokers that the risk may be lower with those for diets estimated to be higher in beta carotene, for example.

MR. GROSSMAN: Well, in your own volume published this year you referred -- Marcel Dekker, I'm sorry, he's the publishers. Tim Byers in the section entitled "Diet as a Factor in the Etiology and Prevention of Lung Cancer" said that there were 27 case controlled studies of lung cancer which uniformly found evidence of the protective effect of dietary vitamin A and/or carotene. Do you recall that?

DR. SAMET: I recall the chapter, yes.

MR. GROSSMAN: And considered together these 27 studies indicate that there is roughly a 50 to 100 percent increase in lung cancer in persons below the 25th percentile of carotene intake as compared with those above the 75th percentile. Do you recall that?

DR. SAMET: Do I recall that specific statement today? No. Do I recall that chapter and that conclusion? Certainly.

MR. GROSSMAN: And you have no reason to disagree with that conclusion, do you?

DR. SAMET: Well, I think the qualification on that conclusion is that most of our evidence on diet and lung cancer comes from studying people who have actively smoked and we have relatively few studies that provide information on people who have not smoked.

MR. GROSSMAN: Didn't that study say that the effect of beta carotene and vitamin...

JUDGE VITTONE: Mr. Grossman, we're coming up a little past the hour here. How much longer do you think you will be?

MR. GROSSMAN: I probably have another 20 minutes, Your Honor.

JUDGE VITTONE: Twenty minutes?

MR. GROSSMAN: Yes.

JUDGE VITTONE: We've gone for an hour and five right now.

MR. GROSSMAN: Well, I believe I'm entitled to two hours. This is taking longer than I anticipated with constant restatements of questions. I'm moving as quickly as I can.

JUDGE VITTONE: I think the answers have been fairly direct and responsive.

MR. GROSSMAN: I'm not complaining about the answers. It's just that it's taken longer to...

JUDGE VITTONE: All right. I would appreciate it if you could...

MR. GROSSMAN: I'm moving as fast as I can.

JUDGE VITTONE: Okay.

MR. GROSSMAN: Doctor, in fact, the article that is in your edited work says that the effect of dietary beta carotene and vitamin A may be lower for active smokers than for others, doesn't it?

DR. SAMET: I believe -- and, again, I'd have to see the article in context, that the principal evidence we have was stratification comparing current and former smokers. Again, because of the dearth of information on never smokers.

MR. GROSSMAN: Now, Doctor, there's also a good deal of information on the effect of dietary fat on cancer available in the epidemiological literature. Is that correct?

DR. SAMET: There are studies of dietary fat intake.

MR. GROSSMAN: Both case control studies and studies comparing different populations across the world with different dietary habits?

DR. SAMET: Correct.

MR. GROSSMAN: Now, are you familiar with the works of Ernst Wynder?

DR. SAMET: Yes.

MR. GROSSMAN: He's certainly no friend of the tobacco industry, I think it's fair to say, isn't it, Doctor?

DR. SAMET: I can't answer that.

MR. GROSSMAN: Well, in the fifties, wasn't he the first researcher to do mouse skin painting and to publish extensively on...

DR. SAMET: I'm aware of Dr. Wynder's work. I don't know if he was the first mouse skin painter or not.

MR. GROSSMAN: Now, Dr. Wynder has published works comparing incidence of lung cancer with dietary fat intake. Are you familiar with those?

DR. SAMET: Only in a peripheral way.

MR. GROSSMAN: Do you receive or generally review the Journal of the National Cancer Institute?

DR. SAMET: I receive it.

MR. GROSSMAN: Are you a subscriber?

DR. SAMET: Yes.

MR. GROSSMAN: Doctor, in Volume 79, No. 4, of the Journal of the National Cancer Institute at page 631, Dr. Wynder, along with James Herbert and Jeffrey Kabat wrote an article called "Association of Dietary Fat and Lung Cancer". In that article, he compared incidence of lung cancer in countries throughout the world with tobacco consumption and with fat consumption and he said the following, or the authors, all three, said the following at page 635: "An interesting observation of this study is that fat calories are more strongly associated with male lung cancer mortality than are tobacco disappearance data." Are you familiar with the study by Dr. Wynder that contains that finding?

DR. SAMET: Actually, I am not. I suspect -- what year is that study?

MR. GROSSMAN: That was 1987 and it's been followed by Dr. Wynder with further studies on the same subject.

DR. SAMET: That particular report I don't know.

MR. GROSSMAN: You are familiar with incidence of lung disease in various countries of the world as part of your studies?

DR. SAMET: Certainly to an extent.

MR. GROSSMAN: You know that the highest level of male smoking in the world is in Japan? As generally reported.

DR. SAMET: Japanese men have a very high rate of active smoking.

MR. GROSSMAN: And there's more active smoking than in the United States in France and Spain and Israel?

DR. SAMET: I'm sorry, there's...

MR. GROSSMAN: France, Spain and Israel all have more active smoking by men than the United States?

DR. SAMET: I don't have the data at my fingertips.

MR. GROSSMAN: You are familiar with Japan, though, and you're familiar that the rates of lung cancer in Japan are far lower than the United States?

DR. SAMET: Yes.

MR. GROSSMAN: And it's been postulated that the reason that lung cancer is far lower in Japan than the United States even though incidence of active smoking is much higher is because of difference in diet?

DR. SAMET: I'm aware that people have postulated that.

MR. GROSSMAN: You have no reason to disagree with that?

DR. SAMET: It's a postulate.

MR. GROSSMAN: It's a postulate that you neither accept nor reject?

DR. SAMET: It would need to be tested.

MR. GROSSMAN: Are you familiar with an epidemiologist named Alvania?

DR. SAMET: Yes, I am.

MR. GROSSMAN: Similarly with Ross Brownson?

DR. SAMET: I'm sorry?

MR. GROSSMAN: Ross Brownson?

DR. SAMET: I know who he is. Yes.

MR. GROSSMAN: And Charles Brown and Christine Swanson, do you know their names as well?

DR. SAMET: Charles Brown I do.

MR. GROSSMAN: Now, Dr. Alvania along with Drs. Brown, Swanson and Brownson, wrote an article in the Journal of the National Cancer Institute, Volume 85, No. 23, December 1, 1993, entitled "Saturated Fat Intake and Lung Cancer Risk Among Non-Smoking Women in Missouri." Are you familiar with that study or the results of it?

DR. SAMET: Yes, I am.

MR. GROSSMAN: Do you recall, Doctor, that in that study of over 600 women in Missouri who were lifetime never smokers and who had been diagnosed with lung cancer it was found that for the highest quintal of fat consumption a risk ratio or an observed ratio for lung cancer, for adenocarcinoma of the lung, was found to be 11.38?

DR. SAMET: Well, I have the article in front of me.

MR. GROSSMAN: All right. Let me point your attention to page 1911.

JUDGE VITTONE: Do you have it, Doctor?

DR. SAMET: Yes, I do. I have that in front of me.

MR. GROSSMAN: All right. Do you se the chart at the top of the page?

DR. SAMET: Yes, I do.

MR. GROSSMAN: And that chart reports observed ratios between saturated fat intake and incidence of adenocarcinoma in lifetime never smokers.

DR. SAMET: No. Where do you come up with lifetime never smokers?

MR. GROSSMAN: The entire article is on lifetime never smokers, isn't it?

DR. SAMET: No. That's a misinterpretation. The article includes a number of long-term former smokers as well. And if you read the footnote to the table, there is an adjustment made for smoking history.

MR. GROSSMAN: All right. Lifetime never smokers and former smokers but it was adjusted for smoking history?

DR. SAMET: Yes. And the number of subjects in the study, I believe you stated 600 and something. It was actually 429 case subjects. I believe we have the same paper.

MR. GROSSMAN: Yes. Of the 429 reported on this column...

DR. SAMET: I'm sorry?

MR. GROSSMAN: Of the 429 reported on this chart on page 1911, 211 are cases of adenocarcinoma?

DR. SAMET: Correct.

MR. GROSSMAN: And 218 are other or unknown cell types of lung cancer?

DR. SAMET: Correct.

MR. GROSSMAN: Now, with regard to the adenocarcinoma cases, after controlling for smoking history and for various other factors including previous lung disease, total calories, interview type and other variables, it was found that the risk ratio for the highest quintal of lifetime history of eating saturated fat was 11.38 for later development of lung cancer.

DR. SAMET: For adenocarcinoma. Correct.

MR. GROSSMAN: And for other types of lung cancer, the reported risk ratio was 3.36?

DR. SAMET: In that quintal.

MR. GROSSMAN: In that quintal. The risk ratio for people with a lifetime history of eating saturated fat at the level of the highest quintal was 11.38 times as likely as the people in the lowest quintal to develop lung cancer?

DR. SAMET: Well, I'm not sure I understand your point...

MR. GROSSMAN: This refers to an increased risk of 11.38.

DR. SAMET: Increased risk. Correct.

MR. GROSSMAN: Eleven point 38 times...

DR. SAMET: The risk of those...

MR. GROSSMAN: Okay. Now, there's never been a reported case control study that you know of that has ever found any risk ratio in that neighborhood for ETS, is that correct?

DR. SAMET: That's correct.

MR. GROSSMAN: So if there were a failure to control for dietary fat intake in an ETS study, that could be an important confounder, is that correct?

DR. SAMET: No, that's not correct. I said a confounder was a cause of the disease. You've shown me one report that shows that dietary fat consumption is associated with lung cancer risk. That is different from making dietary fat a confounder. I said again a confounder is a cause of the disease in its own right whose effect is mingled with that of the agent of interest. And I don't yet identify dietary fat intake, high dietary fat intake, as a cause of lung cancer.

MR. GROSSMAN: When you say you do not yet identify it, are you saying that you do not know whether or not it is a cause by itself of lung cancer?

DR. SAMET: I don't think we have sufficient information.

MR. GROSSMAN: You certainly do not have sufficient information to reject dietary fat intake as a cause of lung cancer, do you?

DR. SAMET: I don't think that's the scientific method, to reject...

MR. GROSSMAN: There is evidence such as the Alvania study upon which a hypothesis could be drawn that dietary fat intake is a causative factor in lung cancer, is there not?

DR. SAMET: You can draw a hypothesis.

MR. GROSSMAN: And there is strong epidemiological evidence, both in cross country studies and in research such as Dr. Alvania's, to support a strong relationship between dietary fat intake and incidence of adenocarcinoma, isn't that correct?

DR. SAMET: I don't think any of the international evidence you mentioned -- again, I'm not familiar with it, is specific for adenocarcinoma.

MR. GROSSMAN: Well, for lung cancer generally.

DR. SAMET: Well, again, I think from what you've described, and I would have to look at the article you've mentioned from 1987, you've described an ecological study which is a useful way for developing -- a useful set of information for developing hypotheses needing further evaluation. And now a hypothesis was apparently advanced in this 1987 article and we're both looking at some data that are supportive of that hypothesis from one study.

MR. GROSSMAN: All right. You have written yourself on a variety of occupational exposures that may be causes of lung cancer, have you not?

DR. SAMET: Correct.

MR. GROSSMAN: And you are aware of literature by others indicating that there are a number of occupational exposures that may cause lung cancer, is that correct?

DR. SAMET: That do and may. Yes.

MR. GROSSMAN: And the list of occupations that have been found to be associated with later development of lung cancer after controlling for smoking include everything from welding to masons to tile setters to janitors and cleaners, to printing workers, to truckers, trucking service people, warehousers and others. Is that correct?

DR. SAMET: It's likely that all such occupations have been mentioned in the literature. Again, I can't answer for each one of those.

MR. GROSSMAN: Your own literature indicates observed risks, increased risks for lung cancer in welders and miners and painters and several others, does it not?

DR. SAMET: Can you tell me what you're referring to?

MR. GROSSMAN: Yes. "Lung Cancer and Occupation in New Mexico," published in the Journal of the National Cancer Institute, Volume 79, No. 4.

DR. SAMET: You're describing the findings in our control study?

MR. GROSSMAN: Yes. And you're one of the authors along with Mary Merchant and Charles Williams.

DR. SAMET: Correct.

MR. GROSSMAN: Now, Doctor, occupational exposures would be an important confounder in lung cancer research and ETS, would it not?

DR. SAMET: No.

MR. GROSSMAN: Why not?

DR. SAMET: Well, I doubt, again, that occupational exposures would have been so prevalent among the women primarily who were included in most of the case controls...

MR. GROSSMAN: I'm not asking about the ETS study, I'm talking now about studies on lung cancer arising from ETS in the workplace.

DR. SAMET: Confounding by such agents would be a potential concern. It would depend on what the exposure patterns were.

MR. GROSSMAN: Now, Doctor, a personal history of respiratory disease has been found to be a potential causative agent of subsequent development of lung cancer, is that not correct?

DR. SAMET: There are a number of studies, including our own, that indicate that certain underlying respiratory conditions are associated with increased risk of lung cancer.

MR. GROSSMAN: Among those would be prior history of tuberculosis or of histoplasmosis or other fungal disease?

DR. SAMET: There is some concern that fibrotic disorders in general may be associated with increased lung cancer risk.

MR. GROSSMAN: And there is concern that fibrotic diseases in general may be associated with development of lung cancer in people who have never smoked.

DR. SAMET: Well, possibly.

MR. GROSSMAN: And similarly there are other respiratory diseases that have been found to be directly related to subsequent development of lung cancer, is that correct?

DR. SAMET: Which diseases?

MR. GROSSMAN: One would be COPD.

DR. SAMET: Persons who have underlying chronic obstructive pulmonary disease do seem to be at increased risk, even given the level of tobacco smoking.

MR. GROSSMAN: And persons who have a family history of lung cancer are at an increased risk of lung cancer, whether or not they smoke, isn't that correct?

DR. SAMET: The literature that I am familiar with on family history is, I think, largely limited to smokers. And, yes, there are -- those with family history are at increased risk.

MR. GROSSMAN: Even after controlling for smoking, those with family histories, particularly parental histories, of lung cancer are at substantially increased risks for lung cancer, isn't that correct?

DR. SAMET: Well, after controlling for smoking in the studies, which again have been almost largely on smokers with lung cancer, a family history has been associated with increased risk.

MR. GROSSMAN: Now, one factor that should be controlled for in a well designed case controlled study on lung cancer should be family history of lung cancer, should it not?

DR. SAMET: I mean, again, it would really depend on how the study was undertaken and what the concern was. I mean, if you're suggesting that family history of lung cancer confounds any study, remember I described a confounder as a factor that is a cause of lung cancer or another disease and its effect is mingled with that of the exposure of interest. That arises -- the confounding arises because of associations in the data. So every factor is not necessarily a confounder in a given study.

MR. GROSSMAN: It may or may not be.

DR. SAMET: It may or may not be.

MR. GROSSMAN: Now, you're familiar with various literature on the almost epidemic of adenocarcinoma in certain areas of China, are you not?

DR. SAMET: I am aware of some of the data on adenocarcinoma in China, not in depth.

MR. GROSSMAN: And you are aware of various case studies indicating that a lifetime of cooking Chinese food can greatly increase risks of adenocarcinoma in non-smokers?

DR. SAMET: I'm aware of case control studies from China showing such associations.

MR. GROSSMAN: For example, you're aware of the study by Lu, I believe a famous study by Lu, published in 1991 showing that the risk ratio for women who cooked Chinese food for 45 years or more was 14.7 for adenocarcinoma?

DR. SAMET: Let me look through my stack here.

MR. GROSSMAN: All right.

(Pause.)

DR. SAMET: It's in my hand.

MR. GROSSMAN: All right. If you'll look on the table, Doctor, I believe it shows the risk ratio for people who cooked Chinese food for less than 30 years as one. For a period of 30 to 45 years as 9.18 and cooked Chinese food for a period in excess of 45 years as 14.7.

DR. SAMET: I have that in front of me.

MR. GROSSMAN: All right. That indicates a very substantial risk from a lifetime of cooking Chinese food?

DR. SAMET: Those are high risks.

MR. GROSSMAN: Now, if a case control study were designed in which the people found to have lung cancer were first generation Chinese women and the people who did not have lung cancer did not include a similar number of first generation Chinese women, the high incidence of adenocarcinoma in non-smoking Chinese women would have to be considered, is that correct?

DR. SAMET: By first generation you are meaning immigrants?

MR. GROSSMAN: I mean immigrants.

DR. SAMET: Immigrants. It would be a factor to consider.

MR. GROSSMAN: Yes. It would be a poorly designed study if it included immigrant Chinese women in the diseased group but not in the control group in similar numbers, is that correct?

DR. SAMET: Well, it would be one of the factors. I'm not sure I like the word poor design but it would certainly be one of the factors that you would want to consider.

MR. GROSSMAN: It would be a substantial confounder.

DR. SAMET: Again, it would depend on patterns in the data so I can't answer that but certainly a potential confounder.

MR. GROSSMAN: Now, Doctor, there are certain hot spots for cancer in the United States. You're familiar with studies on that, aren't you?

DR. SAMET: I have some familiarity with the geographic distribution of cancer in the U.S.

JUDGE VITTONE: Excuse me, Mr. Grossman.

MR. GROSSMAN: I've got probably about five minutes now, Your Honor.

JUDGE VITTONE: That would be fine.

MR. GROSSMAN: Five to ten.

You're familiar with geographic distribution in the United States to a certain extent. One clear cancer hot spot for lung cancer is southern Louisiana, is that correct?

DR. SAMET: That's been historically true. Correct.

MR. GROSSMAN: Historically, the New Orleans to Baton Rouge corridor is one of the great lung cancer hot spots of the United States, correct?

DR. SAMET: I'm almost tempted to ask you to define a great lung cancer hot spot but I won't. The rate's a bit high in that area.

MR. GROSSMAN: Similarly, the Beaumont-Houston area of Texas has been a lung cancer hot spot, as defined in the literature, is that correct?

DR. SAMET: Rates of lung cancer have been high in Harris County.

MR. GROSSMAN: And the Oakland-San Francisco area has been a cancer hot spot in the literature, is that correct?

DR. SAMET: I think so.

MR. GROSSMAN: The Long Beach, California area has been a hot spot for lung cancer, is that correct?

DR. SAMET: I don't know.

MR. GROSSMAN: All right. Now, many of these lung cancer hot spots have arisen irrespective of the underlying degree of smoking in those areas, isn't that correct?

DR. SAMET: That's -- I think -- you'll have to help me with what you're after here.

MR. GROSSMAN: Okay. Let me help you, then. As reported in the morbidity and mortality weekly report of the Massachusetts Medical Society, that's the New England Journal of Medicine publisher, August 19, 1989 and I think similar studies are available elsewhere, Louisiana is a state with a fairly low smoking rate, it's below the median smoking rate in the United States, lower consumption per capita than the average consumption per capita of cigarettes in the United States. I will just represent that to you. And as reported in the same publication on July 28, 1989, in a table prepared by the Center for Disease Control, Louisiana ranks forty-fourth in COPD in the United States. Now, COPD is very closely tied epidemiologically with cigarette smoking, is that correct? Active cigarette smoking.

DR. SAMET: Active cigarette smoking causes COPD.

MR. GROSSMAN: And, in fact, the association between active cigarette smoking and COPD is one of the best described in the literature, is that correct?

DR. SAMET: It's well documented.

MR. GROSSMAN: If COPD were low in Louisiana, it would tend to further reinforce the figures showing that actual consumption of cigarettes were low in Louisiana, would it not?

DR. SAMET: Consistent, yes.

MR. GROSSMAN: Now, the same publication shows not only that Louisiana was forty-fourth in COPD but that it was fifth in lung cancer in the United States. That tends to indicate that there are factors present in Louisiana apart from cigarette smoking that account for a particularly high lung cancer incidence. Is that correct?

DR. SAMET: That's certainly one interpretation of those data.

MR. GROSSMAN: One of the factors that has been postulated is because of the presence of the petrochemical industry in high concentration in the Baton Rouge to New Orleans corridor, is that correct?

DR. SAMET: I am not aware of that.

MR. GROSSMAN: All right. A similar postulate has been made for Oakland, California and Harris County, Texas, which are other areas of high petrochemical industry concentration. Are you familiar with those?

DR. SAMET: I'm familiar with the studies that have been published from Harris County.

MR. GROSSMAN: Now, a well designed epidemiological study attempting to compare incidence of lung cancer among those who were exposed to ETS and those who were not exposed to ETS and attempting to replicate the workplace in the United States as a whole would be based upon a variety of sources that included both cancer hot spots and non-cancer hot spots, Doctor?

DR. SAMET: I'm sorry. Would you repeat that?

MR. GROSSMAN: I'll rephrase the question.

There is reason to believe that there may be one or a variety of factors present in Louisiana and other cancer hot spots apart from cigarette smoking that have given rise to particularly high rates of lung cancer. You acknowledged that a moment ago.

DR. SAMET: You've said that some people have postulated that. That's true certainly.

MR. GROSSMAN: And you have no reason to disagree with that.

DR. SAMET: No.

MR. GROSSMAN: Now, if you were attempting to determine the risk of lung cancer from ETS in the workplace in the United States, would you base your study primarily upon areas in which lung cancer incidence was high and smoking consumption was low?

DR. SAMET: I think the question really would be would other factors in a sense modify the risks of workplace exposure, in this case, the agent of concern.

MR. GROSSMAN: There is a likelihood of more confounders in areas where there is low smoking and high lung cancer incidence than in areas where lung cancer incidence and smoking are both within the norms established in the rest of the country, is that correct?

DR. SAMET: I can't agree with that as you've stated it. Again, we'd have to go back to what a confounder is and I've said that it's a cause of a disease in its own right and in the data at hand associated with exposure of concern. Confounding, as I've said, is always of concern. If there is a potential set of causal factors know, then one would want to consider whether there would be a greater risk of having confounding in a particular study.

MR. GROSSMAN: And if there were a set of potential causing factors known, those factors should either be controlled for or the study should be set up to avoid those additional causative factors?

DR. SAMET: Well, the existence of a potential confounder does not mean that a study is confounded.

MR. GROSSMAN: Well, where observed risks are low, the presence of confounders are more likely to affect the significance of the results presented, is that correct?

DR. SAMET: Well, if you mean statistical significance, the answer is no. Do you mean significance in some other context?

MR. GROSSMAN: I mean in another context.

DR. SAMET: Which is?

MR. GROSSMAN: If the observed risk is low, then the presence of confounders that are uncontrolled for may vitiate the small risk that has been found.

DR. SAMET: Again, I'm not sure what you mean by vitiate but if there is confounding in the data and the risks of the confounders -- let me back up. If there is confounding in the data, of course you want to consider the contribution of confounding to bias and the potential bias and the effect that's been observed.

MR. GROSSMAN: And the lower the observed risk the greater role that confounders and other biases may play in creating that risk. Is that correct?

DR. SAMET: Well, again, the potential for bias as an alternative explanation for an association increases as the level of observed risk declines, depending on the constellation of confounders.

JUDGE VITTONE: Mr. Grossman, wrap it up now, please.

MR. GROSSMAN: I'll just sum up, Your Honor, if I may.

Doctor, I notice in your studies that you were careful not to draw conclusions from any one study but you tend to review many studies before you draw conclusions. Is that correct?

DR. SAMET: Well, I think when I look at scientific evidence on a particular association, I would like to understand the biological evidence and the epidemiological evidence.

MR. GROSSMAN: And you don't look to a single epidemiological case study in order to make a determination of risk ratio or of causation, is that correct?

DR. SAMET: I would not look to a single epidemiological study to make a determination as to causality.

MR. GROSSMAN: And you wouldn't look to a single epidemiological study to make a determination of risk ratio either, would you?

DR. SAMET: I guess it would really depend on the context and the purpose for which I was doing that.

MR. GROSSMAN: If there were many studies available in the epidemiological literature that attempted to determine a risk ratio for exposure to a given substance, you would look at all of those studies before attempting to derive a risk ratio, would you not?

DR. SAMET: Well, I would consider all the evidence and perhaps use some sort of quantitative technique to summarize it.

MR. GROSSMAN: A quantitative technique such as meta-analysis?

DR. SAMET: Such as. Yes.

MR. GROSSMAN: Thank you very much, Doctor.

JUDGE VITTONE: Let's take a short recess, five minutes.

JUDGE VITTONE: Mr. Sirridge?

MR. SIRRIDGE: Thank you, Your Honor.

I am Pat Sirridge, appearing for the same members as yesterday.

Good afternoon, Dr. Samet.

I'd like to spend a few moments, Dr. Samet, talking about the epidemiologic studies dealing with the relationship between environmental tobacco smoke and heart disease.

What is your recollection of the approximate number of studies?

DR. SAMET: Eight, nine, 10 now.

MR. SIRRIDGE: Say 10 or 11?

DR. SAMET: Yes. I would like to look the number up before I give an answer but it's in that range.

MR. SIRRIDGE: All right. It's 10 or 11. You reviewed those studies before you wrote your 1992 article that was in Littman's book, Environmental Toxicants?

DR. SAMET: I reviewed the studies available through approximately 1991.

MR. SIRRIDGE: And the relative risks ranged from, say, below one to almost three in those studies, isn't that true?

DR. SAMET: I don't have the table in front of me but I assume that you've accurately counted that.

MR. SIRRIDGE: And there were reviews that have been published about that time which estimated the overall risk or the average risk at approximately 1.3, is that correct?

DR. SAMET: Can you tell me which reviews you're referring to?

MR. SIRRIDGE: Well, Glantz and Parmley. There were several reviews that tended to...

DR. SAMET: I'm aware of reviews that offered risk estimates and I don't remember the specific numbers.

MR. SIRRIDGE: All right. Do you recall that most of the studies did not report statistically significant increased risks?

DR. SAMET: I don't know about most. I'm aware that some of them did. Yes.

MR. SIRRIDGE: And many of the studies involved small numbers of deaths and different disease end points, isn't that true?

DR. SAMET: Correct.

MR. SIRRIDGE: As an epidemiologist, Dr. Samet, you are obviously interested in how good epidemiologic studies are from a methodologic point of view, isn't that true? Wouldn't that be one of your interests?

DR. SAMET: Well, I'm interested in the methodology of epidemiology.

MR. SIRRIDGE: Yes. And you would be interested in what kind of study population was being looked at and whether that study population was representative or not. Would that be something that you would be interested in studying and observing? You'd want to focus on the study population and make your own determination as to whether it was a representative study population, true?

DR. SAMET: Relative representativity is a matter of what we refer to as the external validity of a study, to whom can the results be generalized. So representativeness may be important for some purposes and not for others.

MR. SIRRIDGE: But it's one of the things that epidemiologists would look at in a study, who the population was.

DR. SAMET: In terms of the findings, certainly. Sure.

MR. SIRRIDGE: And you would want to know whether sufficient data in the case of a coronary heart disease study, you would want to know whether sufficient data had been collected on other risk factors of the study population, true? Besides -- let's just focus in on ETS. If it were an ETS coronary heart disease study, you would be interested to see what other data on cardiovascular risk factors was collected and analyzed, isn't that true?

DR. SAMET: Correct.

MR. SIRRIDGE: And you would want to be certain that the proper analyses were done to rule out potential confounding factors, true?

DR. SAMET: Well, one does not rule out potential confounding factors but one would want to understand the potential role of confounding in the data.

MR. SIRRIDGE: And just be able to identify the existence of potential confounding factors. That would be one of the things you would want to try do to. You would want to see if the authors were at least thinking about potential confounding factors.

DR. SAMET: Confounding is always an issue in interpretation of the data.

MR. SIRRIDGE: Right. And in an ETS study, of course, you would be interested in what their measurement or estimate of exposure was, true?

DR. SAMET: True.

MR. SIRRIDGE: And you would, of course, want to know who the control groups were and whether the exposed groups were classified properly, put into the right categories of exposure, true? That would be another thing that would be important.

DR. SAMET: I would be interested in the quality of the exposure information. Sure.

MR. SIRRIDGE: And I take it, Doctor, you would be especially interested in whether the relative risks reported were reliable in your own opinion, true?

DR. SAMET: I don't use the word reliable as I interpret relative risk. That means repeatable. So that's not a term I would apply to interpretation of a relative risk value per se.

MR. SIRRIDGE: Well, you would certainly focus in on the relative risks reported and try to make a determination in your own mind as to whether that was an accurate or reasonable or explainable relative risk given the dimensions of the study. I don't want to get hung up on reliable, I'm just saying...

DR. SAMET: You used the word accurate, reasonable and explainable, I think, when you...

MR. SIRRIDGE: I don't want to get hung up on certain words.

DR. SAMET: Certainly I would look at what the relative risk value was.

MR. SIRRIDGE: You would look at the relative risk and try to say to yourself does that make sense and is that a real risk or a real association.

DR. SAMET: Again, I would not use a term like real association but I would consider all factors relevant to that particular study in interpreting the relative risk estimate.

MR. SIRRIDGE: And if there was a positive association, wouldn't your interest as an epidemiologist lead you to wonder whether that association was a real association or a true association?

DR. SAMET: Well, I think I would interpret any relative risk value, whether apparently near the null, positive or negative in light of all dimensions of the study. So not only so-called positive results would draw my attention.

MR. SIRRIDGE: And in a study involving heart disease, coronary heart disease, whichever abbreviation you want to use, because of your experience with epidemiology and issues like confounding, in a study of heart disease, you would be concerned about the presence and potential effect of confounding factors.

DR. SAMET: Correct.

MR. SIRRIDGE: With respect to heart disease and its relationship with ETS, Doctor, in conjunction with your 1992 article, you gave some thought to the issue of whether the relative risks reported in those studies fit with current epidemiologic information with respect to the risks of active smoking in coronary heart disease. Do you recall just writing about that particular issue? In other words, how do the risks compare with one another?

DR. SAMET: I recall writing about that.

MR. SIRRIDGE: Do you have that article? Your 1992 article?

DR. SAMET: No, I don't.

MR. SIRRIDGE: Would you like to see it, because I'm going to...

DR. SAMET: Certainly.

(Pause.)

MR. SIRRIDGE: Doctor, I'm going to call your attention to page 253, probably not a great copy, about three-quarters of the way down, a paragraph begins "The emerging evidence"?

DR. SAMET: Yes.

MR. SIRRIDGE: Would you go down about five lines there of that paragraph and where it reads, "The extent of the excess risk associated with passive smoking seems high in view of the relative risks observed in active smokers, approximately two-fold increases." And you cite the U.S. Department of Health and Human Services '83. "This apparent inconsistency in the evidence on passive smoking and heart disease warrants further research." When you said at that time, Doctor, that the relative risks that were reported in those studies which you reviewed for this article were too high in your opinion in comparison with those which had been reported for active smoking and coronary heart disease.

DR. SAMET: Well, it's not for me to judge if they were too high but I was commenting on the fact that they seemed high in relationship to those observed in active smokers where presumably the dose of responsible agents was much higher than for those exposed passively.

MR. SIRRIDGE: Doctor, you would agree that heart disease is a multi-factorial disease?

DR. SAMET: Yes.

MR. SIRRIDGE: And the risk factors discussed at the hearings yesterday for heart disease included the following: age, sex, family history for heart disease, diabetes, high cholesterol, that's both total and high density lipoprotein cholesterol, hypertension, obesity, type A behavior pattern, physical inactivity and/or lack of exercise. Would you want to add any risk factors to that list based on your experience?

DR. SAMET: Well, I'm not a cardiologist nor am I cardiovascular epidemiologist. This is certainly a listing of the usual risk factors for coronary artery disease.

MR. SIRRIDGE: We discussed briefly coffee drinking yesterday as a risk factor for heart disease. Are you aware that coffee drinking has been associated with heart disease?

DR. SAMET: I'm aware that there have been many studies on that association. Yes.

MR. SIRRIDGE: Would you agree that a well designed epidemiologic study on heart disease would try to collect data on as many of these factors as possible?

DR. SAMET: Well, I think first it's important to find out that simply no study is perfect and studies are often done with constraining circumstances and what one would like to do or can do is constrained by reality. If someone gave me an infinite budget and asked me to design a study, of course I would like to consider every factor that's relevant to the outcome of interest.

MR. SIRRIDGE: But in this case, if you have a heart disease study, you would certainly try to collect as much as the budget allowed, as much as the circumstances allowed, of other known risk factors for heart disease, true?

DR. SAMET: If I was setting out on such a study prospectively.

MR. SIRRIDGE: Yes. Doctor, do you recall offhand how many of the coronary heart disease risk factors that we just mentioned were handled in terms of collecting data on those in those ETS and heart disease studies?

DR. SAMET: No.

MR. SIRRIDGE: Would it surprise you to learn that on the average the studies collected data on approximately four of those factors out of about ten?

DR. SAMET: I'm not surprised.

MR. SIRRIDGE: Does that sound consistent with your remberance of the studies?

DR. SAMET: Well, I'm aware that these studies were conducted some using data resources assembled for other purposes and the ideal that we discussed was probably not possible. And, again, as I said, no study is necessarily perfect. Yes.

MR. SIRRIDGE: Now, as an epidemiologist, I was listening to your answers to Mr. Grossman's questions, the issue of confounding was discussed at length and obviously you are interested in the risk factor or risk factor casual factor as part of the confounding issue and you would also be very interested in, of course, the other part of the confounding issue, whether it's related to the issue of exposure or whatever you're studying in the study, correct?

DR. SAMET: Correct.

MR. SIRRIDGE: So it's really a two-fold thing. So in our case here, you would want to be interested whether the confounding factors or risk factors were associated with heart disease, I'm talking about ETS, you would be interested in whether they were associated with heart disease and you would be also interested in how they would be compared between the people who were exposed to ETS and those who were not exposed. Is that true?

DR. SAMET: Yes.

MR. SIRRIDGE: It's your remberance that the studies on ETS and CHD involve exposure to ETS in the home rather than in the workplace?

DR. SAMET: Again, my recollection of these, predominantly, perhaps exclusively, were of home exposure but I don't have all the studies in front of me. I can't attest to that with full certainty.

MR. SIRRIDGE: I understand. In looking at the risk factors that we just mentioned a second ago, Doctor, would you agree that we probably would not be too concerned with age, sex, family history of coronary heart disease and diabetes as potential confounding factors?

DR. SAMET: I can't give a general answer to that question. Confounding is a matter of individual studies.

MR. SIRRIDGE: But would there be -- some of those ten factors that you would be more concerned with from a confounding point of view -- I mean, there's not much you can do about age and diabetes. For example, there's no real evidence that diabetes would be more common in people exposed to ETS versus people not exposed, would there?

DR. SAMET: A priori, I have no reason to think that.

MR. SIRRIDGE: Okay. All I'm trying to do is zero in on the factors which might be potential confounding factors but let's approach it this way. Some of the factors we talked about that might rise to the level of being potential confounding factors would be high cholesterol, hypertension, obesity, lack of physical exercise or inactivity. Would those be the kinds of things in a heart disease study involving ETS that would be potential confounding factors?

DR. SAMET: A simple answer, yes. And, again, it would depend on the study at hand.

MR. SIRRIDGE: And would type A behavior and coffee drinking, would those be potential confounding factors?

DR. SAMET: I'd have to say that those are both very difficult areas of literature which I don't keep up with and I'm not sure we have very strong associations with those factors and coronary artery disease risk. But that's not based on extensive review.

MR. SIRRIDGE: Looking at the studies involved which number about 10 or 11 that we talked about, we'll say 11, and keeping in mind your admonition that there is no perfect study, as I read the studies, Doctor, in terms of hypertension, five out of the 11 studies had information on hypertension.

DR. SAMET: I can't attest to your reading of the studies.

MR. SIRRIDGE: Do you recall whether hypertension was looked at in the studies? Do you have a chart of any kind?

DR. SAMET: No, I do not.

MR. SIRRIDGE: Would it concern you that only five out of 11 of the studies had information on hypertension in terms of their being a confounding factor or problem?

DR. SAMET: I would be concerned, particularly if I had information that suggested that hypertension was more common in those exposed to ETS than non-exposed.

MR. SIRRIDGE: If you knew that five out of the 11 studies had information on serum cholesterol, would that again raise your concern about it being a potential confounding factor?

DR. SAMET: Well, I would have been concerned about all these factors a potential confounders up front.

MR. SIRRIDGE: You're not alone in being concerned. Let me read a statement to you and because I know it's hard to listen and take notes and try to get the question, I will hand up to you what I'm going to read from.

(Pause.)

MR. SIRRIDGE: This is a report from the Congressional Research Service dated March 23, 1994. And I have directed your attention to page 6 of that report, Dr. Samet. Again, it's a very poor copy and I apologize. The paragraph that I'm going to read is as follows:

"The most likely explanation of these large risks from passive smoking epidemiological studies for heart disease is the absence of control for other factors. There are many important causes of heart disease (for example, diet, lack of exercise, lack of preventive health care) that may be engaged in by smokers. That is, there is much evidence that smokers tend to be less concerned about health risks in general. In general, studies do not and perhaps cannot control for many of these factors. If smokers' wives share in these behaviors, the relationships found in the epidemiological studies are spurious."

My question to you, Doctor, is that a reasonable comment on the concern about the potential effect of confounding factors?

DR. SAMET: Well, let me begin by saying that I don't agree with what you just read. Do I agree that there is a potential for confounding through the mechanisms laid out here? Yes.

MR. SIRRIDGE: What don't you agree with in what I read, Doctor?

DR. SAMET: Well, the first sentence that you read said the most likely explanation of these large risks from passive smoking epidemiological studies for heart disease is the absence of control for other factors. I think that's an explanation for them. Whether it's most likely or not, I don't know, but I don't accept the phraseology here. It's an alternative explanation.

MR. SIRRIDGE: So if it read an alternative explanation of these large risks from passive smoking epidemiological studies for heart disease is the absence of control for other factors. That's something you would agree with?

DR. SAMET: Some other factors. I mean, again, as you've pointed out, some of the studies control for some of these potential confounding factors and some don't.

MR. SIRRIDGE: But with the one correction of deleting most likely and putting in alternative, is that a reasonable comment on the potential problems from confounding factors?

DR. SAMET: Epidemiologists look at association bias as always one of the alternative explanations that we consider, as in this instance.

MR. SIRRIDGE: Doctor, are you familiar with the Helsing study?

DR. SAMET: To an extent, yes.

MR. SIRRIDGE: Do you have a copy of it?

DR. SAMET: Yes, I do.

MR. SIRRIDGE: I thought you might. It's probably a mistake to get into a study in a journal which was published at a time when you were the associate editor of the journal but this is just an informational hearing.

DR. SAMET: I'm sorry, could you clarify that comment?

MR. SIRRIDGE: I was saying that I was commenting that you were the associate editor of the American Journal of Epidemiology...

DR. SAMET: Well, let me make clear what an associate editor does. An associate editor of the American Journal of Epidemiology is someone who agrees to agree more manuscripts than the next person and acceptance of this paper because I was involved in it, that would be a misrepresentation of the associate editor's functions which I just laid out.

MR. SIRRIDGE: Absolutely not. My point was that it's a journal that you have a lot of experience with and, in fact, will have even more so now that you're at Johns Hopkins. It was meant to be humorous and not meant to...

DR. SAMET: I just wanted to get that clarification on the record.

MR. SIRRIDGE: I will dispense with all future humorous remarks.

DR. SAMET: Good.

MR. SIRRIDGE: Doctor, you've obviously read this study. Did you refamiliarize yourself with it before today's hearing?

DR. SAMET: It was one of the studies that I looked at again.

MR. SIRRIDGE: And you're aware that that was the study that OSHA used as a basis for its risk assessment.

DR. SAMET: Correct.

MR. SIRRIDGE: And since you read the study, doctor, you know that no data were collected for cholesterol levels, is that true?

DR. SAMET: That's correct.

MR. SIRRIDGE: No data on hypertension.

DR. SAMET: Correct.

MR. SIRRIDGE: No data on diet.

DR. SAMET: Correct.

MR. SIRRIDGE: No diet on obesity or weight.

DR. SAMET: Correct.

MR. SIRRIDGE: No data on exercise habits.

DR. SAMET: Correct.

MR. SIRRIDGE: And you're aware that the study involved only white people?

DR. SAMET: Correct.

MR. SIRRIDGE: Would you have some reluctance as an epidemiologist, doctor, in generalizing a study involving all white people to the entire U.S. population?

DR. SAMET: That would depend on the disease of concern. For some I might, and for some I might not.

MR. SIRRIDGE: What about coronary heart disease?

DR. SAMET: There are differences in the epidemiological features of coronary artery disease in blacks and whites, for example, as I understand it, that may make it difficult to generalize.

MR. SIRRIDGE: So are you saying that it may be difficult to generalize this particular study on all whites involving heart disease to the general U.S. population?

DR. SAMET: I think that's one of those matters where I would want to review the evidence that's relevant to that generalization and make a determination as to whether it was or was not appropriate to extend these findings to groups other than whites. I haven't made such a determination now, sir.

MR. SIRRIDGE: How would you go about that?

DR. SAMET: I would go about that through literature review, examining the evidence on the epidemiological characteristics of coronary artery disease, and the racial and ethnic groups of the United States.

MR. SIRRIDGE: I thought you just told me that you thought racial groups had differences with respect to certain cardiovascular risk factors.

DR. SAMET: I mentioned blacks and whites.

MR. SIRRIDGE: They would have differences, in your view, in certain cardiovascular risk factors.

DR. SAMET: I said there are differences in the epidemiological features of coronary artery disease in blacks and whites that might be relevant to generalization.

MR. SIRRIDGE: Could you give me an example?

DR. SAMET: Yes, the risks of some of the established risk factors, and again, I'm not going to... I simply can't sit here and quote such materials accurately, but the risks of some of the established risk factors seem to be different in blacks and in whites. This is the kind of issue that if a post hearing comment would be helpful, I could provide one, but I can't sit here today as someone who does not work in that area and comment on such a sophisticated issue.

MR. SIRRIDGE: Dr. Samet, there was also discussion of a misclassification issue or methodological problem in the study, in the sense that smoking histories were only taken at the beginning of the study. Do you recall that?

DR. SAMET: The 1963 histories?

MR. SIRRIDGE: Yes.

DR. SAMET: Yes.

MR. SIRRIDGE: And the authors discussed the problems that would result from a change in smoking habits that occurred after 1963, isn't that correct?

DR. SAMET: I have a paragraph in front of me that seems to address that, yes.

MR. SIRRIDGE: What they said was, and I'm sure you're looking at the same paragraph on page 921, on the whole then, this is on the left hand side, halfway down, "On the whole then, our household passive exposure scores based on 1963 census data will tend to be higher than the actual exposures in later years, and to that extent may exaggerate the amount of exposure required to match with a given risk of death from arteriosclerotic heart disease."

DR. SAMET: That's correct.

MR. SIRRIDGE: That means that, what it essentially means is there would be less exposure than there would be if the smoking history remained the same as it was in 1963.

DR. SAMET: Which to me means that the observed relative risks associated with the higher level of exposure are actually the result of a lower level of exposure than they assumed.

MR. SIRRIDGE: Or in fact no exposure for a certain number of years in the study.

Let's just go back. Again, I'm just trying to outline a point here which is mentioned in the study. This study ran from 1963 to 1975. That's where they collected the data, correct?

DR. SAMET: Correct.

MR. SIRRIDGE: If smoking histories changed in 1965, let's say, if a smoking husband stopped smoking in 1965, that person would be listed in the data, in the analysis, as a non-smoker exposed to passive smoking. But the person quit in 1965. There would be ten years of non-exposure in that particular example. That is the problem they're talking about, isn't it?

DR. SAMET: Yes, and I think the implication of that is that if smoking dropped, if the exposure dropped, if the exposure classification was based on that originally, in fact the misclassification resulted in, was associated with a lesser degree of exposure than was actually estimated so that those lesser degrees of exposure were still associated with increased risk.

MR. SIRRIDGE: Wouldn't an alternative explanation be, doctor... Are you familiar with the literature on the reduction of risk of heart disease upon cessation of smoking?

DR. SAMET: Yes.

MR. SIRRIDGE: And that risk drops quickly, doesn't it?

DR. SAMET: It drops during the first year following cessation.

MR. SIRRIDGE: And within five years it is essentially the risk of a non-smoker, isn't that true?

DR. SAMET: Correct.

MR. SIRRIDGE: Let's go back to our example. There was ten years of exposure in this study, out of 12, by the person who was originally listed as a non-smoker exposed to smoking.

DR. SAMET: Start again on that one.

MR. SIRRIDGE: I'm sorry. Going back to my example of the person who's, since the data starts in 1963, and that's all the data they have. A person who's listed as a non-smoker in '63 whose husband is a smoker. In 1965 or late 1964 after the Surgeon General's report, the husband quits. So for the rest of the study, for the next ten-some years, there is no exposure to passive smoking. Yet in the final analysis of the data, that person shows up as a non-smoker who is exposed to passive smoking. And if that person had heart disease, that would be a methodologic problem, wouldn't it? A methodologic weakness.

DR. SAMET: I think what you're pointing out is there could be misclassification of the exposure.

MR. SIRRIDGE: That's correct.

And the authors also noted the limitations of their study because of the lack of information on risk factors, isn't that true?

DR. SAMET: Correct.

MR. SIRRIDGE: We were told the other day, Dr. Samet, that the Helsing study was the best available study on which to base the risk assessment. Due to the methodologic limitations we've been talking about, would you be reluctant to use the Helsing study as a basis for the risk assessment, or would you be concerned about using the Helsing study as the sole basis, numerically, for the risk assessment?

DR. SAMET: OSHA's risk assessment is preliminary, and labeled as such. I think the authors of this study pointed out its limitations and of course any risk assessment done using the Helsing study has to acknowledge these uncertainties and potential limitations.

MR. SIRRIDGE: Would you, as a consultant, advise OSHA to, because of the concerns with the methodology of the Helsing study, to reconsider its use as the basis for the risk assessment?

DR. SAMET: I'd probably advise them to go see a good cardiovascular epidemiologist and talk it over with them.

MR. SIRRIDGE: So you have no concern. You know the problems with the study and you know that it was used for the risk assessment.

DR. SAMET: I stated, you asked me that earlier, and I said that any use of this paper for the risk assessment had to acknowledge its limitations and uncertainties. That is part of doing a risk assessment. Again, as I noted, this is a preliminary risk assessment.

JUDGE VITTONE: Mr. Sirridge, are you about ready to finish up?

MR. SIRRIDGE: Pretty close.

JUDGE VITTONE: Good. How close?

(Laughter)

MR. SIRRIDGE: I'm not going to define terms, Your Honor.

Dr. Samet, one more joke, but that's the way it goes.

JUDGE VITTONE: A joke?

MR. SIRRIDGE: I suppose it's not a joke to you, is it?

(Laughter)

MR. SIRRIDGE: Would you agree, Dr. Samet, that because of the potential effect of confounding factors an excess risk of coronary heart disease in non-smokers has not been established?

DR. SAMET: No. I think that there's a body of evidence showing excess risk. I think that has to be interpreted in light of the whole array of evidence. The potential for confounding to explain it. The understanding of how coronary artery diseases arise, what the role of ETS is in those mechanisms.

MR. SIRRIDGE: My question is really probably more simple than the wording. What I want to know from you is, do you accept the idea that there is an established excess risk for people who are exposed to ETS for heart disease?

DR. SAMET: I told Mr. Grossman that my way of proceeding on such matters is to look at all the evidence, understand it, weigh it, and I have not done that for heart disease. It's outside my area of expertise, and I have not sat back and reviewed a very large body of new experimental data, pathophsyiolgical data, and epidemiological data, and that's the kind of review that I would need to undertake before I gave you an answer to that question.

MR. SIRRIDGE: Let me refer you to your 1992 article on environmental tobacco smoke. I refer you to page 256. It's the page that has references, but there's some text above that.

Did you find the page, doctor?

DR. SAMET: Yes, I did.

MR. SIRRIDGE: The first paragraph, the last two sentences. Actually, the second to the last sentence. The comment is made, "The evidence on cardiovascular disease points to increased risk in non-smokers exposed to ETS."

What did you meant by "points to increased risk"?

I guess what I'm trying to find out is whether you had accepted it as an established excess risk, or whether you were commenting...

DR. SAMET: I was commenting on what was published in the literature, the table that shows these elevated risk elements that are in, I think, the table you already referred to.

MR. SIRRIDGE: Let me ask you today, in 1994, Dr. Samet, do you still feel that the reported risks in the epidemiologic literature for ETS and heart disease seem high in view of the relative risks observed in active smokers.

DR. SAMET: I still do.

MR. SIRRIDGE: Doctor, in your submitted statement to OSHA which I had at one time... I won't worry about quoting it, but you indicated that you did not believe that work place had received specific investigation in terms of ETS and heart disease, and I could find that quote...

MS. SHERMAN: Would you repeat the question? I didn't hear you.

DR. SAMET: Let me go back and get my copy of the statement.

MR. SIRRIDGE: It's on page 12 of Dr. Samet's statement. It is the first full paragraph, about half the way down. It reads, right at the end of that paragraph, "The workplace has not received specific investigation." Does that mean that you were not aware that three of the eleven studies which we've been discussing have data on heart disease and non-smokers exposed to ETS in the work place?

DR. SAMET: When I wrote that, I was really referring to studies designed to look at the workplace exposure as a cause of disease, not the fact that some of the studies may have looked at workplace exposure variables. The specific investigation I guess. Maybe it hinges on what I mean by that and how you interpret it.

MR. SIRRIDGE: Would the lack of data from a specific study which looked at the risks of ETS workplace exposure and heart disease, would the absence of such a study give you some pause in trying to perform a risk assessment of the risk related to exposure to ETS, in the workplace?

DR. SAMET: I think that's a matter of the biology. That is, should there be difference that risks observed at levels of exposure in homes cannot be extended to the workplace. We can take this argument a long way. Do you have to study every kind of workplace? I think it's a biological question in terms of the generalization from home exposure to other locales.

MR. SIRRIDGE: It's a biologic question as to whether you can use data from exposure to ETS in the home for purposes

Again the purpose of assessing the workplace risk?

DR. SAMET: You would want to have some reason a priori to anticipate that the risks of exposure to the same agent in different locations, because of whatever factors you might be concerned about, would lead to a different risk.

MR. SIRRIDGE: But wouldn't the preferable and best way to go about assessing the risk of coronary heart disease from exposure to workplace ETS would be to do that from a study which actually, specifically, focused on the issue of workplace exposure to ETS? Wouldn't that be the best way to do it?

DR. SAMET: I think what may be best and preferable, we've already talked about the real world, and the fact that no study is perfect. What you might do under ideal circumstances were one given unlimited resources and time, may be far different from the resource of evidence that you can turn to in trying to understand the effects of an agent.

MR. SIRRIDGE: Given satisfactory resources, would that be the preferable way to do it?

DR. SAMET: Again, I think we can only put this into a very hypothetical context in which the resources were available to do such a study, and that presumably, probably a large effort, could be mounted. Then I think absent such evidence, one must turn to the evidence at hand and say, "Well, it has limitations. It was done in a home environment. Can it be generalized to another environment?" If yes, why. If not, why not. Those are the questions of biological plausibility, generalizability that I alluded to.

MR. SIRRIDGE: I understand that people want to rely on the espousal studies. My question to you is, if resources was not an issue, isn't the best way to assess risk for workplace exposure to ETS, the best way to do that is to actually have a study which measures and estimates and studies whether people have an excess risk from workplace exposure.

DR. SAMET: One would undertake such a study if they thought that there was a reason to do it. If there were such a reason, you decide that the results at home cannot be extended, then yes, you would want to do such a study.

MR. SIRRIDGE: Thank you.

JUDGE VITTONE: Thank you, Mr. Sirridge.

Mr. Rupp?

MR. RUPP: Can we take a break?

JUDGE VITTONE: Sure. We'll take a two minute break in place.

JUDGE VITTONE: On the record.

Mr. Rupp?

MR. RUPP: Thank you, Your Honor.

For the record, may I say that I am appearing here this afternoon on behalf of the same people on whose behalf I've been appearing all week.

Dr. Samet, you were a member of the, have been a member of the editorial boards or peer review boards of a number of publications, I take it.

DR. SAMET: Correct.

MR. RUPP: Would you briefly describe for me the peer review process that the most prestigious of the journals would typically engage in before deciding whether to publish an article?

DR. SAMET: Typically an article is sent to several reviewers picked for appropriate background and relevant publications themselves. The reviews are received and evaluated by an editor who would look at the article him or herself, and make a decision as to acceptance, rejection, or revision and possible publication pending revisions.

MR. RUPP: When the articles are sent out for review are they sent out on a blinded basis? That is, do the reviewers have any knowledge of the identity of the person who submitted the manuscript?

DR. SAMET: It depends on the journal.

MR. RUPP: Typically not? Is there any pattern that one sees in that respect?

DR. SAMET: I think the American Journal of Public Health usually uses blinded review, a few others do. Probably the majority of them do not.

MR. RUPP: The majority of reviewers would know the identify of the person who had submitted the manuscript?

DR. SAMET: Probably, yes.

MR. RUPP: I take it you also served on the science advisory board of the U.S. Environmental Protection Agency at the time EPA produced its 1922 report on ETS.

DR. SAMET: Correct.

MR. RUPP: Do you recall an appendix to that report that dealt with the misclassification of smoking status and a possible method for approaching misclassification in spousal smoking studies?

DR. SAMET: Yes.

MR. RUPP: Would I be fair if I suggested to you that the SAB peer review, that document at Appendix B?

DR. SAMET: That was part of the report that was submitted to the SAB for its review.

MR. RUPP: Did the SAB review it in a way that such a document would be reviewed in, if it had been submitted to a scientific journal?

DR. SAMET: The process was different. The process of review by the Agency was open to the public and a visible one.

MR. RUPP: And the purposes of the review that was occurring were quite different than the purposes of a review for any of the journals we've been discussing, I take it?

DR. SAMET: Well, again, the purpose of the EPA process was called a peer review. It was to bring to bear the scrutiny of a group of scientists to look at that report.

MR. RUPP: I'd like to ask you a series of questions, if I may, on, again focusing on ETS, and a number of health effect issues that have not yet been discussed this afternoon, and I'd like to do so as briefly as I can.

The health effect issues that are of concern to me are adult pulmonary health including COPD and asthma, reproductive health and irritation. I know you've looked at some of those issues, perhaps not all, and I was listening to the exchanges you had with Mr. Sirridge. Are there any issues in that list about which you feel less qualified or perhaps not fully qualified to discuss with me than others? I know you've written on adult pulmonary health including COPD and asthma. I don't know that you've written on reproductive health or irritation, or perhaps I haven't come across...

DR. SAMET: That's correct.

MR. RUPP: Do you feel qualified to discuss with me the issues of ETS and reproductive health and irritation?

DR. SAMET: Not particularly, no.

MR. RUPP: Would you agree with me as a general proposition, one cannot talk sensibly about adult pulmonary health, and again I'm including COPD and asthma in that general category, without considering the extent of exposure? To any substance.

Let me rephrase the question.

When we're talking about or trying to discuss the issue of whether a particular exposure gives rise to some excess risk of an adverse reproductive effect, isn't one of the first questions you'd ask is how much of the stuff is the person exposed? How long, at what intensity?

DR. SAMET: You said reproductive effects in your question...

MR. RUPP: I'm sorry, I misspoke.

DR. SAMET: I'll make the assumption you...

MR. RUPP: ...I mean to confine all of my questions from here to adult pulmonary health.

DR. SAMET: Certainly one would want to know something about the degree of exposure, yes.

MR. RUPP: In the case of ETS, as well as any other substance having both a gas and a particulate phase, we would also need to consider, I take it, whether the exposure is occurring indoors, what capacity the building ventilation and filtration systems had to address the substance or to remove the substance.

DR. SAMET: I don't agree with that, that it would be necessary to know that to conduct an epidemiological study of ETS and non-malignant respiratory effects.

MR. RUPP: Certainly you would agree I take it, perhaps not, whether any particular particle or gaseous component of the indoor air would be a factor in exposure and how much of a factor would depend upon how quickly the air was being diluted and removed and replaced by new air...

DR. SAMET: I think epidemiological studies have not...

MR. RUPP: I'm not focusing really on epidemiological studies now. I'm really focusing on the more basic proposition. When we're talking about extent of exposure, in a particular case or in the case of a particular individual, one would want to know, I take it, something about the extent of the particular exposure, the capacity of the ventilation system, the circumstances in which the person found himself or herself over any extended period of time.

DR. SAMET: I'm sorry, I understand what you're saying, but I don't have a context in which to give an answer. I might give one answer for an epidemiologic study, another for detailed assessment of exposure to ETS components. So I can't answer the question...

MR. RUPP: Do it in the context of a detailed assessment of extent of exposure, but outside the context of an epidemiologic study. That is you have someone who comes to you on a clinical basis. And you're trying to figure out what might be the cause of her particular form of respiratory distress. What kinds of questions would you ask to the extent that you were pursuing the possibility that ETS might be a factor?

DR. SAMET: I would ask probably a series of questions about their work place, what they do, the nature of the building, sources of pollution within the environment. It's unlikely that an individual patient would have any knowledge of some of the factors that you mentioned.

MR. RUPP: I take it so far as respiratory distress is concerned in all of its various forms, there are a variety of potential causes, so it's not, to the extent you are pursuing a line of inquiry to determine whether there was a predominant cause, a contributing cause, there are a variety of things one would presumably want to ask about.

DR. SAMET: I don't use the term respiratory distress when I either see patients or do epidemiology.

MR. RUPP: Think about it in terms of a patient. As a patient I would think about it in terms of respiratory distress. Use your own term.

DR. SAMET: If someone came to me complaining, a respiratory complaint of some sort.

MR. RUPP: Wheezing. The person was wheezing. I take it you'd ask about a variety of factors that can affect the quality of the air, indoors or outdoors, for that matter.

DR. SAMET: Certainly.

MR. RUPP: I think it was established in the discussion you had with Mr. Sirridge, or it was identified for the record at that time, that you had contributed a chapter to the book edited by Dr. Morton Littman, and the chapter that I'm referring to, the book, rather, is Environmental Toxicants, and the chapter is entitled "Environmental Tobacco Smoke." Did Mr. Sirridge give you a copy of that?

(Pause)

MR. RUPP: So far as ETS and adult pulmonary health is concerned, you wrote at page 242 of that chapter, and I can wait for a moment if you want to turn to that. I'm looking at...

MS. SHERMAN: Can you tell us when that was published?

MR. RUPP: Yes, this is a publication from 1992.

I think this copy is on two sides of the page, and this is on the left hand side of the page. "Consistent evidence of an effective passive smoking on chronic respiratory symptoms in adults has not been found."

And a few lines later you write, "Neither epidemiologic nor experimental studies have established the role of ETS in exacerbating asthma in adults."

Then if I look a bit further, I'm referring now to the bottom of page 243 and the top of page 244, you state, "A conclusion cannot yet be reached on the effects of ETS exposure on lung function in adults." You then call for further research on each of those topics.

Do you see those passages?

DR. SAMET: Yes, I do.

MR. RUPP: And those were your views as of 1992 or 1991 whenever you wrote the manuscript and submitted it to Dr. Littman?

DR. SAMET: Correct.

MR. RUPP: Do those remain your views today?

DR. SAMET: I think there is actually an enlarging body of experimental evidence on exposure if asthmatics who allege ETS sensitivity in fact were placed in a chamber, such persons do respond with what would be gauged as clinically significant reductions among functional workers, Selvagio's group, for example. And I think there is rising evidence from children, and again, all published over the last approximately three or four years, that exposure to ETS exacerbates asthma for those who have it. That conclusion was reached in the EPA report. That conclusion is quite plausible in view of the particulate and potentially gaseous phase components of ETS.

MR. RUPP: That reference is in the case of children, I take it.

DR. SAMET: The EPA report is in the case of children. The Selvagio study was adults.

MR. RUPP: With the exception of asthma which we can return to, then, does this represent, the passages I read to you fairly summarize your views as we sit here today?

DR. SAMET: That was, again, written as of 1991, and there are new reports that have emerged that, again, show association. Several published this year, and I'm aware of other work. So I think the body of evidence on non-malignant respiratory effects is mounting. No group analogous to the EPA report or the Surgeon General has yet reviewed this evidence and made any determination on the weight of the evidence.

MR. RUPP: Let's talk about asthma for just a moment. I think you've written in the past about the problems that clinical investigators have in trying to blind exposure and the problems of stress and queuing from the visual elements of environmental tobacco smoke and try to sort out the effects of those things and the other physiological components. Did Dr. Selvagio and his coworkers at Tulane, were they able to solve those problems?

DR. SAMET: You're going to stress my memory. If I recall, they probably did try and use some sort of masking agents in their protocol, but I cannot answer that question without having the paper in front of me.

MR. RUPP: Do you know what size the room was in the Selvagio experiment, or any notion of what the configuration of the room was?

DR. SAMET: The configuration is described in this article, and I'll have to go look at it.

MR. RUPP: Do you recall what the extent of the exposure was in the Selvagio experiment? Was it real life exposures or did one level of exposure include real life exposures?

DR. SAMET: Again, I would need to look at the levels of whatever markers they used in that particular paper. I don't have that paper with me.

MR. RUPP: My recollection, which may be wrong, and I'd like you to correct me if it is, was not the Selvagio paper published before you wrote this publication?

DR. SAMET: Again, without the paper in front of me I can't answer that question.

MR. RUPP: There is a significant problem, though, is there not, in attempting to determine the effects of ETS exposure on asthmatics in real life conditions when one's only approach, or when the only approach used is basically a chamber, an exposure in a chamber. Unless one is able to discover one way truly to blind exposure.

DR. SAMET: We've gone too many clauses down the line on that question, I'm afraid. Can you repeat it?

MR. RUPP: Yes. Masking of exposure in the investigation of possible reaction of asthmatics to ETS remains an important issue in your mind, does it not?

DR. SAMET: I think the issue in these clinical exposure studies is whether significant decrements in lung function could be produced as a consequence of inability to mask the exposure. I think that probably depends on whether the effect is subtle or rather large, and I don't think that patients tested by well trained technicians are capable of producing consistent large decrements of pulmonary function or respiratory distress if such arises, so it would really depend on the findings.

MR. RUPP: The results that have been reported thus far in the area of adult asthma, have not a number of investigators indicated that they have had great difficulty eliciting any kind of reaction among adult asthmatics in changer settings to ETS?

DR. SAMET: There have been some studies like that, yes.

MR. RUPP: And the Selvagio study is one of those studies, is it not?

DR. SAMET: The Selvagio study documented decrements of lung function of FEV-1, again this is by memory, in a proportion, a significant number, and I again can't remember the numbers.

MR. RUPP: Seven out of 21?

DR. SAMET: Thank you. Of asthmatics who said that they were ETS sensitive and who were challenged.

MR. RUPP: Self declared smoke sensitive asthmatics had levels of ETS exposure that are far above real life exposure levels. Do you recall that aspect of the Selvatio study?

DR. SAMET: We already went over that, and I said I did not have that.

MR. RUPP: Fair enough.

Before making the statements that I had read to you, I take it at that point you had fairly carefully and comprehensively reviewed the available literature pertinent to each of those issues, so that the statements that I read represented a fair analysis of the literature as you understood it or as you believed it to be as of the time you were writing?

DR. SAMET: You're referring to my paper in the Littman book?

MR. RUPP: I am, indeed.

DR. SAMET: I would hope that I'd reviewed the literature.

MR. RUPP: In the same chapter, and I'll try to find the quotation...

(Pause)

MR. RUPP: It;s at the bottom of page 243. you indicate there, and I quote, "An association of [passes moved in] with chronic obstructive pulmonary disease seems biologically implausible, however, since only a minority of active smokers develop this disease and adverse effects of involuntary smoking on lung function in adults have not been consistently observed."

Is that still a fair statement of your views?

DR. SAMET: By chronic obstructive pulminary disease, I'm referring to the disabling impairment of lung function that develops in smokers.

MR. RUPP: COPD as conventionally defined.

DR. SAMET: As conventionally defined, i.e., a sufficient reduction of lung function that one is impaired during daily life. yes.

MR. RUPP: It does represent your view?

DR. SAMET: That still represents my view.

MR. RUPP: Do you know of any study that has investigated the incidents of COPD and ETS in workplace settings at all?

DR. SAMET: The incidents?

MR. RUPP: Yes. Had looked at COPD as a health end point in a workplace setting in connection with exposure to ETS.

DR. SAMET: As opposed to some other...

MR. RUPP: As opposed to some other setting, or opposed to some other substance.

DR. SAMET: Give me a moment on that.

MR. RUPP: Okay.

(Pause)

DR. SAMET: I haven't looked at the literature that way, nor have I brought the world's literature with me, but to my knowledge, I don't think there are such studies.

MR. RUPP: Okay.

Has stress been documented as being a significant factor in the triggering of an asthmatic attack?

DR. SAMET: Stress is certainly discussed as a factor that may trigger asthma attacks. Has stress been well studied as a triggerer of asthma attacks? No. Do clinicians feel that stress may be a trigger? Yes.

MR. RUPP: Does a particular author or article come to mind as particularly illuminating in that respect?

DR. SAMET: No.

MR. RUPP: Or a particular group of investigators, even.

DR. SAMET: There are groups who have investigated this. Again, I didn't come here today prepared to talk about stress and asthma.

MR. RUPP: You had a rather long exchange with Mr. Grossman about the possible impact of biasing and confounding factors in the context of ETS and lung cancer. You do recall that exchange?

DR. SAMET: Yes.

MR. RUPP: Are biasing and confounding factors of potential significance in the case of adult pulmonary diseases from an epidemiologic standpoint? That is, in designing an epidemiologic study, are biasing and confounding factors an element you would want to consider?

DR. SAMET: Well, I think we've sort of gone over tenets of good epidemiology and said that bias with confounding being one bias, always a potential concern.

MR. RUPP: And so far as adult pulmonary disease is concerned, what you would want to control for, I take it, are in particular those exposures or-- well, let's leave it at exposures. Exposures to take one example. That appear to be related or a risk factor for adult pulmonary disease and also seem to be associated in a significant way with ETS? That is, where there was some mixing of the elements.

DR. SAMET: Right. You've given me the definition of confounding and I've said we would be concerned about it. I think the term adult pulmonary disease, I think, is a very general one that I don't use.

MR. RUPP: That you--

DR. SAMET: That I do not use in a broad way.

MR. RUPP: Okay. A number of scientists have written about the danger that a respondent in the pulmonary impairment would tend to over-report exposure to ETS as well as over-report exposure to other substances in the air if asked specifically about those substances. How do you guard against that possibility in your clinical practice? That is, in searching for an answer to what may have caused whatever the person is suffering from, how do you deal with or address the problem of the tendency to over-report, to magnify?

DR. SAMET: You said in my clinical practice.

MR. RUPP: First in your clinical practice and then when you're designing epidemiologic studies.

DR. SAMET: Well, the patient-physician relationship involves trust and as a physician-- and I've been that for many years-- I trust my patients, I try and understand them as people. And in the physician-patient relationship, one hopes that one can trust what information is exchange. Someone is there hopefully seeking diagnosis and treatment and there's a relationship established based on trust. Do I have tools to look for bias in responses that patients give me? No.

MR. RUPP: But the trust is important. That is, that is something you work very hard to develop with your patients, I take it.

DR. SAMET: Correct.

MR. RUPP: So they understand who you are, where you're coming from and that you're there to help them.

DR. SAMET: Well, that I'm there to help them.

MR. RUPP: Would you agree that an epidemiologist undertaking a large-- or a team of epidemiologists undertaking a large population based study doesn't come armed with quite the same advantages as the really good clinician does so far as pre-existing trust of the respond to his concern?

DR. SAMET: Well, the context of information gathering is different.

MR. RUPP: Would you agree that there's a particularly difficult job that an interviewer in an epidemiologic study, perhaps depending in part on the nature of the information that the interviewer is seeking has in trying to ensure that the information is accurate because of the absence of the pre-existing trust?

DR. SAMET: No, I would not predicate potential biases that may affect responses in the epidemiologic context on the lack of a provider-patient relationship. They're different settings.

MR. RUPP: Would it depend more on the nature of the questions being asked?

DR. SAMET: Well, I think-- I'm sorry.

MR. RUPP: Would the nature of the questions being asked be a more significant factor in your view, so far as the reliability of the responses is concerned? Or the nature of your concerns about the reliability of the responses?

DR. SAMET: You've asked me two questions.

MR. RUPP: I think I've asked the same question two different ways for no great purpose, so let me just ask it one way.

Is the nature of the question being asked in an epidemiologic setting of greater significance to you than the issues we've been discussing here the last couple of minutes in determining the extent to which you can rely on the responses being given?

DR. SAMET: I'm going to restate what I think I heard.

MR. RUPP: Okay.

DR. SAMET: Is the nature of the question important in my interpretation of the quality of the information that is obtained? Is that--

MR. RUPP: Very well done. Yes.

DR. SAMET: Okay.

MR. RUPP: Or at least answer that question.

DR. SAMET: You know, clearly, that's one of the determinants or the factors that one would look at in deciding about the quality of information, what has been asked. Some questions are more sensitive than others and some are perhaps more likely to be biased than others.

MR. RUPP: Okay. Now, let me focus again, then, on-- and perhaps this can be almost any disease but I want to ask about it in the context of environmental tobacco smoke. When there's been a good deal of publicity about possible associations of a particular substance with a particular disease and you question after the fact about whether the person was exposed-- and the other factor is the person has been diagnosed with a disease and is asked by a member of a team of epidemiologists whether they have been exposed to the substance over time, would the fact of the publicity be a cause of concern to you in tending to exaggerate or cause the respondent to exaggerate the extent of exposure? In this case, it could be ETS, in another case it could be the dioxin at Love Canal, I really don't care.

DR. SAMET: Well, you're asking a question-- first, I'm always concerned about information bias. Second, could awareness of an association or potential association alter response patterns, it's a possibility.

MR. RUPP: Now, in the case of-- again, because I think it helps to focus things, in the case of ETS, wouldn't one want to, among other things, either look for confirming information from as many different sources as possible-- let's stop there for the moment. I want to ask you about some other possible approaches but wouldn't one first look to see how many ways one could reasonably and within whatever financial constraints you were operating under confirm the information being provided by the respondent?

DR. SAMET: To the extent possible, I think one would like to add to any epidemiologic study whether ETS or any other exposure investigative approaches that may provide some estimate of the validity, which is the technical word, of the information contained.

MR. RUPP: I take it that another-- if there's going to be exaggeration or potential exaggeration of the extent of exposure one would also want to pay particularly careful attention about confounders with respect to which a comparable kind of exaggeration may be possible?

DR. SAMET: Well, we began with an exposure that might be of concern and perhaps known to the public and now we've moved to confounding. I don't know whether such bias in reporting would extend to confounding or not. I'll admit to its possibility but I am not aware of that as a general phenomenon.

MR. RUPP: Let's go back to asthma for a moment. Are you aware of any study that has investigated the epidemiologic-- a study of any sort that has looked at the question of whether there is--

DR. SAMET: Directly, again, without having done-- without looking at the latest work, my answer would probably be not directly.

MR. RUPP: All of the studies that have been reported thus far have been clinical studies, have they not been? So far as ETS is concerned.

DR. SAMET: Well, there's substantial epidemiological data from children with asthma.

MR. RUPP: Yes. Yes. I'm talking about adult pulmonary disease. I'm sorry. I should have made that clear. Excuse me. Adult asthma.

DR. SAMET: Adult asthma. That is probably correct.

MR. RUPP: Why do you suppose no epidemiologic study of adult asthma has yet been undertaken? Any sense at all?

DR. SAMET: I can't speculate about that.

JUDGE VITTONE: Mr. Rupp?

MR. RUPP: Yes. I am winding down. If I could just have another five minutes, that should do it. And perhaps less.

JUDGE VITTONE: Okay.

MR. RUPP: Dr. Samet, let me ask you if you would agree with the following statement which I'm taking from the OSHA preamble in the present rulemaking. Page 15,976. Should I wait a second until you find it?

DR. SAMET: I'm sorry. You said which page?

MR. RUPP: 15,976. And the statement that I'd like to read to you is the following, and I will help you to find it on that page if you have difficulty.

"There is no clear consensus in the medical literature as to the routine clinical use of FEF 2575 and FEF 7575 [measurements]," a word I'm inserting, "or their diagnostic value in independently detecting small airway disease."

Is that a statement with which you agree?

DR. SAMET: Well--

MR. RUPP: It's at the very top of 15,976 on the left-hand side.

DR. SAMET: Well, this statement, the FEF 2575, I think you have to put this into a clinical context and this says clinical use.

MR. RUPP: Yes.

DR. SAMET: I don't think that clinicians would typically in terms of diagnosis in an individual patient-- and I'm again referring to clinicians and individual patients--

MR. RUPP: Right.

DR. SAMET: -- place much emphasis on values of the FEF 25 or FEF 7585.

MR. RUPP: Because of their unreliability or because of the wide margin of variability from one person to another, one time to another?

DR. SAMET: Well, clinicians use the FEV 1, the forced expiratory volume in one second, and the FEV 1/FEC ratio is the primary clinical tool in interpreting spirometry.

MR. RUPP: I note that in many of the studies of adult pulmonary health, and I'm thinking less about asthma now where there haven't really been that many studies, I think we've established, and COPD where there may be one or two studies and no more, in some of the other studies both the studies of functional decrements and incidents of symptoms such as wheezing, cough and so forth, one feature is a substantial number of end points being reported in individual studies. That is, trying to segregate cough from wheezing, from this to that from this, FEV 1, FEF 2575. I think in one of the studies there were 44 different health end points measured. When you have a study of that sort or so much data, does one have to be considered in analyzing those data about spurious findings, positive findings or negative findings with respect to one end point when the P values have not been corrected for multiple comparisons?

DR. SAMET: You've listed the array of respiratory outcome variables that might be derived from a typical survey with a respiratory questionnaire and lung function testing. The usual concern, of course, would be that there would be an exposure and that there might be an effect and this is a set of indicators, let's say, of respiratory health status. Do I think the multiple testing issue per se is of concern here? No, assuming that there was a reasonable a priori basis for using this set of indicators. In other words, one wouldn't do a study and ask extraneous materials and then analyze them and find associations.

MR. RUPP: All right. Now, let's take the same set of circumstances and let's divide into 10 or 15 or 20 different subgroups people who are in this room today, men, women, so that you're looking at the functional decrements or possible functional decrements or other indices of respiratory health within a substantial number of subgroups, 10 or 20. At what point do you start to put up the red flag and say, look, you'd better start looking at your P values because you're doing multiple comparisons and by the very nature of the thing at some point you're going to get something positive and negative wholly spuriously beginning to pop out. The statistics are just going to work that way.

DR. SAMET: Again, speaking to what I think I would do or a quote good epidemiologist would do, one would stratify in ways that had a priori plausibility. In other words--

MR. RUPP: So you know going in that you're going to be looking--

DR. SAMET: One would know going in what to look for, were these stratifications purely arbitrary, then the concern that you've raised might be a concern.

MR. RUPP: Okay. Now, as a good editor who when it falls on your shoulders to decide whether something is going in one of the leading journals and you get a paper in and it has multiple subsets of all sorts of different slices of the same set of data and you have predominantly negative findings but a couple of positive findings in a couple of small subsets or a whole mix, does that start to concern you, whether appropriate corrections have been made for the multiple comparisons that are being undertaken?

DR. SAMET: I think it's really the same interpretative framework which is are the stratifications plausible and do they make sense. I think that would be my basis for interpretation.

MR. RUPP: Would you explain for me, and I think this may be my last question, Your Honor, would you explain for me what the term data dredging or the phrase data dredging means? Is that a phrase--

MS. SHERMAN: What was the term?

MR. RUPP: Data dredging. Data dredging, D-R-E-D-G-I-N-G.

DR. SAMET: It's not a term I use.

MR. RUPP: What would be a term that you would use for the same--

DR. SAMET: But I think what you're referring to is the concept that someone might take a data set, slice it in a number of ways and find something in a particular subset and report that.

MR. RUPP: To keep massaging the data until they could group it in such a way that something positive or negative could be reported.

DR. SAMET: That, I think, is a reasonable definition of the term data dredging, yes.

MR. RUPP: Thank you very much.

JUDGE VITTONE: Thank you.

Why don't we take a very short recess.

JUDGE VITTONE: On the record.

During the recess I was approached by another participant who has a few questions for Dr. Samet.

Sir, would you come to the microphone, please, and identify yourself?

MR. BAYARD: Thank you. My name is Steven Bayard, I work for the Environmental Protection Agency. I will be a witness later on in these hearings for the Environmental Protection Agency.

MS. SHERMAN: Could you talk louder and not so fast?

MR. BAYARD: Do you want me to repeat what I said?

MS. SHERMAN: I caught it, and the Court Reporter caught it.

MR. BAYARD: Thank you, Dr. Samet. I just have a few questions for you.

Dr. Samet, in 1990, you and Dr. Anna Woo Williams published a paper on risk analysis in which you analyzed the data from all the environmental tobacco smoke and lung cancer studies that you could find and specifically analyzed them for dose responses. In that paper, out of the 12 studies in which you had dose responses by intensity of spousal smoking, you found that nine of those, that all of those actually had positive dose response slopes, and that nine of those were statistically significant. Is that fairly accurate?

DR. SAMET: I have the table in front of me and it would appear to be accurate.

MR. BAYARD: Can you think of any biases which might be responsible for that number of significant results?

DR. SAMET: Well, one would have to postulate a pattern of confounding or of misclassification that was dependent on the exposure measure used, which is-- I think it would be difficult to do.

MR. BAYARD: So the answer is it's hard.

What about confounders? Can you think of any confounders that might be responsible for those significant dose response trends in all those studies?

DR. SAMET: Again, one would have to postulate a confounder that was associated with the exposure measure and that is difficult to do in the case of ETS and lung cancer.

MR. BAYARD: You're familiar with the Fontham studies, both the 1991 and the 1994 studies?

DR. SAMET: Yes, I am.

MR. BAYARD: In the 1994 study, Dr. Fontham found significant dose response trends separately for home exposure in lung cancer due to spousal smoking, for work exposure and lung cancer due to spousal smoking, and for social exposure due to spousal smoking.

Now, that I know was not one of the studies you had had in your 1990 paper. Can you think of any reasons or any biases or any confounders that could have been responsible for those response trends?

DR. SAMET: That would be difficult, and these analyses were controlled for a number of potential confounding factors.

MR. BAYARD: So you would-- what do positive dose response or exposure response trends mean to you in terms of a causal association?

DR. SAMET: Well, they're consistent, I think, with our a priori hypothesis with regard to ETS. That is, greater exposure will be associated with greater risk. As it is for active smoking.

MR. BAYARD: But would you say that it's a fairly strong indicator-- the dose response trend is a fairly strong indicator of causal association?

DR. SAMET: Certainly one of the ways that one looks at epidemiological evidence in drawing an interpretation as to causality used in the 1964 Surgeon General's report, for example. And I think, for example, it becomes more difficult to explain a pattern-- to hypothesize a pattern of confounding that would lead to an exposure response relationship as observed here and these exposure response relationships persist after control for confounders.

MR. BAYARD: Thank you. Just one more question, I think. One or two more.

You're familiar with misdiagnosis as a source of bias?

DR. SAMET: I'm familiar with the problems of diagnosing lung cancer and the potential for misclassification, yes.

MR. BAYARD: And how would misdiagnosis as a potential source of bias affect cohort studies of environmental tobaccos smoke and lung cancer?

DR. SAMET: Well, if cases presumed to be lung cancer were in fact primary at other sites that were not associated with ETS, that pattern of misclassification would tend to dilute associations, reduce the magnitude of the association.

MR. BAYARD: So it would tend to be a downward bias.

DR. SAMET: Tat's right. A downward bias.

MR. BAYARD: And how would they affect case control studies?

DR. SAMET: Well, really either context. I think the same pattern, the same would be true.

MR. BAYARD: Okay. I think that's fine.

Thank you very much.

JUDGE VITTONE: Thank you.

Any redirect?

MS. SHERMAN: A little bit.

Dr. Samet, in your experience, can eye irritation and upper respiratory irritation be considered material impairment? And I'm talking about your clinical experience.

DR. SAMET: I've certainly seen patients with sufficient symptomatology affecting airways, irritation primarily, when they come to me that impaired their work performance and affected their quality of life and I would interpret that as material impairment.

MS. SHERMAN: Has anyone-- this is a general question-- has anyone shown a threshold for carcinogens, say perhaps-- okay. Let me just ask you that and see.

DR. SAMET: Well, that's a very difficult question. I think if you look at carcinogens for which we have some studies at relatively low doses-- and, again, that's difficult to specify what low is but in the area of radiation, for example, a threshold for carcinogenesis has not been observed at what are considered lower levels of exposure. I'm not aware of data demonstrating a threshold per se. I think any notions as to threshold would have to draw not only on epidemiology but the mechanisms by which cancer was caused and was a threshold a plausible consideration. In the case of ionizing radiation so far, for example, I think we have abundant data across a range of exposures and we've not seen a threshold.

MS. SHERMAN: Do we know the mechanism for lung cancer?

DR. SAMET: I think the answer to that is we are beginning to understand the molecular mechanisms underlying the occurrence of lung cancer. We certainly know that there are carcinogens that cause lung cancer and I think now with our new tools, the tools of molecular and cellular biology, we're beginning to understand the multiple genetic changes that lead a cell from normalcy to malignancy. Do we have the full picture yet on this? No.

MS. SHERMAN: We had testimony yesterday that ETS is made up of numerous different compounds and I take it that you do believe that a number of these compounds are carcinogens in and of themselves?

DR. SAMET: Yes.

MS. SHERMAN: Is there a difference in your mind between tobacco smoke and ETS? By that I mean is tobacco smoke made up of similar components as environmental tobacco smoke or is it somehow qualitatively different

DR. SAMET: You're referring to mainstream smoke?

MS. SHERMAN: Yes.

DR. SAMET: Well, I think the Surgeon General's report, for example, addressed this issue to an extent. Certainly there are many agents in common, individual components of mainstream smoke and ETS that are similar. Are there differences in some because of the aging of ETS, yes, but many of the same agents associated with disease have been identified in ETS as in mainstream smoke. And this is reviewed in the 1986 report, for example.

MS. SHERMAN: Is it appropriate to assume that the risks associated with tobacco use and heart disease after cessation of smoking drop at a similar rate as the risks associated with ETS exposure and heart disease?

DR. SAMET: Do you mean to say appropriate--

MS. SHERMAN: That was a complex question. I guess what I really mean is if an active smoker ceases smoking and you have their risk of heart disease and then if a passive or involuntary smoker ceases to be exposed to tobacco smoke, would the risks sort of decline at a similar albeit diminished rate? Maybe I made the question harder.

DR. SAMET: I really can't answer that question.

MS. SHERMAN: Okay. Just for my edification, I know that you're the author of numerous articles and even chapters in books, generally speaking, how long does it take between the time you write an article or a chapter like in the Littman book and the time it's actually published and distributed?

DR. SAMET: It's variable. Probably a minimum of a year but often more. In the case of my book on lung cancer, it was held up by the publisher for about a year and so much of the literature review ended about two and a half years before the publication date so it's variable.

MS. SHERMAN: I see. We had some testimony the first day of the hearing or we had some questions the first day of the hearing that referred to a study by McFarland et al. that the way I interpreted the question, the question suggested that the only way of identifying primary lung cancer was through autopsy and the implication was that any epidemiological study that did not rely on autopsy would be flawed. Would you agree or disagree with this?

DR. SAMET: Well, I'm familiar with the McFarland study. I would disagree that the diagnosis of lung cancer has to be made by autopsy. Unfortunately, I've made it far too many times in the living.

MS. SHERMAN: As the primary site?

DR. SAMET: As the primary site.

MS. SHERMAN: So that there are other means of diagnosing primary site lung cancer and if an epidemiological study did not rely on autopsy it would not be fatally flawed?

DR. SAMET: That's correct.

MS. SHERMAN: Do you believe that meta-analysis is the only way to draw a reliable conclusion about what the body of epidemiological literature shows?

DR. SAMET: No, I do not.

MS. SHERMAN: Did EPA rely only meta-analysis to conclude that the epidemiological literature showed an increase risk of lung cancer with exposure to environmental tobacco smoke?

DR. SAMET: The report considers a variety of evidence. The meta-analysis was used for quantitative risk estimation.

MS. SHERMAN: So therefore, did the Scientific Advisory Board say that meta-analysis was only one method of assessing the data and that other data also showed that environmental tobacco smoke was a class A carcinogen? Didn't they conclude that?

DR. SAMET: I'm not sure the Science Advisory Board says that. I think the report itself states within one of the introductory chapters, and, again, I would have to look for that and I can't do it now, that the evidence from active smoking, understanding in cancer there are other considerations, alone would meet the agency's guideline but I think I would have to find that sentence before quoting it with full confidence.

MS. SHERMAN: Well, perhaps it will come to you. We've had a lot of discussion over the last couple of days about the Fontham study and I assume you're fairly familiar with that study.

DR. SAMET: Yes.

MS. SHERMAN: Do you believe that Dr. Fontham adequately controlled for confounders in that study?

DR. SAMET: She did. She controlled for confounding factors that would be-- I think potential confounding factors in women in the United States.

MS. SHERMAN: Are you familiar with, I guess what I would term for want of a better term, the new Fontham study? The one that was recently published?

DR. SAMET: You're referring to the 1994 report, the full study?

MS. SHERMAN: Yes.

DR. SAMET: Yes.

MS. SHERMAN: Does the new Fontham study strengthen the association in your mind between lung cancer and ETS exposure?

DR. SAMET: Well, I think it provides-- I think the association has long been established as causal at this point. I think what the Fontham study does is provides new information on the quantitative risks of ETS exposure.

MS. SHERMAN: And did she-- I assume the answer is yes to this, that she also controlled for confounders in this new study because it's just a part of the old study?

DR. SAMET: It's a continuation. Yes. The same methodology.

MS. SHERMAN: So therefore it's a silly question to ask.

DR. SAMET: Correct. Correct.

MS. SHERMAN: That's all I have.

JUDGE VITTONE: Thank you, Ms. Sherman.

Thank you, Doctor. We appreciate your time and your effort here today. You can step down.

MS. SHERMAN: Did you give your slides to--

DR. SAMET: Yes.

MS. SHERMAN: Okay. Thank you very much.

JUDGE VITTONE: This concludes our scheduled witnesses for today. We have three witnesses scheduled for tomorrow morning: Daniel Ford, M.D.; A. Judson Wells and James Woods. We will be here in this room tomorrow.

MR. RUPP: Your Honor?

JUDGE VITTONE: Yes?

MR. RUPP: May we raise a scheduling issue for tomorrow?

JUDGE VITTONE: I'm sorry. I can't hear you.

MR. RUPP: May we raise a scheduling issue relating to tomorrow at this point before we break?

JUDGE VITTONE: Okay.

MR. RUPP: I think it's going to be very difficult, if not impossible, to get through three witnesses tomorrow, given the nature of the witnesses. I just think it's unrealistic.

I think we are going to find ourselves going much longer than we're going tonight and I think that the pace again, if OSHA's effort is to assemble a productive, useful record, this is not the way to proceed.

I think all of these three people who are scheduled for tomorrow are within 50 or 60 miles of Washington, D.C. What I would like to suggest is that one of them, personally I don't really care which one, be rescheduled for anther time so that we have an adequate time to prepare and to examine, we're not under pressure all day, we don't find ourselves here tomorrow night at nine o'clock. And tomorrow is Friday, in addition to that. So I would like to suggest that with the choice being the agency's that one of these people be called tonight and told not to drive in tomorrow, to be rescheduled at a later date.

JUDGE VITTONE: Ms. Sherman?

MS. SHERMAN: I can take it under advisement. I will tell Mr. Rupp that the schedule of the people scheduled tomorrow are very busy. I don't know when it would be possible to get them back. One of them is already here in a hotel waiting to testify.

MR. RUPP: And I think we should proceed with that person. But I think that the problem-- waiting until tomorrow to know means that many of us are going to have to stay up half the night preparing so our point is we would like to know tonight so that we can prepare, do the preparation that needs to be done and then examine the people who are going to be here for examination.

Now, I think we would be prepared to stay or one of us would be prepared to be in contact with Ms. Sherman if she wants to try to contact the other two individuals tonight and let us know and we can try to let others know but I really would hope that Your Honor would take the request seriously and that something could be done to accommodate in this circumstance. It's been a tough week.

JUDGE VITTONE: Ms. Sherman?

MS. SHERMAN: I can consult with my office and also try to get a hold of the witnesses but I think that perhaps we moved faster toward the end of the day and I don't see any reason why we can't do the same tomorrow.

MR. RUPP: We say that every day and then we find ourselves-- last night we found ourselves here at eight o'clock. Tonight we find ourselves-- and then preparation for the next day begins. Those of us who are asking questions, this is a very difficult pace. We have said this from before the time these proceedings started and each day the notion is that things will get easier tomorrow. They don't get easier tomorrow and tomorrow we can see that we're not going to be able to accommodate those three witnesses.

JUDGE VITTONE: I did some rough calculations while we were sitting here. We started at 9:30 and it was 7:00 when we stopped. We took one hour for lunch. We took an hour for administrative matters and breaks. Took two hours for the witnesses to present their testimony which left about four and a half hours for examination, for all three witnesses and that's primarily the tobacco witnesses but we also had the others, the AFL-CIO, Bowman and so forth.

I guess what I'm trying to say is I think we did fairly well today with respect to the examination and came pretty close to almost a regular eight-hour day here, I guess.

I'm going to leave that up to you. If you can do that, it would be wonderful but what about you guys, as far as keeping to really important stuff so that we can make sure that we can get through at least two of these people?

MR. RUPP: We certainly will continue to try. I will say that in the last two witnesses we faced two diametrically opposed witness styles. In one case, it was very difficult to get him to answer the questions in a reasonably pointed fashion and in the case of this witness it was very difficult-- I mean, it was a fight over the individual words that were used. My sense was often there was no misunderstanding about what the concept was but--

MS. SHERMAN: I would think that that is an improper characterization.

MR. RUPP: I think the questions were fair and reasonable and important.

MS. SHERMAN: I think the questions were so long that it confused the witness.

MR. RUPP: We'll both try. We'll both try. Obviously, this is going to be unresolved.

JUDGE VITTONE: It's the end of the day.

All right. Let's take it up first thing in the morning.

MR. RUPP: Would Ms. Sherman be prepared to call me if you're able to reschedule either of the two gentlemen who are not yet in town and I will try to alert others?

MS. SHERMAN: I will take your phone number or if you would like me to communicate with you if I am able to find out something.

MR. RUPP: Would that be the best way to do it? Who is the witness in the hotel?

MS. SHERMAN: The witness in the hotel is Mr. Wells but I hope you don't ask me which hotel it is because I don't know.

MR. RUPP: No. No. We don't plan to contact Mr. Wells. He will be the first--

MS. SHERMAN: No, what I mean is I don't know where he is. I just got a message that--

MR. RUPP: That he's here?

MS. SHERMAN: That he was here.

MR. RUPP: Okay. Will he be first tomorrow? Can we rely on that?

MS. SHERMAN: I'm not sure what the travel arrangements of the other two are.

MR. RUPP: See, that also presents a problem because there are some people who come in to--

MS. SHERMAN: I can appreciate that and I know Ms. Ward has asked me that also. But as you notice, I've been busy here today, too, and I haven't had a chance to talk to people.

MR. RUPP: Right. Well, could you also let me know that tonight when you call? And I will just wait for your telephone call.

MS. SHERMAN: I will try.

MR. RUPP: I appreciate that.

JUDGE VITTONE: All right. We'll take it up first thing tomorrow morning. We will begin at 9:30 tomorrow morning.
This document's URL is: http://www.tobacco.org/Documents/osha/940922osha.html


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