OSHA: Proposed Standard For Indoor Air Quality: ETS Hearings, September 23, 1994

OSHA: Proposed Standard For Indoor Air Quality: ETS Hearings, September 23, 1994


UNITED STATES DEPARTMENT OF LABOR

OCCUPATIONAL SAFETY AND HEALTH ADMINISTRATION

PUBLIC HEARING

PROPOSED STANDARD FOR INDOOR AIR QUALITY

Friday,

September 23, 1994

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

Witnesses:

Judson Wells 951

Questions:

Pat Sirridge 988

Jeff Furr 1024

John Rupp 1072

James D. Woods 1104

Questions:

Michael Jawer 1139

George Benda 1164

Saneya El-MeKawi 1178

Debra Janes 1180

Lee Hathan 1181

EXHIBITS

EXHIBIT NO. IDENTIFIED RECEIVED

26 1020 1020

27 1072 1072

28 1103 1103 P R O C E E D I N G S

(9:36 a.m.)

JUDGE VITTONE: We finished last night with

Dr. Samet. We will begin this morning, and we have three witnesses on the schedule.

Ms. Sherman?

MS. SHERMAN: I would like to call first on

Mr. Judson Wells.

JUDGE VITTONE: Would Mr. Wells come forward, please. Would you come up here, sir?

Off the record a second.

[Discussion off the record.]

JUDGE VITTONE: Sir, would you identify yourself, please, for the record?

MR. WELLS: My name is A. Judson Wells, and I'm testifying this morning for OSHA.

JUDGE VITTONE: Who are you affiliated with, sir?

MR. WELLS: I guess I'm a freelance consultant, in a way.

JUDGE VITTONE: Okay.

MR. WELLS: I am a half-time volunteer, roughly, for the American Lung Association.

JUDGE VITTONE: All right. You've previously submitted your comments for the record?

MR. WELLS: Yes.

JUDGE VITTONE: Okay. Let me get out of your way, and you can begin your presentation.

MS. SHERMAN: Mr. Wells, let me ask you before you start. Every time you ask to have a slide shown, please identify it by name or number so that the transcript will make some sense.

JUDGE VITTONE: You may begin, Mr. Wells.

A. JUDSON WELLS

MR. WELLS: Yes. As I said, my name is A. Judson Wells. I graduated from Harvard College in 1938 with a summa cum laude degree. I went on at Harvard and finished a PhD there in physical chemistry in 1941.

I was employed in the chemical industry, specifically by E.I. dupont and deNemours Company, from 1941 until 1980.

I worked in chemical research, research management, and general management. From 1969 to 1980, I was director of a business division, with revenues at that time of $125 million. Since 1981, I have served as a volunteer consultant in the smoking and health area for the American Lung Association. For the whole of that time, I have studied the scientific literature on the health effects of passive smoking.

From 1989 to 1983, I was an unpaid consultant to Kenneth G. Brown, Incorporated, a subcontractor to the U.S. Environmental Protection Agency.

Their work leading up to the publication of their report, Respiratory Health Effects of Passive Smoking, Lung Cancer, and other Disorders, I am a co-author of that report.

More recently, I have consulted, again unpaid, for the U.S. Occupational Safety & Health Administration on Health Effects of Passive Smoking, and I am testifying on their behalf today.

In my testimony today I will be covering two topics. One is the Association of Exposure to Environmental Tobacco Smoke, which I will call ETS and heart disease; and, secondly, methods for observe, passive smoking relative risks for the effects of smoker misclassification.

I will also comment on the ETS part of OSHA's preliminary quantitative risk assessment as published in the Federal Register April 5, 1994.

On heart disease, exposure to environmental tobacco smoke, also known as passive or involuntary smoking, results in a number of adverse health effects. Although most of the attention for adults has been directed towards lung cancer, heart disease, at least in terms of probable deaths, is much more important.

The reason is that the percent increase in risk from ETS exposure is about the same for both diseases. Lung cancer among people who have never smoked, is a rare disease, while heart disease among never-smokers is many times more common.

Therefore, the same small fraction of deaths, multiplied by a much larger number of total deaths, results in a large number of deaths attributable to passive smoking.

Over the past six years, there have been five papers in the peer reviewed literature that are known to me and that have assessed the available evidence on adult mortality from passive smoking and heart disease. Each of these papers is appended as part of my testimony, and the five papers are listed in Table 1.

The first is a paper of mine published in December 1988 in the Journal Environment International. The 7 epidemiologic studies then available on passive smoking and heart disease were reviewed.

The relative risks from the 7 studied were pooled to develop a combined risk, which indicates a 30 percent increase in risk for ETS exposure and a predicted 32,000 heart deaths per year in the U.S. among non-smokers that are caused by passive smoking.

The second important peer reviewed paper is that of Glantz and Parmley published in January 1991, in circulation, which is the leading medical journal of the American Heart Association.

They reviewed not only the epidemiologic studies and Wells' death estimate, but also provided a thorough review of the physiology and biochemistry that connects ETS exposure with heart disease. They conclude that, quote: "ETS causes heart disease," unquote.

The third important paper came from Karl Steenland of the National Institute for Occupational Safety & Health, that was in the January 1992 issue of the Journal of the American Medical Association.

He reviewed, again, the epidemiologic studies, now grown to 9, and the biologic plausibility. He then made a risk assessment based on the relative risk from the largest U.S. study, namely, Helsing, et. al, and concluded that if the epidemiologic results are valid, then there 35,000 to 40,000 ischemic heart disease deaths per year in the United States, that are associated with passive smoking.

Ischemic heart disease is that type of heart disease where there is obstruction in the coronary arteries so that part of the heart muscle becomes disabled because of lack of oxygen.

The fourth paper is a medical scientific position statement from the American Heart Association, published in the August 1992 issue of Circulation. The authors, Taylor, Johnson, and Kazemi, reviewed again the available evidence and concluded that, quote, "ETS is a major preventable cause of cardiovascular disease and death," unquote.

The fifth important peer reviewed paper is one of mine, published August 1st, 1994, in the Journal of the American College of Cardiology, another leading medical journal in the heart field.

This paper reviews the newer studies since Glantz and Parmley that support the biologic plausibility of a link between passive smoking and heart disease. Results of the epidemiologic studies, now grown to 13, are again pooled. They indicate a 37 percent increase in ischemic heart disease morbidity, and a 22 percent increase in heart disease death for those exposed to ETS at home versus those not so exposed.

Then, using the EPA's methods of calculating deaths from the relative risks, it is concluded that in 1985, there were 62,000 heart deaths per year in the U.S., caused by passive smoking.

These five papers, covering some 48 pages of medical journal text, cannot not be reviewed in detail here, but the main points will be summarized. There are several ways in which tobacco smoke can affect the heart, even though there is no direct contact between the smoke and the heart itself.

As with lung cancer, active smoking causes heart disease. Therefore, we would expect passive smoking also to cause heart disease but in lesser amounts.

There is one important difference between lung cancer and heart disease as far as ETS exposure is concerned. With lung cancer, the only effect is long-term; say, 20 years exposure before cancer appears. With ETS and heart disease, there are both long-term and very short-term effects, some apparent after only 20 minutes exposure.

Let's look at the short-term effects first.

The platelets in the blood are one of the factors that determine the blood's tendency to coagulate. Platelet sensitivity is a measure of this tendency. Active smokers have a lower platelet sensitivity than non-smokers, meaning that their blood is less resistant to clotting.

The evidence for decreased platelet sensitivity among non-smokers exposed to ETS, comes from the laboratories of J.W. Davis in Kansas City and

H. Sinzinger at Vienna, Austria.

For example, Davis found that non-smokers exposed to only 20 minutes in a hospital lobby, where smoking was allowed, lost about 60 percent of their platelet sensitivity advantage over active smokers.

However, their platelet sensitivity returned to normal shortly after the exposure ceased. Similar results from Burghuber, et al, and Sinzinger's group are shown in Figure 1.

Here, the ETS exposure is also for 20 minutes but at a somewhat higher level. As you can see, the non-smokers have lost about 80 percent of their platelet sensitivity advantage over the smokers. The before and the after, you can see, obviously.

Sinzinger's group also found that after repeated ETS exposures, nonsmokers baseline platelet sensitivity was reduced to a level near to that of smokers. Low platelet sensitivity is a known heart risk factor.

Experiments by Davis with sham cigarettes indicate that the lower platelet sensitivity may be related to the nicotine in this cigarette smoke.

Another short-term effect is that provided by the carbon monoxide in the smoke. Carbon monoxide is the odorless, colorless, toxic gas that also occurs in the exhaust from automobiles.

Carbon monoxide reacts with a hemoglobin in the blood and renders it incapable of transporting oxygen. It is the ability of the blood hemoglobin to carry oxygen from the lungs to the heart, brain and muscles, that sustains life.

Typical ETS atmospheres contain from 3 to 25 parts per million of carbon monoxide resulting in .4 to 5 percent of the hemoglobin being inactivated.

A typical situation would be ETS with 15 parts per million of carbon monoxide resulting in 2 percent of the blood hemoglobin being inactivated.

When 30 percent of the hemoglobin is inactivated, the result is death. With part of the blood hemoglobin inactivated by carbon monoxide from ETS exposure, the heart must work harder. That is, it must pump more blood with the same level of physical exertion.

The carbon monoxide also affects the ability of the heart to process oxygen by attacking some of the proteins and enzymes in the heart muscle that is essential to what is called myocardial/mitochondrial respiration.

Thus, ETS exposure reduces the effective blood supply of the heart, while at the same time reducing the heart's ability to process the blood that it receives.

This results in reduced exercise capability, both in healthy people and particularly in people with existing coronary disease.

Going on now to long-term effects, one theory about how heart attacks arise is, first, there damage to the coronary artery wall; then plaque builds up around the injury, eventually reducing the blood's supply to the heart, and thereby causing the heart attack.

In the platelet experiments that I described earlier, it was also noticed that short-term ETS exposure of nonsmokers results in an increase in endothelial cell carcasses in the blood. This indicates damage to the endothelium, which is the very thin lining of artery walls and blood vessels.

Once the initial damage is done, researchers have found that exposure to cigarette smoke accelerates the growth of these plaques. In other words, not more plaques form but bigger ones form sooner.

These experiments in mice, pigeons, chickens, rabbits and dogs, so far, indicate that it is the poly aromatic hydrocarbons in the smoke that are causing the effect.

The most recent of these papers, namely that by Penn, et al, show a significant increase in plaque development when cockerels were exposed to the smoke from only one cigarette over a 16-week period.

Moreover, one researcher has found through ultrasound experiments that the arterial walls in humans become thicker if the subjects smoke or are exposed to ETS.

Another, I'd say, medium-term effect is that ETS exposure appears to lower the high density or good cholesterol in the blood or to raise the total cholesterol high density cholesterol ratio. These are known heart disease risk factors.

Other researchers have found that ETS exposure reduces plasma ascorbic acid, which is Vitamin C, in nonsmokers by an amount that is 65 percent of the reduction experienced by active smokers.

Thus, we have ample biologic evidence that passive smoking can affect the blood in ways that injurious to the heart and that these effects are often stronger than one would expect considering the difference in dose between active and passive smoking.

To get some idea of the magnitude of the heart risk from passive smoking, one must turn to the epidemiology. In my 1994 paper, I reviewed 13 studies based on over 3,000 cases, where either heart disease or heart death was studied relative to ETS exposure.

This is an enormous data base compared to what is usually available in regulating work place toxins. Five of the studies are U.S. based and the others come from Australia, China, England, Japan, New Zealand, and Scotland.

Eight of the studies are mortality studies, and four of them have data for both males and females, resulting in 12 separate data points that are shown in Figure 2.

The 12 odds ratios or relative risks for prospective studies are platted on a log scale against the statistical weights for each data point. You must remember, the larger studies have larger statistical weight than the smaller studies.

As you can see, for the smaller studies, the ones to the left here, there is considerable scatter. When the statistical weight gets beyond about 20, the odds ratios become very stable in the 1.15, the 1.30 range.

The combined odds ratio for all of the studies, as shown at the right, is 1.22, and is dominated by the large, statistically significant Helsing, et. al study, which comprises 42 percent of the total cases.

Many of the other studies are too small to reach statistical significance at the 95 percent level, but they do indicate appreciable increased risk.

The results of these smaller studies can be pooled to see if, together, they indicate higher statistical significance. When this is done, we find that in mortality studies for both men and women, in the Helsing study is removed, the pool results for the remaining studies, show an odds ratio of 1.26, that is still highly statistically significant.

A new study from Xian, China, not included by OSHA in their proposal in the Federal Register, while too small, 59 cases, to show statistically significant adjusted relative risk, did investigate the heart effects on nonsmoking women exposed to ETS both at home and at work.

For exposure at work, there was an 85 percent increase in risk, with a highly statistically significant trend of increasing risk with increasing amounts of ETS exposure.

Only 8 percent of women in that part of China smoke, but most of the men smoke, and they smoked freely at work, so the study provides an excellent opportunity to judge the effects of ETS exposure at work on heart disease in nonsmokers.

In many of the ETS heart studies, accrued risks were adjusted for various other heart risk factors. The relative risks noted above are the adjusted relative risks after adjusting for such factors as age, blood pressure, cholesterol, personal or family history of heart disease, weight or body mass index, exercise, marital status, education or social status, and diabetes.

Thus, the potentially and most important confounders have been considered in at least some of the studies and found not to explain the observed increased risk.

Comments from the tobacco industry have emphasized the large number of potential confounders and how they might affect the epidemiologic results. Yet, in no study of passive smoking in either heart disease or lung cancer has adjustment for confounders reduced the relative risk to 1.00.

It is evident in my 1994 paper, although adjustment for confounders in some cases raises relative risk and in others lowers the risk, the overall effect is that those studies that adjusted for more potential confounders had higher relative risks than those that adjusted for fewer.

Also in the literature, there are indications that things don't always go in one direction.

For example, LeMarsh, et. al., found that beta carotene intake went down as exposure to ETS went up, and that's a possible confounder for lung cancer. The intake of cholesterol and fat also went down with ETS exposure, and that's a possible protective effect for heart disease.

Lower social class is thought to be a potential adverse confounder for both lung cancer and heart disease, but Humble, et al, and the Evans County, Georgia perspective study, found that higher social status whites had higher passive smoking relative risks for heart disease than did lower social status whites.

Diet is alleged to be an important potential confounder, yet in the EPA report, diet effects in 9 of the passive smoking studies on lung cancer, were investigated. This included all of the studies that contained data on diet effects, including Kalandidi,

et al., and Fontham, et al., that were specifically designed to measure possible confounding by diet. No appreciable effect on the observed relative risk was found.

The heat disease studies have not adjusted for dietary intake as such, but a number of them have adjusted for total cholesterol and high density cholesterol, which should, in part, reflect dietary habits.

Again, no confounding effect was found that nullified the observed passive smoking relative risk.

LeVois and Layard, in their August 10, 1994 submission to OSHA, have presented analyses of the data in the CPS 1 and CPS 2 studies of the American Cancer Society, and also a study based on the national mortality follow back survey, all three of which are purported to show no increase in heart disease relative risk from exposure to ETS.

In none of these analyses was there any adjustment for any heart disease risk factors, other than age and race. This is a serious shortcoming since, as was observed earlier, studies that adjust for more heart risk factors, tend to have higher relative risks.

In terms of the quality tier levels in my 1994 review of Heart Disease and Passive Smoking, there are three studies. These three studies would have been assigned to the lowest tier level, Level 4, and would not have been included in my combined relative risk that was used for the basis of the risk assessment.

The quality tier levels were independent of the size of the studies, which was taken into account by the statistical weight. The CPS 1 study had a rather controversial history as far as passive smoking is concerned.

After Hiriyama and Trichopoulos papers on passive smoking and lung cancer were published in 1981, Lawrence Garfinkel wanted to add a comment on passive smoking to his paper, which was in the National Cancer Institute Journal.

This was a paper on time trends and lung cancer mortality among non-smokers.

Karl Hammond, the former research head of the American Cancer Society, and who had gathered the CPS 1 data in the first place, and his colleague, Ervin Salakoff, both, I believe on the ACS Board at that time, were very opposed to publishing the passive smoking result, so when it was finally published, they expressed their reasons for opposing the publication in a paper in Environmental Research, 1981, Volume 24, pages 444 to 452.

Hammond said that he, and I quote: "Would have liked to estimate lung cancer death rates in relation to the amount of passive smoking among female subjects who never smoked. He" -- and he's referring here to

himself -- "he refrained from attempting to do so for the following reasons.

"Since his perspective study was not designed for that purpose, no special information on the subject was obtained. Information was available on the smoking habits of the husbands of many of the married women in the study but not on the smoking habits of the former husbands of women who were widowed, divorced, separated, or married for a second time.

"More important, in America, at that time, women were not generally barred from public and social gatherings where men were smoking, and smoking husbands who smoked, generally did much, if not most of their smoking, away from home," unquote.

Dr. Hammond and Dr. Salakoff then go on to point out why studies in Greece and Japan are more likely to yield a meaningful result because of the traditional segregation of married women from men, other than their husbands, in those societies.

These criticisms of CPS 1 regarding passive smoking and lung cancer apply at least as much to passive smoking and heart disease. CPS 2 suffers from the same problems. The questionnaire for CPS 2 did include one simple question on ETS exposure that covered current exposure only, at home, work, and other.

However, LeVois and Layard did not avail themselves of any of this information in their analysis.

They relied, instead, as Garfinkel did, on matching spouses on the basis of their individually determined smoking prevalence. So all of Hammond and Salakoff's criticisms of CPS-1 apply to the LeVois and Layard analysis of CPS-2 as well.

Their analysis of the data for the National Mortality Feedback Survey, aside from its failure to adjust for the various heart disease risk factors, relies on the strange choice for controls, namely, persons who died of other diseases, not smoking related.

There is a substantial difference in age of death between the cases and control with the cases living longer.

This NMFS survey may not provide a good basis for making a meaningful estimate of risk of heart disease from passive smoking.

Summarizing the epidemiology that qualified for Tier 3 or better quality rating in my 1994 paper, there is a 20 to 30 percent increase in risk of ischemic heart disease associated with exposure to spousal or household ETS.

There's also strong evidence that the risk from ETS exposure at work are similar to those experienced at home. Also, these increases in risk cannot be accounted for by the other known hard risk factors, and, as I shall note later, they are not accounted for by the misclassification of smokers as non-smokers.

I'll go on now to the effects of smoker misclassification on the passive smoking relative risks.

This part of my testimony, I will be discussing the misclassification and current and past smokers as never smoked, the effects that such misclassification has on the observed relative risks of passive smoking studies.

In doing so, I will be defending Appendix B in the EPA report on ETS and lung cancer. Appendix B describes EPA's methods of dealing with this type of misclassification. I was the author of Appendix B, and the tobacco industry consultants have criticized our methods.

I will deal with the effects of smoker misclassification and heart disease relative risks later.

Why is smoker misclassification an issue? It is known that a small percentage of smokers, if asked if they ever smoked, will say no.

It is also known that smokers tend to marry smokers and nonsmokers tend to marry nonsmokers. Therefore, for a given level of misclassification, more of these real smokers will show up in the group of so-called "never smokers married to the smokers" than the group of "never smokers married to the never smokers".

In the case of lung cancer, the high relative risk among these few misclassified smokers, will raise the average lung cancer risk of the self-reported never smokers, and they will raise it more for those married to the smokers than for those married to the never smokers.

This, then, will create a perceived increase in risk that could be mistaken for a passive smoking effect. There is no real question that such a misclassification effect exists. The real question is how big is it.

The EPA method offer estimating the bias introduced by smoker misclassification was developed by Dr. Walter Stewart of the Johns Hopkins School of Public Health and myself.

Dr. Stewart is an expert in occupational health epidemiology. The method is basically his which I have adapted to passive smoking. Our method involves dividing the misclassified smokers into three groups:

One: The current, regular smokers, with cotinine levels and body fluids, like average, self-reported, current smokers.

The second group are current occasional smokers, and the third group is classified ex-smokers.

This subdivision of the misclassified smokers was first suggested by Peter Lee. Misclassification rates are then developed for each class of misclassifieds, using cotinine data for the current smokers, discordant studies for the ex-smokers.

Cotinine is a longer-lived metabolite of nicotine which has become the biomarker of choice for determining relative levels of ETS exposure.

Proportionate distributions of controls and cases by smoking status of subjects and spouses are developed using demographic data and smoking relative risks. Misclassification rates have been applied to the various subclasses of smokers to estimate the proportions of each category misclassified.

These are then subtracted from the proportions of observed never smokers, yield a proportion of true never smokers among exposed and unexposed cases and controls. In these numbers, the corrected relative risks can be calculated.

Our method has been peer reviewed by EPA's Science Advisory Board. In late 1991, Peter Lee, a consultant to the tobacco industry, came up with an alternative method for estimating the smoker misclassification bias.

As shown on EPA's Appendix B and shown here in Table 2 in condensed form -- this may be a little hard to read -- but basically what it shows is that when the same inputs are used Lee's methods and ours give essentially the same results.

However, Lee's estimates are different, so that his results are different; namely, they come to a much higher bias. There are four important inputs for these calculations. They are, as shown in Table 3, the misclassification rates, the prevalence of smoking among the subjects. The more smokers in the cohort the more will be misclassified.

Three: The relative risks assumed for the misclassified smokers; and,

Four: The marriage concordance among smokers and nonsmokers; that is, the relative degree to which smokers marry smokers and the nonsmokers marry nonsmokers.

Regarding the first important input, namely, the misclassification rates, we used for current smokers, all of the literature data on females, where we could get individual cotinine measurements for each individual from the authors of the papers.

This allowed us to tell exactly how many of the false negatives among the never smokers were really regular smokers and how many were only occasional smokers. We are the only group that has gone to this extent to develop accurate current smoker misclassification rates.

Similar care was taken with the ex-smoker surveys.

We concluded that 1.09 percent of regular smokers would say "never" if asked; also, 24.2 percent of occasional smokers and 11.7 percent of ex-smokers.

Lee used a single, overall misclassification rate which, in effect, was about 30 percent larger than ours. We used smoking prevalence and smoker relative risks that were appropriate for each study. Lee used values that, in some cases, were twice as high as indicated in the studies themselves.

On marriage concordance, he and we used similar values. The overall effect, when these overages were all multiplied together, was that his estimated bias, as I think I showed there on that previous table, was, in some cases, several times as large as ours.

There is evidence that, even in our evidence of the misclassification effect, our corrections are too high. Our data come from some epidemiologic studies but mostly from community survey type studies.

For the regular smokers and the ex-smokers, the two most important classes, the misclassification rates from the community type surveys tend to run about 7 times as large as those from the few epidemiologic studies that we have.

For example, Fontham, et al., is one of the best lung cancer epidemiologic studies. After they went through all of their normal questionnaire procedures, they ran cotinine levels on the remaining subjects who said they never smoked. Among the cases, they found no regular smokers misclassified versus our estimate of 1.09 percent, and about 7 percent of occasional smokers versus our estimate of 24 percent.

Another indication that our bias estimate is high is found in the male data. Here, smoking prevalence are high. When we used male misclassification rates, derived as above for the female rates, namely, from this mixture of community surveys and epidemiologic studies, we found in some studies that we were making corrections for, that the number of smokers misclassified as never smokers, exceeded the number of self-reported never smokers that we had to begin with.

This is evidently impossible; again, indicating that our misclassification rates are too high.

Another reason that our estimates of smoker misclassification bias in the EPA report is too high is that we use too high a smoker relative risk for the misclassified ex-smokers.

The best data on how long ago the misclassified ex-smokers smoked and how much they smoked comes from Micky Briton, in a paper in the International Journal of Epidemiology.

She found that the average interval that a self-reported never smoker last said he or she smoked was 16 years, and the average amount that these misclassified

ex-smokers smoked, was about one-fourth of the amount that the average smoker smokes. These are for people 36 years old at last interview.

These numbers are confirmed qualitiatively by Peter Lee who states that his data indicate that misclassified ex-smokers gave up longer ago and smoked markedly less than self-reported ex-smokers, but he gives no numerical data.

We had used ex-smokers relative risks for smokers who had quit 10 or more years earlier, and that's with that 16-year figure from Micky Briton. We had failed to cut this excess risk to one-fourth to take account of the reduced usage, thus our correction for the ex-smoker group is four times too large.

In a recent submission to OSHA, Mr. Lee has criticized our use of misclassification rates based largely on western data to calculate misclassification bias for Asian studies.

These sites are a market research type study in Japan, based on 400 women, which found, based on cotinine tests, that 22 women said they never smoked but had cotinine levels typical of regular smokers.

Compared with the self-reported regular smokers, there were 78 of those. This is a misclassification rate, in ou type of terms, of 28 percent, compared to our value of 1.09 percent, and that's quite a difference.

These values, based on door-to-door interviews of women age 20 to 50, East Asian data that we have used came from IARC. That's the International Research on Cancer. Specifically, from three epidemiologists who had done passive smoking lung cancer studies in Hong Kong, Sendei, Japan, and in Shanghai; namely, Linda Ku Samuzu and Y.T. Gale.

Their misclassification rate for regular current smokers, also based on cotinine tests, is about 1.2 percent of self-reported current, regular smokers.

The Japanese values is about 2 percent, or about 1/14th of the value that Lee got from his house to house market research style survey.

I had commented earlier about how the misclassification rates obtained from community surveys were higher than we got from the few epidemiologic surveys that were available.

Apparently, these market research type surveys are worse. Lee's survey is reminiscent of the market research style survey done by Ogden, that was included in *the submission of Sears, et al., to EPA in 1992. This study was commissioned by the RJ Reynolds Tobacco Company.

The number in the report are confusing. For example, they claim that 80 occasional smokers were misclassified in the sample that probably only contained about 20 occasional smokers to begin with.

However, their misclassification rate for regular smokers, misclassified as never smokers, is 5.6 percent of the never smokers, or about 12 percent of the current regular smokers.

This is about 11 times the rate we got from our combination of community surveys and epidemiologic studies.

I can't emphasize to strongly that if we are to correct epidemiologic studies accurately, the smoker misclassification, for smoker misclassification, we need smoker misclassification data that are of epidemiologic quality.

Another way in which Lee's Japanese survey differs from the one done by the epidemiologist,

Dr. Shumuzu, is that Lee got almost identical cotinine levels for nonsmokers married to smokers and nonsmokers married to nonsmokers.

Shumuzu, on the other hand, found that nonsmoking women married to smokers had 3-1/2 times the cotinine level of the nonsmokers married to nonsmokers, a result indicating a substantially higher ETS exposure for the women married to the smokers, and much more in line with the results found elsewhere.

Mr. Lee also claims that marriage concordance of smokers with smokers and nonsmokers with nonsmokers, increases with the amount smoked and cites his own data as evidence.

In his 1992 book, Environmental Tobacco Smoke and Mortality, he quotes a study by Coultas, et al., where the concordance declined with the amount smoked for females. No other data for females reported.

My analysis of the data of Sutton, which is his paper in the Annals of Human Biology, 1980, plus Private Communications from Dr. Sutton, indicates that concordance declines with increasing age of the subjects, a view concurred with by data Lee describes of Venders, et al.

Thus, for the ages at which death by passive smoking occurs -- that means age 60s and 70s -- concordance values could be substantially lower.

Also, one must be very careful to design accurately which level of smoking is being considered since concordance values of ever smokers and ex-smokers are lower than for current smokers.

We believe that the concordance values we have used are reasonable and that there is very little evidence that concordance increases enough the smoking level to explain the dose response effects that are observed in these passive smoking studies.

Yet, a measure of the impact of these corrections on the lung cancer relative risks, Dr. Stewart and I pooled a relative risk from 25 of the lung cancer studies in the EPA report. The EPA had divided the epidemiologic studies on ETS exposure and lung cancer into four quality tier levels, based on scores for various factors, either included in or excluded from the various studies.

They based their lung cancer risk assessment on the top three quality tiers. We also used their quality assignments and drew our 25 studies from the top three tiers. That's essentially all of the studies. These were all studies on females.

We then corrected each of the studies for smoker misclassification and pooled the corrected relative risk. The pooled uncorrected risk was 1.40; the pooled corrected risk was 1.37. So, for a lung cancer, the overall effect is smaller.

For studies in western countries, where females smoking prevalence is high, the corrections are larger.

For Asian and other countries and other studies and conservative societies, where female smoking is low, the corrections are very small.

In the Fontham, et al., study, on which OSHA's lung cancer risk assessment is based, the correction for smoker misclassification is very small because the authors were able to eliminate most of the current smokers from the study by cotinine tests.

For heart disease, there is an even smaller correction for smoker misclassification. The reason is that the relative risk for active smoking for heart disease is much lower than for lung cancer. It's about 1.7 relative risk versus about 4 worldwide for lung cancer in females, or about 8 in recent U.S. studies.

This lower relative risk carries over to the smokers' misclassified as never smokers, thus lowering the correction.

In my recent paper on Passive Smoking and Heart Disease, the pooled heart relative risk for females was lowered only from 1.25 to 1.24 by the smoker misclassification correction.

For males, the correction was larger -- 1.38 to 1.30 -- because of the larger proportion of smokers.

Again, these corrections are probably too large by a factor of 2 to 4, for the reasons I mentioned earlier.

I would like to comment briefly on the OSHA Preliminary Risk Assessment.

The passive smoking risk assessments that have been carried out so far, both for lung cancer and for heart disease, have covered the entire U.S. population. This risk assessment by OSHA is the first, to my knowledge, that is restricted entirely to work place exposure.

Although I might differ on some of the details, the assume methodology is well conceived, and results are reasonable.

OSHA has used, as a lung cancer relative risk, the occupational risk of 1.34 for women, in a preliminary report by Fontham, et al.

This is, without doubt, the best U.S. study and is an appropriate choice. However, the final report for that study is now available, so the updated occupational relative risk of 1.39, with 95 percent confidence interval of 1.11 to 1.74 should be used.

William Butler, in his August 1994 submission to OSHA, has challenged the use of the Fontham study for lung cancer, and proposed the Brownson, et al., study insisted, primarily because the Brownson study is larger than the preliminary version of the Fontham study.

However, the final version of the Fontham study is now out, and it is larger than the Brownson study, so that argument now goes in reverse.

Further, the Fontham study had in person rather than telephone interviews, 83 percent direct interviews with cases versus 35 percent for Brownson.

Urine samples from most of the participants versus no urine samples for Brownson, and information to allow for adjustment for age, study area, education level, fruit, vegetable, and vitamin supplement intake, dietary cholesterol intake, family history of lung cancer, and high risk occupation; whereas Brownson adjusted only for age and previous lung disease. Thus, the Fontham study is, by far, the better study.

Butler characterizes the Brownson study as negative as far as work place exposure is concerned and noting an odds ratio of .90.

However, if one compares the odds ratio from his Table 5 to the highest quartile of exposure with that for the lowest quartile, certainly a legitimate way to look at the data, one notes an increased risk of 1.83 or 83 percent for the higher -- that's for the highest quartile versus the lowest quartile.

Or for the higher half relative to the lower half, 1.30 over .6 equals 1.97, which is a 97 percent increase of risk for the higher half of the exposure group.

Even including the non-exposed denominator, the highest two quartiles of exposure show increased risk of 1.44.

For heart disease, OSHA used the relative risk for household ETS exposure from the largest U.S. heart study, namely, Helsing, et al. This, again, is appropriate.

However, an alternative analysis of the data, based on a somewhat different mathematical model, appears in Sandler, et al. Relative risk for males at 1.31, is the same in both papers; the relative risk for females is slightly different; namely, 1.19 in Sandler versus 1.24 in Helsing.

I talked to Dr. Sandler about this, and she advises that these two estimates are statistically equivalent. You just use different statistical models. So, an average of say 1.21 might be appropriate for the female relative risk.

OSHA's discussion of why the household exposure data can be used for the occupational exposure is appropriate and well done. Major support for OSHA's position that there is an adverse heart effect from ETS exposure at the work place, comes from the new He, et al., paper from Xian, China, that was mentioned earlier.

This very recent study covers females only. Although the number of cases is not large, this is an excellent paper, with about 15 heart disease risk factors, including all of the important ones, either adjusted for or accounted for.

These authors found a relative risk for spousal ETS exposure of 1.24, not significant but very similar to the combined result of home exposure for all of the other studies.

In addition, they found that almost statistically significant relative risk for work place exposure of 1.85 with a highly statistically significant upward trend as work place exposure increased.

As I noted earlier, Xian is a good place to study the effects of ETS exposure on the heart, because very few women smoke there, about 8 percent, thereby cutting down on background and misclassification effects.

Most of the men smoke and they smoke freely, both at home and at work. The higher work place relative risk may result from higher exposure than is typical for U.S. work places, but this paper indicates strongly that ETS exposure at work can indeed result in coronary heart disease just as the Fontham, et al., paper suggests the same for lung cancer.

Although the risk elevations from Fontham, et al. and Helsing, et al., are small, the results are statistically significant at the 95 percent level. When the risks are applied to the large number of people exposed, a very large public health risk is indicated.

The risk assessments for the total population, it is customary to adjust the relative risk upward to account for exposure and background ETS.

This is done in order to estimate the relative risk relative to a hypothetical population that has no ETS exposure at all. However, in OSHA's case, where they are trying to determine the effect of work place exposure alone, using relative risk without adjusting for background, is more appropriate.

In the final draft, some discussion of the point may be in order.

OSHA may have underestimated the number of nonsmoking workers exposed to ETS work based on the Cummings data in the OSHA Table 4-9.

Those exposed to work but not at home totalled 48.67 percent, but an additional 29.2 percent said they were exposed both home and at work. Therefore, the OSHA range should be from 18.81 percent to 79.89 percent.

OSHA used an incidence rate for lung cancer for nonsmokers. With a low survival rate, this is almost equivalent to a mortality rate. However, they used a mortality rate for heart disease, therefore, the risk assessments in Table 4-10 and surrounding text are inconsistent.

They are disease estimates for lung cancer and death estimates for heart disease. Since the incidence rate for heart disease is about three times the mortality rate, the true number of workers exposed to ETS who -- and I quote their report -- "will develop heart disease," unquote, could be about 3 times the number of 7 to 16 per thousand mentioned in the text and shown on Table 4-10.

Perhaps Table 4-10 should be amended to show three cases: lung cancer incidence, heart disease deaths, and heart disease incidence.

The reason that the heart disease numbers are so large, relative to lung cancer, is as I said earlier that lung cancer among nonsmokers is a rare disease, so even with an appreciable increase in risk from ETS exposure, the number of lung cancer deaths from ETS exposure is about 3000 in the U.S., small relative to the number for heart disease, which is like 35,000 to 50,000.

However, the ETS lung cancer deaths are still enormous when compared to those from what EPA usually regulates, such as asbestos at about 15 deaths per year, or vinyl chloride at about 27 deaths per year.

With heart disease, the underlying death or incidence rate for nonsmokers is large. The death rate is about 3 per 1000, versus .121 per thousand for lung cancer, or about 25 times as large as the rate for lung cancer.

So when this large rate is multiplied by even a small increase in risk from ETS exposure, very large numbers result.

Leaving the epidemiology aside, it seems to me that it's unwise to have American workers exposed to fumes, such as ETS, that are known to depress significantly blood platelet sensitivity and high density cholesterol and to damage the linings of blood vessels, and, furthermore, which contains appreciable amounts of a known poison, such as carbon monoxide.

In conclusion, OSHA is to be commended for quantifying these work place risks. They are real, and they need to be attended to.

Thank you.

JUDGE VITTONE: Thank you, Mr. Wells.

Let me ask for a show of who would like to question Mr. Wells. Will the people please stand?

(Pause)

JUDGE VITTONE: Five people.

Let me get an idea of what you're asking for in terms of time. First, Mr. Sirridge?

MR. SIRRIDGE: About an hour.

JUDGE VITTONE: The gentleman here?

VOICE: Somewhere around an hour.

JUDGE VITTONE: Mr. Rupp?

MR. RUPP: About an hour.

JUDGE VITTONE: The gentleman, I'm sorry, I've forgotten your name.

MR. LOWE: Lowe. Probably half an hour.

JUDGE VITTONE: The gentleman from EPA?

VOICE: Ten minutes.

JUDGE VITTONE: Let's take a five minute recess here. It's now 10:43, and we will be back in five minutes.

JUDGE VITTONE: On the record.

Our first questioner is Mr. Sirridge.

Mr. Sirridge, would you identify yourself again for the record please?

MR. SIRRIDGE: Yes. My name is Pat Sirridge, and I will be asking questions on behalf of the same numbers that I used yesterday and the day before.

MS. SHERMAN: Could you speak up, Mr. Sirridge?

MR. SIRRIDGE: Yes. My name is Pat Sirridge, and I'll be asking questions on behalf of the same numbers of participants who filed comments that I used in previous days.

DR. WELLS: I wasn't here yesterday, so I didn't hear that list.

MR. SIRRIDGE: I can read the 17 numbers off, if that would help you.

DR. WELLS: Would you do that, please?

JUDGE VITTONE: Mr. Wells, would you keep that microphone as close as possible to you so we can make sure we get you recorded, and also everybody can hear your voice.

MR. SIRRIDGE: I'm asking questions on behalf of docket numbers 51, 153, 34, 35, 71, 74, 161, 95, 246, 57, 85, 274, 38, 180, 147 and 264.

MS. SHERMAN: Mr. Sirridge, perhaps it would be helpful if you have the names of the people who those numbers represent, if Mr. Wells wants to hear that.

MR. SIRRIDGE: I'm very confused by this process. We just had a very long discussion about trying to shorten things, and I don't think that either of you are helping that process.

DR. WELLS: I guess I'd just like to know where these questions are coming from in general. Are you a lawyer?

MR. SIRRIDGE: Yes, I'm a lawyer.

JUDGE VITTONE: Mr. Wells. Mr. Sirridge is an attorney. He is representing, who's your primary client?

MR. SIRRIDGE: Philip Morris.

JUDGE VITTONE: Philip Morris, and a number of other people who have filed statements with respect to this particular Proposed Rule.

DR. WELLS: That's very helpful. Thank you.

MR. SIRRIDGE: Sorry, I guess I should have clarified that.

Dr. Wells, did you volunteer to be a consultant to the Occupational Safety and Health Administration?

DR. WELLS: I really don't remember whether they approached me or what.

MR. SIRRIDGE: Did you hear about the OSHA rulemaking process from Mr. Repace?

DR. WELLS: I don't remember, really, where I heard it.

MR. SIRRIDGE: But you have worked with Mr. Repace on issues relating to the Environmental Protection Agency risk assessment, isn't that true?

DR. WELLS: Well, I worked for Ken Brown, and Jim Repace was in EPA, but I never really worked that closely with him on that. I worked for Steven Bayard very closely.

MR. SIRRIDGE: But you corresponded with and had discussions with Mr. Repace about issues involving environmental tobacco smoke for many years.

DR. WELLS: Yes.

MR. SIRRIDGE: In fact, he offered comments, and you exchanged correspondence in conjunction with your very first paper on ETS and risk back in 1988.

DR. WELLS: Perhaps.

MR. SIRRIDGE: You acknowledge him in the footnote.

DR. WELLS: Yeah. Mr. Repace and I are in somewhat different fields. I work more on relative risks and health effects. He works more on exposure. But if he has a paper that he'd like to have somebody look at he'll send it to several people, and sometimes sends them to me, but not very often.

MR. SIRRIDGE: And you, of course, know Dr. Glantz?

DR. WELLS: Yes.

MR. SIRRIDGE: And you've had many discussions with Dr. Glantz over the years about issues relating to ETS?

DR. WELLS: Yes.

MR. SIRRIDGE: This recent article, Dr. Wells, that was published in the Journal of the American College of Cardiology...

DR. WELLS: Yes.

MR. SIRRIDGE: That's the journal that Dr. Glantz is an editor of, is that correct?

DR. WELLS: I believe he's an associate editor.

MR. SIRRIDGE: Did Dr. Glantz suggest that you submit that article to the Journal of the American College of Cardiology?

DR. WELLS: The paper was done by request as a review article, and the request came from Dr. Parmley who is the editor of that journal.

MR. SIRRIDGE: And Dr. Parmley is the co-author with Dr. Glantz on numerous papers relating to ETS, is that correct?

DR. WELLS: Yes, that's true, but you've got to remember, Dr. Parmley is no activist. He's a very well respected past president of the American College of Cardiologists, and is widely known around the world as a very level headed, non-activist type of researcher.

MR. SIRRIDGE: Did Dr. Glantz provide you with comments and suggestions with respect to your review article?

DR. WELLS: No. Not to my knowledge.

MR. SIRRIDGE: Was he one of the peer reviewers?

DR. WELLS: I don't know. You don't know who the peer reviewers are in a well peer reviewed journal.

MR. SIRRIDGE: Dr. Wells, you've made no secret that you're a volunteer for the American Lung Association.

DR. WELLS: Yes, sir.

MR. SIRRIDGE: Would you agree that that organization has been on the forefront of anti-smoking activities in the United States?

DR. WELLS: The mission of the American Lung Association is to fight lung disease, and since smoking causes lung disease in enormous amounts, naturally...

MR. SIRRIDGE: They would be on the forefront.

DR. WELLS: They're in the forefront in that area, right.

MR. SIRRIDGE: One of your assignments at the American Lung Association has been to network in the passive smoking field.

DR. WELLS: That's right.

MR. SIRRIDGE: I guess that's what we're talking about when you're visiting with Mr. Repace and Dr. Glantz and Dr. Samet and other people in the field, is that correct?

DR. WELLS: You've got to remember that I've developed quite a group of people that I network with all around the world -- Switzerland, Sweden, New Zealand, Japan. When you single out Glantz and Repace, that's misleading. I have at least as intimate associations with several other people, and peripheral associations with many people around the world. I network very well.

MR. SIRRIDGE: You've networked, I guess, with Kyle Steenland of the National Institution of...

DR. WELLS: I've never met Steenland. He and I have discussed things over the telephone.

MR. SIRRIDGE: You're acknowledged in his publication.

DR. WELLS: Yeah.

MR. SIRRIDGE: Dr. Wells, you originally trained as a chemist?

DR. WELLS: That's right.

MR. SIRRIDGE: You're obviously not an MD or a cardiologist.

DR. WELLS: No.

MR. SIRRIDGE: And you're not an epidemiologist.

DR. WELLS: No.

MR. SIRRIDGE: And you've never conducted an epidemiologic study on coronary heart disease.

DR. WELLS: No.

MR. SIRRIDGE: You've never conducted an epidemiologic study on environmental tobacco smoke.

DR. WELLS: No, but of course that's not the area I work in, either.

MR. SIRRIDGE: And you've not conducted an epidemiologic study on any issue, true?

DR. WELLS: That's true, but completely unnecessary for the work I do.

MR. SIRRIDGE: But many of the papers that you publish, of course, are reviewing epidemiologic studies and commenting on them, is that true?

DR. WELLS: That's right, yes.

MR. SIRRIDGE: Dr. Wells, have you ever studied any other health issue in depth except environmental tobacco smoke?

DR. WELLS: No.

MR. SIRRIDGE: Have you ever undertaken a review or published an article on a public health issue other than ETS?

DR. WELLS: No.

MR. SIRRIDGE: Dr. Wells, could you name for me five or six of the major prospective studies in the field of coronary heart disease etiology?

DR. WELLS: I don't... That's not my area.

MR. SIRRIDGE: Well, Dr. Wells, don't you think it would have been helpful for you to review those prospective studies on heart disease etiology before you embarked on your job of...

DR. WELLS: I've read review articles.

MR. SIRRIDGE: But you've never reviewed the major prospective studies on cardiovascular epidemiology.

DR. WELLS: I don't think that's necessary in my work.

MR. SIRRIDGE: Your latest article, Dr. Wells, the 1994 article, again mentions the available epidemiologic studies on ETS and heart disease.

DR. WELLS: That's right.

MR. SIRRIDGE: I was a little confused this morning, your slides said 12 studies, and yet you mentioned 13 in your remarks.

DR. WELLS: I think I added the Lavechia study.

MR. SIRRIDGE: You added it to your discussion and it was not in the article?

DR. WELLS: No, it's not. I wasn't aware of it. As a matter of fact, I wasn't aware of the second Hayes study in its final form, either.

MR. SIRRIDGE: But you included that in your review and it's in the table.

DR. WELLS: Yes, but based on the abstract only. And there is a substantial difference between the abstract result and the result in the final paper.

MR. SIRRIDGE: The final paper is the one that's been published in the British Medical Journal?

DR. WELLS: Yes, I think that's where it was. It came out in early 1994, and I missed it. But you understand, when I work out of my home, I don't catch everything. People have to tell me later on. But I have figured out what effect those papers have on the results in the 1994 paper. And if you like, I'll' include that in a post-hearing written statement if you want.

MR. SIRRIDGE: You've already included, it seems to me, all the He-2 results, the one from 1994. Feel free to include the results from Lavechia in your submissions.

DR. WELLS: As I said, in the He-1994 result is different from the abstract. It has a lower relative risk per household exposure. So this would affect some of the numbers in my 1994 paper.

MR. SIRRIDGE: And these were the numbers that you were commenting on this morning about these secondhand...

DR. WELLS: I was using the numbers out of the paper.

MR. SIRRIDGE: The final paper?

DR. WELLS: Yeah. But they don't affect that risk assessment because they aren't U.S. studies. The risk assessment was based on the U.S. studies.

MR. SIRRIDGE: Yes.

Do you remember out of those 12 studies, the 12 studies in your chart that you had the slide on this morning, do you remember how many of those reported a statistically significant relative risk for environmental tobacco smoke and coronary heart disease?

DR. WELLS: No, I don't. But of course the whole idea is you pool the smaller studies to see what all of them look like when you put them all together.

MR. SIRRIDGE: But you'll agree with me that the large majority of them did not produce...

DR. WELLS: They aren't large enough. They're perfectly good studies, but you can't get statistical significance out of individual small studies. Now the Helsing study is statistically significant.

MR. SIRRIDGE: It was a quite large study.

DR. WELLS: Yeah, and I think...

MR. SIRRIDGE: 1358 deaths.

DR. WELLS: I think Hirayama may have been. There are several of them that are either almost statistically significant or not. And of course, then that all depends on how you define statistical significance.

If you dig back into Rothenberger who is one of the outstanding epidemiologists in this country, he says using 95 percent significance levels to decide something is or is not statistically significant is a lot of baloney. You have to look at the quality of the study. You want some reasonable statistical significance, but 95 percent itself is essentially meaningless.

MR. SIRRIDGE: But the scientific journals and medical publications...

DR. WELLS: They all use it. Rothenberger says that's all a bunch of bunk...

MR. SIRRIDGE: Is this Rothenberger or Kenneth Rothman?

DR. WELLS: Yeah. Yeah, he's pretty well known.

MR. SIRRIDGE: True.

Dr. Wells, you rated your studies one to four, based on the number and importance of the risk factors that were included in the study, and the corrections that were made to those.

DR. WELLS: Right.

MR. SIRRIDGE: The Helsing study, which is really the same study as the Sandler study...

DR. WELLS: Right.

MR. SIRRIDGE: That rated a number three.

DR. WELLS: Right.

MR. SIRRIDGE: One would be the best. Two, three, four would be the worst.

DR. WELLS: Right.

MR. SIRRIDGE: So it was on the less reliable end.

DR. WELLS: Well, that was a prospective study that was started years and year ago before anybody had any idea we were going to get into a controversy on heart disease and passive smoking. But I think the point I made, Mr. Sirridge, earlier, was that when you aggregated all the rest of the studies where they did test for a lot of these things, you get the same result as Helsing got. So I think it's still a very good study.

MR. SIRRIDGE: But don't individual studies stand on their own merits in terms of whether they took and gathered information on coronary risk factors and then did the proper analysis? The study has to stand on its own in terms of its own methodology, isn't that true?

DR. WELLS: You'll have to go over that again. I missed it.

MR. SIRRIDGE: Well, we'll get to that on the factors that were included in the studies. But there was a variety in those studies in terms of the information they gathered and the analysis they were able to do to adjust for the various risk factors for heart disease.

DR. WELLS: I suppose so, if you say so.

MR. SIRRIDGE: The dose response information in those studies varied, didn't it?

DR. WELLS: Well, it always varies depending on the size of the study and so on.

MR. SIRRIDGE: The majority of the women's studies did show a dose response.

DR. WELLS: Yes.

MR. SIRRIDGE: And the majority of the men's studies did not show a dose response.

DR. WELLS: It could be. I can't remember the majority. It was a smaller number.

MR. SIRRIDGE: It was two out of five that showed a dose response for men.

DR. WELLS: You see, men normally seem to be exposed to more background ETS than women do, in general. It's harder to get a good signal in the men's area. So I wouldn't think that would be unusual. I think it's easier to do a good study on females, particularly if you do it in Greece or Japan or some place, as I said in my talk, where female smoking prevalence is low. Because then you don't get a lot of this background that muddies things up. But it's hard to do that with men. Men are out in society all the time, and they are exposed to a lot of ETS, other than their wives' cigarette smoke. So I'm not surprised that the male results are "iffier" than the female results.

MR. SIRRIDGE: You mentioned Japan and Greece, and you certainly have other sociological and other environmental issues to worry about in those countries.

DR. WELLS: Those are minor matters, though, compared to the fact that you get much less background and a much clearer signal in the ETS.

MR. SIRRIDGE: Dr. Wells, in your paper in 1994, this most recent one, you've concluded that there is a 20 percent to a 70 percent excess risk for ischemic heart disease due to ETS. Do you recall that?

DR. WELLS: Yes.

MR. SIRRIDGE: What's the difference between heart disease, arteriosclerotic heart disease, and ischemic heart disease?

DR. WELLS: I think those are just terms that those various authors used.

MR. SIRRIDGE: Have you examined the death certificate information in any of those studies to determine whether the designations in those categories were verifiable and could be used consistently by all the researchers?

DR. WELLS: I go strictly by what's in the papers, plus whatever I can get from the authors if I want further information.

MR. SIRRIDGE: Now a 70 percent excess risk is the same excess risk that's reported by the Surgeon General for overall risk for smokers for heart disease.

DR. WELLS: Yeah, but of course that's based on average never-smokers, not non-exposed never-smokers.

MR. SIRRIDGE: Were you aware that the relative risks reported for non-smokers exposed to ETS have been described as being high? compared to the risk which has been associated with smokers.

DR. WELLS: Yes, and I'm a little surprised at that myself. But I said in my testimony that the platelet sensitivity in a 20 minute exposure went down, what did we lose 60 percent of the platelet sensitivity advantage of non-smokers over smokers, was lost on that short an exposure, and the vitamin C, remember I told you about that, it was down 65 percent. I think, as I understood what Dr. Glantz said the other day, apparently the heart system seems to saturate much faster from relatively slight exposures to ETS, and then the rest of the exposure that you get from active smoking doesn't seem to add that much burden to the heart.

MR. SIRRIDGE: Are you aware...

DR. WELLS: That's just from looking at the numbers. I can't give you a mechanism.

MR. SIRRIDGE: Because the mechanism is still a hypothesis or a theory, isn't that true?

DR. WELLS: That's the question, you know. Are we going to sacrifice American workers because we think this epidemiology is all wrong? My guess is that the epidemiology is right, and we ought to look after the workers.

MR. SIRRIDGE: Let's take a look at that epidemiology, but before we go, are you aware that Dr. Samet said yesterday that he believes that the relative risks seem high compared to those...

DR. WELLS: I didn't hear what Dr. Samet said.

MR. SIRRIDGE: Well, he wrote the same thing back in 1992. I don't know if you're familiar with that publication. It was an article entitled, "Environmental Tobacco Smoke." It was published in 1992 by Dr. Jonathan Samet in a book called, "Environmental Toxicants."

DR. WELLS: Yeah, I've missed that one. You have to remember, though, that Dr. Samet's a very cautious epidemiologist. I've known him for a number of years, and usually I'm about five years ahead of him.

MR. SIRRIDGE: Five years ahead of him in age, or...

(Laughter)

DR. WELLS: I figure out what's happening, and about five years later Dr. Samet begins to agree with me. (Laughter)

MR. SIRRIDGE: Let's go back to the Helsing study. You're aware that in your testimony this morning, that it was used for a basis for the risk assessment.

DR. WELLS: Yeah, yeah, I was aware of it.

MR. SIRRIDGE: And you're, of course, aware that it has a number of methodologic limitations.

DR. WELLS: Well, you know, as I've said, any prospective study they started that long ago isn't going to be the perfect answer to passive smoking and heart disease in 1994. But it's a pretty good study just the same.

MR. SIRRIDGE: But since they started in 1963 before much of the epidemiologic work on coronary heart disease, they did not control for six of the important risk factors which have been identified.

DR. WELLS: That's right. We said it was Level 3 in my paper.

I think what you have to look at is the fact that it does agree with all the rest of them put together, so what you're using when you use the Helsing paper, you're really using all of the studies, because they're equivalent.

MR. SIRRIDGE: Well, looking at the other 11 studies, how many of those other 11 studies... Well let's just group them all as 12. How many of the 12 studies controlled for lack of exercise or physical inactivity?

DR. WELLS: That's all in the paper there.

MR. SIRRIDGE: Well, would you agree that it's one out of 12?

DR. WELLS: As these studies have gone along, what they're doing is controlling for more and more factors, because, you know, everybody's talking about confounders.

MR. SIRRIDGE: And how many of the papers controlled for Type A behavior pattern?

DR. WELLS: I think one or two, probably.

MR. SIRRIDGE: Just one.

DR. WELLS: Was it?

MR. SIRRIDGE: And that was the Chinese study, amazingly enough.

DR. WELLS: Well, they do some good work in China.

MR. SIRRIDGE: How many of the studies broke down cholesterol in terms of its LDL and HDL components?

DR. WELLS: I can't remember. I think, though, the thing to remember is that as they controlled for more studies, on average, they found higher relative risks. And I think that's very important. In other words, as they begin to control for more of these things, they're finding the risks are higher than in the studies where very few things were controlled.

MR. SIRRIDGE: But don't the relative risks often go down when the start adjusting for...

DR. WELLS: Some do and some don't. All I'm saying is that on average, the ones that control for more risks, more factors had higher relative risks than the ones that were controlled for fewer. That's a very important point.

MR. SIRRIDGE: Now, only about half the studies controlled for hypertension, does that sound right?

DR. WELLS: I guess, if you say so.

MR. SIRRIDGE: About the same number for cholesterol?

DR. WELLS: Well, should we get the paper out and look at it?

MR. SIRRIDGE: That'd be just great. You probably have it, don't you?

DR. WELLS: You know, I can't remember all this stuff, but we can certainly dig the paper out and we can look at it.

MR. SIRRIDGE: It's on Table 1.

DR. WELLS: Now I've got to find the...

MR. SIRRIDGE: I had a hard time with all those abbreviations of yours.

DR. WELLS: Well, that's just the journal, you know. They uh, okay, let's go.

MR. SIRRIDGE: Table 1.

DR. WELLS: Table 1.

MR. SIRRIDGE: I said about half of the studies controlled for cholesterol.

MS. SHERMAN: Excuse me, which paper are we...

MR. SIRRIDGE: I'm sorry, Dr. Well's paper, August 1994, Journal of the American College of Cardiology.

MS. SHERMAN: Thank you.

MR. SIRRIDGE: You're welcome.

JUDGE VITTONE: What page is that?

MR. SIRRIDGE: It's on page 548, and I believe it's appended to his statement that he submitted. I think it's the last...

DR. WELLS: I guess eight of them were for cholesterol, and I can't remember how many of them were high density and how many were just total cholesterol.

MR. SIRRIDGE: But wouldn't you also be counting the Spenson study twice there? I mean, that's really the same study, isn't it? The last thing on your list there.

DR. WELLS: Yeah. Right.

MR. SIRRIDGE: You're counting that twice. It's really the same study.

DR. WELLS: Yeah, yeah.

MR. SIRRIDGE: Less than half of them controlled for family history of coronary heart disease.

DR. WELLS: Yeah. As I've said, some of these are older studies before they started collecting this information.

MR. SIRRIDGE: But isn't the point, Dr. Wells, that most of the studies did not solve the confounding problem, and didn't, well, didn't solve the confounding problem or resolve it?

DR. WELLS: Well, that depends on how you look at it. Nobody's ever found the confounder that really depressed these risks, consistently across the board and in a way that eliminated the risk.

MR. SIRRIDGE: It's hard to find a confounder when no one collects the data.

DR. WELLS: Yeah, that's what we were discussing before. Are we going to imperil American workers because we haven't found some other confounding factors? What we've found are a whole flock of them here, and as we've found more of them, the risks have gone up, not down.

MR. SIRRIDGE: Well, Dr. Samet said yesterday that when you're dealing with a relative risk like 1.2, 1.3, right in that range, you should be more concerned with confounding factors, because that's a very low risk in epidemiologic terms.

DR. WELLS: You should be concerned, but you shouldn't be misled to the point where if you haven't found one that doesn't work, you say, well, we're not going to accept any of these data. You know, I worked for DuPont, and the way I remember it was that when you had a suspected material, it was guilty until proven innocent. The purveyor had to go out and prove the stuff was safe.

Now what we seem to be trying to do here is to try to, you know, to prove that the stuff is, that it's the other way around. I've never seen such things. It amazes me, frankly.

MR. SIRRIDGE: Well, the burdens of proof are in various places, and many of them are regulated by law, so, we'll let that just take it's course.

Dr. Wells, based on your submission and your remarks this morning, I take it you're in favor of OSHA enacting the Proposed Rule on ETS in the workplace.

DR. WELLS: I generally stay out of policy.

MR. SIRRIDGE: I'm saying, you're testifying in favor of the Rule, though?

DR. WELLS: Yeah, I'm testifying in favor of the science, so to speak, but... I may have some personal opinions, but I'm not very active in trying to get policies affected one way or the other.

MR. SIRRIDGE: Let me ask you, Dr. Wells, what would be, or what will be the reduction in risk for coronary heart disease, mortality, and morbidity if OSHA were to implement the Proposed Rule on ETS in the workplace?

DR. WELLS: I haven't any idea. I think I've said in my paper there, though, that the reduced exposure to smoking... It looked to me like the heart deaths may have gone from 62,000 down to 49,000 or whatever it was, but that was kind of a horseback estimate. But part of it was based on assuming less ETS exposure, you know. If there's a risk for ETS exposure, you know, if there's less exposure, why the number of deaths eventually is going to go down.

MR. SIRRIDGE: Well, as far as you know, there is no published data or quantified data on the reduction of risk from coronary heart disease mortality or morbidity related to the elimination of ETS in the workplace.

DR. WELLS: Well, we certainly know from those platelet sensitivity experiments that if you, if people are not, you know, if they're removed from the ETS exposure, the platelet sensitivity goes back up to normal. And in the lipid tests with cholesterol, they've found there, I think, that when smokers quit smoking, their lipid level goes back up to what's normal. So certainly, you'd expect logically if the exposure to ETS is removed, that the deaths from heart disease from that source are going to go down. That seems logical to me.

MR. SIRRIDGE: But there's no quantifiable, there's no computated number or reduction of risk that you're aware of.

DR. WELLS: Well, I suppose one could be calculated, but no, I don't know of one.

MR. SIRRIDGE: Dr. Wells, your calculations on the environmental tobacco smoke risk in your 1994 paper that we've been discussing are based on spousal or household exposure to ETS.

DR. WELLS: That's right.

MR. SIRRIDGE: In how many of those 12 studies you reviewed for your conclusions was the exposure verified by either the measurement of ETS or by measuring some kind of biomarker in the nonsmokers?

DR. WELLS: That's not the way those studies are done. That doesn't mean the studies are invalid. The studies are perfectly good, they just don't do that sort of thing.

MR. SIRRIDGE: Let's just say they take questionnaire data.

DR. WELLS: Yeah, but you know, there's just no practical way to do what you're talking about.

MR. SIRRIDGE: Doctor, what about the data on workplace exposure to ETS? How many studies have such data in them that you've reviewed?

DR. WELLS: Well, normally I don't pay much attention to workplace data, because, you know, if people, the turnover, and all that kind of business, and I've concentrated more on the home exposure. But I did get into the heart workplace exposure the other day, prompted by Peter Lee's comment that there were no statistically significant data. But I did run a little meta-analysis on the papers where we did have data on workplace exposure.

MR. SIRRIDGE: And which papers were those?

DR. WELLS: What's that?

MR. SIRRIDGE: Which papers were those?

DR. WELLS: Butler, Dobson, the new He paper, Jackson, and Svendson. And when you run that meta-analysis, what you get is a relative risk of 1.37 for both sexes combined, with a 95 percent confidence limit from 1.10 to 1.71, which is a very highly statistically significant result. So I guess what you could say offhand about the heart result is that such workplace data as we have agrees essentially with the home exposure data. It's a little bit higher relative risk, but basically the same.

MR. SIRRIDGE: Now, I just have a couple of questions about the studies you included. Did you include the Lee study?

DR. WELLS: I looked through Lee's paper, and I couldn't find anything in there on workplace.

MR. SIRRIDGE: Well, I believe he does have...

DR. WELLS: What there is is a combination of home, work, and other, but I couldn't find any way to disentangle the workplace exposure from the other two exposures.

MR. SIRRIDGE: In the Jackson data you have, that's not in a peer-review publication...

DR. WELLS: No, that's in a thesis.

MR. SIRRIDGE: ...in the open literature, is it?

DR. WELLS: Yeah, but what I find is that if I don't include stuff like that, then people accuse me of publication bias and selectivity and all that kind of stuff. So generally what I do is I try to include everything I know about, whether it's plus or minus or what.

MR. SIRRIDGE: Well, isn't it true that the biggest study, largest study by far that has workplace data is the Dobson study?

DR. WELLS: No, I don't think so.

MR. SIRRIDGE: In terms of this.

DR. WELLS: Yes, the statistical weights that I have are... the Butler study has the higher statistical weights, and for women, for example, that says a 1.86 relative risk.

MR. SIRRIDGE: What I'm talking about is numbers of deaths, numbers of cases.

DR. WELLS: Well, I'm not talking about that. I'm talking about the statistical weight, which is much more important than the number of cases. I mean, you must realize that.

MR. SIRRIDGE: But it certainly has a very low power percentage as rated by Dr. Glantz, doesn't it, the Butler study?

DR. WELLS: Could be, but the workplace data is pretty, uh, apparently has better statistical weight than any of the rest of them.

MR. SIRRIDGE: The Dobson study has the largest number of deaths in a study that has workplace findings, workplace data, and its conclusion was that there was no statistically significant excess risk. In fact, there was not an excess risk at all, was there?

DR. WELLS: Well, what you've got to remember, remember all that discussion about publication bias in some of these things? In smaller studies, you're always going to get a lot of scatter, and you're going to have some plus studies and some minus studies, and so what I imagine is that the Dobson study just shows that the normal publication bias scatter is there. But the other four studies all show positive relative risks.

MR. SIRRIDGE: I'm not following you on Dobson, because it is the third largest study of the twelve in your table. You have Sandler, Helsing...

DR. WELLS: We're talking about the workplace data, not the...

MR. SIRRIDGE: Well, I'm just talking about, it sure makes the largest workplace study by far, in terms of numbers of deaths.

DR. WELLS: Not according to the statistical significant of the data and the statistical...

MR. SIRRIDGE: I'm just looking at your Table Number 1 that we were talking about a minute ago.

DR. WELLS: Where? That has nothing to do with workplace.

MR. SIRRIDGE: Well, I'm looking at number of deaths in the study.

DR. WELLS: I don't know that's for home exposure. I don't know how many deaths they had in the workplace data.

MR. SIRRIDGE: But suffice it to say the authors concluded they did not have an excess risk for lung cancer based on workplace ETS exposure.

DR. WELLS: Yeah, they made that conclusion. All I'm saying is that when you aggregate all of the studies, you get a relative risk of 1.37.

MR. SIRRIDGE: Doctor, you're...

DR. WELLS: ...using the same procedures that are used in the paper.

MR. SIRRIDGE: Many times you have quoted the American Heart Association and their finding in respect to ETS, or their opinion with respect to ETS and heart disease, in fact you mentioned it this morning as one of your...

DR. WELLS: I wouldn't say many times, but yeah, I have quoted that. I think they're a responsible group.

MR. SIRRIDGE: In fact, you led off your 1994 paper, first sentence, talking about the American Heart Association publication, do you recall that?

DR. WELLS: Yeah.

MR. SIRRIDGE: That was based on a recommendation from the Council on Cardiopulmonary and Critical Care.

DR. WELLS: Right.

MR. SIRRIDGE: Who was on that council?

DR. WELLS: I haven't any idea.

MR. SIRRIDGE: Do you know whether there is an epidemiologist on that council?

DR. WELLS: I assume it's a responsible group. I don't know any of those authors, either. In my networking, I've never somehow tied in with Johnson, and who ever else those authors, Taylor and Kesmi. I don't know...

MR. SIRRIDGE: You never heard of those guys.

DR. WELLS: No, they're all strangers to me.

MR. SIRRIDGE: Well, would it surprise you that none of them are epidemiologists or statisticians?

DR. WELLS: That's not my area. That's the American Heart Association's problem.

MR. SIRRIDGE: Did you know that Dr. Samet reviewed the same evidence that this group from the American Heart Association reviewed at about the same time and reached a different conclusion, or at least reached a quite different conclusion?

DR. WELLS: No, I...

MR. SIRRIDGE: Well, let me read...

DR. WELLS: I assume the Heart Association knows more about hearts than John Samet does. He's a cancer expert.

MR. SIRRIDGE: But you wouldn't know it based on your knowledge on who wrote the recommendation? The three gentlemen?

DR. WELLS: I told you, I take these papers as they appear, and this is a very qualified group, I assume, or they wouldn't have that job.

MR. SIRRIDGE: Course you know their conclusion. This is early '92 that the paper came out, and the Council on Cardiopulmonary and Critical Care has concluded that environmental tobacco smoke is a major preventable cause of cardiovascular disease and death. That's what they wrote early '92.

DR. WELLS: Right.

MR. SIRRIDGE: Dr. Samet reviewed the same evidence in '92 and wrote the following. "The evidence...

DR. WELLS: Is this a question?

MR. SIRRIDGE: It is going to be a question.

JUDGE VITTONE: Mr. Wells, just wait a second. He's going to ask you a question to try to get some information.

DR. WELLS: Okay.

MR. SIRRIDGE: The evidence, this is Dr. Samet, the evidence on cardiovascular disease points to increased risk in nonsmokers exposed to ETS. Now my question is could the anti-tobacco position and agenda of the American Heart Association have the affected their view of the evidence?

DR. WELLS: I haven't any idea.

MR. SIRRIDGE: And isn't a fact...

DR. WELLS: I'm not a member of the American Heart Association, I have very little contact with them.

MR. SIRRIDGE: When did you personally decide that ETS caused heart disease?

DR. WELLS: What's that?

MR. SIRRIDGE: When did you personally decide that ETS caused heart disease?

DR. WELLS: Well, I guess around 1984. I mean, I didn't decide, but the evidence was starting blow that away.

MR. SIRRIDGE: You'd reached an opinion or judgement yourself.

DR. WELLS: Yeah, you know how these things go, they grow on you as time goes by. I gave a seminar at Harvard University in 1984, I think, where I was already starting to express the idea that maybe heart disease caused ETS. And I told you, I'm always five years ahead of Samet. I think what you ought to do is to quote what he says three years from now.

MR. SIRRIDGE: Well, let me ask you this. We've talked quite about the He Study from China...

DR. WELLS: Right.

MR. SIRRIDGE: ...that was just published in 1994 in a British medical journal. Isn't it true that the authors themselves stand, say in that paper, that ETS as a cause of heart disease is still controversial?

DR. WELLS: I don't know, I can't remember that.

MR. SIRRIDGE: Well, would it surprise you if they said that in 1994 with all the evidence you've talked about?

DR. WELLS: No, I would say, you know, it's certainly controversial to the extent that the tobacco industry is making it controversial.

MR. SIRRIDGE: Well, do you think Dr. He and his colleagues are members of the tobacco industry?

DR. WELLS: No, I think there are other people who still have some doubts, but you know how that is, you can't get 100 percent consensus on anything in this country.

MR. SIRRIDGE: Thank you, Dr. Wells.

DR. WELLS: Okay.

JUDGE VITTONE: Thank you, Mr. Sirridge. We have several other people who have asked us questions, but we are coming close to 12:00, and the Department of Labor has asked that we break exactly at 12:00 for lunch, and we will return at 1:15. But before we break, there are a couple of things. First, a little housekeeping matter: the exhibit number for Mr. Wells' testimony, is that 25 or 26?

DR. WELLS: 26.

(The document referred to was marked for identification as Exhibit No. 26 and received in evidence.)

JUDGE VITTONE: And Mr. Wells, excuse me is it Mr. Wells, or Dr. Wells?

DR. WELLS: I have a PhD in physical chemistry.

JUDGE VITTONE: Dr. Wells, then.

DR. WELLS: Well, you can call me whatever you want.

JUDGE VITTONE: Dr. Wells. Do you have copies of your slides, sir, that we can attach to the testimony?

DR. WELLS: Yes.

JUDGE VITTONE: Or is that, or are they already, no they're not, they're different in what you had in your prepared testimony.

MS. SHERMAN: I believe he has copies to submit.

DR. WELLS: Well maybe I didn't get the figures, but I've got copies of them if you want them.

JUDGE VITTONE: Well, we make copies for the official transcripts, so if you could provide those. If you have them today, that's fine, if not, if you could provide them within a week, I'd appreciate it. They'll be Exhibit 26 and Exhibit 26 plus the slides will be received into the record of these proceedings. Let me ask you one question quickly. Do you have a copy of your testimony there? This is a small matter, but I want to...

DR. WELLS: I think I have. Here it is.

JUDGE VITTONE: Look at Page 14.

DR. WELLS: Yes.

JUDGE VITTONE: Page 14 at the very top there, it begins, "Regular smokers misclassified versus our estimate of 1.09 percent."

DR. WELLS: Yeah.

JUDGE VITTONE: And the next line says, "and about 10 percent of occasional smokers."

DR. WELLS: Right.

JUDGE VITTONE: Maybe I misheard you, but I thought you said 7 percent.

DR. WELLS: I did.

JUDGE VITTONE: You said seven percent.

DR. WELLS: Yes, and I'll tell you what the difference is.

JUDGE VITTONE: Okay. But is it seven, not 10.

DR. WELLS: It's seven.

JUDGE VITTONE: Okay. If you just want to state for the record, real quickly.

DR. WELLS: The difference is that the Fontham paper came out in two versions. There was a preliminary version, and there was a final version. Well, the 10 percent had been calculated based on the preliminary version, but they didn't find any more of those misclassified smokers. But they added a lot of denominator, so what I wanted to get into the record was the result from the final paper, and that reduces that to seven percent.

JUDGE VITTONE: Okay, but seven percent is the accurate figure.

DR. WELLS: Right.

JUDGE VITTONE: I just wanted to make sure. I don't know how important that is...

DR. WELLS: I need also to change the footnote number from 21 to 22 to get it over under the final paper basis.

JUDGE VITTONE: Okay, would you make sure that that correction is made to the file copy for the record.

One other brief matter before we break. We had an extended, not very extended, off-the-record discussion concerning the course of this hearing for the rest of the day.

I made an offer, Ms. Sherman, that I would certainly be willing to hold hearings tomorrow, if you wanted to, in order to add any witness that we have had to drop.

If you would let us know after the lunch break whether you want to take me up on that so we can make any plans for that, I would appreciate it. And we will resume at 1:15.

A F T E R N O O N S E S S I O N

(1:24 p.m.)

JUDGE VITTONE: We finished with Mr. Sirridge before the lunch break, and I think we're ready to proceed, Dr. Wells. I'm sorry, sir. I've forgotten your name.

MR. FURR: Jeff Furr.

JUDGE VITTONE: Okay, Mr. Furr.

Are you ready to go forward, sir?

MR. FURR: I am.

Good afternoon, Your Honor, Dr. Wells.

As I said, my name is Jeff Furr. I'm a lawyer from North Carolina, with the law firm of Womble, Carlyle, Sandridge & Rice. My principle client here is the RJ Reynolds Tobacco Company, but I'm also representing 10 other clients.

Would you like the numbers?

JUDGE VITTONE: No, I don't think the numbers would do me much good.

MR. FURR: Would you like for me to name them?

JUDGE VITTONE: Well, what sort of people are they?

MR. FURR: The National License Beverage Association; the Ohio License Beverage Association; the

Oregon Smokers Rights, and a number of individuals: Sarah R. Mahler, William Pfeiffer, Jr.; L. Susan Alsop; Faye D. Eberhardt; Roth Associates, Inc., and Ken Risk.

JUDGE VITTONE: Thank you.

MR. FURR: This afternoon, I am going to primarily ask you questions regarding smoking status misclassification.

You and Dr. Stewart have developed a method for adjusting the ETS epidemiologic studies, to account for the bias introduced by smoking status misclassification.

That method was published in Appendix B to the 1992 ETS Risk Assessment.

Is it fair to describe that methodology as a model?

DR. WELLS: Well, it's sort of a mathematical model.

MR. FURR: If I call it the Wells Model during the course of this examination, would you know what I'm talking about?

DR. WELLS: Well, I suppose you're talking about what's expounded in that Appendix B.

MR. FURR: That's correct.

DR. WELLS: Has the model been published anywhere?

DR. WELLS: Not beyond that Appendix B. You have to remember that Dr. Stewart and I are both unpaid in this area. In his case, particularly, he has to spend his primary time on his funded projects, so it's been very difficult for Dr. Stewart to get enough time to review this thing to the point where we could get it into what we consider publishable shape.

We have submitted it, and we have had a peer review of it, and we're in the process of answering the questions raised by the people who peer reviewed.

MR. FURR: Have you been told whether it's going to be published?

DR. WELLS: Well, it hasn't been accepted yet, because --

MR. FURR: Okay. Thank you.

DR. WELLS: -- we have to have answers.

MR. FURR: I want to ask you some questions about how that model works. There are a number of parameters in that model, aren't there?

DR. WELLS: Oh, yes.

MR. FURR: Do you know how many?

DR. WELLS: No. But, as you can tell from Appendix B, we certainly tried to get data sources to support most of those parameters to the extent we possibly could.

MR. FURR: Okay. A friend of mine attempted to count the parameters and told me that he counts at least 66 parameters. Would that number surprise you?

DR. WELLS: No.

MR. FURR: I want to ask you some questions about the --

DR. WELLS: But I don't think that's an issue.

MR. FURR: Well, okay.

DR. WELLS: We did the very best we could, and we've obviously done much better than anybody else has done.

MR. FURR: Let's talk about the nature of the parameters that go into that model.

Most of those parameters are in the nature of a statistic, aren't they? And when I say "statistic," I mean, while you provide a point estimate, it's really a number that has a certain variability associated with it.

DR. WELLS: Yes.

MR. FURR: For instance, you use the percentage of 1.09 percent as the estimate for the rate at which current regular smokers misclassify their smoking status as never smokers. You calculated that rate by combining the number of studies.

All of those studies did not find the same rate of misclassification, did they?

DR. WELLS: No.

MR. FURR: In fact, they range from 0.8 percent in the Cumming study, up to almost 5 percent in the Coultas study. Is that correct?

DR. WELLS: That number sounds high for the Coultas. As I remember it, it was more like 3-1/2.

MR. FURR: Okay. So we range from 0.8

percent --

DR. WELLS: It was at a range, as you say, and that is, office, why I said that there's such a difference between what I call the community survey studies and the ones that are an epidemiological grid.

MR. FURR: Okay. And that range causes there to be variability in the point estimate that you calculated for that parameter.

Let me try another one.

In your misclassification adjustment for each study, you use a relative risk number for active smoking that you have determined to be appropriate for use in that specific study.

DR. WELLS: That's right.

MR. FURR: And you use the point estimate for that, but that relative risk actually contains some variability and can be described with confidence intervals, can't it?

MS. SHERMAN: Excuse me a moment. We've gotten a report from the back of the room that the audience is having a hard time hearing Mr. Wells. Perhaps you could grab another microphone, or maybe we can turn it up or something.

Sorry.

DR. WELLS: That's okay. Is that better?

MR. FURR: Dr. Wells, we're talking about the parameters in your model and how many of them are statistics in nature, and they have variability associated with them, and we were talking about the relative risk for active smoking that you use that's specific to each individual study to adjust it, and that's a statistic with variability around it, that can be described by confidence intervals.

DR. WELLS: That's right.

MR. FURR: Another input parameter in your model is the concordance ratio between spouses with respect to their smoking habits. The value that you use for that concordance ratio you derived from combining a number of studies, correct?

DR. WELLS: 4, actually.

MR. FURR: For 4?

DR. WELLS: Not very many.

MR. FURR: Did all 4 of them find the same concordance ratio?

DR. WELLS: No.

MR. FURR: So the point estimate that you derived for those 4 studies had some variability associated with it?

DR. WELLS: Right.

MR. FURR: There are a lot of other parameters in your model that have variability, aren't there?

DR. WELLS: That's right.

MR. FURR: All right. Would you look with me at Table 2 to your testimony that you gave here today.

DR. WELLS: Yes.

MR. FURR: I would like to focus on the far right-hand column, that has been labeled EPA inputs.

DR. WELLS: Right.

MR. FURR: That column contains the degree of bias that the EPA calculated for specific epidemiologic studies because of smoking status misclassification.

DR. WELLS: Right.

MR. FURR: In fact, those numbers were calculated using your model. You may have calculated them?

DR. WELLS: Yes, I probably did.

MR. FURR: You don't provide any confidence intervals around those numbers, do you?

DR. WELLS: No.

MR. FURR: There is variability associated with those numbers, isn't there?

DR. WELLS: That's right.

MR. FURR: Based on the EPA report and the additional materials that you provided to us here today, we don't have any way of knowing how much variability is associated with those point estimates for bias for a particular study, do we?

DR. WELLS: That would be pretty hard to figure.

MR. FURR: It would be, but you haven't done that, have you?

DR. WELLS: No. Because I don't -- I don't think it would lead anywhere.

JUDGE VITTONE: Mr. Furr --

DR. WELLS: Yes, sir.

JUDGE VITTONE: -- I'm going to do exactly the opposite to you what I've done to other people. Could you back off that microphone a little?

MR. FURR: Certainly.

So looking at your published work, we cannot tell how much variability is associated with the point estimates that you have calculated or bias introduced by smoking misclassification for any given study.

DR. WELLS: Well, obviously, it's either going to be higher or lower.

MR. FURR: It could be lower, couldn't it?

DR. WELLS: Yes. It could be higher, it could be lower.

MR. FURR: It could be higher.

You could calculate a 95 percent confidence interval around these point estimates, couldn't you?

DR. WELLS: That would be a very difficult calculation, probably beyond my capability. I have very limited computer power.

MR. FURR: You're not a statistician, either, are you?

DR. WELLS: No.

MR. FURR: A statistician could do this?

DR. WELLS: I don't think there would be anything gained by it, because you still have to come back to the point estimates to figure out probably what's going on.

MR. FURR: But you don't know that, because you haven't done that, have you?

DR. WELLS: What's that?

MR. FURR: You haven't done that. You haven't calculated the variability.

DR. WELLS: Well, we tried in the EPA report, and if you look in there, you will find some estimates, but it's a footless exercise, basically.

You eventually have to come back to the point estimates in order to make any sense out of it.

MR. FURR: So is it your testimony that calculating the variability associated with these point estimates would not provide any useful information?

DR. WELLS: I don't think so, no.

MR. FURR: All right. Thank you. Let's talk about something different now.

DR. WELLS: If you look at Lee's estimates, he has the same problem. You know, he says that it's higher than mine.

MR. FURR: Dr. Wells, we're done with it. Let's move on and try to keep things moving.

DR. WELLS: Well, it bears on the point.

MR. FURR: I'm not going to ask anymore questions about that.

DR. WELLS: It bears on the point.

JUDGE VITTONE: Dr. Wells, Ms. Sherman will have an opportunity to ask you any clarifying questions after we complete the examination of these people -- of the gentlemen in the office.

Go ahead, Mr. Furr.

MR. FURR: Thank you, Your Honor.

In the Wells Model, you used 1.90 percent as the percentage of current regular smokers who will misreport themselves as never smokers. Correct?

DR. WELLS: That's right.

MR. FURR: And you use 24.2 percent as the percentage of occasional smokers who will misreport themselves as never smokers.

You derived those rates by examining data contained in these studies that you list in Table B-3 of Appendix B to the 1992 risk assessment. Correct?

DR. WELLS: Right.

MR. FURR: And there are six studies there but nine different data bases, something like that?

DR. WELLS: Something like that.

MR. FURR: And they include the Coultas study?

DR. WELLS: Um-hum.

MR. FURR: Cumming's?

DR. WELLS: Um-hum.

MR. FURR: Pierce. Lee. Hattow and Riboli.

DR. WELLS: Two Hattow studies.

MR. FURR: Two Hattow.

DR. WELLS: And there's several pieces of the Riboli study.

MR. FURR: And that's the sum total of the data that you examined in calculating your misclassification rates?

DR. WELLS: Yes. As I said, they were the only data bases we could find where we could get individual cotinine levels for the women.

MR. FURR: Let's talk about those levels. Those levels do not appear in the published reports of those studies, do they?

DR. WELLS: No. I had to write to the authors, and that's one reason that I couldn't get anymore because some of the people I wrote to, either the data were lost or they wouldn't send them to me.

MR. FURR: So none of that data appears in the peer reviewed literature?

DR. WELLS: No, none of it.

MR. FURR: For example --

DR. WELLS: Well, some of it does, because the Lee stuff is in great detail in his letter to Lancet.

MR. FURR: Most of the data doesn't appear in the peer reviewed literature, does it?

DR. WELLS: The Hattow studies, as I remember, there's enough detail in the published paper so that you could derive what I have there.

MR. FURR: Does the data from the Coultas study appear in the peer review literature?

DR. WELLS: No. He sent me his data sheets.

MR. FURR: In fact, the data you have reported having been sent to you by Coultas is different than the data that appears in the published work, isn't it?

DR. WELLS: That's true, and I'm not sure I understand why that it is.

MR. FURR: We don't either.

DR. WELLS: But it isn't much different. It's pretty close.

MR. FURR: Does the data that you use from the Cumming's study appear in the peer review literature?

DR. WELLS: No. He sent me his data sheets also.

MR. FURR: Would the same be true for the Pierce study?

DR. WELLS: Well, the Pierce study is a little complicated because that was done in Australia, and the lady that has that data set now is Petra McGaskill, but I wrote to her and she sent me a very tight, very fine detail on that study.

MR. FURR: Has that data been published in the peer review literature?

DR. WELLS: You mean the detail?

MR. FURR: Yes, sir.

DR. WELLS: No, not to my knowledge.

MR. FURR: What about the data from the Riboli study; has it been published in the peer review literature?

DR. WELLS: No, not the misclassification data. We got that directly from Riboli, who of course was a senior author on that paper on the cotinine studies.

MR. FURR: All this data that we've been talking about was made available to you through personal correspondence?

DR. WELLS: Well, not the -- the Riboli study came to EPA, and they gave it to me. The Pierce data, the Cumming's data and the Coultas data, I got directly from the authors, and I also got some help from the Hattow group.

MR. FURR: If the RJ Reynolds Tobacco Company were to request that you provide that data to them so that they could have an opportunity to examine the data --

DR. WELLS: Oh, sure.

MR. FURR: -- would you provide that?

DR. WELLS: Yes, if you could get permission from those authors.

MR. FURR: Let's talk about the data that should be used to calculate the classification rate for adjustment of the epidemiologic studies. Shouldn't the data that is used to make that adjustment be representative of the populations that were studied in the epidemiologic studies?

DR. WELLS: That would be helpful if you can find enough data to do that, yes.

MR. FURR: In this case, we're really talking about the adjustments that you've made to the studies of females in the United States, the spousal smoking female U.S. studies; correct?

DR. WELLS: Right.

MR. FURR: So, preferably, you would have data that is representative of that group?

DR. WELLS: That would nice --

MR. FURR: Isn't that correct?

DR. WELLS: -- if we had enough. Yes.

MR. FURR: That's true because the tendency to misreport smoking status may vary among populations?

DR. WELLS: Well, it's possible, but we haven't discovered much variation.

MR. FURR: It may vary culturally, don't you think?

DR. WELLS: Possible, but the Asian data are very similar to the U.S. data.

MR. FURR: Why do people misreport their smoking status?

DR. WELLS: I haven't any idea.

MR. FURR: So if you don't know the factors that cause people to do it, it's very difficult to reach the conclusion that it won't vary across different populations, isn't it?

DR. WELLS: I'm just telling you what the numbers say.

MR. FURR: Okay.

DR. WELLS: A lot of this could be just clerical errors.

MR. FURR: We do agree that it would be preferable to use data that is representative of the epidemiologic studies to make a misclassification adjustment, don't we?

DR. WELLS: Yes. As I said this morning, the main thing to do is to get data that is of a quality of the epidemiologic studies.

You know, that Japanese study of Peter Lee and that Sears study are obviously not of epidemiological quality and should --

MR. FURR: We're going to talk about that later.

DR. WELLS: -- and shouldn't be considered in trying to estimate these misclassification rates.

MR. FURR: Well, let's focus on the studies that you did use, for a moment.

Isn't it true that the authors of the Cumming's study, in the published report, state that the generalizability of the Cumming's data is, quote, "limited due to the self-selection of the study population."

DR. WELLS: That particular group is limited because it's an Hispanic group, and Hispanic groups are known to misclassify themselves more often than what you might call mainstream groups, so that value is on the high side of the ones that I quote.

One reason I included it was to give some deal for the minority groups in the United States.

MR. FURR: So that the record is clear, the answer to my question was a yes, wasn't it? Then you explained your answer?

DR. WELLS: Yes.

MR. FURR: Isn't it true that the authors of the Coultas study state in the report that, quote, "Because our study was of a minority group, generalizability about the prevalence of deception on smoking habits may be limited."

DR. WELLS: Yes. That's what I just said, yes.

MR. FURR: No, I'm talking about the Coultas study now.

DR. WELLS: That's what I'm talking about.

MR. FURR: Don't the authors make that statement with respect to the Coultas study? Let me back up.

I initially asked you about the Cummings study.

DR. WELLS: Let me tell you what I said.

What I said was the Coultas study is on Hispanics. Hispanics are a minority and minorities, in the studies we've seen, misclassify themselves at a higher rate than the mainstream part of the population.

I knew when I put that study in there that it was on the high side, but I thought we ought to have some minority representation in the list, and that's why that study is in there.

MR. FURR: And so if you were going to make a misclassification bias adjustment to an epidemiologic study that included a large percentage of Hispanics, you should use a higher misclassification rate, shouldn't you?

DR. WELLS: That's probably right.

MR. FURR: Okay. I may have misspoke. I meant for the first study I asked you about to be the Cumming's study. Isn't it true, also, that the authors of the Cumming's study have stated that the generalizability of their data is, quote, limited?

DR. WELLS: Well, possible, yeah. But that's probably a more representative group than -- you know, it's hard to find representative groups in this area.

MR. FURR: Do you think you have insight into the generalizability of that data set beyond what Cumming's,

et al, have?

DR. WELLS: Well, I don't know. You know, I've been looking at the whole of it, and it seems to me that's probably as much in the middle as any that I've seen.

MR. FURR: SIr, is your answer that you don't know?

DR. WELLS: Well, I've studied a lot of this data.

MR. FURR: Let's talk about another study -- the Hattow, et al., study -- that is included in your Table B-3. That was a study that was restricted to white pregnant women, wasn't it?

DR. WELLS: Right.

MR. FURR: Those women exhibited unusual cotinine levels, didn't they?

DR. WELLS: Right.

MR. FURR: Not necessarily representative of the general female population in the U.S.?

DR. WELLS: Well, what you have to do, cotinine studies in pregnant women are lower than they are in the general population. Since we were using percentages of the current smoker, cotinine level, we therefore used lower cutoff points for that study, and I think, under those conditions, it's quite valid.

I also have a letter here from that research group saying they think the same thing.

MR. FURR: Dr. Wells, can I ask you something? We have to make a clear record here. So when I ask you a question, you need to try to respond to the question that I ask first, and then if you want to explain your answer that's perfectly acceptable, and I appreciate that. Okay?

DR. WELLS: Right.

MR. FURR: In your Table B-3 that you used to calculate the misclassification rates, you also included data from foreign countries, including data from the Pierce, Lee and Riboli studies, correct?

DR. WELLS: Right.

MR. FURR: Have you made any effort to determine whether there are any new data that meet the requirements you've imposed or including data in the calculation of misclassification rates?

DR. WELLS: I don't know of any that I would consider quality that matches epidemiologic studies.

MR. FURR: That wasn't the restriction you placed on studies for inclusion in Table B-3, was it?

DR. WELLS: Well, we needed more data, so I did include community survey type studies.

MR. FURR: And there are additional data of that nature now available, aren't there?

DR. WELLS: Not that I'm aware of, no.

MR. FURR: Have you reviewed the comments of the RJ Reynolds Tobacco Company to the OSHA docket in this proceeding?

DR. WELLS: I don't know what you're referring to.

MR. FURR: My understanding is that it is a follow up report on the data that the RJ Reynolds Tobacco Company presented partially in 1992 to the Environmental Protection Agency. Have you reviewed the final report on that data?

DR. WELLS: No, I haven't seen any such report.

MR. FURR: So you don't know whether that data would meet the standards that you've set for inclusion in your analysis or not, do you?

DR. WELLS: From what I've seen of studies that are done by market research groups, I would guess that that's probably not anywhere near epidemiologic quality. I would think that the RJ Reynolds Company would be better off if they hired some qualified epidemiologists independent of the company to make such studies, rather than going around hiring market research groups.

MR. FURR: Dr. Wells, have you reviewed the submission of Reynolds?

DR. WELLS: I reviewed the --

MR. FURR: You have not reviewed the submission of Reynolds in this proceeding, have you?

DR. WELLS: I reviewed the 1992 one.

MR. FURR: You have not reviewed the final submission, have you?

DR. WELLS: I haven't seen it.

MR. FURR: And you don't know the quality of the data contained in that study, do you?

DR. WELLS: Well, the quality of the original study wasn't very good.

MR. FURR: I'm talking about the submission to this docket in this proceeding. You have not reviewed that study, have you?

DR. WELLS: No.

MR. FURR: Okay. There are a number of other studies that contain data relevant to the rate of misclassifications, aren't there?

DR. WELLS: Yes.

MR. FURR: You mentioned this morning in your testimony, Peter Lee. You know Peter Lee, don't you?

DR. WELLS: Well, I know of him.

MR. FURR: Yes. You reviewed his work, obviously?

DR. WELLS: Very thoroughly.

MR. FURR: You're aware that he's identified at least 10 addition cotinine studies that can be utilized to calculate the misclassification rate that are not included in your Table B-3, aren't you?

DR. WELLS: Yes. And I've been over that last, and either there are studies that weren't available to me or there were studies that were not gender specific. In other words, there were good reasons for leaving each one of those out, as far as I was concerned.

MR. FURR: If the studies were not available to, how can you know there's a good reason for now leaving them out of your table?

DR. WELLS: I can't put them in the table if I can't get ahold of the data.

MR. FURR: Mr. Lee appears to have been able to get a hold of the data.

DR. WELLS: Well, maybe he could.

MR. FURR: You reviewed the studies. What information you have about the studies, you have reviewed, haven't you?

DR. WELLS: What's that?

MR. FURR: You have reviewed the information that you have about those studies, haven't you?

DR. WELLS: Yes. Most of them are not gender specific.

MR. FURR: Okay. You know that, in fact, in eight of those studies, the Peter Lee incorporates into his analysis that are no contained in your Table B-3 that the misclassification rates are higher than the mean rates in the studies that are included in your table?

DR. WELLS: That's possible. That doesn't mean, though, that they met my criteria.

MR. FURR: If you had taken those studies into consideration and included them in your calculation of a misclassification rate, the rate you derived would have been higher than that that you did, based only on the information in Table B-3.

DR. WELLS: Let me go back our earlier question.

MR. FURR: You need to answer this question, and then --

DR. WELLS: Well, I'd rather go back to the earlier one, if that's all right with the Judge.

JUDGE VITTONE: It would be a lot more orderly if you can respond to this question. I'll give you a chance to clarify.

DR. WELLS: Now, what?

JUDGE VITTONE: Repeat the question.

DR. WELLS: Can he repeat the question.

MR. FURR: You know, then, that if you had taken those studies into consideration, that the values that you derived from misclassification rates would have been higher than those that you derived based only on the studies contained in Table B-3 of the EPA Appendix?

DR. WELLS: You use studies with higher misclassification rates, you get higher biases. But I repeat, I took those studies into consideration.

MR. FURR: Did you ever attempt to calculate a misclassification rate based on all 16 of those studies in Peter Lee's table?

DR. WELLS: I repeated Peter Lee's mathematics of that study, yes.

MR. FURR: What value did you obtain?

DR. WELLS: I can't remember.

MR. FURR: If I were to represent to you that the value that would be obtained using your methodology is approximately 3.7 percent, the current regular smokers misclassifying themselves as nonsmokers, would you accept that?

DR. WELLS: I have no basis.

MR. FURR: In your written comments --

DR. WELLS: I didn't get a chance to go back to the earlier question.

MR. FURR: Your Honor --

JUDGE VITTONE: Why don't you just hold that thought, and then -- okay?

DR. WELLS: It's very pertinent to the discussion.

JUDGE VITTONE: I appreciate that, sir, but I will give you an opportunity to clarify it.

MS. SHERMAN: Dr. Wells, why don't you write it down right now?

DR. WELLS: What?

MS. SHERMAN: The point that you wish to make it.

DR. WELLS: Well, it bears on --

MR. FURR: Your Honor, really, this is what we're trying to avoid.

JUDGE VITTONE: Dr. Wells, you will have an opportunity.

Go ahead, Mr. Furr.

MR. FURR: Dr. Wells, in the written comments that you provided and then again in your oral testimony here today, you've made some statements with respect to the impact of smoking status misclassification upon your summary risk calculations for all of the epidemiologics combined in some form of meta analysis. Is that correct?

DR. WELLS: Yes.

MR. FURR: Have you made an analysis that the impact of smoking status misclassification would have on that summary risk estimate if you used a value of between 3 and 4 percent to the rate of misclassification of current regular smokers as nonsmokers?

DR. WELLS: I have not.

MR. FURR: Would it surprise you to learn that if you use a value of approximately 3.5 the summary risk estimate becomes 1.0?

DR. WELLS: I know that from what Peter Lee has done, but I have also pointed out all the errors of

Peter Lee's work which effectively nullifies that kind of an estimate.

MR. FURR: I want to turn to a different topic, if we could. I want to ask you some questions about the use of cotinine measurements to discern individual smoking status.

In the written statement that you submitted in this proceeding, you state that, by reviewing the community survey and the epidemiologic data with respect to the individual level of cotinine in female study subjects, that is the information that we discussed earlier, that you

could -- and I quote here -- "tell exactly how many of the false negatives among the never smokers were really regular smokers and how many were only occasional smokers."

Do all smokers absorb nicotine into their circulation at the same rate or to the same extent?

DR. WELLS: No, but it all averages out.

MR. FURR: In fact, the amount of nicotine that a smoker absorbs is dependent on a number of factors, isn't it?

DR. WELLS: I'm not much into what the smokers absorb.

MR. FURR: Do you have any expertise or knowledge about the pharmacokinetics of nicotine in smokers?

DR. WELLS: I read a few papers, but I'm not an expert in that area.

MR. FURR: Well, we may be able to shortcut a lot of this. Is it your testimony that you do not have the knowledge or expertise to provide an opinion with respect to the pharmacokinetics of nicotine in smokers?

DR. WELLS: No, I don't have that kind of expertise.

MR. FURR: Do you have that type of expertise to provide opinions with respect to pharmacokinetics of nicotine in nonsmokers?

DR. WELLS: No. I just take the data people give me.

MR. FURR: So, in the scheme contained in your model, concerning individual smoking status based on cotinine measures, you have set up a number of values for use. Correct?

DR. WELLS: Right.

MR. FURR: Your scheme is that if an individual's serum cotinine level or salivary, for that matter, is 10 to 30 percent of the mean reported for current regular smokers, you classify that person as an occasional smoker?

DR. WELLS: That's right.

MR. FURR: Correspondingly, if an individual's serum or salivary cotinine level is 10 percent of that reported -- of the mean found in self-reported current smokers --

DR. WELLS: Right.

MR. FURR: -- that person is classified as a nonsmoker?

DR. WELLS: That's right.

MR. FURR: Is it your testimony that you do not have the knowledge or expertise to evaluate the validity of that scheme you've set up in your model?

DR. WELLS: Well, I can do easily well on something like that. Those cutoff points were suggested originally by Peter Lee. He probably doesn't know much more about nicotine pharmacokinetics than I do, but the point is that whether you choose 10 percent or 5 percent, you get basically the same bias calculation at the end, anyway.

Because as you go down in cutoff point from 10 percent to 5 percent, what happens, of course, is that the cotinine -- average cotinine level -- goes down for those occasional smokers from 16 percent to about 13 percent.

So you get more occasional smokers if you use the lower cutoff point, but you get a lower calculated relative risk for those smokers. One offsets the other, and you end up with just about the -- almost identically the same bias calculation that way with 5 percent cutoff that you get with 10 percent cutoff.

You don't need a knowledge of pharmacokinetics to figure that out.

MR. FURR: Well, let's explore that a little bit.

What you're telling me is that the misclassification rate that is derived depends on where you set the cutoff points?

DR. WELLS: That's right. If you're somebody who is doing a study where he wants to eliminate all possible smokers from his cohort, you use a lower cutoff point, like 5 percent.

If you're interested in distinguishing non-smokers from smokers, then the people that have done those studies use cutoff points closer to 10 percent. See, there are different objectives in those studies.

MR. FURR: Right. But the number that you end up deriving from misclassification rate, depends on where you set those cutoff points?

DR. WELLS: Yes. But the ones we have used are well substantiated by the average cotinine levels of those groups. The 30 percent cutoff point -- you see, what happens is, the misclassified smokers tend to bunch lower in the group than the average self-reported smoker.

So if that cutoff point above 30 percent is regular smokers, the average cotinine level for those misclassified smokers, is the same as all of the self-reported smokers, including the ones that are light, occasional, and almost zero because they bunch down toward the lower end of that range.

So, really, they're very well validated cutoff points. Actually, we could have used a 35 percent cutoff point, and then still, within the average cotinine level of self-reported current smokers.

MR. FURR: What do you mean when you say an current, occasional smoker?

DR. WELLS: In my terms, it's somebody whose cotinine level is between 10 and 30 percent of self-reported current smokers.

MR. FURR: Using your scheme, isn't it correct that a current regular smoker of 6 cigarettes per day would be classified as an occasional smoker?

DR. WELLS: If his cotinine level lay between 10 and 30 percent, it would.

MR. FURR: On average, isn't that where you would expect his cotinine level to lay?

DR. WELLS: I don't understand your question.

MR. FURR: On average, doesn't a current regular smoker of approximately 6 cigarettes per day generate a steady state, serum cotinine level in the range of 30 to 90 nanograms per milliliter?

DR. WELLS: I don't know.

MR. FURR: You don't know.

DR. WELLS: No.

MR. FURR: You're not familiar with the literature on the subject, I take it?

DR. WELLS: Well, as we said in the paper there, implicit in this discussion, and it's the same thing that Peter Lee uses, the level of cotinine is a measure of probably the level of carcinogenicity. One's a surrogate for the other. We have no other thing to rely on.

MR. FURR: You really base your cutoffs on those used by Peter Lee, don't you?

DR. WELLS: Yes. Peter Lee -- Peter's contributed something to this literature, I must say, and that was one of the things that he contributed.

MR. FURR: And you don't have, independently, any expertise or knowledge with respect to whether those cutoffs make any sense from a pharmacokinetic perspective?

DR. WELLS: I don't think they have to, as long as you're making the assumption that the carcinogenicity varies with the cotinine level.

MR. FURR: Is that a yes or no?

DR. WELLS: I told you originally --

MR. FURR: As I asked you earlier, you need to first try to answer my question, and then I appreciate your explanation. But this record is going to be unclear if you immediately go into an explanation and do not address the question that I pose.

DR. WELLS: Yes. But I've told you several times I have no special pharmacokinetic knowledge. You keep asking that question over and over again.

MR. FURR: Do you know what the plasma half-life of cotinine is?

DR. WELLS: About 48 hours, something like that.

MR. FURR: The plasma half-life of cotinine is 48 hours?

DR. WELLS: Well, it's longer than nicotine, and it's --

MR. FURR: What's the plasma half-life of nicotine?

DR. WELLS: Well, it's shorter.

MR. FURR: It's what?

DR. WELLS: As I said in my testimony, the biomarker of choice today, in these studies, is

cotinine --

MR. FURR: Dr. Wells, my question --

DR. WELLS: -- and there's nothing --

MR. FURR: -- is what is the --

DR. WELLS: -- I can do about that.

MR. FURR: -- plasma half-life of nicotine?

JUDGE VITTONE: Gentlemen, gentlemen.

MR. FURR: I don't think that's a --

JUDGE VITTONE: Gentlemen.

MR. FURR: -- it doesn't matter whether you think it's a relevant question.

JUDGE VITTONE: Gentlemen. All right, let's calm it down.

Dr. Wells, let him get his question out, and let him get an answer out.

DR. WELLS: I answered the question, sir.

JUDGE VITTONE: Okay.

DR. WELLS: I said it was shorter than cotinine.

MR. FURR: How short? One hour, five hours, ten hours, how short?

DR. WELLS: I would guess probably on the order of 20 percent.

MR. FURR: 20 percent shorter?

DR. WELLS: No. 20 percent of.

MR. FURR: Of the half -- of what?

DR. WELLS: Half-life of cotinine.

MR. FURR: If a current regular smoker of a pack a day is deprived of cigarettes or stopped smoking for one reason or another, how long does it take your serum cotinine level to decrease to that which would be classified as a nonsmoker under your guidelines?

DR. WELLS: I suppose several days, but I'm not an expert in this area.

MR. FURR: So you do not know?

DR. WELLS: Well, I guess so, yes. That was my estimate, but I wouldn't hold me to it.

MR. FURR: How does the use of cotinine levels allow you to discern a former smoker from a lifelong, never smoker?

DR. WELLS: Say that again?

MR. FURR: How do cotinine levels allow you to discern a former smoker from a lifelong, never smoker?

DR. WELLS: You can't do that.

MR. FURR: In fact, someone could quit for only a few days after being a lifelong pack a day smoker, and based on their cotinine levels, you would not be able to identify them as such, would you?

DR. WELLS: That's right.

MR. FURR: Do you know what the average serum cotinine level is in self-reported current regular smokers?

DR. WELLS: Well, it depends on what body fluid you're talking about.

MR. FURR: Serum.

DR. WELLS: I'd have to look.

[Pause.]

MR. FURR: That's okay. You don't need to look it up. If you don't know off the top of your head, that's fine. I'll accept that.

DR. WELLS: Well, urine is 1200 and, as I remember, serum is around 300.

MR. FURR: Thank you.

You have made a number of arguments in your written testimony and in your oral testimony today with respect to why you believe your estimate of misclassification may be too high.

DR. WELLS: That's right.

MR. FURR: One of those is that the Fontham study found a very low rate of misclassification.

DR. WELLS: Um-hum.

MR. FURR: A second is that your model, in essence, produces nonsensical results for male misclassification.

DR. WELLS: Right.

MR. FURR: And a third is your belief that the community surveys report data that may be too high because those values are different from those found in the epidemiologic studies?

DR. WELLS: The ones I've been able to see, yes.

MR. FURR: Let's talk about the Fontham study for a minute.

DR. WELLS: Um-hum.

MR. FURR: Have you reviewed the Fontham study?

DR. WELLS: Yes.

MR. FURR: Have you reviewed the questionnaire that was used in the Fontham study?

DR. WELLS: No.

MR. FURR: Have you discussed the study with

Dr. Fontham?

DR. WELLS: Sometime ago. Well, not really.

MR. FURR: But you're familiar with the procedures and methodology in the study?

DR. WELLS: In general, yes.

MR. FURR: Has Dr. Fontham provided you any data from the study?

DR. WELLS: Not to me, no. I think she provided some data to the EPA.

MR. FURR: Your belief is that she provided data to EPA?

DR. WELLS: Right.

MR. FURR: Do you know who at EPA she would have provided that data to?

DR. WELLS: Probably Steven Bayard.

MR. FURR: Steven Bayard.

Do you know what kind of data it was?

DR. WELLS: As I remember, what we got from her was data on background. In other words, comparing cotinine levels of people exposed to ETS compared to people who weren't exposed, or said they weren't.

MR. FURR: Is this data that was not included in the published reports?

DR. WELLS: As far as I know, yes.

MR. FURR: What form was the data in? Was it raw data or was it tabulated information?

DR. WELLS: I don't remember.

MR. FURR: Back to the Fontham study.

Isn't it true that the procedures that were used for identifying and eliminating possible smokers from the self-reported never smokers in the Fontham smokers, were more rigorous than those used in the other American epidemiologic studies?

DR. WELLS: Probably, yes.

MR. FURR: Consequently, wouldn't you have expected fewer misreporters of smoking status to make it through that screening procedure and be detected with the cotinine assay?

DR. WELLS: Yes, I think that's true.

MR. FURR: Isn't it likely that subjects that are diagnosed with lung cancer have some motivation to quit smoking?

DR. WELLS: Well, I guess some of them do. I don't know.

MR. FURR: Well, there is data addressing this point, isn't there?

DR. WELLS: Not that I'm familiar with.

MR. FURR: Are you familiar with the work of Cabat and Wynder?

DR. WELLS: Oh, yes.

MR. FURR: Did they not report that lung cancer cases tend to deny their smoking history more than controls with non-smoking related diseases.

DR. WELLS: Yes, that's right.

MR. FURR: You don't have any reason to doubt that observation, do you?

DR. WELLS: Well, I think one of the tables there in Appendix B compared discordant answers of lung cancer cases with the general community studies. What we found was that the misclassification rates from the lung cancer studies were a good deal lower than the ones from the community studies.

So it's possible that the Cabat and Wynder thing just was a chance reversal.

MR. FURR: The misclassification rates from the epidemiologic lung cancer studies are based from rates found in cases that have been diagnosed with cancer, aren't they?

DR. WELLS: Yes, that's right.

MR. FURR: For several years now, most American hospitals have been smoke free, haven't they?

DR. WELLS: Well, not at the time that most of this data was gathered.

MR. FURR: Isn't it true that hospital bound populations who smoke are constrained from smoking and have limited physical opportunities to smoke?

DR. WELLS: Well, I don't know. My brother-in-law, when he had lung cancer, he smoked right up to the end in the hospital.

MR. FURR: I understand that's an anecdote --

DR. WELLS: That's anecdotal.

MR. FURR: -- but my question is, generally speaking.

DR. WELLS: I wouldn't be able to answer that.

MR. FURR: You stated earlier that you have reviewed the reports by Fontham, et al., both in the 1991 and the 1994 reports?

DR. WELLS: Um-hum.

MR. FURR: Well, isn't it true that they suggested that because of the cases health problems, that the cases who misreport their smoking status may be less likely than free-moving controls to be still smoking and therefore less likely to be detected by cotinine measurements?

DR. WELLS: It may be in there. I don't remember.

MR. FURR: Let's talk about another of your rationales as to why your misclassification rate may be too high. That's the male data.

Isn't it possible that the odd results that you obtained when you tried to adjust the male data from misclassification may be a result of an error in your model?

DR. WELLS: Well, at the same -- no, I don't think that's really likely.

MR. FURR: But is it possible?

DR. WELLS: Well, anything's possible, but I don't think it's very likely.

MR. FURR: Let's go to another of your rationale's as to why your value may be too high.

JUDGE VITTONE: Mr. Furr, let me ask you a question. How much longer?

MR. FURR: Five to ten minutes.

JUDGE VITTONE: Thanks.

MR. FURR: Thank you.

With respect to this inconsistency between the community survey data and the epidemiologic data on misclassification rates, what is the basis for your conclusion that the data from the epidemiologic studies are more reliable or representative than the data from the community survey studies?

DR. WELLS: I'm just reporting how they came out. I really don't know. But as we said earlier this morning, when qualified epidemiologists do these things, they seem to get more penetrating results than people who do it more on a fly-by-night basis.

MR. FURR: So your judgment as to which of the data bases is more reliable is based solely on who conducted the studies?

DR. WELLS: On their training and background and so on.

MR. FURR: There is nothing methodologically or procedurally about the two sets of studies that suggest that one should be more reliable than another, is there?

DR. WELLS: Well, it depends. You know, if you stand on a street corner and just ask people as they go by whether they smoke or they don't, you're not going to get very reliable results.

MR. FURR: Well, both types of studies, in fact, use questionnaires --

DR. WELLS: Right.

MR. FURR: -- to assess self-reported smoking status, don't they?

DR. WELLS: Yes.

MR. FURR: And both types of studies use cotinine measurements and compare them to those responses? Isn't that correct?

DR. WELLS: That --

MR. FURR: I'm sorry. I didn't hear the answer.

DR. WELLS: The fact remains that

epidemiologists --

MR. FURR: Please, Dr. Wells, you need to answer my question before you give an explanation.

DR. WELLS: Well, superficially, they're the same. Let's put it that way. They are the same procedurally, superficially.

MR. FURR: Okay. Thank you.

Dr. Wells, isn't it true that in the Proposed Rule that OSHA has put forth that there are no analyses to determine the degree to which smoking status misclassification may have affected the relative risk as reported by the investigators?

DR. WELLS: As far as I know, that's true.

MR. FURR: And that goes for both heart disease and lung cancer?

DR. WELLS: I believe so, yes.

MR. FURR: Do you have an opinion as to whether misclassification bias of smoking status could also be causing a spurious increase in the work place epidemiologic data?

DR. WELLS: I think that would have to be looked into.

MR. FURR: There's really no data available on that issue now? Is that correct?

DR. WELLS: I'd have to think about that.

MR. FURR: Dr. Wells, do you always perform your own statistical analyses or do you have people that work with you?

DR. WELLS: Well, you understand what I do is simple, but I don't have anybody that works with me, no.

MR. FURR: Is the method that you have used to effectuate the Wells model, has it been reduced to a computer program, or is it based on a computer program?

DR. WELLS: Yes. I have an old Osborne I bought in 1978, and I have set up some of those calculations on that computer.

MR. FURR: And so you have some computer program related to this misclassification model then?

DR. WELLS: Well, it just follows the arithmetic that's in Appendix B. It's pretty simple.

MR. FURR: Would you be willing to make that program available to others?

DR. WELLS: If they want it, yeah, but there's nothing much to it.

MR. FURR: I only have one more question, I hope.

JUDGE VITTONE: All right.

MR. FURR: I was intrigued by something that you said this morning when Mr. Sirridge was examining you.

DR. WELLS: Um-hum.

MR. FURR: As I understood it, you were discussing your experience at dupont, when you were still working there. You said that when a chemical became a suspect chemical, there was cause to be concern about the health effects of that chemical; that the approach utilized was that the chemical was presumed to be guilty until proven innocent. Is that a fair description of what you said?

DR. WELLS: No. What I was doing there was quoting a man named Goldstein, I think he is, who's a real expert in the area of regulatory affairs, as I understood it, which I am not.

But I was really quoting him, where he said that, from a regulator's point of view, suspect material should be guilty until proven innocent.

MR. FURR: Okay.

DR. WELLS: I will comment on my dupont experience, though, and that is, when we found that beta naphthylamine caused bladder cancer, we stopped manufacturing it. We were, to my personal experience, very careful about what things we exposed our workers to.

MR. FURR: In fact, that's really the frame of mind orientation that you have brought with you to your evaluation of the ETS data, isn't it?

DR. WELLS: Well, you're correct there, to some degree, because I look on ETS just like any of the work place carcinogens, and it would seem to me that we ought to be regulating them the way we do vinyl chloride or asbestos or any of the work place carcinogens, and I've felt that way for some time. That's correct.

MR. FURR: Thank you very much, Dr. Wells.

DR. WELLS: I never got a chance to answer that question.

JUDGE VITTONE: You'll have an opportunity later, hopefully.

JUDGE VITTONE: Thank you, Mr. Furr.

Who is next? Mr. Rupp.

Okay. Let's take a --

MS. SHERMAN: Your Honor, I believe you told

Dr. Wells he could answer the question and I think he made a note of it. Perhaps just for the sake of the record, you could allow him to answer it now.

JUDGE VITTONE: I will always allow him to answer the question and to issue any clarification he wants,

Ms. Sherman. But if he would like to do it now, that would be fine with me, too.

Dr. Wells, go ahead.

DR. WELLS: What we were talking about was Peter Lee's list of acceptable studies --

JUDGE VITTONE: Yes, sir.

DR. WELLS: -- and my list. One of the studies on Peter Lee's list is Haddow, 1987; and one of the co-authors on that study was a fellow named Knight. I have a letter here from Knight, and let me describe the study that

Peter Lee thinks should be included.

MR. FURR: Your Honor, I don't see how this could be relevant to anything that I asked. Not responsive.

JUDGE VITTONE: Well, that's --

MR. FURR: If he wants to explain this data later, can't he do it later on direct, from Ms. Sherman, if that's what she wants to talk about?

DR. WELLS: This is very pertinent to this question.

MR. FURR: If it's pertinent, if it's related, to the subject of this hearing, I'm going to allow him to put it in the record.

JUDGE VITTONE: All right. Go ahead. Now, would you like to read it or would you prefer to put it in?

DR. WELLS: I'm just going to read a little piece of it.

JUDGE VITTONE: Go ahead.

DR. WELLS: We're talking about the 1987

study --

JUDGE VITTONE: Let me just -- they're going to ask to see the entire letter at some point, so you're --

DR. WELLS: Yes, that's all right.

JUDGE VITTONE: All right. Go ahead and read the part that you want.

DR. WELLS: "In our report" -- he's referring to the study that Peter Lee thinks we ought to use -- the answer to a question on a laboratory slip to obtain information on smoking behavior -- "this laboratory slip is used for the primary purpose of obtaining clinical information for a neural tube defect screening program.

"The question on smoking was asked for research purposes only. The laboratory slip can be filled out by the physician or physician's office staff as well as by the woman herself. In some cases, the laboratory slip can be filled out weeks or months in advance of the actual drawing of the blood sample.

"Our intent was to assess the usefulness of a simple question as a screen for identifying women who smoke in pregnancy and to use this information for studying the effects on smoking and pregnancy outcome.

"We specifically avoid to intervene to collect missing results or to correct misclassification errors because we wish to simulate as much as possible what actually happens in a routine clinical practice.

"Given these limitations, the use of information in this paper to assess the degree of misclassification of smokers as nonsmokers is of doubtful reliability."

He goes on to explain why the other two studies are of epidemiological quality. This is the point that I've been trying to make this morning and trying to make now. This is simply a study that is not of epidemiological quality. These that Lee is including on his list, is the kind of think that muddies up the water in this area.

We're trying to stick to high-quality work.

MR. FURR: Your Honor, I don't have anymore questions now, but you have anticipated correctly. The time we would like to see the exhibit is now, or at least sometime today, so that we could have an opportunity to examine it.

I would like to reserve the right to pose further questions to Mr. Wells, based only on this exhibit, if it occurs to us that we need to do some follow up, because we haven't seen this exhibit yet.

JUDGE VITTONE: For the sake of the record, I would like to have a copy of the letter made a part of the record, the quoted portion of it. If you could make that copy available, Dr. Wells, we could mark it as Exhibit 27.

(The document referred to was marked for identification as Exhibit 27 and received in evidence.)

Would you make that available, in the meantime, to Mr. Furr?

DR. WELLS: It's the only copy I have.

JUDGE VITTONE: Okay. We'll have copies made or you can provide them at a later date. But make that available to Mr. Furr right now, if you would.

We're going to take a five-minute recess, and we'll come right back. Okay.

Thank you.

[Recess]

JUDGE VITTONE: Mr. Rupp, you're next in line.

MR. RUPP: Thank you very much, Your Honor.

Good afternoon, Dr. Wells.

DR. WELLS: Good afternoon.

MR. RUPP: My name is John Rupp, and I represent a variety of individuals who have submitted statements in this proceeding on behalf of the Tobacco Institute.

About a quarter of your printed statement and a good portion of your oral presentation this morning related to a variety of biological theories that have been advanced to explain how ETS -- exposure to ETS -- might be a cause of cardiovascular disease.

I take it you remember that part of your presentation?

DR. WELLS: Right.

MR. RUPP: I'd like to pursue that with you, if I may, and I'm going to ask you to do something for me because this, I think, will help to make both the questions I'm asking and your responses more understandable to us all.

I'd like to begin by asking you to assist me by drawing a simple schematic of an artery with the major portions.

The parts that I am particularly interested in are the endothelium, the tunica intima, the tunica media, and the adventitia, because I think those are the parts that have been implicated and that we've been discussing -- we only need to discuss.

DR. WELLS: You know, I'd rather not do that because I'm not an expert in that area.

MR. RUPP: Would it help you if I did the schematic and then we could talk about it from there?

DR. WELLS: Well, it won't get us very far because I don't know that much about hearts. I'm just quoting what other people have said when I commented on that damage to the endothelium.

MR. RUPP: You have no independent basis for judgment on any of those issues?

DR. WELLS: No. Not on that, no.

MR. RUPP: Well, would you suggest that OSHA not rely on your statements in that area but, instead, any primary statements upon which you rely?

DR. WELLS: I think Glantz and Parmley are experts. I think you could rely on what they say, and what I've been doing mostly is quoting them in a couple of review articles I've read.

MR. RUPP: I see.

Do you have any basis for assessing the expertise of Drs. Glantz and Parmley in this area; that is, if they said that the heart was green, would you know that that is not so? Or that the tunica media was green?

DR. WELLS: As I said, Dr. Parmley is well regarded, a past president of the American College of Cardiology, and I assume he knows more or less what he's talking about.

MR. RUPP: But you have no basis for assessing whether the statements that he or anyone else with respect to heart disease is concerned is correct, accurate, correct, controversial, uncontroversial?

DR. WELLS: No. All I was trying to do is relate the findings of Sinzinger and Burghuber to what is, I assume, a fairly well established idea as to one of the causative steps in heart disease.

MR. RUPP: Okay. If I pursued with you a line of questions that tried to illuminate for us all the stages and the development of arteriosclerotic plaque, is that a discussion you could have with me or you're just not qualified to discuss it?

DR. WELLS: I don't think I can, no. I suggest you have that conversation with Dr. Glantz.

MR. RUPP: Okay. What about in the area of platelet sensitivity? Could we talk about some of the technical aspects of platelet sensitivity and the variety of studies that are available in that area?

DR. WELLS: I doubt that that would profit us much because all I know is about what I said in the statement. That is, platelet sensitivity goes down, and it's known that that's not a good idea.

MR. RUPP: All right. Well, you have read, with respect to platelet sensitivity, the study by Burghuber and coworkers?

DR. WELLS: Yes.

MR. RUPP: Okay. Let me ask you a couple of questions about that.

DR. WELLS: This has been a long time ago when I read that.

MR. RUPP: Well, I'm trying to -- I'll try to stay as close as I can to the presentation you made today, so I assume that that will at least ring some bells.

I'd like you, first, because you presented some of the results or what you thought were the results of that study in the presentation this morning and in your printed statements, let's begin by talking for a moment about how that study was set up.

What did that study involve? How did those investigators approach your task?

DR. WELLS: I don't remember.

MR. RUPP: Would it remind you if I said that what they did was to place nonsmokers in a room, measuring either 18 square meters or 18 meters cubed? There's some uncertainty on this point.

DR. WELLS: Yes, there's some confusion there. I remember that.

MR. RUPP: Right.

And expose them for 20 minutes to air polluted with the smoke of 30, quote, "heavy brand," unquote cigarettes. Does that --

DR. WELLS: Yes. I said this morning that there was heavier than normal exposure.

MR. RUPP: Yes.

DR. WELLS: Remember?

MR. RUPP: Yes.

And that there were 22 people in the room in question?

DR. WELLS: I don't remember that.

MR. RUPP: You do remember that there were 30 heavy brand cigarettes smoked within that period?

DR. WELLS: No. What I remember was it was heavier exposure than you would expect in what I call a normal smokey room, but the Davis results, though, were in a hospital lobby that just had smokers in it.

MR. RUPP: Okay. Well, let's talk about Davis in a couple minutes. Let me finish up and see if we can figure out what the significance or lack thereof the Burghuber study is.

Do you recall that adenosine diphosphate was used by the Burghuber investigators to induce irreversible platelet aggregation in that study?

DR. WELLS: I'm not an expert in what causes platelets to coagulate.

MR. RUPP: Let me try this, then.

Do you have any knowledge, either from your reading of the Burghuber study or from any other source, concerning what the exposure levels to tobacco smoke were within the 18 square meter or 18 meter cubed room was?

DR. WELLS: All I can really tell you is that in the Davis data, where it was a normal exposure, you lost 60 percent of the platelet sensitivity advantage over smokers.

MR. RUPP: Okay.

DR. WELLS: In the Burghuber case, it was 80 percent. As I said, it was a heavier exposure than normal.

MR. RUPP: Are you qualified by training or in any other way to tell me about the process that leads to platelet sensitivity or what the impact or significance of platelet sensitivity is, so far as the development of arteriosclerotic lesions are concerned?

DR. WELLS: No.

MR. RUPP: Do you have any expertise or knowledge that would help us understand the impact of ADP in stimulating or causing platelet sensitivity to occur?

DR. WELLS: No.

MR. RUPP: Do you have any knowledge that would permit you to determine what impact various doses of chemicals would have on platelet sensitivity?

DR. WELLS: No. This is not my area. What I did is took those papers as they were and reported the results.

MR. RUPP: Okay. Do you know what kind of correlation one finds in the literature, if there is one at all, between platelet aggregation or sensitivity and the atherogenic potential of an agent?

DR. WELLS: All I know is that I understood that cardiologists don't like to have your platelet sensitivity go down.

MR. RUPP: But you have no --

DR. WELLS: Because, you know, it leads to blood clotting, at least I said this morning. Blood clots can form, can cause heart attacks.

MR. RUPP: You think platelet sensitivity --

DR. WELLS: That's pretty simple, but that's about the state of my knowledge.

MR. RUPP: Well, do you know whether the current literature documents a relationship between platelet sensitivity and the development of arteriosclerotic plaque or lesions or anything of the sort?

DR. WELLS: No.

MR. RUPP: Do you know whether active smoking studies show a correlation between smoking and thrombi incidents -- the incidence of a thrombus?

DR. WELLS: No. All I know is that the general consensus is is that active smoking causes heart attacks.

MR. RUPP: Okay. Are you at all aware of studies by Hare, Dolin, Peto, Handley, Barbash, and Bicari, that it looked at active smoking and thrombi incidents?

DR. WELLS: No.

[Pause.]

MR. RUPP: Well, let's then move to the Davis study.

I take it what Davis and coworkers did was to look at endothelial cell damage, and ask the question whether endothelial cell damage could be induced by exposure to ETS. Is that your understanding of that study?

DR. WELLS: My understanding is that what they found, I don't know what they looked for, but what they found was more endothelial cell carcasses in the blood.

I don't think they cut out any arteries or things like that to see whether there was damage; but you know if you're going to find endothelial cell carcasses in increased levels in the blood, they must have come from somewhere; and presumably they came from the endothelium, and so you could presume, I guess, some damage.

MR. RUPP: Well, I'm interested in your use of the word presumed, because you know that the method that was used in the Davis study was based upon a method first developed of leuco-concentration first developed by Hadlivik and Rossman [ph] which isolates only presumed endothelial cells, not necessarily actual endothelial carcasses in the blood?

DR. WELLS: You're going beyond my knowledge.

Didn't Burghuber pick up endothelial cell damage, too? I mean carcasses.

MR. RUPP: I'll have to review that study myself. Perhaps we both should.

DR. WELLS: Yes, maybe we both should. I think, as I remember --

MR. RUPP: Focusing still on the Davis study, do you know whether Davis and coworkers considered confounding by perceptual reactivity to ETS or the fact that several vasoactive compounds have been shown to cause an increase in endothelial cell count?

That is, the variety of things, the variety of insults, the variety of agents and conditions that can cause an increased endothelial cell count in blood, quite apart from a deific agent, unless the exposure to those other agents also was carefully controlled?

DR. WELLS: Well, I guess so, but you know, if you walk in, as they did, put a person in a smoky lobby for 20 minutes and the endothelial cell count went up, and then you take them away and it goes back down again, that's all he found as far as I know.

MR. RUPP: Would you know what impact --

DR. WELLS: So what would you have the control for? I don't understand.

MR. RUPP: Do you know what the conditions were of those people prior to their entry into the experiment, for example?

DR. WELLS: I suppose they were just normal people.

MR. RUPP: But do you know?

DR. WELLS: Well, no, I don't know.

MR. RUPP: I really would like you to be -- try to stay with what you think you know, and then we'll -- because that will shorten things, or may lengthen things, depending on what you can answer.

DR. WELLS: Yes.

MR. RUPP: If I were to suggest to you that one can tell nothing about endothelial cell count without carefully controlling for possible confounders, including a variety of vasoactive compounds, would you have any basis for disputing that claim or my statement?

DR. WELLS: Well, just being --

MR. RUPP: Answer as much as you can yes or no, and then I'll be happy to hear --

DR. WELLS: -- as an old research man, I would say that the chances that that really is necessary in the simple experiment Davis ran, it is probably very, very low.

MR. RUPP: Well, I'll bet you know from your days in industry that some things that appear easy and simple to laymen are known by those who are students of the matter, to be not quite as simple as they sometimes appear.

DR. WELLS: That's true, but I don't know of anybody that's really attacked that Davis paper in a peer-reviewed way.

MR. RUPP: Have you done a comprehensive analysis of the literature to see whether --

DR. WELLS: No.

MR. RUPP: -- the data reported in that study has been discussed by anyone, and another perspective on that data provided?

DR. WELLS: No, but usually my friends tip me off sooner or later, because I don't have any literature base.

MR. RUPP: No one has tipped you off thus far?

DR. WELLS: No.

MR. RUPP: Okay. Then can we talk for a moment about the uptake and composition of lipids? Is that an area in which you feel any expertise at all?

DR. WELLS: Well, I know like everybody else that low high-density cholesterol is bad, and a high ratio of total cholesterol to high-density cholesterol is bad. That's about the level of my knowledge.

MR. RUPP: Okay, let's pick up on that point for a moment and follow it through and see how far we go. And I'm going to try to summarize what I think you were saying there and see if this was correct.

Is it now quite clear that what was once regarded as a danger of cholesterol is more precisely the danger of high LDL and low HDL cholesterol?

DR. WELLS: Yes.

MR. RUPP: And is that something you feel you know quite certainly?

DR. WELLS: I just know what the doctor says.

MR. RUPP: Okay. Do you know whether that developing knowledge over the past several years has caused researchers to look back at their interpretation of any data that had appeared in the literature before that knowledge became public?

DR. WELLS: No, I don't know anything about that.

MR. RUPP: I think certainly OSHA and I thought you, but perhaps not, had referred to a study by Moscowitz on blood lipoprotein. Do you know anything of that study?

DR. WELLS: Well, it was in the Glantz and Parmley paper, and they reviewed the thing fairly extensively, as I remember, and I was relying pretty much on their analysis.

MR. RUPP: Okay. Do you know what happens when we apply our recently-developed knowledge about the various forms of cholesterol to the results reported by Moscowitz which focuses, of course, upon adolescent children whose parents smoke.

If you look at the LDL and the HDL separately, do you know whether the results reported by Moscowitz are in a normal range, a range of elevation or a range of depression?

DR. WELLS: No.

MR. RUPP: Do you know whether LDL cholesterol levels are known to be affected by a variety of factors such as diet, alcohol consumption and physical activity?

DR. WELLS: Yes.

MR. RUPP: And that's something you've been told by people?

DR. WELLS: I assume so, yes.

MR. RUPP: You assume so?

DR. WELLS: Well, I've heard that's the case. It's sort of hearsay.

MR. RUPP: Do you know whether chemical composition of plasma LDL can be modulated by lifestyle factors?

DR. WELLS: No, I don't have any firsthand knowledge of that.

MR. RUPP: I have a series of questions that relate to increased proliferation of smooth muscle cells. In a few of the other studies, you've discussed --

DR. WELLS: Can I --

MR. RUPP: Let me finish, and then I'll let you talk.

And also on oxygen supply and cardiac function, I am more than happy to ask those questions of you, and I thought they would be appropriate in light of your statement.

But if you believe that you do not have expertise to answer detailed questions, I will not ask; and I leave the matter up to you.

DR. WELLS: Yes. Can I go back to your previous question?

MR. RUPP: You sure can.

DR. WELLS: I looked at those two childhood studies, and it seemed to me --

MR. RUPP: The Moscowitz studies?

DR. WELLS: The Moscowitz and there's another one; I've forgotten the author on the other one. But it is possible that both of those could be confounded, as you say, by lifestyle factors.

MR. RUPP: Right.

DR. WELLS: I think the thing that has impressed me more is this report from White on adult exposure in the workplace. Because there, what he found, is there's a significantly reduced level of high-density HDL for the adults that were exposed to ETS in the workplace compared to ones that weren't exposed, and a significantly increased ratio of total cholesterol to high-density cholesterol.

Now you see there's a lot less opportunity for the lifestyle to influence a workplace result, and I think this leads me to believe that possibly those results on children are probably not confounded by the lifestyle, because the children's results and this workplace result are very, very similar.

MR. RUPP: Well, if I asked you a series of questions that attempted to elucidate the impact and relationship between a variety of lifestyle factors on the cholesterol species about which we've been speaking, would you be able to answer those questions or would you refer me to an expert in the area?

DR. WELLS: I probably would not be able to answer those questions.

MR. RUPP: All right. Wouldn't it be fair, and wouldn't you yourself advise OSHA, so far as possible biological mechanisms of effect; ETS and cardiovascular health is concerned, that they should be relying on someone who is an expert, who is qualified by training and experience to evaluate the pertinent literature, who has read comprehensively the literature that applies to the points that are at issue?

DR. WELLS: Well, it depends on what kind of advice they're looking for. You know, if they're interested in mechanisms, that would be true.

MR. RUPP: That's really where the focus of my question is.

DR. WELLS: Yes.

MR. RUPP: Now if I were to say to you for example that if you'd sit down with me for 15 minutes or a half hour,

MR. RUPP: Wouldn't it be fair and wouldn't you, yourself, advise OSHA, so far as possible biological mechanisms of effect, ETS and cardiovascular health is concerned, that they should be relying on someone who is an expert, who is qualified by training and experience to evaluate the pertinent literature, who has read comprehensively the literature that applies to the points that are at issue?

DR. WELLS: Well, it depends on what kind of advice they're looking for. If they're interested in mechanisms, that would be true.

MR. RUPP: That's really where the focus of my question is.

DR. WELLS: Yes.

MR. RUPP: Now if I were to say to you, for example, if you'd sit down with me for 15 minutes or a half an hour, me and a real expert, since I'm not a cardiologist either, I can convince you that these proposed biological mechanisms are nonsense.

Sitting there as you are now, you couldn't be certain whether I could do that or not do that, could you?

DR. WELLS: I guess I don't quite understand your question.

MR. RUPP: That is, isn't it true that one needs a good deal of background training and expertise to be able even to deal adequately with some of the basic concepts and interactions that researchers have been studying for years and years?

That this is a very complex area, that one's evaluative powers are almost in proportion to the amount of background and fundamental knowledge one has? Would you agree?

DR. WELLS: Well, as I said, if you're interested in mechanisms, that's probably true. If you're just interested in the kind of thing I've been talking about, I don't think that's necessary.

MR. RUPP: Do you know whether carbon monoxide concentrations and the effect of carbon monoxide on health has been studied extensively, or is this an emerging area of science?

DR. WELLS: I think it's probably been going on for some time.

MR. RUPP: Are you aware that the current threshold limit value for CO in the workplace is 25 parts per million?

DR. WELLS: No, I was not.

MR. RUPP: You stated in your testimony this morning that typical ETS atmospheres contain from three to 25 parts per million of CO, do I recall that correctly? I'll give you a moment to review.

DR. WELLS: Say that again?

MR. RUPP: Three to 25 parts per million CO?

DR. WELLS: I think I said three to 50.

MR. RUPP: Three to 50? Okay.

DR. WELLS: I can't remember though, it's just data I got out of the Surgeon General's report.

MR. RUPP: Okay. Now I note that recent field studies undertaken and reported at Oakridge National Laboratory have found CO concentrations in smoking areas to be less than 0.5 ppm above the CO concentration in nonsmoking areas. Do you have any basis for disputing, and that was on the basis, I must say, of personal monitoring studies.

DR. WELLS: I'm not familiar with the study.

MR. RUPP: Have you ever undertaken a personal monitoring study?

DR. WELLS: No, this isn't my area.

MR. RUPP: How about an area monitoring study?

DR. WELLS: I've done none of those things, no.

MR. RUPP: Okay. Have you attempted to look comprehensively at background exposure levels of CO in workplace environments with and without smoking?

DR. WELLS: As I said, I've gotten these data out of the Surgeon General's report. That's my source on CO levels and smoky rooms. I assume --

MR. RUPP: Do you know what the background level was in those rooms before the smoking began?

DR. WELLS: I assume they made a very thorough search, so I thought it was a good source.

MR. RUPP: Well, CO is ubiquitous in the environment, is it not? It's produced by a whole host of sources.

DR. WELLS: Yes, but I think they've been finding that cigarettes are an important source.

MR. RUPP: Do you know that as a fact, or is that just something you've heard?

DR. WELLS: Well, I read the analyses of cigarette smoke and so on, vapor phase, and so on.

MR. RUPP: CO is found in cigarette smoke.

DR. WELLS: Oh, yeah.

MR. RUPP: Well, when a cigarette is smoked in a room like this, do you have any idea what impact that would have on the level of CO in this room?

DR. WELLS: Well, not really, but of course it would depend on how many people were smoking. If everybody in the room was smoking, it would probably make quite an impact.

MR. RUPP: But you don't know what the actual level would be.

DR. WELLS: No. I don't think I have to know in order to read the Surgeon General's report.

MR. RUPP: Maybe so, and maybe not. That's the answer to that. You don't know what the background level was in the figures that you've cited, though, that were unrelated to smoking.

DR. WELLS: They are listed in there in the report.

MR. RUPP: Okay. Are you aware of a 1985 report by the United States Environmental Protection Agency which states:

"EPA has reviewed the available epidemiologic data relating to hypothesis of an association between elevated carboxyhemoglobin or carbon monoxide exposure and the risk of heart attack, sudden death, and the progression of arteriosclerosis and has found them to be inconclusive."

DR. WELLS: Yes, well, that sounds reasonable. I think what you have to remember is that people that you really have to worry about are the ones that are walking around with a heart condition that they don't know they've got.

MR. RUPP: Is that because you have studied literature and could respond to the type of questions I'm asking if I limited myself to people who have impaired myocardial function? Or is that your notion as a layman?

DR. WELLS: No, the CO literature that we've been talking about here does have a number of experiments where people who already had heart conditions were put on exercise machines, and so on, and they've found that the amounts of CO that we normally found in a really smoky room does affect their exercise performance.

MR. RUPP: And which studies are you thinking about?

DR. WELLS: Well, there's Alrat, there's several of them.

MR. RUPP: Aranow?

DR. WELLS: Yes, that was one of them.

MR. RUPP: Guoya, Akova.

DR. WELLS: I don't remember that one.

MR. RUPP: Sheps? Have you read the Sheps study in that area?

DR. WELLS: There again, my report is basically an update of new stuff since Stan Glantz, and Bill Parmley did their study in 1992, and that's part of my testimony.

So I think the thing to do is look through that, and then there's this Leone study that's a new one from Italy, and it basically confirms what the earlier studies have said, that is that CO levels at that general level have an adverse affect on people with a heart condition.

MR. RUPP: Whether that's so or not, you have no independent basis for knowing.

DR. WELLS: No, as I said this morning, I generally take these peer-reviewed scientific papers at face value. In my situation I can't investigate every research paper and do it over again. That wouldn't make any sense.

MR. RUPP: And you can't be an expert in every area, I understand that.

DR. WELLS: I work hard at what I do, but basically it's sitting home reading the literature.

MR. RUPP: Okay, are you sufficiently familiar with the results from the Aranow study and the methodological design in that study to have a discussion with me about that study?

DR. WELLS: All I remember is that was very controversial at the time, but then years later, other studies came along that basically duplicated that study, and its reputation has revived.

JUDGE VITTONE: Mr. Rupp, let me ask you, where are we?

MR. RUPP: I thought we'd take an hour. I think I have now taken about 20 minutes. I hope another ten.

JUDGE VITTONE: No, I think you've taken 30.

MR. RUPP: Thirty? Well, I'll try to wrap it up as quickly as I can, Your Honor, if you'd indulge me for another few minutes.

JUDGE VITTONE: Okay.

MR. RUPP: With respect to the Aranow study, are you aware, for example, that Aranow and co-workers recorded premature ventricular contraction only after exercise? Would you know what significance that would have one way or the other?

DR. WELLS: Sounds bad.

MR. RUPP: Does to me, too. Aranow hypothesized that one of the things that might be involved in causing the effects that he was reporting was lactate. Are you aware that lactate is produced primarily by exercising skeletal rather than cardiac muscles?

DR. WELLS: No.

MR. RUPP: Do you know whether Aranow made any effort to control for confounders?

DR. WELLS: I don't know that, either. No.

MR. RUPP: Are you aware of the more recent study in the same area by Shep and co-workers which was designed to test the Aranow hypothesis?

DR. WELLS: I haven't been into the detail of these studies for some time, frankly. If you want to write out some questions, I could try to give you some answers in the post-hearing on a written basis, but to ask my questions about the details in those papers right now is --

MR. RUPP: You're not going to be able to help me?

DR. WELLS: I don't think so.

MR. RUPP: If I may have about 15 seconds, Your Honor?

JUDGE VITTONE: Sure.

MR. RUPP: Dr. Wells, have you reviewed in any kind of a comprehensive fashion the available literature on the relationship between stress and cardiovascular disease?

DR. WELLS: No.

MR. RUPP: Okay. And one final series of questions. And again, I don't mean to take you into areas that you're not comfortable, so if you're not, and I do have some detailed questions, you just tell me and I will stop. My understanding is that researchers at Oakridge National Laboratory, as well as the United States Environmental Protection Agency, have reported that carbon monoxide concentrations in environments where smoking is allowed have been generally less than 1.5 parts per million higher in nonsmoking areas than in smoking areas, that is the gap between the two has generally been below 1.5 parts per million.

DR. WELLS: I think we talked about that before. I hadn't seen the papers, so I don't have any basis for disputing your knowledge. I refer you, though to the Surgeon General's report where they're reporting much bigger values.

MR. RUPP: All right. Do you have knowledge or expertise that would permit you to calculate what the impact of various exposure levels to CO might have, from whatever source, on blood carboxyhemoglobin levels?

DR. WELLS: I have there in my testimony what little I know, which I got from a couple of sources, one was a review article, and the other was another article.

MR. RUPP: But again, would it be fair to say that you have no independent basis for judging the validity or invalidity of those?

DR. WELLS: No.

MR. RUPP: Trusting the authors' --

DR. WELLS: I think there's one thing you have to remember, and that is that some of these tests, like the one that Aranow ran and Alrat and so on, they often don't reach equilibrium carbon monoxide levels. But somebody's exposed eight hours at work very likely would.

So that the parts per million or the percent hemoglobin in some of those experiments, you could reach that percent hemoglobin with a longer exposure at a lower level. So you've got to be a little careful when you're talking about CO levels and parts per million.

MR. RUPP: Is that something you know, or is that something you've been told?

DR. WELLS: No, that's just from looking at the literature. And of course I know a fair amount about carbon monoxide just from my chemical experience.

MR. RUPP: Sure. Do you know what kind of sampling times were involved in the studies undertaken by Oakridge National Laboratory, as well as the studies summarized by Oakridge National Laboratory, the Surgeon General, and the United States Environmental Protection Agency?

DR. WELLS: No, I've been relying primarily on the Surgeon General's report.

MR. RUPP: Okay. Thank you very much. I appreciate it. Thank you, Your Honor.

JUDGE VITTONE: Thank you, Mr. Rupp. Mr. Lowe?

MR. LOWE: Your Honor, most of the questions I intended to ask Dr. Wells have already been presented. In the interest of saving time, I'm not going to ask any questions. Thank you.

JUDGE VITTONE: Bless you.

MS. JINOT: Dr. Bayard had to leave, so he won't be asking any questions.

JUDGE VITTONE: Okay. Do you work with

Dr. Bayard?

MS. JINOT: Yes.

JUDGE VITTONE: Do you want to ask his questions for him?

MS. JINOT: (Unintelligible.)

JUDGE VITTONE: I'm sorry, what's your name?

MS. JINOT: Jennifer Jinot.

JUDGE VITTONE: If he wants to submit his questions in writing, if he still has them, maybe they've already been asked. All right, redirect.

MS. SHERMAN: We have no questions, Your Honor.

JUDGE VITTONE: Dr. Wells, anything you want to add before I let you get off of this hot spot?

DR. WELLS: No, I think I've had enough for today, thank you.

JUDGE VITTONE: Thank you, sir. You may step down.

MS. SHERMAN: Did you submit your documents to the record, Mr. Wells?

DR. WELLS: What's that?

MS. SHERMAN: Did you submit your documents, your slides, etc. to the court reporter?

JUDGE VITTONE: Can you do that? If you have them now, that would be fine, if not, if you could do it within a week?

DR. WELLS: I think I could give them to you right now.

MS. SHERMAN: What exhibit number are we up to?

JUDGE VITTONE: 26 is his exhibit number for his testimony and slides, 27 will be the letter that he quoted from in the course of Mr. Furr's examination.

(The document referred to was marked for identification as Exhibit 28 and received in evidence.)

MS. SHERMAN: Okay, so the next number is 28?

JUDGE VITTONE: The next number will be 28.

MS. SHERMAN: Okay.

JUDGE VITTONE: I have, I'll give them to you at the end, I have his slides.

MS. SHERMAN: Do we have the letter also in that package?

JUDGE VITTONE: No, I don't. I think he's going to have to make copies to provide it, right, Dr. Wells?

MS. SHERMAN: He already did.

JUDGE VITTONE: Oh, you already did? Okay. So the letter --

DR. WELLS: The letter is dated October 23, 1990. It's a two-page letter signed by George Jay Knight, Ph.D., addressed to Dr. Wells. It's on the letterhead of the Foundation for Blood Research of Scarborough, Maine.

MS. SHERMAN: Your Honor, could we have a short break between Mr. Wells and Mr. Woods?

JUDGE VITTONE: Okay, five minutes.

JUDGE VITTONE: Okay. Let's go on the record, please.

Mr. Tyson, you wanted to raise a procedural matter.

MR. TYSON: Yes, sir.

I just wanted to make a point of clarification with respect to the agreement reached yesterday with respect to the rescheduling of the Philip Morris testimony that was originally scheduled for the 30th of September.

The Government has indicated a problem with the effect of the rescheduling of having tobacco companies back to back on subsequent days or successive days.

I just want to note for the record that I have talked to the folks at RJR and within those first two weeks of December any time that the Government would like to schedule the Philip Morris presentation and the RJR presentation is acceptable. So within that timeframe, we have a two-week period, we are happy at any time in there that the Government wants to put us.

JUDGE VITTONE: Okay. And you've talked about that with counsel for the Government and you both agree on that?

MR. TYSON: Yes. And RJR has agreed.

MS. SHERMAN: Yes. And we also will talk about rescheduling individual people at the beginning of next week.

JUDGE VITTONE: Individuals meaning?

MS. SHERMAN: Some of our witnesses.

JUDGE VITTONE: Some of your own witnesses.

MR. TYSON: That's acceptable.

JUDGE VITTONE: Okay.

We will have somebody next Friday, then? On the 30th? Isn't that next Friday?

MS. SHERMAN: We will try.

JUDGE VITTONE: Okay.

MR. TYSON: I can't be here next Friday, so it's fine with me if there isn't one. I mean, that's what started this problem.

JUDGE VITTONE: Okay. All right. Thank you very much.

MR. TYSON: We're in agreement on that? We're clear?

MS. SHERMAN: Yes, I think so.

MR. TYSON: Thank you, Your Honor. I appreciate that.

JUDGE VITTONE: You're welcome.

Dr. Woods, would you state your name and your affiliation, please?

DR. WOODS: My name is James E. Woods.

JUDGE VITTONE: Try that other microphone. I don't think that one works.

DR. WOODS: I am James E. Woods, Professor of Building Construction, at Virginia Polytechnic Institute and State University.

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

DR. WOODS: That's correct.

JUDGE VITTONE: Okay. And you have previouslyÍsubmitted a statement for the record on AugustÍ12, 1994?

DR. WOODS: Yes, sir.

JUDGE VITTONE: Okay.

And you are going to have a slide presentation, too, right?

DR. WOODS: Yes. Overheads. Right.

JUDGE VITTONE: Overheads. Okay.

Your testimony will be 28, Exhibit No. 28, with the slides, for the record.

(The document referred to was marked for identification as Exhibit No. 28 and was received in evidence.)

JUDGE VITTONE: Okay. If you are ready to go forward, sir, if you want to use that stand up there, that would be fine.

JAMES E. WOODS, PH.D.

PROFESSOR OF BUILDING CONSTRUCTION

VIRGINIA POLYTECHNIC INSTITUTE AND STATE UNIVERSITY

DR. WOODS: I will try to identify the overheads by number as I walk through these.

Your Honor, OSHA and participants in this hearing, I am pleased to be here this afternoon. As I mentioned, I am a professor of building construction and Director of the Indoor Environment Program at Virginia Tech. I have been there five years. Before that, I spent six years as senior staff scientist and senior engineering manager at Honeywell Corporation. Previous to that, for nine years, I was a professor of mechanical engineering architecture at Iowa State University.

My background is that I have a Bachelor's degree in mechanical engineering from the University of New Mexico, a Master's of physiological science and a Ph.D. in mechanical engineering from Kansas State University.

Before I did my graduate work at Kansas State, I had worked in industry for both Johnson Control Company and also for Enviroco, Inc., which is a manufacturer of cleaning equipment.

I have served as a member of EPA's Science Advisory Board, as a member of the Building Research Board for the National Research Council, as a member of the Science Advisory Committee for the Center of Indoor Air Research and as a member of the Technical Advisory Committee for the American Lung Association.

I have also served as a consultant to NIOSH and several government agencies and corporations.

I am a fellow in the American Society of Heating, Refrigerating and Air Conditioning Engineers and am currently a member of the continuing education committee and technical committees 2.1, which is physiology and human environment, and 4.3, ventilation requirements and infiltration. I am also a charter member of the International Academy of Indoor Air Sciences.

I offer this testimony in support of the OSHA proposed rulemaking on indoor air quality and indoor work environment. It must be noted, however, that the opinions I express here are mine and do not necessarily represent the expressions of Virginia Polytechnic Institute and State University.

This is overhead 2.

I intend to present this testimony in two parts.

At the request of OSHA, I have reviewed eh previous research and other work that I have done relative to the Notice for Public Rulemaking, primarily as a backup for the fact that some of the material that I have conducted was cited in the preamble for the notice.

I also intend to make specific comment with regards to paragraphs A, B and C of the proposed regulatory text.

I do not intend to present testimony with regard to paragraphs D on to the end of the regulatory text.

The first thing I would like to do is give a summary of opinions, kind of tell you what I'm going to tell you and then tell you and then come back and tell you what I told you. And I'm going to try to get this done within 45 minutes or as close to that as I possibly can.

There is a set of opinions throughout the testimony and I've tried to bullet those up front.

The first is that the health of a building degrades analogous to that of human health. I think if you keep that in perspective in dealing with the way that buildings perform that it helps people on both sides of the equation understand what's going on.

As I will show you possibly, it's my opinion that possibly 20 percent of U.S. office workers are exposed to conditions that manifest a sick building syndrome.

That mitigation and control requires a systematic approach to achieve and maintain healthy buildings.

That thermal environmental controls strongly influence perceived air quality, that the cost avoidance potential exists for tens of billions of dollars per year that can be realized in the proper control of buildings.

That costs associated with litigation, in my experience, which is extremely limited, but I have seen costs now well in excess of several million dollars, these can be avoided through responsible and accountable control.

The diagnostic procedures exist and are evolving to enable a concept that I call continuous accountability.

That implementation of the proposed rule is feasible and practical at this time and that those held accountable must have the training, and I would add the authority, to fulfill their responsibilities.

Recent focus of my research has looked at an interaction of two concepts that I will present this afternoon. It's an approach for the systematic characterization, evaluation and control of indoor environments. These two concepts are continuous degradation of buildings and the second would be interception of that continuous degradation through a concept that we call continuous accountability.

Overhead 6 gives a rationale for this continuous degradation.

I first presented this at the International Conference on Indoor Air Quality and Climate in Toronto in 1990 and it's based on three previous studies that I had published. One is a national survey of office workers that I will tell you about that was conducted while I was at Honeywell. We published that at the previous International Indoor Air Quality Conference on Climate in Berlin in 1987. In Stockholm in 1988 at the first Healthy Building Conference I presented an analysis and characterization of 30 problem buildings and then in 1989 in a chapter of a book on building associated illnesses I had a chapter on costs associated with owning and operating buildings. And in that I developed an analysis on national cost implications for owning and operating problem buildings.

An overview of the concept of this continuous degradation which appears in the Notice for Public Rulemaking was first presented in 1988 and then in 1989. We were able to put some more numbers on our estimate of the distribution of these buildings and then actually put it together in 1990.

At the time that we first did this, according to the 1983 DOE data, there were about four million non-industrial, non-residential buildings in the United States. Based on the national survey that I'll tell you about plus a World Health Organization study, we first began to look at this number of 20 to 30 percent of the building population as being characterized as problem buildings which left a residual of 70 to 80 percent as buildings without real problems.

The work that I conducted and reported on the 30 problem buildings indicated that these split into about two-thirds of the problem buildings being characterized as sick building syndrome and the other one-third of the problem building set being characterized as building related illness.

For the sake of time, if you look at the written testimony, the definitions that we're using for sick building syndrome and building related illness are in there, so unless there's a question in that regard, I am not going to spend time defining those.

In the 1989 paper on cost avoidance, we were able to postulate that 10 to 20 percent of the building stock exists as undetected problem buildings which gives a residual of 50 to 70 percent of the existing building stock as potentially being healthy buildings.

So that's eh basis that we have for the concept of continuous degradation.

I do need to mention one more thing here, that what we find is through proactive work that it is possible to achieve and maintain a healthy building stock, that during normal decay of the performance of the building it's likely that the performance is going to degrade to what I call the first level of degradation or undetected problem building category.

If it's not intercepted at this point, further decay into the problem category first as sick building syndrome and then if it is not mitigated at that point ultimate decay to the third level of building related illness plus sick building syndrome.

One additional point is in my experience I have not seen a building related illness case that did not have simultaneously a population of people that manifest as sick building syndrome. They have the symptoms associated with that which again lends support to the concept of this continuous degradation.

In 1993, in the International Conference on Indoor Air Quality and Climate in Helsinki we presented a concept with regard to putting together a set of performance criteria. And what this amounts to is that the desired response that we have in the non-residential, non-industrial sector can be evaluated in terms of human response and we have four domains of those responses: environmental perceptual, personal perceptual, environmental effective and personal effective. There is an example given in the written testimony with regard to stuffiness that you will find, you can evaluate the room as stuffy. I feel that there is from a personal perceptual standpoint, I feel a stuffiness, it's unacceptable and I feel sick. Those would beÍ-- you can do that with thermal, you can do that with lighting or acoustics or any of the parameters.

Now, from an engineering perspective, it's very difficult to control at this level of human response correctly because of all the extraneous factors that influence human response, so what we do from an engineering standpoint is try to control exposure.

The primary factors that are controlled are thermal, air quality, illumination and acoustics.

The exposure terms, then, must relate as closely as possible to what the human responses are and also in terms of control through the systems.

Now, the systems can be evaluated in terms of structure, envelope of services or enclosed spaces. Those systems control the sources of indoor and outdoor stresses or loads, thermal loads, contaminant loads, acoustic loads, lighting loads, et cetera.

So we're looking for the systems, then, to control these loads to provide acceptable exposures so that we can achieve the desired human response. The important part of this model is that it must rest on a platform of economics, so the technical feasibility is one aspect but it also has to be practically employed.

What I would like to do that is somewhat different than the format that I have in the written testimony is to try to put this together in a format that may make some sense.

What I've tried to do in this is look at those two concepts, degradation of the buildings versus what the criteria are that we can evaluate that degradation. So the first two would be in terms of human response and exposure where we degrade from a minimum level of discomfort to mild discomfort to acute discomfort that the epidemiologists call the symptoms associated with sick building syndrome, to clinical science associated with building related illness.

From an environmental standpoint, the desired effect is to produce a transparent environment. In office spaces or educational facilities or hospitals, people do not want to think about the environment. They want to think about what they're doing in that space and once that begins to degrade and they think about what's going on in the building, this is basically the type of information, then, that has to be responded to.

So the first level of degradation that we can characterize, then, is that up to 20 percent of the people in the building or the space will begin to perceive hampered performance, that the environment is bad enough that they can feel that they are just not producing the way that they want to. When we get to the problem building category, that number seems to exceed 20 percent.

From a social managerial standpoint, we find that the feeling of confidence in the management of the facility is really pretty good in the healthy building. People feel like management is taking care of them.

Once we begin this degradation process, this number seems to be somewhere in the 20 to 50 percent range and then once we get over into the problem area it tends to exceed 50 percent of the people that feel that the management doesn't really care much about the occupant in the space and I'll show you some of the data on that in a few minutes.

With regard to exposure, what we look for, then, is full compliance with a healthy building, we begin to see just marginal compliance and finally non-compliance.

Now, Hans Selye calls this area of exposure control eustress or crib stress, stress without distress. If you have no stress imposed on your physiological system, you will fatigue that system. So there has to be some dynamic. But once that begins to degrade, we get into a condition of what I will call general distress because you can't quite find the source of the problem but once we get over to building related illness and sources are identifiable, then we have both specific and general distress.

On overhead 10, in a continuation of that overview, we look at system performance. We move from full compliance to marginal to non-compliance with criteria. And, again, for the sake of time, I am not going to talk about the specifics of those criteria. They're in the written testimony. If you have questions, I'll be glad to answer the questions but I'll not go over those specifics.

With regard to economic performance, we move from full compliance, again, with the criteria to increasing operating and maintenance costs, a concept of decreased productivity or decreasing productivity because of the hampered performance. When we get over to the sick building syndrome, we begin to see measurable lost time. You also have a major cost with regard to the stigma of a sick building.

When we get to the BRI, not only do we have measurable lost time, we begin to have increased insurance costs and increased litigation costs.

Now, in both cases, what happens is that we find that the degree of difficulty and the costs associated with recovering the undetected problem building category and moving it back to healthy buildings is really in the normal cost of doing business and that's what most people try to do.

One of the problems here is beginning to deny or neglect the fact that people are beginning to complain and that complaint is festering and when that happens the degree of difficulty becomes much higher and the cost of recovering this is quite high. Not only do we have to deal with the technical problem but the social problems to regaining a building's good name or the goodwill of that building is very expensive.

When we get to the cost of litigation, as many of you lawyers know, that cost is just skyrocketing at this particular time, and so these litigation costs are extremely expensive.

Now, what I would like to do, then, with that background is walk through the national survey for a few minutes. Again, the details of it, what I want to do now is give you some supporting documentation. I'll try to highlight a couple of the bullets but basically that's, again, in the written report. But one of the points I want to make here is that this was done while I was at Honeywell. I was still Senior Staff Scientist at the time and we were trying to figure out on an international basis what made sense with regard to a business opportunity in the field of indoor air quality and so we needed to get the best possible answer that we thought we could on this point and so a scientific study was commissioned. It was a stratified random sample in nine demographic areas of the United States. In this particular study, we had 600 respondents that were contacted at home by random digital dialing. The respondents were screened to represent the type of population that was expected in offices so that two-thirds were men, one-third women; they were 18 years old; they had to spend at least 20 hours of work in the office and there were supposed to be at least five co-workers with them in that building.

We looked at the range of sampling errors and we looked at numbers from 600 down to 100 and tried to match those up.

This was initially published as a Honeywell analysis report in 1985 and then it was published at the Indoor Air Quality Conference in Berlin in 1987.

Maybe the most important finding, I'm not sure that's true but I think it is, with regard to air quality, what we found was that of the 600 people that responded 24Ípercent felt dissatisfied with the air quality in those office spaces. We have absolutely no idea what building they were in. They may have been in nine buildings. All those people could have been one in each of the nine demographic areas. Probably not. But they were called at home so there is no way to go back and find out what building they were in.

Secondly, 20 percent of the people felt that either often or sometimes they had difficulty doing their work because of the air quality in their office.

Now, another important finding from that is to look at the 20 percent of the people who perceived hampered performance and look at their concern. They were either seriously or very seriously concerned with these symptoms as problems. These are very representative of the type of symptoms that you would see with sick building syndrome and what we find is that the percentage of people that are seriously or very seriously concerned are significantly above that 20 percent that's used as a trigger for diagnostics in sick building syndrome.

So this basically indicates that those 20 percent that felt hampered also had serious concerns about this set of symptoms, which gave us validation, we felt, of the fact that that was so much higher than what we would normally expect that the numbers seemed to validate that.

Now, another point here, it's also in the written testimony, is if we look at the physical factors of people we're concerned about, these 20 percent, the ones that were most prominent, where at least 50 percent of those 20 percent indicated serious or very serious concern, most of these were either thermal or a combination of air quality and thermal. The only one that showed up as a significant air quality factor that I would call not thermally related would be cigarette smoke.

In overhead 15, we look at the other 12 factors and we see a few in here that are thermal or air quality, thermal or both but most of these are in the air quality area, so air quality alone as a point source or as a specific factor without the interactions seems to be in this lower range where the combination of thermal and air quality seems to be the stronger indicator of problems in these buildings.

Again, I don't know if you can read these numbers, and I'm not going to even ask you to do that, but what I've tried to do in this particular point is give you a breakdown of the numbers with regard to the percent dissatisfied and the percent of hampered either often or sometimes.

Some of the interesting points, I think, that you'll find here is in regard to the location of the people with regard to whether they felt hampered in their performance or not.

This is number 17. One of the important factors, we found a significantly greater number of women that were dissatisfied and perceived hampered performance and so the question was why and I think these data really begin to indicate that the women that responded were confined into their space more than men were, their career path was very different and the type of space that they were in was quite different than men. And when you put those two factors together, I don't have the data here to show you that but when we controlled for that there was very little difference in the dissatisfaction and the hampered performance between men and women.

With regard to the age and type of work area, this seems to refute a lot of the literature that's out there today with regard to age. What we see typically in the literature is the new buildings are the ones that are causing people to get sick and this did not indicate that; that in fact there was a significant difference between the buildings that were less than 10 years old and those that were more than 20 years old in both the dissatisfaction factor and the performance factor.

There is also with regard to the type of space that they're in a significant difference in both of these factors.

Windows, of interest here, there is a significant difference if the windows are not there. But if the windows are there with regard to both of these numbers, I'm not sure you can say a whole lot. It looks like if they're open often that the dissatisfaction factor goes down but I can't see anything here with regard to hampered performance. So if windows are present, that's important.

With dissatisfaction, it may be important as to whether they can open it but with regard to performance, it's not as clear.

A major point, and I want to come back to this later when we look at the litigation issue, is the perceived effects of heating, ventilating and air conditioning equipment. When we looked at the type of air distribution system, what we found is that if the system was constant volume, if the air was on all the time and we asked them to tell us about how the air is in the space, if there is a constant flow of air you can see both dissatisfaction and the performance factor is low. If it's a variable air volume system, the dissatisfaction factor increases 100 percent. And when we go up to the off/on systems, the little heat pump systems with the thermostat like in your home that cycles on and off, the number goes up again so that the on/off systems are two and a half times, they are going to increase the dissatisfaction level by a factor of about two and a half. And that seems to be holding true in the types of investigations I've been involved in also.

Now, with regard to the perceived concerns of management, what we found overall is 30 percent of the people felt that management was not very or not at all concerned about air quality.

Now, I have to tell you that this is a study, the survey was conducted in 1984, okay? And there may be a modification to that but this is the data that we're using right now as the benchmark data and, to my knowledge, we do not have another study that allows us to have any better data than this at this point, so I think OSHA has used, in my opinion, probably the definitive study like this that's out there. Unfortunately, we need more.

Again, you find women have a greater concern about management than the men did. Interesting here, if the people perceived the air quality in their office as excellent, the percent of people that felt management was not very or not at all concerned was very low, 14 percent. But it goes up three times if they feel that the air quality is only fair or poor and I think that is an area that we really need to look at at this particular point. We see a big change in the crowdedness of the area and we also see a significant change if they're in an open area, the big pits that people have to work in.

Now, on overhead 22, I will give you the full set of overheads for the record but I'm kind of skipping some now so we can get through the time, we reported in 1988 an investigation or an analysis of 30 buildings that I had access to the data at that time because we were actively doing diagnostics on buildings around the country.

Of those buildings, two-thirds of those were characterized as sick building syndrome and one-third as building related illness.

The types of stressors that we found in those buildings are that 75 percent of the time they were characterized as chemical or particulate contaminants and almost always odors.

Thermal problems existed in about 55 percent of our investigations.

Microbial contaminants about 45 percent of the cases and non-thermal humidity problems about 30 percent of the cases.

Now, this is a significant difference from what NIOSH reports and I think you will find other people reporting higher numbers than NIOSH does also. Microbial contamination is a very important problem and it can be mitigated but from this part of the country to the tip of Texas in particular, we're in a hot humid climate and mold is a major problem in the summertime.

If we go up to the northern part of the country, mold becomes a problem in the wintertime. Mold is a problem. How you control it and what the factors are may have some demographics that need to be dealt with but this is a very important problem to deal with.

We also reported in '89, I reported in '89 a comparison of two studies. Gary Robertson had also reported work at the 1988 conference and so I've tried to do a parallel analysis of this.

We found reasonable agreement in the numbers with regard to system problems and equipment problems that you could say are design related. He did not report problems on the operation side but this is, I feel, a very important factor and OSHA, in my opinion, directly addresses this, that in 90 percent of the cases, the problem buildings that we investigated, we found control problems.

Now, realize I was working for a control company. You can imagine how they were feeling about this, okay? But it was dealt with very forthrightly in that regard.

We found two factors. One is the systems are over-complex, people are not trained to be able to deal with the control systems that are installed. Or the other side of the problem is that there is an over-aggressive energy management program that's been instituted and the implications of those energy management strategies have not been studied with regard to environmental quality.

We found 75 percent of the problems involved inadequate maintenance. In 60 percent of the cases, we found that there were significant changes in the loads imposed on the systems but the capacities of the systems had not been modified to correspond with the changes in the loads.

These are all solvable types of problems.

In this regard, we also have tried to characterize what we called healthy buildings. These factors, again, are directly addressed in the Notice for Proposed Rulemaking.

JUDGE VITTONE: What number is that?

DR. WOODS: The number of this one is 24. Thank you.

I'm going to redefine that in a little while when I show you another diagnostic technique that we're looking at but we feel that by complying with the human response, the systems and the service factors that the opportunity of preventing problem buildings increases considerably.

With regard to the economics, I wanted toÍ-- again, this is in the material, so I want to just highlight this. There are conflicts among the various players in the design, construction and operations of buildings. And if you go through this, you will begin to see, for example, let me just take one case and that would be the rented or leased space. At $15 to $50 a square foot, the tenant is going to try to get as small a space as possible but the building owner wants the whole building rented, so there's a conflict on how do you deal with that particular problem.

Crowding, we found, doubles the percent of perceived hamperedÍ-- of the people that perceived hampered performance and crowding also impacts load. We found load imbalance in 60 percent of the buildings. So of the 20 to 30 percent of the problem buildings or 20 to 30 percent of the total population, 12 to 18 percent maybe accounted for because of that particular conflict.

I want to look at a couple of other numbers quickly. The numbers that I had based our analysis on were generated by the same source that OSHA is using in their data base. In 1983, DOE reportedÍ-- or U.S. Energy Information Office reported four million buildings, four and a half in 1989. We anticipate the net growth of the building population increases about 2 percent a year. That fits right in there.

Now, what we have looked at here are four as examples, four of the categories of buildings that are mentioned in the NOPR. And if we just look at offices, educational facilities and health care facilities, we account for about 58 percent of the building stock.

Now, public assembly buildings adds another 14Ípercent and lodging adds another 3 percent. So we're up to 70-some percent of the building stock in just looking at those categories.

On number 27, I tried to spread those buildings against the stages of degradation, to begin to look at the number of buildings that are likely to be in each of these four stages of degradation.

If we look at the examples of national cost avoidance in problem buildings, I have modified the '89 paper a little bit because I'm using the new numbers of the stock, but if we look at 30 percent of the 675,000 office buildings in the United States with an average flow area of 13,000 square feet, and we look at a cost factor of salary of $200 per square foot per year, if half of the 20 percent of the people that perceived hampered performance lose three days a year out of an expected 12 days per year, the national cost impact is about $3 billion. And we can do the same thing with administrative services and hospitals, we get another .4.

In addition to that, if the patient has to stay in the hospital an extra day because of building related nosocomial infection, that adds another $3.5 billion.

In the mercantile and food and sales area, we look at a range in here of 2 to 70 billion dollars a year national cost avoidance.

Okay. Now, if we compare these numbers against what OSHA is estimating in here of 30 percent of 4.5 million buildings with a productivity loss of 3 percent, we see a net cost impact of $15.4 billion. My opinion is that that scenario seems to fit very well within the total type of scenario that you can generate in this area. It seems to be, if anything, a conservative number.

I want to turn my attention a little bit to an area that I have not previously reported. The information in the testimony is reported for the first time. As I indicated, I was asked by OSHA to kind of look back at the research that I've been doing, so please understand I'm giving you a biased viewpoint of the world according to Woods, okay?

This is stuff that I've been involved in directly.

I want to give you an overview of 11 cases pertaining to sick building syndrome and building related illness that I've been involved in since about 1982. The first time I began to be called about this type of problem was in '82. I've seen four office buildings, four schools, two courthouses and a hospital. The outcomes, three office building cases were tried before juries. There have been two judgments, one with negligence without medical damages; one negligence with medical damages; one was settled during trial. It was being tried on strict liability rather than negligence. One office building case settled before trial. One school settled before trial, three schools are pending. One courthouse settled before trial, one is pending. And one hospital case settled before trial.

On overhead 30, I give you a characterization of those 11 buildings. I was really surprised to see this number but 10 of the 11 were owned or leased by government agencies. Only one was truly in the private sector. And I have to say even in that one case there were government agencies in the building. They were not involved in the case.

Six of the buildings were owned. Two were leased for full occupancy and two were leased for partial occupancy.

Of the 11, four of the buildings were speculative office buildings, three had absentee owners. Of particular interest here, two of those buildings were owned by insurance companies as part of their portfolio of investments.

Two had on-site facility management under contract with the owners, one was owner occupied and managed.

Of the other seven facilities, five had off-site campus management. One courthouse had on-site management under contract with the owner. One hospital had on-site management by the owner.

Now, if we look at the human response factors, we see 11 of the cases were associated with sick building syndrome without BRI. Eight of the cases were BRI with sick building syndrome.

I think the lesson learned there is with the clinical signs and the evidence of clinical signs, people are more prone to file a suit.

With regard to exposure, four of the buildings characterized as an issue regarding occupancy of a new building. Six were issues involving occupancy during renovation or fit-out. Only one of the buildings did not involve some kind of construction.

If we look at the HVAC systems, if you go back and think a bit about that national survey, what we find is that two of the buildings has constant air volume systems, five had variable air volume systems, and six had on/off control, which fit pretty well with what that indication had been.

Now, it seems that there are two primary issues that are forcing litigation. One is premature occupancy at substantial completion, the other is occupancy during renovation.

The premature occupancy at substantial completion should be alleviated if the process is rigorously followed in signing off on a form called the AIA Document G704, which is the date of substantial completion. The contractor signs it, says we're ready for occupancy, gives it to the architect who looks at it, generates a punch list and says with the exception of these punch list items I agree, it's habitable, it's ready to use for its intended purpose. Then it's given to the owner and the owner says, yes, I agree with these, I accept responsibility for the performance of the building. It's amazing to me how often we do not find that document in these litigation cases.

Now, in the new buildings, primarily what we're finding are chemical exposures as the issue. That's not true in renovation. It may be particulate, it may be mold. During the reconstruction or the ventilation period, you don't know what you're going to get when you drop out the ceiling in some of these spaces.

Typically, what happens is that the areas are not properly isolated, so the occupants in the surrounding area become exposed to what's going on in that construction zone. The same type of thing happens in tenant fit-out.

The churn rate today is something like 18 months. About every 18 months to 24 months, offices are going to change. People are going to move out, new people are going to move in, et cetera, so there is always this type of system going on in these buildings.

Now, if we begin to think about the other side of this, rather than the degradation, if we look at the accountabilityÍ--

JUDGE VITTONE: Excuse me, Dr. Woods?

DR. WOODS: Yes?

JUDGE VITTONE: How much longer do you think you need?

DR. WOODS: I think I can finish in about 10 minutes.

JUDGE VITTONE: Okay.

DR. WOODS: There's a five-step process that we've looked at and it's in the document that indicates that throughout the life cycle of a building if the performance criteria are properly defined that accountability can be assigned throughout the life cycle of the building. It can be tested in these phases by using the concept of building diagnostics. Again, that's explained in the written documents but there are four points in building diagnostics that are really important to understand. One is the knowledge of what to measure in the building and the availability of the appropriate instrumentation, to be able to interpret your own data and have the capability of predicting the performance over time. Typically this is not available to building managers. It's becoming more available but there is a training effort needed in this regard.

This flow chart just basically shows how these things come together so that you can use this diagnostic procedure but the important thing here is that you absolutely have to have a set of performance documents, performance criteria, so you can evaluate the building.

That's a very important part of what Section C of the regulatory text addresses.

I was asked to talk a little bit about what the cost of these diagnostics are. The current methods of diagnostics typically can be explained in a three-phase process. My experience is that with the one-day, what I call a one-day walkthrough, we can usually identify problems in 70 percent of the cases. It takes maybe two people one day to go through and at a rate of $100 to $200 an hour, you're probably looking at an expense of $2000 to $4000.

If you need to go to the next stage with a more detailed engineering analysis, we can get up to about 90 percent of the problem buildings, identifying the causes. It probably take two person weeks and we'd get a factor of five increase on that.

If it's necessary to do the exposure assessment, you also have to do simultaneous system analysis and so that raises the cost again. So it's a step-wise process. You don't always have to go in and do this type of diagnostic. Most of the time you can deal with this type of a situation and provide adequate assurance that the building is performing properly.

Now, what we have been doing recently is looking at a new technique of diagnostics where we use the performance criteria but we also categorize and in order to try to minimize false negatives and false positive errors, we're using three categories instead of four. The important point here is that it's a little more rigorous and it gives us a little more power than being able to diagnose what's going on in the buildings.

This is a set of data that we took in several buildings. It represents about 45 sites where we evaluated against the performance criteria that we have in the testimony. And what we found is only 7 percent complied with all the criteria the first time through. Eleven percent missed on one and we put that in the marginal criteria which basically says that additional diagnostics are necessary before we can classify it as a healthy building.

If there's two or more criteria missed, the probability of getting into the problematic area goes up tremendously, which basically indicates that we've got a problem with being able to use these criteria to evaluate what needs to be done to bring the building back into shape.

Now, if we look at those three studies together, what this begins to indicate is that our original estimate of 20 to 30 percent probably holds. The new procedure, this should be 51 percent. There's an error here. I'm sorry. That should be 51 percent. So it moves over into this range just a little bit. But probably going back in and doing additional diagnostics, some of these buildings are going to move over into the marginal area or moveÍ-- some of these marginals are going to move over here.

The important point here, I think, is what OSHA is trying to do is draw a line down here. They're saying this is what we're trying to prevent, working in this area is very productive and cost effective.

JUDGE VITTONE: Dr. Wells, let me ask you a question.

DR. WOODS: Yes.

JUDGE VITTONE: You just made some markings on that chart.

DR. WOODS: Yes.

JUDGE VITTONE: The one you just marked. You just made some marks on that chart. Is what you said there reflected in your written testimony?

DR. WOODS: It is not. What I've tried to do is condense and bring the information together. It's reflected but I think I may have enhanced it a little bit here.

JUDGE VITTONE: Okay. That chart is called "Evidence of Continuous Degradation". Everything to the leftÍ--

DR. WOODS: Everything to the left of the line that I drew here is in that problem category that is the subject of the notice.

JUDGE VITTONE: So that would be problematic buildings, everything to the left.

DR. WOODS: Right.

JUDGE VITTONE: Okay. And everything to the right isÍ--

DR. WOODS: Those would be eh buildings that are not yet in the problematic area that in my opinion would be those that are performing adequately.

JUDGE VITTONE: So UPB, commercial buildings, everything to the right.

DR. WOODS: Yes, sir.

MS. SHERMAN: Mr. Woods, you will make a similar mark on the hard copy that you submit for the record?

DR. WOODS: Sure. Absolutely.

MS. SHERMAN: Thank you.

DR. WOODS: I'm almost done.

JUDGE VITTONE: Thank you.

DR. WOODS: With regard to responsibility authority and accountability, I've written this in the testimony but I just want to highlight that I believe it's very important to consider this chain of custody of accountability throughout the lifetime of the building, that by identifying the performance criteria that it's possible then to identify who in the stage of that building's life has the primary accountability for its performance.

Continuous accountability enables interception of the degradation before the onset of problem buildings and that, I think, is the point that you were making, Your Honor, that I was trying to show on the slide.

Now, the final point here, I think, that in addition to education and training, it's really important that authority be given to those people that are responsible for the performance of the buildings. Oftentimes you go into the building and they'll say, yes, we know it but we don't have any way to getÍ-- we don't have a budget, we can't deal with the problem. So authority to be able to implement the performance according to the criteria that's established also needs to be presented.

Now, finally, I think in summary of the testimony, what I've tried to do here is to indicate that the proposed IAQ compliance program is needed and practical; that the diagnostic procedures are available that enable cost effective implementation of the compliance program and that employer accountability provides a high probability of intercepting building degradation before the onset of problem buildings and resultant health impairment.

I just want to finish with a couple of comments with regard to the specifics in the document itself, regulatory comments, I don't have anything to add to the written comments. But with regard to the definitions, one point that I find that OSHA should address is the additional definition of sick building syndrome, that the basis for much of the work that's done in the preamble is consideration of sick building syndrome.

I endorse in principle the proposed definition of designated person and, as I mentioned, I recommend that this definition be modified to empower the person with authority to take the necessary measures.

I would also recommend that because of the confusion of what we're dealing with from a health perspective in non-industrial buildings, that health be defined as clearly as possible and that material impairment of health, a definition of material impairment of health, consistent with that definition of health in the non-industrial building sector be defined.

I think with that regard I'll just leave the written testimony to stand with regard to paragraph C and take questions.

JUDGE VITTONE: Thank you, Dr. Woods.

Can I have a show of who has questions for Dr.ÍWoods? Two?

Mr. Rupp?

MR. RUPP: Your Honor, I may or may not have questions. I'm trying to figure it out.

JUDGE VITTONE: Okay.

The gentleman over here to my left, would you identify yourself?

Come forward and identify yourself, please. YouÍcan leave your jacket off. It's Friday afternoon, it's after four.

Dr. Woods, I do have one question for you. I guess I assume from what your testimony is if you want to stay healthy stay out of government buildings?

(Laughter.)

DR. WOODS: I really didn't want to say that. I'm not sure what to make of that at this point. I think probably that within the government sector that recourse may not be as readily available as it is in the non-government sector. I'm just not sure. It just turns out in those 11 cases that's the way it came out.

JUDGE VITTONE: I've got a feeling I've probably had offices in a couple of those buildings.

Why don't you come forward, sir, and identify yourself for the record?

Let me ask, is anybody going to need these slides?

Okay.

MR. JAWER: I am Michael Jawer with Building Owners and Managers Association. We're number one on OSHA's list. And as I may need more than 10 minutes for the questions that I have, I would like to mention that I have the proxy of one of the other organizations on the list, the Institute of Real Estate Management, which is number 68 on the list.

JUDGE VITTONE: How much time do you think you're going to need?

MR. JAWER: I will need 20 minutes at most. And I will try to keep it closer to 10. But if I should go over 10Í--

JUDGE VITTONE: All right. Let me ask the gentleman who also raised his hand back there on the rightÍ-- 10 minutes?

All right. Why don't you go first and then we'll follow with the second gentleman.

No, you. Why don't you go first, okay?

MR. JAWER: I would just like to mention for the record, if I do go beyond the 10 minutes, the question I will be asking will be on behalf of BOMA.

Dr. Woods, you didn't mention here today and I didn't see it in your written comments whether you support what is undoubtedly the most controversial of OSHA's proposals and that is the provisions to limit environmental tobacco smoke exposure in buildings.

Do you support those provisions?

DR. WOODS: As I mentioned probably in the written testimony, I support the scope of the document that is expressed in part A of the intent. So, yes, I support the document.

MR. JAWAR: The environmental tobacco smoke provisions, I believe, are in paragraph E of the OSHA proposal. Do you support the provisions in that section?

DR. WOODS: What I was asked to testify about was regarding the concept that's defined in A, B and C. I was not asked to comment on paragraphs D on. And so from that regard, I'm not prepared to testify or to give comment on that.

MR. JAWAR: Very well. So just to clarify, you do support the gist of paragraphs A, B and C but not necessarily the following paragraphs?

DR. WOODS: Well, I'm not in a position to make any comment on the others at this point.

MR. JAWAR: All right. I would like to ask you some questions about eh 1985 Honeywell tech analysis report that you spend some time on called "Indoor Air Quality, A National Survey of Office Worker Attitudes." In your written comments to OSHA, you mentioned this beginning on page 6, you were involved in the preparation and the analysis of this survey for Honeywell at that time?

DR. WOODS: That's correct.

MR. JAWAR: It was quite an earnest effort to sample office workers across the country. Just to refresh our collective memory, it was administered to 600 office workers, 18 years of age or older who currently work or at that time who worked outside their home more than 20 hours a week in an office or an office-type setting in which five or more persons were employed. One of the conclusions in this benchmark survey on air quality in the office was that, and I quote, "Office workers do consider air quality an important ingredient in creating a productive working environment but they do not consider it a critical problem." Did you mention this conclusion of the survey in the recent submission to the OSHA docket?

DR. WOODS: That was the -- are you talking about the actual report?

MR. JAWAR: The actual report.

DR. WOODS: Yes. I looked -- we evaluated that actual report and what I am trying to comment as objectively as possible is their interpretation was that as long as -- it would be 76 percent felt that it was okay, that was good enough. Our evaluation was that was not good enough.

MR. JAWAR: Our evaluation?

DR. WOODS: At Honeywell at the time. When we wrote the paper. So we took the data and presented the results of the data. We also looked at that report and their comment with regard to that and we put a more rigorous interpretation to the data.

MR. JAWAR: So the analysis that was contained within the report, you were not involved in the preparation of that analysis?

DR. WOODS: That analysis was done by an independent survey research house.

MR. JAWAR: Okay. I'd like to read a brief paragraph from that analysis. It states, "Respondents were first asked to consider a number of things that may contribute to making an office or work area a productive place in which to work. More than two out of three respondents cited lighting, 87 percent; temperature, 78 percent; and air quality, 68 percent as 'very important factors' affecting the office environment. Not far behind is overall housekeeping, how clean and orderly the office is, which is mentioned as very important by 63 percent of office workers." Again, in your docket submission to OSHA, did you mention these other conclusions, these other factors, in particular that lighting and temperature were cited by a higher percentage of respondents than indoor air quality as affecting their perceptions of the office environment?

DR. WOODS: Let me try to answer it this way. I have included the tech analysis report in the material that I have submitted to OSHA, so they have that information. What I was particularly interested in then and continue to be at this point are the interactive effects of thermal, lighting, acoustics, air quality. What we have been focusing on are the thermal/air quality interactions as primarily affected by the HVAC system, so when we begin to look at systems, there is no way that we try to ignore thermal. We don't ignore the lighting component. But from a standpoint of being able to deal with the issues of how HVAC systems impact or how the mechanical systems in the building impact performance, the concentration has been on the thermal/air quality interaction.

MR. JAWAR: In the materials that you've submitted to OSHA, is this analysis portion of the Honeywell report included? Does OSHA have this particular information?

DR. WOODS: Yes, it is.

MR. JAWAR: So I take it that your views were different at that time than the folks who prepared this particular analysis because you were focused, as you mentioned, on indoor air quality, HVAC and thermal issues as paramount among the top three issues that were mentioned by the respondents in this survey rather than lighting, rather than housekeeping, for example. You believe that indoor air quality, of these factors, is deserving of federal regulation among those different factors?

DR. WOODS: As it impacts health of the occupants, yes, sir.

MR. JAWAR: There is another mention that over half of the respondents said that the size of the office or workspace and quiet are of paramount importance and over 41 percent felt that distance to co-workers was very important in helping to create a productive environment. Are these other factors that you consider to be important in perceptions of indoor air quality?

DR. WOODS: Yes. In fact, I tried to address that in my testimony.

MR. JAWAR: On page 2 of your written comments to OSHA, you state, and this is the third full paragraph, "The results from our study of 30 problem buildings support and provide field validation of the national survey." Were those buildings, those 30 buildings that you've characterized as problem buildings, selected at random?

DR. WOODS: They were not. Those were problem buildings that we had been retained to investigate, so there was nothing random about them.

MR. JAWAR: How can you then conclude that the results of that study, which was a specific population of buildings that you knew were problem buildings, the results provide field validation of the national survey which was a random survey?

DR. WOODS: That's a good point. What we're trying to concentrate on are the 20 percent of the people that felt hampered, okay? So that in a sense defined the subset that we're calling a problem building, the 20 to 30 percent. The 20 percent hampered, the 24 percent dissatisfied, the number of symptoms, the factors that we found that people were common on tended to validate that subset of the national survey. So from that standpoint, I felt it clearly validated it.

MR. JAWAR: It validated that subset rather than the national survey overall without qualification.

DR. WOODS: That's right. That's right.

MR. JAWAR: All right. On page 23 of your written comments to OSHA, and this is the third full paragraph, you mentioned this in your presentation, that since 1982 you have provided consultation and expert opinion on 11 cases in which occupants who claimed they had suffered deleterious effects from indoor exposures filed lawsuits against tenants, building owners, manufacturers, contractors and designers. Did you physically investigate those buildings on site, those 11 situations?

DR. WOODS: I think I've been to each one of those. Yes.

MR. JAWAR: And, as you mentioned, four of those cases involved occupant exposures in office buildings, four were exposures in schools, two in courthouses, and one hospital. And then further you mentioned that 10 of those 11 were owned or leased by government agencies so that only one of the 11 buildings was a privately owned and leased facility.

DR. WOODS: Right.

MR. JAWAR: Is that correct?

DR. WOODS: That's correct.

MR. JAWAR: Would you hazard a guess as to why there was this overwhelming preponderance, and you were asked the question before, I'm not sure it was on the record, of publicly owned or leased space showing up in these lawsuits?

DR. WOODS: I think that's the same question that was asked and I am perplexed by it. I'm not sure I know what that means. If you look at the subset of speculative office buildings, the four speculative office buildings that were in there, it happens in four of the 11. Now, some of those were leased to government agencies, one was the private leasing. So I don't think we have enough data there to be able to draw to the point of being able to say we understand that all government buildings are inferior to all private buildings or vice versa. I don't think I want to stretch it that far. I do think that from the information I've gathered in doing the analysis in preparation for these cases that occupants in governmental agencies don't feel that they have the same recourse. They can't pick up and leave. In a BOMA class A building, if people don't like what's going on, they're going to -- they're going to make comments to the point that either it gets changed or the owner of that building is going to be without a tenant. And I think in the federal agency basis -- well, I can tell you, let me just expand on that just a minute. I've been involved both in litigation and in some cases that are not in litigation in federal office buildings in the D.C. area and in both cases the lease for the building is running somewhere between $7.00 and $17.00 per square foot per year. And I doubt if you could go rent the same kind of space for $30 a square foot a year. This puts a terrible burden on both sides. The agency can't afford to move out because they're locked into a budget.

Are you talking about the actual report?

MR. JAWER: Yes.

DR. WOODS: We evaluated that actual report, and I'm trying to comment as objectively as possible. Their interpretation was that as long as 76 percent felt that it was okay, that was good enough. Our evaluation was that was not good enough.

MR. JAWER: Our evaluation being?

DR. WOODS: Honeywell at the time. When we wrote the paper. So we took the data and presented the results of the data. We also looked at that report and their comment with regard to that, and we put a more rigorous interpretation to the data.

MR. JAWER: So the analysis that is contained within the report, you were not involved in the preparation of that analysis?

DR. WOODS: That analysis was done by an independent survey research house.

MR. JAWER: I'd like to read a brief paragraph from that analysis that states, "Respondents were first asked to consider a number of things that may contribute to making an office or work area a productive place in which to work. More than two out of three respondents cited lighting, 87 percent; temperature, 78 percent; and air quality 68 percent as 'very important factors' affecting the office environment. Not far behind is overall housekeeping, how clean and orderly the office is, which is mentioned as very important by 63 percent of office workers."

Again, in your docket submission to OSHA did you mention these other conclusions, these other factors? In particular, that lighting and temperature were cited by a higher percentage of respondents than indoor air quality as affecting their perceptions of the office environment?

DR. WOODS: Let me try to answer it this way. I have included the Technalysis Report in the material that I have submitted to OSHA, so they have that information. What I was particularly interested in then, and continue to be at this point, are the interactive effects of thermal lighting, acoustics, air quality. What we've been focusing on are the thermal air quality interactions as primarily affected by the HVAC system. So when we begin to look at systems, there's no way that we'd try to ignore thermal. We don't ignore the lighting component. But from the standpoint of being able to deal with the issues of how HVAC systems impact or how the mechanical systems in the building impact performance, the concentration has been on the thermal air quality interaction.

MR. JAWER: In the materials that you've submitted to OSHA, is this analysis portion of the Honeywell report included? Does OSHA have this particular information?

DR. WOODS: Yes, it is.

MR. JAWER: So I take it that your views were different at that time than the folks who prepared this particular analysis, because you were focused, as you mentioned, on indoor air quality, HVAC, and thermal issues as paramount among the top three issues that were mentioned by the respondents in this survey, rather than lighting, rather than housekeeping, for example. You believe that indoor air quality, of these factors, is deserving of federal regulation among those different factors?

DR. WOODS: As it impacts health of the occupants, yes, sir.

MR. JAWER: There is another mention that over half of the respondents said that the size of the office or work space and quiet are of paramount importance, and another 41 percent felt that distance to co-workers was very important in helping to create a productive environment. Are these other factors that you considered to be important in perceptions of indoor air quality?

DR. WOODS: Yes. In fact I tried to address that in my testimony.

MR. JAWER: On page two of your written comments to OSHA, you state, and this is the third full paragraph, "The results from our study of 30 problem buildings support and provide field validation of the national survey."

Were those 30 buildings that you've characterized as problem buildings, selected at random?

DR. WOODS: They were not. Those were problem buildings that we had been retained to investigate, so there's nothing random about them.

MR. JAWER: How can you then conclude that the results of that study, which was a specific population of buildings that you knew were problem buildings, the results provide field validation of the national survey which was a random survey?

DR. WOODS: That's a good point. What we're trying to concentrate on are the 20 percent of the people that felt hampered. So that, in a sense, defined the subset that we're calling the problem building. The 20 to 30 percent. The 20 percent hampered, the 24 percent dissatisfied, the number of symptoms, factors that we found that people were commenting on tended to validate that subset of the national survey. So from that standpoint, I felt that it clearly validated it.

MR. JAWER: It validated that subset rather than the national survey overall without qualification.

DR. WOODS: That's right.

MR. JAWER: On page 23 of your written comments to OSHA, and this is the third full paragraph, and you mentioned this in your presentation, that since 1982 you provided consultation and expert opinion on 11 cases in which occupants who claimed they had suffered deleterious effects from indoor exposures, filed lawsuits against tenants, building owners, manufacturers, contractors, and designers.

Did you physically investigate those buildings on site, those 11 situations?

DR. WOODS: I think I've been to each one of those, yes.

MR. JAWER: And as you mentioned, four of those cases involved occupant exposures in office buildings; four were exposures in schools; two in courthouses; and one hospital. Then further, you mentioned that ten of those 11 were owned or leased by government agencies, so that only one of the 11 buildings was a privately owned and leased facility. Is that correct?

DR. WOODS: That's correct.

MR. JAWER: Would you hazard a guess as to why there was this overwhelming preponderance? And you were asked the question before, I'm not sure if it was on the record, of publicly owned or leased space showing up in these lawsuits.

DR. WOODS: I think that's the same question that Your Honor asked. I'm perplexed by it. I'm not sure I know what that means. If the subset of speculative office buildings, the four speculative office buildings that were in there, it happens that four of the 11. Some of those were leased to government agencies; one was the private leasing. I don't think we have enough data there to be able to draw to the point of being able to say we understand that all government buildings are inferior to all private buildings or vice versa. I don't think I want to stretch it that far. I do think that from the information I've gathered in doing the analysis in preparation for these cases, that occupants in governmental agencies don't feel that they have the same recourse. They can't pick up and leave in a BOMA class A building. If people don't like what's going on, they're going to make comments to the point that either it gets changed or the owner of that building is going to be without a tenant. I think in the federal agency basis... Let me just expand on that just a minute.

I've been involved both in litigation and in some cases that are not in litigation in federal office buildings in the D.C. area. In both cases, the lease for the building is running somewhere between $7 and $17 per square foot per year. I doubt if you could go rent the same kind of space for $30 a square foot a year. This puts a terrible burden on both sides. The agency can't afford to move out because they're locked into a budget. The owner of the building is locked into not being able to have any movement at all to be able to maintain because the cost is so low, and he may be actually wanting to get rid of that particular agency because he could rent for a higher rate.

So again, I've tried to address that in this conflict of players situation, but that would be maybe one way to expand that piece of information that's coming out of this.

MR. JAWER: There is a market incentive, for example, that may be absent on the public sector side? That's one interpretation.

DR. WOODS: I think that may be true, because most of the government space, most of it is long term lease.

MR. JAWER: Let me move on, because I've got a few other questions, and I'll try to be brief.

In the Honeywell survey of the people who were contacted in this random phone survey, what percentage worked in privately owned, privately leased office space?

DR. WOODS: I don't think we asked that question. I don't think I have an answer for that.

MR. JAWER: Did some of those calls go to public buildings? Occupants in public buildings? Occupants who worked in public buildings?

DR. WOODS: Bear with me just a minute. I may have that information.

MR. JAWER: For that matter, I'm interested to know whether the calls also went to workers in schools, colleges, universities, retail stores, restaurants, hospitals, or elder health care facilities.

(Pause)

DR. WOODS: The closest I think we can come to, and it's on Overhead #16, is that 382 of the 600 were in owner occupied spaces as they reported, and 187 were in rented or leased spaces. This survey, to my knowledge, did not ask whether they were in private or public sector. I don't think we know that.

MR. JAWER: Were there questions to get at whether they worked in particular types of facilities, restaurant, shopping mall...

DR. WOODS: That was screened out immediately. They told me the number. It was well in excess of 1,000 people that were called. If they didn't fit the screening category, the phone call was terminated.

MR. JAWER: Was there an estimated size of the office buildings that people worked in that were covered in this survey? An average square footage estimated, or people were asked to estimate.

DR. WOODS: Not that I recall.

Let me go back to your previous comment for just a minute, because I may have misstated my answer.

We did not ask if the office they were in was in a hospital or a school or a spec building. It was an office environment.

MR. JAWER: So it could have been responding about conditions in a school or a hospital or...

DR. WOODS: Sure. If that's where you were going with the question. I want to be sure that...

MR. JAWER: Yes, I appreciate that, because I was not certain whether that was the answer.

DR. WOODS: Right. We would have included anybody that was in an office environment, so that would have been schools, hospitals, public buildings, private buildings, whatever.

MR. JAWER: In one of the overheads you estimated that the average office building size is 13,000 square feet.

DR. WOODS: Right.

MR. JAWER: How do you get that number?

DR. WOODS: To the best of my... There's two numbers, I think one of them is yours, or was yours at the time I was doing this. The other is out of the US Energy Information. I believe 13,000. I've also heard the number 14,000.

MR. JAWER: Are you aware that according to information reported by BOMA International members who represent about half the available commercial office space in the country today, the typical private sector office building is 190,000 square feet?

DR. WOODS: Oh, yeah. Let me clarify what we're talking about. We're talking about anything that people call an office. It could be a trailer, it could be a mobile home. It could be anything that is established for business. What we find on a national basis, Honeywell had the same numbers because of the work that they were doing in the different sector of their business. So if you look at all buildings across the population, all sizes of buildings, the prominent number of buildings is a very, very small building. Another statistic that comes out along this same line is only about 20 percent of the commercial buildings that are in place today were designed by an architect/engineering team.

MR. JAWER: So based on, there's a considerable discrepancy between the typical class A, class B office building owned and operated by BOMA members, and the estimated size of any building with an office, with office space in it that you were using for your calculations.

DR. WOODS: Absolutely.

MR. JAWER: So the 13,000 number does not really represent accurately the typical office building in downtown USA.

DR. WOODS: Yes, it does. In suburban USA, in shopping mall USA, etcetera. What we're trying to look at from the standpoint of the mean size, and you can get this out of the US Energy Information Data, that the average size of all buildings, commercial buildings, is about that number.

MR. JAWER: All buildings. The 13,000 does not represent your typical class A or class B office building.

DR. WOODS: That's correct.

MR. JAWER: The Honeywell survey asked people their age, their income, their gender. Did it ask them their smoking status?

DR. WOODS: It did.

MR. JAWER: Did it ask them about their susceptibility to allergies?

DR. WOODS: I don't remember if it did that or not. If you look in the back of the report, the demographic information is in there.

MR. JAWER: I didn't see smoking status of susceptibility...

DR. WOODS: Smoking status is there. I don't remember about whether allergies was or not.

DR. WOODS: I also didn't see a question about the relative position that they have in the office in which they worked. Was that asked?

Proximates? Political structure, the hierarchy.

MR. JAWER: The person who works in the mailroom. I'm just trying to get an idea of whether you asked their job titles or their position, relatively speaking, in the hierarchy of that office.

DR. WOODS: We did, and that's been factored. I tired to show some of that information. If you look at the gender difference overhead, or I think in the written testimony.

(Pause)

MR. JAWER: Besides gender, did these other demographic or personal factors... Because I understand about gender, how that affected the response, and you suggested some reasons why. Were there differences in responses based on some of these other factors? Smoking for instance, whether they smoke, the proximity to people who smoked, susceptibility to allergies during the time the phone survey was conducted, that sort of thing.

DR. WOODS: I don't recall that we factored that out. The data is there. We can get that information out. I haven't pulled it out.

MR. JAWER: Were any of these random calls followed up by actual visits to any of these buildings?

Could those complaints that were reported by survey respondents have been due to specific contaminant sources in their workplace. For example, carpeting, office acid from carpets, fumes if there was painting going on; emissions from Crestwood Furnishings, copiers,

or laser printers, although laser printers probably weren't too common in 1984 or 1985. Solvents, pesticides, that sort of thing, could they have been due to practices such as occupant smoking or cooking in the workplace, to practices such as blocking their air vents if they felt they were too warm or too cold, which was evidently one of the strong concerns voiced; fouled trash cans in the facility. Could their complaints have been due to any or all of those factors?

DR. WOODS: Right. If you look on page eight of the written testimony, you'll see that the 12 factors where 36 percent or less of the people had serious or very serious concern. If you look at the lower factors -- fumes from trucks, buses, cars, gas vapor from office machines, computer terminals, irritating chemicals such as formaldehyde, fumes from the factory workshop, paint fumes. I'd consider all those point sources. Those tend to be point sources.

MR. JAWER: But these, again, were their perceptions. They weren't based on an actual visit to the work site.

DR. WOODS: That's correct.

MR. JAWER: If no attempt was made to determine the cause of these perceptions concerning indoor air quality in the office environment, how could one reasonably conclude that any of the buildings that those people worked in was "sick", and I put quote around that word, or potentially "sick"? How can you make that jump?

DR. WOODS: What we did in the paper that we presented at Berlin was to hypothesize that 20 to 30 percent of the occupancy space had conditions, had reported conditions from this that were consistent with sick building syndrome as manifested by those symptoms.

Then in the '88 paper, what I began to look at is that study, coupled with the World Health Organization Study that had reported essentially the same thing in that time frame. So those two studies -- the World Health Organization committee study and our survey, was the basis for forming the hypothesis that I work on now, that 20 to 30 percent are in the problem building category.

MR. JAWER: Again, I'm having difficulty. I can understand an hypothesis that 20 or X percent of people may be working in spaces where the indoor air quality is less than ideal, but how does one conclude, as OSHA has evidently in its preamble on page 16006 where it says, "Based on the information submitted to the docket, OSHA assumed that 30 percent of the buildings have indoor air quality problems."

Would you conclude that 30 percent of buildings are sick, the buildings themselves, as opposed to sources in the buildings?

DR. WOODS: It's a semantic issue, and let me try to answer it this way. From the standpoint of diagnostics in trying to characterize where the buildings fit in this distribution in the population, different methods of diagnostics, different rules are likely to be followed. Whether you're going to use more stringent criteria or less stringent criteria.

For example, on the healthy building side, because there's not an a prior assumption of a problem building, you probably would use more relaxed standards. Or performance criteria, excuse me.

In a problem building you would use more rigorous criteria to investigate the problem. So from a diagnostic standpoint, it's very helpful to be able to make that distinction. What I've seen in work since the time of this report that we published in '87, is I tried to indicate towards the end of my presentation here, if anything, indicates that we've got more problems than this number indicates. That the problematic building, not the problem building but the problematic building is 51 percent from the small set that we've got right now.

MR. JAWER: With all due respect I suggest, and I'd be interested in your reaction, that the difference is more than semantic because it seems from the Honeywell survey that there are a variety of sources, there are a variety of factors influencing perceptions of indoor air quality. The perception, when it reaches the press, the perception when it reaches the regulatory stage is that 20 to 30 percent of buildings themselves are sick, which is, in our estimation as building owners and managers, a much vastly different perception than even X percent of buildings with unidentified problems.

I'll just lead into a question. There's a definition of sick building syndrome that you offered on page four of your response to OSHA's 1991 request for information. And it says Sick Building Syndrome is suspected when occupant complaints of certain symptoms associated with acute discomfort -- headaches, fatigue, eye irritation, etcetera -- persist for more than two weeks in frequency, significantly greater than 20 percent in the area of the building, or in the entire building. The cause or causes of the complaints are not recognizable. And a substantial percentage of the complainant's report almost immediate relief upon exiting from the building.

Is it appropriate in your opinion for OSHA to regulate an issue such as this, a "syndrome" that is chiefly recognized by the lack of identifiable causes?

DR. WOODS: In my opinion it is, absolutely it is.

This definition of sick building syndrome, which is also on page 12 of my testimony, came from the Building Research Board study on policies and procedures for indoor air quality that was published I think in 1987. As I indicated, I was chair of that committee for the National Research Council. Your predecessor from Beaumont was on that committee, who signed off on that definition and has participated in that report.

At that time, BOMA was on the committee, represented. We did not have comments to the contrary from BOMA that they disagreed with this definition.

MR. JAWER: You know organizations are evolving and ever changing, especially in the association field. Our comments are on the docket, but just to... our current comments are on the docket. But just to reemphasize, despite the fact that causes of sick building syndrome are unidentified, you do support a regulatory approach at this time?

DR. WOODS: I do, indeed. Yes.

MR. JAWER: Thank you.

JUDGE VITTONE: Thank you.

The gentleman back here on the right.

MR. BENDA: Thank you, Your Honor.

I'm George Benda, Chelsea Group, Ltd. My docket number is 173.

DR. WOODS: I'm sorry, George. I'm a neophyte to this. What does that mean, your docket number is...

MR. BENDA: That means that the number I use...

JUDGE VITTONE: It's just where he filed. That's just the number that was assigned when his filing...

DR. WOODS: I don't have to worry about it.

JUDGE VITTONE: No, you don't have to worry about it.

(Laughter)

MR. BENDA: That wasn't a question.

(Laughter)

MR. BENDA: I'll do my best to keep these very brief, Your Honor.

JUDGE VITTONE: Thank you.

MR. BENDA: My first question relates to design issues, Dr. Woods. In your testimony on page 13 under system problems, you attribute building designs with inadequate outdoor air as a cause of problems in 75 percent of problem cases, and the numbers don't matter, the location doesn't matter, but the issue really is if these are design problems, could you take a moment and explain how the proposed OSHA rules address design problems?

DR. WOODS: Absolutely.

I think one of the reasons I am so supportive of this is the concept that the employer as defined, is very broad. The employer in this case represents the building owner, it could be the tenant. In turn, the pressure is going to be to the contractor and to the designer. If the employer knows that they're going to be held accountable, you can bet that the accountability is going to transfer. That's why I've tried to talk about, on continuous accountability, the concept of chain of custody. So if in the design non-compliance of performance criteria is identified and is taken care of at that point, we're not going to have a problem. In diagnostics, you can diagnose a virtual building with almost the same certainty that you can diagnose an actual building if you go... And people will do that in quality assurance or team reviews or peer review of design. That's all in there to be able to address this.

So I think what this does is it puts the design community at notice that everybody will be held accountable. I think it's a very powerful step forward.

MR. BENDA: I guess to focus down a little bit, my reading of the Rule suggests that the primary thing that a building owner would see is that he has to restore the building to design conditions, the codes and standards applicable in the design conditions. And if the design conditions then were not...

MS. SHERMAN: Could you speak a little bit louder, sir? We're having trouble hearing you.

MR. BENDA: I apologize.

JUDGE VITTONE: Thank you.

MR. BENDA: If the design conditions of the building, if the designer didn't do a good job to get to the root of it, and there is evidence to suggest that's a fairly frequent thing, then in that instance how does the Rule respond, how does that really help resolve those kinds of problems?

DR. WOODS: Let me try to answer that by going back to my comments on Section 3ii.

MR. BENDA: What page of your...

DR. WOODS: That would be on 39. Section 4.

In 3ii, I've tried to distinguish... There's a statement that either single line schematics or as-built construction documents are required. What I've tried to indicate there is these are not synonymous, and both are probably needed.

If we go over to Section 4, I believe that three of the documents that are in Section 4, the as built documents -- not the constructed or design documents, but the systems as currently existing; the operations and maintenance manuals and water treatment logs ought to be required, and those should be moved to Section 3-5, those required documents.

As builts should give you information with regard to the present loads that are on the building. The present loads may not at all represent what the design was. As I indicated, in 60 percent of the cases, of those 30 buildings that we investigated, and I can tell you I'm seeing that all the time, a good example is that EPA building that started out with 30-some air handling units, and by the time the litigation occurred, there were over 120. People didn't even know where all the 120 were in the building.

Now the loads changed and something was done about it, but it wasn't documented. Accurate documentation of what the current status is makes a huge difference in being able to provide assurance that the building is going to perform according to its desired intent. Desired intent and design intent sometimes are the same, but they've changed over time.

MR. BENDA: Thank you.

The second set of questions I have relates to commissioning issues, and it really...

MS. SHERMAN: Can you talk louder, sir?

MR. BENDA: The second set of questions relates to commissioning issues. It, again, goes to the same kinds of questions. Your litigation record talked about premature occupancy in four of the 11 cases. Could you elaborate on how building commissioning could have prevented those IAQ problems? And then in the context of these same kind of design questions, a question of design and as builts and schematics, how could commissioning, per se, overcome those problems as opposed to design record keeping.

DR. WOODS: Is that a set up question or what?

(Laughter)

DR. WOODS: Commissioning is a very important aspect that, it's a technology that's being transferred into the building sector. We've been doing formal building commissioning probably for less than ten years in buildings.

My experience in Virginia has been rather good in regard to the Department of Engineering and Buildings now beginning to consider this for the state-owned buildings.

Commissioning is defined basically in guideline one in ASHRAE consists of three parts; assimilation of material, perturbation of the system after it's been designed and balanced; and adequate training of the operating personnel. So commissioning as really practice professionally, starts probably at the schematic design stage, the 30 percent stage of design. There's an early buy-in, everybody understands that there's going to be a commissioner, which is like a quality control check. That commissioner is going to look at design decisions at the schematic stage, at the 60 percent stage at the 90 percent stage, and try to correct problems at that point.

Once the building is under construction, the commissioner will periodically inspect the building. After it's been tested, adjusted, and balanced and calibrated, the control systems have been calibrated, possibly after the certificate of occupancy has been issued, a final evaluation of the performance of the building will be done during the warning period. In my vision of commissioning, it's a subset of diagnostics. It's diagnostics that occurs in the short time frame between schematic design and turnover to the building owner. The diagnostics continues throughout the life time of the building. So this is one phase of a quality assurance program.

Extremely important, I've recommended in my testimony that that guideline be considered. I've introduced information with regard to a study that we did on the evaluation, the cost effectiveness of commissioning. I've given that to OSHA for their literature. Including an appendix where we have a prototype commissioning specification in construction specification and institute format.

So again, it's part of this big picture of being able to provide for this compliance program and I think it's very compatible with what OSHA has promulgated from their Proposed Rule.

MR. BENDA: Let me take you one more step. Have you ever heard of building commissioning being done during the life of a building? In essence, recommissioning of a building?

DR. WOODS: As a matter of fact, yes. I think this is the diagnostic phase. I've written and lectured on the concept of commissioning a renovation project. That is much more extensive than a new building from the standpoint that you have to decommission, you have go to through a formal stage of decommissioning the area to be renovated. You have to recommission the area where people are moved into because the loads have changed in that space. After the building is isolated and the work has been done, then you recommission not only the renovated area, but the area that people have moved back out of. So the commissioning process or diagnostic process or whatever we want to call that assurance aspect of compliance with criteria is very important. It's of paramount importance to this document.

MR. BENDA: Dr. Woods, I'd like to carry you to another level of opinion, which is, do you think it's possible that the concept of commissioning and periodic recommissioning of buildings might be a good substitute for the reliance on original design and local codes as a foundation for an indoor air quality regulation?

DR. WOODS: I'd really have to think that through. I really don't want to answer that on the spur of the moment. It's a good question, but I'm not sure I'm prepared to answer that right now. I'm going to beg that one.

MR. BENDA: All right.

My next group of questions relates to your endorsement of the definition of employer and the designated person. As you've mentioned, you endorse the broad concept of employer. And additionally, during your discussion of litigation information, it sounded as if many of the buildings would be multi-tenant buildings, or at least would be leased buildings as opposed to owner occupied buildings.

DR. WOODS: Certainly.

MR. BENDA: Could you give an example in a multi-tenant building -- obviously not owner occupied -- of how definitions of employer and designated person might work under the proposed rule, and what changes you might make to improve that practicality of that.

DR. WOODS: In a multi-tenant building as I see it, there are probably several employers. And probably levels of designated persons. So the tenant of the space could have one level. That tenant holds a responsibility. This is, again, what I've tried to identify, the chain of custody, and the five steps of continuous accountability.

MR. BENDA: But if I can focus you just a little bit. In the Rule, as proposed, it does not allow for those levels of designated persons, is that correct?

DR. WOODS: I'm not sure that that's true. I think probably there's enough flexibility in that that it does include that. I think that you could definitely look at that aspect.

In the final Rule it may be more clearly defined. But I think the broad concept of employer, including this concept of chain of custody, the Rule as defined is flexible enough to handle that. That's what I've tried to recommend is that they deal with this chain of custody.

MR. BENDA: The provisions of the Rule specifically require that the designated person pay attention to the maintenance of the building and so forth, and observe certain aspects of the activities of maintaining and so forth. In that ranking of designated persons, I at least didn't see anything which suggested that he wouldn't have in a multi-tenant building, for example, a requirement of 20 people observing a maintenance activity.

DR. WOODS: As far as the building is concerned, there is certainly going to be a designated person for that building. The owner, ultimately, has the final responsibility for the performance of that building.

MR. BENDA: Do you feel the current Rule is clear enough on that issue?

DR. WOODS: It needs to be refined, I think. The concept and, as I've indicated, I think the concept is good. The flexibility is there. The breadth of incorporating all of the players is there, and I think the final Rule could take, it could refine that and make it clearer, sure.

MR. BENDA: Let me turn to ne last question set, and this relates to the items which trigger an employer response to a complaint. You argue, and reinforced in your verbal testimony as you did on page 38 of your written testimony, that SBS should be included in the definition.

First, do you mean to imply that the trigger for an employer to respond to an IAQ concern expressed by an employee should be an employee complaint about SBS as well as it would be about BRI?

DR. WOODS: Well before SBS occurs, that's why this complaint log is so important. Again, let me try to be specific on that.

MR. BENDA: Dr. Woods, if I can narrow it just slightly. The specific requirement in the Rule, and I apologize, I don't have the cite in the Rule, asks that an employer respond when an employee complains of building-related illness. That's very specific, and sets that threshold. Would you see that for that requirement it would be restated as saying that the employer would have to respond for a complaint of a building-related illness or sick building syndrome?

DR. WOODS: Absolutely. If you look at page 41 of my written testimony, the paragraph just before summary.

MR. BENDA: Yes.

DR. WOODS: The employer is required to establish a written record," I think that means a log, "of employee complaints or symptoms (associated with SBS)?"

My point there is that assuming that the definition of SBS has been incorporated, then we would incorporate, I would recommend incorporating the triggering with SBS. Or clinical signs of illness associated with BRI.

MR. BENDA: Just to make my point a tiny bit clearer, it's not the logging, it's the investigation of the building that I'm talking about that's required as a result of that...

DR. WOODS: Certainly.

MR. BENDA: Let me go on from there, I think you've answered that question very clearly.

I guess the next set of questions relate to the skill of the designated person, the role of that person in taking complaints and so forth. I apologize, but I believe that the way the OSHA regulatory text reads, that that person might be receiving the same training as a mechanical person. That's the only training that's really spelled out in the regulatory text. As you know, that training is only one-half hour. Do you believe that a lay person with only one-half hour of training would be able to diagnose a sick building syndrome case or a building-related illness case from an employee complaint?

DR. WOODS: That's an excellent point, and we've wrestled with this. Let's take the five to 13,000 square foot little building out in the middle of nowhere that somebody's renting. Who is the employer? It would be the person on that building. Who's responsible for that? The designated person is going to have to be identified. That identified person is going to have, will have to have the credentials and the background to be able to understand the complaint log, to be able to respond adequately to the complaint log and to have a deep enough understanding in the performance of the system to understand the relationship.

I think that training is also part of what's in the document and what I've recommended. Training will be necessary. I don't think it's extensive, if they understand that these complaints have to be taken seriously, that maintenance has to be done rigorously, that forms have to be kept up, that you really need to have the as builts, that the maintenance manuals need to be looked at once in awhile. It doesn't take a registered engineer, a PhD or a registered architect to do that.

MR. BENDA: But will one half hour of training be sufficient to do that?

DR. WOODS: I'm not sure I would recommend one-half hour of whatever. I think that needs to be looked at. I don't remember seeing one-half hour anywhere.

MR. BENDA: It's the assumption in the equation in which the training calculation is based.

The next step in that is the question of triggering action by the building owner, and from the information I've gathered, I believe that in most of its industrial regulations, OSHA typically requires a medical opinion about an occupational illness before an employer need take action. But the standard within this rule is a complaint. Do you agree with those two statements?

DR. WOODS: Absolutely. It's a different environment. The action, if you remember what Your honor asked me about, that line that I drew down. OSHA is trying to prevent crossing that line into the problem building area. The action should be taken to the right of that, well before an impairment of health. I think what this Rule does is it says by doing this, by taking this action, by using the procedure that's established in Section C, that you deal with this undetected problem building category and you bring it to the healthy building category which is at little or no cost. And you prevent it from degrading to level two or the sic building syndrome. Or absolutely endorse that. I think that's where the action should be, and not wait until somebody has a physical impairment. You're trying to prevent that physical impairment.

MR. BENDA: Then just to summarize that, you do not think it would be reasonable to require a medical opinion relating to an SBS or ERI complaint prior to the time that a building owner is required to investigate the conditions in his building.

DR. WOODS: I do not think that's a prerequisite, no. That's after the horse has left the barn.

MR. BENDA: That's the extent of my questions, Your Honor.

Thank you very much.

JUDGE VITTONE: Thank you very much.

Mr. Rupp?

MR. RUPP: I have no questions.

JUDGE VITTONE: Thank you, sir.

Do you have any Redirect?

MS. SHERMAN: A couple of questions, Your Honor.

MS. EL-MEKAWI: Dr. Woods, does the continuous building degradation concept apply to all types of buildings like hotels, hospitals, schools?

DR. WOODS: Yes, it does.

MS. EL-MEKAWI: Can we make this generalization?

DR. WOODS: Absolutely, yes. It can work...

MS. EL-MEKAWI: And restaurants?

DR. WOODS: Sure.

MS. EL-MEKAWI: Consequently, is it applicable to generalize a 30 percent problem estimate to all these types of buildings?

DR. WOODS: I'm getting a terrible echo. I didn't get the question.

MS. EL-MEKAWI: Is it applicable to generalize the 30 percent problem estimate of problem buildings to these types of buildings?

DR. WOODS: In my opinion, it is. Yes.

MS. EL-MEKAWI: You mentioned that the half hour estimate for training is insufficient to train the designated person. How many hours do you suggest or would recommend?

DR. WOODS: Again, I think I'm not ready to answer that on the spot. With regard to being able to look at the complaint log and understand the significance when a complaint is filed, what that means with regard to systems, having enough understanding of a system...

It seems to me that the training for a building operator ought to be at least as much as an auto mechanic. Auto mechanics, good auto mechanics, take a lot more than a half hour training.

MS. EL-MEKAWI: Do you know what percentage of buildings in your study of the 30 problem buildings were public versus private? Just an estimate.

DR. WOODS: It's been so long ago since I looked at those 30 buildings... My sense is that more than half would have been in the private sector.

MS. EL-MEKAWI: Do you happen to know how many office buildings are represented by BOMA?

DR. WOODS: I can speculate. I don't know. Do you want me to speculate?

MS. EL-MEKAWI: Please.

Office building category is 14 percent of the total buildings that we see in there. My information that I've looked at over the years indicates that about half of the buildings in the United States are owned by some form of government. I got that information when I was a member of the Building Research Board. There are statistics, I believe, that are available from the... It's a committee under the Building Research Board that represents federal agencies, and I forget the name of it offhand.

But there's an amazingly high percentage of total office buildings that are owned by the government, what we call office buildings.

So if 14 percent of the buildings are offices and half of those are government, my guess would be that we're talking somewhere around 10 percent or less of the total buildings out there would be represented by BOMA. We can get a direct answer here, I think, in a minute, but that's my speculative guess.

MS. EL-MEKAWI: Thank you.

JUDGE VITTONE: Anything else?

MS. JANES: This is Debra Janes.

With the scope of our standard applying to all different types of buildings and what not, with your theory of continuous degradation of buildings, do you feel it's necessary for all buildings to have regular operating and maintenance plans so that they can track what's going on in their facility?

DR. WOODS: Only the buildings that have people in them.

(Laughter)

MR. HATHAN: Lee Hathan with OSHA.

Mr. Woods, my question is in regard to Mr. Benda's question regarding the merits of ventilating to original design intent if that original design was questionable, I believe, is how his question was.

What I'd like to ask you is that OSHA, when it looked at this issue, it looked at feasibility, and within that issue of feasibility, it led us in that direction of as a minimum designing to what the buildings were capable of with the existing equipment, etcetera. From that feasibility standpoint, are there other alternatives, or is OSHA on the right track in that direction?

DR. WOODS: The concern I think that I would have with that is if... Let me give you an example of a hospital.

Most of the hospitals have parts that were designed and built before the turn of the century. There are a few hospitals that were built brand new within the last ten years, but most hospitals have evolved over many years.

I've been involved in several hospitals where we had to look at what code pertained, and it turns out that there are many codes that pertain, it depends on the phase

of the construction that existed at the time. And

parts of it have been renovated, maybe not sufficiently that they had to upgrade to the code at the time of the renovation. So I think that if you only look at the code as a minimum, that that probably isn't sufficient, that you really have to understand what the performance of the building is at the time of occupancy. In my opinion, the building code, it's a design parameter, something that you dealt with at the time of design. What you're dealing with now is exposure to occupants in real time and you've got to provide assurance that there's adequate performance, ventilation, source control, whatever it is in the present time, not what happened 20 or 30 or 40 years ago.

MR. RUPP: Okay. I'll accept that answer. Thank you.

JUDGE VITTONE: Anything else?

MS. SHERMAN: We have no further questions, Your Honor.

JUDGE VITTONE: Thank you very much.

MS. SHERMAN: Did Dr. Woods submit his slides as corrected to the docket?

DR. WOODS: I have to make that one --

JUDGE VITTONE: Would you make that one correction, please, or one mark on there?

And if I haven't done it, just to make sure I have, Exhibit 28, which is Dr. Woods' testimony and his slides, will be received into the record.

MS. SHERMAN: Your Honor, I would like to be heard on your earlier suggestion of having a Saturday hearing.

JUDGE VITTONE: Okay.

MS. SHERMAN: I've checked with the available witnesses that we have and we can't find a witness for tomorrow so I would like to respectfully decline your offer to provide a hearing tomorrow.

JUDGE VITTONE: All right. Thank you very much, Ms. Sherman. It's a standing offer. Any Saturday except November 5th.

We will recess in a few seconds here. Just for the record, I would like everyone to understand, we are going to resume on Monday at 9:30, September 26th, in Hearing Room B at the Interstate Commerce Commission at 1201 Constitution Avenue, N.W. We will be there at 9:30.


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