OSHA: Proposed Standard For Indoor Air Quality: ETS Hearings, January 11, 1995
OSHA: Proposed Standard For Indoor Air Quality: ETS Hearings, January 11, 1995
UNITED STATES DEPARTMENT OF LABOR
OCCUPATIONAL SAFETY AND HEALTH ADMINISTRATION
PUBLIC HEARING
PROPOSED STANDARD FOR INDOOR AIR QUALITY
Wednesday, January 11, 1995
Department of Labor
Washington, D.C.
The above-entitled matter came on for hearing, pursuant to notice, at 9:50 a.m.
BEFORE: HONORABLE JOHN VITTONE
Administrative Law Judge
AGENDA
PAGE
Holcomb Environmental Services
Larry Holcomb 10717
Questions:
Ms. Sherman 10741
Mr. Haviland 10839
Mr. McNeely 10857
Mr. Gross 10866
San Francisco Hotel Association
Glen Galfond
Jay Tansing
Questions:
Ms. Sherman 10874
Ms. Collia 10902
Mr. Sandman 10908
Mr. Rupp 10946
EXHIBITS
EXHIBIT NO. IDENTIFIED RECEIVED
217 10740 10740
218 10871 10871
219 10871 10871
220 10874 10874
P R O C E E D I N G S
9:50 a.m.
JUDGE VITTONE: On the record.
I'm going to take Mr. Holcomb, because I held him over from yesterday. As I understand it, he's got to get out of town today, too.
Is there anything else I've got to take up before we get started here?
You're Mr. Galfond?
MR. GALFOND: Yes.
Just a scheduling issue, something we've been talking about. I was under the understanding, I was told yesterday I was first up today. Now things change, I understand that. I just want to fix a time, because I can't stay here all day. I could do it, say at 3:30, if we could pick a time. But there may be scheduling conflicts because I made some other arrangements.
JUDGE VITTONE: Mr. Holcomb has got about a 35 minute presentation.
How long is your...
MS. SHERMAN: Your Honor, the problem, as I understand it, is this. Mr. Galfond has a meeting at 2:00. I don't think there will be time after Mr. Holcomb to have Mr. Galfond come on and present everything by 2:00. So I think what he's asking is, he can be back here at 3:30. I think it's safe to say that we will be long finished with Mr. Holcomb by then. So if you don't have any objection, I wouldn't have any objection to this arrangement, in the interest of staying on schedule.
JUDGE VITTONE: Anybody have any problem coming back at 3:30 if we finish up with Mr. Holcomb? I would hope we'd finish up with Mr. Holcomb well before 3:30.
Mr. Rupp?
MR. RUPP: How much time does Ms. Sherman have for Price Waterhouse?
MS. SHERMAN: I'd say about an hour, perhaps a little bit more.
JUDGE VITTONE: As I understand it, they've already given their direct presentation, as I recall, you're just here for examination.
MR. GALFOND: Correct.
MS. SHERMAN: That is correct.
JUDGE VITTONE: Who else has questions for Mr. Galfond.
Mr. McNeely. How long?
MR. McNEELY: Between 30 and 45 minutes.
JUDGE VITTONE: I saw two hands...
MR. McNEELY: It was the same, a team.
JUDGE VITTONE: But total about 30 minutes or so.
Mr. Rupp?
MR. RUPP: Ten or 15.
JUDGE VITTONE: Anybody else?
MR. GALFOND: If it would help, I could probably push it up to 3:15 or something like that.
JUDGE VITTONE: Let's make it 3:30.
MR. GALFOND: Thank you.
JUDGE VITTONE: Be back at 3:30.
Mr. Holcomb, why don't you come on down.
Was there something else? Mr. Andrade.
MR. ANDRADE: Another scheduling matter, Your Honor. As I discussed with you a few minutes ago, Dr. Clayton is not feeling well and will not be here to testify tomorrow.
JUDGE VITTONE: Dr. Clayton, as I understand it, he had pneumonia?
MR. ANDRADE: He had pneumonia over Christmas, and we were hoping that he'd be up to, but we met with him, and he isn't up to testifying tomorrow. I apologize for the short notice, but it's one of those situations.
JUDGE VITTONE: Do you want to reschedule him?
MR. ANDRADE: The doctors have said it would take about six to eight weeks as the normal period of recovery. We could keep that as an option, but I'm not sure that it's going to work out that he'll be able to do it at any time within the confines of the remainder of the hearing. I understand, with the schedule, we might finish up sometime the third week in February or the second week in February, depending on how things go. So I don't want to ask to have him rescheduled only to find out that his recuperative period is longer than anticipated, and that he can't appear. Then we'll be in the same position of him having to cancel.
If you want to keep that open as an option, we'll be glad to do that as well, but we won't necessarily be requesting to be rescheduled, understanding that he may not be up to physically.
JUDGE VITTONE: Okay. He's the older gentleman I saw?
MR. ANDRADE: He's 70 years old, Your Honor.
JUDGE VITTONE: That's tomorrow.
I've also just received another letter from ICF Kaiser asking that they be scheduled for the week of January 23rd. Dr. Greenfield, I guess it is.
MS. SHERMAN: I believe, Your Honor, that we've already rescheduled them to appear first on Monday, the 23rd of January.
JUDGE VITTONE: So that's been taken care of.
MS. SHERMAN: Yes.
JUDGE VITTONE: So he's out.
That leaves tomorrow with only Mr. Newell, Consultants in Toxicology?
VOICE: (Inaudible comment)
JUDGE VITTONE: Who?
MS. SHERMAN: No, Mr. Gillam apparently is going to appear on the 13th. They called in and said that.
JUDGE VITTONE: What about the Steelworkers?
MS. KAPLAN: They're appearing on Friday, the 20th.
MS. SHERMAN: My understanding is the Steelworkers will appear on Friday, January 20th. I believe we put a new schedule out front and gave one to you yesterday afternoon.
JUDGE VITTONE: Okay.
Then everybody understands we go through Mr. Holcomb today, this morning, and whatever the break is, we will be back at 3:30 for Mr. Galfond from Price Waterhouse.
Mr. Holcomb, would you state your full name please, and the name of your organization?
DR. HOLCOMB: Good morning, Judge, OSHA staff. My name is Larry C. Holcomb. I am a Vice President at Holcomb Environmental Services at 17375 Garfield Road, Olivet, Michigan.
JUDGE VITTONE: You have overhead slides and...
DR. HOLCOMB: I have clear transparencies, and Mr. Hall said he'd be glad to do that for me.
JUDGE VITTONE: Let me get out of your way, and you can begin.
DR. HOLCOMB: I want to be very clear that I was invited by the Tobacco Institute to review the OSHA proposal for rulemaking, and that I have submitted comments in August. I submitted an additional list of all of the references that I used at a later date. And I have given the staff a copy of what my main comments will be today, including a set of the overhead clear transparencies that I intend to use.
My background, I have a PhD in Zoology from Michigan State University in 1963. That entailed advanced coursed in human physiology, mammalian physiology, biochemistry, and chemistry, and a lot of work in embryology and histology and anatomy. I have taught in universities largely to pre-medical and pre-dental students for 11 years, succeeding my stay at Michigan State in the largely pre-medical and dental students in the area of embryology and histology, physiology, comparative anatomy, and I completed research at that same time.
My PhD thesis was on reproductive physiology in mink where we looked at the effects of doses of progesterone, on reproductive impact of various doses of progesterone.
I worked for three years for the United Nations in East Africa, and then I came back to my home state, Michigan. I worked for the Michigan Department of Natural Resources in the area of waste management, and looking at the various risks or lack thereof, from a variety of resource management of waste -- both hazardous and solid waste.
I then worked for the Michigan Toxic Substance Control Commission for five and a half years, and directed the staff there, and looked at every possible potential toxic substance problem one can imagine from the PBB, the polybromated biphenyl incident in cattle there, to workers on assembly lines, to indoor air quality and the whole gamut. In that role we did on a daily basis risk assessment or lack thereof, due to exposure.
Following that in 1986, and since then, we have our own consulting company. There are six of us. It's a small company operating in a rural area of Michigan, and we do exactly the same kinds of work as I did when I worked for the state. That is largely interpretation of toxicological data and exposure data from air, water, soil, whether it's dermal exposure, inhalation exposure, or ingestion exposure, including foodstuffs.
That gives you, I believe, a general background for me, and up to date.
What I'd like to do today is to review with you largely the information with regard to exposure, either the lack of information that I see in the OSHA document, the proposed rules, or some suggestions about what the literature shows.
What I'm going to present is that first of all, OSHA has failed to substantiate its claim about the risk to human health presented by environmental tobacco smoke, in terms of relating exposure to symptoms or disease.
Secondly, I believe that OSHA's assumptions about workplace exposures and dose levels of ETS are not valid. Dose-related information will show that workers exposed to ETS receive insignificant concentrations. Other sources of the same materials contribute much larger exposures.
Thirdly, I believe that OSHA has chosen an inappropriate mitigation strategy for ETS. I will demonstrate that ventilation meeting ASHRAE Standard 62-1989 will reduce significant exposure of workers to ETS and indeed to all other sources.
(Slide No. 1)
I was a bit surprised when I read the OSHA proposed Preamble and suggested rules, because I had submitted voluminous information with regard to exposure in areas where there was smoking compared to areas where there was no smoking. Subsequent to that submittal, however, I published in 1993 in Environment International, a review of all of the indoor air quality data published in North America since 1980. So it entailed about 41 different studies, and includes a lot of information other than what OSHA has looked at.
I'm going to concentrate first on indoor air quality and ETS concentration and exposure as I outlined in that area.
(Slide No. 2)
I would like to first concentrate on the concept of dose, which is, to me, the overlying issue here. OSHA has used this concept in assessing risk, in development of permissible exposure levels with regard to rulemaking on other substances, but has failed to do so for ETS.
If you look at dosimetric calculations, and this is the way I want to look at it. I've looked at some of the previous testimony and I have no argument with how people assess dose, but I'm going to take the concentration of the respirable particulates, for instance, in indoor air, and give you the mean difference in smoking and non-smoking areas.
You might legitimately say how can you do that? I don't think I could do that if I had just a handful of studies, but I've got 41 studies. All of the data subsequent to that that I have given you in my earlier submittal, papers even beyond my 1993 paper, show the same sort of thing.
Furthermore, you need to know the duration of exposure, what's the time allocation in various areas where one might be exposed. Thirdly, the respiration rate.
We used light work or resting. You could use more active ventilation rates if you wanted to in terms of respiratory volumes. And for percent of retention, I used all of the data that was available to that time, both papers by Hiller, which indicated an 11 percent retention. So I'm taking exposure beyond just concentration of the air and breathing it in. I'm taking it to the point where you either retain it or you breathe it back out.
The dose then, that I've calculated, is the concentration times the duration, times the respiration rate, times the percent retention.
(Slide No. 3)
Interestingly enough, I looked at some of the earlier CAP study material from California in terms of time allocation in my 1993 paper, but in addition, several other sources that showed time allocation of various environments. What this slide does is show you where people spend their time. This is the entire population, not just the workplace population. But generally, you can see that home awake and home asleep certainly make up the majority of the time. If you're going to be exposed, if you are exposed to ETS in the home, you're exposed a whole lot more in terms of duration of time than you are anyplace else.
In terms of overall work exposures, males only have around 20 percent of their time at work, and females less than that, close to 12 percent.
There are other places that were exposed, sometimes in travel, sometimes in bars or bar-like atmospheres. I'm not claiming here that the average time that people spend in bars is 3.8 percent. What I am claiming, that if you include bowling alleys, discotheques, bars, and those like atmosphere where smoking density may be heavier, that that is the amount of time I would allocate to that.
(Slide No. 4)
From the data summarized in the 1993 paper, if you look at the mean difference in micrograms per cubic meter on the left column, going from zero to 120 micrograms per cubic meter of respirable particulates, these are respirable particulates less than or equal to five microns in diameter. Remember that ETS represents those mostly in the area of less, far less, than one micron in diameter.
In homes, the mean difference between non-smoking and smoking homes is 27.2 micrograms per cubic meter. For offices and public places, about 22. So there's a slight difference. A little edge. More in the home, and concentration, than in office places.
In restaurants, it's slightly higher. In bars and taverns, as you would expect, it's even higher. There's very little data for transportation. A little bit of data for trains.
Remember, this does not necessarily mean that all of the difference in respirable particulates here is due to ETS. I think if one has a lot of data and has reviewed a low, that you're fairly close, and I think I'm fairly close here.
If you look at the ultraviolet particulate matter data or the salanisol data or the FPM data that is more tobacco-specific, they jive very well. They're very closely correlated with these kinds of numbers.
I'd like to now turn to adverse effects. OSHA asserts that cardiovascular disease, pulmonary effects, cancer effects, genotoxic and reproductive disorders result from exposure to ETS and they set forth exhibits in their document as evidence.
As I will demonstrate, the exhibits used by OSHA have no evidence demonstrating adverse effects from ETS exposure.
(Slide No. 5)
I'd like to deal briefly... I submitted earlier much more detailed information...
Trying to put this in perspective a bit in terms of the respirable particulates in the terms of retained dose, without going to a lot of explanation, let me say this. The worst case example is a workplace... A worst case male, that's the fifth one down, where the dose would be about 108 micrograms per day. The dose per year almost 40 in terms of milligrams per years. And cigarette equivalents per year, a little less than four.
Now do I take a lot of stock in cigarette equivalents? Not necessarily. I think it's a mechanism to give some indication of the amount of respirable particulate that a non-smoker would take in and retain compared to a direct cigarette smoker. This assumes that the direct cigarette smoker retains around 10.6 milligrams per cigarette. So you can see that at any rate the doses, regardless if our retention is ten percent or 20 percent or 30 percent, it's going to make very little different. You already have the data to show it was around 11 percent, and if you use that, the doses are very, very small and insignificant in terms of potential health impact.
(Slide No. 6)
There were several cardiovascular effects claimed by OSHA and I've reviewed that data. I've reviewed the papers. This is just a summary of that information.
There were 18 exhibits where the exposure levels were 15 to 1,000 parts per million carbon monoxide, generally greater than 30 parts per million, with a carboxyhemoglobin level ranging between .4 and 15 percent, seven of those studies. Real life exposures, as I have documented very well and others have too, are around one to six parts per million. The OSHA permissible exposure level is 50 parts per million.
These exposure levels to animals or to people have no resemblance to real life exposures. In three of the exhibits that OSHA used, benzo(a)pyrene, B(a)P or benzo(a)pyrene or dimethylbenzanthrazene, DMBA. The doses given to the animals were 2.4 to 2400 milligrams per kilogram. Not micrograms, not nannograms. This is in milligrams per kilogram. Real life levels of exposure in air are around 0.7 nannograms per cubic meter in smoking areas. The OSHA permissible exposure level is 0.2 milligrams, not nannograms or micrograms. 0.2 milligrams per cubic meter.
There were two exhibits that had nicotine exposure levels of 30 to 1103 micrograms per cubic meter when in fact the exposure levels in offices and public places are around six micrograms per cubic meter and the OSHA PEL is 500.
There were two exhibits that showed that the respirable particulate level associated with experiments on cardiovascular disease were 4,000 to 60,000 micrograms per cubic meter, when in fact real life concentration levels of ETS-derived respirable particulates range probably somewhere between 20 and 30 micrograms per cubic meter, or less.
Let me have the next slide, please, with regard to pulmonary effects.
(Slide No. 7)
There were several pulmonary effects claimed by OSHA, and I've summarized the information that I submitted in my full documentation. The exhibits are noted there, where no exposure assessment was given. We don't know whether it was direct smoking-like activity, we don't know what the concentrations were. There were no cotinine, no nicotine measurements.
In additional exhibits, it was very evident from the data that was in the papers that it was either at direct smoking levels or very concentrated sidestream smoke. No resemblance to reality.
In a couple more exhibits, the carbon monoxide levels were between 15 and 4100 parts per million. People would die at that level. Animals would die at that level, at 4100 parts per million. No resemblance to reality.
In three more exhibits, the carboxyhemoglobin levels were 9.4 to 28 percent. If you look at ETS-exposed persons, about the highest carboxyhemoglobin level increase you could get would be about 0.1 percent. These have no resemblance at all to real life situations.
I'd like Overhead eight, please.
(Slide No. 8.)
I'd like to now deal with cancer effects claimed by OSHA.
This is a summary of information that I submitted earlier that shows exhibits where there was highly concentrated smoke, either direct smoking-like activity to the animals or people, or very concentrated sidestream.
In three additional exhibits there were lung implants of concentrated smoke tars.
As an environmental toxicologist, I can tel you that this has no resemblance to reality. If you concentrate anything that has any good potential for being toxic and implant it on the tissue, you're going to cause an adverse reaction -- no matter what it is. If it's potentially hazardous at a high concentration, you're going to cause an adverse reaction. So that has no resemblance to reality in terms of causing a cancer effect.
There were two additional exhibits by Coggins & Associates that became, were the only exhibits that came close to reality where they exposed rats to 100 micrograms or 1,000 or 10,000 micrograms per cubic meter of respirable particulates. I believe they came to the conclusion that 10,000 micrograms would be a no observable effect level, or adverse effect level. And certainly no effect at all at 1,000 micrograms per cubic meter. Even the lowest dose level that they used is some five to ten times higher than the normal concentrations one would have in indoor air.
What I'm surprised at, more than anything else, is that one of the best studies, best couple of studies that were submitted to OSHA and OSHA used, were downgraded or somewhat, even chastised by OSHA, as perhaps being something that they couldn't really count on.
None of the exhibits used by OSHA for cardiovascular or pulmonary or cancer effects is evidence of exposure to ETS conditions except for the Coggins studies on rats. In these examples, there were no adverse effects.
OSHA reports that exposure to materials such as benzo(a)pyrene and nitrosamines from ETS will lead to the adverse impacts they purport to occur as a result of such exposure. However, doses of these materials from other sources are much higher, much, much higher, than from ETS exposure.
If I could have Overhead nine, please.
(Slide No. 9)
This clear transparency will show you a summary of data that I submitted in my August 1993 submission.
If you will look at the data and find 0.7 nannograms per cubic meter of benzo(a)pyrene in indoor air perhaps as a result of ETS exposure, the weekly dose would be about 8.8 nannograms per week from food. From EPA databases and FDA databases, you can easily define 860 nannograms per week from food alone. From drinking water, from fresh vegetables, highly variable, but up to close to 40,000 nannograms per week if you're at the high end. From charbroiled meat, certainly, a good opportunity for heavy doses, and from ambient air, especially in urban air, you're submitted to a lot of possible doses.
It appears no matter how liberal or conservative we want to be, that less than one percent of benzo(a)pyrene exposure could possibly be due to ETS exposure.
Could I have Overhead ten, please?
(Slide No. 10)
I'd like to now look at the nitrosamine data. There is not a lot of nitrosamine data. Nitrosamines are not easily measured in indoor air because they are so minuscule in terms of concentration. But if you look at the NDMA nitrosamine, the nitrosodimethylamine, dose from ETS and other sources, the only information we have suggests that there may be 20 to 30 nannograms per cubic meter in a very smoky environment. The weekly dose, you have on the right hand column, you can get it from tap water, distilled water. If you're a beer drinker you can get a whole lot of NDMA.
I'm not suggesting to you that you stop drinking beer or alcoholic beverages, because even those doses are very low. But what I am showing you is that foodstuffs and beer, interiors of new cars, urban air, fried fish, cured meats, cosmetics, and this is not an exhaustive list, give you exposures to NDMA, very large exposures compared to what you could possibly get from ETS exposures.
(Slide No. 11)
Then if you look at the other nitrosamine that there is any readily available information on, if you look at NDEA, you find the same thing.
MS. SHERMAN: This is Slide 11?
DR. HOLCOMB: This is Slide 11, yes. Slide 11 shows you the possible ETS concentrations, as low as zero to 30 nannograms per cubic meter. Again, only taken in very smoky environments. Not taken in an office or general workplace setting. You can see that tapwater or beer, interiors of new cars or fried foods will also produce these same kinds of materials.
If I could have that one off, and I'll go to number 12 and 13 in just a moment.
What it suggests to me is this. That for most persons certainly less than one percent, perhaps only 1/1000ths of one percent, but certainly less than one percent of the nitrosamines that one encounters in terms of exposure, could possibly be from ETS exposure.
Now I'd like to turn to environmental tobacco smoke and indoor air quality.
OSHA reports that indoor air quality is poor, resulting in adverse health impacts, especially when environmental tobacco smoke is present.
If I could have that next one, number 12, Overhead 12.
(Slide No. 12)
I've looked at all the North American indoor air quality concentration values since 1980. This is what we find. If you look at the concentration for respirable particulates, and this is in workplace environments -- offices and public places, you see the difference in smoking and non-smoking in micrograms per cubic meter, for respirable particulates. You see the OSHA permissible exposure level and you see the percent of the PEL in indoor air in smoking and non-smoking areas, right about one percent of the permissible exposure level.
If you look at carbon monoxide, the levels are nearly identical. In fact this data occurs very frequently throughout the literature. There is very little increase in carbon monoxide due to increased exposure in ambient indoor air.
Can you get an increase? Absolutely. But the data shows that day in and day out the concentrations are very low.
For nicotine, you can see the differences. They could be less than that, but around six micrograms per cubic meter in smoking environments, and compared to the PEL, it's very insignificant, around one percent of permissible exposure level.
For nitrogen dioxide, there's very little data available for smoking versus non-smoking environments. But at any rate, what it does show us is that the levels that we do encounter are rather low, unless there's a very unusual point source.
For formaldehyde, the same thing. Very, very little contribution of ETS to formaldehyde levels. And the smoking and non-smoking levels are very low. For benzo(a)pyrene, extremely low levels compared to the OSHA PEL, whether in smoking or non-smoking environments. And for sulfur dioxide, around 1.6 percent overall in indoor air.
If I could have the next slide, Overhead 13.
(Slide No. 13)
I'd like to now look at some of the organic chemicals like the volatile organic compounds. You can see there is not the database that we'd like to see in this area, but what is available shows us that for benzene and trichloroethylene and some of the other commonly found VOC's in indoor air, that the concentrations are very low compared to the OSHA PEL, always less than one percent. Usually, perhaps, around 1/100th to 1/1000th of one percent.
What these data demonstrate overall are that ETS contributes a very small percentage of the materials in indoor air. Furthermore, whether in smoking or non-smoking areas, the concentrations of measured substances are generally less than one percent of the OSHA permissible exposure levels. I know someone is going to ask me, do I hold a lot of faith in the OSHA permissible exposure levels? I do in this regard.
If these values that we were finding in indoor air were even close to the OSHA permissible exposure levels, I would begin to express some concern. They are not. They are not even close to the OSHA permissible exposure levels. Generally, less than one percent. And when they are more than one percent, they are materials that generally show a threshold level of effect. For instance, like carbon monoxide.
If I could have Slide 14, please.
(Slide No. 14)
I would like to give you just a little additional information. I know that some of this may have been brought to the attention of OSHA staff, but these are some of the more recent papers in the literature since I did my review, and I'd like to just bring them to your attention and discuss a bit what I think they mean.
These are additional recent papers concerning exposure to cigarettes in experimental situations. The Takenawa Report, looking at mutagenic effects in rats. Look at the exposure level -- 25,000 micrograms per cubic meter of concentrated sidestream. Not diluted, aged sidestream. Not environmental tobacco smoke. But concentrated, fresh sidestream.
Penn et al in their 1994 report with their arteriosclerotic plaque development in cockerels, not really an animal I'd want to use in studies with ETS, but even if you did, look at the levels. 2480 micrograms per cubic meter of sidestream smoke.
Witschi et al did some respiratory cell kinetic work in hamsters. Some of the lower values concentrated sidestream, though, at 1,000 micrograms per cubic meter. They don't know what... They got some small effects on cells there, they don't know what it means. But again, it's some 40 times higher, even then, that what we usually encounter in indoor air.
Sun et al looked at atherosclerosis in rabbits. Look at the sidestream smoke concentrations -- way beyond reality. Having nothing to do with reality.
Ji et al in 1994, respirable cell impacts in post-natal rabbits. Concentrated sidestream smokes at 1,000 micrograms per cubic meter. They reported very subtle, if any effect there. They don't know what it means. Again, it's a higher levels than you would expect.
Hockhertz et al looked at cell immune system in humans, using concentrated ETS, respirable particulates at nearly 2800 micrograms per cubic meter. Again, nothing at reality.
If I could have the next slide please, Overhead 15.
(Slide No. 15)
You have seen some of these before. The Heavner paper you may or may not have seen. It's one that's just coming out in Environment International, I believe, this month, in the first issue. It's VOC exposure in homes attributable to ETS exposure. What they found was that overall in smoking homes versus non-smoking homes, that the total VOC, about 5.5 percent of total VOC exposure was attributable to ETS. About 13.2 of the benzene, 12.6 of styrene. And as you can expect, from tobacco smoke you would expect a higher percentage of things like pyridines at 40.7 percent. But all of these levels were very, very low in small microgram per cubic meter levels, but it does show you the amount attributable to ETS.
In other words, there are a whole lot of other sources of these, and if they are of any problem at all, we ought to be looking at why they are there, ad what we may be able to do to control them, if indeed, they're a problem at those levels.
Phillips et al looked at general ETS exposures in humans. They looked at total solid particulates, but what they found was that the TSP was about 142 micrograms per cubic meter from all sources, and around four from ETS exposure, so very low exposures from ETS.
I understand that Dr. Hedge will, if he has not already, be appearing here before you, or submitted material. But one of his latest papers does show that there is no effect on carbon monoxide, as I would expect from the other studies I reviewed, in smoking areas or non-smoking areas of buildi