Tobacco Documents Online

Comments on EPA Review drafts uHealth Effects of Passive Smoking: Assessment of Lung cancer in adults and respiratory disorders in Children." and "Environmental Tobacco smoke : a guide to workplace smoking policies". R.C.Brown, Medical Research Council Toxicology Unit, Woodmansterne Road, Carshalton, Surrey, UK Introduction There is no doubt that exposure to other people's tobacco smoke is irritating and objectionable; the risk assessment document attempts to show that it is also harmful while the guide to workplace policies is written to support control of smoking at work. However the risks from exposure to environmental tobacco smoke (ETS) are small and, as can be seen from the detailed analysis of the cancer risk felt necessary in this document, are not universally accepted. It is not my intention to comment on the mathematics of this analysis or the content and design of the studies analysed but I do feel that I must comment on some aspects of policy raised by these docu- ments. The implications of acceptance of this report are profound not only in the prevention of exposure to ETS but also in determining society's reaction to other perceived risks. Respiratory disorders in children The risk assessment notes that the children of smokers suffer more respiratory disease than do those of non-smokers. The reason for this phenomenon are not clear. Among possible causes are exposure to ETS, class differences and exposure to greater levels of respiratory disease by contact with their smoking parents. There is enormous scope for more studies on these possibilities and conclusions are not possible at this point 1

Lung cancer risk in adults 1. It might be appropriate to consider whether meta-analyses are ever appropriate in making final conclusions as to the existence or absolute magnitude of a risk. This report is itself a meta-analysis and quotes other similar reports in support of its findings - yet these are not independent studies being themselves meta-analyses of the same data. Since sometimes the same authors have contributed to apparently different reports any agreement is hardly surprising. However often repeated the results of such studies will not become more powerful. The use of meta-analysis as a tool for summing small effects rather than for designing new more powerful surveys will undoubtably be used to justify economies in funding which will lead to fewer good surveys and less "good science". 2.Little effort is made to identify those studies contributing most authority to the overall findings. If meta-analysis is to be used it should be supported by recalculation for all possible subsets of data so as to identify those studies contributing most to the statistical significance of the overall analysis. If those studies are themselves flawed then so is the overall analysis. The removal of outlying results from such calculations is usual and an apposite example can be seen in Repace & Lowry1 where values for the cigarette equivalent exposure of passive smokers are omitted for various reasons. Perhaps all meta-analyses should omit those studies giving extreme values for risk ratios: a genuine effect will withstand such robust analysis. 3. A great deal is made of the fact that sidestream smoke contains more toxic and carcinogenic material than does mainstream smoke2 and from the context it is suggested that this is one reason for the risks claimed to be associated with ETS. This causes several inconsistencies. If the risk from tobacco smoke in both -------------------- t.e.g. Repace, J.L & Lowry, A.H. (1990) Risk assessment methodologies in passive smoking. J.Risk Anal. 10 no.1 2. See particularly 'Environmental tobacco smoke; a guide to workplace smoking policies". p 8 2

smokers and non-smokers is proportional to exposure then there is no need to invoke this property of ETS. However if passive smokers are affected disproportionately then the increased potency of ETS can not be the explanation. Active smokers are also exposed to their own passive smoke, indeed they are at the centre of any diffusion gradient of smoke and in many cases hold the source close to their breathing zone between puffs. One must also assume that active smokers spend less time in smoke free areas than do non-smokers and so are exposed to more ETS. Correcting the incidence of lung cancer in active smokers by including their risk from passive smoke would be difficult but should be attempted before the detailed calculations of risk based on cigarette equivalents. 4. The results leading to the suspected hazardous nature of environmental tobacco smoke are largely based on exposures occurring in the home - there are few data concerning possible hazards elsewhere. This is important, because at=home exposures may differ markedly from public exposure. Hirayama has stressed the importance of proximity to the source of the smoke - and this is quoted in this report 1,2. Hirayama appears to regard passive smoking as exposure at a distance of 1-1.5 metres from the source. Outside the home it is quite likely that exposures occur at a far greater distance and that the substances and concentrations to which anybody is exposed in the workplace or public building differ markedly from those in a small (Japanese) house shared with a smoker. If this is the case (and the question is worth study) it is clearly inappropriate to utilise studies based on at-home exposures as the source for the adoption of control measures in other places. In most cases the identification of a risk leads to control of the exposure causing that risk and, if possible, any control of the toxicant would then be widened to other related, exposures. This is not the case in this study where the supposed demonstration of hazard in one setting would be used to justify the control of 1. Health Effects of passive smoking: assessment of lung cancer in animals and respiratory disorders in children. p 3-39: OD Q 2. Hirayama, T.(1984) Prev.Med. 13:680-690 CCM11 3

quite different exposures leaving the original (domestic) exposures alone. Surely the logical consequence of accepting this report should be the health risk warnings on packets such as "smoking can damage your spouse's health" rather than the concentration on control of workplace exposures. 5. While accepting the theoretical point that there may be no threshold for carcinogenic effects this is not a practical view point for the control of carcinogens: in any case would not be true for other health effects. Most authorities would doubt the wisdom of attempting to control a material without suitable methods for monitoring and measuring exposure. If suitable methods do not yet exist then attempts at control are premature. In the "guide to workplace policies" work on suspended particulates and other measures of smoke exposure are discussed but again the results quoted are mainly from studies of domestic exposures and it is notable that proximity to source is not mentioned explicitly as a dose determinant. However in the review document 1 the importance of proximity to source and the small living spaces enjoyed by the Japanese are invoked to explain Hirayama's results. Despite this no attempt is made to compare these domestic exposures to those in the workplace or suggest control levels. Surely an action level of zero is neither possible nor practical. 6. If we now accept that the resolution of epidemiological methods is such that exposures with relative risks of under 1.5 should be prevented then many other materials may have to come under legislative control. Has any previous control measure been adopted with this level of increased risk? 7. A list of the toxic materials in ETS, some animal and other results with these components, and the possible use of these results to model the effects of ETS are given - does this add to the analysis in this document? Most of the components mentioned are widespread and indeed this list of components of tobacco smoke could (with the exception of nicotine) be equally applied to most smokes, exhaust fumes or pyrolysis products. I would recommend much more 1.Effects of passive smoking: assessment of lung cancer in animals and respiratory disorders in children. p 3-39: -4-

research on the effects of these compounds both alone and in combinations but the present list must mean that the suggested controls should apply to other sources of airborne carcinogens such as car exhausts, bonfires, barbecues etc. If the EPA accept that there should be zero emission of these materials from tobacco smoke how will they avoid pressure to eradicate (not control) other emissions? 8. The acceptance of this report could lead to the attribution to passive smoking of many lung cancers that are in fact due to other as yet unidentified causes. Such attribution will lead to less effort being put into the identification of any novel hazards leading to lung cancer. This has happened with other materials. Mesothelioma has been usually attributed to asbestos exposure and as with ETS there is an almost universal exposure to asbestos this has made it difficult to identify any other causes for this rare tumour. There is now reason to believe that perhaps half of the mesotheliomas are not associated with asbestos and the problems caused by firmly held preconceptions can be seen by the exhaustive search for asbestos exposure when endemic mesotheliomas were found in Turkey~ . -------------------- 1.Rohl, A.N.. Langer A.M., Moncure, G.,Selikoff, U., & Fischbein, A. Science 216: 518-520 -5