Tobacco Documents Online

ENVIRONMENTAL TOBACCO SMOKE Environmental tobacco smoke is among the~ingle pollutants targeted specifically for control in the Proposed Rules. This term refers to the mixture of sidestrcam smoke and exhaled mainstream smoke that contaminates air in spaces where smoking is taking place. Although referre~l to as though it w~r~ a single agent, ETS is a complex mixture of particles and gases that is known to have many of the same toxic and carcinogenic components that are present in the mainstream smoke inhaled by the active smoker (U.S. Department of Health and Human Services 1986; U.S. Environmental Protection Agency 1992). Markers of tobacco smoke can be measured in smoking-contaminated air, e.g.., nicotine, and uptake of ETS components by nonsmokers has been shown using cotinine and other biomarkers. Active smoking has diverse adverse effects including being a cause of cancer and a number of non-malignant conditions as well. This evidence has been comprehensively reviewed in the Reports of the Surgeon General on smoking and health. In regard to exposures of adult nonsmokers in the workplace to ETS, the literature on active smoking indicates a basis for concern about risk for lung cancer and for heart disease. Active cigarette smoking has long been established as a cause of lung cancer, with the risk varying with the number of cigarettes smoked per day and the duration of smoking, as well as other aspects of smoking behavior and the type of product smoked (U.S. Department of Health and Human Services 1982; U.S. Department of Health and Human Services 1989). The risk for coronary heart disease is also increased by cigarette smoking with the risk d.ependtng most directly on being a current smoker and the number of cigarettes smoked per day (U.S. Department of Health and Human Services 1983; U.S. Department of Health and Human Services 1990). In fact, a substantial epidemiologic literature indicates increased risk for lung cancer in never smokers exposed to ETS (U.S. Environmental Protection Agency 1992). These epidemiologic studies are largely of the case-control design, comparing exposures of never smokers with lung cancer to those of control never smokers without lung cancer. The principal exposure variable assessed in these studies has been marriage to a smoker, based on the as.,,umption that never smokers married to smokers sustain greater exposure at home than ne~er smokers married to never smokers. The ~elght of the evidence ind)ca~es increased lung cancer risk for II T102321399

never smokers married to smokers; the causal nature of this association is further supported by l~res~nt understanding of respiratory carcinogenesis CU.S. Department of Health and Human Services 1986; U.S. Environmental Protection Agency 1992). Only a few stu~dies have addressed exposure to ETS in the workplace and a precise estimate of the risk of workplace exposure is not available. It would be anticipated that the risk would be variable among workplaces, depending on the level .of contamination and the duration of exposure. There is no r~ason to assume that an agent, tobacco smoke, that has been shown to be a carcinogen when actively inhaled during active smoking and passively inhaled at home, would not be a carcinogen when involuntarily inhaled in the workplace. For coronary heart disease, the epidemiologic evidence on passive smoking is less abundant, but does indicate increased risk (American Heart Association 1992). Mechanisms have been postulated on the basis by which ETS could cause coronary heart disease and the American Heart Association has concluded that ETS is a cause of coronary heart disease in adults. The workplace has not received specific investigation. Other effects of ETS exposure have been identified and considered to have a causal relationship to exposure (l~a~ional Research Council and Committee on Passive Smoking 1986; U.S. Department of Health and Human Services 1986; U.S. Environmental Protection Agency 1993). Children exposed to ETS are at increased risk for lower respiratory illnesses during the first years of life. Additionally, they have increased rates of respiratory symptoms and the lung function of exposed children increases at a lesser rate than for unexposed children. The status of children with asthma is adversely affected by ETS (U.S. Environmental Protection Agency 1992) and ETS is a suspect cause of asthma. ETS exposure could plausibly exacerbate asthma in adults as well. Some studies have indicated that exposure of adults to ETS may also adversely lung function and produce respiratory symptoms, although the evidence has not been judged conclusive (Samet, Cain et al. 1991). THE POTENTIAL BENEFITS OF THE PROPOSED RULES The Proposed Rules have two elements, a broad strategy oriented towards achieving acceptable indoor air quality through a compliance program designed to assure indoor air quality through buitdin~ operation and control approache.~ directed at individual potlutant.~ or groups of pollutants including ETS. These Proposed 12 T102321400

Rules are offm'cd at a rirnc when there arc evident gaps in our understm~ding of indoor air quality and health. Nevertheless, the I~oposed Rules offer approaches that build on both the scientific evidence on indoor air pollution and health and on the field -- exl~ricnce of persons who operate buildings and evaluate buildings with problems. Benefits for health of the workforce can reasonably be anticipated even though any quantitative estimates of the burden of morbidity and mortality caused by indoor air pollution in the ............ work place are subject to diverse uncertainties. For ETS, exposures can be completely avoided by prohibiting smoking and the alternative strategy of separate smoking areas under negative pressure should minimize exposure of nonsmokers to ETS. OSHA can reasonably project avoidance of the burden of morbidity and mortality associated with ETS with implementation of the Proposed Rules. 13 Tffi2321401

REFERENCES American Heart Association (1992). "Environmental tobacco smoke and cardiovascular disease. A position paper from the Council on Cardiopulmonary and Criticial Care, Am~rican Heart Association.:' Circulation 86: 699-702. American Thoracic Society (1990). "Environmental controls and lung disease." Am. Rev. Respir. Dis. 142: 915-939. Berglund, B. and T. Lindvall (1990). Sensory criteria for healthy buildings. Indoor Air '90. the Fifth International Conference on Indoor Air Quality and Climate, Ottawa, Canada, Burge, S., ~. Hedge, et al. (1987). "Sick building syndrome: a study of 4373 office workers." Ann. Qccu_o~ Hvg. 31: 493-504. Coultas, D. B. and W. E. Lambert (1991). Carbon monoxide. Indoor air: a health perspective. Baltimore, MD, Johns Hopkins Uni.versity Press. 187-208. Health Effects Institute Asbestos Research Literature Review Panel (1991). Asbestos in public and commercial buildings. Cambridge, MA, Health Effects Institute Asbestos Research. Institute of Medicine. Committee on the Health Effects of Indoor Allergens (1993). Indoor Allergens. Assessing and Controllino_ Adverse Health Effects. Washington, D.C. National Academy Press. Marbury, M. C. and J. E. J. Woods (1991). Building-related illne~'s. Indoor air ppll¢lion: ~ he;~lth perspective. Baltimore,MD, Johns Hopkins University Press. 306-322. Molhave, L. (1992). Volatile organic compounds and the sick building syndrome. ]Environmenti~l Toxi¢~an~; Heman Expo~¢res and Their Health Effects. New York, Van Nostrand Reinhold. 633-46. National Asthma Education Program (1991). Guidelines for the diagnosi.~ and management of asthma. Bethesda, MD. Department of Health and Human Services. 14 TI02321402

National Research Council. Committee on Passive Smoking (1986). Environmental Tobacco Smoke: Measuring Exposures aud Assessin~ Heal~h Effects. Washington, DC, National Academy Press. Samet, J. M.; W. S. Cain, et al. (1991). Environmental tobacco smoke. Indoor air potIudon: a health perspective. Baltimore, MD, Johns Hopkins University Press. 131-169. Samet. J.M (1993). Indoor air pollution: a public health perspective. Indoor Air3: 219-226. Spengler, J. D. and J. M. Samet (199I). A perspective on indoor and outdoor air pollution. Indoor Air Pollution. a Health Perspective. Baltimore, MD, Johns Hopkins University Press. 1-29. U.S. Department of Health and Human Services (1982). The health consea_uences of smoking: cancer. A. report of the Surgeo.n General. Washington, DC, U.S. Government Printing Office. - U.S. Department of Health and Human Services (1983). The Health Consequences of Smoking: Cardio.v.ascular Disease. Rockville, MD, U.S. Govrnment Printing Office. A Report of the SUrgeon General. U.S. Department of Health and Human Services (1984). The health conseqoence$ of ~moking: chronic .obstructive pulmonary disease. report of the Surgeon General. Washington, DC, U.S. Government Printing Office. A U.S. Department of Health and Human Services (1986). The Health Consea_uences of lnvolontary Smoking. a Report of the Sorgeon General. Washington, DC, U.S. Government Printing Office. U.S. Department of Health and Human Services (1989). Reducino_ the heallh consequences of smoking: 25 years of progress, A report of lhe Surgeon General. DHHS Publioati0n No. (CDC) 89-8411. Washington, DC, U. S. Government Printing Office. U.S. Department of Health and Human Services (1990). The Health Benefits of Smoking Cessation; a Report of the Surgeon General. DHHS Publicatio.n NO. (CDC) 90-g416. U.S. Environmental Protection. Agenc.~ (1992). t5 TI02321403

Resoiratorv Health Effects of Passive Srnokin~: Lun~ caa¢~ and Other Disorders. EPA/600/6-90/006F. Washington, DC, U.S. EPA. U.S. Environmental Protection Agency (1993). Respiratory Health Effects of Passive Smoking: Lun~ Cancer and 0ther_Disorders. Washington, D.C., National Institutes of Health. Weissman, D. N. and M. R Schuyler (1991). Biological agents and allergic diseases. Indoor ~ oollution. A health oerst~ective. Baltimore, MD, Johns HoI-..ns University Pross. 285-305. Woods, J. E., G. M. Drewry, et al. (1987). Office worker.perceptions of indoor air quality effects on discomfort and performance. Indoor Air "87. .Proceedings of lhe 4th International Conference on Indoor Air and Climate. 17-21 August. Berlin (West), Institute for Water, Soil and Air Hygiene. 464-468. 16 TI02321404

Tatlle 1 A ckts~fioation of the adverse effeots of indoor air poat,~t~on. C3~ly evident dises~es: Disease for which the usual methods o~ clinical evalum~ "on c~ establ~ ~ ~ link to an indoor ~ polluter. disease is exacerbated by indoor air pollution. Inc~ased gisk for di.gease: Diseases for which-epidemiological or other evidence establishes increased risk in exposed individuals. However, the usual clinical methods indicative of injury typically cannot establish the causal link in an individual patient. Physiological impairment: Transient or persistem effects on a measure of physiological functioning which are of insufficient magnitude to cause clinical disease. Symptom responses: Subjectively reported responses which van be linked to indoor pollutants or are attributed to indoor pollutants. Perception of unacceptable indoor air quality: Ser~.sing of indoor air quality as uncomfortable to an unacceptable degree. Perception of exposure to indoor air pollutants: Awareness of exposure to one or more pollutants with an unacceptable level of concern about exposure. T102321405

T~le 2 Selected ex~nl~ of clin~cally evident ~ise~se linked to indoor air pollution. Carbon mo~v~ide poisoning Hemorrhagic Imeumonitis~ from high level of NO: Hyp~rs~sitivitT pneumonitis and humidifer fever Legionella pne~unonia Cat- and mite-induced asthma T102321406

Table 3 ~ ~ of exposure-disease a~ons for indoor air pollutar~ Euvironmental Tobacco Smok~: Lung cancer, increased lower re~iramoj illness in infants Benzene: Leukemia Asbestus: Lung cancer and mesothelioma. Formaldehyde: Nasal cancer. T102321407

Vmti~o~ Type Dry Eyes BloCked No~ Dry Thr~ ~ * ~ource: Dala from Table 5 in Burge, eta]., I987. TI02321408