Tobacco Documents Online

3 limiting or banning environmental tobacco smoke in the workplace, the evidence of the grave danger of tobacco smoke to American workers was just beginning to emerge. The U.S. Surgeon General and the National Research Council of the National Academy of Sciences had both declared that ETS caused lung cancer and other diseases in healthy nonsmokers. Unfortunately, OSHA did not find the determinations of these two eminent bodies to constitute sufficient evidence of the grave danger of tobacco smoke, and OSHA in 1989 declined to issue an emergency temporary standard, a decision which was upheld by the court in ASH v. OSHA No.89-1656 (D.C. Cir. May 10, 1991) 59 U.S.L.W.2728. Subsequently, on February 26, 1992, ASH filed a Petition requesting a rulemaking regulating passive tobacco smoke under OSHA's general workplace standards, 29 U.S.C. §655(b) and 29 CFR §1911.3. Then on March 10, 1992, ASH initiated a request for rulemaking under OSHA's Cancer Policy. These petitions have been docketed respectively as No. 991 and No. 3-1030. (Attachment 6 and Attachment 7, incorporated herein by reference) Then on July 31, 1992, ASH filed another Cancer Petition requesting a rulemaking proceeding under OSHA's Cancer Policy, 29 CFR Part 1990. That petition contained additional evidence of the hazardous nature of tobacco smoke and included many of the more recent scientific studies which further documented the urgent need for OSHA to ban tobacco smoke in the workplace. (Attachment 8, incorporated herein by reference)

4 When OSHA denied that Petition for the issuance of a standard regulating environmental tobacco smoke as a potential occupational carcinogen by a letter dated October 30, 1992, ASH petitioned the U.S. Court of Appeals for the District of Columbia Circuit on December 22, 1992 to review and set aside the determinations contained in the letter. On May 20, 1993, the Court ruled in ASH's favor and refused to dismiss the lawsuit as requested by OSHA. Additionally, the Court held that OSHA's October 30, 1992 letter "meets the criteria of a final, reviewable order," and also directed OSHA to respond to the Court by July 19, 1993 on further proceedings. (Attachment 9, ASH v. U.S. Department of Labor, No. 92-1661(D.C. Cir.)). Subsequent to the filing of ASH's petitions, the EPA released its final report on "Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders" on January 8, 1993.. It contained more than 200 studies of the dangers of environmental tobacco smoke which had been published and peer reviewed subsequent to ASH's 1987 request for an emergency regulation. (See Appendix Item 2). As previously stated, then Secretary Martin herself realized that the evidence of the grave danger of tobacco smoke was now so massive that an emergency temporary regulation was the appropriate measure for OSHA to take. That was six months ago. What the Secretary of Labor considered so serious she wanted to regulate immediately, remains unregulated.

5 Even though her successor Secretary of Labor Robert B. Reich is said, through counsel, to have ordered OSHA to proceed expeditiously, no proposed rulemaking has been undertaken either on the Department's own initiative or in response to the various petitions filed by ASH. While ASH appreciates that it takes time for a new administration to get organized, lives are nonetheless at continued risk from exposure to ETS. Consequently, due to the grave danger of the risk posed by Environmental Tobacco Smoke, Action on Smoking and Health is filing this new Emergency Temporary Standard Petition to prompt OSHA to finally promulgate a regulation prohibiting tobacco smoke in the workplace. C. Cancer Evidence Has Accumulated In addition to the earlier reports of the U.S. Surgeon General and the National Research Council of the National Academy of Sciences, (Attachment 8:Exhibits 15 and 20 respectively) there is a growing body of evidence on the carcinogenicity of environmental tobacco smoke. This evidence includes: 1. EPA report The recently released EPA report on "Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders" represents the latest and most comprehensive assessment to date of the grave danger of environmental tobacco smoke. The report concludes that ETS is a human lung carcinogen, responsible for approximately 3,000 lung cancer deaths a year among U.S. nonsmokers. (Attachment 1, p.1-1) In announcing the release of the study then EPA Administrator William K. Reilly noted that the

6 "risk assessment adds new peer-reviewed evidence to the growing health consensus that smoking is not just a health danger for smokers, but a significant risk for non-smokers.... " (Attachment 10) He stated further that: Tobacco smoke has long been recognized as a major cause of death and disease, especially lung cancer and chronic respiratory disease in smokers. In recent years there has been concern that non-smokers may also be at increased risk as a result of their exposure to the smoke exhaled by smokers and given off by the burning end of cigarettes, pipes or cigars. This smoke contains more than 4,000 substances, at least 43 of which cause cancer in humans or animals and many of which are strong eye or respiratory irritants. The lung cancer findings in EPA's assessment are based on several important analytical findings: first, the chemical and physical similarity of ETS to that inhaled by smokers; second, the known lung carcinogenicity of tobacco smoke to smokers; third, the known exposure to ETS and uptake by the human body; and fourth, a thorough and comprehensive review of more than 30 studies in both the Untied States and abroad that examined the relationship between lung cancer and exposure to secondhand smoke in people who never smoked, usually the spouses of smokers. EPA concluded from the total "weight of evidence" of all the studies that ETS increases the risk of lung cancer in non-smokers. The EPA concluded that ETS should be classified as a known human carcinogen. As a known human carcinogen the EPA officially designated ETS as a "Group A carcinogen," the Agency's category of greatest scientific certainly for carcinogens. (Attachment 1, pp.1- 3, 1-4, 1-8, 4-28, 5-68 and 6-29) The EPA clearly determined that ETS constitutes a grave danger to nonsmokers and one for which no safe lower level of exposure is known or believed to exist.

7 2. National Institute for Occupational Safety and Health In 1991 the National Institute for Occupational Safety and Health (NIOSH) concluded that environmental tobacco smoke "is potentially carcinogenic to occupationally exposed workers." (Attachment 8:Exhibit 2) Most significantly, NIOSH reached this conclusion after careful review of the then existing research, including reports of the Surgeon General of the United States and numerous epidemiological studies of nonsmokers exposed to ETS. Noting that it considered OSHA's Cancer Policy the most appropriate for identifying occupational carcinogens, NIOSH went on to state that it "considers ETS to be a potential occupational carcinogen in conformance with the OSHA carcinogen policy (29 CFR 1990]." NIOSH made the results of its research and analysis publicly known in June 1991 by issuing its Current Intelligence Bulletin 54 (CIB 54), entitled "Environmental Tobacco Smoke in the Workplace". (Attachment 8:Exhibit 2) In CIB 54, NIOSH recommended that "the risk of developing cancer should be decreased by minimizing exposure to ETS", and that employers should reduce ETS exposures to the "lowest feasible concentration." (Attachment 8:Exhibit 2, p.12) In outlining how ETS exposure can be reduced to the lowest feasible level, NIOSH noted that ETS is most effectively controlled simply by eliminating tobacco use from the workplace. Quoting the Surgeon General's 1986 report on involuntary smoking, NIOSH reiterated that, "the simple separation of smokers and nonsmokers

8 within the same airspace may reduce, but does not eliminate, the exposure of nonsmokers to ETS." Recognizing that "ETS can spread throughout the airspace of all workers," when smoking is allowed in indoor worksites, ?aIOSH concluded that "[t]he most direct and effective method of eliminating ETS from the workplace is to prohibit smoking in the workplace." (Attachment 8: Exhibit 2, p.13) Given that OSHA's Cancer Policy specifies NIOSH as one of the three agencies it suggests OSHA may want to confer with to obtain recommendations regarding "the identification, classification, or regulation of any potential occupational carcinogen," 29 CFR 1990.104, 29 CFR 1990.106(b)(2), it appears NIOSH's finding that environmental tobacco smoke is a potential occupational carcinogen should be given considerable weight and deference by OSHA. 3. National Cancer Institute The National Cancer Institute has concluded that ETS is carcinogenic. In fact, "it is the official position of this Department that nonsmoker exposure to tobacco smoke, at those levels commonly found in indoor environments where smoking is permitted, increases the risk of lung cancer and possibly other chronic diseases. We know of no valid arguments to the contrary." (Attachment 8:Exhibit 3) 4. Pertinent New Lung Cancer Studies Additional pertinent studies on the respiratory health m effects of passive smoking were released after the cutoff date for ~ O inclusion in the EPA report. The newest studies are considered W „.a m

9 consistent with the EPA report's conclusion that ETS exposure increases the risk of lung cancer in nonsmokers. As stated in the addendum to the report: Two of the new studies are case-control studies of ETS and lung cancer in U.S. female nonsmokers (Stockwell et al., 1992; Brownson et al., 1992). Stockwell et al. conclude that "long-term exposure to [ETS) increases the risk of lung cancer in women who have never smoked." Similarly, Brownson et al. conclude, "Ours and other recent studies suggest a small but consistent increased risk of lung cancer from passive smoking." In an autopsy study of Greeks who had died of causes other than respiratory diseases, Trichopoulos et al. (1992) found an increase in "epithelial, possibly precancerous, lesions" in the lungs of nonsmoking women who were married to smokers. The authors concluded that their results "provide support to the body of evidence linking passive smoking to lung cancer...."(Attachment 1, p.ADD-1) 5. Cervical And Other Cancer Risks ETS causes cancers in sites in the body other than the lung, including the cervix. Cigarette smoking and exposure to passive smoke as risk factors for cervical cancer have been described in a paper by Slattery and others in a population-based case-control study conducted in Utah. For smokers who are also exposed to ambient tobacco smoke, the risk estimate associated with passive smoke exposure for 3 or more hours per day was 2.96. The increased risk from passive smoking was even greater in women who were not smokers--3.43. (Attachment 8:Exhibit 40) Thus, in addition to lung cancer, ETS presents a very serious risk of cervical cancer for women. A number of other studies have found passive smoking to significantly increase risks at body sites other than the lung and

10 cervix, including those studies cited in the Report of the National Research Council "Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects". Thus, passive smoking is associated with tumors of the brain, nasal sinus, breast, endocrine glands, hematopoietic tissues and also leukemia and lymphoma. (Attachment 8:Exhibit 20, pp.250-256) D. Evidence Of The Grave Danger Of ETS To The Heart Has Also Grown The Interagency Task Force on Environmental Cancer, Heart, and Lung Disease Workshop on ETS concluded that the effects of ETS on the heart might present an even greater risk than its cancer causing effects on the lungs. "EPA Indoor Air Facts No. 5". (Attachment 8:Exhibit 10) Subsequent research, some of which has been summarized in NIOSH Bulletin CIB 54 pp. 9-11, has confirmed the deleterious effects of ETS on the heart. (Attachment 8:Exhibit 2) Since that publication, George Howard of the Bowman Gray School of Medicine in Winston-Salem, N.C. has released a new study that clarifies how ETS contributes to heart disease. That study found that exposure to environmental tobacco smoke significantly narrows the arteries of nonsmokers, thereby making them more prone to clogging by cholesterol, and increasing their risk of heart disease. Addressing the Annual Meeting of the American Heart Association, Howard said that researchers also found that the more hours per week a person was exposed to secondhand smoke the narrower the arteries became. People who had never smoked and who

11 said that they were not exposed to secondhand smoke had the least artery narrowing. (Attachment 8:Exhibit 41 and 42) Additionally, in another recent study which specifically focused on the workplace, researchers at the University of California in Los Angeles found that exposure to tobacco smoke also increased the risk of heart disease by raising the cholesterol levels of nonsmokers. The findings, which were presented by UCLA physiologist James White at the Eighth World Conference on Tobacco or Health, and which used carbon dioxide (CO) as an index of cigarette smoke in the workplace, showed that carbon dioxide levels were nearly three times higher in offices with smokers compared with smokefree offices. The researchers found that passive smokers had greater CO levels during the workday. Increased carbon dioxide caused the passive smokers to have higher total cholesterol levels and "significantly depressed" high-density lipoprotein (so-called good cholesterol) than nonsmokers. Women also had higher levels of low- density lipoprotein (so called bad cholesterol). Recognizing that high total cholesterol and low HDL levels are considered risk factors for heart disease, the study concluded that "nonsmoking workers are at increased risk of developing coronary heart disease resulting from exposure to second-hand tobacco smoke." They estimated that ETS "increased heart disease risk by ~ 10 to 15 percent in men and between 26 and 39 percent in women". ~ O .~ W N

12 Urging workplace smoking bans, White predicted "that in 10 years smoking will be prohibited in all indoor public facilities. Tobacco smoke is dangerous stuff." (Attachment 8:Exhibit 43 and 44) In addition, A. Judson Wells in "An Estimate of Adult Mortality in the United States from Passive Smoking" (Attachment 8:Exhibit 36) has calculated that 32,000 deaths each year from heart disease are attributable to passive smoking. Two other recent studies have reinforced the fact that the risk of death from heart disease due to environmental tobacco smoke exposure is even greater than for lung cancer. The first study by Stanton A. Glantz and William W. Parmley on "Passive Smoking and Heart Disease" concluded that there is a 10 times greater risk of death from ETS-induced heart disease than lung cancer and that "these (heart disease) deaths contribute greatly to the estimated 53,000 deaths annually from passive smoking." (Attachment 8:Exhibit 45, p.10) Of these 53,000 ETS deaths annually, 37,000 are attributable to heart disease compared to 3,700 for lung cancer. (Attachment 8:Exhibit 45, p.4) Glantz and Parmley also noted that "nonsmokers [are] more sensitive to lower exposures to cigarette smoke than are smokers." The second study by Kyle Steenland of NIOSH which was released just last year summarized the findings by Glantz and Parmley and then reviewed some newer experimental and epidemiologic studies, all of which reinforced the earlier findings the ETS has a very adverse effect on the heart. Arriving at an estimate of 35,000 to 40,000 heart disease deaths attributable to ETS among never-smokers