标题：The Impact of Clean Indoor Air Exemptions and Preemption Policies on the Prevalence of a Tobacco-Specific Lung Carcinogen Among Nonsmoking Bar and Restaurant Workers
摘要：Objectives. We studied the impact of clean indoor air law exemptions and preemption policies on the prevalence of a tobacco-specific lung carcinogen—4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)—among nonsmoking bar and restaurant workers. Methods. secondhand smoke were compared with results from participants who were exposed to it. Results. Participants exposed to workplace secondhand smoke were more likely to have any detectable level of NNAL ( P =.005) and higher mean levels of NNAL ( P < .001) compared with nonexposed participants. Increased levels of NNAL were also associated with hours of a single workplace exposure ( P =.005). Conclusions. Nonsmoking employees left unprotected from workplace secondhand smoke exposure had elevated levels of a tobacco-specific carcinogen in their bodies. All workers—including bar and restaurant workers—should be protected from indoor workplace exposure to cancer-causing secondhand smoke. Epidemiological studies have shown that exposure to secondhand smoke among non-smokers increases their risk of lung cancer, heart disease, and asthma, perinatal complications such as sudden infant death syndrome and low birthweight, and other chronic and acute diseases. 1 – 7 Research has also shown that nonsmoking workers exposed to work-place secondhand smoke are at elevated risk for these diseases. 2 , 5 , 7 – 11 This evidence of increase in disease risk among nonsmokers exposed in the workplace has led to the passage of clean indoor air acts that ban smoking in indoor work environments. Such laws now protect a large majority of workers from indoor secondhand smoke 12 , 13 and have the added benefit of facilitating smoking cessation among smokers in workplaces where smoking has been prohibited. 14 – 17 In spite of the progress made in protecting workers from secondhand smoke exposure, at the time of this study, only 11 states had comprehensive clean indoor air acts that banned smoking in all indoor workplaces. 18 In the other 39 states, clean indoor air acts exempt certain workplaces, especially bars and restaurants. 19 , 20 As a result of the exemptions, millions of food service workers are at elevated risk of secondhand smoke exposure. 12 , 21 , 22 Smoky bars and restaurants also create the impression that smoking is an acceptable behavior, 23 especially among young people who frequent these types of establishments. In the absence of statewide clean indoor air acts that include bars and restaurants, the tobacco control community adopted a strategy to protect nonsmoking workers by passing local comprehensive clean indoor air ordinances. 24 – 26 Not only do these local ordinances protect workers in their jurisdictions, but enactment of a substantial number of local ordinances in a state also can facilitate the passage of statewide comprehensive clean indoor air laws. Indeed, in California, the first state to totally ban smoking in restaurants and bars, the statewide law followed the enactment of hundreds of local ordinances. The tobacco industry responded to the tobacco control community’s strategy of passing of local ordinances that restrict smoking in public places by using its influence to promote passage of state-level preemption laws that eliminate local jurisdictions’ authority to regulate tobacco. 24 , 25 , 27 , 28 As of 2004, 19 states had at least 1 preemptive provision in their clean indoor air legislation, and the Centers for Disease Control and Prevention’s (CDC) assessment is that since 1999, almost no progress had been made toward the 2010 goal 29 of eliminating all preemptive state smoke-free indoor air laws. 30 Oregon is one state that currently has both a preemptive provision and exemptions in its clean indoor air legislation. Oregon’s statewide comprehensive Tobacco Prevention and Education Program began in 1997 with dedicated funds from a voter-mandated tobacco tax increase. In accordance with guidance from the CDC, 22 , 31 Oregon’s Tobacco Prevention and Education Program funded local (county-level) coalitions to create smoke-free environments, including support for local clean indoor air ordinances that had no exemptions. Indeed, beginning in 1997, several Oregon cities passed local clean indoor air ordinances that had no exemptions. The passage of these local ordinances and the indication that more local ordinances without exemptions were forthcoming led to the enactment of a statewide clean indoor air law in 2001. This law included exemptions for bars and restaurants with areas posted “off limits” to minors and preemptive provision that prohibited passage of more stringent local clean indoor air ordinances. When preemption was legislated, however, previously enacted local ordinances that prohibited smoking in all indoor workplaces, including all bars and restaurants, were permitted to remain in place. The fact that some nonsmoking food service workers in Oregon are protected from secondhand smoke by local ordinance, while others cannot be protected because of clean indoor air exemptions and preemption, provides an opportunity to assess the extent to which these policies create a health disparity among the unprotected nonsmoking workers. To test for this possible disparity, we examined the prevalence of metabolites of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) among nonsmoking food service workers in Oregon communities where such workers were either protected or not protected from secondhand smoke. A potent carcinogen, NNK has an important role in the induction of lung cancer in smokers. 32 – 35 In rodents, NNK has been shown to induce adenocarcinoma of the lung, 34 , 36 , 37 the same type of tumor most prevalent among nonsmokers exposed to secondhand smoke. 38 , 39 The presence of NNK and its bio-markers in the human body is specific to tobacco use or tobacco smoke exposure. 35 , 38 , 40 , 41 Therefore, its presence cannot be attributed to other factors. 34 , 35 , 38 A number of studies have documented the urinary biomarkers for NNK: 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and its glucuronides (NNAL- O -Gluc and NNAL- N -Gluc), which demonstrate NNK uptake and metabolism in nonsmokers exposed to secondhand smoke. Specifically, increases in levels of NNAL have been detected among (1) nonsmoking subjects experimentally exposed to secondhand smoke 42 ; (2) nonsmoking female spouses of smokers 38 ; (3) nonsmoking children exposed in homes and cars 41 ; (4) nonsmoking patrons exposed during a 4-hour casino visit 43 ; (5) nonsmoking hospital workers who performed some of their duties in areas where patients smoke 44 ; and (6) nonsmoking food service workers exposed to workplace secondhand smoke. 45 In the latter study, there were significant increases in total NNAL on working days compared with nonworking days, which strongly suggests that workplace exposure to secondhand smoke increases NNK levels among nonsmoking workers. The 2 studies of NNK among nonsmokers exposed in the workplace 44 , 45 employed relatively small sample sizes (n < 21) and have not shown that workplace exposure to secondhand smoke increases the proportion of workers with NNK metabolite levels above the limit of detection. In addition, no studies have assessed increases in NNK levels within a single workshift exposure. Our study’s sample size and analytic approach allowed us to address both issues. We hypothesized that (1) those participants working in establishments where smoking is allowed would be more likely to have any detectable level and higher levels of NNAL in their urine, compared with those workers protected from workplace secondhand smoke by local ordinances and (2) among those exposed to secondhand smoke at work, levels of total urinary NNAL would rise between the beginning and end of a workshift. In addition to analyzing participants’ pre- and postworkshift urine samples for total NNAL, we supplemented the NNAL analyses with tests for cotinine and nicotine, as previous research has shown that levels of these tobacco metabolites increase with workplace exposure. 22 , 46 – 50
