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      Air pollution in Boston bars before and after a smoking ban

      research-article
      1 , 2 , , 1 , 1
      BMC Public Health
      BioMed Central

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          Abstract

          Background

          We quantified the air quality benefits of a smoke-free workplace law in Boston Massachusetts, U.S.A., by measuring air pollution from secondhand smoke (SHS) in 7 pubs before and after the law, comparing actual ventilation practices to engineering society (ASHRAE) recommendations, and assessing SHS levels using health and comfort indices.

          Methods

          We performed real-time measurements of respirable particle (RSP) air pollution and particulate polycyclic aromatic hydrocarbons (PPAH), in 7 pubs and outdoors in a model-based design yielding air exchange rates for RSP removal. We also assessed ventilation rates from carbon dioxide concentrations. We compared RSP air pollution to the federal Air Quality Index (AQI) and the National Ambient Air Quality Standard (NAAQS) to assess health risks, and assessed odor and irritation levels using published SHS-RSP thresholds.

          Results

          Pre-smoking-ban RSP levels in 6 pubs (one pub with a non-SHS air quality problem was excluded) averaged 179 μg/m 3, 23 times higher than post-ban levels, which averaged 7.7 μg/m 3, exceeding the NAAQS for fine particle pollution (PM 2.5) by nearly 4-fold. Pre-smoking ban levels of fine particle air pollution in all 7 of the pubs were in the Unhealthy to Hazardous range of the AQI. In the same 6 pubs, pre-ban indoor carcinogenic PPAH averaged 61.7 ng/m 3, nearly 10 times higher than post-ban levels of 6.32 ng/m 3. Post-ban particulate air pollution levels were in the Good AQI range, except for 1 venue with a defective gas-fired deep-fat fryer, while post-ban carcinogen levels in all 7 pubs were lower than outdoors.

          Conclusion

          During smoking, although pub ventilation rates per occupant were within ASHRAE design parameters for the control of carbon dioxide levels for the number of occupants present, they failed to control SHS carcinogens or RSP. Nonsmokers' SHS odor and irritation sensory thresholds were massively exceeded. Post-ban air pollution measurements showed 90% to 95% reductions in PPAH and RSP respectively, differing little from outdoor concentrations. Ventilation failed to control SHS, leading to increased risk of the diseases of air pollution for nonsmoking workers and patrons. Boston's smoking ban eliminated this risk.

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          Most cited references32

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          The health consequences of involuntary exposure to tobacco smoke; a report of the Surgeon General

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            Secondhand smoke exposure and risk following the Irish smoking ban: an assessment of salivary cotinine concentrations in hotel workers and air nicotine levels in bars.

            To investigate whether the Irish smoking ban has had an impact on secondhand smoke (SHS) exposures for hospitality workers. Before and after the smoking ban a cohort of workers (n = 35) from a sample of city hotels (n = 15) were tested for saliva cotinine concentrations and completed questionnaires. Additionally, a random sample (n = 20) of city centre bars stratified by size (range 400-5000 square feet), were tested for air nicotine concentrations using passive samplers before and after the ban. Salivary cotinine concentrations (ng/ml), duration of self reported exposures to secondhand smoke, air nicotine (microg/cubic metre). Cotinine concentrations reduced by 69%, from 1.6 ng/ml to 0.5 ng/ml median (SD 1.29; p < 0.005). Overall 74% of subjects experienced decreases (range 16-99%), with 60% showing a halving of exposure levels at follow up. Self reported exposure to SHS at work showed a significant reduction from a median 30 hours a week to zero (p < 0.001). There was an 83% reduction in air nicotine concentrations from median 35.5 microg/m3 to 5.95 microg/m3 (p < 0.001). At baseline, three bars (16%) were below the 6.8 microg/m3 air nicotine significant risk level for lung cancer alone; at follow up this increased to 10 (53%). Passive smoking and associated risks were significantly reduced but not totally eliminated. Exposure to SHS is still possible for those working where smoking is still allowed and those working where smoke may migrate from outdoor areas. Further research is required to assess the true extent and magnitude of these exposures.
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              Passive smoking and heart disease. Epidemiology, physiology, and biochemistry.

              The evidence that ETS increases risk of death from heart disease is similar to that which existed in 1986 when the US Surgeon General concluded that ETS caused lung cancer in healthy nonsmokers. There are 10 epidemiological studies, conducted in a variety of locations, that reflect about a 30% increase in risk of death from ischemic heart disease or myocardial infarction among nonsmokers living with smokers. The larger studies also demonstrate a significant dose-response effect, with greater exposure to ETS associated with greater risk of death from heart disease. These epidemiological studies are complemented by a variety of physiological and biochemical data that show that ETS adversely affects platelet function and damages arterial endothelium in a way that increases the risk of heart disease. Moreover, ETS, in realistic exposures, also exerts significant adverse effects on exercise capability of both healthy people and those with heart disease by reducing the body's ability to deliver and utilize oxygen. In animal experiments, ETS also depresses cellular respiration at the level of mitochondria. The polycyclic aromatic hydrocarbons in ETS also accelerate, and may initiate, the development of atherosclerotic plaque. Of note, the cardiovascular effects of ETS appear to be different in nonsmokers and smokers. Nonsmokers appear to be more sensitive to ETS than do smokers, perhaps because some of the affected physiological systems are sensitive to low doses of the compounds in ETS, then saturate, and also perhaps because of physiological adaptions smokers undergo as a result of long-term exposure to the toxins in cigarette smoke. In any event, these findings indicate that, for cardiovascular disease, it is incorrect to compute "cigarette equivalents" for passive exposure to ETS and then to extrapolate the effects of this exposure on nonsmokers from the effects of direct smoking on smokers. These results suggest that heart disease is an important consequence of exposure to ETS. The combination of epidemiological studies with demonstration of physiological changes with exposure to ETS, together with biochemical evidence that elements of ETS have significant adverse effects on the cardiovascular system, leads to the conclusion that ETS causes heart disease. This increase in risk translates into about 10 times as many deaths from ETS-induced heart disease as lung cancer; these deaths contribute greatly to the estimated 53,000 deaths annually from passive smoking. This toll makes passive smoking the third leading preventable cause of death in the United States today, behind active smoking and alcohol.
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                Author and article information

                Journal
                BMC Public Health
                BMC Public Health
                BioMed Central (London )
                1471-2458
                2006
                27 October 2006
                : 6
                : 266
                Affiliations
                [1 ]Department of Public Health and Family Medicine, Tufts University School of Medicine, 136 Harrison Ave.; Boston, MA 02111, USA
                [2 ]Repace Associates, 101 Felicia Lane, Bowie, MD 20720, USA
                Article
                1471-2458-6-266
                10.1186/1471-2458-6-266
                1637107
                17069654
                29289456-1686-4bcf-9eb4-670b11509757
                Copyright © 2006 Repace et al; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 28 April 2006
                : 27 October 2006
                Categories
                Research Article

                Public health
                Public health

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