Contribution Of Environmental Tobacco Smoke Research Articles

A quantitative method for assessing smoke associated molecular damage in lung cancers.

While tobacco exposure is the cause of the vast majority of lung cancers, an important percentage arise in lifetime never smokers. Documenting the precise extent of tobacco induced molecular changes may be of importance. Also, the contribution of environmental tobacco smoke (ETS) is difficult to assess. We developed and validated a quantitative method to assess the extent of tobacco related molecular damage by combing the most characteristic changes associated with tobacco smoke, the tumor mutation burden (TMB) and type of molecular changes present in lung cancers. Using maximum entropy (MaxEnt) as a classifier, we developed a F score. F score values >0 were considered to show evidence of tobacco related molecular damage, while values ≤0 were considered to lack evidence of tobacco related molecular damage. Compared to the stated patient tobacco exposure histories, the F scores had sensitivity, specificity and accuracy values of 85-87%. Using this method, we analyzed public data sets of lung adenocarcinoma (LUAD), lung squamous cell (LUSC) and small cell lung cancer (SCLC). Less than 10% of LUSCs and SCLCs had negative F scores, while 27% to 35% of LUADs had positive scores. The F score showed a highly significant downward trend when LUADs were subdivided into the following categories: ever, reformed ≤15 years, reformed >15 years and never smokers. Most of the examined bronchial carcinoids (a lung cancer type not associated with smoke exposure) had negative F scores. In addition, most LUADs with EGFR mutations had negative F scores, while almost all with KRAS mutations had positive scores. We have established and validated a quantitative assay that will be of use in assessing the presence and degree of smoke associated molecular damage in lung cancers arising in ever and never smokers.

Environmental Tobacco Smoke and Airway Obstruction in Children With Sickle Cell Anemia

The contribution of environmental tobacco smoke (ETS) exposure to pulmonary morbidity in children with sickle cell anemia (SCA) is poorly understood. We tested the hypothesis that children with SCA and ETS exposure would have an increased prevalence of obstructive lung disease and respiratory symptoms compared with children with SCA and no ETS exposure. Parent reports of ETS and respiratory symptom frequency were obtained for 245 children with SCA as part of a multicenter prospective cohort study. One hundred ninety-six children completed pulmonary function testing. Multivariable regression models were used to evaluate the associations between ETS exposure at different time points (prenatal, infant [birth to 2 years], preschool [2 years to first grade], and current) and lung function and respiratory symptoms. Among the 245 participants, a high prevalence of prior (44%) and current (29%) ETS exposure was reported. Of the 196 children who completed pulmonary function testing, those with parent-reported infant and current ETS exposure were more likely to have airway obstruction (defined as an FEV1/FVC ratio below the lower limit normal) compared with unexposed children (22.0% vs 3.1%, P < .001). Those with ETS exposure also had a lower forced expiratory flow, midexpiratory phase/FVC ratio (0.82 vs 0.97, P = .001) and were more likely to have evidence of bronchodilator responsiveness (23% vs 11%, P = .03). Current and prior ETS exposure and in utero smoke exposure were associated with increased frequency of respiratory symptoms. ETS exposure is associated with evidence of lower airway obstruction and increased respiratory symptoms in SCA.

Quantification of Environmental Tobacco Smoke Contribution on Outdoor Particulate Aliphatic and Polycyclic Aromatic Hydrocarbons

The objective of this study was to identify and quantify the sources of fine particulate aliphatic and polycyclic aromatic hydrocarbons (PAHs) in an urban area in southeastern Europe. A total of 91 urban PM2.5 samples were analyzed by gas chromatography coupled with mass spectrometry for alkanes and PAHs. Exploratory statistical tools were applied to resolve a decreased number of components based on the variation of measurements. Molecular markers and diagnostic ratios were examined to assign retained components to specific sources. The contributions of the sources were estimated by multivariate linear regression. Sources of aliphatic and PAHs hydrocarbons included primary particles from traffic (3.9 ng/m(3) for alkanes and 240 pg/m(3) for PAHs), evaporative fugitive (4.0 ng/m(3) for alkanes and 93 pg/m(3) for PAHs), and unburnt fuels and oil residues (1.1 ng/m(3) for alkanes and 230 pg/m(3) for PAHs). For the first time, we quantified the contribution of environmental tobacco smoke (ETS), which accounted for 5.2 ng/m(3) of alkanes and 128 pg/m(3) of PAHs. The findings of this study underlined the persistence of ETS and possible exposures to significant quantities of tobacco residues outdoors. Tobacco smoke is known to induce adverse respiratory and cardiovascular illnesses and increased risk for cancer.

Smoking, environmental tobacco smoke, and risk of renal cell cancer: a population-based case-control study

BackgroundKidney and renal pelvis cancers account for 4% of all new cancer cases in the United States, among which 85% are renal cell carcinomas (RCC). While cigarette smoking is an established risk factor for RCC, little is known about the contribution of environmental tobacco smoke (ETS) to RCC incidence. This study assesses the role of smoking and ETS on RCC incidence using a population-based case-control design in Florida and Georgia.MethodsIncident cases (n = 335) were identified from hospital records and the Florida cancer registry, and population controls (n = 337) frequency-matched by age (+/- 5 years), gender, and race were identified through random-digit dialing. In-person interviews assessed smoking history and lifetime exposure to ETS at home, work, and public spaces. Home ETS was measured in both years and hours of exposure. Odds ratios and 95% confidence intervals were calculated using logistic regression, controlled for age, gender, race, and BMI.ResultsCases were more likely to have smoked 20 or more pack-years, compared with never-smokers (OR: 1.35, 95% CI: 0.93 – 1.95). A protective effect was found for smoking cessation, beginning with 11–20 years of cessation (OR: 0.39, 95% CI: 0.18–0.85) and ending with 51 or more years of cessation (OR: 0.11, 95% CI: 0.03–0.39) in comparison with those having quit for 1–10 years. Among never-smokers, cases were more likely to report home ETS exposure of greater than 20 years, compared with those never exposed to home ETS (OR: 2.18; 95% CI: 1.14–4.18). Home ETS associations were comparable when measured in lifetime hours of exposure, with cases more likely to report 30,000 or more hours of home ETS exposure (OR: 2.37; 95% CI: 1.20–4.69). Highest quartiles of combined home/work ETS exposure among never-smokers, especially with public ETS exposure, increased RCC risk by 2 to 4 times.ConclusionThese findings confirm known associations between smoking and RCC and establish a potential etiologic role for ETS, particularly in the home. Differences in methods of retrospective measurement of lifetime smoking and ETS exposure may contribute to discrepancies in measures of associations across studies, and should be addressed in future research.

Assessment and Management of Residential Radon Health Risks: A Report from the Health Canada Radon Workshop

Epidemiologic studies of uranium miners and other underground miners have consistently shown miners exposed to high levels of radon to be at increased risk of lung cancer. More recently, concern has arisen about lung cancer risks among people exposed to lower levels of radon in homes. The current Canadian guideline for residential radon exposure was set in 1988 at 800 Bq/m3. Because of the accumulation of a considerable body of new scientific evidence on radon lung cancer risks since that time, Health Canada sponsored a workshop to review the current state-of-the-science on radon health risks. The specific objectives of the workshop were (1) to collect and assess scientific information relevant to setting national radon policy in Canada, and (2) to gather information on social, political, and operational considerations in setting national policy. The workshop, held on 3–4 March 2004, was attended by 38 invited scientists, regulators, and other stakeholders from Canada and the United States. The presentations on the first day dealt primarily with scientific issues. The combined analysis of North American residential radon and lung cancer studies was reviewed. The analysis confirmed a small but detectable increase in lung cancer risk at residential exposure levels. Current estimates suggest that radon in homes is responsible for approximately 10% of all lung cancer deaths in Canada, making radon the second leading cause of lung cancer after tobacco smoking. This was followed by a perspective from an UNSCEAR (United Nations Scientific Committee on the Effects of Atomic Radiation) working group on radon. There were two presentations on occupational exposures to radon and two presentations considered the possibility of radon as a causative factor for cardiovascular disease and for cancer in other organs besides the lung. The possible contribution of environmental tobacco smoke to lung cancers in nonsmokers was also considered. Areas for future research were identified. The second day was devoted to policy and operational issues. The presentations began with a perspective from the U.S. Environmental Protection Agency, followed by a history of radon policy development in Canada. Subsequent presentations dealt with the cost-effectiveness of radon mitigation, Canadian building codes and radon, and a summary of radon standards from around the world. Provincial representatives and a private consultant were given opportunities to present their viewpoints. A number of strategies for reducing residential radon exposure in Canada were recognized, including testing and mitigation of existing homes (on either a widespread or targeted basis) and changing the building code to require that radon mitigation devices be installed at the time a new home is constructed. The various elements of a comprehensive national radon policy were set forth. This workshop was sponsored by the Radiation Protection Bureau of Health Canada, and was held in collaboration with the McLaughlin Centre for Population Health Risk Assessment at the University of Ottawa. We are grateful to Anar Baweja, Barry Hauck, Sonia Johnson, Ed Korpach, and Trevor Stocki for support in organizing and carrying out the workshop. Jack Cornett, Director of the Radiation Protection Bureau, is thanked for his support and encouragement to the workshop. Most of all, we thank all those who attended the workshop and shared their views.

The Contribution of Environmental Tobacco Smoke to Indoor Pollution in Pubs and Bars

Smoking is currently allowed in most UK pubs and bars and smoking policies are self regulated by the hospitality industry through the Public Places Charter, which encourages the provision of non-smoking areas and improved ventilation. In this study monitoring of environmental tobacco smoke (ETS) has been conducted in 60 pubs and bars in the Greater Manchester area to determine the effectiveness of different smoking policies. The ETS markers RSP (as PM2.5), UVPM, FPM, SolPM and nicotine were sampled at several locations in each establishment, using portable monitoring cases and analysed using established methods. ETS concentrations were significantly lower in non-smoking areas in comparison to smoking areas, with reductions of between 27-69%. Bar areas had similar levels to smoking areas. The proportion of particles (RSP) that could be attributed to ETS was considerable even in non-smoking areas (43-55%) indicating that smoking was the major source of particles in these environments. The use of mechanical and/or air cleaning systems resulted in lower average concentrations of ETS markers in comparison to use of extractor fans or natural ventilation, but these differences were not statistically significant.

Variations in the estimation of the contribution of environmental tobacco smoke (ETS) to respirable (≤5 µm) indoor air particulates obtained by the use of different analytical methods

Several methods are in use for the identification of the contribution of particulate associated environmental tobacco smoke (ETS) and sidestream smoke to an atmosphere. These include the measurement of respirable suspended particulates (RSP), measurements of the total UV absorption and total fluorescence emission of a methanol extract of collected particulates and the use of specific marker compounds such as solanesol and scopoletin. Use of these methods gave values for the contribution of particulate ETS to total respirable (< or = 5 microns) particulates in the ranges 8.3-124.7% for smokers' houses and 9.6-121.2% for smokers' offices, respectively. However, using what we consider to be the most reliable methodology, based on the measurement of solanesol, the average contribution of particulate ETS to total respirable (< or = 5 microns) particulates for smokers' houses was 21.7% and for smokers' offices was 23.3%.

Use of volatile tracers to determine the contribution of environmental tobacco smoke to concentrations of volatile organic compounds in smoking environments

Three volatile nitrogen-containing compounds, 3-ethenylpyridine (3-EP), pyridine and pyrrole, were investigated as potential tracers for determining the contribution of environmental tobacco smoke (ETS) to concentrations of volatile organic compounds (VOCs) in indoor environments with smoking. The source emission rates of the three tracers and ten selected VOCs in ETS were first measured in a room-size environmental chamber for a market-weighted selection of six commercial cigarettes. The ratios of the emission rates of the tracers to the emission rates of the selected VOCs were calculated and compared among the six brands. The utility of the tracers was then evaluated in a field study conducted in five office buildings. Samples for VOCs were collected in designated smoking areas and adjoining non-smoking areas, air change rates were measured, and smoking rates were documented. Concentrations of the three tracers in the smoking areas were calculated using a mass-balance model and compared to their measured concentrations. Based on this comparison, 3-EP was selected as the most suitable tracer for the volatile components of ETS, although pyrrole is also potentially useful. Using 3-EP as the tracer, the contributions of ETS to the measured concentrations of the selected VOCs in the smoking areas were estimated by apportionment. ETS was estimated to contribute 57% to 84% (4.1 to 26 μg m −3) of the formaldehyde concentrations, 44–69% (0.9 to 5.8 μg m −3) of the 2-butanone concentrations, 37 to 58% (1.3 to 8.2 μg m −3) of the benzene concentrations, and 20 to 69% (0.5 to 3.0 μg m −3) of the styrene concentrations. The fractional contributions of ETS to the concentrations of acetone, toluene, ethylbenzene, xylene isomers, and d-limonene were all less than 50%.

Urinary mutagenic activity in workers exposed to diesel exhaust

We measured postshift urinary mutagenicity (mutu; n = 306 samples) on a population of railroad workers (n = 87) with a range of diesel exhaust exposures. Postshift urinary mutagenicity was determined by a sensitive microsuspension procedure using Salmonella strain TA98 +/- S9. Number of cigarettes smoked on the study day and urinary cotinine were highly correlated with postshift urinary mutagenicity. Diesel exhaust exposure was measured over the work shift by constant-flow personal sampling pumps. Respirable particle concentrations were adjusted for the contribution of environmental tobacco smoke, as estimated from nicotine concentration on treated filters. The relative ranking of jobs by this adjusted respirable particle concentration (ARP) was correlated with relative contact the job groups have with operating diesel locomotives. After adjustment for cigarette smoking (active and passive) in multiple regressions, there was no independent association of diesel exhaust exposure, as estimated by ARP, with postshift urinary mutagenicity among smokers or nonsmokers. An important finding is the detection of "baseline" mutagenicity in most of the nonsmoking workers. Despite the use of individual measurements of diesel exhaust exposure, the absence of a significant association in this study may be due to the low levels of diesel exposure, the lack of a specific marker for diesel exhaust exposure, and/or urinary mutagenicity levels from diesel exposure below the limit of sensitivity for the mutagenicity assay.

Method for assessing the contribution of environmental tobacco smoke to respirable suspended particles in indoor environments

Abstract The development of a method providing an upper limit for the ETS contribution to indoor concentrations of RSP is reported. This upper limit is termed ultraviolet particulate matter (UVPM). Air is drawn at 2 L min−1 through an inertial impactor separating at 3.5 μm, the RSP is collected on a membrane filter, and analyzed gravimetrically. Filters and collected material are then extracted in methanol, and the absorbance of the extraqt is measured spectrophotometrically at 325 nm. UVPM mass is computed from a calibration curve based upon ETS particulate matter collected in an environmental chamber.

An investigation of the contribution of environmental tobacco smoke to the air in betting shops

Abstract This paper investigates levels of some Environmental Tobacco Smoke (ETS) related constituents and volatile organic compounds found in the air of six betting shops. The levels of ETS constituents were found to be very low. Moreover, the study shows the important influence of the outdoor air on the air inside these betting shops.