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BackgroundDiesel exhaust has been considered to be a probable lung carcinogen based on studies of occupationally exposed workers. Efforts to define lung cancer risk in these studies have been limited in part by lack of quantitative exposure estimates.ObjectiveWe conducted a retrospective cohort study to assess lung cancer mortality risk among U.S. trucking industry workers. Elemental carbon (EC) was used as a surrogate of exposure to engine exhaust from diesel vehicles, traffic, and loading dock operations.MethodsWork records were available for 31,135 male workers employed in the unionized U.S. trucking industry in 1985. A statistical model based on a national exposure assessment was used to estimate historical work-related exposures to EC. Lung cancer mortality was ascertained through the year 2000, and associations with cumulative and average EC were estimated using proportional hazards models.ResultsDuration of employment was inversely associated with lung cancer risk consistent with a healthy worker survivor effect and a cohort composed of prevalent hires. After adjusting for employment duration, we noted a suggestion of a linear exposure-response relationship. For each 1,000-µg/m³ months of cumulative EC, based on a 5-year exposure lag, the hazard ratio (HR) was 1.07 [95% confidence interval (CI): 0.99, 1.15] with a similar association for a 10-year exposure lag [HR = 1.09 (95% CI: 0.99, 1.20)]. Average exposure was not associated with relative risk.ConclusionsLung cancer mortality in trucking industry workers increased in association with cumulative exposure to EC after adjusting for negative confounding by employment duration.

BackgroundFew studies have directly assessed the association of secondhand smoke (SHS) with cardiovascular disease-related inflammatory markers, and the findings are inconsistent.ObjectivesWe assessed the association between SHS exposure and the inflammatory markers high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and soluble intercellular adhesion molecule-1 (sICAM-1) in 199 nonsmoking U.S. trucking industry workers.MethodsParticipants provided blood samples either by mail (blood drawn at local health care provider near home) or at the work site (blood drawn by research staff on-site) and completed a health and work history questionnaire at the time of blood draw. Exposure to SHS was measured by plasma cotinine concentrations. We used multivariate regression analyses to assess the associations between levels of cotinine and inflammatory markers.ResultsThe median cotinine level was 0.10 ng/mL (interquartile range, 0.04-0.23 ng/mL). The odds ratios of elevated hs-CRP (above highest CRP tertile, 1.5 mg/L) were 2.85 [95% confidence interval (CI), 1.03-7.89] for the high-cotinine group (> 0.215 ng/mL) and 2.80 (95% CI, 1.11-7.10) for the moderate-cotinine group (0.05-0.215 ng/mL), compared with the low-cotinine group (< 0.05 ng/mL), adjusting for age, sex, race, educational level, obesity, previous smoking history, job title, and medical history. Plasma cotinine levels were not associated with IL-6 or sICAM-1.ConclusionsSHS exposure, as assessed by plasma cotinine, was positively associated with hs-CRP in this group of blue-collar workers. The strength of the association with hs-CRP depended on the cut points selected for analysis.

BackgroundAlthough the smoking rate in the United States is declining because of an increase of smoke-free laws, among blue-collar workers it remains higher than that among many other occupational groups.ObjectivesWe evaluated the factors influencing workplace secondhand smoke (SHS) exposures in the U.S. unionized trucking industry.MethodsFrom 2003 through 2005, we measured workplace SHS exposure among 203 nonsmoking and 61 smoking workers in 25 trucking terminals. Workers in several job groups wore personal vapor-phase nicotine samplers on their lapels for two consecutive work shifts and completed a workplace SHS exposure questionnaire at the end of the personal sampling.ResultsMedian nicotine level was 0.87 microg/m3 for nonsmokers and 5.96 microg/m3 for smokers. As expected, smokers experienced higher SHS exposure duration and intensity than did nonsmokers. For nonsmokers, multiple regression analyses indicated that self-reported exposure duration combined with intensity, lack of a smoking policy as reported by workers, having a nondriver job, and lower educational level were independently associated with elevated personal nicotine levels (model R2 = 0.52). Nondriver job and amount of active smoking were associated with elevated personal nicotine level in smokers, but self-reported exposure, lack of a smoking policy, and lower educational level were not.ConclusionsDespite movements toward smoke-free laws, this population of blue-collar workers was still exposed to workplace SHS as recently as 2005. The perceived (reported by the workers), rather than the official (reported by the terminal managers), smoking policy was associated with measured SHS exposure levels among the nonsmokers. Job duties and educational level might also be important predictors of workplace SHS exposure.

BackgroundAn elevated risk of lung cancer in truck drivers has been attributed to diesel exhaust exposure. Interpretation of these studies specifically implicating diesel exhaust as a carcinogen has been limited because of limited exposure measurements and lack of work records relating job title to exposure-related job duties.ObjectivesWe established a large retrospective cohort of trucking company workers to assess the association of lung cancer mortality and measures of vehicle exhaust exposure.MethodsWork records were obtained for 31,135 male workers employed in the unionized U.S. trucking industry in 1985. We assessed lung cancer mortality through 2000 using the National Death Index, and we used an industrial hygiene review and current exposure measurements to identify jobs associated with current and historical use of diesel-, gas-, and propane-powered vehicles. We indirectly adjusted for cigarette smoking based on an industry survey.ResultsAdjusting for age and a healthy-worker survivor effect, lung cancer hazard ratios were elevated in workers with jobs associated with regular exposure to vehicle exhaust. Mortality risk increased linearly with years of employment and was similar across job categories despite different current and historical patterns of exhaust-related particulate matter from diesel trucks, city and highway traffic, and loading dock operations. Smoking behavior did not explain variations in lung cancer risk.ConclusionsTrucking industry workers who have had regular exposure to vehicle exhaust from diesel and other types of vehicles on highways, city streets, and loading docks have an elevated risk of lung cancer with increasing years of work.

OBJECTIVE: Isocyanates (di- and poly-), important chemicals used worldwide to produce polyurethane products, are a leading cause of occupational asthma. Respiratory exposures have been reduced through improved hygiene controls and [...]

Background: Few studies have directly assessed the association of secondhand smoke (SHS) with cardiovascular disease-related inflammatory markers, and the findings are inconsistent. Objectives: We assessed the association between SHS exposure and the inflammatory markers high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and soluble intercellular adhesion molecule-1 (sICAM-1) in 199nonsmoking U.S. trucking industry workers. Methods: Participants provided blood samples either by mail (blood drawn at local health care provider near home) or at the work site (blood drawn by research staff on-site) and completed a health and work history questionnaire at the time of blood draw. Exposure to SHS was measured by plasma cotinine concentrations. We used multivariate regression analyses to assess the associations between levels of cotinine and inflammatory markers. Results: The median cotinine level was 0.10 ng/mL (interquartile range, 0.04-0.23 ng/mL). The odds ratios of elevated hs-CRP (above highest CRP tertile, 1.5 mg/L) were 2.85 [95% confidence interval (CI), 1.03-7.89] for the high-cotinine group (> 0.215 ng/mL) and 2.80 (95% CI, 1.11-7.10) for the moderate-cotinine group (0.05-0.215 ng/mL), compared with the low-cotinine group (< 0.05 ng/mL), adjusting for age, sex, race, educational level, obesity, previous smoking history, job title, and medical history. Plasma cotinine levels were not associated with IL 6 or sICAM 1. Conclusions: SHS exposure, as assessed by plasma cotinine, was positively associated with hs CRP in this group of blue-collar workers. The strength of the association with hs-CRP depended on the cut points selected for analysis. [ABSTRACT FROM AUTHOR]

Background: Although the smoking rate in the United States is declining because of an increase of smoke-free laws, among blue-collar workers it remains higher than that among many other occupational groups. Objectives: We evaluated the factors influencing workplace secondhand smoke (SHS) exposures in the U.S. unionized trucking industry. Method s: From 2003 through 2005, we measured workplace SHS exposure among 203 nonsmoking and 61 smoking workers in 25 trucking terminals. Workers in several job groups wore personal vapor-phase nicotine samplers on their lapels for two consecutive work shifts and completed a workplace SHS exposure questionnaire at the end of the personal sampling. Results: Median nicotine level was 0.87 μg/m³ for nonsmokers and 5.96 μg/m³ for smokers. As expected, smokers experienced higher SHS exposure duration and intensity than did nonsmokers. For nonsmokers, multiple regression analyses indicated that self-reported exposure duration combined with intensity, lack of a smoking policy as reported by workers, having a nondriver job, and lower educational level were independently associated with elevated personal nicotine levels (model R² = 0.52). Nondriver job and amount of active smoking were associated with elevated personal nicotine level in smokers, but self-reported exposure, lack of a smoking policy, and lower educational level were not. Conclusions: Despite movements toward smoke-free laws, this population of blue-collar workers was still exposed to workplace SHS as recently as 2005. The perceived (reported by the workers), rather than the official (reported by the terminal managers), smoking policy was associated with measured SHS exposure levels among the nonsmokers. Job duties and educational level might also be important predictors of workplace SHS exposure. [ABSTRACT FROM AUTHOR]

BACKGROUND: Epidemiologic studies of air pollution have demonstrated a link between long-term air pollution exposures and mortality. However, many have been limited to city-specific average pollution measures or spatial or land-use regression exposure models in small geographic areas. OBJECTIVES: Our objective was to develop nationwide models of annual exposure to particulate matter < 10 μm in diameter (PM10) and nitrogen dioxide during 1985?2000. METHODS: We used generalized additive models (GAMs) to predict annual levels of the pollutants using smooth spatial surfaces of available monitoring data and geographic information system-derived covariates. Model performance was determined using a cross-validation (CV) procedure with 10% of the data. We also compared the results of these models with a commonly used spatial interpolation, inverse distance weighting. RESULTS: For PM10, distance to road, elevation, proportion of low-intensity residential, high-intensity residential, and industrial, commercial, or transportation land use within 1 km were all statistically significant predictors of measured PM10 (model R2 = 0.49, CV R2 = 0.55). Distance to road, population density, elevation, land use, and distance to and emissions of the nearest nitrogen oxides-emitting power plant were all statistically significant predictors of measured NO2 (model R2 = 0.88, CV R2 = 0.90). The GAMs performed better overall than the inverse distance models, with higher CV R2 and higher precision. CONCLUSIONS: These models provide reasonably accurate and unbiased estimates of annual exposures for PM10 and NO2. This approach provides the spatial and temporal variability necessary to describe exposure in studies assessing the health effects of chronic air pollution. [ABSTRACT FROM AUTHOR]