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      Exposure-Response Estimates for Diesel Engine Exhaust and Lung Cancer Mortality Based on Data from Three Occupational Cohorts

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          Abstract

          Background: Diesel engine exhaust (DEE) has recently been classified as a known human carcinogen.

          Objective: We derived a meta-exposure–response curve (ERC) for DEE and lung cancer mortality and estimated lifetime excess risks (ELRs) of lung cancer mortality based on assumed occupational and environmental exposure scenarios.

          Methods: We conducted a meta-regression of lung cancer mortality and cumulative exposure to elemental carbon (EC), a proxy measure of DEE, based on relative risk (RR) estimates reported by three large occupational cohort studies (including two studies of workers in the trucking industry and one study of miners). Based on the derived risk function, we calculated ELRs for several lifetime occupational and environmental exposure scenarios and also calculated the fractions of annual lung cancer deaths attributable to DEE.

          Results: We estimated a lnRR of 0.00098 (95% CI: 0.00055, 0.0014) for lung cancer mortality with each 1-μg/m 3-year increase in cumulative EC based on a linear meta-regression model. Corresponding lnRRs for the individual studies ranged from 0.00061 to 0.0012. Estimated numbers of excess lung cancer deaths through 80 years of age for lifetime occupational exposures of 1, 10, and 25 μg/m 3 EC were 17, 200, and 689 per 10,000, respectively. For lifetime environmental exposure to 0.8 μg/m 3 EC, we estimated 21 excess lung cancer deaths per 10,000. Based on broad assumptions regarding past occupational and environmental exposures, we estimated that approximately 6% of annual lung cancer deaths may be due to DEE exposure.

          Conclusions: Combined data from three U.S. occupational cohort studies suggest that DEE at levels common in the workplace and in outdoor air appear to pose substantial excess lifetime risks of lung cancer, above the usually acceptable limits in the United States and Europe, which are generally set at 1/1,000 and 1/100,000 based on lifetime exposure for the occupational and general population, respectively.

          Citation: Vermeulen R, Silverman DT, Garshick E, Vlaanderen J, Portengen L, Steenland K. 2014. Exposure-response estimates for diesel engine exhaust and lung cancer mortality based on data from three occupational cohorts. Environ Health Perspect 122:172–177;  http://dx.doi.org/10.1289/ehp.1306880

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          The global burden of disease due to outdoor air pollution.

          Aaron J. Cohen, H. Ross Anderson, Bart Ostro … (2005)
          As part of the World Health Organization (WHO) Global Burden of Disease Comparative Risk Assessment, the burden of disease attributable to urban ambient air pollution was estimated in terms of deaths and disability-adjusted life years (DALYs). Air pollution is associated with a broad spectrum of acute and chronic health effects, the nature of which may vary with the pollutant constituents. Particulate air pollution is consistently and independently related to the most serious effects, including lung cancer and other cardiopulmonary mortality. The analyses on which this report is based estimate that ambient air pollution, in terms of fine particulate air pollution (PM(2.5)), causes about 3% of mortality from cardiopulmonary disease, about 5% of mortality from cancer of the trachea, bronchus, and lung, and about 1% of mortality from acute respiratory infections in children under 5 yr, worldwide. This amounts to about 0.8 million (1.2%) premature deaths and 6.4 million (0.5%) years of life lost (YLL). This burden occurs predominantly in developing countries; 65% in Asia alone. These estimates consider only the impact of air pollution on mortality (i.e., years of life lost) and not morbidity (i.e., years lived with disability), due to limitations in the epidemiologic database. If air pollution multiplies both incidence and mortality to the same extent (i.e., the same relative risk), then the DALYs for cardiopulmonary disease increase by 20% worldwide.
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            An overview of methods for calculating the burden of disease due to specific risk factors.

            Kyle Steenland, Ben G. Armstrong (2006)
            There are a number of measures that quantify the public health burden due to specific risk factors for specific diseases. Although these measures are of importance for policymakers, epidemiologists do not often calculate them or may be unfamiliar with some of the issues involved when they do. The primary measure of interest is the attributable fraction (AF), representing the fraction of cases or deaths from a specific disease that would not have occurred in the absence of exposure to a specific risk factor either in the exposed population or the population as a whole. AFs can be multiplied by the total number of cases of a given disease to obtain a "body count"--the absolute number of preventable cases due to a specific risk factor. Two other measures of public health burden, used in conjunction with AFs, are attributable years-of-life-lost and attributable disability-adjusted life-years. We provide an overview of the AF and related measures and discuss some of the specific issues involved in calculating AFs. These issues include calculating the variance of AFs (such as Monte Carlo sensitivity methods), biases arising from some formulas for the AF, sources of data for calculating AFs, dependence of AFs on basic decisions about what exposure-disease associations are causal, and extrapolation from the source population to the target population.
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              Associations of ambient air pollution with chronic obstructive pulmonary disease hospitalization and mortality.

              Michael Brauer, Chris Carlsten, J. FitzGerald … (2013)
              Ambient air pollution has been suggested as a risk factor for chronic obstructive pulmonary disease (COPD). However, there is a lack of longitudinal studies to support this assertion. To investigate the associations of long-term exposure to elevated traffic-related air pollution and woodsmoke pollution with the risk of COPD hospitalization and mortality. This population-based cohort study included a 5-year exposure period and a 4-year follow-up period. All residents aged 45-85 years who resided in Metropolitan Vancouver, Canada, during the exposure period and did not have known COPD at baseline were included in this study (n = 467,994). Residential exposures to traffic-related air pollutants (black carbon, particulate matter <2.5 μm in aerodynamic diameter, nitrogen dioxide, and nitric oxide) and woodsmoke were estimated using land-use regression models and integrating changes in residences during the exposure period. COPD hospitalizations and deaths during the follow-up period were identified from provincial hospitalization and death registration databases. An interquartile range elevation in black carbon concentrations (0.97 × 10(-5)/m, equivalent to 0.78 μg/m(3) elemental carbon) was associated with a 6% (95% confidence interval, 2-10%) increase in COPD hospitalizations and a 7% (0-13%) increase in COPD mortality after adjustment for covariates. Exposure to higher levels of woodsmoke pollution (tertile 3 vs. tertile 1) was associated with a 15% (2-29%) increase in COPD hospitalizations. There were positive exposure-response trends for these observed associations. Ambient air pollution, including traffic-related fine particulate pollution and woodsmoke pollution, is associated with an increased risk of COPD.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Environ Health Perspect
                Journal ID (iso-abbrev): Environ. Health Perspect
                Journal ID (publisher-id): EHP
                Title: Environmental Health Perspectives
                Publisher: National Institute of Environmental Health Sciences
                ISSN (Print): 0091-6765
                ISSN (Electronic): 1552-9924
                Publication date (Electronic): 22 November 2013
                Publication date (Print): February 2014
                Volume: 122
                Issue: 2
                Pages: 172-177
                Affiliations
                [1 ]Division of Environmental Epidemiology, Institute for Risk Assessment Sciences, Utrecht University, Utrecht, the Netherlands
                [2 ]Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA
                [3 ]Pulmonary and Critical Care Medicine Section, Medical Service, Veterans Affairs Boston Healthcare System; Channing Division of Network Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
                [4 ]Section of Environment and Radiation, International Agency for Research on Cancer, Lyon, France
                [5 ]Department of Environmental and Occupational Health, Rollins School of Public Health, Emory University, Atlanta, Georgia, USA
                Author notes
                Address correspondence to R. Vermeulen, Yalelaan 2, 3584 CM Utrecht, the Netherlands. Telephone: 31-30-253-9448. E-mail: R.C.H.Vermeulen@ 123456uu.nl
                Article
                Publisher ID: ehp.1306880
                DOI: 10.1289/ehp.1306880
                PMC ID: 3915263
                PubMed ID: 24273233
                SO-VID: 7d7de5dd-ff5b-4906-9e63-2c10cd4d260a
                License:

                Publication of EHP lies in the public domain and is therefore without copyright. All text from EHP may be reprinted freely. Use of materials published in EHP should be acknowledged (for example, “Reproduced with permission from Environmental Health Perspectives”); pertinent reference information should be provided for the article from which the material was reproduced. Articles from EHP, especially the News section, may contain photographs or illustrations copyrighted by other commercial organizations or individuals that may not be used without obtaining prior approval from the holder of the copyright.

                History
                Date received : 02 April 2013
                Date accepted : 21 November 2013
                Date: 22 November 2013
                Date: 01 February 2014
                Categories
                Subject: Research

                ScienceOpen disciplines: Public health
                Data availability:
                ScienceOpen disciplines: Public health

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