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Diesel exhaust exposure and the risk of lung cancer--a review of the epidemiological evidence.

ABSTRACT: To critically evaluate the association between diesel exhaust (DE) exposure and the risk of lung cancer, we conducted a systematic review of published epidemiological evidences. To comprehensively identify original studies on the association between DE exposure and the risk of lung cancer, literature searches were performed in literature databases for the period between 1970 and 2013, including bibliographies and cross-referencing. In total, 42 cohort studies and 32 case-control studies were identified in which the association between DE exposures and lung cancer was examined. In general, previous studies suffer from a series of methodological limitations, including design, exposure assessment methods and statistical analysis used. A lack of objective exposure information appears to be the main problem in interpreting epidemiological evidence. To facilitate the interpretation and comparison of previous studies, a job-exposure matrix (JEM) of DE exposures was created based on around 4,000 historical industrial measurements. The values from the JEM were considered during interpretation and comparison of previous studies. Overall, neither cohort nor case-control studies indicate a clear exposure-response relationship between DE exposure and lung cancer. Epidemiological studies published to date do not allow a valid quantification of the association between DE and lung cancer.

SUBMITTER: Sun Y

PROVIDER: S-EPMC3945540 | biostudies-literature | 2014 Jan

REPOSITORIES: biostudies-literature

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Diesel exhaust exposure and the risk of lung cancer--a review of the epidemiological evidence.

Sun Yi Y Bochmann Frank F Nold Annette A Mattenklott Markus M

International journal of environmental research and public health 20140127 2

To critically evaluate the association between diesel exhaust (DE) exposure and the risk of lung cancer, we conducted a systematic review of published epidemiological evidences. To comprehensively identify original studies on the association between DE exposure and the risk of lung cancer, literature searches were performed in literature databases for the period between 1970 and 2013, including bibliographies and cross-referencing. In total, 42 cohort studies and 32 case-control studies were ide ...[more]

PMID: 24473109

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Project description:BackgroundMost studies of the association between diesel exhaust exposure and lung cancer suggest a modest, but consistent, increased risk. However, to our knowledge, no study to date has had quantitative data on historical diesel exposure coupled with adequate sample size to evaluate the exposure-response relationship between diesel exhaust and lung cancer. Our purpose was to evaluate the relationship between quantitative estimates of exposure to diesel exhaust and lung cancer mortality after adjustment for smoking and other potential confounders.MethodsWe conducted a nested case-control study in a cohort of 12 315 workers in eight non-metal mining facilities, which included 198 lung cancer deaths and 562 incidence density-sampled control subjects. For each case subject, we selected up to four control subjects, individually matched on mining facility, sex, race/ethnicity, and birth year (within 5 years), from all workers who were alive before the day the case subject died. We estimated diesel exhaust exposure, represented by respirable elemental carbon (REC), by job and year, for each subject, based on an extensive retrospective exposure assessment at each mining facility. We conducted both categorical and continuous regression analyses adjusted for cigarette smoking and other potential confounding variables (eg, history of employment in high-risk occupations for lung cancer and a history of respiratory disease) to estimate odds ratios (ORs) and 95% confidence intervals (CIs). Analyses were both unlagged and lagged to exclude recent exposure such as that occurring in the 15 years directly before the date of death (case subjects)/reference date (control subjects). All statistical tests were two-sided.ResultsWe observed statistically significant increasing trends in lung cancer risk with increasing cumulative REC and average REC intensity. Cumulative REC, lagged 15 years, yielded a statistically significant positive gradient in lung cancer risk overall (P (trend) = .001); among heavily exposed workers (ie, above the median of the top quartile [REC ≥ 1005 μg/m(3)-y]), risk was approximately three times greater (OR = 3.20, 95% CI = 1.33 to 7.69) than that among workers in the lowest quartile of exposure. Among never smokers, odd ratios were 1.0, 1.47 (95% CI = 0.29 to 7.50), and 7.30 (95% CI = 1.46 to 36.57) for workers with 15-year lagged cumulative REC tertiles of less than 8, 8 to less than 304, and 304 μg/m(3)-y or more, respectively. We also observed an interaction between smoking and 15-year lagged cumulative REC (P (interaction) = .086) such that the effect of each of these exposures was attenuated in the presence of high levels of the other.ConclusionOur findings provide further evidence that diesel exhaust exposure may cause lung cancer in humans and may represent a potential public health burden.

Project description:ObjectivesEpidemiological research on the association between diesel exhaust exposure and lung cancer risk has some methodological challenges that give rise to different conclusions and intense debates. This raises the question about the role of selective citation and of citation bias in particular. Our aim was to investigate the occurrence and prevalence of selective citation in this field.DesignCitation analysis.SettingWeb of Science Core Collection.ParticipantsWe identified 96 publications in this network, with 4317 potential citations. For each publication, we extracted characteristics such as study conclusion and funding source. Some of these characteristics are related to the study content: study design, sample size, method of diesel exposure assessment, type of diesel technology under investigation, and whether smoking had been adjusted for.Primary and secondary outcome measuresWhether a citation occurs or not, measured and analysed according to the preregistered protocol. Exploratively we analysed the association between funding source and study conclusion.ResultsMethodological content of a study was clearly related to citation, studies using more sophisticated methods were more likely to be cited. There was some evidence for citation bias: supportive publications had a higher chance of being cited than non-supportive ones, but after adjustment for study quality, this effect decreased substantially (adjusted OR 1.3, 95% CI 1.0 to 1.7). Explorative analyses indicated that three quarters of non-profit funded publications had a supportive study conclusion against only one quarter of the industry-funded publications.ConclusionsThere is evidence for selective citation within this field, but the evidence for citation bias was weak. It seems that factors related to the methodology had more impact on citation than the conclusion of a study. Interestingly, publications that were funded by industry were more skeptical about a causal relationship between diesel exhaust and lung cancer compared to non-profit-funded publications.

Project description:Exposure to diesel exhaust emissions (DEE) is strongly linked to innate immune injury and lung injury, but the role of macrophage chemoattractant CXCL17 in the lung damage caused by DEE exposure remains unclear. In this study, whole-body plethysmography (WBP), inflammatory cell differential count, and histopathological analysis were performed to assess respiratory parameters, airway inflammation, and airway injury in C57BL/6 male mice exposed to DEE for 3 months. qRT-PCR, IHC (immunohistochemistry), and ELISA were performed to measure the CXCL17 expression in airway epithelium or BALF (bronchoalveolar lavage fluid) following DEE/Diesel exhaust particle (DEP) exposure. Respiratory parameters, airway inflammation, and airway injury were assessed in CXCL17-overexpressing mice through adeno-associated virus vector Type 5 (AAV5) infection. Additionally, an in vitro THP-1 and HBE co-culture system was constructed. Transwell assay was carried out to evaluate the effect of rh-CXCL17 (recombinant human protein-CXCL17) on THP-1 cell migration. Flow cytometry and qRT-PCR were conducted to assess the impacts of rh-CXCL17 on apoptosis and inflammation/remodeling of HBE cells. We found that the mice exposed to DEE showed abnormal respiratory parameters, accompanied by airway injury and remodeling (ciliary injury in airway epithelium, airway smooth muscle hyperplasia, and increased collagen deposition). Carbon content in airway macrophages (CCAM), but not the number of macrophages in BALF, increased significantly. CXCL17 expression significantly decreased in mice airways and HBE after DEE/DEP exposure. AAV5-CXCL17 enhanced macrophage recruitment and clearance of DEE in the lungs of mice, and it improved respiratory parameters, airway injury, and airway remodeling. In the THP-1/HBE co-culture system, rh-CXCL17 increased THP-1 cell migration while attenuating HBE cell apoptosis and inflammation/remodeling. Therefore, CXCL17 might attenuate DEE-induced lung damage by recruiting and activating pulmonary macrophages, which is expected to be a novel therapeutic target for DEE-associated lung diseases.

Project description:BackgroundWith the exception of lung cancer, the health effects associated with diesel exhaust for other cancers and nonmalignant health outcomes are not well understood.ObjectivesWe extended the mortality follow-up of the Diesel Exhaust in Miners Study, a cohort study of 12,315 workers, by 18 y (ending 31 December 2015), more than doubling the number of observed deaths to n=4,887, to evaluate associations between mortality and diesel exhaust exposure.MethodsQuantitative estimates of historical exposure to respirable elemental carbon (REC), a surrogate for diesel exhaust, were created for all jobs, by year and facility, using measurements collected from each mine, as well as historical measurements. Standardized mortality ratios (SMRs) and hazard ratios (HRs) were estimated for the entire cohort and by worker location (surface, underground).ResultsWe observed an excess of death for cancers of the lung, trachea, and bronchus (n=409; SMR=1.24; 95% CI: 1.13, 1.37). Among workers who ever worked underground, where the majority of diesel exposure occurred, excess deaths were evident for lung, trachea, and bronchus cancers (n=266; SMR=1.26; 95% CI: 1.11, 1.42). Several nonmalignant diseases were associated with excess mortality among workers ever-employed underground, including ischemic heart disease (SMR=1.08; 95% CI: 1.00, 1.16), cerebrovascular disease (SMR=1.22; 95% CI: 1.04, 1.43), and nonmalignant diseases of the respiratory system (SMR=1.13; 95% CI: 1.01, 1.26). Continuous 15-y lagged cumulative REC exposure <1,280 μg/m3-y was associated with increased lung cancer risk (HR=1.93; 95% CI: 1.24, 3.03), but the risk declined at the highest exposures (HR=1.29; 95% CI: 0.74, 2.26). We also observed a significant trend in non-Hodgkin lymphoma (NHL) risk with increasing 20-y lagged cumulative REC (HRTertile3 vs. Tertile1=3.12; 95% CI: 1.00, 9.79; p-trend=0.031).DiscussionIncreased risks of lung cancer mortality observed in the original study were sustained. Observed associations between diesel exposure and risk of death from NHL and the excesses in deaths for diseases of the respiratory and cardiovascular system, including ischemic heart disease and cerebrovascular disease, warrant further study and provide evidence of the potential widespread public health impact of diesel exposure. https://doi.org/10.1289/EHP12840.

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Diesel exhaust exposure and the risk of lung cancer--a review of the epidemiological evidence.

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Diesel exhaust exposure and the risk of lung cancer--a review of the epidemiological evidence.

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