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Background Exposures to volatile organic compounds could influence glycemic regulation. This study examines hemoglobin A1c (HbA1c) in a cohort of oil spill cleanup workers up to 6 years post-exposure in relation to benzene, toluene, ethylbenzene, and xylenes (BTEX) exposures, individually and as a mixture, as well as a separate estimation of the aggregate sum of BTEX (total BTEX). Methods Data for this analysis are from the Gulf Long-term Follow-up (GuLF) Study– a prospective cohort of workers involved in the 2010 Deepwater Horizon oil spill cleanup. HbA1c and medication information were obtained at Home Visit and Clinical Exam phases 1–3 years and up to 6 years post-exposure, respectively. Cumulative inhalation exposure to the individual BTEX chemicals and to total BTEX were estimated using a job-exposure matrix linking air measurements to detailed individual worker cleanup work histories. We used Tobit regression models to examine associations between exposure to the chemicals and latent, untreated HbA1c, accounting for medication-reduced HbA1c. We used quantile g-computation to examine exposure to the mixture of BTEX chemicals and HbA1c. Results In results examining Home Visit HbA1c we observed no discernable patterns but found suggestive evidence of an association with total BTEX. In results for Clinical Exam HbA1c, we did not observe monotonic patterns, but rather an inverted-U pattern with elevations in Q2 or Q3 or no clear pattern. Similarly, in results for final HbA1c adjusting for initial HbA1c, total BTEX difference estimates showed an inverted-U pattern in point estimates across Q2 (0.24 95%CI (0.14, 0.34)), Q3 (0.13 95%CI (0.03, 0.24)), and Q4 (0.00 95% CI (-0.11, 0.10)), compared to Q1. Conclusion Exposures to the moderate levels of the BTEX chemicals observed in this study population, individually and as an aggregate, may be associated with elevated HbA1c up to 6 years after exposure, with an inverted-U pattern.

ObjectivesTrichloroethylene, a chlorinated solvent widely used for metal degreasing, is classified by the International Agency for Research on Cancer as a kidney carcinogen. Other chlorinated solvents are suspected carcinogens, most notably the cleaning solvent perchloroethylene, although it is unclear whether they are associated with kidney cancer. We investigated kidney cancer associations with occupational exposure to 6 chlorinated solvents (trichloroethylene, perchloroethylene, 1,1,1-trichloroethane, carbon tetrachloride, chloroform, and methylene chloride) within a case–control study using detailed exposure assessment methods.MethodsCases (n=1217) and controls (n=1235) provided information on their occupational histories and, for selected occupations, on tasks involving potential exposure to chlorinated solvents through job-specific interview modules. Using this information, an industrial hygienist assessed potential exposure to each solvent. We computed ORs and 95% CIs for different exposure metrics, with unexposed participants as the referent group.Results1,1,1-trichloroethane, carbon tetrachloride, chloroform, and methylene chloride were not associated with kidney cancer. Among jobs with high exposure intensity, high cumulative hours exposed to perchloroethylene was associated with increased risk, both overall (third tertile vs unexposed: OR 3.1, 95% CI 1.3 to 7.4) and after excluding participants with ≥50% exposure probability for trichloroethylene (OR 3.0, 95% CI 0.99 to 9.0). A non-significant association with high cumulative hours exposed to trichloroethylene was observed (OR 1.7, 95% CI 0.8 to 3.8).ConclusionsIn this study, high exposure to perchloroethylene was associated with kidney cancer, independent of trichloroethylene. Additional studies are needed to further investigate this finding.

ObjectiveTo examine the relation between congenital heart defects (CHDs) in offspring and estimated maternal occupational exposure to chlorinated solvents, aromatic solvents and Stoddard solvent during the period from 1 month before conception through the first trimester.MethodsThe study population included mothers of infants with simple isolated CHDs and mothers of control infants who delivered from 1997 through 2002 and participated in the National Birth Defects Prevention Study. Two methods to assess occupational solvent exposure were employed: an expert consensus-based approach and a literature-based approach. Multiple logistic regression was used to calculate adjusted ORs and 95% CIs for the association between solvent classes and CHDs.Results2951 control mothers and 2047 CHD case mothers were included. Using the consensus-based approach, associations were observed for exposure to any solvent and any chlorinated solvent with perimembranous ventricular septal defects (OR 1.6, 95% CI 1.0 to 2.6 and OR 1.7, 95% CI 1.0 to 2.8, respectively). Using the literature-based approach, associations were observed for: any solvent exposure with aortic stenosis (OR 2.1, 95% CI 1.1 to 4.1) and Stoddard solvent exposure with d-transposition of the great arteries (OR 2.0, 95% CI 1.0 to 4.2), right ventricular outflow tract obstruction defects (OR 1.9, 95% CI 1.1 to 3.3) and pulmonary valve stenosis (OR 2.1, 95% CI 1.1 to 3.8).ConclusionsThe authors found evidence of associations between occupational exposure to solvents and several types of CHDs. These results should be interpreted in light of the potential for misclassification of exposure.

With the exception of lung cancer, the health effects associated with diesel exhaust for other cancers and nonmalignant health outcomes are not well understood. We 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 , to evaluate associations between mortality and diesel exhaust exposure. Quantitative 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). We observed an excess of death for cancers of the lung, trachea, and bronchus ( ; ; 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 ( ; ; 95% CI: 1.11, 1.42). Several nonmalignant diseases were associated with excess mortality among workers ever-employed underground, including ischemic heart disease ( ; 95% CI: 1.00, 1.16), cerebrovascular disease ( ; 95% CI: 1.04, 1.43), and nonmalignant diseases of the respiratory system ( ; 95% CI: 1.01, 1.26). Continuous 15-y lagged cumulative REC exposure was associated with increased lung cancer risk ( ; 95% CI: 1.24, 3.03), but the risk declined at the highest exposures ( ; 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 ( ; 95% CI: 1.00, 9.79; ). Increased 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.

Diesel exhaust (DE) is classified as a probable human carcinogen. Aims were to describe the major occupational uses of diesel engines and give an overview of personal DE exposure levels and determinants of exposure as reported in the published literature. Measurements representative of personal DE exposure were abstracted from the literature for the following agents: elemental carbon (EC), particulate matter (PM), carbon monoxide (CO), nitrogen oxide (NO), and nitrogen dioxide (NO 2 ). Information on determinants of exposure was abstracted. In total, 3528 EC, 4166 PM, 581 CO, 322 NO, and 1404 NO 2 measurements were abstracted. From the 10,001 measurements, 32% represented exposure from on-road vehicles and 68% from off-road vehicles (30% mining, 15% railroad, and 22% others). Highest levels were reported for enclosed underground work sites in which heavy equipment is used: mining, mine maintenance, and construction (EC: 27–658  μ g/m 3 ). Intermediate exposure levels were generally reported for above-ground (semi-) enclosed areas in which smaller equipment was run: mechanics in a shop, emergency workers in fire stations, distribution workers at a dock, and workers loading/unloading inside a ferry (generally: EC<50  μ g/m 3 ). Lowest levels were reported for enclosed areas separated from the source, such as drivers and train crew, or outside, such as surface mining, parking attendants, vehicle testers, utility service workers, surface construction and airline ground personnel (EC<25  μ g/m 3 ). The other agents showed a similar pattern. Determinants of exposure reported for enclosed situations were ventilation and exhaust after treatment devices. Reported DE exposure levels were highest for underground mining and construction, intermediate for working in above-ground (semi-) enclosed areas and lowest for working outside or separated from the source. The presented data can be used as a basis for assessing occupational exposure in population-based epidemiological studies and guide future exposure assessment efforts for industrial hygiene and epidemiological studies.

To obtain information on the safety and efficacy of the gluten-free/casein-free (GFCF) diet, we placed 14 children with autism, age 3–5 years, on the diet for 4–6 weeks and then conducted a double-blind, placebo-controlled challenge study for 12 weeks while continuing the diet, with a 12-week follow-up. Dietary challenges were delivered via weekly snacks that contained gluten, casein, gluten and casein, or placebo. With nutritional counseling, the diet was safe and well-tolerated. However, dietary challenges did not have statistically significant effects on measures of physiologic functioning, behavior problems, or autism symptoms. Although these findings must be interpreted with caution because of the small sample size, the study does not provide evidence to support general use of the GFCF diet.

ObjectivesTo inform the potential human carcinogenicity of acrylonitrile, we estimate associations between acrylonitrile exposures and lung cancer mortality in US workers with the objectives of (1) assessing potential for healthy worker survivor bias and (2) adjusting for this bias while assessing the expected lung cancer mortality under different hypothetical occupational exposure limits on acrylonitrile exposure using the parametric g-formula.MethodsWe used data from a cohort of 25 460 workers at facilities making or using acrylonitrile in the USA. We estimated HRs to quantify associations between employment and lung cancer mortality, and exposure and leaving employment. Using the parametric g-formula, we estimated cumulative lung cancer mortality at hypothetical limits on acrylonitrile exposure.ResultsRecent and current employment was associated with lung cancer, and exposure was associated with leaving employment, indicating potential for healthy worker survivor bias. Relative to no intervention, reducing the historical exposure under limits of 2.0, 1.0 and 0.45 parts per million would have been expected to reduce lung cancer mortality by age 90 by 4.46 (95% CI 0.78 to 8.15), 5.03 (95% CI 0.96 to 9.11) and 6.45 (95% CI 2.35 to 10.58) deaths per 1000 workers, respectively. A larger lung cancer mortality reduction would be expected under elimination of exposure: 7.21 (95% CI 2.72 to 11.70) deaths per 1000 workers.ConclusionsHealthy worker survivor bias likely led to underestimation of excess risk. Our results corroborate previous study findings of an excess hazard of lung cancer among the highest exposed workers.

The 2010 disaster led to the largest ever marine oil spill. Individuals who worked on the spill were exposed to toxicants and stressors that could lead to adverse effects. The GuLF STUDY was designed to investigate relationships between oil spill exposures and multiple potential physical and mental health effects. Participants were recruited by telephone from lists of individuals who worked on the oil spill response and clean-up or received safety training. Enrollment interviews between 2011 and 2013 collected information about spill-related activities, demographics, lifestyle, and health. Exposure measurements taken during the oil spill were used with questionnaire responses to characterize oil exposures of participants. Participants from Gulf states completed a home visit in which biological and environmental samples, anthropometric and clinical measurements, and additional health and lifestyle information were collected. Participants are being followed for changes in health status. Thirty-two thousand six hundred eight individuals enrolled in the cohort, and 11,193 completed a home visit. Most were young (56.2% ≤ 45 years of age), male (80.8%), lived in a Gulf state (82.3%), and worked at least 1 day on the oil spill (76.5%). Workers were involved in response (18.0%), support operations (17.5%), clean-up on water (17.4%) or land (14.6%), decontamination (14.3%), and administrative support (18.3%). Using an ordinal job exposure matrix, 45% had maximum daily total hydrocarbon exposure levels ≥ 1.0 ppm. The GuLF STUDY provides a unique opportunity to study potential adverse health effects from the oil spill.

Background: With the exception of lung cancer, the health effects associated with diesel exhaust for other cancers and nonmalignant health outcomes are not well understood. Objectives: We 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. Methods: Quantitative 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). Results: We 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 [micro]g/[m.sup.3]-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 ([HR.sub.Tertile3vs. Tertile1] =3.12; 95% CI: 1.00, 9.79; p-trend = 0.031). Discussion: Increased 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.