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Background: During the 2010 Deepwater Horizon (DWH) disaster, response and cleanup workers were potentially exposed to toxic volatile components of crude oil. However, to our knowledge, no study has examined exposure to individual oil spill-related chemicals in relation to cardiovascular outcomes among oil spill workers. Objectives: Our aim was to investigate the association of several spill-related chemicals [benzene, toluene, ethylbenzene, xylene, n-hexane (BTEX-H)] and total hydrocarbons (THC) with incident coronary heart disease (CHD) events among workers enrolled in a prospective cohort. Methods: Cumulative exposures to THC and BTEX-H across the cleanup period were estimated via a job-exposure matrix that linked air measurement data with self-reported DWH spill work histories. We ascertained CHD events following each worker's last day of cleanup work as the first self-reported physician-diagnosed myocardial infarction (MI) or a fatal CHD event. We estimated hazard ratios (HR) and 95% confidence intervals for the associations of exposure quintiles (Q) with risk of CHD. We applied inverse probability weights to account for bias due to confounding and loss to follow-up. We used quantile g-computation to assess the joint effect of the BTEX-H mixture. Results: Among 22,655 workers with no previous MI diagnoses, 509 experienced an incident CHD event through December 2019. Workers in higher quintiles of each exposure agent had increased CHD risks in comparison with the referent group (Q1) of that agent, with the strongest associations observed in Q5 (range of HR = 1.14-1.44). However, most associations were nonsignificant, and there was no evidence of exposure-response trends. We observed stronger associations among ever smokers, workers with Conclusions: Higher exposures to volatile components of crude oil were associated with modest increases in risk of CHD among oil spill workers, although we did not observe exposure-response trends. https://doi.org/10.1289/EHP11859, Introduction The 2010 Deepwater Horizon (DWH) disaster was the largest marine oil spill in U.S. history. (1) An estimated 4.9 million barrels of crude oil were discharged into the Gulf [...]

Grilled, barbecued, and smoked meat intake, a prevalent dietary source of polycyclic aromatic hydrocarbon (PAH) carcinogens, may increase the risk of incident breast cancer. However, no studies have examined whether intake of this PAH source influences survival after breast cancer. We interviewed a population-based cohort of 1508 women diagnosed with first primary invasive or in situ breast cancer in 1996 and 1997 at baseline and again approximately five years later to assess grilled/barbecued and smoked meat intake. After a median of 17.6 years of follow-up, 597 deaths, of which 237 were breast cancer related, were identified. Multivariable Cox regression was used to estimate adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for mortality as related to prediagnosis intake, comparing high (above the median) to low intake, as well as postdiagnosis changes in intake, comparing every combination of pre-/postdiagnosis intake to low pre-/postdiagnosis intake. All statistical tests were two-sided. High prediagnosis grilled/barbecued and smoked meat intake was associated with increased risk of all-cause mortality (HR = 1.23, 95% CI = 1.03 to 1.46). Other associations were noted, but estimates were not statistically significant. These include high prediagnosis smoked beef/lamb/pork intake and increased all-cause (HR = 1.17, 95% CI = 0.99 to 1.38, Ptrend = .10) and breast cancer-specific (HR = 1.23, 95% CI = 0.95 to 1.60, Ptrend = .09) mortality. Also, among women with continued high grilled/barbecued and smoked meat intake after diagnosis, all-cause mortality risk was elevated 31% (HR = 1.31, 95% CI = 0.96 to 1.78). Further, breast cancer-specific mortality was decreased among women with any pre- and postdiagnosis intake of smoked poultry/fish (HR = 0.55, 95% CI = 0.31 to 0.97). High intake of grilled/barbecued and smoked meat may increase mortality after breast cancer.

BackgroundRecently, the International Agency for Research on Cancer (IARC) Programme for the Evaluation of Carcinogenic Risks to Humans has been criticized for several of its evaluations, and also for the approach used to perform these evaluations. Some critics have claimed that failures of IARC Working Groups to recognize study weaknesses and biases of Working Group members have led to inappropriate classification of a number of agents as carcinogenic to humans.ObjectivesThe authors of this Commentary are scientists from various disciplines relevant to the identification and hazard evaluation of human carcinogens. We examined criticisms of the IARC classification process to determine the validity of these concerns. Here, we present the results of that examination, review the history of IARC evaluations, and describe how the IARC evaluations are performed.DiscussionWe concluded that these recent criticisms are unconvincing. The procedures employed by IARC to assemble Working Groups of scientists from the various disciplines and the techniques followed to review the literature and perform hazard assessment of various agents provide a balanced evaluation and an appropriate indication of the weight of the evidence. Some disagreement by individual scientists to some evaluations is not evidence of process failure. The review process has been modified over time and will undoubtedly be altered in the future to improve the process. Any process can in theory be improved, and we would support continued review and improvement of the IARC processes. This does not mean, however, that the current procedures are flawed.ConclusionsThe IARC Monographs have made, and continue to make, major contributions to the scientific underpinning for societal actions to improve the public's health.

Background: During the 2010 Deepwater Horizon (DWH) disaster, controlled burning was conducted to remove oil from the water. Workers near combustion sites were potentially exposed to increased fine particulate matter [with aerodynamic diameter [less than or equal to] 2.5 [micro]m (P[M.sub.2.5])] levels. Exposure to P[M.sub.2.5] has been linked to decreased lung function, but to our knowledge, no study has examined exposure encountered in an oil spill cleanup. Objective: We investigated the association between estimated P[M.sub.2.5] only from burning/flaring of oil/gas and lung function measured 1-3 y after the DWH disaster. Methods: We included workers who participated in response and cleanup activities on the water during the DWH disaster and had lung function measured at a subsequent home visit (n = 2,316). P[M.sub.2.5] concentrations were estimated using a Gaussian plume dispersion model and linked to work histories via a job-exposure matrix. We evaluated forced expiratory volume in 1 s (FEV1; milliliters), forced vital capacity (FVC; milliliters), and their ratio (FEV1/FVC; %) in relation to average and cumulative daily maximum exposures using multivariable linear regressions. Results: We observed significant exposure-response trends associating higher cumulative daily maximum P[M.sub.2.5] exposure with lower FEV1 (p-trend = 0.04) and FEV1/FVC (p-trend = 0.01). In comparison with the referent group (workers not involved in or near the burning), those with higher cumulative exposures had lower FEV1 [-166.8 mL, 95% confidence interval (CI): -337.3, 3.7] and FEV1/FVC (-1.7, 95% CI: -3.6, 0.2). We also saw nonsignificant reductions in FVC (high vs. referent: -120.9, 95% CI: -319.4, 77.6; p-trend = 0.36). Similar associations were seen for average daily maximum P[M.sub.2.5] exposure. Inverse associations were also observed in analyses stratified by smoking and time from exposure to spirometry and when we restricted to workers without prespill lung disease. Conclusions: Among oil spill workers, exposure to P[M.sub.2.5] specifically from controlled burning of oil/gas was associated with significantly lower FEV1 and FEV1/FVC when compared with workers not involved in burning. https://doi.org/10.1289/EHP8930, Introduction The 2010 Deepwater Horizon (DWH) disaster was the largest marine oil spill in U.S. history (National Commission on the BP Deepwater Horizon Oil Spill and Offshore Drilling 2011). An [...]

Styrene, benzene, toluene, ethylbenzene, and xylenes (SBTEX) are established neurotoxicants. SBTEX contains hazardous air pollutants (HAPs) that are released from the petrochemical industry, combustion process, transport emission, and solvent usage sources. Although several SBTEX toxic assessment studies have been conducted, they have mainly relied on ambient measurements to estimate exposure and limit their scope to specific locations and observational periods. To overcome these spatiotemporal limitations, an air quality modeling system over the US Gulf region was created, predicting the spatially and temporally enhanced SBTEX modeling concentrations from May to September 2012. Due to the incompleteness of SBTEX in the official US Environmental Protection Agency (EPA) National Emission Inventory (NEI), the Hazardous Air Pollutions Imputation (HAPI) program was used to identify and estimate the missing HAP emissions. The improved emission data were processed to generate the chemically speciated hourly gridded emission inputs for the Comprehensive Air Quality Model with Extensions (CAMx) chemical transport model to simulate the SBTEX concentrations over the Gulf modeling region. SBTEX pollutants were modeled using the Reactive Tracer feature in CAMx that accounts for their chemical and physical processes in the atmosphere. The data show that the major SBTEX emissions in this region are contributed by mobile emissions (45 %), wildfire (30 %), and industry (26 %). Most SBTEX emissions are emitted during daytime hours (local time 14:00–17:00), and the emission rate in the model domain is about 20–40 t h -1 , which is about 4 times higher than that in the nighttime (local time 24:00–04:00, about 4–10 t h -1). High concentrations of SBTEX (above 1 ppb) occurred near the cities close to the I-10 interstate highway (Houston, Beaumont, Lake Charles, Lafayette, Baton Rouge, New Orleans, and Mobile) and other metropolitan cities (Shreveport and Dallas). High styrene concentrations were co-located with industrial sources, which contribute the most to the styrene emissions. The HAPI program successfully estimated missing emissions of styrene from the chemical industry. The change increased total styrene emissions by 22 %, resulting in maximum ambient concentrations increasing from 0.035 to 1.75 ppb across the model domain. The predicted SBTEX concentrations with imputed emissions present good agreement with observational data, with a correlation coefficient (R) of 0.75 (0.46 to 0.77 for individual SBTEX species) and a normalized mean bias (NMB) of -5.6 % (-24.9 % to 32.1 % for the individual SBTEX species), suggesting their value for supporting any SBTEX-related human health studies in the Gulf region. The SBTEX data were published at Zenodo (10.5281/zenodo.7967541) (Wang et al., 2023), and the HAPI tool was also published at Zenodo (10.5281/zenodo.7987106) (Wang and Baek, 2023). [ABSTRACT FROM AUTHOR]