Dataset Information

Estimating population exposure to ambient polycyclic aromatic hydrocarbon in the United States - Part II: Source apportionment and cancer risk assessment.

ABSTRACT: A revised Community Multiscale Air Quality (CMAQ) model was developed to simulate the emission, reactions, transport, deposition and gas-to-particle partitioning processes of 16 priority polycyclic aromatic hydrocarbons (PAHs), as described in Part I of the two-part series. The updated CMAQ model was applied in this study to quantify the contributions of different emission sources to the predicted PAH concentrations and excess cancer risk in the United States (US) in 2011. The cancer risk in the continental US due to inhalation exposure of outdoor naphthalene (NAPH) and seven larger carcinogenic PAHs (cPAHs) was predicted to be significant. The incremental lifetime cancer risk (ILCR) exceeds 1×10-5 in many urban and industrial areas. Exposure to PAHs was estimated to result in 5704 (608-10,800) excess lifetime cancer cases. Point sources not related with energy generation and the oil and gas processes account for approximately 31% of the excess cancer cases, followed by non-road engines with 18.6% contributions. Contributions of residential wood combustion (16.2%) are similar to that of transportation-related sources (mostly motor vehicles with small contributions from railway and marine vessels; 13.4%). The oil and gas industry emissions, although large contributors to high concentrations of cPAHs regionally, are only responsible of 4.3% of the excess cancer cases, which is similar to the contributions of non-US sources (6.8%) and non-point sources (7.2%). The power generation units pose the most minimal impact on excess cancer risk, with contributions of approximately 2.3%.

SUBMITTER: Zhang J

PROVIDER: S-EPMC6205197 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature

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Estimating population exposure to ambient polycyclic aromatic hydrocarbon in the United States - Part II: Source apportionment and cancer risk assessment.

Zhang Jie J Wang Peng P Li Jingyi J Mendola Pauline P Sherman Seth S Ying Qi Q

Environment international 20160906

A revised Community Multiscale Air Quality (CMAQ) model was developed to simulate the emission, reactions, transport, deposition and gas-to-particle partitioning processes of 16 priority polycyclic aromatic hydrocarbons (PAHs), as described in Part I of the two-part series. The updated CMAQ model was applied in this study to quantify the contributions of different emission sources to the predicted PAH concentrations and excess cancer risk in the United States (US) in 2011. The cancer risk in the ...[more]

PMID: 27613001

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Project description:BackgroundPolycyclic aromatic hydrocarbons (PAHs) are ubiquitous organic compounds associated with chronic disease in epidemiologic studies, though the contribution of PAH exposure on fatal outcomes in the U.S. is largely unknown.ObjectivesWe investigated urinary hydroxylated PAH metabolites (OH-PAHs) with all-cause and cause-specific mortality in a representative sample of the U.S. population.MethodsStudy participants were ≥20 years old from the National Health and Nutrition Examination Survey 2001-2014. Concentrations (nmol/L) of eight OH-PAHs from four parent PAHs (naphthalene, fluorene, phenanthrene, pyrene) were measured in spot urine samples at examination. We identified all-cause, cancer-specific, and cardiovascular-specific deaths through 2015 using the National Death Index. We used Cox proportional hazards regression to estimate adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between ΣOH-PAHs and mortality endpoints. We assessed potential heterogeneity by age, gender, smoking status, poverty, and race/ethnicity. Additionally, we examined the overall mixture effect using quantile g-computation.ResultsIn 9,739 eligible participants, there were 934 all-cause deaths, 159 cancer-specific deaths, and 108 cardiovascular-specific deaths (median 6.75 years follow-up). A log10 increase in ΣOH-PAHs was associated with higher all-cause mortality (HRadj = 1.39 [95%CI: 1.21, 1.61]), and possibly cancer-specific mortality (HRadj = 1.15 [95%CI: 0.79, 1.69]), and cardiovascular-specific mortality (HRadj = 1.49 [95%CI: 0.94, 2.33]). We observed substantial effect modification by age, smoking status, gender, and race/ethnicity across mortality endpoints. Risk of cardiovascular mortality was higher for non-Hispanic blacks and those in poverty, indicating potential disparities. Quantile g-computation joint associations for a simultaneous quartile increase in OH-PAHs were HRadj = 1.15 [95%CI: 1.02, 1.31], HRadj = 1.41 [95%CI: 1.05, 1.90], and HRadj = 0.98 [95%CI: 0.66, 1.47] for all-cause, cancer-specific, and cardiovascular-specific mortalities, respectively.DiscussionOur results support a role for total PAH exposure in all-cause and cause-specific mortality in the U.S. population.

Dataset Information

Estimating population exposure to ambient polycyclic aromatic hydrocarbon in the United States - Part II: Source apportionment and cancer risk assessment.

Publications

Estimating population exposure to ambient polycyclic aromatic hydrocarbon in the United States - Part II: Source apportionment and cancer risk assessment.

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