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Polychlorinated Biphenyls and Pulmonary Hypertension

同族 全国健康与营养检查调查 医学 人口 参考剂量 风险评估 体质指数 生理学 环境卫生 内科学 毒理 环境化学 化学 生物 计算机安全 计算机科学
作者
Hamza Assaggaf,Changwon Yoo,Roberto Lucchini,Stephen M. Black,Munerah Hamed,Faisal Minshawi,Quentin Felty
出处
期刊:International Journal of Environmental Research and Public Health [Multidisciplinary Digital Publishing Institute]
卷期号:19 (8): 4705-4705 被引量:2
标识
DOI:10.3390/ijerph19084705
摘要

Polychlorinated biphenyls (PCBs) are persistent environmental pollutants that were banned because of their potential carcinogenicity. Population studies have shown that PCBs are associated with lung toxicity and hypertension. The objective of this study was to evaluate whether higher exposure to PCB congeners is associated with the risk of pulmonary hypertension. Serum levels of PCBs in 284 subjects with combined risk factors for pulmonary arterial hypertension (PAH) were compared to 4210 subjects with no risk for PAH using the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2004. The major findings from this study include significantly higher PCB levels in PAH subjects compared to non-PAH subjects; for example, the geometric mean (GM) of PCB74 was 15.91 (ng/g) (14.45-17.53) vs. 11.48 (ng/g) (10.84-12.16), respectively. Serum levels of PCB congeners showed an increasing trend in the age group 20-59 years as PCB180 GM was 19.45 (ng/g) in PAH vs. 12.75 (ng/g) in the control. A higher body burden of PCB153 followed by PCB138, PCB180, and PCB118 was observed. Estimated age, race, BMI, and gender-adjusted ORs for PCB congener levels in subjects with the combined risk factors for PAH compared to controls was significant; for example, PCB99 (OR: 1.5 (CI: 1.49-1.50). In summary, these findings indicate that exposure, as well as body burden estimated based on lipid adjustment of PCBs, were higher in people with risk factors for PAH, and PCB congeners accumulated with age. These findings should be interpreted with caution because of the use of cross-sectional self-reported data and a small sample size of subjects with combined risk factors for pulmonary arterial hypertension. Nonetheless, our finding emphasizes a need for a comprehensive environmental molecular epidemiologic study to determine the potential role of environmental exposures to PCBs in the development of pulmonary arterial hypertension.

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