Hyun-Woo Kim1, Sin Kam2, Duk-Hee Lee3. 1. Department of Family Medicine, Daegu Medical Center, 157 Pyungli-ro, Seo-Gu, Daegu 703-713, Republic of Korea. 2. Department of Preventative Medicine, School of Medicine, Kyungpook National University, 680 Gukchaebosang-ro, Jung-gu, Daegu 700-842, Republic of Korea. 3. Department of Preventative Medicine, School of Medicine, Kyungpook National University, 680 Gukchaebosang-ro, Jung-gu, Daegu 700-842, Republic of Korea. Electronic address: lee_dh@knu.ac.kr.
Abstract
BACKGROUND: Polycyclic aromatic hydrocarbons (PAHs) may be obesogens. However, the role of PAHs independent of environmental tobacco smoke (ETS) is unclear, and the interaction between PAHs and ETS remains unknown. METHODS: We performed cross-sectional analyses of urinary concentrations of PAH metabolites, body mass index (BMI), and waist circumference (WC) in 1985 people aged 6-18 years using data from the 2003-2008 U.S. National Health and Nutrition Examination Survey. ETS exposure level was measured as serum cotinine level. RESULTS: PAH metabolites were positively associated with BMI and WC in both the ETS-unexposed and ETS-exposed groups. The adjusted odds ratios for general obesity defined by age- and sex-specific BMI≥95th percentile across the quartiles of total PAH metabolites were 1, 4.51, 2.57, and 8.09 (Ptrend=0.003) in the ETS-unexposed group and 1, 2.02, 1.83, and 3.86 (Ptrend<0.001) in the ETS-exposed group. However, the association of PAH metabolites with obesity became stronger as serum cotinine levels increased (Pinteraction<0.05). Among those with high ETS exposure, the adjusted odds ratios for general obesity across quartiles of total PAH metabolites were 1, 2.89, 5.26, and 16.29 (Ptrend<0.001). Compared to the low PAH-exposure group without exposure to ETS, the high ETS- and high PAH-exposure group had 33.85- and 17.64-fold greater risks of general and central obesity, respectively. CONCLUSION: Environmental exposure to PAHs may be associated with childhood obesity irrespective of ETS. In particular, simultaneous exposure to PAHs and ETS may substantially increase the risk of obesity.
BACKGROUND:Polycyclic aromatic hydrocarbons (PAHs) may be obesogens. However, the role of PAHs independent of environmental tobacco smoke (ETS) is unclear, and the interaction between PAHs and ETS remains unknown. METHODS: We performed cross-sectional analyses of urinary concentrations of PAH metabolites, body mass index (BMI), and waist circumference (WC) in 1985 people aged 6-18 years using data from the 2003-2008 U.S. National Health and Nutrition Examination Survey. ETS exposure level was measured as serum cotinine level. RESULTS:PAH metabolites were positively associated with BMI and WC in both the ETS-unexposed and ETS-exposed groups. The adjusted odds ratios for general obesity defined by age- and sex-specific BMI≥95th percentile across the quartiles of total PAH metabolites were 1, 4.51, 2.57, and 8.09 (Ptrend=0.003) in the ETS-unexposed group and 1, 2.02, 1.83, and 3.86 (Ptrend<0.001) in the ETS-exposed group. However, the association of PAH metabolites with obesity became stronger as serum cotinine levels increased (Pinteraction<0.05). Among those with high ETS exposure, the adjusted odds ratios for general obesity across quartiles of total PAH metabolites were 1, 2.89, 5.26, and 16.29 (Ptrend<0.001). Compared to the low PAH-exposure group without exposure to ETS, the high ETS- and high PAH-exposure group had 33.85- and 17.64-fold greater risks of general and central obesity, respectively. CONCLUSION: Environmental exposure to PAHs may be associated with childhood obesity irrespective of ETS. In particular, simultaneous exposure to PAHs and ETS may substantially increase the risk of obesity.
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