Purpose: Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental toxic compounds formed from incomplete combustion of carbon-containing materials, cigarette smoking, and food cooking. The genotoxic effects of PAHs have been widely studied. However, their nongenotoxic effects such as their impacts on glucose and metabolic homeostasis have not been well examined.
Methods: We used the National Health and Nutritional Examination Survey (NHANES) 2001-2008 to investigate the associations between eight monohydroxy urinary metabolites of four PAHs and glucose homeostasis as well as metabolic syndrome in 1,878 nondiabetic participants aged 18 years or older.
Results: In linear regression models, increased level of 2-PHEN was significantly associated with increased insulin resistance (β coefficient 0.05 ± 0.02), and increased concentrations of 3-FLUO (β coefficient -0.02 ± 0.01) were significantly associated with decreased β-cell function (all p<0.05) after controlling for selected covariates. In addition, increased concentrations of 2-FLUO (OR=1.25, 95% CI: 1.04-1.51), 1-PHEN (OR=1.36, 95% CI: 1.09-1.70), and 2-PHEN (OR: 1.49, 95% CI: 1.22-1.83) were significantly associated with a higher prevalence of the metabolic syndrome after adjusting for covariates. Consistent results were observed in the subgroup analysis among nonsmokers.
Conclusions: Our findings suggest that environmental exposure to PAHs independent of cigarette smoking is associated with insulin resistance, β-cell dysfunction, and increased prevalence of metabolic syndrome.
Keywords: Insulin resistance; Metabolic syndrome; NHANES; OH-PAHs; Polycyclic aromatic hydrocarbons (PAHs); β-Cell function.
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