Atmospheric nitrated polycyclic aromatic hydrocarbons (NPAHs), which have been shown to have adverse health effects such as carcinogenicity, are formed in part through nitration reactions of their parent polycyclic aromatic hydrocarbons (PAHs) in the atmosphere. However, little is known about heterogeneous nitration rates of PAHs by gaseous NO2 on natural mineral substrates, such as desert dust aerosols. Herein by employing kinetic experiments using a flow reactor and surface analysis by Fourier transform infrared spectroscopy with pyridine adsorption, we demonstrate that the reaction is accelerated on acidic surfaces of mineral dust, particularly on those of clay minerals. In support of this finding, we show that levels of ambient particle-associated NPAHs in Beijing, China, significantly increased during heavy dust storms. These results suggest that mineral dust surface reactions are an unrecognized source of toxic organic chemicals in the atmosphere and that they enhance the toxicity of mineral dust aerosols in urban environments.

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Chlorinated polycyclic aromatic hydrocarbons (Cl-PAHs) have recently been found in the environment at relatively high concentrations. However, their toxicological information has not been well documented. In this study, a 24 hr in vivo experiment was conducted to evaluate the sex-dependent difference of the acute toxicological effects of 7-chlorinated benz[a]anthracene (7-ClBaA) as a model Cl-PAH. 7-ClBaA or its parent chemical, BaA, was once orally administered to male or female ICR mice at concentrations of 1, 10, and 100 mg/kg body weight. The relative liver weights of the males were significantly increased at the highest dose of both chemicals compared to the vehicle controls, but the weights were comparable among all groups in the females. The plasma 7-ClBaA level was similar in both sexes, but significantly higher than that of BaA. 7-ClBaA dose-dependently induced expression of the genes Cyp1a1, 1a2, and 1b1 in the liver and lung, and these stimulations were significantly higher in both organs and genders at a dose of 100 mg/kg 7-ClBaA compared with an equivalent amount of BaA, except in the case of hepatic Cyp1a2 and 1b1 and pulmonary Cyp1a2 in the female mice. The results suggest that acute toxicity of 7-ClBaA is gender-and organ-specific, and female mice might be less sensitive to acute toxicity of both 7-ClBaA and BaA than the males.