Pulmonary Inflammation and DNA Adducts in Rats Inhaling Diesel Exhaust or Carbon Black

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Abstract
Inhaled diesel exhaust has been shown to be carcinogenic to rats. Two mechanisms have been suggested: a genotoxic effect of organic compounds associated with the diesel soot, and an epigenetic effect resulting from large accumulations of particles that produce chronic inflammation and epithelial proliferation in the lung. To gain insights into the possible roles of these two mechanisms, we compared inflammatory responses and DNA adducts in lungs of rats exposed to diesel exhaust (33% extractable organic compounds by mass) and carbon black (0.04% extractable), which are similar carbonaceous particles with virtually no organic compounds. Male rats were exposed 7 h/day, 5 days/wk for 12 wk to diesel exhaust or carbon black, both at a concentration of 70.0 mg/m3, or to filtered air: Both diesel exhaust and carbon black exposures caused mild inflammation in the lung, as evidenced by increases in numbers of neutrophils and in the protein content of bronchoalveolar lavage fluids. The levels of DNA adducts, as measured by 32P postlabeling, were increased more by exposure to diesel exhaust than to carbon black. Although it remains unclear whether the carcinogenicity of diesel exhaust is related primarily to DNA injury or primarily to the loading of the lung with particles, our findings are consistent with an initiation-promotion mechanism that involves both DNA damage and lung inflammation.

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