ToxSci Advance Access originally published online on November 24, 2004
Toxicological Sciences 2005 84(1):81-87; doi:10.1093/toxsci/kfi043
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Toxicological Sciences vol. 84 no. 1 © Society of Toxicology 2005; all rights reserved.
Carcinogenic Activity of Cigarette Smoke Gas Phase and Its Modulation by Beta-Carotene and N-Acetylcysteine
Center for Health and the Environment, University of California, Davis, One Shields Avenue, Davis, California 95616
Received October 5, 2004; accepted November 15, 2004
Male strain A/J mice were exposed for six hours a day, five days a week for six months to either full tobacco smoke or to tobacco smoke drawn through a HEPA filter that removed more than 99% of particulate matter. After another four months in air, the animals were sacrificed and lung tumors were counted for calculation of multiplicities and incidences. Analysis of the chamber atmospheres showed that in the filtered smoke the concentrations of polycyclic aromatic hydrocarbons and tobacco smoke specific nitrosamines were reduced to from below 18% to even nondetectable levels of the original values measured in the unfiltered smoke. Aldehydes and other volatile organic compounds such as 1,3-butadiene, benzene, or acrolein were reduced to about 50 to 90% of the concentrations found in unfiltered smoke. Some potentially carcinogenic metals reached levels in filtered smoke ranging from 77% to less than 1% found in full smoke. The mice exposed to the filtered smoke atmosphere had practically identical lung tumor multiplicities and incidence as had the animals exposed to full smoke, significantly higher than in air exposed controls. Diets containing 0.5% ß-carotene or 0.4% N-acetylcysteine afforded some chemoprevention. It was tentatively concluded that 1,3-butadiene might be an important contributor to lung tumorigenesis in this mouse model of tobacco smoke carcinogenesis.
Key Words: tobacco smoke; mice; strain A/J mice; lung tumors; 1,3-butadiene.
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