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GENOTOXICITY OF TEN CIGARETTE SMOKE CONDENSATES IN FOUR TEST SYSTEMS: COMPARISONS AMONG ASSAYS AND CONDENSATES
Citation:
DEMARINI, D. M., R. GUDI, A. SZKUDLINSKA, M. RAO, L. RECIO, M. KEHL, P. E. KIRBY, G. POLZIN, AND P. I. RICHTER. GENOTOXICITY OF TEN CIGARETTE SMOKE CONDENSATES IN FOUR TEST SYSTEMS: COMPARISONS AMONG ASSAYS AND CONDENSATES. Presented at 38th Annual Meeting of the Environmental Mutagen Society, Atlanta, GA, October 20 - 24, 2007.
Impact/Purpose:
Here we report on the genotoxicity of 10 CSCs prepared from commercial cigarettes.
Description:
The particulate fraction of cigarette smoke, cigarette smoke condensate (CSC), is genotoxic in many short-term in vitro tests and carcinogenic in rodents. However, no study has evaluatedd a set of CSCs prepared from a diverse set of cigarettes in a variety of short-term genotoxicity tests. Here we report on the genotoxicity of 10 CSCs prepared from commercial cigarettes that ranged from ultra-low tar (≤6.5 mg) to full flavor (>14.5 mg), a reference cigarette blended to be representative of a U.S. low tar cigarette, and also experimental cigarettes constructed of a single tobacco type. All cigarettes were machine smoked by the Federal Trade Commission (FTC) method, and one was also smoked by the Massachusetts intense method. The CSCs were tested in the presence of Aroclor-induced, rat-liver S9 mix in the Salmonella plate-incorporation assay in the frameshift strains TA98 and YG1041, the micronucleus and comet assays in L578Y/Tk+/-7.3.2C mouse lymphoma cells, and an assay for chromosomal aberrations in CHO-K1 cells. All 10 CSCs were mutagenic in both strains of Salmonella, and their potencies ranked similarly between the two strains, ranging over 7 fold. All 10 CSCs induced micronuclei, and their potencies ranged over 3 fold. All CSCs but one induced DNA damage (comet assay), and their potencies ranged over 20 fold. All CSCs but one induced chromosomal aberrations, and their potencies ranged over 4 fold. The smoking-machine conditions did not produce a consistent effect on the genotoxic potency of the CSCs across the assays. There was no relationship among the genotoxic potencies of the CSCs across the assays, and a qualitative advantage of the addition of the other assays to the Salmonella assay was not supported by our findings. Because of compensatory smoking habits and other factors, measurements of mutagenic activity of CSCs in any of the assays used in the present study have qualitative, but not quantitative value in assessing risk of cigarette types and cigarette smoking to human health.