Occupational exposure to unburnt bidi tobacco elevates mutagenic burden among tobacco processors.

The nature of mutagenic burden due to occupational exposure to tobacco flakes and dust was determined among 20 female tobacco processors (TP) and 20 matched controls (C) by testing urinary mutagenicity in the Ames assay. In addition, urinary cotinine was estimated as a marker of tobacco absorption. Workers and controls were sub-divided into those with no tobacco habit (NH) and those habituated to the use of masheri (a pyrolysed form of tobacco) as a dentifrice (MH). Cotinine was not detected in samples from C-NH while the mean urinary cotinine levels in TP-NH and TP-MH were significantly higher than that in C-MH (3.46 +/- 0.95 and 3.57 +/- 0.46 versus 1.80 +/- 0.58 mM/M creatinine; P < 0.02). The majority of the urine samples from C-NH were non-mutagenic in the presence or absence of rat liver S9 while those from C-H were mutagenic to TA98 and TA102 strains upon metabolic activation. On the other hand, direct mutagenicity to TA98, TA100 and TA102 strains respectively was noted in 6/10, 5/10 and 8/10 samples from TP-NH and 7/10, 4/10 and 3/10 samples from TP-M. Generally, beta-glucuronidase treatment reduced or abolished the mutagenic potential of workers' urine samples indicating that glucuronide conjugates may have partially contributed to direct mutagenicity. Experiments using scavengers of reactive oxygen species revealed that direct mutagenicity in TA102 strain was mediated mainly via hydroxyl radicals. The results clearly demonstrate that tobacco processors are exposed to a wide spectrum of mutagens that cause frame-shift, base pair substitution and oxidative damage.