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 mutagenicity in the Ames assay. In addition, urinary continine 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 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 higer 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-MH were mutagenic to TA98,TA100 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-MH. Generally, ß-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 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

Mutagenic potential of Indian tobacco products

The mutagenic potential of aqueous extracts of masheri (ME), chewing tobacco alone (CTE) and a mixture of chewing tobacco plus lime (CTLE) was tested using the Ames assay. ME exhibited mutagenicity in Salmonella typhimurium TA98 upon metabolic activation with aroclor-1254-induced rat liver S9, while nitrosation rendered it mutagenic in TA100 and TA102. CTE exhibited borderline mutagenicity in the absence or presence of S9 in TA98 and TA100 and after nitrosation in TA102, while nitrosation led to doubling of TA98 and TA100 revertants. In contrast, CTLE exhibited direct mutagenicity in TA98, TA100 and TA102, was mutagenic to TA98 upon S9 addition and induced mutagenic responses in all three tester strains after nitrosation. Experiments using scavengers of reactive oxygen species (ROS) suggested that CTLE-induced oxidat-ive damage in TA102 was mediated by a variety of ROS. The high mutagenic potency of CTLE vis a vis that of CTE may be attributed to changes in the pH leading to differences in the amount and nature of compounds extracted from tobacco. Thus, exposure to a wide spectrum of tobacco-derived mutagcns and promutagens may play a critical role in the development of oral cancer among users of tobacco plus lime

Occupational exposure to tobacco and resultant genotoxicity in bidi industry workers

In India, over 3 million workers employed in the bidi industry receive massive, chronic exposure to unburnt tobacco, mainly by the cutaneous and nasopharyngeal routes. While the hazards of habitual tobacco usage are well established, very little information is available about the effects of occupational tobacco exposure. In the present study, tobacco processing plant workers (TPPW) and bidi rollers (BR) with or without tobacco habits were monitored for occupation-related exposure to tobacco and resultant genotoxicity. Salivary cotinine levels were determined as an index of tobacco exposure and micronucleated buccal epithelial cell (MNC) frequency was recorded as a genotoxic endpoint. Occupational tobacco exposure led to the detection of cotinine in the saliva of 19% of BR and 100% of TPPW with no tobacco habit (NH). The greater degree of exposure in TPPW was evident from the significantly higher mean salivary cotinine level in TPPW-NH as compared to BR-NH (2.86 ± 0.48 vs. 0.84 ± 0.26 μg/ml; p < 0.01). The effect of occupational exposure was also evident in TPPW and BR with the masheri habit. A moderate but statistically significant increase in MNC frequency was observed in habit-free as well as masheri-habituated TPPW and BR as compared with the respective controls. The findings provide preliminary evidence for the clastogenic effects of occupational tobacco exposure

Mutagenicity of processed bidi tobacco: possible relevance to bidi industry workers

The genotoxic potential of bidi tobacco was evaluated by mutagenicity testing of aqueous, aqueous: ethanolic, ethanolic and chloroform extracts of processed tobacco used in the manufacture of 'bidis', indigenous forms of cigarettes smoked in India. The Salmonella/mammalian microsome test (Ames assay) was used to detect mutagenicity in tester strains TA98, TA100 and TA102. The extracts were tested in the absence and presence of metabolic activation using liver S9 from rat and hamster, and following in vitro nitrosation with sodium nitrite at acidic pH. All the extracts were non-mutagenic in the absence of nitrosation. The nitrosated aqueous extract was mutagenic in strains TA98 and TA100. While weak mutagenicity was elicited by the nitrosated aqueous: ethanolic extract in TA100, the nitrosated ethanolic extract induced a 3-fold increase in the number of revertants in the same strain. Moreover both these extracts elicited a strong mutagenic response in TA102, while the chloroform extract was non-mutagenic even after nitrite treatment. The present study indicates that workers employed in the bidi industry are exposed to potentially mutagenic and genotoxic chemicals in the course of their occupation

Biological monitoring of bidi industry workers occupationally exposed to tobacco

Ambient and biological monitoring was undertaken among tobacco processors who are chronically exposed to tobacco particulates via nasopharyngeal and cutaneous routes. Ambient monitoring revealed that the inspirable dust concentration was 150-fold higher in the tobacco factory than in the control environment, and was associated with chronic bronchitis in workers. Increased systemic exposure to tobacco constituents was evident from the high levels of cotinine, thioethers, promutagens and direct acting mutagens in workers' urine. The mean glutathione level and glutathione S-transferase activity were significantly lower in the peripheral blood lymphocytes of workers; however, the frequency of the GSTM1 null allele was similar to that in controls. A significant increase in chromosomal damage was noted in target and non-target cells of tobacco processors. In view of the association between tobacco use and several non-communicable diseases, the findings of the present study indicate an urgent need to minimize tobacco exposure among the processors