Cancers of the colon are most common in the Western world. In majority of these cases, there is no familial history and sporadic gene damage seems to play an important role in the development of tumors in the colon. Studies have shown that environmental factors, especially diet, play an important role in susceptibility to GI tract cancers. Consequently, environmental chemicals that contaminate food or diet during its preparation becomes important in the development of GI cancers. Polycyclic aromatic hydrocarbons (PAHs) are one such family of ubiquitous environmental toxicants. These pollutants enter the human body through consumption of contaminated food, drinking water, inhalation of cigarette smoke, automobile exhausts, and contaminated air from occupational settings. Among these pathways, dietary intake of PAHs constitutes a major source of exposure in humans. Although many reviews and books on PAHs and their ability to cause toxicity and breast or lung cancer have been published, aspects on contribution of diet, smoking and other factors towards development of digestive tract cancers and strategies to assess risk from exposure to PAHs have received much less attention. This review, therefore, focuses on dietary intake of PAHs in humans, animal models, and cell cultures used for GI cancer studies along with epidemiological findings. Bioavailability and biotransformation processes, which influence the disposition of PAHs in body and the underlying causative mechanisms of GI cancers, are also discussed. The existing data gaps and scope for future studies is also emphasized. This information is expected to stimulate research on mechanisms of sporadic GI cancers caused by exposure to environmental carcinogens.

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Many anti-neoplastic drugs are used globally during chemotherapy in the treatment of cancer. However, occupational exposure to anti-cancer drugs can represent a potential health risk to humans. Investigations on the genotoxicity of these drugs are inconsistent. Further, information on the genotoxic potential of anti-neoplastic drugs in medical personnel from India is not available. Hence, the aim of this study was to carry out genotoxicity monitoring of nurses from the oncology department of a hospital in South India, occupationally exposed to anti-neoplastic drugs under routine working conditions. The level of genome damage was determined in whole blood with the comet assay as well as micronucleus test (MNT) and in buccal epithelial cells with MNT alone of 60 nurses handling anti-neoplastic drugs and 60 referents matched for age and sex. Urinary cyclophosphamide (CP), used as a marker for drug absorption, was also measured in the urine of the nurses. The DNA damage observed in the lymphocytes of exposed nurses was significantly higher than the controls. Similarly, a significant increase in micronuclei (MN) frequency with peripheral blood lymphocytes and buccal cells was observed in the exposed nurses compared to controls (P < 0.05). Multiple regression analysis showed that occupational exposure and age had a significant effect on mean comet tail length as well as on frequency of MN. The mean value of CP in urine of the nurses handling anti-neoplastic drugs was (mean +/- standard deviation; 0.44 +/- 0.26 microg/ml). Our study has shown that increased genetic damage was evident in nurses due to occupational exposure to anti-neoplastics. This data corroborate the need to maintain safety measures to avoid exposure and the necessity of intervention in the case of exposure when using and handling anti-neoplastic drugs.

Information on potential genetic damage in humans after exposure to waste anaesthetic gases in Indian hospitals is scarce. To evaluate the possible genotoxic effects of waste anaesthetic gases, the chromosomal aberrations analysis and comet assay were studied in peripheral blood lymphocytes in 45 operating room personnel currently employed at a hospital in South India. In addition, the micronucleus test on buccal epithelial cells was also carried out in the same subjects. The exposed group was compared with a group of 45 non-exposed group, matched by age, sex, alcohol consumption and smoking habits. The results showed a statistically significant increase in DNA damage by the comet assay in the exposed group. Chromosome aberrations and micronucleus frequencies also increased significantly in the study subjects in comparison to the controls. Analysis of variance showed that smoking had a significant effect on DNA mean tail length, whereas alcohol consumption, duration of exposure to anaesthetic agents, age and gender had no significant effect. All the confounding factors had significant effect by the micronucleus test. However, smoking, alcohol consumption, age, gender and years of exposure showed no significant effect by the chromosome aberrations test. The results of our study suggest that exposure to waste anaesthetic gases has the potential to cause changes in the human genome.

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