Essay: Tobacco related cancer

Tobacco related cancer is the most common malignancy, and one of the most lethal. The role of tobacco smoking in the etiology of cancer disease has been well known for many decades, and any approach aimed at expediting the detection of population sub-groups at increased risk should be considered a high priority task. It may be possible to use genotoxicity assays to identify which sub-groups of smokers are more susceptible to the DNA-damaging effect of cigarette smoke and/or which level of smoking produces significant increases in mutation over base-line. Many of the substances contained in cigarette smoke are genotoxic causing carcinogenesis in man and therefore cytogenetic damage seems to be an excellent biomarker for determining the effect of exposure to chromosome-damaging agents in smoke.
Anderson et al. (1988) found no influence of smoking on chromosome aberrations. However, many reports confirm significant effect of smoking on chromosome aberrations (Obe and Herha 1978; Lambert et al. 1978; Vijaylaxmi and Evans 1982: Yadav and Thakur 2000b; Yadav et al. 2001b, c). Smokers engaged in different occupations like farming and workers in industries are exposed to variety of chemicals. Most of chemicals used by industry workers and pesticide sprayers have produced chromosomal damage in human somatic cells (Van Bao et al. 1974; Fredga et al. 1982; Rita et al. 1987; Sharma and Sobti 1988; Rupa et al. 1989; Yadav and Kaushik 1996a;Yadav and Seth 1998a,b; Yadav et al. 2001a, b, c).
The analysis of chromosomal aberrations has gained increasing popularity as an in vitro genotoxicity test and an assay for human genotoxic exposure and effect. The main reasons for this development are obvious. The scoring of the Giemsa stained Chromosomal aberrations is simpler, requires shorter training and is less time consuming.
Sierra et al (2004) showed that the frequency was significantly higher in smokers than in non-smokers showing the highest number of Chromosomal Aberrations (CA) among heavy smokers (>20 pack-years). In addition, a significant positive correlation was found between the frequency of CA and the intensity of smoking in pack-years. The present report confirms these findings. Two studies on chromosomal aberrations in leukocyte cultures, smokers (Uma et al. 2011) and tobacco related oral cancer (Uma et al. 2014 a) and two studies on the micronucleus assay in the exfoliative buccal cells of tobacco related oral cancer conducted by Uma et al (2014 b,c) on the Pondicherry population showed a significant elevation of chromosomal damage indicating the population to be at a high risk for cancer.
A number of studies have been designed to evaluate the potential influence of background factors such as gender, age, or smoking habit on Chromosomal aberrations frequency. Many of these studies suffer from a poor assessment of exposure, and subjects are often roughly classified as smokers versus non-smokers, without considering the levels of cigarette consumption. The evaluation of smoking cessation is even more difficult, because former smokers sometimes are included in the group of current smokers, and sometimes with non-smokers. The planning and high-quality information regarding smoking habit is the best approach to understand the possible use of Chromosomal aberrations as a marker of exposure/effect on the chromosomes of tobacco smokers.
Keeping the above criteria in mind , in the present study all the samples ( Smoker and Non Smokers) was taken from a small village population with agricultural background , low social strata, with a mean age of 40 years, same sex and smoking habits ( exclusively active smokers only ) based on their smoking index.
The results showed that among the smokers there were aberrant chromosomes with breaks and fragments in smokers of smoking index greater than 300 (Table 2 ) indicating that smoker who smoked more than 20 cigarettes per day suffer greater genotoxic effects in their lymphocytes caused by cigarette smoke constituents than their other nonsmoking and smoking counterparts (smoker I and II) and further indicating a high risk of carcinogenic activity in them. Thus, there is a significant positive correlation in the frequency of Chromosome aberration and the intensity of smoking in heavy smokers (smoker group III) (Sierra et al, 2004) making this group of smokers more prone to cancer in immediate future.
Conclusion
This study has been performed as a small community service, to verify, not only the genotoxic effect of cigarette smoke on chromosomes based on the smoking index, but also efforts have been taken to tell the agricultural people of the small village in Pondicherry, the real ill-effect it would cause in due course of time like lung cancer , coronary artery disease, chronic obstructive pulmonary diseas , hypertension and oral carcinoma and also to reinforce smoking cessation in them.
The present study indicates that the genotoxic effects in lymphocytes of the agricultural population of smokers who smoke more than 20 cigarettes per day are most likely caused by cigarette smoke constituents indicating that they fall under the category of high risk group to neoplastic disease in near future. Such findings may provide scientific evidence to encourage national campaigns to prevent tobacco consumption and devise intervention strategies that might reduce the persisting morbidity and mortality from smoking related cancer.