Evaluation of Chromosome Aberrations in Subjects Exposed to Environmental Tobacco Smoke in Tamilnadu, India V. Balachandar Æ B. Lakshman Kumar Æ K. Suresh Æ K. Sasikala Received: 19 September 2007 / Accepted: 4 June 2008 / Published online: 15 July 2008 Ó Springer Science+Business Media, LLC 2008 Abstract Numerous expert panels have concluded that there is sufficient evidence to classify involuntary smoking (or passive smoking) as carcinogenic to humans. The aim of this study is to establish whether passive smoking increases the frequency of chromosomal aberrations (CA) in peripheral blood lymphocytes compared to controls in Tamil Nadu, India. In the present study, CA increased with an increase in environmental tobacco smoke (ETS) and active smoke exposure period in passive smokers quanti- fied on the basis of serum cotinine levels. The passive subjects were compared with healthy normal controls to validate the results. In conclusion, these data are compat- ible with the current knowledge on the mechanisms of carcinogenesis of tobacco-related cancers, occurring not only in active smokers but with a high biological plausi- bility also in passive smokers. Keywords Passive smoking Á Chromosomal aberrations Á Serum cotinine It has been estimated that the annual mortality associated with cigarette smoking was 3 million in 1990, 4 million in 1998, and is expected to rise up to 8.4 million in 2020 (WHO 2002). In India, the smoking habits in lower and middle socio-economic class are more common among men than women (Gupta 1996; WHO 1997). Cigarette smoking is responsible for the vast majority of lung cancers and is associated with cancers of the mouth, pharynx, larynx, oesophagus, stomach, pancreas, kidney, ureter, bladder, colon and uterine cervix. Interestingly, exhaustive report on health consequences of involuntary smoking by the United States Surgeon General (DHHS 1984) and reports by the United States Environmental Protection Agency (US EPA 1992) highlighted the increased risks of several diseases similar to those seen among smokers, in persons exposed to passive smoking or environmental tobacco smoking (ETS) at home or at work place. Passive smoke exposure is a cause of cardiovascular disease, can- cer, and respiratory disease (DHHS 2006; Hozawa et al. 2006). Most of the chemicals found in cigarette smoke are genotoxic (IARC 1986), and therefore, chromosome dam- age appears to be an excellent biomarker for determining the effect of exposure to smoking. The chromosomal aberrations (CA) assay is important for monitoring the populations exposed to genotoxic agents because it allows the evaluation of the entire genome to identify mutagenic and carcinogenic chemicals (Au et al. 1998). Therefore, the analysis of CA in peripheral blood lymphocytes can be used as a biomarker of health outcome, measuring genetic damage due to exposure that results from non-repaired primary lesions. Numerous studies have been conducted using the CA assay to monitor the effect of cigarette smoking but the results are inconsistent. While a large population study indicated that CA frequencies in lym- phocytes were not increased by smoking (Bender et al 1988) another showed that smoking caused a 10–20% increase (NST 1990). The spouse, child and close associates face the conse- quence without being directly involved in active smoking. One of the very difficult tasks in most studies on passive smoking is to quantify an ETS and active smoke exposure. The number of cigarettes was the best measure of exposure to husbands’ smoking, while exposure at workplace was more V. Balachandar (&) Á B. L. Kumar Á K. Suresh Á K. Sasikala Division of Human Genetics, Department of Zoology, Bharathiar University, Coimbatore 641046, India e-mail: geneticbala@yahoo.co.in 123 Bull Environ Contam Toxicol (2008) 81:270–276 DOI 10.1007/s00128-008-9489-3