Secondary Cigarette Smoke Causes DNA Damage: Susceptibility for Disease Development

editorial

Indian Pediatr 2012;49: 948-949

Secondary Cigarette Smoke Causes DNA Damage: Susceptibility for Disease Development

Basu Dev Banerjee and Smita Jain

Environmental Biochemistry and Molecular Biology Laboratory, Department of Biochemistry, University College of Medical Sciences, University of Delhi, and Guru Teg Bahadur Hospital, Delhi, India.
Email: [email protected]

Exposure to secondary cigarette smoke, also called environmental tobacco smoke (ETS) or second hand smoke occurs when a person (non-smoker) encounters smoke either produced from burning cigarette or exhaled from smoker. ETS is a significant health problem in children worldwide. Cigarette smoke inhalation causes cancer in various organs and smoking during pregnancy harms both mother and baby, initially retarding intrauterine development with several side-effects [1]. Various respiratory diseases such as asthma and bronchiolitis can be seen in children, even at low-level exposure to environmental cigarette smoke [2, 3]. Cigarette smoke contains several reactive oxygen species (ROS) which may damage lipids, proteins, DNA, carbohydrates and other biomolecules. Most ROS have a short half-life and cause damage locally except H2O2 which has a relatively long half-life and can travel long distances causing DNA damage at distant sites. Increased production of ROS leads to an imbalance between the oxidative forces and the antioxidant defence systems, favoring an oxidative stress or injury. ROS can influence cell survival and genomic stability.

Exposure to cigarette smoke is a significant health problem in Turkey with the prevalence of 81.6% in home and 85.9% outside the home in the children aged 13-15-years [4]. Cigarette smoke contains various substances which stimulate the increased productivity of free radicals in vivo and thus disturb the oxidant: antioxidant homeostasis. Free radicals after binding to macro-molecules oxidize them and lead to the production of adducts which interfere with normal cellular processes. The authors have demonstrated increased oxidative stress and DNA damage in cigarette smoke-exposed group; however, the total antioxidants level remained unaltered. Moreover, high cotinine levels in urine as observed after exposure to cigarette smoke were found to be significantly correlated with total oxidative stress (TOS), oxidative stress index (OSI) and DNA damage. DNA damage induced by ROS may contribute to increased mutation rates, genome instability, apoptosis and associated tissue regeneration and cell proliferation [5].

The intensity of smoke induced oxidative damage varies with the degree or frequency of exposure to cigarette smoke. Measuring the degree of passive smoking is of critical importance regarding the toxic effect and various health problems such as asthma and bronchiolitis, which are prevalent in children. The authors have shown significantly higher DNA damage and OSI in the group exposed to more than 10 cigarettes per day (although the statistical value was low because the number in the group was low) as compared to group exposed to <10 cigarettes per day. Effect of secondary cigarette smoke on TAS was not evident in either of the exposure groups. This unresponsiveness of TAS can be explained on the basis of inter-individual genetic variation which is reflected in differential antioxidant capacities in different individuals of a population [6]. This study has shown that secondary cigarette smoke is common and harmful in children and may increase the risk of carcinogenesis by inducing oxidative stress and DNA damage. The study has proved that OS and DNA damage are correlated events and together may enhance the risk of cancer in genetically predisposed individuals. The only limitation was insufficient number of control cases besides the widespread exposure to second hand cigarette smoke in the study population. Several multi-centric or large cohort studies aimed at determining the relationship between DNA damage occurring in children exposed to cigarette smoke and the development of cancer are further required to validate the findings of the present study. Moreover, this study will lay foundation for identifying potential ill-effects of passive smoking with reference to health and diseases which are otherwise overlooked in present scenario.

Competing interests: None stated; Funding: Nil.

References

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