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Indian Pediatr 2012;49: 948-949 |
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Secondary Cigarette Smoke Causes DNA Damage:
Susceptibility for Disease Development
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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]
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E xposure 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.
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