A vast array of data suggests that early age of smoking onset enhances the risk for development of lung cancer in adulthood. Initiation of smoking at a young age may influence the development of lung cancer because of its effect on duration of smoking. Early onset of smoking also may serve as an independent risk factor. It may increase the likelihood that smoking occurs during a critical period of development that enhances susceptibility to the adverse effects of cancer causing agents in cigarette smoke, thereby facilitating the initiation of the carcinogenic process. While evidence for the latter hypothesis derives from a variety of sources, definitive proof has proven elusive. Whether or not early age of smoking serves as an independent risk factor for lung carcinogenesis, the consensus of the public health community is that prevention of smoking onset at a young age and early cessation are keys to stemming the current lung cancer pandemic. Population approaches to tobacco prevention and control, such as measures contained in the World Health Organization Framework Convention Tobacco Control Treaty, offer the best opportunity, on the scale needed, to create a smoke-free world and bring an end to the pandemic of tobacco-related disease. 1. Introduction Cigarette smoking has been called a pediatric disease [1]. Worldwide, between 82,000 and 99,000 young people begin smoking every day, 80% of them from low-income countries [2]. If current trends continue, more than 200 million young people under the age of 20 will die prematurely from tobacco-related diseases. More immediate effects on child health include higher rates of cough, fatigue and shortness of breath, and shortness of breath on exertion than youth who do not smoke. Those who smoke also are more prone to allergies, respiratory and ear infections, enhanced risk of asthma, and impaired lung growth [2]. In addition to immediate effects of cigarette smoking, early age at initiation of smoking increases the risk of lung cancer [3] and cardiovascular disease [4] during their life time. Of the organ sites at which smoking is known to cause cancer, smoking-associated genotoxic effects have been found for oral nasal, esophagus, pharynx, lung, pancreas, myeloid organs, bladder/ureter, and uterine cervix [2]. In addition to permanent changes in DNA, the reversibility of cancer risk after smoking cessation implies a role for epigenetic factors in carcinogenesis [2]. Initiation of cigarette smoking in childhood and adolescence plays a role in the development of lung cancer by virtue of its contribution to
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