Abstract
In addition to the well-known link between smoking and lung cancer, large epidemiological studies have shown a relationship between smoking and cancers of the nose, oral cavity, oropharynx, larynx, esophagus, pancreas, bladder, kidney, stomach, liver, colon and cervix, as well as myeloid leukemia. Epidemiological evidence has reported a direct link between exposure of non-smokers to environmental tobacco smoke and disease, most notably, lung cancer. Much evidence demonstrates that carcinogenic-DNA adducts are useful markers of tobacco smoke exposure, providing an integrated measurement of carcinogen intake, metabolic activation, and delivery to the DNA in target tissues. Monitoring accessible surrogate tissues, such as white blood cells or bronchoalveolar lavage (BAL) cells, also provides a means of investigating passive and active tobacco exposure in healthy individuals and cancer patients. Levels of DNA adducts measured in many tissues of smokers are significantly higher than in non-smokers. While some studies have demonstrated an association between carcinogenic DNA adducts and cancer in current smokers, no association has been observed in ex or never smokers. The role of genetic susceptibility in the development of smoking related-cancer is essential. In order to establish whether smoking-related DNA adducts are biomarkers of tobacco smoke exposure and/or its carcinogenic activity we summarized all data that associated tobacco smoke exposure and smoking-related DNA adducts both in controls and/or in cancer cases and studies where the effect of genetic polymorphisms involved in the activation and deactivation of carcinogens were also evaluated. In the future we hope we will be able to screen for lung cancer susceptibility by using specific biomarkers and that subjects of compared groups can be stratified for multiple potential modulators of biomarkers, taking into account various confounding factors.
Highlights
Tobacco is the single most preventable cause of death in the world today, it has been estimated to have killed more than five million people in 2008 and will be responsible for the death of more than eight million by 2030 [1]
Since the aim of this review is the evaluation of carcinogenic-DNA adducts as biomarkers of tobacco smoke exposure and its carcinogenic activity we reported studies that measured smokingrelated DNA adducts as biomarkers of tobacco smoke exposure both in cancer cases and healthy smokers and non-smoker subjects [18,19,20,21,22,23,24,25]
In our review we considered studies that took into account the effect of genetic polymorphisms involved in the activation and deactivation of carcinogens on DNA adduct levels
Summary
Tobacco is the single most preventable cause of death in the world today, it has been estimated to have killed more than five million people in 2008 and will be responsible for the death of more than eight million by 2030 [1]. While many countries have adopted consistent policies against its use in public places, there are still approximately 1.3 billion smokers in the world and hundreds of millions of smokeless tobacco users. Cigarette smoking causes 30% of all cancer mortality in developed countries, and smokeless tobacco use is an important cause of cancer, in southern Asia [2]. The strongest carcinogens present in tobacco smoke are polycyclic aromatic hydrocarbons (PAH), N-nitrosamines, aromatic amines, aldehydes, benzene and butadiene. Cigarette smoke products can be divided into particulate and gas phases. The particulate phase contains nicotine, nitrosamines [4(methylnitrosamino)-1-(3-pyridyl)-1-butanone], N-nitrosonornicotine, metals, polycyclic aromatic hydrocarbons (PAH) and carcinogenic amines (4-aminobiphenyl). The gas phase contains carbon monoxide, carbon dioxide, benzene, ammonia, formaldehyde, hydrogen cyanide, N-nitrosodimethylamine and N-nitrosodiethylamine [3]
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