Abstract
243 ISSN 1758-1966 10.2217/LMT.12.37 © 2012 Future Medicine Ltd Lung Cancer Manage. (2012) 1(4), 243–246 Arsenic is a well-established human carcinogen. Due to its wide distribution throughout the Earth’s crust, arsenic contamination of drinking water and food is a threat to global human health. In fact, arsenic in drinking water has been considered as the largest mass poisoning in mankind, affecting approximately 160 million people in more than 70 countries. Since 1958, the WHO has lowered the maximum allowable arsenic concentration in drinking water from 0.2 to 0.01 mg/l, based on concerns regarding its carcino genicity to humans due to chronic low-dose exposure [101]. Multiple organs are targets for arsenicinduced carcinogenesis, including skin, liver, kidney, bladder and lung. Accumulating data suggest that lung cancer is the main cause of arsenic-related mortality. Evidence for the relationship between arsenic and lung cancer comes mainly from countries where arsenic is a major public health issue, such as in Bangladesh, India, Taiwan, Argentina and Chile. Arsenic can also act synergistically with other lung carcinogens, such as tobacco, increasing the risk of developing lung cancer by 25-times compared with the nonexposed [1,2]. Similar effects have been described in populations chronically exposed to low concentrations of arsenic. For example, in the USA, low-level exposure may contribute to more than 5000 lung cancer cases per year [3]. Lung tumors associated with arsenic are histologically similar to those derived from tobacco smoke. However, based on emerging differences at epidemiological and molecular levels, these tumors might be considered as different biological entities [4]. The widespread arsenic contamination around the world makes this metalloid a major non-tobacco agent associated with lung cancer. Considering the magnitude of
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