Arsenic

Inorganic arsenic has been known as a human carcinogen for decades. The first evidence suggesting arsenic could cause cancer occurred in 1977.50 During this time, arsenic was being applied directly to the skin as a treatment for psoriasis, which resulted in the development of skin cancers.51 Arsenic is released into the atmosphere from both natural and anthropogenic sources, the latter being responsible for the majority of emissions released.51 The production of arsenic in the Unites States has been banned since 1985; however, it is still imported for use. The current concern lies in being exposed to arsenic through food and drinking water. Additionally, individuals may be exposed to arsenic compounds through air emissions from industrial facilities that manufacture pesticides, glass, and cigarette tobacco, smelting operations, and the burning of fossil fuels.2

Studies from around the world have linked exposure to arsenic with the formation of skin, lung, and bladder cancers. There is also increasing evidence that arsenic increases the risk of developing cancers of the kidney, liver, and colon. The majority of epidemiologic studies have focused on populations with contaminated groundwater/drinking water. Many of these populations have higher incidences of lung cancers in comparison to control populations.52,53 More recently, there is concern that ingestion of arsenic through contaminated food sources and ambient air pollution may be additional routes of exposure.

The means by which arsenic causes cancer is not well understood. Multiple mechanisms have been proposed and include both genotoxic and nongenotoxic modes of action.51 Arsenic does not interact with DNA, but indirectly causes chromosome aberrations, genomic instability, and aberrant DNA methylation in promoter regions of genes. In animal studies, arsenic induces the formation of ROS, which may alter regulation of DNA repair and cell-cycle progression.54,55 The generation of ROS by arsenic can have a profound effect on signal transduction pathways. Growth factor receptors [epidermal growth factor receptor (EGFR), platelet-derived growth factor (PDGF), vascular endothelial growth factor (VEGF)], G proteins (Ras, C-src), kinases [extracellular regulated kinase (ERK), c-Jun NH2-terminal kinase (JNK), p38], and nuclear transcription factors [NFkb, AP-1, hypoxia-inducible factor 1 (HIF-1)] have all been suggested as targets of arsenic-induced oxidative damage through mechanisms that are still poorly understood.56 Arsenic can also affect these pathways independent of free radical generation by direct interaction with these proteins. Alterations in these signaling pathways can have profound effects on cell proliferation, apoptosis, differentiation, and transformation.57

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