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In the late 1960s, arsenic-rich drinking water was found to induce carcinogenesis, and arsenic contamination became an international environmental health issue. The pleiotropic nature of arsenic-induced toxicity has become evident due to several epidemiological studies which have demonstrated and defined exposure levels relevant to human health. Evidence from these epidemiological studies suggests that arsenic simultaneously causes the promotion and progression of several diseases, including lung cancer (National Research Council, 1999). In addition to the ability of arsenic alone to induce carcinogenesis, there is also compelling evidence that arsenic acts synergistically with other carcinogens, such as tobacco or polycyclic aromatic hydrocarbons (IARC, 2004; Rossman, 2003). The complexity of the interaction of arsenic with other carcinogens, coupled with the evidence supporting multiple modes of actions, makes the mechanisms surrounding arsenic-induced carcinogenesis in the human lung unclear. Arsenic has been shown to be a potent activator of diverse signal transduction pathways even at subcytotoxic exposures. Until recently, few models of low-level arsenical-induced cancer have been established in animals, so in vitro methods have been widely used to study subcytotoxic arsenic exposures. In this issue of Toxicological Sciences, Andrews et al. identifies the involvement in both Beas-2B cells and human lung tumors of the epidermal growth factor receptor (EGFR) pathway following exposure to arsenic. This comparison between in vitro methods and human lung tissue makes this study a valuable contribution to the investigation into the mode of action behind arsenical-induced lung cancer. The highlighted article by Andrews et al. reports the activation of the EGFR (EGFR/ErbB1/HER1) pathway by arsenic at contamination levels which are pertinent to the U.S. population. In this study, arsenic exposure (0.01–10lM sodium arsenite) was shown to increase levels of EGFR phosphorylation, increase the levels of the pro-ligand heparin-binding EGF (HB-EGF), and also increase the protein levels of downstream cyclin D1, and extracellular signal-regulated kinase (p-ERK) in human bronchial epithelial cells (Beas-2B cells). EGFR belongs to the ErbB/HER-family of tyrosine kinase

Potential Clinical Significance of EGFR-Mediated Signaling following Inorganic Arsenic Exposure in Human Lung