ToxSci Advance Access originally published online on April 15, 2009
Toxicological Sciences 2009 109(2):169-171; doi:10.1093/toxsci/kfp071
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© The Author 2009. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Potential Clinical Significance of EGFR-Mediated Signaling following Inorganic Arsenic Exposure in Human Lung
S. C. Johnson & Son, Inc., 1525 Howe St., Racine, Wisconsin 53403
For correspondence via Fax: 262-260-3752. E-mail: kyleeeblin@yahoo.com, keeblin@scj.com
Received March 30, 2009; accepted March 31, 2009
| The first 10% of the full text of this article appears below. |
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