Commentary

Commentary: mechanistic considerations for associations between formaldehyde exposure and nasopharyngeal carcinoma

Chad M Thompson¹ and Roland C Grafström^2,3

¹  ToxStrategies, Inc, 23501 Cinco Ranch Blvd, Suite G265, Katy, TX 77494, USA

²  Institute of Environmental Medicine, Karolinska Institutet, SE-171 77 Stockholm, Sweden

³  VTT Technical Research Centre of Finland, Medical Biotechnology, PO Box 106, FI-20521 Turku, Finland

author email corresponding author email

Environmental Health 2009, 8:53doi:10.1186/1476-069X-8-53

Published:	25 November 2009

Abstract

Occupational exposure to formaldehyde has been linked to nasopharyngeal carcinoma. To date, mechanistic explanations for this association have primarily focused on formaldehyde-induced cytotoxicity, regenerative hyperplasia and DNA damage. However, recent studies broaden the potential mechanisms as it is now well established that formaldehyde dehydrogenase, identical to S-nitrosoglutathione reductase, is an important mediator of cGMP-independent nitric oxide signaling pathways. We have previously described mechanisms by which formaldehyde can influence nitrosothiol homeostasis thereby leading to changes in pulmonary physiology. Considering evidences that nitrosothiols govern the Epstein-Barr virus infection cycle, and that the virus is strongly implicated in the etiology of nasopharyngeal carcinoma, studies are needed to examine the potential for formaldehyde to reactivate the Epstein-Barr virus as well as additively or synergistically interact with the virus to potentiate epithelial cell transformation.