Mechanistic and dose considerations for supporting adverse pulmonary physiology in response to formaldehyde
- National Center for Environmental Assessment, Office of Research and Development, U.S. Environmental Protection Agency, 1200 Pennsylvania Avenue, NW, 8623-P, Washington, DC, 20460 (United States)
- Institute of Environmental Medicine, Karolinska Institutet, SE-171 77 Stockholm (Sweden)
Induction of airway hyperresponsiveness and asthma from formaldehyde inhalation exposure remains a debated and controversial issue. Yet, recent evidences on pulmonary biology and the pharmacokinetics and toxicity of formaldehyde lend support for such adverse effects. Specifically, altered thiol biology from accelerated enzymatic reduction of the endogenous bronchodilator S-nitrosoglutathione and pulmonary inflammation from involvement of Th2-mediated immune responses might serve as key events and cooperate in airway pathophysiology. Understanding what role these mechanisms play in various species and lifestages (e.g., child vs. adult) could be crucial for making more meaningful inter- and intra-species dosimetric extrapolations in human health risk assessment.
- OSTI ID:
- 21180502
- Journal Information:
- Toxicology and Applied Pharmacology, Vol. 233, Issue 3; Other Information: DOI: 10.1016/j.taap.2008.09.011; PII: S0041-008X(08)00394-3; Copyright (c) 2008 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0041-008X
- Country of Publication:
- United States
- Language:
- English
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