Mechanisms of Formaldehyde Respiratory Effects Explored

Toxicology and Applied PharmacologyVolume 233, Issue 3, 15 December 2008, Pages 355-359
Mechanistic and dose considerations for supporting adverse pulmonary physiology in response to formaldehyde
Chad M. Thompsona, , , Ravi P. Subramaniama and Roland C. Grafströmb, c
aNational Center for Environmental Assessment, Office of Research and Development, U.S. Environmental Protection Agency, 1200 Pennsylvania Avenue, NW, 8623-P, Washington, DC, 20460, USA
bInstitute of Environmental Medicine, Karolinska Institutet, SE-171 77 Stockholm, Sweden
cVTT Technical Research Centre of Finland, Medical Biotechnology, P.O. Box 106, FI-20521 Turku, Finland
Abstract
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.
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BrooklynDodger(s) comment: This publication co-authored by EPA again suggests that EPA is laying on ammunition for an upcoming battle over a risk assessment for formaldehyde. Apparently some investigators have generated a controversy over formaldehyde as a risk factor for asthma, so EPA has sought to explore the other side of the argument. Apparently, the mechanistic extrapolation market has been cornered by the other guys in the US, so EPA went to Scandinavia for collaborators.