Mechanistic and dose considerations for supporting adverse pulmonary physiology in response to formaldehyde

Chad M. Thompson (Corresponding Author), Ravi P. Subramaniam, Roland Grafström

Research output: Contribution to journalArticleScientificpeer-review

22 Citations (Scopus)


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.
Original languageEnglish
Pages (from-to)355-359
JournalToxicology and Applied Pharmacology
Issue number3
Publication statusPublished - 2008
MoE publication typeA1 Journal article-refereed



  • Formaldehyde
  • Asthma
  • S-nitrosoglutathione
  • Dosimetry
  • ADH3

Cite this