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

Chad M. Thompson; Ravi P. Subramaniam; Roland Grafström

doi:10.1016/j.taap.2008.09.011

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

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

VTT Technical Research Centre of Finland

Research output: Contribution to journal › Article › Scientific › peer-review

26 Citations (Scopus)

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.

Original language	English
Pages (from-to)	355-359
Journal	Toxicology and Applied Pharmacology
Volume	233
Issue number	3
DOIs	https://doi.org/10.1016/j.taap.2008.09.011
Publication status	Published - 2008
MoE publication type	A1 Journal article-refereed

Keywords

Formaldehyde
Asthma
S-nitrosoglutathione
Dosimetry
ADH3

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.taap.2008.09.011

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title = "Mechanistic and dose considerations for supporting adverse pulmonary physiology in response to formaldehyde",

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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AU - Thompson, Chad M.

AU - Subramaniam, Ravi P.

AU - Grafström, Roland

PY - 2008

Y1 - 2008

N2 - 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.

AB - 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.

KW - Formaldehyde

KW - Asthma

KW - S-nitrosoglutathione

KW - Dosimetry

KW - ADH3

U2 - 10.1016/j.taap.2008.09.011

DO - 10.1016/j.taap.2008.09.011

M3 - Article

SN - 0041-008X

VL - 233

SP - 355

EP - 359

JO - Toxicology and Applied Pharmacology

JF - Toxicology and Applied Pharmacology

IS - 3

ER -

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

Abstract

Keywords

UN SDGs

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