Landscape fire smoke airway exposure impairs respiratory and cardiac function and worsens experimental asthma.

Gomez, HM; Haw, TJ; Ilic, D; Robinson, P; Donovan, C; Croft, AJ; Vanka, KS; Small, E; Carroll, OR; Kim, RY; Mayall, JR; Beyene, T; Palanisami, T; Ngo, DTM; Zosky, GR; Holliday, EG; Jensen, ME; McDonald, VM; Murphy, VE; Gibson, PG; Horvat, JC

Landscape fire smoke airway exposure impairs respiratory and cardiac function and worsens experimental asthma.

Gomez, HM Haw, TJ Ilic, D Robinson, P Donovan, C

Croft, AJ Vanka, KS Small, E Carroll, OR Kim, RY Mayall, JR Beyene, T Palanisami, T Ngo, DTM Zosky, GR Holliday, EG Jensen, ME McDonald, VM Murphy, VE Gibson, PG Horvat, JC

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Publisher:: MOSBY-ELSEVIER
Publication Type:: Journal Article
Citation:: J Allergy Clin Immunol, 2024, 154, (1), pp. 209-221.e6
Issue Date:: 2024-07

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Field	Value	Language
dc.contributor.author	Gomez, HM
dc.contributor.author	Haw, TJ
dc.contributor.author	Ilic, D
dc.contributor.author	Robinson, P
dc.contributor.author	Donovan, C https://orcid.org/0000-0003-4558-329X
dc.contributor.author	Croft, AJ
dc.contributor.author	Vanka, KS
dc.contributor.author	Small, E
dc.contributor.author	Carroll, OR
dc.contributor.author	Kim, RY
dc.contributor.author	Mayall, JR
dc.contributor.author	Beyene, T
dc.contributor.author	Palanisami, T
dc.contributor.author	Ngo, DTM
dc.contributor.author	Zosky, GR
dc.contributor.author	Holliday, EG
dc.contributor.author	Jensen, ME
dc.contributor.author	McDonald, VM
dc.contributor.author	Murphy, VE
dc.contributor.author	Gibson, PG
dc.contributor.author	Horvat, JC
dc.date.accessioned	2024-12-17T00:09:54Z
dc.date.available	2024-02-22
dc.date.available	2024-12-17T00:09:54Z
dc.date.issued	2024-07
dc.identifier.citation	J Allergy Clin Immunol, 2024, 154, (1), pp. 209-221.e6
dc.identifier.issn	0091-6749
dc.identifier.issn	1097-6825
dc.identifier.uri	http://hdl.handle.net/10453/182603
dc.description.abstract	BACKGROUND: Millions of people are exposed to landscape fire smoke (LFS) globally, and inhalation of LFS particulate matter (PM) is associated with poor respiratory and cardiovascular outcomes. However, how LFS affects respiratory and cardiovascular function is less well understood. OBJECTIVE: We aimed to characterize the pathophysiologic effects of representative LFS airway exposure on respiratory and cardiac function and on asthma outcomes. METHODS: LFS was generated using a customized combustion chamber. In 8-week-old female BALB/c mice, low (25 μg/m3, 24-hour equivalent) or moderate (100 μg/m3, 24-hour equivalent) concentrations of LFS PM (10 μm and below [PM10]) were administered daily for 3 (short-term) and 14 (long-term) days in the presence and absence of experimental asthma. Lung inflammation, gene expression, structural changes, and lung function were assessed. In 8-week-old male C57BL/6 mice, low concentrations of LFS PM10 were administered for 3 days. Cardiac function and gene expression were assessed. RESULTS: Short- and long-term LFS PM10 airway exposure increased airway hyperresponsiveness and induced steroid insensitivity in experimental asthma, independent of significant changes in airway inflammation. Long-term LFS PM10 airway exposure also decreased gas diffusion. Short-term LFS PM10 airway exposure decreased cardiac function and expression of gene changes relating to oxidative stress and cardiovascular pathologies. CONCLUSIONS: We characterized significant detrimental effects of physiologically relevant concentrations and durations of LFS PM10 airway exposure on lung and heart function. Our study provides a platform for assessment of mechanisms that underpin LFS PM10 airway exposure on respiratory and cardiovascular disease outcomes.
dc.format	Print-Electronic
dc.language	eng
dc.publisher	MOSBY-ELSEVIER
dc.relation.ispartof	J Allergy Clin Immunol
dc.relation.isbasedon	10.1016/j.jaci.2024.02.022
dc.rights	info:eu-repo/semantics/openAccess
dc.subject	1107 Immunology
dc.subject.classification	Allergy
dc.subject.classification	3204 Immunology
dc.subject.mesh	Animals
dc.subject.mesh	Female
dc.subject.mesh	Smoke
dc.subject.mesh	Mice, Inbred BALB C
dc.subject.mesh	Asthma
dc.subject.mesh	Male
dc.subject.mesh	Mice
dc.subject.mesh	Particulate Matter
dc.subject.mesh	Mice, Inbred C57BL
dc.subject.mesh	Lung
dc.subject.mesh	Wildfires
dc.subject.mesh	Disease Models, Animal
dc.subject.mesh	Lung
dc.subject.mesh	Animals
dc.subject.mesh	Mice, Inbred BALB C
dc.subject.mesh	Mice, Inbred C57BL
dc.subject.mesh	Mice
dc.subject.mesh	Asthma
dc.subject.mesh	Disease Models, Animal
dc.subject.mesh	Smoke
dc.subject.mesh	Female
dc.subject.mesh	Male
dc.subject.mesh	Particulate Matter
dc.subject.mesh	Wildfires
dc.subject.mesh	Animals
dc.subject.mesh	Female
dc.subject.mesh	Smoke
dc.subject.mesh	Mice, Inbred BALB C
dc.subject.mesh	Asthma
dc.subject.mesh	Male
dc.subject.mesh	Mice
dc.subject.mesh	Particulate Matter
dc.subject.mesh	Mice, Inbred C57BL
dc.subject.mesh	Lung
dc.subject.mesh	Wildfires
dc.subject.mesh	Disease Models, Animal
dc.title	Landscape fire smoke airway exposure impairs respiratory and cardiac function and worsens experimental asthma.
dc.type	Journal Article
utslib.citation.volume	154
utslib.location.activity	United States
utslib.for	1107 Immunology
pubs.organisational-group	University of Technology Sydney
pubs.organisational-group	University of Technology Sydney/Faculty of Science
pubs.organisational-group	University of Technology Sydney/Faculty of Science/School of Life Sciences
utslib.copyright.status	open_access	*
dc.rights.license	This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0). To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/
dc.date.updated	2024-12-17T00:09:52Z
pubs.issue	1
pubs.publication-status	Published
pubs.volume	154
utslib.citation.issue	1

Abstract:

BACKGROUND: Millions of people are exposed to landscape fire smoke (LFS) globally, and inhalation of LFS particulate matter (PM) is associated with poor respiratory and cardiovascular outcomes. However, how LFS affects respiratory and cardiovascular function is less well understood. OBJECTIVE: We aimed to characterize the pathophysiologic effects of representative LFS airway exposure on respiratory and cardiac function and on asthma outcomes. METHODS: LFS was generated using a customized combustion chamber. In 8-week-old female BALB/c mice, low (25 μg/m3, 24-hour equivalent) or moderate (100 μg/m3, 24-hour equivalent) concentrations of LFS PM (10 μm and below [PM10]) were administered daily for 3 (short-term) and 14 (long-term) days in the presence and absence of experimental asthma. Lung inflammation, gene expression, structural changes, and lung function were assessed. In 8-week-old male C57BL/6 mice, low concentrations of LFS PM10 were administered for 3 days. Cardiac function and gene expression were assessed. RESULTS: Short- and long-term LFS PM10 airway exposure increased airway hyperresponsiveness and induced steroid insensitivity in experimental asthma, independent of significant changes in airway inflammation. Long-term LFS PM10 airway exposure also decreased gas diffusion. Short-term LFS PM10 airway exposure decreased cardiac function and expression of gene changes relating to oxidative stress and cardiovascular pathologies. CONCLUSIONS: We characterized significant detrimental effects of physiologically relevant concentrations and durations of LFS PM10 airway exposure on lung and heart function. Our study provides a platform for assessment of mechanisms that underpin LFS PM10 airway exposure on respiratory and cardiovascular disease outcomes.

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http://hdl.handle.net/10453/182603