Maternal Particulate Matter Exposure Impairs Lung Health and Is Associated with Mitochondrial Damage.

Wang, B; Chan, Y-L; Li, G; Ho, KF; Anwer, AG; Smith, BJ; Guo, H; Jalaludin, B; Herbert, C; Thomas, PS; Liao, J; Chapman, DG; Foster, PS; Saad, S; Chen, H; Oliver, BG

Maternal Particulate Matter Exposure Impairs Lung Health and Is Associated with Mitochondrial Damage.

Wang, B Chan, Y-L Li, G Ho, KF Anwer, AG Smith, BJ Guo, H Jalaludin, B Herbert, C Thomas, PS Liao, J Chapman, DG Foster, PS Saad, S Chen, H

Oliver, BG

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Publisher:: MDPI AG
Publication Type:: Journal Article
Citation:: Antioxidants (Basel, Switzerland), 2021, 10, (7), pp. 1029-1029
Issue Date:: 2021-06-25

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Field	Value	Language
dc.contributor.author	Wang, B
dc.contributor.author	Chan, Y-L
dc.contributor.author	Li, G
dc.contributor.author	Ho, KF
dc.contributor.author	Anwer, AG
dc.contributor.author	Smith, BJ
dc.contributor.author	Guo, H
dc.contributor.author	Jalaludin, B
dc.contributor.author	Herbert, C
dc.contributor.author	Thomas, PS
dc.contributor.author	Liao, J
dc.contributor.author	Chapman, DG
dc.contributor.author	Foster, PS
dc.contributor.author	Saad, S
dc.contributor.author	Chen, H https://orcid.org/0000-0001-6883-3752
dc.contributor.author	Oliver, BG
dc.date.accessioned	2021-08-20T07:56:00Z
dc.date.available	2021-06-24
dc.date.available	2021-08-20T07:56:00Z
dc.date.issued	2021-06-25
dc.identifier.citation	Antioxidants (Basel, Switzerland), 2021, 10, (7), pp. 1029-1029
dc.identifier.issn	2076-3921
dc.identifier.issn	2076-3921
dc.identifier.uri	http://hdl.handle.net/10453/150189
dc.description.abstract	Relatively little is known about the transgenerational effects of chronic maternal exposure to low-level traffic-related air pollution (TRAP) on the offspring lung health, nor are the effects of removing such exposure before pregnancy. Female BALB/c mice were exposed to PM<sub>2.5</sub> (PM<sub>2.5,</sub> 5 µg/day) for 6 weeks before mating and during gestation and lactation; in a subgroup, PM was removed when mating started to model mothers moving to cleaner areas during pregnancy to protect their unborn child (Pre-exposure). Lung pathology was characterised in both dams and offspring. A subcohort of female offspring was also exposed to ovalbumin to model allergic airways disease. PM<sub>2.5</sub> and Pre-exposure dams exhibited airways hyper-responsiveness (AHR) with mucus hypersecretion, increased mitochondrial reactive oxygen species (ROS) and mitochondrial dysfunction in the lungs. Female offspring from PM<sub>2.5</sub> and Pre-exposure dams displayed AHR with increased lung inflammation and mitochondrial ROS production, while males only displayed increased lung inflammation. After the ovalbumin challenge, AHR was increased in female offspring from PM<sub>2.5</sub> dams compared with those from control dams. Using an in vitro model, the mitochondria-targeted antioxidant MitoQ reversed mitochondrial dysfunction by PM stimulation, suggesting that the lung pathology in offspring is driven by dysfunctional mitochondria. In conclusion, chronic exposure to low doses of PM<sub>2.5</sub> exerted transgenerational impairment on lung health.
dc.format	Electronic
dc.language	eng
dc.publisher	MDPI AG
dc.relation	http://purl.org/au-research/grants/nhmrc/APP1158186
dc.relation.ispartof	Antioxidants (Basel, Switzerland)
dc.relation.isbasedon	10.3390/antiox10071029
dc.rights	info:eu-repo/semantics/openAccess
dc.title	Maternal Particulate Matter Exposure Impairs Lung Health and Is Associated with Mitochondrial Damage.
dc.type	Journal Article
utslib.citation.volume	10
utslib.location.activity	Switzerland
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Strength - CHT - Health Technologies
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Life Sciences
pubs.organisational-group	/University of Technology Sydney/Centre for Health Technologies (CHT)
utslib.copyright.status	open_access	*
dc.date.updated	2021-08-20T07:55:56Z
pubs.issue	7
pubs.publication-status	Published
pubs.volume	10
utslib.citation.issue	7

Abstract:

Relatively little is known about the transgenerational effects of chronic maternal exposure to low-level traffic-related air pollution (TRAP) on the offspring lung health, nor are the effects of removing such exposure before pregnancy. Female BALB/c mice were exposed to PM_2.5 (PM_2.5, 5 µg/day) for 6 weeks before mating and during gestation and lactation; in a subgroup, PM was removed when mating started to model mothers moving to cleaner areas during pregnancy to protect their unborn child (Pre-exposure). Lung pathology was characterised in both dams and offspring. A subcohort of female offspring was also exposed to ovalbumin to model allergic airways disease. PM_2.5 and Pre-exposure dams exhibited airways hyper-responsiveness (AHR) with mucus hypersecretion, increased mitochondrial reactive oxygen species (ROS) and mitochondrial dysfunction in the lungs. Female offspring from PM_2.5 and Pre-exposure dams displayed AHR with increased lung inflammation and mitochondrial ROS production, while males only displayed increased lung inflammation. After the ovalbumin challenge, AHR was increased in female offspring from PM_2.5 dams compared with those from control dams. Using an in vitro model, the mitochondria-targeted antioxidant MitoQ reversed mitochondrial dysfunction by PM stimulation, suggesting that the lung pathology in offspring is driven by dysfunctional mitochondria. In conclusion, chronic exposure to low doses of PM_2.5 exerted transgenerational impairment on lung health.

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http://hdl.handle.net/10453/150189