Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/91344
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dc.contributorDepartment of Civil and Environmental Engineeringen_US
dc.creatorWang, Ben_US
dc.creatorChan, YLen_US
dc.creatorLi, Gen_US
dc.creatorHo, KFen_US
dc.creatorAnwer, AGen_US
dc.creatorSmith, BJen_US
dc.creatorGuo, Hen_US
dc.creatorJalaludin, Ben_US
dc.creatorHerbert, Cen_US
dc.creatorThomas, PSen_US
dc.creatorLiao, Jen_US
dc.creatorChapman, DGen_US
dc.creatorFoster, PSen_US
dc.creatorSaad, Sen_US
dc.creatorChen, Hen_US
dc.creatorOliver, BGen_US
dc.date.accessioned2021-11-03T06:52:52Z-
dc.date.available2021-11-03T06:52:52Z-
dc.identifier.issn2076-3921en_US
dc.identifier.urihttp://hdl.handle.net/10397/91344-
dc.language.isoenen_US
dc.publisherMolecular Diversity Preservation International (MDPI)en_US
dc.rights© 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).en_US
dc.rightsThe following publication Wang, B.; Chan, Y.-L.; Li, G.; Ho, K.F.; Anwer, A.G.; Smith, B.J.; Guo, H.; Jalaludin, B.; Herbert, C.; Thomas, P.S.; et al. Maternal Particulate Matter Exposure Impairs Lung Health and Is Associated with Mitochondrial Damage. Antioxidants 2021, 10, 1029 is available at https://doi.org/10.3390/antiox10071029en_US
dc.subjectAir pollutionen_US
dc.subjectAsthmaen_US
dc.subjectLung functionen_US
dc.subjectMitochondrial dysfunctionen_US
dc.subjectReactive oxygen speciesen_US
dc.titleMaternal particulate matter exposure impairs lung health and is associated with mitochondrial damageen_US
dc.typeJournal/Magazine Articleen_US
dc.identifier.volume10en_US
dc.identifier.issue7en_US
dc.identifier.doi10.3390/antiox10071029en_US
dcterms.abstractRelatively 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 PM2.5 (PM2.5, 5 µg/day) for 6 weeks before mating and during gestation and lactation; in a subgroup, PM was re-moved 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. PM2.5 and Pre-exposure dams exhibited airways hyper-responsiveness (AHR) with mucus hyperse-cretion, increased mitochondrial reactive oxygen species (ROS) and mitochondrial dysfunction in the lungs. Female offspring from PM2.5 and Pre-exposure dams displayed AHR with increased lung inflammation and mitochondrial ROS production, while males only displayed increased lung in-flammation. After the ovalbumin challenge, AHR was increased in female offspring from PM2.5 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 PM2.5 exerted transgenerational impairment on lung health.en_US
dcterms.accessRightsopen accessen_US
dcterms.bibliographicCitationAntioxidants, July 2021, v. 10, no. 7, 1029en_US
dcterms.isPartOfAntioxidantsen_US
dcterms.issued2021-07-
dc.identifier.scopus2-s2.0-85108605660-
dc.identifier.artn1029en_US
dc.description.validate202110 bcvcen_US
dc.description.oaVersion of Recorden_US
dc.identifier.FolderNumberOA_Scopus/WOS, a1497en_US
dc.identifier.SubFormID45172-
dc.description.fundingSourceRGCen_US
dc.description.fundingSourceOthersen_US
dc.description.fundingTextStrategic Focus Area scheme of The Research Institute for Sustainable Urban Development at The Hong Kong Polytechnic Universityen_US
dc.description.pubStatusPublisheden_US
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