Maternal particulate matter exposure impairs lung health and is associated with mitochondrial damage

Baoming Wang, Yik Lung Chan, Gerard Li, Kin Fai Ho, Ayad G. Anwer, Bradford J. Smith, Hai Guo, Bin Jalaludin, Cristan Herbert, Paul S. Thomas, Jiayan Liao, David G. Chapman, Paul S. Foster, Sonia Saad, Hui Chen, Brian G. Oliver

Research output: Journal article publicationJournal articleAcademic researchpeer-review

6 Citations (Scopus)


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 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.

Original languageEnglish
Article number1029
Issue number7
Publication statusPublished - Jul 2021


  • Air pollution
  • Asthma
  • Lung function
  • Mitochondrial dysfunction
  • Reactive oxygen species

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology


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