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

• Main Authors: Baoming Wang (Author), Yik-Lung Chan (Author), Gerard Li (Author), Kin Fai Ho (Author), Ayad G. Anwer (Author), Bradford J. Smith (Author), Hai Guo (Author), Bin Jalaludin (Author), Cristan Herbert (Author), Paul S. Thomas (Author), Jiayan Liao (Author), David G. Chapman (Author), Paul S. Foster (Author), Sonia Saad (Author), Hui Chen (Author), Brian G. Oliver (Author)
• Format: Book
• Published: MDPI AG, 2021-06-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.
• Notes: 10.3390/antiox10071029; 2076-3921
• Keywords: air pollution; lung function; reactive oxygen species; mitochondrial dysfunction; asthma; Therapeutics. Pharmacology; RM1-950
• Source: Antioxidants, Vol 10, Iss 7, p 1029 (2021)

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.