Sex difference in bronchopulmonary dysplasia of offspring in response to maternal PM2.5 exposure

[Display omitted] •Maternal PM2.5 exposure altered BPD-related consequences in offspring.•BPD-related consequences could recover during postnatal development.•The male offspring were more sensitive to maternal PM2.5 exposure than the female. The adverse effects of fine particulate matters (PM2.5) on respiratory diseases start in utero. In order to investigate whether maternal PM2.5 exposure could lead to bronchopulmonary dysplasia (BPD) in offspring, PM2.5 was collected in Taiyuan, Shanxi, China during the annual heating period. Mice were mated and gestation day 0 (GD0) was considered the day on which a vaginal plug was observed. The plug-positive mice received 3 mg/kg b.w. PM2.5 by oropharyngeal aspiration every other day starting on GD0 and throughout the gestation period. Offspring were sacrificed at postnatal days (PNDs) 1, 7, 14 and 21. We assessed some typical BPD-like symptoms in offspring. The results showed that maternal PM2.5 exposure caused low birth weight, hypoalveolarization, decreased angiogenesis, suppressed production of secretory and surfactant proteins, and increased inflammation in the lungs of male offspring. However, maternal PM2.5 exposure induced only hypoalveolarization and inflammation in the lungs of female offspring. Furthermore, these alterations were reversed during postnatal development. Our results demonstrated that maternal exposure to PM2.5 caused reversible BPD-related consequences in offspring, and male offspring were more sensitive than females. However, these alterations were reversed during postnatal development.