Maternal particulate matter exposure during pregnancy affected offspring’s lung health

Abstract

In humans, maternal particulate matter (PM) exposure during pregnancy is known to negatively affect offspring’s lung. Most murine models used to investigate mechanisms with high doses. The aim of this study was to develop a low dose in-utero exposure model to investigate the effect on offspring’s lung health. Female BALB/c mice were divided into SHAM, PM and PM cessation groups. PM group was exposed to PM1 (5ug/day) before mating for 6 weeks, during gestation and lactation. PM cessation group only exposed during the pre-gestational period. Lung were collected from both dams and male offspring at age of postnatal day P1, P20 and 13 weeks. Lung function were tested in the dams and bronchoalveolar lavage fluid was assessed for inflammation. Oxidative stress (MnSOD), mitophagy (Drp-1, Opa-1, Parkin1 and PINK1), autophagy (LC3A/B-I, II), pro-inflammatory mediator (NF-KB, MAPK signalling pathway (ERK1,2, JNK1,2 and P38)), and inflammasome NLRP3 were measured by western blotting. In the dams, PM exposure caused airway hyperresponsiveness and increased infiltration of macrophages and neutrophils into the lung. This was accompanied by increased oxidative stress, inflammasome, autophagy and MAPK siganaling pathway activation, some of which were reduced in the ceseation group. In P1 and P20 offspring, Mitophagy and MAPK signalling casecades markers were increased by maternal PM exposure, which were reduced in the ceseation group. At 13 weeks, the offspring from PM exposed dams had more macrophages in the BALF. p-JNK2 level in the PM group was higher than the SHAM. Compared to the PM group, PM cessation group had lower Drp-1. Conclusion: PM exposure caused adverse effects in the lungs of dams and offspring.