Maternal Exposure to PM_2.5 Affects Fetal Lung Development at Sensitive Windows

Abstract

Lung development continues from the embryonic period to adulthood. Previous epidemiological studies have noted that maternal exposure of atmospheric pollutants during the sensitive windows disturbed the lung development and increased the risk of lung diseases after birth, but the experimental evidence was insufficient. In the present study, we exposed plug-positive mice to PM2.5 (3 mg/kg b.w.) by oropharyngeal aspiration every other day, and intended to test whether maternal PM2.5 exposure affected prenatal lung development in the offspring. First, maternal PM2.5 exposure decreased embryo weight and crown-rump length at E18.5 but not in earlier developmental stages (E0–E16.5). Second, maternal PM2.5 exposure did not prevent lung-bud and tracheal specification, and did not cause abnormalities in branching morphogenesis, distal lung epithelium, and mesenchyme differentiation in earlier stages of lung development (E0–E16.5). However, the exposure significantly disturbed the distal lung epithelium and mesenchyme differentiation of lung, led to reduced intact rings of trachea, and suppressed the expression of lung development-related genes (Nkx2.1, Tbx4, Tbx5, and Sox9) at E18.5. Finally, we found that the exposure not only increased PM2.5-bound metal content (Pb and Cu) but also caused inflammatory response in the placenta, which transmitted from the mother to the fetus and contributed to the developmental abnormalities.

Fetotoxicity of Nanoparticles: Causes and Mechanisms

“…So far, numerous studies have indisputably demonstrated that maternal exposure to nanomaterials during gestation result in fetotoxicity, including adverse prenatal effects on the fetus [10][11][12][13][14][15][16][17], neurotoxicity [18][19][20][21][22][23], reproductive toxicity [24][25][26][27][28], immunotoxicity [29][30][31][32] and respiratory toxicity [29,[33][34][35] in offspring or even in adulthood [16][17][18]36]. The direct translocation of NPs or indirect interference from maternal damage-induced maternal mediators and placental mediators contributes to the fetotoxicity induced by prenatal exposure to NPs [37,38].…”

Bisphenol A Analogs Induce Cellular Dysfunction in Human Trophoblast Cells in a Thyroid Hormone Receptor-Dependent Manner: In Silico and In Vitro Analyses

“…Homogeneity of variance (HV) among groups was analyzed with Levene’s test. A two-tailed Student’s t test was used to compare the results between two groups as we described previously . Differences in all tests were considered significant when p < 0.05.…”

Environmental Air Pollutants Inhaled during Pregnancy Are Associated with Altered Cord Blood Immune Cell Profiles

“…Air pollution exposure during pregnancy has been linked to placental inflammation and impairment of placental function [ 67 ]. PM 2.5 exposure may cause inflammatory responses in the placenta, which may be transmitted from the mother to the fetus and contribute to the development of abnormalities [ 68 , 69 ].…”