Exposure to particulate matter, prenatal depressive symptoms and HPA axis dysregulation

BACKGROUND: The prevalence of depression during pregnancy is on the rise, affecting women's well-being and their children's health outcomes. Preliminary studies suggest that exposure to air pollution during pregnancy may play a role in development of depressive symptoms. In addition, pollution has been linked to dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, our brain's primary stress response system. The purpose of this study was to examine the association of air pollution exposure during pregnancy to prenatal depressive symptoms. We also evaluated whether cortisol, the hormonal endpoint of HPA activation, mediated the relationship between exposure to pollution and prenatal depression. METHODS: Women were recruited in obstetric clinics during their third trimester of pregnancy. They completed the Patient Health Questionnaire-9 to assess depression and provided salivary samples at 4 times during the day for 2 days. Four measures of cortisol were calculated from salivary assays: average cortisol level, cortisol awakening response (CAR), diurnal cortisol slope (DCS), and area under the curve (AUC(G)). We acquired data on particulate matter with a diameter of (2.5) μm (PM(2.5)) or less within each woman's residential area from public records of the air quality control district. Structural equation modeling was used to analyze the aims. RESULTS: Increased prenatal exposure to PM(2.5) across pregnancy was associated with more severe depressive symptoms during the 3rd trimester (β = 0.14, p = 0.02). Greater PM(2.5) exposure also had significant relationships with both higher cortisol AUC(G) (β = 15.933, p = 0.005) and average cortisol levels (β = 0.018, p = 0.023) among women. However, no cortisol parameter appeared to mediate the relationship between PM(2.5) exposure and depressive symptoms. CONCLUSIONS: Findings suggest pregnancy may be a critical window of sensitivity to PM(2.5) exposure that escalates depression risk and induces activation of the HPA axis, evidenced in greater overall cortisol concentration. Further research is needed to identify mechanisms underlying the effects of particulate matter, especially potential methylation of glucocorticoid or serotonin transporter genes that may elicit changes in both depression and the stress response system. In addition, assessment of depression appears warranted for pregnant women in regions known for high pollution.