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. 2021 May 11;18(10):5062.
doi: 10.3390/ijerph18105062.

Air Pollution, Neonatal Immune Responses, and Potential Joint Effects of Maternal Depression

Jill Hahn  1 , Diane R Gold  2   3 , Brent A Coull  3   4 , Marie C McCormick  1 , Patricia W Finn  5   6 , David L Perkins  7   8   9 , Sheryl L Rifas Shiman  10 , Emily Oken  10 , Laura D Kubzansky  1
Affiliations

Air Pollution, Neonatal Immune Responses, and Potential Joint Effects of Maternal Depression

Jill Hahn et al. Int J Environ Res Public Health. .

Abstract

Prenatal maternal exposure to air pollution may cause adverse health effects in offspring, potentially through altered immune responses. Maternal psychosocial distress can also alter immune function and may increase gestational vulnerability to air pollution exposure. We investigated whether prenatal exposure to air pollution is associated with altered immune responses in cord blood mononuclear cells (CBMCs) and potential modification by maternal depression in 463 women recruited in early pregnancy (1999-2001) into the Project Viva longitudinal cohort. We estimated black carbon (BC), fine particulate matter (PM2.5), residential proximity to major roadways, and near-residence traffic density, averaged over pregnancy. Women reported depressive symptoms in mid-pregnancy (Edinburgh Postnatal Depression Scale) and depression history by questionnaire. Immune responses were assayed by concentrations of three cytokines (IL-6, IL-10, and TNF-α), in unstimulated or stimulated (phytohemagglutinin (PHA), cockroach extract (Bla g 2), house dust mite extract (Der f 1)) CBMCs. Using multivariable linear or Tobit regression analyses, we found that CBMCs production of IL-6, TNF-a, and IL-10 were all lower in mothers exposed to higher levels of PM2.5 during pregnancy. A suggestive but not statistically significant pattern of lower cord blood cytokine concentrations from ever (versus never) depressed women exposed to PM2.5, BC, or traffic was also observed and warrants further study.

Keywords: air pollution; chemical stressors; cord blood mononuclear cells; cytokines; immune system; intergenerational effects; maternal prenatal depression; non-chemical stressors; social determinants of health.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Percent difference in cord blood cytokine concentrations per μg/m3 increase in PM2.5 exposure. Unstimulated (Med) IL-10 was analyzed using Tobit regression; others were analyzed using linear regression. Models were adjusted for maternal age, race/ethnicity, education, household income, child sex, the season of birth, pre-pregnancy BMI, and smoking. PM2.5 exposure was averaged over pregnancy.
Figure 2
Figure 2
Effect estimates * for the association of air pollution and cytokine concentrations (in unstimulated (Med) cord blood lymphocytes or for those stimulated with phytohemagglutinin (PHA), cockroach antigen (Bla), or dust mite antigen (Der)), in ever and never depressed women. Open circles: never-depressed mothers. Closed diamonds: ever-depressed mothers. Unstimulated IL-10 was analyzed using Tobit regression; TNF-α and IL-6 were analyzed using linear regression. Outcomes were log-transformed for analysis. Models were adjusted for maternal age, race/ethnicity, education, household income, child sex, the season of birth, pre-pregnancy BMI, and smoking. * For PM2.5 and BC, (effect estimate × 100) is approximately the % change in cytokine concentration for a 1-unit increase in air pollution. For proximity to road and traffic density, the effect estimate is the % change in cytokine concentration for a 1% increase in air pollution.
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