Exposure to environmental chemicals and perinatal psychopathology Original paper

What was reviewed?

This paper reviewed the growing body of literature examining how exposure to environmental chemicals, such as endocrine-disrupting chemicals (EDCs), heavy metals, pesticides, and air pollutants, contributes to perinatal psychopathology, particularly depression and anxiety during pregnancy and postpartum. The review assessed human and animal studies that link prenatal and early postnatal environmental exposures to altered neurobiology, behavior, and emotional outcomes, including disruptions of the gut-brain axis and inflammatory pathways.

Who was reviewed?

The review synthesized findings from both clinical populations of pregnant and postpartum individuals and preclinical animal models that explore mechanisms behind environmentally linked psychopathology. The human studies included pregnant and postpartum women exposed to chemicals such as bisphenol A (BPA), phthalates, lead, cadmium, and particulate matter. Animal studies allowed researchers to investigate mechanisms like neuroinflammation, HPA-axis disruption, neurogenesis, and microbiota alterations under controlled exposure conditions.

What were the most important findings?

The review emphasized that perinatal exposure to environmental chemicals significantly contributes to the risk of developing depression and anxiety. Mechanistically, the most consistent findings link chemical exposures with heightened neuroinflammation, dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, and altered monoamine signaling, particularly in serotonin pathways. Several chemicals also disrupted the gut microbiota, implicating the gut-brain axis in environmentally driven psychopathology.

Heavy metals like lead and cadmium induced microglial activation and inflammatory cytokine production, contributing to anxiety- and depression-like behaviors. EDCs such as BPA and phthalates disrupted estrogen and glucocorticoid signaling, which are vital for mood regulation during the perinatal period. Importantly, both human and animal studies showed changes in gut microbial composition associated with these exposures. For example, exposure to BPA reduces microbial diversity and suppresses beneficial genera like Lactobacillus and Bifidobacterium, while increasing pathobionts like Proteobacteria. These microbial shifts were frequently linked to increased gut permeability, systemic inflammation, and behavioral alterations relevant to perinatal mood disorders.

What are the greatest implications of this review?

This review highlights a critical intersection between environmental health, neurobiology, and the microbiome in shaping perinatal mental health. For clinicians, these findings underscore the need to consider environmental exposures as modifiable risk factors when assessing and treating pregnant and postpartum patients with mood disorders. Integrating environmental history into mental health screening could improve early detection and prevention strategies. Additionally, supporting gut microbial health through targeted nutritional and probiotic interventions may mitigate some of the inflammatory and neurochemical consequences of environmental toxicants. The evidence also supports advocacy for public health policies aimed at reducing pregnant women’s exposure to harmful environmental chemicals, particularly in vulnerable and underserved populations. Ultimately, these insights offer a strong rationale for multidisciplinary approaches in maternal mental health care that incorporate environmental toxicology, microbiome science, and neuropsychology.