The joint effects of prenatal pesticide exposure and psychosocial factors on epigenetic age trajectories and child psychopathology in a south african birth cohort - pregnancy is a critical period…

The National Institute of Environmental Health Sciences awarded Emory University $148,614 on February 16, 2026, under the Environmental Health program (CFDA 93.113) to investigate the joint effects of prenatal pesticide exposure and psychosocial factors on epigenetic age trajectories and child psychopathology in a South African birth cohort.

The study uses advanced environmental mixture methods to analyze longitudinal data from the Drakenstein Child Health Study, a low-resource-setting birth cohort. Aim 1 investigates joint effects of prenatal urinary pesticide metabolite levels and psychosocial factors on child psychopathology at 6.5 years of age, hypothesizing that combined effects will be associated with increased psychopathology and will exceed individual effects of pesticides or psychosocial stressors alone. Aim 2 assesses joint effects on epigenetic age acceleration trajectories as a proposed mechanism linking combined environmental and psychosocial exposures to behavioral outcomes. The research addresses a gap in understanding how psychosocial stressors exacerbate harmful pesticide effects in low-resource settings with high burden of co-occurring exposures.

Performance occurs in Georgia, with a period of performance from February 16, 2026, through November 4, 2027. This is a Project Grant assistance type. Emory University's Office of Sponsored Programs serves as the recipient.

The joint effects of prenatal pesticide exposure and psychosocial factors on epigenetic age trajectories and child psychopathology in a south african birth cohort - pregnancy is a critical period for neurodevelopment, with the developing fetus particularly vulnerable to environmental toxicants and maternal psychosocial stressors. Prenatal pesticide exposure, an established neurotoxicant, has been linked to an increased risk of child psychopathology, including anxiety, mood disorders, and attention-deficit/ hyperactivity disorder. Preliminary studies indicate that the harmful effects of environmental toxins are exacerbated by psychosocial stressors, which lower the developing brain's threshold for neurotoxicity. This issue is particularly pronounced in low-resource settings, defined as areas with limited access to health services or infrastructure, and experience high burden of CO-occurring exposures. However, little is known about how psychosocial stressors may exacerbate the harmful effects of pesticide exposures on child psychopathology. Epigenetic age acceleration, a biomarker of biological aging, is proposed as a mechanism underlying the impact of combined environmental and psychosocial exposures on behavioral outcomes. This study aims to investigate the joint effects of prenatal pesticide exposure and psychosocial factors on trajectories of epigenetic age acceleration and subsequent child psychopathology. Utilizing advanced environmental mixture methods, the study will leverage longitudinal data from the drakenstein child health study (dchs), a birth cohort from a low-resource setting. Aim 1: investigate the joint effects of prenatal urinary pesticide metabolite levels and psychosocial factors on child psychopathology at 6.5 years of age. We hypothesize that these joint effects will be associated with increased child psychopathology and that their magnitude will exceed the individual effects of pesticides or psychosocial factors. Aim 2: assess the joint effects of prenatal urinary pesticide metabolite levels and psychosocial factors on longitudinal changes in epigenetic age acceleration at 1, 3, and 5 years of age. We hypothesize that these joint exposures will affect the trajectories of epigenetic age acceleration. Aim 3: determine the relationship between epigenetic age acceleration trajectories and child psychopathology at 6.5 years of age and explore whether epigenetic age acceleration mediates the association between prenatal exposures and child psychopathology. We hypothesize that changes in epigenetic age acceleration will be associated with increased psychopathology and that epigenetic age acceleration will mediate the effects of joint exposures on child psychopathology. This research will enhance our understanding of how environmental toxicants and psychosocial stressors interact during a sensitive developmental period, particularly in communities that experience high burden of exposure. The findings could inform early detection and prevention strategies to improve child brain health outcomes.