First-trimester maternal erythrocyte acetylcholinesterase activity and neurodevelopmental outcomes at 6 months among children of smallholder horticultural growers in the Southern Highlands of Tanzania

Agricultural intensification in Tanzania's Southern Highlands has increased reliance on organophosphate pesticides, raising concern about maternal–fetal exposure and infant neurodevelopment. Evidence from other settings links prenatal organophosphate exposure to poorer cognitive, motor, and behavioural outcomes in childhood, but data from sub-Saharan African smallholder communities, particularly at early infancy, remain scarce. A comparative cross-sectional study was conducted among 337 mother–child pairs recruited from reproductive and child health clinics in four districts of Iringa and Njombe regions, Tanzania — 220 from a priori pesticide-exposed districts (Kilolo, Makambako) and 117 from comparison districts (Njombe Town, Iringa Municipal). Maternal pesticide exposure was assessed via erythrocyte acetylcholinesterase (AChE) activity measured during the first trimester and classified as low or high/moderate inhibition, alongside a structured pesticide-use inventory classified by IRAC/FRAC/HRAC systems. Infant neurodevelopment was assessed at approximately six months using the Malawi Developmental Assessment Tool (MDAT) across four domains (gross motor, fine motor, language and hearing, social) and a composite outcome. Associations were estimated using parsimonious multivariable Firth penalized logistic regression, including a prespecified pesticide exposure-by-child sex interaction term, with secondary district-stratified models. Pesticide use was dominated by organophosphates, particularly chlorpyrifos and profenofos, as well as pyrethroids and neonicotinoids, with frequent use of pesticide mixtures, including neonicotinoid–organophosphate combinations (24.3%). Overall, 38.3% of mothers had moderate or high AChE inhibition. Most infants demonstrated normal neurodevelopment at six months, with 88.4% having normal composite development and 94.7–97.3% showing normal development across individual domains. High maternal AChE inhibition/high pesticide exposure was associated with higher odds of mild or delayed composite neurodevelopment (AOR = 2.94, 95% CI: 1.02–8.33; p = 0.045). A significant pesticide exposure-by-child-sex interaction was also observed (AOR = 4.30, 95% CI: 1.05–17.56; p = 0.042), suggesting that the association between maternal pesticide exposure and neurodevelopment may differ by child sex. Maternal secondary/tertiary education was associated with lower odds of mild or delayed composite neurodevelopment (AOR = 0.47, 95% CI: 0.22–1.00; p = 0.050), while increasing maternal age was associated with lower odds of language and hearing delay (AOR = 0.86, 95% CI: 0.74–0.99; p = 0.042). Maternal pesticide exposure was substantial among women in horticultural communities, and high maternal AChE inhibition was associated with increased odds of mild or delayed composite neurodevelopment at six months. The significant exposure-by-child-sex interaction suggests possible sex differences in susceptibility, although the estimate was imprecise and requires confirmation. Longitudinal studies incorporating repeated and pesticide-specific exposure measurements, longer neurodevelopmental follow-up, and adequately powered sex-stratified analyses are warranted. Strengthening safer pesticide-use practices, antenatal occupational exposure counselling, and developmental surveillance is recommended in horticultural communities.