In the vegetable-growing highlands of southern Tanzania, where smallholder farms feed much of the nation, a new study has found that pregnant women with stronger signs of pesticide poisoning during early pregnancy were nearly three times more likely to have infants showing mild or delayed neurodevelopment at six months of age. The research, published in BMC Pediatrics, is among the first to connect a biochemical marker of pesticide exposure measured in the first trimester with developmental outcomes in early infancy within a sub-Saharan African smallholder farming population, a setting where such data have long been missing.
The study was led by Peter M. Chilipweli and Elias C. Nyanza of the Catholic University of Health and Allied Sciences in Mwanza, together with Aiwerasia Vera Ngowi of Muhimbili University of Health and Allied Sciences and Karim Manji, also of Muhimbili. Their team recruited 337 mother–child pairs from reproductive and child health clinics across four districts in the Iringa and Njombe regions. Of these, 220 came from districts classified in advance as pesticide-exposed — Kilolo and Makambako, both centers of intensive horticulture — while 117 came from comparison districts, Njombe Town and Iringa Municipal, where agricultural chemical use is expected to be lower.
The central measurement was erythrocyte acetylcholinesterase activity, assessed during the first trimester of pregnancy. Acetylcholinesterase is the enzyme that breaks down acetylcholine, the neurotransmitter released at nerve synapses, and organophosphate insecticides work precisely by inhibiting this enzyme, causing overstimulation of nerve pathways. Because red blood cell acetylcholinesterase mirrors the enzyme found at nerve endings, its activity in maternal blood serves as a widely used proxy for the body’s internal dose of organophosphate exposure. The researchers classified each mother as having either low inhibition or high or moderate inhibition of the enzyme. Overall, 38.3 percent of the mothers showed moderate or high inhibition, a strikingly high burden of biological exposure in a general population of pregnant women rather than a group of occupationally selected workers.
Alongside the blood measurements, the team administered a structured pesticide-use inventory, classifying the products farmers reported using according to the international IRAC, FRAC and HRAC classification systems for insecticides, fungicides and herbicides. The picture that emerged was one of heavy reliance on organophosphates, particularly chlorpyrifos and profenofos, alongside pyrethroids and neonicotinoids. Notably, 24.3 percent of the reported use involved pesticide mixtures, including combinations of neonicotinoids with organophosphates — a pattern of co-formulation and co-application that toxicologists increasingly worry about, since different chemical classes can interact in ways that single-compound risk assessments do not capture.
When the infants reached approximately six months of age, the researchers assessed their development using the Malawi Developmental Assessment Tool, an instrument designed and validated for African settings that evaluates four domains: gross motor function, fine motor function, language and hearing, and social behavior. The overall picture was reassuring at the population level. Most infants — 88.4 percent — showed normal composite development, and across the individual domains, between 94.7 and 97.3 percent scored within normal ranges. Yet beneath that generally healthy surface, the statistical analysis revealed a consistent signal tied to prenatal exposure.
Using parsimonious multivariable Firth penalized logistic regression — a technique chosen because it produces more stable estimates when outcomes are imbalanced and sample sizes are modest — the researchers found that high maternal acetylcholinesterase inhibition, indicating high pesticide exposure, was associated with roughly triple the odds of mild or delayed composite neurodevelopment in the infants, with an adjusted odds ratio of 2.94 and a 95 percent confidence interval of 1.02 to 8.33, reaching statistical significance at p equal to 0.045. The confidence interval was wide, reflecting the modest number of delayed cases, but the association aligned with a substantial body of evidence from other parts of the world.
Perhaps the most intriguing finding was a significant interaction between pesticide exposure and the sex of the child, with an adjusted odds ratio of 4.30 and a 95 percent confidence interval of 1.05 to 17.56, at p equal to 0.042. This suggests that the relationship between maternal pesticide exposure and infant neurodevelopment may differ for boys and girls, echoing a recurring theme in the environmental health literature, where male fetuses have often appeared more vulnerable to neurotoxic insults, although the direction and magnitude of sex differences vary across studies. The authors themselves are careful to note that this particular estimate was imprecise and requires confirmation in larger, adequately powered, sex-stratified analyses before firm conclusions can be drawn.
The study also identified protective social factors. Mothers who had completed secondary or tertiary education had lower odds of having an infant with mild or delayed composite development, with an adjusted odds ratio of 0.47 and a confidence interval of 0.22 to 1.00, just crossing the threshold of significance at p equal to 0.050. Increasing maternal age was associated with lower odds of language and hearing delay, with an adjusted odds ratio of 0.86 per year of age and a confidence interval of 0.74 to 0.99 at p equal to 0.042. These findings underscore that developmental risk in such communities is shaped by a web of influences — schooling, maternal experience, household environment — that interact with chemical exposures rather than operating in isolation.
The broader context gives the findings weight. Agricultural intensification in Tanzania’s Southern Highlands has driven a marked increase in reliance on organophosphate pesticides, and evidence from cohorts such as the CHAMACOS study of farmworker families in California has linked prenatal organophosphate exposure to poorer cognitive, motor and behavioral outcomes in childhood. What has been missing is data from low- and middle-income countries, and especially from sub-Saharan African smallholder communities, where women often work in the fields themselves, handle concentrates without adequate personal protective equipment, and face exposure through spraying, mixing, re-entering treated plots and laundering contaminated clothing. This study provides a rare, early-window measurement in exactly that population, and it does so using an objective biomarker rather than self-reported exposure alone.
The authors emphasize that the cross-sectional design, the single exposure measurement in the first trimester, and the wide confidence intervals all counsel caution, and they call for longitudinal studies incorporating repeated, pesticide-specific exposure measurements, longer neurodevelopmental follow-up and properly powered sex-stratified analyses. Still, the practical implications are immediate. The team recommends strengthening safer pesticide-use practices in horticultural communities, providing antenatal counseling on occupational exposure, and building developmental surveillance into routine reproductive and child health services so that infants at elevated risk are identified early. The work was funded by Tanzania’s Ministry of Education, Science and Technology through the Higher Education for Economic Transformation Project, and approved by the Catholic University of Health and Allied Sciences and Bugando Medical Centre Research Ethics and Review Committee. For the farming families of Iringa and Njombe, the message is that the first weeks of pregnancy may be a critical window in which pesticide exposure leaves measurable traces in an infant’s developing nervous system — and that protecting mothers in those early months is an investment in the next generation’s minds.
Subject of Research: Prenatal organophosphate pesticide exposure and infant neurodevelopment in Tanzanian smallholder farming communities
Article Title: First-trimester maternal erythrocyte acetylcholinesterase activity and neurodevelopmental outcomes at 6 months among children of smallholder horticultural growers in the Southern Highlands of Tanzania
Article References: Chilipweli, P. M., Nyanza, E. C., Ngowi, A. V., & Manji, K. (2026). First-trimester maternal erythrocyte acetylcholinesterase activity and neurodevelopmental outcomes at 6 months among children of smallholder horticultural growers in the Southern Highlands of Tanzania. BMC Pediatrics. https://doi.org/10.1186/s12887-026-07698-2
Image Credits: AI Generated
DOI: 10.1186/s12887-026-07698-2
Keywords: acetylcholinesterase, organophosphate pesticides, chlorpyrifos, neurodevelopment, Malawi Developmental Assessment Tool, prenatal exposure, smallholder horticulture, Tanzania, infant health, occupational exposure, child sex differences, public health
Cite Scienmag News
Harold Sullivan. (September 26, 2026). Pesticide Exposure in Pregnancy Linked to Early Infant Development Delays in Tanzania. Scienmag. https://scienmag.com/pesticide-exposure-in-pregnancy-linked-to-early-infant-development-delays-in-tanzania/
Harold Sullivan. "Pesticide Exposure in Pregnancy Linked to Early Infant Development Delays in Tanzania." Scienmag, 26 September 2026, https://scienmag.com/pesticide-exposure-in-pregnancy-linked-to-early-infant-development-delays-in-tanzania/. Accessed 26 September 2026.
Harold Sullivan. "Pesticide Exposure in Pregnancy Linked to Early Infant Development Delays in Tanzania." Scienmag. September 26, 2026. https://scienmag.com/pesticide-exposure-in-pregnancy-linked-to-early-infant-development-delays-in-tanzania/

