Genotoxic and epigenetic effects of prenatal and early-childhood pesticide exposure: a systematic review and meta-analysis
1
Institute of Public Health, United Arab Emirates University, Al Ain, United Arab Emirates
2
Department of Anatomy and Embryology, Benha University, Benha, Egypt
3
Department of Physiology, Benha University, Moshtohor, Egypt
4
Department of Statistics, Benha University, Benha, Egypt
5
Central Clinical Pathology Labs, Ministry of Health and Population, Cairo, Egypt
Popul. Med. 2026;8(Supplement Supplement 1):A442
ABSTRACT
BACKGROUND:
Exposure to pesticides at early stages of life is a global environmental health concern, yet the genotoxic mechanisms potentially linking these exposures to adverse health outcomes remain incompletely characterized. This study aims to systematically review and meta-analyze evidence for genotoxic effects of early-life pesticide exposure.
METHODS:
Following PRISMA guidelines we searched four databases for studies of prenatal/childhood pesticide exposure reporting primary DNA damage, cytogenetic damage, DNA methylation, or gene-expression outcomes. Risk of bias was assessed with the Newcastle–Ottawa Scale. Random-effects meta-analyses estimated pooled effect sizes and explored subgroup heterogeneity.
RESULTS:
Twenty-eight studies met inclusion criteria. Meta-analysis revealed substantial DNA damage in pesticide-exposed groups (Cohen's d=4.85, 95%CI=3.31-6.39), with stronger effects in maternal and cord blood than in children's blood. Cytogenetic damage showed consistent increase in agricultural versus urban areas, though with significant heterogeneity in effect magnitude. Pathway-specific gene expression analysis revealed significant downregulation of DNA damage/repair genes (-1.08, 95%CI:-1.20,-0.96) and distinct biological responses across inflammatory, oxidative stress, and cell signaling pathways. DNA methylation responses varied by pesticide class, with o,p'-DDT consistently associated with hypermethylation. Pronounced sex-specific effects and genetic susceptibility emerged as important effect modifiers.
CONCLUSIONS:
The evidence supports substantial genotoxic and epigenetic alterations following early-life pesticide exposure, highlighting mechanistic pathways that may underlie adverse health outcomes and reinforcing the need for effective environmental health policies during critical developmental windows.
Exposure to pesticides at early stages of life is a global environmental health concern, yet the genotoxic mechanisms potentially linking these exposures to adverse health outcomes remain incompletely characterized. This study aims to systematically review and meta-analyze evidence for genotoxic effects of early-life pesticide exposure.
METHODS:
Following PRISMA guidelines we searched four databases for studies of prenatal/childhood pesticide exposure reporting primary DNA damage, cytogenetic damage, DNA methylation, or gene-expression outcomes. Risk of bias was assessed with the Newcastle–Ottawa Scale. Random-effects meta-analyses estimated pooled effect sizes and explored subgroup heterogeneity.
RESULTS:
Twenty-eight studies met inclusion criteria. Meta-analysis revealed substantial DNA damage in pesticide-exposed groups (Cohen's d=4.85, 95%CI=3.31-6.39), with stronger effects in maternal and cord blood than in children's blood. Cytogenetic damage showed consistent increase in agricultural versus urban areas, though with significant heterogeneity in effect magnitude. Pathway-specific gene expression analysis revealed significant downregulation of DNA damage/repair genes (-1.08, 95%CI:-1.20,-0.96) and distinct biological responses across inflammatory, oxidative stress, and cell signaling pathways. DNA methylation responses varied by pesticide class, with o,p'-DDT consistently associated with hypermethylation. Pronounced sex-specific effects and genetic susceptibility emerged as important effect modifiers.
CONCLUSIONS:
The evidence supports substantial genotoxic and epigenetic alterations following early-life pesticide exposure, highlighting mechanistic pathways that may underlie adverse health outcomes and reinforcing the need for effective environmental health policies during critical developmental windows.
| eISSN: | 2654-1459 |
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