# Impact of Pesticide Use on Gut Microbiota and Health: A Systematic Review of Findings in Both Humans and Animal Models

**Authors:** Iria Osa-Subtil, Teolincacihuatl Romero-Rosales, María José Dios-Duarte

PMC · DOI: 10.3390/jox16020041 · 2026-02-25

## TL;DR

This review explores how pesticide exposure affects gut microbiota and health in humans and animals, highlighting the need for reduced exposure and further research.

## Contribution

The paper systematically reviews evidence linking pesticide exposure to gut microbiota changes and health effects in both humans and animal models.

## Key findings

- Prenatal pesticide exposure is associated with adverse fetal development outcomes.
- Pesticide exposure alters gut microbiota, affecting metabolic, immune, and nervous system functions.
- Animal studies reveal mechanisms like oxidative stress and inflammation linked to pesticide exposure.

## Abstract

Background/objective: The widespread use of pesticides in modern agriculture has raised increasing concern about their potential adverse effects on human health. Exposure to these compounds has been linked to multiple negative health outcomes. This systematic review aims to evaluate and synthesise the available scientific evidence on the effects of pesticide exposure on human health during agricultural production—with particular emphasis on alterations in gut microbiota and intestinal membrane permeability—by integrating results from experimental and observational studies conducted on animals and humans. Methods: This systematic review was conducted in accordance with PRISMA guidelines. A systematic literature search was carried out using the main databases Medline/PubMed, Embase and Web of Science, introducing the search algorithm “pesticides” AND “gut microbiota”, from which a total of seven systematic reviews that met our inclusion criteria were found and subsequently analysed. The quality assessment was based on the principles of evidence-based medicine. This systematic review was registered in the OSF. Results: The findings indicate that prenatal exposure to pesticides is linked to adverse outcomes in foetal development. Additionally, pesticide exposure affects metabolic, immune, and nervous system function due to alterations in gut microbiota composition and membrane permeability. Evidence from animal model studies complements human data by providing insight into the underlying biological mechanisms, such as oxidative stress, liver dysfunction, alterations in hormonal signalling and activation of the inflammatory response. Conclusions: Public health strategies should prioritise reducing pesticide exposure, strengthening environmental protection and supporting further research on gut microbiota modulation and intestinal membrane permeability. Such measures may contribute to the prevention and mitigation of pesticide-related health disorders. Limitations: Human data are insufficient to establish clear causal relationships. Moreover, substantial variability among pesticide types and the difficulty of distinguishing the effects of complex mixtures from those of individual compounds complicate interpretation of the findings.

## Full-text entities

- **Genes:** Tnfrsf1a (tumor necrosis factor receptor superfamily, member 1a) [NCBI Gene 21937] {aka CD120a, FPF, TNF-R, TNF-R-I, TNF-R1, TNF-R55}, Ache (acetylcholinesterase) [NCBI Gene 11423], Cxcl15 (C-X-C motif chemokine ligand 15) [NCBI Gene 20309] {aka Il8, Scyb15, lungkine, weche}, Tnf (tumor necrosis factor) [NCBI Gene 21926] {aka DIF, TNF-a, TNF-alpha, TNFSF2, TNFalpha, Tnfa}, NR1H4 (nuclear receptor subfamily 1 group H member 4) [NCBI Gene 9971] {aka BAR, FXR, HRR-1, HRR1, PFIC5, RIP14}, GPBAR1 (G protein-coupled bile acid receptor 1) [NCBI Gene 151306] {aka BG37, GPCR19, GPR131, M-BAR, TGR5}
- **Diseases:** health disorders (OMIM:603663), autism spectrum disorder (MESH:D000067877), neurosensory impairment (MESH:D006319), enterohepatic disorders (MESH:D009358), neurological defects (MESH:D009421), reproductive disorders (MESH:D060737), vascular dysfunction (MESH:D002561), Low body mass (MESH:C536030), Neurodevelopmental disorders (MESH:D002658), endotoxic (MESH:D012772), Weight gain (MESH:D015430), Impaired energy metabolism (MESH:D008659), liver toxicity (MESH:D056486), injury to (MESH:D014947), auditory alterations (MESH:D004408), Insulin resistance (MESH:D007333), dyskinesia (MESH:D004409), chronic (MESH:D002908), autistic traits (MESH:D001321), intestinal diseases (MESH:D007410), hyper-mobility (MESH:D014086), Low body weight (MESH:D001835), kidney disease (MESH:D007674), non-alcoholic fatty liver disease (MESH:D065626), cancer (MESH:D009369), Social interaction impairment (MESH:C563663), Obesity (MESH:D009765), type 2 diabetes (MESH:D003924), metabolic and neurological diseases (MESH:D001928), deficits in social interaction (MESH:D009461), hepatic metabolism disorders (MESH:D008107), lipid (MESH:D011017), cardiovascular disease (MESH:D002318), immune dysfunction (MESH:D007154), toxicity (MESH:D064420), Glucose intolerance (MESH:D018149), Asthma (MESH:D001249), Dysbiosis (MESH:D064806), systemic (MESH:D015619), Neurodevelopmental defects (MESH:D065886), colitis (MESH:D003092), prostate, ovarian and kidney diseases (MESH:D010049), Communication deficits (MESH:D003147), cognitive and motor impairment (MESH:D003072), respiratory or neuromuscular toxicity (MESH:D020511), hepatic lipid metabolism disorders (MESH:D052439), impaired locomotor activity (MESH:D001523), neuroinflammation (MESH:D000090862), metabolic syndrome (MESH:D024821), liver dysfunction (MESH:D017093), atherogenic (MESH:D050197), mitochondrial dysfunction (MESH:D028361), diabetes (MESH:D003920), prostate disease (MESH:D011469), hepatic and cardiovascular alterations (MESH:D018376), Neurological impairments (MESH:D009422), endocrine disruption (MESH:D004700), Hypo (MESH:D052456), Behavioural abnormalities (MESH:D000014), neuro behavioural deficits (MESH:D001289)
- **Chemicals:** Pyrethroids (MESH:D011722), TG (MESH:D013866), LH (MESH:D007986), cholesterol (MESH:D002784), neonicotinoid pesticides (-), organophosphate (MESH:D010755), GABA (MESH:D005680), fatty acid (MESH:D005227), glutamine (MESH:D005973), bile acid (MESH:D001647), retinol (MESH:D014801), carbamate (MESH:D002219), blood sugar (MESH:D001786), Ammonium glufosinate (MESH:C003121), LPSs (MESH:D008070), organochlorine compounds (MESH:D006843), carbohydrate (MESH:D002241), Propamocarb (MESH:C033205), propionate (MESH:D011422), triglyceride (MESH:D014280), Short-chain fatty acids (MESH:D005232), Lipid (MESH:D008055), glucose (MESH:D005947), butyrate (MESH:D002087), Chlorpyrifos (MESH:D004390), acetate (MESH:D000085), Imidacloprid (MESH:C082359)
- **Species:** Bifidobacterium (genus) [taxon 1678], Mus musculus (house mouse, species) [taxon 10090], Bacteria Latreille et al. 1825 (Bacteria stick insect, genus) [taxon 629395], gut metagenome (species) [taxon 749906], Rattus norvegicus (brown rat, species) [taxon 10116], Homo sapiens (human, species) [taxon 9606], Lactobacillus (genus) [taxon 1578]
- **Mutations:** A-A2
- **Cell lines:** C57BL/6 — Mus musculus (Mouse), Transformed cell line (CVCL_C0MU)

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC13010730/full.md

---
Source: https://tomesphere.com/paper/PMC13010730