Neural tube defects (NTDs) are the second most common congenital anomaly and have been widely associated with exposure to pesticides. This systematic review which analyzes the association between parental exposure to pesticides and NTDs was conducted in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines. The search strategy was designed considering the population, exposure, controls, outcomes, and study design (PECOS). The inclusion criteria were epidemiological studies involving pesticides exposure during embryonic development, written in English, Portuguese, or Spanish, and performed in 12 databases. Based on the eligibility criteria, 16 articles were selected for analysis. The most frequently assessed NTDs were anencephaly and spina bifida, with 14 studies investigating each of these conditions. The assessment of pesticide exposure was based on parental occupation and residential proximity to agricultural fields. Studies differed regarding the pesticides assessed, exposure windows, and parents exposed. Regarding the outcomes, it was observed that geographic proximity to agricultural fields and a greater association with family members exposed to pesticides were found in mothers and neonates with NTDs. In relation to occupational exposure, some articles found an association with NTDs, while others did not. Therefore, an analysis of the available evidence suggests that pesticides are a risk factor in the development of NTDs.

Weeds have acquired resistance to commonly used herbicides, and to replace them, new products, including those of natural origin, have been produced. This study evaluated the neurotoxicity, cytotoxicity, and changes in the antioxidant system caused by Natural Herbicide (NH) in SH-SY5Y neuroblastoma cells and HaCaT dermal cells. SH-SY5Y and HaCaT cells were exposed to three concentrations of NH (NH1: 0.6; NH2: 1.56; and NH3: 3.12 µL/mL) for 24 and 72 h. In the SH-SY5Y cell line, the highest concentration of NH (NH3) caused cytotoxicity at both 24 and 72 h. At 24 h, the NH3 group increased the SOD. In the NH2 and NH3 groups, there was also an increase in AChE activity after 24 h of exposure. The NH1 group led to an increase in GSH after 72 h of exposure. As for the HaCaT strain, there was cytotoxicity and an increase in SOD and GSH at all NH concentrations and for both periods analyzed (24 h and 72 h). GST was reduced after exposure to NH2 and NH3. Thus, NH showed cytotoxicity in neural and dermal cells (SH-SY5Y and HaCaT, respectively). These results show that NH altered cellular homeostasis, and the evaluation of other toxicity mechanisms is important to clarify its safety.

Exposure to pesticides during embryonic development can cause damage to health, especially when they are complex mixtures. This study evaluated the lethality, teratogenic effects, antioxidant system, and neurotoxicity in zebrafish (Danio rerio) embryos during a 96 h exposure to the herbicides dicamba (DIC) and glyphosate (GLY), alone and in a mixture. The embryos were exposed to 18 (D1) and 72 (D2) mg/L of DIC, 6 (G1) and 22 (G2) mg/L of GLY, and mixtures M1 (18 mg/L of DIC + 6 mg/L of GLY) and M2 (72 mg/L of DIC + 22 mg/L of GLY). The LC₅₀ was 88.1 mg/L and 285.8 mg/L for GLY and DIC, respectively. M2 showed greater lethality at 48 and 72 h. The mixtures increased teratogenic effects. Generalized edema, predominant in embryos exposed to DIC, reached its maximum incidence between 48 and 72 h and then decreased. M1 delayed hatching by 72 h, while M2 accelerated it by 48 h. Yolk sac edema was significant in M1. Herbicides affected the antioxidant system differently: DIC reduced SOD activity, while GLY increased it. Additionally, DIC and M2 increased acetylcholinesterase activity, indicating neurotoxicity. This is the first study to report the effects of these herbicide mixtures on zebrafish embryos, highlighting the complexity and severity of their impact on embryonic development. Therefore, the importance of the controlled use of these pesticides is emphasized to avoid harmful effects on non-target organisms.

Pesticides are among the most widely used environmental contaminants worldwide, resulting in continuous human exposure primarily through dietary intake. As a major site of contact following oral exposure, the gastrointestinal tract represents a relevant target for pesticide-associated toxicity. Although accumulating evidence indicates that pesticides can alter intestinal structure and function, the toxicological mechanisms underlying these effects have not been critically integrated. This narrative review evaluates experimental studies in rodent models investigating the intestinal toxicity of herbicides, insecticides, and fungicides, with particular emphasis on the convergence and heterogeneity of the reported mechanisms. Across the studies reviewed, recurrent alterations included oxidative imbalance, inflammatory activation, epithelial barrier disruption, changes in intestinal permeability, mitochondrial dysfunction, and genotoxicity. However, the occurrence and magnitude of these responses varied according to pesticide class, compound, dose, exposure duration, formulation, and experimental model, and the available evidence does not support a universal mechanistic sequence. By comparatively integrating these findings, this review highlights shared and pesticide-specific intestinal responses while distinguishing recurrent associations from established causal relationships. Important knowledge gaps remain regarding chronic low-dose exposure, pesticide mixtures, sex-specific susceptibility, recovery after exposure, and the translational relevance of experimental findings to humans. Overall, this review provides a critical framework for interpreting pesticide-associated intestinal toxicity and identifies priorities for future experimental and translational research.