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The use of pesticides has become a worldwide concern, and Brazil is one of the countries that release the most pesticides and is affected by them. These chemical substances, when in contact with the human body, can cause health problems such as nephrotoxicity, neurodegeneration, and even cancer. This study investigates how direct and indirect pesticide exposure interferes with acetylcholinesterase (AChE) and hematological parameters. This cross-sectional study was conducted in Sergipe, Brazil, and included 378 participants. The impact of pesticides on AChE and hematological parameters in individuals exposed to these agents was evaluated. Triazine (TZ) and Organochlorine (OC) classes combination generated the lowest AChE. A lower mean for AChE for individuals directly exposed to pesticides (p < 0.05) was observed. Men and younger individuals tended to have lower levels of AChE, as did individuals who declared themselves black or yellow or did not declare any ethnicity. As for hematological alterations, micronuclei (MN) were detected in 12.2% of farmers and 8.7% of families and neighborhoods. We found that AChE values tended to increase with the number of platelets and red blood cells (RBC). Still, we did not detect any other relationships between AChE and the type of exposure with hematological parameters. These findings contribute to evaluating the impact of pesticide exposure on human health. Thus, it allows us to infer that individuals directly exposed to pesticides tend to have lower levels of AChE, demonstrating the need to monitor these clinical parameters in individuals exposed to these agents and seek to identify the profile of this population., (© The Author(s) 2025. Published by Oxford University Press on behalf of the Society of Environmental Toxicology and Chemistry. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

Diabetes mellitus is a metabolic syndrome that has grown globally to become a significant public health challenge. Hypothesizing that the plasma membrane protein, transient receptor potential ankyrin-1, is a pivotal target in insulin resistance, we investigated the mechanism of action of cinnamaldehyde (CIN), an electrophilic TRPA1 agonist, in skeletal muscle, a primary insulin target. Specifically, we evaluated the effect of CIN on insulin resistance, hepatic glycogen accumulation and muscle and adipose tissue glucose uptake. Furthermore, the in vitro role of CIN in glucose uptake and intracellular signaling was determined in insulin-resistant rats whose calcium influx was analyzed. Moreover, the serum lipid profile was assessed following short-term CIN treatment in rats, and lipid tolerance was analyzed. The effects of CIN on insulin resistance were mediated by TRPA1, with downstream signaling involving the activation of PI3-K, MAPK, PKC, as well as extracellular calcium and calcium release from intracellular stores. Additionally, cytoskeleton integrity was required for the complete action of CIN on glucose uptake in muscle. CIN also ameliorated the serum lipid profile and improved triglyceride tolerance following acute vivo exposure.