During the past decades, farmers in low to middle-income countries have increased their use of pesticides, and thereby the risk of being exposed to potentially genotoxic chemicals that can cause adverse health effects. Here, the aim was to investigate the correlation between exposure to pesticides and genotoxic damage in a Bolivian agricultural population. Genotoxic effects were assessed in peripheral blood samples by comet and micronucleus (MN) assays, and exposure levels by measurements of 10 urinary pesticide metabolites. Genetic susceptibility was assessed by determination of null frequency of GSTM1 and GSTT1 genotypes. The results showed higher MN frequency in women and farmers active ≥8 years compared to their counterpart (P < 0.05). In addition, age, GST genotype, alcohol consumption, and type of water source influenced levels of genotoxic damage. Individuals with high exposure to tebuconazole, 2,4-D, or cyfluthrin displayed increased levels of genotoxic damage (P < 0.05–0.001). Logistic regression was conducted to evaluate associations between pesticide exposure and risk of genotoxic damage. After adjustment for confounders, a significant increased risk of DNA strand breaks was found for high exposure to 2,4-D, odds ratio (OR) = 1.99 (P < 0.05). In contrast, high exposure to pyrethroids was associated with a reduced risk of DNA strand breaks, OR = 0.49 (P < 0.05). It was also found that high exposure to certain mixtures of pesticides (containing mainly 2,4-D or cyfluthrin) was significantly associated with increased level and risk of genotoxic damage (P < 0.05). In conclusion, our data show that high exposure levels to some pesticides is associated with an increased risk of genotoxic damage among Bolivian farmers, suggesting that their use should be better controlled or limited.
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The authors warmly thank all the people in the communities who participated in this study and the people who contacted them, Rubén Araujo (Pastoral Social Cáritas Corocoro, La Paz) and Angela del Callejo (Universidad Mayor de San Simón, Cochabamba). We are also grateful to Pablo Almaraz for their technical assistance, to the members of Toxicology Genetics unit at the Genetic Institute (Universidad Mayor de San Andrés, La Paz) and all workers at the local health care centers for their assistance during the field activities. We thank Karin Leander (Karolinska Institutet, Stockholm) for assistance with statistical analysis. This work was supported by the Swedish International Development Cooperation Agency [grant number 7500055309], the Swedish Research Council [grant number 2016-05799], and the Genetic Institute, Universidad Mayor de San Andrés, Bolivia.
This work was supported by the Swedish International Development Cooperation Agency [grant number 7500055309 ], the Swedish Research Council [grant number 2016-05799 ], and the Genetic Institute, Universidad Mayor de San Andrés, Bolivia .
© 2019 The Authors