Glyphosate - HH-RA.org

Bibliography Tag: glyphosate

Cattani et al., 2017

Cattani, D., Cesconetto, P. A., Tavares, M. K., Parisotto, E. B., De Oliveira, P. A., Rieg, C. E. H., Leite, M. C., Prediger, R. D. S., Wendt, N. C., Razzera, G., Filho, D. W., & Zamoner, A., “Developmental exposure to glyphosate-based herbicide and depressive-like behavior in adult offspring: Implication of glutamate excitotoxicity and oxidative stress,” Toxicology, 2017, 387, 67-80. DOI: 10.1016/j.tox.2017.06.001.

ABSTRACT:

We have previously demonstrated that maternal exposure to glyphosate-based herbicide (GBH) leads to glutamate excitotoxicity in 15-day-old rat hippocampus. The present study was conducted in order to investigate the effects of subchronic exposure to GBH on some neurochemical and behavioral parameters in immature and adult offspring. Rats were exposed to 1% GBH in drinking water (corresponding to 0.36% of glyphosate) from gestational day 5 until postnatal day (PND)-15 or PND60. Results showed that GBH exposure during both prenatal and postnatal periods causes oxidative stress, affects cholinergic and glutamatergic neurotransmission in offspring hippocampus from immature and adult rats. The subchronic exposure to the pesticide decreased L-[(14)C]-glutamate uptake and increased (45)Ca(2+) influx in 60-day-old rat hippocampus, suggesting a persistent glutamate excitotoxicity from developmental period (PND15) to adulthood (PND60). Moreover, GBH exposure alters the serum levels of the astrocytic protein S100B. The effects of GBH exposure were associated with oxidative stress and depressive-like behavior in offspring on PND60, as demonstrated by the prolonged immobility time and decreased time of climbing observed in forced swimming test. The mechanisms underlying the GBH-induced neurotoxicity involve the NMDA receptor activation, impairment of cholinergic transmission, astrocyte dysfunction, ERK1/2 overactivation, decreased p65 NF-kappaB phosphorylation, which are associated with oxidative stress and glutamate excitotoxicity. These neurochemical events may contribute, at least in part, to the depressive-like behavior observed in adult offspring. FULL TEXT

Cai et al., 2017

Cai, Wenyan, Ji, Ying, Song, Xianping, Guo, Haoran, Han, Lei, Zhang, Feng, Liu, Xin, Zhang, Hengdong, Zhu, Baoli, & Xu, Ming, “Effects of glyphosate exposure on sperm concentration in rodents: A systematic review and meta-analysis,” Environmental Toxicology and Pharmacology, 2017, 55, 148-155. DOI: 10.1016/j.etap.2017.07.015.

ABSTRACT:

BACKGROUND: Correlation between exposure to glyphosate and sperm concentrations is important in reproductive toxicity risk assessment for male reproductive functions. Many studies have focused on reproductive toxicity on glyphosate, however, results are still controversial. We conducted a systematic review of epidemiological studies on the association between glyphosate exposure and sperm concentrations of rodents. The aim of this study is to explore the potential adverse effects of glyphosate on reproductive function of male rodents.

METHODS: Systematic and comprehensive literature search was performed in MEDLINE, TOXLINE, Embase, WANFANG and CNKI databases with different combinations of glyphosate exposure and sperm concentration. 8 studies were eventually identified and random-effect model was conducted. Heterogeneity among study results was calculated via chi-square tests. Ten independent experimental datasets from these eight studies were acquired to synthesize the random-effect model.

RESULTS: A decrease in sperm concentrations was found with mean difference of sperm concentrations (MDsperm)=−2.774×106/sperm/g/testis(95%CI=−0.969 to −4.579) in random-effect model after glyphosate exposure. There was also a significant decrease after fitting the random-effect model: MDsperm=−1.632×106/sperm/g/testis (95%CI=−0.662 to −2.601).

CONCLUSIONS: The results of meta-analysis support the hypothesis that glyphosate exposure decreased sperm concentration in rodents. Therefore, we conclude that glyphosate is toxic to male rodent’s reproductive system. FULL TEXT

Bai and Ogbourne, 2016

Bai, S. H., & Ogbourne, S. M., “Glyphosate: environmental contamination, toxicity and potential risks to human health via food contamination,” Environmental Science and Pollution Research, 2016, 23(19), 18988-19001. DOI: 10.1007/s11356-016-7425-3.

ABSTRACT:

Glyphosate has been the most widely used herbicide during the past three decades. The US Environmental Protection Agency (EPA) classifies glyphosate as ‘practically non-toxic and not an irritant’ under the acute toxicity classification system. This classification is based primarily on toxicity data and due to its unique mode of action via a biochemical pathway that only exists in a small number of organisms that utilise the shikimic acid pathway to produce amino acids, most of which are green plants. This classification is supported by the majority of scientific literature on the toxic effects of glyphosate. However, in 2005, the Food and Agriculture Organisation (FAO) reported that glyphosate and its major metabolite, aminomethylphosphonic acid (AMPA), are of potential toxicological concern, mainly as a result of accumulation of residues in the food chain. The FAO further states that the dietary risk of glyphosate and AMPA is unlikely if the maximum daily intake of 1 mg kg(-1) body weight (bw) is not exceeded. Research has now established that glyphosate can persist in the environment, and therefore, assessments of the health risks associated with glyphosate are more complicated than suggested by acute toxicity data that relate primarily to accidental high-rate exposure. We have used recent literature to assess the possible risks associated with the presence of glyphosate residues in food and the environment. FULL TEXT

von Ehrenstein et al., 2019

von Ehrenstein, O. S., Ling, C., Cui, X., Cockburn, M., Park, A. S., Yu, F., Wu, J., & Ritz, B., “Prenatal and infant exposure to ambient pesticides and autism spectrum disorder in children: population based case-control study,” BMJ, 2019, 364, l962. DOI: 10.1136/bmj.l962.

ABSTRACT:

OBJECTIVE: To examine associations between early developmental exposure to ambient pesticides and autism spectrum disorder.

DESIGN: Population based case-control study.

SETTING: California’s main agricultural region, Central Valley, using 1998-2010 birth data from the Office of Vital Statistics.

POPULATION: 2961 individuals with a diagnosis of autism spectrum disorder based on the Diagnostic and Statistical Manual of Mental Disorders, fourth edition, revised (up to 31 December 2013), including 445 with intellectual disability comorbidity, were identified through records maintained at the California Department of Developmental Services and linked to their birth records. Controls derived from birth records were matched to cases 10:1 by sex and birth year.

EXPOSURE: Data from California state mandated Pesticide Use Reporting were integrated into a geographic information system tool to estimate prenatal and infant exposures to pesticides (measured as pounds of pesticides applied per acre/month within 2000 m from the maternal residence). 11 high use pesticides were selected for examination a priori according to previous evidence of neurodevelopmental toxicity in vivo or in vitro (exposure defined as ever v never for each pesticide during specific developmental periods).

MAIN OUTCOME MEASURE: Odds ratios and 95% confidence intervals using multivariable logistic regression were used to assess associations between pesticide exposure and autism spectrum disorder (with or without intellectual disabilities) in offspring, adjusting for confounders.

RESULTS: Risk of autism spectrum disorder was associated with prenatal exposure to glyphosate (odds ratio 1.16, 95% confidence interval 1.06 to 1.27), chlorpyrifos (1.13, 1.05 to 1.23), diazinon (1.11, 1.01 to 1.21), malathion (1.11, 1.01 to 1.22), avermectin (1.12, 1.04 to 1.22), and permethrin (1.10, 1.01 to 1.20). For autism spectrum disorder with intellectual disability, estimated odds ratios were higher (by about 30%) for prenatal exposure to glyphosate (1.33, 1.05 to 1.69), chlorpyrifos (1.27, 1.04 to 1.56), diazinon (1.41, 1.15 to 1.73), permethrin (1.46, 1.20 to 1.78), methyl bromide (1.33, 1.07 to 1.64), and myclobutanil (1.32, 1.09 to 1.60); exposure in the first year of life increased the odds for the disorder with comorbid intellectual disability by up to 50% for some pesticide substances.

CONCLUSION: Findings suggest that an offspring’s risk of autism spectrum disorder increases following prenatal exposure to ambient pesticides within 2000 m of their mother’s residence during pregnancy, compared with offspring of women from the same agricultural region without such exposure. Infant exposure could further increase risks for autism spectrum disorder with comorbid intellectual disability. FULL TEXT

Zhang et al., 2019a

Zhang, Luoping, Rana, Iemaan, Shaffer, Rachel M., Taioli, Emanuela, & Sheppard, Lianne, “Exposure to Glyphosate-Based Herbicides and Risk for Non-Hodgkin Lymphoma: A Meta-Analysis and Supporting Evidence,” Mutation Research/Reviews in Mutation Research, In Press, 2019. DOI: 10.1016/j.mrrev.2019.02.001.

ABSTRACT:

Glyphosate is the most widely used broad-spectrum systemic herbicide in the world. Recent evaluations of the carcinogenic potential of glyphosate-based herbicides (GBHs) by various regional, national, and international agencies have engendered controversy. We investigated whether there was an association between high cumulative exposures to GBHs and increased risk of non-Hodgkin lymphoma (NHL) in humans. We conducted a new meta-analysis that included the most recent update of the Agricultural Health Study (AHS) cohort published in 2018 along with five case-control studies. Using the highest exposure groups when available in each study, we report the overall meta-relative risk (meta-RR) of NHL in GBH-exposed individuals was increased by 41% (meta-RR = 1.41, 95% CI, confidence interval: 1.13–1.75). For comparison, we also performed a secondary meta-analysis using high-exposure groups with the earlier AHS (2005), and we determined a meta-RR for NHL of 1.45 (95% CI: 1.11–1.91), which was higher than the meta-RRs reported previously. Multiple sensitivity tests conducted to assess the validity of our findings did not reveal meaningful differences from our primary estimated meta-RR. To contextualize our findings of an increased NHL risk in individuals with high GBH exposure, we reviewed available animal and mechanistic studies, which provided supporting evidence for the carcinogenic potential of GBH. We documented further support from studies of malignant lymphoma incidence in mice treated with pure glyphosate, as well as potential links between GBH exposure and immunosuppression, endocrine disruption, and genetic alterations that are commonly associated with NHL. Overall, in accordance with evidence from experimental animal and mechanistic studies, our current meta-analysis of human epidemiological studies suggests a compelling link between exposures to GBHs and increased risk for NHL. FULL TEXT

Wozniak et al., 2018

Wozniak, E., Sicinska, P., Michalowicz, J., Wozniak, K., Reszka, E., Huras, B., Zakrzewski, J., & Bukowska, B., “The mechanism of DNA damage induced by Roundup 360 PLUS, glyphosate and AMPA in human peripheral blood mononuclear cells – genotoxic risk assessement,” Food and Chemical Toxicology, 2018, 120, 510-522. DOI: 10.1016/j.fct.2018.07.035.

ABSTRACT:

Glyphosate is the most heavily applied among pesticides in the world, and thus human exposure to this substance continues to increase. WHO changed classification of glyphosate to probably cancerogenic to humans, thus there is urgent need to assess in detail genotoxic mechanism of its action. We have assessed the effect of glyphosate, its formulation (Roundup 360 PLUS) and its main metabolite (aminomethylphosphonic acid, AMPA) in the concentration range from 1 to 1000muM on DNA damage in human peripheral blood mononuclear cells (PBMCs). The cells were incubated for 24h. The compounds studied and formulation induced DNA single and double strand-breaks and caused purines and pyrimidines oxidation. None of compounds examined was capable of creating adducts with DNA, while those substances increased ROS (including (*)OH) level in PBMCs. Roundup 360 PLUS caused damage to DNA even at 5muM, while glyphosate and particularly AMPA induced DNA lesions from the concentration of 250muM and 500muM, respectively. DNA damage induced by glyphosate and its derivatives increased in order: AMPA, glyphosate, Roundup 360 PLUS. We may conclude that observed changes were not associated with direct interaction of xenobiotics studied with DNA, but the most probably they occurred through ROS-mediated effects. FULL TEXT

Ward, 2018

Ward, E. M., “Glyphosate Use and Cancer Incidence in the Agricultural Health Study: An Epidemiologic Perspective,” Journal of the National Cancer Institute, 2018, 110(5), 446-447. DOI: 10.1093/jnci/djx247.

ABSTRACT:

Not Available. FULL TEXT

Varayoud et al., 2017

Varayoud, J., Durando, M., Ramos, J. G., Milesi, M. M., Ingaramo, P. I., Munoz-de-Toro, M., & Luque, E. H., “Effects of a glyphosate-based herbicide on the uterus of adult ovariectomized rats,” Environmental Toxicology, 2017, 32(4), 1191-1201. DOI: 10.1002/tox.22316.

ABSTRACT:

Glyphosate is the active ingredient of several herbicide formulations. Different reports suggest that glyphosate-based herbicides (GBHs) may act as endocrine disruptors. We evaluated the potential estrogenic effects of a GBH formulation using the uterotrophic assay. Adult ovariectomized rats were sc injected for 3 consecutive days with: saline solution (vehicle control), 2.10(-5) g E2 /kg/day (uterotrophic dose; UE2 ), 2.10(-7) g E2 /kg/day (nonuterotrophic dose; NUE2), or 0.5, 5, or 50 mg GBH/kg/day of the. Twenty-four hours after the last injection, the uterus was removed and weighed and processed for histopathology and mRNA extraction. Epithelial cell proliferation and height and expression of estrogen-responsive genes were evaluated (estrogen receptors, ERalpha and ERbeta; progesterone receptor, PR; complement 3, C3). Uterine weight and epithelial proliferation were not affected by GBH. However, the luminal epithelial cell height increased at GBH0.5. ERalpha mRNA was downregulated by all GBH doses and E2 groups, whereas PR and C3 mRNA were diminished by GBH0.5. GBH5-, GBH50-, and UE2 -treated rats showed downregulated ERalpha protein expression in luminal epithelial cells, while the receptor was upregulated in the stroma. GBH upregulated ERbeta (GBH0.5-50) and PR (GBH5) expressions in glandular epithelial cells, similar effect to that of NUE2 group. These results indicate that, although the uterine weight was not affected, GBH modulates the expression of estrogen-sensitive genes. (c) 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1191-1201, 2017.

Valle et al., 2018

Valle, A. L., Mello, F. C. C., Alves-Balvedi, R. P., Rodrigues, L. P., & Goulart, L. R., “Glyphosate detection: methods, needs and challenges,” Environmental Chemistry Letters, 2018. DOI: 10.1007/s10311-018-0789-5.

ABSTRACT:

Glyphosate is considered toxicologically harmful and presents potential association with human carcinogenesis and other chronic diseases, including mental and reproductive behaviors. The challenges to analyse and demonstrate its toxicity are likely due to its metal-chelating properties, the interference of organic compounds in the environment, and similarity with its by-products. Whereas there is a link with serious health and environmental problems, there is an absence of public health policies, which is probably due to the difficulties in detecting glyphosate in the environment, further complicated by the undetectable hazard in occupational safety and health. The historical lenient use of glyphosate in transgenic-resistant crops, corroborated by the fact that it is not easily detected, creates the “Glyphosate paradox”, by which it is the most widely used herbicide and one of the most hardly determined. In this review, we revisited all available technologies for detection and quantification of glyphosate, including their drawbacks and advantages, and we further discuss the needs and challenges. Briefly, most of the technologies require high-end equipments and resources in low throughput, and none of them are adequate for real-time field tests, which may explain the lack of studies on occupational health associated with the chemical hazard. The real-time detection is an urgent and highly demanded need to improve public policies. FULL TEXT

Townsend et al., 2017

Townsend, M., Peck, C., Meng, W., Heaton, M., Robison, R., & O’Neill, K., “Evaluation of various glyphosate concentrations on DNA damage in human Raji cells and its impact on cytotoxicity,” Regulatory Toxicology and Pharmacology, 2017, 85, 79-85. DOI: 10.1016/j.yrtph.2017.02.002.

ABSTRACT:

Glyphosate is a highly used active compound in agriculturally based pesticides. The literature regarding the toxicity of glyphosate to human cells has been highly inconsistent. We studied the resulting DNA damage and cytotoxicity of various glyphosate concentrations on human cells to evaluate DNA damaging potential. Utilizing human Raji cells, DNA damage was quantified using the comet assay, while cytotoxicity was further analyzed using MTT viability assays. Several glyphosate concentrations were assessed, ranging from 15 mM to 0.1 muM. We found that glyphosate treatment is lethal to Raji cells at concentrations above 10 mM, yet has no cytotoxic effects at concentrations at or below 100 muM. Treatment concentrations of 1 mM and 5 mM induce statistically significant DNA damage to Raji cells following 30-60 min of treatment, however, cells show a slow recovery from initial damage and cell viability is unaffected after 2 h. At these same concentrations, cells treated with additional compound did not recover and maintained high levels of DNA damage. While the cytotoxicity of glyphosate appears to be minimal for physiologically relevant concentrations, the compound has a definitive cytotoxic nature in human cells at high concentrations. Our data also suggests a mammalian metabolic pathway for the degradation of glyphosate may be present. FULL TEXT

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