Perinatal exposure to glyphosate-based herbicide alters the thyrotrophic axis and causes thyroid hormone homeostasis imbalance in male rats

Souza, Janaína Sena de; Kizys, Marina M. L.; Conceição, Rodrigo Rodrigues da; Glebocki, Gabriel; Romano, Renata Marino; Ortiga-Carvalho, Tânia M.; Giannocco, Gisele; Silva, Ismael Dale Cotrim Guerreiro da; Silva, Magnus R. Dias da; Romano, Marco Aurélio; Chiamolera, Maria Izabel

doi:10.1016/j.tox.2016.11.005

Cited by 76 publications

(53 citation statements)

References 62 publications

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“…Gene expression of mouse cortical neurons was altered by certain fungicides and resembled transcriptional changes thought to underlie development of autism spectrum disorder 214. Translational research connecting toxicological and animal studies with findings from epidemiological studies is needed to identify the specific modes of action of pesticides relevant for the pathogenesis of autism spectrum disorder 6566676869…”

Section: Discussionmentioning

confidence: 99%

Prenatal and infant exposure to ambient pesticides and autism spectrum disorder in children: population based case-control study

Ehrenstein

Ling

Cui

et al. 2019

BMJ

216

165

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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.

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Section: Discussionmentioning

confidence: 99%

Prenatal and infant exposure to ambient pesticides and autism spectrum disorder in children: population based case-control study

Ehrenstein

Ling

Cui

et al. 2019

BMJ

216

165

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“…The reanalysis in this review show an inconsistent increase in thyroid C-cell adenomas and/or carcinomas in male and female SD rats and thyroid follicular cell adenomas in male SD rats. De Souza et al [94] exposed male Wistar rats to the GBH Roundup Transorb from gestational day18 to postnatal day 5 and examined the animals for thyroid hormone effects at postnatal day 90. They saw dose-dependent decreases in thyroid stimulating hormone but no changes in circulating triiodothyronine or thyroxine.…”

Section: Related Findings From the Peer-reviewed Literaturementioning

confidence: 99%

A comprehensive analysis of the animal carcinogenicity data for glyphosate from chronic exposure rodent carcinogenicity studies

Portier

2020

Environ Health

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Since the introduction of glyphosate-tolerant genetically-modified plants, the global use of glyphosate has increased dramatically making it the most widely used pesticide on the planet. There is considerable controversy concerning the carcinogenicity of glyphosate with scientists and regulatory authorities involved in the review of glyphosate having markedly different opinions. One key aspect of these opinions is the degree to which glyphosate causes cancer in laboratory animals after lifetime exposure. In this review, twenty-one chronic exposure animal carcinogenicity studies of glyphosate are identified from regulatory documents and reviews; 13 studies are of sufficient quality and detail to be reanalyzed in this review using trend tests, historical control tests and pooled analyses. The analyses identify 37 significant tumor findings in these studies and demonstrate consistency across studies in the same sex/species/strain for many of these tumors. Considering analyses of the individual studies, the consistency of the data across studies, the pooled analyses, the historical control data, non-neoplastic lesions, mechanistic evidence and the associated scientific literature, the tumor increases seen in this review are categorized as to the strength of the evidence that glyphosate causes these cancers. The strongest evidence shows that glyphosate causes hemangiosarcomas, kidney tumors and malignant lymphomas in male CD-1 mice, hemangiomas and malignant lymphomas in female CD-1 mice, hemangiomas in female Swiss albino mice, kidney adenomas, liver adenomas, skin keratoacanthomas and skin basal cell tumors in male Sprague-Dawley rats, adrenal cortical carcinomas in female Sprague-Dawley rats and hepatocellular adenomas and skin keratocanthomas in male Wistar rats.

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“…Levels of TSH were decreased in exposure groups, however levels of both T3 and T4 were unaffected. This curious lack of TH hormone effects, despite TSH and target gene changes, may reflect changes in TSH set-point resulting from differential gene programming in rats during the fetal period (131). Due to the removal of patent protection for glyphosate in 2000, many new glyphosate-based herbicides arrived on the pesticide market.…”

Section: In Vivo Evidence Of Thyroid Disruptionmentioning

confidence: 99%

Pesticides With Potential Thyroid Hormone-Disrupting Effects: A Review of Recent Data

et al. 2019

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Plant Protection Products, more commonly referred to as pesticides and biocides, are used to control a wide range of yield-reducing pests including insects, fungi, nematodes, and weeds. Concern has been raised that some pesticides may act as endocrine disrupting chemicals (EDCs) with the potential to interfere with the hormone systems of non-target invertebrates and vertebrates, including humans. EDCs act at low doses and particularly vulnerable periods of exposure include pre-and perinatal development. Of critical concern is the number of pesticides with the potential to interfere with the developing nervous system and brain, notably with thyroid hormone signaling. Across vertebrates, thyroid hormone orchestrates metamorphosis, brain development, and metabolism. Pesticide action on thyroid homeostasis can involve interference with TH production and its control, displacement from distributor proteins and liver metabolism. Here we focused on thyroid endpoints for each of the different classes of pesticides reviewing epidemiological and experimental studies carried out both in in vivo and in vitro. We conclude first, that many pesticides were placed on the market with insufficient testing, other than acute or chronic toxicity, and second, that thyroid-specific endpoints for neurodevelopmental effects and mixture assessment are largely absent from regulatory directives.

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Perinatal exposure to glyphosate-based herbicide alters the thyrotrophic axis and causes thyroid hormone homeostasis imbalance in male rats

Cited by 76 publications

References 62 publications

Prenatal and infant exposure to ambient pesticides and autism spectrum disorder in children: population based case-control study

Prenatal and infant exposure to ambient pesticides and autism spectrum disorder in children: population based case-control study

A comprehensive analysis of the animal carcinogenicity data for glyphosate from chronic exposure rodent carcinogenicity studies

Pesticides With Potential Thyroid Hormone-Disrupting Effects: A Review of Recent Data

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