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Bibliography Tag: endocrine disruptors

Gasnier et al., 2009.

Gasnier C, Dumont C, Benachour N, Clair E, Chagnon MC, Séralini GE, “Glyphosate-based herbicides are toxic and endocrine disruptors in human cell lines,” Toxicology, 2009, 262:3. DOI: 10.1016/j.tox.2009.06.006.

ABSTRACT: Glyphosate-based herbicides are the most widely used across the world; they are commercialized in different formulations. Their residues are frequent pollutants in the environment. In addition, these herbicides are spread on most eaten transgenic plants, modified to tolerate high levels of these compounds in their cells. Up to 400 ppm of their residues are accepted in some feed. We exposed human liver HepG2 cells, a well-known model to study xenobiotic toxicity, to four different formulations and to glyphosate, which is usually tested alone in chronic in vivo regulatory studies. We measured cytotoxicity with three assays (Alamar Blue, MTT, ToxiLight), plus genotoxicity (comet assay), anti-estrogenic (on ERalpha, ERbeta) and anti-androgenic effects (on AR) using gene reporter tests. We also checked androgen to estrogen conversion by aromatase activity and mRNA. All parameters were disrupted at sub-agricultural doses with all formulations within 24h. These effects were more dependent on the formulation than on the glyphosate concentration. First, we observed a human cell endocrine disruption from 0.5 ppm on the androgen receptor in MDA-MB453-kb2 cells for the most active formulation (R400), then from 2 ppm the transcriptional activities on both estrogen receptors were also inhibited on HepG2. Aromatase transcription and activity were disrupted from 10 ppm. Cytotoxic effects started at 10 ppm with Alamar Blue assay (the most sensitive), and DNA damages at 5 ppm. A real cell impact of glyphosate-based herbicides residues in food, feed or in the environment has thus to be considered, and their classifications as carcinogens/mutagens/reprotoxics is discussed.

Defarge et al., 2016

Defarge N, Takács E, Lozano VL, Mesnage R, Spiroux de Vendômois J, Séralini GE, Székács A, “Co-Formulants in Glyphosate-Based Herbicides Disrupt Aromatase Activity in Human Cells below Toxic Levels,” International Journal of Environmental Research and Public Health, 2016, 13:3.


Pesticide formulations contain declared active ingredients and co-formulants presented as inert and confidential compounds. We tested the endocrine disruption of co-formulants in six glyphosate-based herbicides (GBH), the most used pesticides worldwide. All co-formulants and formulations were comparably cytotoxic well below the agricultural dilution of 1% (18-2000 times for co-formulants, 8-141 times for formulations), and not the declared active ingredient glyphosate (G) alone. The endocrine-disrupting effects of all these compounds were measured on aromatase activity, a key enzyme in the balance of sex hormones, below the toxicity threshold. Aromatase activity was decreased both by the co-formulants alone (polyethoxylated tallow amine-POEA and alkyl polyglucoside-APG) and by the formulations, from concentrations 800 times lower than the agricultural dilutions; while G exerted an effect only at 1/3 of the agricultural dilution. It was demonstrated for the first time that endocrine disruption by GBH could not only be due to the declared active ingredient but also to co-formulants. These results could explain numerous in vivo results with GBHs not seen with G alone; moreover, they challenge the relevance of the acceptable daily intake (ADI) value for GBHs exposures, currently calculated from toxicity tests of the declared active ingredient alone.  FULL TEXT

Collotta et al., 2013

Collotta, M, Bertazzi, PA, Bollati, V, “Epigenetics and pesticides,” Toxicology, 2013, 307, DOI: 10.1016/j.tox.2013.01.017.

ABSTRACT: Pesticides, a wide class of environmental contaminants, may cause both acute and delayed health effects in exposed subjects. These effects can range from simple irritation of the skin and eyes to more severe effects such as affecting the nervous system, the reproductive system and cancer. The molecular mechanisms underlying such effects are still under investigation. Epigenetics is the study of heritable changes in gene expression that occur without a change in the DNA sequence. Several epigenetic mechanisms, including DNA methylation, histone modifications and microRNA expression, can be triggered by environmental factors.We review current evidences indicating that epigenetic modifications may mediate pesticide effects on human health. In vitro, animal, and human investigations have identified several classes of pesticides that modify epigenetic marks, including endocrine disruptors, persistent organic pollutants, arsenic, several herbicides and insecticides. Several investigations have examined the effects of environmental exposures and epigenetic markers, and identified toxicants that modify epigenetic states. These modifications are similar to the ones found in pathological tissue samples. In spite of the current limitations, available evidence supports the concept that epigenetics holds substantial potential for furthering our understanding of the molecular mechanisms of pesticides health effects, as well as for predicting health-related risks due to conditions of environmental exposure and individual susceptibility.  FULL TEXT

Agopian et al, 2013b

Agopian AJ, Lupo PJ, Canfield MA, Langlois PH, “Case-control study of maternal residential atrazine exposure and male genital malformations,” American Journal of Medical Genetics Part A, 2013, 161A:5, doi: 10.1002/ajmg.a.35815.

ABSTRACT: Exposure to endocrine disrupting chemicals has been associated with risk for male genital malformations. However, residential prenatal exposure to atrazine, an endocrine disrupting pesticide, has not been evaluated. We obtained data from the Texas Birth Defects Registry for 16,433 cases with isolated male genital malformations and randomly selected, population-based controls delivered during 1999-2008. County-level estimates of atrazine exposure from the United States Geological Survey were linked to all subjects. We evaluated the relationship between estimated maternal residential atrazine exposure and risk for male genital malformations in offspring. Separate unconditional logistic regression analyses were conducted for hypospadias, cryptorchidism, and small penis. We observed modest, but consistent, associations between medium-low and/or medium levels of estimated periconceptional maternal residential atrazine exposure and every male genital malformation category evaluated (e.g., adjusted odds ratio for medium compared to low atrazine levels and all male genital malformations: 1.2, 95% confidence interval: 1.1-1.3). Previous literature from animal and epidemiological studies supports our findings. Our results provide further evidence of a suspected teratogenic role of atrazine. FULL TEXT

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