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A growing body of research suggests that dysbiosis of the gut microbiota induced by environmental pollutants, such as pesticides, could have a role in the development of metabolic disorders. We have examined the long-term effects of 3 doses of the Roundup(R) herbicide (made of glyphosate and formulants) on the gut microbiota in male and female Sprague-Dawley rats. A total of 141 bacteria families were identified by a 16S sequencing analysis approach. An OPLS-DA analysis revealed an increased Bacteroidetes family S24-7 and a decreased Lactobacillaceae in 8 out of the 9 females treated with 3 different doses of R (n = 3, for each dose). These effects were confirmed by repetitive sequence-based PCR fingerprinting showing a clustering of treated females. A culture-based method showed that R had a direct effect on rat gut microbiota. Cultivable species showed different sensitivities to R, including the presence of a high tolerant or resistant strain identified as Escherichia coli by 16S rRNA sequencing. The high tolerance of this E. Coli strain was explained by the absence of the EPSPS gene (coding glyphosate target enzyme) as shown by DNA amplification. Overall, these gut microbiome disturbances showed a substantial overlap with those associated with liver dysfunction in other studies. In conclusion, we revealed that an environmental concentration of R (0.1 ppb) and other two concentrations (400 ppm and 5,000 ppm) have a sex-dependent impact on rat gut microbiome composition and thus warrants further investigation. Keywords: Glyphosate, Roundup, Gut microbiome, Pesticides, Toxicity

Everything began with the discovery that pesticides have long had unintended side effects on non-target species, which is illustrated by Ponepal et al [...]

Organic and non-organic equivalent corresponding type of foods were assessed for pollutants, polycyclic aromatic hydrocarbons (PAHs), pesticides and heavy metals. In total, 35 samples of sausages and cheeses were tested from three western European countries, Spain, France, and Germany. These samples were chosen because they are meat and milk products presenting some bioaccumulation capacity. Petroleum residues were demonstrated in pesticide formulants. These include polycyclic aromatic hydrocarbons (PAHs) and metals. We measured in these human foods 800 pesticides, 24 PAHs, using accredited methods, as well as eleven metals and elements. Pesticides’ measurements were performed either by gas or liquid chromatography, followed by mass spectrometry, according to regulatory standard methods, that were measured over the threshold of 10 μg/kg for this reason. This could be insufficient to detect all toxic contaminations. Metals were analysed by high frequency induced plasma emission spectrometry and mass spectrometry after pressurized digestion. PAHs were assessed by gas and/or high-performance liquid chromatography with reverse phase polarity and if necessary double mass spectrometry. The raw data are summarized in Tables 1 and 2. The dataset can be reused for statistical analyses by the scientific community to evidence food pollution and to be compared with other measurements.

Endocrine disruption (ED) and endocrine disruptors (EDs) emerged as scientific concepts in 1995, after numerous chemical pollutants were found to be responsible for reproductive dysfunction. The World Health Organization established in the United Nations Environment Programme a list of materials, plasticizers, pesticides, and various pollutants synthesized from petrochemistry that impact not only reproduction, but also hormonal functions, directly or indirectly. Cells communicate via either chemical or electrical signals transmitted within the endocrine or nervous systems. To investigate whether hormone disruptors may also interfere directly or indirectly with the development or functioning of the nervous system through either a neuroendocrine or a more general mechanism, we examined the scientific literature to ascertain the effects of EDs on the nervous system, specifically in the categories of neurotoxicity, cognition, and behaviour. To date, we demonstrated that all of the 177 EDs identified internationally by WHO are known to have an impact on the nervous system. Furthermore, the precise mechanisms underlying this neurodisruption have also been established. It was previously believed that EDs primarily function via the thyroid. However, this study presents substantial evidence that approximately 80 % of EDs operate via other mechanisms. It thus outlines a novel concept: EDs are also neurodisruptors (NDs) and can be collectively termed endocrine and nervous disruptors (ENDs). Most of ENDs are derived from petroleum residues, and their various mechanisms of action are similar to those of “spam” in electronic communications technologies. Therefore, ENDs can be considered as an instance of spam in a biological context.

Toxicological investigations of pesticides largely focus on the declared active ingredient, which constitutes only between a few percent to around 50% of the total formulation. The complete formulations are unknown. For each declared active ingredient, there are dozens or hundreds of formulations. We demonstrate that petroleum has always been and is still always in pesticides. Gas chromatography and mass spectrometry (GC-MS) were applied for 24 pesticides. The measured compounds were the 16-priority polycyclic aromatic hydrocarbons (PAHs). The ratio of the PAHs to the threshold of toxicity was from 2.16 to 8288 times. The levels and distribution of PAHs per pesticide were different. Petroleum residues appear to be a waste product. The declared active component is taken alone for toxicity calculations, such as the acceptable daily intake (ADI). The PAHs with 2–3 cycles are more represented in pesticides than those with 4–6 cycles, which underlines that the petroleum residues appear to come mainly from crude unburned material. The ADI should be divided by 1000 if it is considered that petroleum residues amplify the toxicity by 1000. The admixture of PAHs in pesticides can be highly carcinogenic or toxic in the long term, even more than the declared active ingredient itself.

We analysed 14 recently marketed pesticides for consumers, available in France, Germany, and Poland. They were supposed to be glyphosate-free herbicides; glyphosate was banned for sale to the public in 2019. Measurements of 36 metals, 16 polycyclic aromatic hydrocarbons, 6 essential minerals, and glyphosate plus aminomethyl phosphonic acid, were performed in a laboratory accredited for regulatory purposes. The technologies used were respectively inductively coupled plasma mass spectrometry, gas-chromatography coupled with mass spectrometry, and high-performance liquid chromatography. These data can be used by scientists, the public, and regulatory bodies.

Glyphosate (G)-based herbicidal formulations, such as the most commonly used one, Roundup (R), are major pesticides used worldwide on food and feed. Pregnant women may be frequently exposed to R compounds. These are composed of G, which is declared as the active principle, and other products contained in formulations, named formulants, which have been declared as inerts and diluents by the manufacturers. These formulants have, in fact, been demonstrated to be much more toxic than G, in particular to placental and embryonic human cells. In this work, we thus compared the effect of G and a GT+ formulation named R, using placental perfusion ex vivo. R, but not G alone, was demonstrated to alter the placental permeability of a known small model molecule, antipyrine. Similar results were observed for the fetal venous flow rate. The transfer of G alone increases with time, but is significantly decreased in presence of its formulants. The perfusion of R provokes a destruction of fetal vessels, as demonstrated by immunohistochemistry. Formulants obviously alter the fetal-placental circulation and placental integrity according to time of exposure. Therefore, G does not appear to be the main toxic agent of R. Formulants, although undeclared, include polyoxyethanolamines, PAHs, or heavy metals, and may be responsible for this toxicity. These compounds are also present in other pesticides. The progressive blood flow reduction due to the toxic compounds of formulations may diminish the nutrient supply to the fetus, alter the development, and may enhance the poisoning effects. Although these are preliminary results, they could at least partially explain some adverse pregnancy outcomes in mothers exposed to pesticides or other environmental pollutants. The debate on glyphosate alone is proven insufficient for the understanding of the toxicity.

Background: Dietary exposure to environmental pollutants in humans is an important public health concern. While long-term fasting interrupts the dietary exposure to these substances, fat mobilization as an energy source may also release bioaccumulated substances. This was, to our knowledge, only investigated in obese people decades ago. This study explored the effects of 10-days fasting on the excretion of heavy metals and glyphosate.Methods: Urinary levels of arsenic, chromium, cobalt, lead, nickel, mercury and glyphosate were measured before and after 10 fasting days in 109 healthy subjects. Additionally, hair analysis was done before and ten weeks after fasting in 22 subjects.Results: Fasting caused a decrease in body weight, and in urinary arsenic (by 72%) and nickel (by 15%) concentrations. A decrease in lead hair concentrations (by 30%) was documented. Urinary mercury levels were unchanged for chromium, cobalt and glyphosate, which were undetectable in most of the subjects. Additionally, fatigue, sleep disorders, headache and hunger were reduced. Body discomfort symptoms diminished four weeks after food reintroduction.Conclusions: The results of this study provide the first insights into the changes in heavy metal excretion caused by long-term fasting. Further studies focusing on the kinetics of efflux between different compartments of the body are needed.Clinical Trial Registration:https://www.drks.de/drks_web/navigate.do?navigationId=trial.HTML&TRIAL_ID=DRKS00016657, identifier: DRKS00016657.

A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has not been fixed in the paper.

Chronic health effects are increasing in the world such as cancers, hormonal, reproductive, nervous, or immune diseases, even in young people. During regulatory toxicological subchronic tests to prevent these on mammalian health, prior commercialization of chemicals, including pesticides and drugs, or GMOs, some statistically significant findings may be revealed. This discussion is about the need to investigate the relevant criteria to consider those as biologically significant. The sex differences and the non linear dose or time related effects should be considered in contrast to the claims of a Monsanto-supported expert panel about a GMO, the MON 863 Bt maize, but also for pesticides or drugs, in particular to reveal hormone-dependent diseases and first signs of toxicities.

The quality of diets in rodent feeding trials is crucial. We describe the contamination with environmental pollutants of 13 laboratory rodent diets from 5 continents. Measurements were performed using accredited methodologies. All diets were contaminated with pesticides (1-6 out of 262 measured), heavy metals (2-3 out of 4, mostly lead and cadmium), PCDD/Fs (1-13 out of 17) and PCBs (5-15 out of 18). Out of 22 GMOs tested for, Roundup-tolerant GMOs were the most frequently detected, constituting up to 48% of the diet. The main pesticide detected was Roundup, with residues of glyphosate and AMPA in 9 of the 13 diets, up to 370 ppb. The levels correlated with the amount of Roundup-tolerant GMOs. Toxic effects of these pollutants on liver, neurodevelopment, and reproduction are documented. The sum of the hazard quotients of the pollutants in the diets (an estimator of risk with a threshold of 1) varied from 15.8 to 40.5. Thus the chronic consumption of these diets can be considered at risk. Efforts toward safer diets will improve the reliability of toxicity tests in biomedical research and regulatory toxicology.