Vineis, 2019
Vineis, P.; “Public Health and Independent Risk Assessment;” American Journal of Public Health, 2019, 109(7), 978-980; DOI: 10.2105/AJPH.2019.305142.
Samet, 2019
Samet, J. M.; “Expert Review Under Attack: Glyphosate, Talc, and Cancer;” American Journal of Public Health, 2019, 109(7), 976-978; DOI: 10.2105/AJPH.2019.305131.
Morabia, 2019
Morabia, A.; “Fighting Independent Risk Assessment of Talc and Glyphosate: Whose Benefit Is It Anyway?;” American Journal of Public Health, 2019, 109(7), 955-956; DOI: 10.2105/AJPH.2019.305144.
Rodenberg, 2019
Rodenberg, H.; “Reliance, Not Responsibility: Relations Between Science and Industry;” American Journal of Public Health, 2019, 109(7), 980-981; DOI: 10.2105/AJPH.2019.305125.
Schaden et al., 2020
Schaden, Helmut Burtscher, Clausing, Peter, & Van Scharen, Hans. “Factsheet: Dangerous Confidence in ‘Good Laboratory Practices,'” February 11, 2020, Corporate Europe Observatory and PAN Germany.
SUMMARY:
Our authorisation system for chemicals is based on the principle that manufacturers must prove, by means of scientifc studies, that their products do not pose unacceptable risks to public health and the environment. It is therefore also the responsibility of manufacturers to commission certifed contract laboratories to carry out the toxicological studies necessary for the approval procedure. As a guarantee against manipulation and falsifcation of these “regulatory” studies, regulatory authorities worldwide rely on the certifed standard of “Good Laboratory Practice” (GLP). This standard provides for strict documentation requirements and regular internal and external controls. However, the current fraud scandal involving a German contract laboratory certifed according to GLP, shows that this trust is unlikely to be justifed. According to reports, GLP studies have been manipulated and falsifed there since 2005.
- Recent research now shows that LPT has also produced studies that were part of the study package for the EU-wide approval of glyphosate in December 2017: One in seven studies in this package, which was the basis to grant re-approval for glyphosate, came from LPT. These fndings are worrying in two ways: – On the one hand, there is the fundamental question of whether the risk assessments for medicines, pesticides and chemicals based on LPT studies can be trusted.
- Even more worrying is the general realisation that laboratories, despite the supposedly “tamper-proof” GLP standard, are apparently able to falsify studies over years and decades without being noticed by the control authorities.
The classifcation of glyphosate as “non-carcinogenic” and “not genotoxic“o is based, among other things, on the European authorities’ full confdence in the GLP system. In the EU assessment proces GLP studies were automatically classifed as reliable; This in stark contrast with the numerous “non-GLP studies” from university research, peer reviewed and published, most of which reported evidence of a genotoxic effect and an increased risk of lymphatic cancer in users of glyphosate, were disqualifed by the authorities as “unreliable“.
The LPT counterfeiting scandal reveals the failure of a regulatory system, that places the commissioning and preparation of studies in the hands of industry. At the same time, it confrms the urgency of a fundamental reform of this system for identifying the risks of chemicals, as called for by the European coalition “Citizens for Science in Pesticide Regulation” in October 2018. FULL TEXT
Wang et al., 2020
Wang, G. H., Berdy, B. M., Velasquez, O., Jovanovic, N., Alkhalifa, S., Minbiole, K. P. C., & Brucker, R. M.; “Changes in Microbiome Confer Multigenerational Host Resistance after Sub-toxic Pesticide Exposure;” Cell Host & Microbe, 2020; DOI: 10.1016/j.chom.2020.01.009.
ABSTRACT:
The gut is a first point of contact with ingested xenobiotics, where chemicals are metabolized directly by the host or microbiota. Atrazine is a widely used pesticide, but the role of the microbiome metabolism of this xenobiotic and the impact on host responses is unclear. We exposed successive generations of the wasp Nasonia vitripennis to subtoxic levels of atrazine and observed changes in the structure and function of the gut microbiome that conveyed atrazine resistance. This microbiome-mediated resistance was maternally inherited and increased over successive generations, while also heightening the rate of host genome selection. The rare gut bacteria Serratia marcescens and Pseudomonas protegens contributed to atrazine metabolism. Both of these bacteria contain genes that are linked to atrazine degradation and were sufficient to confer resistance in experimental wasp populations. Thus, pesticide exposure causes functional, inherited changes in the microbiome that should be considered when assessing xenobiotic exposure and as potential countermeasures to toxicity. FULL TEXT
Janssens and Stoks, 2017
Janssens, L., & Stoks, R.; “Stronger effects of Roundup than its active ingredient glyphosate in damselfly larvae;” Aquatic Toxicology, 2017, 193, 210-216; DOI: 10.1016/j.aquatox.2017.10.028.
ABSTRACT:
Pesticides are causing strong decreases in aquatic biodiversity at concentrations assumed safe by legislation. One reason for the failing risk assessment may be strong differences in the toxicity of the active ingredient of pesticides and their commercial formulations. Sublethal effects, especially those on behaviour, have been largely ignored in this context, yet can be equally important as lethal effects at the population and ecosystem levels. Here, we compared the toxicity of the herbicide Roundup and its active ingredient glyphosate on survival, but also on ecologically relevant sublethal traits (life history, behaviour and physiology) in damselfly larvae. Roundup was more toxic than glyphosate with negative effects on survival, behaviour and most of the physiological traits being present at lower concentrations (food intake, escape swimming speed) or even only present (survival, sugar and total energy content and muscle mass) following Roundup exposure. This confirms the toxicity of the surfactant POEA. Notably, also glyphosate was not harmless: a realistic concentration of 2mg/l resulted in reduced growth rate, escape swimming speed and fat content. Our results therefore indicate that the toxicity of Roundup cannot be fully attributed to its surfactant, thereby suggesting that also the new generation of glyphosate-based herbicides with other mixtures of surfactants likely will have adverse effects on non-target aquatic organisms. Ecotoxicological studies comparing the toxicity of active ingredients and their commercial formulations typically ignore behaviour while the here observed differential effects on behaviour likely will negatively impact damselfly populations. Our data highlight that risk assessment of pesticides ignoring sublethal effects may contribute to the negative effects of pesticides on aquatic biodiversity. FULL TEXT
Van Stempvoort et al., 2014
Van Stempvoort, D. R., Roy, J. W., Brown, S. J., & Bickerton, G.; “Residues of the herbicide glyphosate in riparian groundwater in urban catchments;” Chemosphere, 2014, 95, 455-463; DOI: 10.1016/j.chemosphere.2013.09.095.
ABSTRACT:
The herbicide glyphosate and its putative metabolite aminomethylphosphonic acid (AMPA) have been found in urban streams, but limited information is available on their presence in urban riparian groundwater. Information is also lacking regarding the source of AMPA in these urban settings (glyphosate metabolite or wastewater), and whether, if present, glyphosate residues in urban riparian groundwater contribute significantly to urban streams. Glyphosate and AMPA were detected in shallow riparian groundwater at 4 of 5 stream sites in urban catchments in Canada and each were found in approximately 1 in 10 of the samples overall. Frequency of observations of glyphosate and AMPA varied substantially between sites, from no observations in a National Park near the Town of Jasper Alberta, to observations of both glyphosate and AMPA in more than half of the samples along two short reaches of streams in Burlington, Ontario. In these two catchments, AMPA was correlated with glyphosate, rather than the artificial sweetener acesulfame, suggesting that the AMPA is derived mainly from glyphosate degradation rather than from wastewater sources. Land use, localized dosage history, depth below ground and other factors likely control the occurrence of detectable glyphosate residues in groundwater. FULL TEXT
Romano et al., 2010
Romano, R. M., Romano, M. A., Bernardi, M. M., Furtado, P. V., & Oliveira, C. A.; “Prepubertal exposure to commercial formulation of the herbicide glyphosate alters testosterone levels and testicular morphology;” Archives of Toxicology, 2010, 84(4), 309-317; DOI: 10.1007/s00204-009-0494-z.
ABSTRACT:
Glyphosate is a herbicide widely used to kill weeds both in agricultural and non-agricultural landscapes. Its reproductive toxicity is related to the inhibition of a StAR protein and an aromatase enzyme, which causes an in vitro reduction in testosterone and estradiol synthesis. Studies in vivo about this herbicide effects in prepubertal Wistar rats reproductive development were not performed at this moment. Evaluations included the progression of puberty, body development, the hormonal production of testosterone, estradiol and corticosterone, and the morphology of the testis. Results showed that the herbicide (1) significantly changed the progression of puberty in a dose-dependent manner; (2) reduced the testosterone production, in semineferous tubules’ morphology, decreased significantly the epithelium height (P < 0.001; control = 85.8 +/- 2.8 microm; 5 mg/kg = 71.9 +/- 5.3 microm; 50 mg/kg = 69.1 +/- 1.7 microm; 250 mg/kg = 65.2 +/- 1.3 microm) and increased the luminal diameter (P < 0.01; control = 94.0 +/- 5.7 microm; 5 mg/kg = 116.6 +/- 6.6 microm; 50 mg/kg = 114.3 +/- 3.1 microm; 250 mg/kg = 130.3 +/- 4.8 microm); (4) no difference in tubular diameter was observed; and (5) relative to the controls, no differences in serum corticosterone or estradiol levels were detected, but the concentrations of testosterone serum were lower in all treated groups (P < 0.001; control = 154.5 +/- 12.9 ng/dL; 5 mg/kg = 108.6 +/- 19.6 ng/dL; 50 mg/dL = 84.5 +/- 12.2 ng/dL; 250 mg/kg = 76.9 +/- 14.2 ng/dL). These results suggest that commercial formulation of glyphosate is a potent endocrine disruptor in vivo, causing disturbances in the reproductive development of rats when the exposure was performed during the puberty period. FULL TEXT
Guerrero Schimpf et al., 2017
Guerrero Schimpf, M., Milesi, M. M., Ingaramo, P. I., Luque, E. H., & Varayoud, J.; “Neonatal exposure to a glyphosate based herbicide alters the development of the rat uterus;” Toxicology, 2017, 376, 2-14; DOI: 10.1016/j.tox.2016.06.004.
ABSTRACT:
Glyphosate-based herbicides (GBHs) are extensively used to control weeds on both cropland and non-cropland areas. No reports are available regarding the effects of GBHs exposure on uterine development. We evaluated if neonatal exposure to a GBH affects uterine morphology, proliferation and expression of proteins that regulate uterine organogenetic differentiation in rats. Female Wistar pups received saline solution (control, C) or a commercial formulation of glyphosate (GBH, 2mg/kg) by sc injection every 48h from postnatal day (PND) 1 to PND7. Rats were sacrificed on PND8 (neonatal period) and PND21 (prepubertal period) to evaluate acute and short-term effects, respectively. The uterine morphology was evaluated in hematoxylin and eosin stained sections. The epithelial and stromal immunophenotypes were established by assessing the expression of luminal epithelial protein (cytokeratin 8; CK8), basal epithelial proteins (p63 and pan cytokeratin CK1, 5, 10 and 14); and vimentin by immunohistochemistry (IHC). To investigate changes on proteins that regulate uterine organogenetic differentiation we evaluated the expression of estrogen receptor alpha (ERalpha), progesterone receptor (PR), Hoxa10 and Wnt7a by IHC. The GBH-exposed uteri showed morphological changes, characterized by an increase in the incidence of luminal epithelial hyperplasia (LEH) and an increase in the stromal and myometrial thickness. The epithelial cells showed a positive immunostaining for CK8, while the stromal cells for vimentin. GBH treatment increased cell proliferation in the luminal and stromal compartment on PND8, without changes on PND21. GBH treatment also altered the expression of proteins involved in uterine organogenetic differentiation. PR and Hoxa10 were deregulated both immediately and two weeks after the exposure. ERalpha was induced in the stromal compartment on PND8, and was downregulated in the luminal epithelial cells of gyphosate-exposed animals on PND21. GBH treatment also increased the expression of Wnt7a in the stromal and glandular epithelial cells on PND21. Neonatal exposure to GBH disrupts the postnatal uterine development at the neonatal and prepubertal period. All these changes may alter the functional differentiation of the uterus, affecting the female fertility and/or promoting the development of neoplasias. FULL TEXT