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EU’s Re-approval of Glyphosate: The Role of Science and the Competence of Member States
Published in Stefania Negri, Environmental Health in International and EU Law, 2019
Moreover, a clearer understanding of the role of MSs in the decision-making for active substances could push them to take full responsibility in granting national authorisations for the marketing and use of pesticides. In fact, MSs only have the competence to authorise or not the final products; in particular, according to article 1, paragraph 4, of the Regulation, MSs are asked to rely on the precautionary principle in case of scientific uncertainty as to the risks with regard to human or animal health and the environment posed by PPPs to be authorised in their territory. Thus, following the adoption of Regulation (EU) 2017/2324 that has renewed the authorisation of glyphosate, MSs has been asked to keep monitoring if the pesticides containing such active substance are safe or not. In accordance with the latter Regulation, some MSs have adopted stricter rules for the use of glyphosate-based herbicides, but none of them have totally banned the marketing and the use of all glyphosate-containing products58. In France, for example, the sale and use of Roundup 360 (an herbicide containing glyphosate) has been banned in January 2019 as a consequence of a court ruling stating that French regulators had committed an error of assessment in the light of precautionary principle when they had authorised the marketing and use of this herbicide.59
The Role of Light and Electromagnetic Fields in Maintaining Vascular Health
Published in Aruna Bakhru, Nutrition and Integrative Medicine, 2018
Once in the vasculature, the surfactants and glyphosate, working in concert, will cause a similar effect in the vascular wall. This will open up vascular leaks allowing the poisons to infiltrate the pleural cavity, along with blood plasma and small proteins. This will cause pleural effusion and allow access of the poisons to the heart and lungs via the interstitial fluids. The danger becomes acute when cardiac cells over-express the Na-K pump, because this leads to long QT syndrome, arrhythmias such as tachycardia and bradycardia (slow heart rate), and cardiac arrest. These are well-known consequences of acute poisoning by glyphosate-based herbicides [56].
Pesticides and Chronic Diseases
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
Reports of neural defects and craniofacial malformations from regions where glyphosate-based herbicides (GBH) are used lead people to undertake an embryological approach to explore the effects of low doses of glyphosate in development. Xenopus laevis embryos were incubated with 1/5000 dilutions of a commercial GBH. The treated embryos were highly abnormal with marked alterations in cephalic and neural crest development and shortening of the anterior posterior (A–P) axis. Alterations on neural crest markers were later correlated with deformities in the cranial cartilages at tadpole stages. Embryos injected with pure glyphosate showed very similar phenotypes. Moreover, GBH produced similar effects in chicken embryos, showing a gradual loss of rhombomere domains, reduction of the optic vesicles, and microcephaly. This suggests that glyphosate itself was responsible for the phenotypes observed, rather than a surfactant or other component of the commercial formulation. A reporter gene assay revealed that GBH treatment increased endogenous retinoic acid (RA) activity in Xenopus embryos and cotreatment with a RA antagonist rescued the teratogenic effects of the GBH. Therefore, they conclude that the phenotypes produced by GBH are mainly a consequence of the increase of endogenous retinoid activity. This is consistent with the decrease of Sonic hedgehod (Shh) signaling from the embryonic dorsal midline, with the inhibition of OTX2 expression and with the disruption of cephalic neural crest development. The direct effect of glyphosate on early mechanisms of morphogenesis in vertebrate embryos opens concerns about the clinical findings from human offspring in populations exposed to GBH in agricultural fields.
The use of combined high-fructose diet and glyphosate to model rats type 2 diabetes symptomatology
Published in Toxicology Mechanisms and Methods, 2021
Oluwafemi Ezekiel Kale, Mary Vongdip, Temitope Funmi Ogundare, Odutola Osilesi
There is a paucity of data regarding renal effects in animals exposed to GP formulations. However, recent studies have suggested the potential toxicity of acute renal failure following GP ingestion (Cho et al. 2019; Wang et al. 2019). Most recently, Trasande et al. (2020) reported GP intoxication causing kidney injury in infants and young children. Studies that will help in understanding the toxicological effect of GP in the renal system and how this may contribute to the development of IR formation are being investigated. For instance, authors that administered low doses of GP in rats of both sexes have reported serum changes indicative of potential kidney effects (El-Shenawy 2009; Owagboriaye et al. 2019). In this study, we obtained decreased creatinine, BUN, and UA levels following high FRC administrations. Contrastingly, GP2 alone increases creatinine and UA but not BUN in the treated rats. The combinations, however, resulted in further increase creatinine and UA levels in the treated animals while BUN remained lowered throughout the experiment. Other reports on the deleterious effects following glyphosate-based herbicide ingestion have been reported in both retrospective as well as animal studies and form current evidence that supports these findings (El-Shenawy 2009; Jayasumana et al. 2015; Cho et al. 2019; Wang et al. 2019). The potential of FRC-GP to produce altered renal function, in particular hyperuricemia, demonstrates the possible role it may play in T2D formation when exploring further.
The impact and toxicity of glyphosate and glyphosate-based herbicides on health and immunity
Published in Journal of Immunotoxicology, 2020
Cindy Peillex, Martin Pelletier
Glyphosate (N-phosphomethyl[glycine]), is an organophosphorus compound with herbicide properties discovered in 1970. It is a competitive inhibitor of the 5-enolpyruvylshikimate-3-phosphate synthase, an enzyme involved in aromatic amino acid biosynthesis in plants and microorganisms (Figure 1(A)) (Steinrücken and Amrhein 1984). In 1974, Monsanto started its commercialization as a broad-spectrum herbicide. This first glyphosate-based herbicide (GBH), RoundUp®, and the others that followed such as Glyphogan®, Touchdown®, or Glifloglex®, are mixtures of glyphosate and various adjuvants used to boost its penetration in plants and enhance its activity (Williams et al. 2000). Most of them are surfactants, such as polyethoxylated tallow amine (POEA). First used as a desiccant and in the pretreatment of crops, RoundUp® utilization spreads dramatically since 1995 with the development of RoundUp®-resistant plants (Benbrook 2016). Glyphosate is now the most used herbicide globally, and its usage keeps increasing with the emergence of weed resistance, from 16 million kg spread in the world in 1994 to 79 million kg spread in 2014, including 15% in the United States alone (Benbrook 2016).
Acute exposure of glyphosate-based herbicide induced damages on common carp organs via heat shock proteins-related immune response and oxidative stress
Published in Toxin Reviews, 2021
Yuanyuan Li, Weikai Ding, Xiaoyu Li
Glyphosate-based herbicide (GBH) is one of the most frequently used herbicides in the world (Nwani et al.2013). Glyphosate can be metabolized by glyphosate oxidoreductase to produce aminomethylphosphonic acid (AMPA) and glyoxylate, and also can be metabolized by several bacteria to produce sarcosine which is then converted to glycine and ammonia by sarcosine oxidase (Brewster et al.1991). The metabolites of glyphosate ultimately breaks down to carbon dioxide, water, and phosphonic acid. The toxicity of GBH in humans and animals is controversial worldwidely, as its mode of action is the inhibition of 5-enolpyruvoylshikimate-3-phosphate synthase, a key enzyme of shikimate pathway, which is absent in animals (Mottier et al.2013), so animals cannot be considered as target organisms and GBH has often been considered relatively nontoxic for them (Giesy et al.2000, Williams et al.2000). However, due to its high water solubility (12 g L − 1 at 25 °C), long half-life in the environment (vary from a few days to 60 days), and extensively use (Vereecken 2005), it is frequently detected in aquatic ecosystems, sometimes at high concentrations (0.1–0.7 mg/L) (Botta et al.2009, Puértolas et al.2010) and many cases of acute poisoning and death of animals have been reported over the past few decades (Paganelli et al.2010, Guilherme et al.2012, Koller et al.2012), therefore, its toxicity must be studied thoroughly. Even though the negative impacts of GBH on different aquatic organisms about biochemical and physiological parameters have been studied, but there are few literatures available on the immunotoxicity in fish caused by glyphosate (Çavaş and Könen 2007, Modesto and Martinez 2010b, Kreutz et al.2010, 2011, Kondera et al.2018), and the effects of glyphosate-induced immunotoxicity in fish were not completely elucidated.