Roundup, Not the Harmless Pesticide Monsanto Schlepped to You

[Toxed2lossKeymaster 20p]

Jeffery Smith interviews Stephanie Seneff, PhD, a Senior Research Scientist at MIT, on her research into the devastating effects of glyphosate (Roundup) and GMO crops. They discuss the metabolic pathways that are damaged and the host of 21st Century diseases that are being proliferted by it. The video is an hour and twenty minutes, but well worth it. This info effects everyone. It’s NEED TO KNOW!

• This topic was modified 2 years, 4 months ago by  Toxed2loss.
• This topic was modified 2 years, 4 months ago by  Toxed2loss.
• This topic was modified 2 years, 4 months ago by  Toxed2loss.

[Toxed2lossKeymaster 20p]

Glyphosate poisoning

While there is no longer a question that glyphosate products are toxic to mammals (1-16), Its really difficult to find information using a search engine, that substantiates the damage (atypical to the label) that I received following the glyphosate product exposure I received in March of 2013. So in case anybody else is looking, I’m collecting research here.

First off is a list of symptoms that the researchers attributed to deliberate ingestion of a large quantity of glyphosate product, followed by those with less direct exposures. If you’re immune system compromised you get the symptoms of direct exposure with trace amounts… If you’re a normally healthy person, even minimal exposures accummulate, and degrade your health. At some point you end up with a disease that you can’t pinpoint to one specific exposure. Thats because it was accumulative. Thats also why the symptoms of those with Toxic Injuries (TI) vary so much. Their condition is a result of a great many exposures to a wide variety of toxic substances. Each toxic substance has it’s own set of symptoms. Their conditions are not static but fluctuate as they recover from, and get exposed to new, toxic substances. The majority of people who claim environmental illness, chemical hypersensitivity, or TILT (Toxin Induced Loss of Tolerance) arrived at their condition by accumulation of many small exposures over many years. They just didn’t have enough acute symptoms at the time of each exposure to realize they were being poisoned. They were unable to connect the dots. In the beginning they most likely thought they were getting a cold, flu, had food poisoning or were suffering with “allergies.” So, here we go, documented adverse effects to glyphosate products not necessarily on the label…

“Gastrointestinal corrosive effects, with mouth, throat and epigastric pain and dysphagia are common. Renal and hepatic impairment are also frequent and usually reflect reduced organ perfusion. Respiratory distress, impaired consciousness, pulmonary oedema, infiltration on chest x-ray, shock, arrythmias, renal failure requiring haemodialysis, metabolic acidosis and hyperkalaemia may supervene in severe cases. Bradycardia and ventricular arrhythmias are often present pre-terminally. Dermal exposure to ready-to-use glyphosate formulations can cause irritation and photo-contact dermatitis has been reported occasionally; these effects are probably due to the preservative Proxel (benzisothiazolin-3-one). Severe skin burns are very rare. Inhalation is a minor route of exposure but spray mist may cause oral or nasal discomfort, an unpleasant taste in the mouth, tingling and throat irritation. Eye exposure may lead to mild conjunctivitis,”1

“They exhibit a variety of mechanisms of toxicity including dose-dependent cell membrane damage, uncoupling of oxidative phosphorylation, and disruption of acetylcoenzyme A metabolism… Adjuvants in the formulations may have contributed to some of the features observed. Vomiting, abdominal pain, diarrhea, and, occasionally, gastrointestinal hemorrhage were early effects. When present, hypotension was predominantly due to intravascular volume loss, although vasodilation and direct myocardial toxicity may have contributed in some cases. Neurotoxic features included coma, hypertonia, hyperreflexia, ataxia, nystagmus, miosis, hallucinations, convulsions, fasciculation, and paralysis. Hypoventilation occurred not infrequently, usually in association with central nervous system depression, but respiratory muscle weakness was a factor in the development of respiratory failure in some patients. Myopathic symptoms including limb muscle weakness, loss of tendon reflexes, and myotonia were observed and increased creatine kinase activity was noted in some cases. Other clinical features reported included metabolic acidosis, rhabdomyolysis, renal failure, increased aminotransferase activities, pyrexia, and hyperventilation. Twenty-two of 66 patients died. FEATURES FOLLOWING DERMAL AND INHALATIONAL EXPOSURE:…Substantial dermal exposure has been reported to cause mild gastrointestinal irritation after a latent period followed by progressive mixed sensory-motor peripheral neuropathy. Mild, transient gastrointestinal and peripheral neuromuscular symptoms have also occurred after occupational inhalation exposure, with or without dermal exposure.”4

“the incidence of clinical complications was (in rank order) as follows: hypotension, 47.1%; mental deterioration, 38.6%; respiratory failure, 30.0%; acute kidney injury, 17.1%; and arrhythmia, 10.0%. These complications were influenced by the volume of surfactant and not the type of surfactant-ingredient in the herbicide product. Two patients died of refractory shock, metabolic acidosis, and respiratory failure. “5

One of the short comings of these studies is that they rely on “subjects that received medical treatment.” Those of us that are TI generally can’t access medical treatment. So like me, their conditions are unreported, or undocumented, in the established medical paradigm. The western medical system would insist on treating TIs with toxic chemicals and methods. That would kill us in our weaked/poisoned state. So we don’t go in, and our reactions are not documented. The government, especially the agencies that are involved with toxic chemicals and pesticides, use that “lack of substantiated evidence” as “proof” that the pesticides aren’t harmful, and that there isn’t an epidemic of pesticide poisoning. In fact, if you call a poison control center and report adverse reactions to a glyphosate product exposure they disregard your call if your symptoms are not concomitant with the symptoms on the product label.14

“Many doctors, however, based on Monsanto’s advertising that glyphosate is not a cholinesterase inhibitor, refuse to test RoundUp poisoning victims for cholinesterase inhibition, so even anecdotal evidence is not readily available.”21

The product label is extremely limited and does not reflect the array of symptoms documented in the independent research literature. The fact is that most glyphosate products are 100 times more toxic than the label indicates. Sayer Ji, of Green Med Info wrote an excellent article on that subject; you can access it here link

From my exposures to glyphosate products I have experienced the following symptoms from these citations: Gastrointestinal corrosive effects, with mouth, throat and epigastric pain and dysphagia (my tongue, mouth, throat swell, I can’t swallow, or get food past my LES for extended periods following exposures, food that I manage to get in does not move or digest), regurgitation & vomiting. Renal and hepatic impairment ( severe liver and kidney pain and inflammation, distention of upper abdomen, unable to urinate, or severly reduced amount for 2-3 days), Respiratory distress, impaired consciousness, pulmonary oedema (I find it difficult to breathe, am spacey, and have chest pain and pressure). I’ve experienced bradycardia, arrhythmia and tachycardia. It causes my skin & mucous membranes to burn, tingle and become numb or extremely painful. Cognitive impairment. I get conjunctivitis and impaired vision. Weakness, lack of energy. I looked up “oxidative phosphorylation” its part of the ATP (energy production in the cells) cycle, so that is just a scientific definition of “lack of energy. It intrigued me because of the phosphorus component and what I’m learning about remineralizing teeth and the calcium-phosphorus imbalance that leads to tooth decay.(Yikes! A Cavity!) Which I’m also experiencing. Since I’ve had acetylcholinesterase poisoning and am certified (ATSDR) in the detection and recognition of those symptoms, I can validate that I suffer with those (again. I won’t list them here). I have symptoms that are not mentioned here, like the achalasia( which is related to acetylcholingeric damage. 17, 18 I also get ataxia (staggering gate), and fasciculation (rapid, short, repetitive muscle spasms). Pyrexia just means fever, without infection. I get that. Peripheral neuropathy is numbness, burning, pain and tingling in the extremities. I get that. Nose bleeds 9; following the major glyphosate exposure I had in the spring of 2013 I had nose bleeding so bad it was drowning and choking me. I also experience sore teeth, gums and jaw.

I treated my symptoms with a high organic dairy fat (fat trapping of toxins, moderates glucose/insulin response, provides slow burning energy & vitamins A & D), high sugar diet (for porphria and to boost ATP) w/raw organic eggs (nutrient dense food, high in glutathione precursors) , with high amounts of buffered C. I was using C buffered (alkalizing) with calcium, however the calcium makes the achalasia (dysphagia + spasming of the muscle between the esophagus and stomach) worse, and I switched to C buffered with magnesium. Magnesium is a muscle relaxant, and most people are magnesium defficient. I was not consuming much phosphorus, because I couldn’t digest or retain meat. I was unaware of the phosphorus connection to both the glyphosate phospholipid disruption (24,25) and the importance of phosphorous in tooth enamel. I did begin adding in bone broth once I was able to retain food and get some liquids past my LES. I was injecting 16 ml glutathione solution every 3 days and receiving from my MD IV C, B & D every 2 weeks at the end of the season. While it appears the right course of action, according to the biological literature, I’m concerned with the problems I’m having with my teeth. So I started this research to figure out how to deal with both issues, and to find out if its the glyphosate product poisoning that is contributing to the weakening of my enamel. My neighbors are spraying glyphosate again. Some notify, so I can leave. Some don’t. The literature contains very little on treatments for glyphosate product poisoning. Here’s what I’ve found so far:

“In addition to supportive care, alkaline diuresis to enhance herbicide elimination should be considered in all seriously poisoned patients.” 4

“prompt fluid replacement therapy seems critical in the initial management of such exposures. Patients’ airway should also be secured to avoid aspiration and subsequent respiratory failure.” 10

“Our results show that the effects of glyphosate containing compounds are pH-dependent and that they inhibit intracellular transport through disassembly of the cytoskeleton possibly by interfering with intracellular Ca(2+)-balance.”11

As glyphosate has been found to behave like organophosphates (4,20, 22, 23, 26) some hospitals have tried treatments for glyphosate poisoning as though it was acetylcholine poisoning from OPs. However those chemicals are toxic, and I found atropine containing foods (salsa, tomato, peppers, potato) to exacerbate the dysphagia and achalasia. Just before spray season started (2014) I was beginning to be able to add tomatoes & pepper foods back in.

I’ve researched OP treatments as well. Here are the citations and non chemical treatments that have shown efficacy,

“Orally administered AC (activated charcoal) can adsorb many toxicants in the gastrointestinal tract, particularly large non-polar compounds, and would logically be an effective treatment for OP poisoning… the sooner after ingestion it is given, the more toxicant will be bound and effectively neutralized. Specific commercial preparations of powdered AC are given as a 20% suspension in tap water at a dosage of 5 g of the slurry/kg BW, by gavage or stomach tube in the animals. Repeat doses can be given every 4-6 hours. Sedation and the use of a cuffed endotracheal tube are needed to avoid aspiration (Osweiler, 1996; Parton, 2001)… Bioremediation is the use of microorganisms, plants (often called phytoremediation), or biologically active agents to degrade, sequester, or conjugate environmental pollutants (such as OPs). Advantages of bioremediation include ease and timing of application, ability to target specific pollutants, decreased sludge volume, and decreased ecological hazard. There is potential to use enzymatic treatment in bioremediation, and this technology is currently at the laboratory stage of development (Alexander, 1999). Oxygenation is the most frequent first step in the biotransformation of pesticides and other organic xenobiotics. Many of these reactions are mediated by oxidative enzymes, e.g., cytochrome P450s, peroxidases, and polyphenol oxidases.The most extensively studied oxidative enzymes in plants and animals are the P450s, which are the most important enzymes in Phase I pesticide metabolism (Barrett, 2000). Cytochrome P450s are hemethiolate proteins that have been characterized in animals, plants, bacteria, and filamentous fungi. Organophosphorus hydrolase (OPH), isolated from soil microorganisms from diverse geographic locations, has been shown to hydrolyze various OPs significantly (Cho et al., 2002). Plants and microorganisms produce a wide range of oxidative enzymes (e.g., peroxidase, polyphenoloxidase, laccase, and tyrosinase) other than P450s that catalyze the polymerization of various anilines and phenols (Dec and Bollag, 2000).”19

What I gathered from this last citation is that I needed to add activated charcoal powder (make sure it is from coconut shell) in water, immediately after exposure, and that the coffee enemas recommended to me by my acupuncturist (to raise glutathione levels) are equally important for their polyphenols, and OP scavenging ability. I had been doing enzymes (my TI began in 1996 with OP poisoning by Monitor, an insecticide used to control Colorado Potato Beetles in potatoes. I was surveying a potatoe field when an arial applicator arrived and sprayed the field. Yes, he saw me.), however, they were encapsulated and I could not retain them. I had the same problem with chlorella capsules. I tried emptying the caps onto a spoonful of yogurt, which resulted in gagging and vomiting. Dark green vegetables (especially organic broccoli) are excellent sources of these same compounds, however, with the achalasia, I was unable to retain those as well, until I could relax the LES enough to get liquids in. I added them to my bone broth. As I progressed to being able to eat more solids I included well cooked broccoli in homemade organic cheese sauce. Whey protein is often recommended for treatment to people with chronic illness and immune system compromise. Unfortunately the commercial products are highly processed and contain free glutamate (MSG). The best form of whey to consume is organic, raw, full fat dairy yogurt. The clear, light yellow liquid that separates is whey. Organic, full fat organic cheese has remnants of whey, as its the solids pressed with the whey removed. Its also full of probiotics and enzymes.

As I get the chance, and find additional literature I’ll add it to this thread. I sincerely hope this information helps you to make healthier choices in your own lives. I hope it illustrates the importance of organic agriculture and the labeling of GMO crops.

Bibliography
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1.”Toxicol Rev. 2004;23(3):159-67.
Glyphosate poisoning.
Bradberry SM1, Proudfoot AT, Vale JA.
Author information

Abstract
Glyphosate is used extensively as a non-selective herbicide by both professional applicators and consumers and its use is likely to increase further as it is one of the first herbicides against which crops have been genetically modified to increase their tolerance. Commercial glyphosate-based formulations most commonly range from concentrates containing 41% or more glyphosate to 1% glyphosate formulations marketed for domestic use. They generally consist of an aqueous mixture of the isopropylamine (IPA) salt of glyphosate, a surfactant, and various minor components including anti-foaming and colour agents, biocides and inorganic ions to produce pH adjustment. The mechanisms of toxicity of glyphosate formulations are complicated. Not only is glyphosate used as five different salts but commercial formulations of it contain surfactants, which vary in nature and concentration. As a result, human poisoning with this herbicide is not with the active ingredient alone but with complex and variable mixtures. Therefore, It is difficult to separate the toxicity of glyphosate from that of the formulation as a whole or to determine the contribution of surfactants to overall toxicity. Experimental studies suggest that the toxicity of the surfactant, polyoxyethyleneamine (POEA), is greater than the toxicity of glyphosate alone and commercial formulations alone. There is insufficient evidence to conclude that glyphosate preparations containing POEA are more toxic than those containing alternative surfactants. Although surfactants probably contribute to the acute toxicity of glyphosate formulations, the weight of evidence is against surfactants potentiating the toxicity of glyphosate. Accidental ingestion of glyphosate formulations is generally associated with only mild, transient, gastrointestinal features. Most reported cases have followed the deliberate ingestion of the concentrated formulation of Roundup (The use of trade names is for product identification purposes only and does not imply endorsement.) (41% glyphosate as the IPA salt and 15% POEA). There is a reasonable correlation between the amount ingested and the likelihood of serious systemic sequelae or death. Advancing age is also associated with a less favourable prognosis. Ingestion of >85 mL of the concentrated formulation is likely to cause significant toxicity in adults. Gastrointestinal corrosive effects, with mouth, throat and epigastric pain and dysphagia are common. Renal and hepatic impairment are also frequent and usually reflect reduced organ perfusion. Respiratory distress, impaired consciousness, pulmonary oedema, infiltration on chest x-ray, shock, arrythmias, renal failure requiring haemodialysis, metabolic acidosis and hyperkalaemia may supervene in severe cases. Bradycardia and ventricular arrhythmias are often present pre-terminally. Dermal exposure to ready-to-use glyphosate formulations can cause irritation and photo-contact dermatitis has been reported occasionally; these effects are probably due to the preservative Proxel (benzisothiazolin-3-one). Severe skin burns are very rare. Inhalation is a minor route of exposure but spray mist may cause oral or nasal discomfort, an unpleasant taste in the mouth, tingling and throat irritation. Eye exposure may lead to mild conjunctivitis, and superficial corneal injury is possible if irrigation is delayed or inadequate. Management is symptomatic and supportive, and skin decontamination with soap and water after removal of contaminated clothing should be undertaken in cases of dermal exposure.”

2. Spectrum of corrosive esophageal injury after intentional paraquat or glyphosate-surfactant herbicide ingestion.
Chen HH, Lin JL, Huang WH, Weng CH, Lee SY, Hsu CW, Chen KH, Wang IK, Liang CC, Chang CT, et al.
Int J Gen Med. 2013; 6:677-83. Epub 2013 Aug 14

3. Glyphosate, hard water and nephrotoxic metals: are they the culprits behind the epidemic of chronic kidney disease of unknown etiology in Sri Lanka?
Jayasumana C, Gunatilake S, Senanayake P.
Int J Environ Res Public Health. 2014 Feb 20; 11(2):2125-47. Epub 2014 Feb 20.

4. J Toxicol Clin Toxicol. 2000;38(2):111-22.
Mechanisms of toxicity, clinical features, and management of acute chlorophenoxy herbicide poisoning: a review.
Bradberry SM1, Watt BE, Proudfoot AT, Vale JA.
Author information

“Abstract
INTRODUCTION:
Chlorophenoxy herbicides are used widely for the control of broad-leaved weeds. They exhibit a variety of mechanisms of toxicity including dose-dependent cell membrane damage, uncoupling of oxidative phosphorylation, and disruption of acetylcoenzyme A metabolism. Between January 1962 and January 1999, 66 cases of chlorophenoxy herbicide poisoning following ingestion were reported in the literature. FEATURES FOLLOWING INGESTION: Adjuvants in the formulations may have contributed to some of the features observed. Vomiting, abdominal pain, diarrhea, and, occasionally, gastrointestinal hemorrhage were early effects. When present, hypotension was predominantly due to intravascular volume loss, although vasodilation and direct myocardial toxicity may have contributed in some cases. Neurotoxic features included coma, hypertonia, hyperreflexia, ataxia, nystagmus, miosis, hallucinations, convulsions, fasciculation, and paralysis. Hypoventilation occurred not infrequently, usually in association with central nervous system depression, but respiratory muscle weakness was a factor in the development of respiratory failure in some patients. Myopathic symptoms including limb muscle weakness, loss of tendon reflexes, and myotonia were observed and increased creatine kinase activity was noted in some cases. Other clinical features reported included metabolic acidosis, rhabdomyolysis, renal failure, increased aminotransferase activities, pyrexia, and hyperventilation. Twenty-two of 66 patients died. FEATURES FOLLOWING DERMAL AND INHALATIONAL EXPOSURE: Substantial dermal or inhalational 2,4-dichlorophenoxyacetic acid exposure has occasionally led to systemic features but no such reports have been published in the last 20 years and no fatalities have been reported at any time. Substantial dermal exposure has been reported to cause mild gastrointestinal irritation after a latent period followed by progressive mixed sensory-motor peripheral neuropathy. Mild, transient gastrointestinal and peripheral neuromuscular symptoms have also occurred after occupational inhalation exposure, with or without dermal exposure.
MANAGEMENT:
Limited clinical data suggest that hemodialysis produces similar herbicide clearance to alkaline diuresis without the need for urine pH manipulation and the administration of substantial amounts of intravenous fluid in an already compromised patient.
CONCLUSIONS:
While chlorophenoxy herbicide poisoning is uncommon, ingestion of a chlorophenoxy herbicide can result in serious and sometimes fatal sequelae. In severe cases of poisoning, alkaline diuresis or hemodialysis to increase herbicide elimination should be considered.”

5. Clin Toxicol (Phila). 2011 Dec;49(10):892-9. doi: 10.3109/15563650.2011.626422. Epub 2011 Nov 11.
Surfactant volume is an essential element in human toxicity in acute glyphosate herbicide intoxication.
Seok SJ1, Park JS, Hong JR, Gil HW, Yang JO, Lee EY, Song HY, Hong SY.
Author information

“Abstract
BACKGROUND:
Glyphosate, one of the most commonly used herbicides worldwide, has been considered as minimally toxic to humans. However, clinical toxicologists occasionally encounter cases of severe systemic toxicity. The purpose of this study was to determine the effect of glyphosate-surfactants (“glyphosate-surfactant toxicity”) in patients with acute glyphosate intoxication.
METHODS:
In all, 107 patients (69 men and 38 women, aged 52.3 ± 15.5 years) with acute glyphosate intoxication were enrolled in this study. From their medical records, we identified the formulation of ingested glyphosate products and derived clinical parameters, which focused on clinical outcome, admission days, duration in the intensive care unit, development of respiratory failure, cardiovascular deterioration, renal failure, altered mental status, and convulsions. The effect of surfactants on clinical complications was also assessed.
RESULTS:
For surfactant ingestion volumes of 8 mL, the incidence of clinical complications was (in rank order) as follows: hypotension, 47.1%; mental deterioration, 38.6%; respiratory failure, 30.0%; acute kidney injury, 17.1%; and arrhythmia, 10.0%. These complications were influenced by the volume of surfactant and not the type of surfactant-ingredient in the herbicide product. Two patients died of refractory shock, metabolic acidosis, and respiratory failure. However, the final clinical outcomes of the surviving patients were benign, and cardiovascular, respiratory, kidney, and mental functions were fully restored to normal levels.
CONCLUSIONS:
Our results indicate that treatment of patients with acute glyphosate herbicide intoxication should take into account the volume and not the type of surfactants in herbicide formulations.”

6. Effect of intravenous lipid emulsion in patients with acute glyphosate intoxication.
Gil HW, Park JS, Park SH, Hong SY.
Clin Toxicol (Phila). 2013 Sep-Oct; 51(8):767-71. Epub 2013 Jul 19.

7. Predicting acute complicated glyphosate intoxication in the emergency department.
Moon JM, Chun BJ.
Clin Toxicol (Phila). 2010 Aug; 48(7):718-24.

8. Determination of glyphosate and AMPA in blood and urine from humans: about 13 cases of acute intoxication.
Zouaoui K, Dulaurent S, Gaulier JM, Moesch C, Lachâtre G.
Forensic Sci Int. 2013 Mar 10; 226(1-3):e20-5. Epub 2013 Jan 3.

9. Vet Hum Toxicol. 1997 Jun;39(3):147-51.
The oral and intratracheal toxicities of ROUNDUP and its components to rats.
Adam A1, Marzuki A, Abdul Rahman H, Abdul Aziz M.
Author information

Abstract
The toxicities of ROUNDUP and its component chemicals, glyphosate (N-phosphonomethylglycine) and polyoxyethyleneamine (POEA), were determined at 0, 1, 3, 6 and 24 h following administration to rats. The intratracheal administration of glyphosate (0.2 g/kg), POEA (0.1 g/kg), a mixture of glyphosate (0.2 g/kg) + POEA (0.1 g/kg), or ROUNDUP (containing 0.2 g/kg glyphosate and 0.1 g/kg POEA) elicited immediate respiratory effects which were more severe and which lasted longer in the groups receiving the POEA-containing preparations than in the glyphosate alone group. By 1 h, all test preparations had caused deaths, but more occurred from the POEA-containing preparations than from glyphosate. The po administration of POEA (1 g/kg), the mixture of glyphosate (2 g/kg) +POEA (1 g/kg), or ROUNDUP (containing 2 g/kg glyphosate and 1 g/kg POEA) produced diarrhea and blood-stained weeping from noses. Death was only seen from POEA at 24 h. Glyphosate (2 g/kg po) produced transient diarrhea without nose bleeds; POEA caused diarrhea at 1 h; and the mixture of POEA + glyphosate produced diarrhea later that increased in severity with time. Bloody nose secretions were seen only with the preparations that contained POEA. No deaths, respiratory effects or bloody nose secretions occurred in controls given saline. Both POEA and glyphosate caused lung hemorrhages and lung epithelial cell damage with po or intratracheal exposures. These results indicate POEA and preparations that contained POEA were more toxic than glyphosate.

10. Clin Toxicol (Phila). 2009 Aug;47(7):670-7. doi: 10.1080/15563650903140399.
The epidemiology of glyphosate-surfactant herbicide poisoning in Taiwan, 1986-2007: a poison center study.
Chen YJ1, Wu ML, Deng JF, Yang CC.

“BACKGROUND:
Glyphosate-surfactant herbicide (GlySH) is widely used in agriculture and has been associated with numerous toxicities following oral ingestion. However, there are many controversies with regard to the exact causes and determinants of developing severe/death outcome after exposure to GlySH.
METHODS:
We conducted an analysis of all GlySH exposures reported to the Taiwan National Poison Control Center between 1986 and 2007. Patients’ baseline characteristics and clinical data were reviewed and analyzed.
RESULTS:
A total of 2,186 patients were eligible for analysis. Most of the exposures were related to oral ingestion (n = 2,023, 92.5%) and attempted suicide (n = 1,631, 74.6%). The mean age of exposure was 42.8 +/- 18.6 years. One hundred patients developed severe effects and 146 patients died following oral GlySH exposure, resulting in a case fatality rate of 7.2%. Shock (n = 85, 58.2%) and respiratory failure (n = 34, 23.3%) accounted for most fatalities. Four out of eight patients with injection exposure manifested severe (n = 3) or fatal outcome (n = 1). In a multivariate logistic regression analysis, increasing age, larger amount of exposure, longer elapsed time to presentation, attempted suicide, receipt of atropine therapy, and being exposed in certain calendar years were positively associated with the severity of poisoning following oral GlySH exposure.
CONCLUSION:
Age, ingested amount, delayed presentation, and reason for exposure were likely to be determinants of the severity of GlySH exposure. Because shock is the major cause of death and usually develops early after GlySH exposure, prompt fluid replacement therapy seems critical in the initial management of such exposures. Patients’ airway should also be secured to avoid aspiration and subsequent respiratory failure.”

11. Toxicol In Vitro. 2010 Apr;24(3):795-802. doi: 10.1016/j.tiv.2009.12.020. Epub 2009 Dec 29.
Effects of Roundup and glyphosate formulations on intracellular transport, microtubules and actin filaments in Xenopus laevis melanophores.
Hedberg D1, Wallin M.
Author information

“Abstract
Glyphosate containing herbicides, such as Roundup, are commonly used and generally considered to be safe. However, some toxic effects are found on amphibians in vivo and human and mouse cells in vitro. In this study the effects of Roundup, glyphosate, glyphosateisopropylamine and isopropylamine were studied on intracellular transport by measuring aggregation capacity in Xenopus laevis melanophores. The chemicals inhibited retrograde transport of melanosomes in the range of 0.5-5mM. Cellular morphology and localization of microtubules and actin filaments were affected as determined by immunocytochemistry. Both glyphosate and Roundup decreased pH in the media. Acidic pH inhibited melanosome transport and altered microtubule and actin morphology in the absence of chemicals, while transport inhibiting concentrations of glyphosate, Roundup and glyphosateisopropylamine disassembled both microtubules and actin filaments. At physiological pH the effects of Roundup decreased whereas glyphosate failed to inhibit transport. Physiological pH decreases glyphosate lipophilicity and its diffusion into the cytoplasm. The Roundup formulation contains surfactants, such as POEA (polyetylated tallow amine) that increases membrane permeability allowing cellular uptake at physiological pH. Our results show that the effects of glyphosate containing compounds are pH-dependent and that they inhibit intracellular transport through disassembly of the cytoskeleton possibly by interfering with intracellular Ca(2+)-balance.
Copyright (c) 2010 Elsevier Ltd. All rights reserved.”

12. Forensic Sci Int. 2013 Mar 10;226(1-3):e20-5. doi: 10.1016/j.forsciint.2012.12.010. Epub 2013 Jan 3.
Determination of glyphosate and AMPA in blood and urine from humans: about 13 cases of acute intoxication.
Zouaoui K1, Dulaurent S, Gaulier JM, Moesch C, Lachâtre G.
Author information

“Abstract
Acute intoxications after ingesting glyphosate are observed in suicidal or accidental cases. Despite low potential toxicity of this herbicide, a number of fatalities and severe outcomes are reported. Indeed, some authors have described the clinical features associated with blood and urine concentrations following intoxication. The purpose of this study is to describe the clinical feature and determinate the utility of the glyphosate concentration in blood and urine and the dose taken for predicting clinical outcomes. In 13 glyphosate poisoning cases treated in our laboratory within 7 years period from 2002 to 2009, we registered clinical observations and collected blood and urine samples to HPLC-MS-MS analysis. We classified our patients by the intoxication severity using simple clinical criteria. We obtained clinical observations from 10 patients and the others three patients were treated in forensic cases. Among the 10 patients, one was asymptomatic, 5 had mild to moderate poisoning and 2 had severe poisoning. There were 6 deaths whose 3 were forensic cases. The most common symptoms were oropharyngeal ulceration (5/10), nausea and vomiting (3/10). The main altered biological parameters were high lactate (3/10) and acidosis (7/10). We also noted respiratory distress (3/10), cardiac arrhythmia (4/10), hyperkaleamia, impaired renal function (2/10), hepatic toxicity (1/10) and altered consciousness (3/10). In fatalities, the common symptoms were cardiovascular shock, cardiorespiratory arrest, haemodynamic disturbance, intravascular disseminated coagulation and multiple organ failure. Blood glyphosate concentrations had a mean value of 61 mg/L (range 0.6-150 mg/L) and 4146 mg/L (range 690-7480 mg/L) respectively in mild-moderate intoxication and fatal cases. In the severe intoxication case for which blood has been sampled, the blood glyphosate concentration was found at 838 mg/L. Death was most of the time associated with larger taken dose (500 mL in one patient) and high blood glyphosate concentrations. To predict clinical outcomes and to guide treatment support in patients who ingested glyphosate, blood concentrations of this compound and the taken dose have been useful.
Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.”

13. Toxicology. 2013 Nov 16;313(2-3):122-8. doi: 10.1016/j.tox.2012.09.006. Epub 2012 Sep 21.
Ethoxylated adjuvants of glyphosate-based herbicides are active principles of human cell toxicity.
Mesnage R1, Bernay B, Séralini GE.
Author information

1University of Caen, EA2608, Institute of Biology, Risk Pole CNRS, Esplanade de la Paix, 14032 Caen, Cedex, France; CRIIGEN, 40 rue de Monceau, 75008 Paris, France.

“Abstract
Pesticides are always used in formulations as mixtures of an active principle with adjuvants. Glyphosate, the active ingredient of the major pesticide in the world, is an herbicide supposed to be specific on plant metabolism. Its adjuvants are generally considered as inert diluents. Since side effects for all these compounds have been claimed, we studied potential active principles for toxicity on human cells for 9 glyphosate-based formulations. For this we detailed their compositions and toxicities, and as controls we used a major adjuvant (the polyethoxylated tallowamine POE-15), glyphosate alone, and a total formulation without glyphosate. This was performed after 24h exposures on hepatic (HepG2), embryonic (HEK293) and placental (JEG3) cell lines. We measured mitochondrial activities, membrane degradations, and caspases 3/7 activities. The compositions in adjuvants were analyzed by mass spectrometry. Here we demonstrate that all formulations are more toxic than glyphosate, and we separated experimentally three groups of formulations differentially toxic according to their concentrations in ethoxylated adjuvants. Among them, POE-15 clearly appears to be the most toxic principle against human cells, even if others are not excluded. It begins to be active with negative dose-dependent effects on cellular respiration and membrane integrity between 1 and 3ppm, at environmental/occupational doses. We demonstrate in addition that POE-15 induces necrosis when its first micellization process occurs, by contrast to glyphosate which is known to promote endocrine disrupting effects after entering cells. Altogether, these results challenge the establishment of guidance values such as the acceptable daily intake of glyphosate, when these are mostly based on a long term in vivo test of glyphosate alone. Since pesticides are always used with adjuvants that could change their toxicity, the necessity to assess their whole formulations as mixtures becomes obvious. This challenges the concept of active principle of pesticides for non-target species.”

14. J Toxicol Clin Toxicol. 2002;40(7):885-92.
An analysis of glyphosate data from the California Environmental Protection Agency Pesticide Illness Surveillance Program.
Goldstein DA1, Acquavella JF, Mannion RM, Farmer DR.
Author information

Abstract
Glyphosate is among the pesticides most frequently reported to the California EPA Pesticide Illness Surveillance Program. We analyzed glyphosate-related calls to the Pesticide Illness Surveillance Program in order to assess the number of reports involving systemic symptoms and to better understand the nature and severity of reported cases. Data on glyphosate and other pesticides are available for the years 1982-1997 including: type of exposure (agricultural/other); target organ(s) affected (skin/eye/respiratory/systemic); exposure(s); an assessment of causal relationship (possible, probable, or definite); and limited medical text. Of 815 total glyphosate calls, most involved topical irritation of the eye (n = 399), skin (n = 250), upper airway (n = 7), or combinations of these sites (n = 32) without systemic symptoms. Of the 187 systemic cases, only 22 had symptoms recorded as probably or definitely related to glyphosate exposure alone. The reported symptoms were not severe, expected to be limited in duration, and frequently inconsistent with the route of exposure and/or previous experience with glyphosate. We conclude that call volume is not a reliable indicator of the actual incidence or severity of glyphosate-related incidents in California.”

15. Toxicology. 2009 Aug 21;262(3):184-91. doi: 10.1016/j.tox.2009.06.006. Epub 2009 Jun 17.
Glyphosate-based herbicides are toxic and endocrine disruptors in human cell lines.
Gasnier C1, Dumont C, Benachour N, Clair E, Chagnon MC, Séralini GE.
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“6Abstract
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.”

17. Tang Jinxia, Lu Cunhui (1979) The influence of electroacupuncture anaesthesia on cholinergic transmitters in patients and rats. Proceedings of Nat Symp Acupunt Moxib Acupunct Anaesthesia, Beijing June 1-5.

18. Wang Caiyuan, Yu Bi, Liu Xiaochun (1979) The influence of acupuncture on the acetylcholine level in various regions of rat brain. Proceedings Nat Symp Acupunct Moxib Acupunct Anaesthesia, Beijing, June 1-5.

19. Importance and toxicological effects of organophosphorus pesticides: A comprehensive review M. Kazemi1*, A. M. Tahmasbi1, R. Valizadeh1, A. A. Naserian1, A. Soni2 and M. M. Moheghi1 Department of Animal Science, Excellence Center for Animal Science, Faculty of Agriculture, Ferdowsi University of Mashhad

20. Viragh C, Kovach IM, Pannell L, 1999. Small Molecular Products of Dealkylation in Soman-Inhibited Electric Eel Acetylcholinesterase. American Chemical Society, June 11, 1999.

21. Sawada Y, Nagai Y, Ueyama M, Yamamoto I, 1988. Probable toxicity of surface-active agent in commercial herbicide containing glyphosate. Lancet. 1988 Feb 6;1(8580):299.

22. (Servizi JA, Gordon RW, Martens DW, 1987. Acute toxicity of Garlon 4 and Roundup herbicides to salmon, Daphnia, and trout.
Bull Environ Contam Toxicol. 1987 Jul;39(1):15-22.

23. “In a 1993 article on organophosphate poisoning, British researcher, T. C. Marrs, indicated that “certain OPs are exploited for their anticholinesterase effects, including defoliants such as ‘DEF’, herbicides such as glyphosate.” The article goes on to say that the cholinergic syndrome is “caused by acetylcholinesterase inhibition.” PANUPS, 1999. Glyphosate May Harm Beneficial Organisms, October 27, 1999 – Marrs, TC, 1993. Organophosphate poisoning. Pharmacol Ther 1993; 58(1): 51-66

24. “cholinesterases are readily phosphorylated at the active site serine by a variety of organophosphorus agents (OP) and carbamates.” http://www.ensam.inra.fr/cholinesterase/chem/chemInhibition2.html. The ESTHER “Chemical Mechanism of Acetylcholinesterase Inhibition” introduction

25. Goldberg I, Mateles RI , 1975. Growth of Pseudomonas C on C1 compounds: enzyme activities in extracts of Pseudomonas C cells grown on methanol, formaldehyde, and formate as sole carbon sources. J Bacteriol 1975 Apr;122(1):47-53)

26.
RoundUp and Cholinesterase Inhibition, http://www.naturescountrystore.com/roundup/page7.html

• This reply was modified 1 year, 5 months ago by  Toxed2loss.
• This reply was modified 1 year, 5 months ago by  Toxed2loss.
• This reply was modified 1 year, 5 months ago by  Toxed2loss.
• This reply was modified 1 year, 5 months ago by  Toxed2loss.
• This reply was modified 1 year, 5 months ago by  Toxed2loss.

[Toxed2lossKeymaster 20p]

I found this on westonaprice.org Note the “mouth swelling.”

“SOY TRAGIC

Soy is not only toxic in its own right; in addition, the way it is cultivated adds further toxins to the environment. The tragic proving ground for these two facts is the Argentinian Pampas, which used to be dotted with dairy and vegetable farms, but now is blanketed with large-scale genetically engineered soybean monoculture. Fifty-six percent of Argentina’s cultivated land is now planted with Roundup Ready soy beans with the result that 190 million liters of glyphosate (the active ingredient in the herbicide Roundup) are sprayed in Argentina annually. The practice is leading not only to the dieoff of trees but also to serious disorders in human beings! The immediate symptoms in the spray zone are dizziness, allergic reactions, itching, mouth swelling and general malaise. People are warned to stay inside when spraying is underway, but they report getting sick anyway. Authorities are turning a deaf ear—why would they disrupt Argentina’s major export crop—but some scientists are speaking out. For example, Andres Carrasco of the Argentine Ministry of Science has found that glyphosate exposure can cause defects in the brain, intestines and hearts of amphibian fetuses, and these results can be applied to humans. The work of Carrasco and others indicates that soy causes endocrine disruption, developmental and reproductive toxicity, DNA damage, neurotoxicity and cancer—especially in the poorly nourished who are forced to eat a lot of soy.”

[Toxed2lossKeymaster 20p]

I also found on Dr. Mercola’s article about glyphosate in breast milk (even in mothers that ate organic and tried to avoid chemicals) that glyphosate was originally patented as a chelator. A chelator grabs minerals out of the body tissues. It would grab calcium first. That would mean weakened enamel and bones.

[Toxed2lossKeymaster 20p]

More research linking glyphosate exposure (and other toxic chemicals) and achalasia,

“In relationship to strong chemicals (possibly harmful), 19 patients (58%) reported the contact. The most frequent were herbicides reported by 9 patients (27%) in which 4 (12%) declared use of liquids derived from glyphosate; 3 (9%) had intense contact with thinner and 2 (6%) reported contact with powdered lime (one accidental ingestion). Other chemicals reported were kerosene, paint remover, PVC glue, resins, stain remover, sulfates, diesel, bleach and strong acids.”

“Idiopathic esophageal achalasia: a study of etiology and profile of the patients” Gustavo Carvalho de Oliveira; Luiz Roberto Lopes; João de Souza Coelho-Neto
ABCD, arq. bras. cir. dig. vol.23 no.1 São Paulo Jan./Mar. 2010, http://dx.doi.org/10.1590/S0102-67202010000100004

[Toxed2lossKeymaster 20p]

A ground breaking report came out in the Lancet, research showing Glyphosate is a “probable carcinogen.”

http://www.thelancet.com/journals/lanonc/article/PIIS1470-2045%2815%2970134-8/abstract

• This reply was modified 5 months, 4 weeks ago by  Toxed2loss.

[PattyvaughnParticipant 197p]

I really hope “mainstream science” is finally ready to recognize how bad this stuff is and that it is finally going the way of DDT and other banned substances.

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