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Mesnage et al., 2015

R. Mesnage, N. Defarge, J. Spiroux de Vendomois, G.E. Seralini, “Potential toxic effects of glyphosate and its commercial formulations below regulatory limits,” Food and Chemical Toxicology, 2015, 84, DOI: 10.1016/J.FCT.2015.08.012.

ABSTRACT:

Glyphosate-based herbicides (GlyBH), including Roundup, are the most widely used pesticides worldwide. Their uses have increased exponentially since their introduction on the market. Residue levels in food or water, as well as human exposures, are escalating. We have reviewed the toxic effects of GlyBH measured below regulatory limits by evaluating the published literature and regulatory reports. We reveal a coherent body of evidence indicating that GlyBH could be toxic below the regulatory lowest observed adverse effect level for chronic toxic effects. It includes teratogenic, tumorigenic and hepatorenal effects. They could be explained by endocrine disruption and oxidative stress, causing metabolic alterations, depending on dose and exposure time. Some effects were detected in the range of the recommended acceptable daily intake. Toxic effects of commercial formulations can also be explained by GlyBH adjuvants, which have their own toxicity, but also enhance glyphosate toxicity. These challenge the assumption of safety of GlyBH at the levels at which they contaminate food and the environment, albeit these levels may fall below regulatory thresholds. Neurodevelopmental, reproductive, and transgenerational effects of GlyBH must be revisited, since a growing body of knowledge suggests the predominance of endocrine disrupting mechanisms caused by environmentally relevant levels of exposure. FULL TEXT

Marc et al., 2004

Julie Marc, Robert Belle, Julia Morales, Patrick Cormier, and Odile Mulner-Lorillon, “Formulated Glyphosate Activates the DNA-Response Checkpoint of the Cell Cycle Leading to the Prevention of G2/M Transition,” Toxicological Sciences, 2004, 82, DOI:10.1093/TOXSCI/KFH281.

ABSTRACT:

A glyphosate containing pesticide impedes at 10 mM glyphosate the G2/M transition as judged from analysis of the first cell cycle of sea urchin development. We show that formulated glyphosate prevented dephosphorylation of Tyr 15 of the cell cycle regulator CDK1/cyclin B in vivo, the end point target of the G2/M cell cycle checkpoint. Formulated glyphosate had no direct effect on the dual specific cdc25 phosphatase activity responsible for Tyr 15 dephosphorylation. At a concentration that efficiently impeded the cell cycle, formulated glyphosate inhibited the synthesis of DNA occurring in S phase of the cell cycle. The extent of the inhibition of DNA synthesis by formulated glyphosate was correlated with the effect on the cell cycle. We conclude that formulated glyphosate’s effect on the cell cycle is exerted at the level of the DNA-response checkpoint of S phase. The resulting inhibition of CDK1/cyclin B Tyr 15 dephosphorylationleads to prevention of the G2/M transition and cell cycle progression. FULL TEXT

Jayasumana et al., 2015a

Channa Jayasumana, Sarath Gunatilake, and Sisira Siribaddana, “Simultaneous exposure to multiple heavy metals and glyphosate may contribute to Sri Lankan agricultural nephropathy,” BMC Nephrology, 2015, 16:103, DOI 10.1186/s12882-015-0109-2.

ABSTRACT:

BACKGROUND: Sri Lankan Agricultural Nephropathy (SAN), a new form of chronic kidney disease among paddy farmers was first reported in 1994. It has now become the most debilitating public health issue in the dry zone of Sri Lanka. Previous studies showed SAN is a tubulo-interstitial type nephropathy and exposure to arsenic and cadmium may play a role in pathogenesis of the disease.

METHODS: Urine samples of patients with SAN (N = 10) from Padavi-Sripura, a disease endemic area, and from two sets of controls, one from healthy participants (N = 10) from the same endemic area and the other from a non-endemic area (N = 10; Colombo district) were analyzed for 19 heavy metals and for the presence of the pesticide- glyphosate.

RESULTS: In both cases and the controls who live in the endemic region, median concentrations of urinary Sb, As, Cd, Co, Pb, Mn, Ni, Ti and V exceed the reference range. With the exception of Mo in patients and Al, Cu, Mo, Se, Ti and Zn in endemic controls, creatinine adjusted values of urinary heavy metals and glyphosate were significantly higher when compared to non-endemic controls. Creatinine unadjusted values were significant higher for 14 of the 20 chemicals studied in endemic controls and 7 in patients, compared to non-endemic controls. The highest urinary glyphosate concentration was recorded in SAN patients (range 61.0-195.1 μg/g creatinine).

CONCLUSTIONS: People in disease endemic area exposed to multiple heavy metals and glyphosate. Results are supportive of toxicological origin of SAN that is confined to specific geographical areas. Although we could not localize a single nephrotoxin as the culprit for SAN, multiple heavy metals and glyphosates may play a role in the pathogenesis. Heavy metals excessively present in the urine samples of patients with SAN are capable of causing damage to kidneys. Synergistic effects of multiple heavy metals and agrochemicals may be nephrotoxic. FULL TEXT

Jayasumana et al., 2014

Channa Jayasumana, Sarath Gunatilake, and Priyantha Senanayake, “Glyphosate, Hard Water and Nephrotoxic Metals: Are They the Culprits Behind the Epidemic of Chronic Kidney Disease of Unknown Etiology in Sri Lanka?,” International Journal of Environmental Research and Public Health, 2014, 11, DOI:10.3390/IJERPH 110202125.

ABSTRACT:

The current chronic kidney disease epidemic, the major health issue in the rice paddy farming areas in Sri Lanka has been the subject of many scientific and political debates over the last decade. Although there is no agreement among scientists about the etiology of the disease, a majority of them has concluded that this is a toxic nephropathy. None of the hypotheses put forward so far could explain coherently the totality of clinical, biochemical, histopathological findings, and the unique geographical distribution of the disease and its appearance in the mid-1990s. A strong association between the consumption of hard water and the occurrence of this special kidney disease has been observed, but the relationship has not been explained consistently. Here, we have hypothesized the association of using glyphosate, the most widely used herbicide in the disease endemic area and its unique metal chelating properties. The possible role played by glyphosate-metal complexes in this epidemic has not been given any serious consideration by investigators for the last two decades. Furthermore, it may explain similar kidney disease epidemics observed in Andra Pradesh (India) and Central America. Although glyphosate alone does not cause an epidemic of chronic kidney disease, it seems to have acquired the ability to destroy the renal tissues of thousands of farmers when it forms complexes with a localized geo environmental factor (hardness) and nephrotoxic metals. FULL TEXT

Guyton et al., 2015

Kathryn Z Guyton, Dana Loomis, Yann Grosse, Fatiha El Ghissassi, Lamia Benbrahim-Tallaa, Neela Guha, Chiara Scoccianti, Heidi Mattock, Kurt Straif, on behalf of the International Agency for Research on Cancer Monograph Working Group, “Carcinogenicity of tetrachlorvinphos, parathion, malathion, diazinon, and glyphosate,” The Lancet, 2015, 16, DOI: 10.1016/S1470-2045(15)70134-8.

ABSTRACT:

Not Avaialble

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IARC, 2017

International Agency for Research on Cancer. “IARC monographs on the evaluation of carcinogenic risks to humans, volume 112. Glyphosate,” IARC; 2017.

ABSTRACT:

The IARC Monographs identify environmental factors that can increase the risk of human cancer. These include chemicals, complex mixtures, occupational exposures, physical agents, biological agents, and lifestyle factors. National health agencies can use this information as scientific support for their actions to prevent exposure to potential carcinogens. FULL TEXT

Center for Food Safety, 2012

Center for Food Safety, “Exposure to Herbicide Residues and Herbicide-Resistant Crops,” November 2012.

ABSTRACT:

Not Available

FULL TEXT

Hartzler et al., 2006

Bob Hartzler, Chris Boerboom, Glenn Nice, Peter Sikkema, “Understanding Glyphosate To Increase Performance: The Glyphosate, Weeds, and Crops Series,” Purdue Extension, 2006.

ABSTRACT:

Glyphosate and Roundup Ready® crops are popular because they provide consistent, broad spectrum weed control with minimal risk of crop injury. On occasion, however, growers experience poor weed control with glyphosate, generally because of application or weather-related factors. This publication examines the factors that affect glyphosate performance and offers management strategies to minimize fluctuations in its effectiveness. FULL TEXT

EPA, 2015

Environmental Protection Agency, “Updated Screening Level Usage Analysis (SLUA) Report for Glyphosate Case PC #s(103601, 103604, 103607, 103608, 103613,and417300),” Office of Chemical Safety and Pollution Prevention, October 22, 2015.

ABSTRACT:

This memorandum transmits an updated Screening Level Usage Analysis (SLUA) report for the glyphosate case (previously completed in 2007). The usage data in the updated SLUA (2015) are an amalgamation of USDA/NASS and Private Pesticide Market Research data from 2005 to 2014. The new SLUA (2015) shows a decrease in usage, in terms of pounds a.i. and/or percent crop treated on apples, apricots, artichokes, avocados, broccoli, caneberries, cauliflower, grapefruit, garlic, nectarines, oranges, pasture, peaches, pears, pecans, and tangelos. The usage data did not change for cantaloupes, carrots, celery, lemons, oats, green beans, and pumpkins. The new SLUA (2015) shows an increase in usage, in terms of pounds a.i. and/or percent crop treated on the remainder of the SLUA crops. FULL TEXT

EPA, 1999d

Environmental Protection Agency, “Reassessed Group 3 Tolerances By Pesticide,” 1999.

ABSTRACT:

Lists the tolerances for multiple pesticides that were re-assessed between 1997-1999, including glyphosate. FULL TEXT

Bibliography Index