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Bibliography Tag: glyphosate

EPA, 1979

Environmental Protection Agency, Petition proposing the establishment of tolerance for residues of glyphosate, November 13, 1979.

SUMMARY:

Petition by Monsanto Agricultural Products, Inc. requests the establishment of a tolerance for residues of glyphosate and its metabolite in stone fruit at 0.2 ppm and refers to an ADI of 0.05 mg/kg/day.  FULL TEXT

EPA, 1975

Environmental Protection Agency, “Request for the establishment of final tolerances,” for Pesticide Petition # 5F1536, 1975.

SUMMARY:

Request for the establishment of final tolerances for combined negligible residues of the herbicide N-phosphonomethyl glycine (glyphosate) and its metabolite aminomethyl phosphonic acid in or on forage grasses (crop group) and soybean forage and hay at 0.2 ppm; and various crops grains and soybeans at 0.1 ppm.  FULL TEXT

Franz, 1974

Franz, John E., “N. Phosphonomethyl-glycine Phytotoxicant Compositions,” U.S. Patent 3,799,758, March 26, 1974.

ABSTRACT:

N-phosphonomethylglycine and novel derivatives thereof useful as phytotoxicants or herbicides.

FULL TEXT

EPA, 1993

Environmental Protection Agency, “Reregistration Eligibility Decision (RED): Glyphosate,” Office of Prevention, Pesticides, and Toxic Substances, September 1993.

ABSTRACT:

All pesticides sold or distributed in the United States must be registered by EPA, based on scientific studies showing that they can be used without posing unreasonable risks to people or the environment. Because of advances in scientific knowledge, the law requires that pesticides which were first registered years ago be reregistered to ensure that they meet today’s more stringent standards. In evaluating pesticides for reregistration, EPA obtains and reviews a complete set of studies from pesticide producers, describing the human health and environmental effects of each pesticide. The Agency imposes any regulatory controls that are needed to effectively manage each pesticide’s risks. EPA then reregisters pesticides that can be used without posing unreasonable risks to human health or the environment. When a pesticide is eligible for reregistration, EPA announces this and explains why in a Reregistration Eligibility Decision (RED) document. This fact sheet summarizes the information in the RED document for glyphosate.  FULL TEXT

EPA, 2016b

Environmental Protection Agency, “Glyphosate Issue Paper: Evaluation of Carcinogenic Potential,” EPA’s Office of Pesticide Programs, September 12, 2016.

ABSTRACT:

Not Available

FULL TEXT

Walsh et al., 2000

Lance P. Walsh, Chad McCormick, Clyde Martin, and Douglas M. Stocco, “Roundup Inhibits Steroidogenesis by Disrupting Steroidogenic Acute Regulatory (StAR) Protein Expression,” Environmental Health Perspectives, 2000, 108.

ABSTRACT:

Recent reports demonstrate that many currently used pesticides have the capacity to disrupt reproductive function in animals. Although this reproductive dysfunction is typically characterized by alterations in serum steroid hormone levels, disruptions in spermatogenesis, and loss of fertility, the mechanisms involved in pesticide-induced infertility remain unclear. Because testicular Leydig cells play a cmcial role in male reproductive function by producing testosterone, we used the mouse MA-10 Leydig tumor cell line to study the molecular events involved in pesticide-induced alterations in steroid hormone biosynthesis. We previously showed that the organochlorine insecticide lindane and the organophosphate insecticide Dimethoate directly inhibit steroidogenesis in Leydig cells by disrupting expression of the steroidogenic acute regulatory (StAR) protein. StAR protein mediates the rate-limiting and acutely regulated step in steroidogenesis, the transfer of cholesterol from the outer to the inner mitochondrial membrane where the cytochrome P450 side chain cleavage (P450scc) enzyme initiates the synthesis of all steroid hormones. In the present study, we screened eight currendy used pesticide formulations for their ability to inhibit steroidogenesis, concentrating on their effects on StAR expression in MA-10 cells. In addition, we determined the effects of these compounds on the levels and activities of the P450scc enzyme (which converts cholesterol to pregnenolone) and the 3p-hydroxysteroid dehydrogenase (3P-HSD) enzyme (which converts pregnenolone to progesterone). Of the pesticides screened, only the pesticide Roundup inhibited dibutyryl [(Bu)2]cAMP-stimulated progesterone production in MA-10 cells without causing cellular toxicity. Roundup inhibited steroidogenesis by disrupting StAR protein expression, further demonstrating the susceptibility of StAR to environmental pollutants.   FULL TEXT

Monsanto, 2015b

Monsanto, “Roundup Ready Plus 2015 Weed Management Recommendations and Incentives: Plains, Midwest, and Northeast,” 2015.

ABSTRACT:

Not Available

FULL TEXT

Monsanto, 2015

Monsanto, “Roundup Ready Plus 2015 Weed Management Recommendations and Incentives: Midsouth and Southeast,” 2015.

ABSTRACT:

Not Available

FULL TEXT

Erickson and Bomgardner, 2015

Britt E. Erickson, Melody M. Bomgardner, “Resistant weeds, fears of health effects drive market for alternatives to widely used herbicide,” Chemical and Engineering News, 2015, 93:37.

ABSTRACT:

Not Available

FULL TEXT

Landrigan and Benbrook, 2015

Phillip Landrigan and Charles Benbrook, “GMOs, Herbicides, and Public Health,” Commentary in New England Journal of Medicine, 2015, 373:8, DOI: 10.1056/NEJMp1505660.

ABSTRACT:

Not Available

FULL TEXT

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