Pesticide Exposure - HH-RA.org

Bibliography Tag: pesticide exposure

Hill et al., 1995

Hill RH Jr, Head SL, Baker S, Gregg M, Shealy DB, Bailey SL, Williams CC, Sampson EJ, Needham LL, “Pesticide Residues of Adults Living in the United States: Reference Range Concentrations,” Environmental Research, 1995, 71:2, DOI: 10.1006/ENRS.1995.1071.

ABSTRACT:

We measured 12 analytes in urine of 1000 adults living in the United States to establish reference range concentrations for pesticide residues. We frequently found six of these analytes: 2,5-dichlorophenol (in 98% of adults); 2,4-dichlorophenol (in 64%); 1-naphthol (in 86%); 2-naphthol (in 81%); 3,5,6- trichloro-2-pyridinol (in 82%); and pentachlorophenol (in 64%). The 95th percentile concentration (95th PC) for 2,5-dichlorophenol (indicative of p-dichlorobenzene exposure) was 790 micrograms/liter; concentrations ranged up to 8700 micrograms/liter. 2,4-Dichlorophenol concentrations ranged up to 450 micrograms/ liter, and the 95thPC was 64 micrograms/liter. 1-Naphthol and 2-naphthol (indicative of naphthalene exposure) had 95thPCs of 43 and 30 micrograms/liter, respectively; concentrations of 1-naphthol ranged up to 2500 micrograms/liter. Chlorpyrifos exposure was indicated by 3,5,6-tricholoro-2-pyridinol concentrations of 13 (95thPC) and 77 micrograms/liter (maximum observed). Pentachlorophenol had a 95thPC of 8.2 micrograms/liter. Other analytes measured included 4-nitrophenol (in 41%); 2,4,5-trichlorophenol (in 20%); 2,4,6-trichlorophenol (in 9.5%); 2,4-dichlorophenoxyacetic acid (in 12%); 2-isopropoxyphenol (in 6.8%); and 7-carbofuranphenol (in 1.5%). The 95thPCs of these analytes were < 6 micrograms/liter. p-Dichlorobenzene exposure is ubiquitous; naphthalene and chlorpyrifos are also major sources of pesticide exposure. Exposure to chlorpyrifos appears to be increasing. Although pentachlorophenol exposure is frequent, exposure appears to be decreasing. These reference range concentrations provide information about pesticide exposure and serve as a basis against which to compare concentrations in subjects who may have been exposed to pesticides. FULL TEXT

EPA, 2012

EPA, “Index to Pesticide Chemical Names, Part 180 Tolerance Information, and Food and Feed Commodities (by Commodity),” Office of Pesticides Programs, 2012.

ABSTRACT:

Not Available

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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

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

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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

EPA, 1992a

Code of Federal Regulations, “Pesticide Tolerances and Food and Feed Additive Regulations for Glyphosate” (Summary), 40 CFR §§ 180-186, 1992

ABSTRACT:

SUMMARY: This document establishes tolerances and food and feed additive regulations for the combined residues of the herbicide glyphosate (N-(phosphonomethyl)glycine) and its metabolite aminomethyl phosphonic acid. The specific proposals are: an amended tolerance in or on the raw agricultural commodities (RACs) soybeans from 6 parts per million (ppm) to 20 ppm; a tolerance on soybean straw at 20 ppm; a food additive regulation proposing increases in tolerances for the processed human food instant tea from 4.0 ppm to 7.0 ppm; a feed additive regulation for citrus molasses at 1 ppm; and amended feed additive tolerances for dried citrus pulp from 0.4 ppm to 1 ppm and soybean hulls from 20 ppm to 100 ppm. These regulations were requested by the Monsanto Co. and would establish the maximum permissible residues of the herbicide in or on these RACs, this processed human food, and these animal feed commodities. FULL TEXT

EPA, 2016

Code of Federal Regulations, “Glyphosate; tolerances for residues,” 40 CFR § 180.364, 2016.

ABSTRACT:

Tolerances are established for residues of glyphosate, including its metabolites and degradates, in or on the commodities listed below resulting from the application of glyphosate, the isopropylamine salt of glyphosate, the ethanolamine salt of glyphosate, the dimethylamine salt of glyphosate, the ammonium salt of glyphosate, and the potassium salt of glyphosate. Compliance with the following tolerance levels is to be determined by measuring only glyphosate (N-(phosphonomethyl)glycine).

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