Critical Evaluation of Cancer Risk from 2,4-D

Gandhi, Renu; Wandji, Serge-Alain; Snedeker, Suzanne M.

doi:10.1007/978-1-4612-1156-3_1

Cited by 13 publications

(13 citation statements)

References 90 publications

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“…Their results suggested that some mixtures, especially nitrate plus either pesticide, had effects not detected from exposure to the individual chemicals. Thus, when assessing environmental exposure involving mixtures of pesticides, single chemical evaluations of toxicity (e.g., Gandhi et al 2000; Muir et al 1991), although they provide useful information, generally have little practical value when assessing normal environmental exposure involving mixtures of pesticides.…”

Section: Discussionmentioning

confidence: 99%

Pesticides in Surface Drinking-Water Supplies of the Northern Great Plains

Donald

Cessna

Sverko

et al. 2007

Environ Health Perspect

157

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BackgroundHuman health anomalies have been associated with pesticide exposure for people living in rural landscapes in the northern Great Plains of North America.ObjectiveThe objective of this study was to investigate the occurrence of 45 pesticides in drinking water from reservoirs in this area that received water primarily from snowmelt and rainfall runoff from agricultural crop lands.MethodsWater from 15 reservoirs was sampled frequently during the spring pesticide application period (early May to mid-August) and less frequently for the remainder of the year. Drinking water was sampled in early July. Sample extracts were analyzed for pesticide content using mass spectrometric detection.ResultsWe detected two insecticides and 27 herbicides in reservoir water. Consistent detection of a subset of 7 herbicides suggested that atmospheric deposition, either directly or in rain, was the principal pathway from fields to the reservoirs. However, the highest concentrations and number of herbicides in drinking water were associated with runoff from a localized 133-mm rainfall over 15 days toward the end of spring herbicide application. Water treatment removed from 14 to 86% of individual herbicides. Drinking water contained 3–15 herbicides (average, 6.4).ConclusionsWe estimated the mean annual calculated concentration of herbicides in drinking water to be 75 ng/L (2,4-dichlorophenoxy)acetic acid, 31 ng/L (2-chloro-4-methylphenoxy)acetic acid, 24 ng/L clopyralid, 11 ng/L dichlorprop, 4 ng/L dicamba, 3 ng/L mecoprop, and 1 ng/L bro-moxynil. The maximum total concentration of herbicides in drinking water was 2,423 ng/L. For the seven herbicides with established drinking water guidelines, all concentrations of the individual chemicals were well below their respective guideline. However, guidelines have not been established for the majority of the herbicides found in drinking water or for mixtures of pesticides.

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Section: Discussionmentioning

confidence: 99%

Pesticides in Surface Drinking-Water Supplies of the Northern Great Plains

Donald

Cessna

Sverko

et al. 2007

Environ Health Perspect

157

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“…Although the use of a wide range of assays for mutagenicity and genotoxicity, previous studies have revealed conflicting or even opposite results of the genotoxic potential of 2,4-D (Gandhi et al, 2000). These inconsistencies, as suggested by Kaya et al (1999), could be most probably due to: (1) the use of both pure compounds and commercial formulations with unknown impurities; and/or (2) the differential sensitivities of the specific systems/endpoints used.…”

Section: Discussionmentioning

confidence: 99%

Herbicide 2,4‐dichlorophenoxyacetic acid (2,4‐D)‐induced cytogenetic damage in human lymphocytes in vitro in presence of erythrocytes

Soloneski

González

Reigosa

et al. 2007

Cell Biology International

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The genotoxic effects of 2,4-D and its commercial derivative 2,4-D DMA were studied by measuring sister chromatid exchange (SCE), cell-cycle progression and mitotic index in human whole blood (WBC) and plasma leukocyte cultures (PLC). Concentrations of 10, 25, 50 and 100 microg herbicide/ml were used during 72 h. In WBC, a significant increase in SCE frequency was observed within the 10-50 microg 2,4-D/ml and 25-100 microg 2,4-D DMA/ml dose range. Contrarily, in PLC, none of the concentrations employed affected the SCEs frequency. A significant delay in cell proliferation was observed in WBC after treatments with 25 and 50 microg 2,4-D/ml and 50 and 100 microg 2,4-D DMA/ml. In PLC, only 100.0 microg 2,4-D/ml altered cell-cycle progression. For both chemicals, a progressive dose-related inhibition of mitotic activity was observed. The results demonstrated that the presence of erythrocytes in the culture system modulated the DNA and cellular damage inflicted by 2,4-D and 2,4-D DMA into human lymphocytes in vitro as well as both 2,4-D and 2,4-D DMA were more potent genotoxic agents in the presence of human red cells.

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“…Furthermore, the results of experimental studies in laboratory animals did not support a causal association between exposure these three compounds and cancer development. Similarly, Gandhi et al [41] developed a critical evaluation of cancer risk from 2,4-D and found that there was no evidence for carcinogenicity of 2,4-D, although there was some suggestive evidence for NHL as an outcome, but without a plausible mode of action.…”

Section: Introductionmentioning

confidence: 99%

A Systematic Review of Carcinogenic Outcomes and Potential Mechanisms from Exposure to 2,4-D and MCPA in the Environment

Stackelberg

2013

Journal of Toxicology

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Chlorophenoxy compounds, particularly 2,4-dichlorophenoxyacetic acid (2,4-D) and 4-chloro-2-methylphenoxy)acetic acid (MCPA), are amongst the most widely used herbicides in the United States for both agricultural and residential applications. Epidemiologic studies suggest that exposure to 2,4-D and MCPA may be associated with increased risk non-Hodgkins lymphoma (NHL), Hodgkin's disease (HD), leukemia, and soft-tissue sarcoma (STS). Toxicological studies in rodents show no evidence of carcinogenicity, and regulatory agencies worldwide consider chlorophenoxies as not likely to be carcinogenic or unclassifiable as to carcinogenicity. This systematic review assembles the available data to evaluate epidemiologic, toxicological, pharmacokinetic, exposure, and biomonitoring studies with respect to key cellular events noted in disease etiology and how those relate to hypothesized modes of action for these constituents to determine the plausibility of an association between exposure to environmentally relevant concentrations of 2,4-D and MCPA and lymphohematopoietic cancers. The combined evidence does not support a genotoxic mode of action. Although plausible hypotheses for other carcinogenic modes of action exist, a comparison of biomonitoring data to oral equivalent doses calculated from bioassay data shows that environmental exposures are not sufficient to support a causal relationship. Genetic polymorphisms exist that are known to increase the risk of developing NHL. The potential interaction between these polymorphisms and exposures to chlorophenoxy compounds, particularly in occupational settings, is largely unknown.

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Critical Evaluation of Cancer Risk from 2,4-D

Cited by 13 publications

References 90 publications

Pesticides in Surface Drinking-Water Supplies of the Northern Great Plains

Pesticides in Surface Drinking-Water Supplies of the Northern Great Plains

Herbicide 2,4‐dichlorophenoxyacetic acid (2,4‐D)‐induced cytogenetic damage in human lymphocytes in vitro in presence of erythrocytes

A Systematic Review of Carcinogenic Outcomes and Potential Mechanisms from Exposure to 2,4-D and MCPA in the Environment

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