The Clastogenic Potential of Triazine Herbicide Combinations Found in Potable Water Supplies

Taets, Carrie; Aref, Susanne; Rayburn, A. Lane

doi:10.2307/3433963

Cited by 7 publications

(8 citation statements)

References 8 publications

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“…The evidence indicating that atrazine is genotoxic was reviewed in 1994 and found to be either negative or equivocal 19. However, more recently, other work has suggested that triazines may cause chromosome breakage (clastogenicity) in Chinese hamster ovary (CHO) cells in vitro 20–22. In addition, in earlier work, not included in the evaluation in Reference 19, it was suggested that certain plants convert it into a mutagen23–26 such as N ‐nitrosoatrazine.…”

Section: Resultsmentioning

confidence: 99%

“…Several papers have been published on the genotoxicity of triazines since the review by Brusick 19. Chromosome damage was reported as increased clastogenicity caused by triazines, using flow cytometric analysis in CHO cells 20–22. The measures of clastogenicity were twofold: the CV (coefficient of variation) of the G1 peak of whole cells and the change in CV of the largest chromosome in the flow karyotype.…”

Section: Resultsmentioning

confidence: 99%

“…The increase in CV is due to chromosomal breakage causing an uneven distribution of DNA in daughter cells. In one such publication22 the triazines atrazine, cyanazine and simazine were tested alone and in combination, at two concentrations: the MCL (maximum contaminant level) and the highest concentration detected in Illinois water supplies. These concentrations were 3 ppb and 18 ppb, respectively, for atrazine, which served as the positive control based on the earlier work 20, 21.…”

Section: Resultsmentioning

confidence: 99%

See 2 more Smart Citations

A risk assessment of atrazine use in California: human health and ecological aspects

Gammon

Aldous

Carr

et al. 2005

Pest Management Science

166

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A risk assessment of the triazine herbicide atrazine has been conducted by first analyzing the toxicity database and subsequently estimating exposure. Margins of safety (MOS) were then calculated. Toxicity was assessed in animal studies and exposure was estimated from occupational and dietary sources. In acute toxicity studies, atrazine caused developmental toxicity in the rabbit [no observed effect level (NOEL) 5 mg kg(-1) day(-1)] and cardiotoxicity in a dog chronic study (NOEL 0.5 mg kg(-1) day(-1)); cancer (mammary glands) resulted from lifetime exposure. The mammary tumors, which occurred specifically in female Sprague-Dawley rats, were malignant, increased in a dose-dependent manner and were also observed with other, related triazines. Evidence for a genotoxic basis for these tumors was either equivocal or negative. Triazines have been shown to be clastogenic in Chinese hamster ovary cells, in vitro, but without showing a convincing dose/response relationship. Atrazine can be converted into genotoxic N-nitrosoatrazine in the environment or the digestive system, suggesting that N-nitrosamines derived from triazines could be oncogenic. However, it was concluded that N-nitrosotriazines are unlikely to play a significant role in triazine-induced rat mammary gland tumors. An endocrine basis for the mammary tumors, involving premature aging of the female SD rat reproductive system, has been proposed. A suppression of the luteinizing hormone surge during the estrus cycle by atrazine leads to the maintenance of elevated blood levels of 17beta-estradiol (E2) and prolactin. The mechanism for tumor development may include one or more of the following: the induction of aromatase (CYP19) and/or other P450 oxygenases, an antagonist action at the estrogen feedback receptor in the hypothalamus, an agonist action at the mammary gland estrogen receptor or an effect on adrenergic neurons in the hypothalamic-pituitary pathway. None of these has been excluded as a target because there has been a lack of a rigorous attempt to address the mechanism of action for mammary tumors at the molecular level. The potential occupational exposure to atrazine was assessed during mixing, loading and application. Absorbed daily dosage values were 1.8-6.1 microg kg(-1) day(-1). The MOS values (animal NOEL/human exposure) for short-term (acute) exposure were 820-2800. Longer-term occupational exposure and risk were also calculated. Detectable crop residues are generally absent at harvest. Theoretical calculations of acute dietary exposure used tolerance levels, along with secondary residues, and water, for which there is a maximum contamination level; atrazine plus the three main chlorotriazine metabolites were combined. MOS values were above 2000 for all population subgroups. Dietary exposure to atrazine is therefore extremely unlikely to result in human health hazard. Recent publications have reported a possible feminization of frogs, measured in laboratory and field studies. This is assumed to be due to the induction of aromatase, but no meas...

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

A risk assessment of atrazine use in California: human health and ecological aspects

Gammon

Aldous

Carr

et al. 2005

Pest Management Science

166

View full text Add to dashboard Cite

show abstract

“…The triazine pesticide atrazine has caused chromosomal damage in Chinese hamster ovary cells (28) and been associated with elevated rates of intrauterine growth retardation in communities with contaminated drinking waters (29). However, there is conflicting evidence as to whether atrazine is mutagenic in cultured human cell lines (30)(31)(32)(33).…”

Section: Discussionmentioning

confidence: 99%

An exploratory analysis of the effect of pesticide exposure on the risk of spontaneous abortion in an Ontario farm population.

Arbuckle

Lin

Mery

2001

Environ Health Perspect

250

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The toxicity of pesticides on human reproduction is largely unknown--particularly how mixtures of pesticide products might affect fetal toxicity. The Ontario Farm Family Health Study collected data by questionnaire on the identity and timing of pesticide use on the farm, lifestyle factors, and a complete reproductive history from the farm operator and eligible couples living on the farm. A total of 2,110 women provided information on 3,936 pregnancies, including 395 spontaneous abortions. To explore critical windows of exposure and target sites for toxicity, we examined exposures separately for preconception (3 months before and up to month of conception) and postconception (first trimester) windows and for early (< 12 weeks) and late (12-19 weeks) spontaneous abortions. We observed moderate increases in risk of early abortions for preconception exposures to phenoxy acetic acid herbicides [odds ratio (OR) = 1.5; 95% confidence interval (CI), 1.1-2.1], triazines (OR = 1.4; 95% CI, 1.0-2.0), and any herbicide (OR = 1.4; 95% CI, 1.1-1.9). For late abortions, preconception exposure to glyphosate (OR = 1.7; 95% CI, 1.0-2.9), thiocarbamates (OR = 1.8; 95% CI, 1.1-3.0), and the miscellaneous class of pesticides (OR = 1.5; 95% CI, 1.0-2.4) was associated with elevated risks. Postconception exposures were generally associated with late spontaneous abortions. Older maternal age (> 34 years of age) was the strongest risk factor for spontaneous abortions, and we observed several interactions between pesticides in the older age group using Classification and Regression Tree analysis. This study shows that timing of exposure and restricting analyses to more homogeneous endpoints are important in characterizing the reproductive toxicity of pesticides.

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“…Many studies have evaluated potential hazards of atrazine in rats, freshwater mollusks, and other animals [11–15]. However, few studies have examined potential interactions between triazine herbicides and insecticide mixtures.…”

Section: Introductionmentioning

confidence: 99%

Effects of atrazine and cyanazine on chlorpyrifos toxicity in Chironomus tentans (Diptera: Chironomidae)

Jin-Clark

Lydy

Zhu

2002

Enviro Toxic and Chemistry

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Toxicities of two triazine herbicides (atrazine and cyanazine) and an organophosphate insecticide (chlorpyrifos) were evaluated individually and with each herbicide in binary combination with chlorpyrifos using fourth-instar larvae of the aquatic midge, Chironomus tentans. Chlorpyrifos at 0.25 microg/L resulted in an effect in less than 10% of midges in 48-h acute toxicity bioassays. Neither atrazine nor cyanazine alone at relatively high concentrations (up to 1,000 microg/L) caused significant acute toxicity to C. tentans. However, atrazine and cyanazine caused significant synergistic effects on the toxicity of chlorpyrifos when midges were exposed to mixtures of atrazine or cyanazine (10, 100, 1,000 microg/L) with chlorpyrifos (0.25 microg/L). At fixed concentrations (200 microg/L) of the herbicides, toxicity of chlorpyrifos was enhanced by 1.8- and 2.2-fold by atrazine and cyanazine, respectively, at the 50% effective concentration levels. Although atrazine and cyanazine are not effective inhibitors of acetylcholinesterase (AChE) in vitro, the synergism of the two triazine herbicides with chlorpyrifos was associated with increased in vivo inhibition of AChE in midges. We observed a positive correlation between the degree of inhibition of AChE and the concentration of atrazine or cyanazine in the presence of a fixed concentration of chlorpyrifos. It is possible that these herbicides may affect cytochrome P450 enzymes to confer synergistic effects on the toxicity of chlorpyrifos.

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The Clastogenic Potential of Triazine Herbicide Combinations Found in Potable Water Supplies

Cited by 7 publications

References 8 publications

A risk assessment of atrazine use in California: human health and ecological aspects

A risk assessment of atrazine use in California: human health and ecological aspects

An exploratory analysis of the effect of pesticide exposure on the risk of spontaneous abortion in an Ontario farm population.

Effects of atrazine and cyanazine on chlorpyrifos toxicity in Chironomus tentans (Diptera: Chironomidae)

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