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In February 1999, the Office of Environmental Health Hazard Assessment and the California Environmental Protection Agency teamed up to draft the Public Health Goal for Atrazine In Drinking Water.


The Office of Environmental Health Hazard Assessment (OEHHA) has developed a Public Health Goal (PHG) of 0.00015 mg/L (0.15 µg/L or 0.15 ppb) for atrazine in drinking water. The current California MCL is 3 pbb for atg/L or 0.15 ppb) for atrazine in drinking water. The current California MCL is 3 pbb for atrazine in drinking water. The PHG is based on mammary tumors (adenocarcinoma and fibroadenoma) observed in females in a carcinogenicity study in Sprague-Dawley rats (70/sex/dose) fed atrazine at dietary concentrations of 0, 10, 70, 500, or 1,000 ppm for 24 months and using a linear dose response approach with a carcinogenic slope factor (CSF) of 0.23 (mg/kg-day) -1. In F344 rats, a significantly higher incidence of benign mammary tumors was found in the high dose males and a significantly positive trend test was observed for leukemia and lymphoma in females. Atrazine had no carcinogenic effects in a mouse carcinogenicity study. Epidemiological studies are equivocal. The exact mechanism of mammary tumor formation is not known. Atrazine is positive in a number of mutagenicity studies. It disrupts the estrous cycle in female rats, but it is not directly estrogenic. It decreases triiodothyronine (T3) levels in rats and causes thyroid hyperplasia. Decreases in luteinizing hormone (LH), progesterone and estradiol levels were also observed in rats administered atrazine or its metabolite diaminochlorotriazine. The most sensitive endpoint for non-carcinogenic effects is cardiomyopathy, observed in a one-year dog study. The NOEL for this effect is 0.48 mg/kg. Based on the NOAEL of 0.48 mg/kg, the non-cancer health protective concentration is 0.0034 mg/L (3 ppb). Atrazine is readily absorbed from the gastrointestinal tract and excreted via urine (≥70%) and feces (≥20%). It is metabolized via stepwise oxidative P-450 dealkylation to de-ethyl or de-isopropyl and then to diaminochlorotriazine. The toxicity of these metabolites is essentially similar to the parent compound.

To read the full report, click here (PDF).

In 2005, a study by the California EPA was published called:  A risk assessment of atrazine use in California: human health and ecological aspects stating that “Although some studies have claimed that atrazine exposure results in an elevated risk of prostate cancer, the published literature is inconclusive with respect to cancer incidence.”

To read the study in full, click here.