ATRAZINE AND ITS METABOLITES 

Atrazine is a selective systemic herbicide of the chlorotriazine class, used for the control 

of annual broadleaf and grassy weeds. Atrazine and its chloro-s-triazine metabolites— 

deethyl-atrazine (DEA), deisopropyl-atrazine (DIA) and diaminochlorotriazine 

(DACT)—have been found in surface water and groundwater as a result of the use of 

atrazine as a pre-emergent or early post-emergent herbicide. The metabolite 

hydroxyatrazine is more commonly detected in groundwater than in surface water. 

Guideline values 0.1 mg/l for atrazine and its chloro-s-triazine metabolites 

0.2 mg/l for hydroxyatrazine 

Occurrence Concentrations rarely exceed 2 μg/l and are commonly well below 

0.1 μg/l 

Group ADI for atrazine and its 

chloro-s-triazine metabolites 

0–0.02 mg/kg body weight based on the NOAEL for atrazine of 1.8 

mg/kg body weight per day identified on the basis of luteinizing 

hormone surge suppression and subsequent disruption of the estrous 

cycle seen at 3.6 mg/kg body weight per day in a 6-month study in rats, 

using a safety factor of 100

ADI for hydroxyatrazine 0–0.04 mg/kg body weight based on the NOAEL of 1.0 mg/kg body 

weight per day identified on the basis of kidney toxicity at 7.8 mg/kg 

body weight per day in a 24-month study in rats, and using a safety 

factor of 25, based on kinetic considerations 

Limit of detection Atrazine: 1 ng/l, isotope dilution MS with solid-phase extraction; 

10 ng/l, GC/MS with solid-phase extraction; 50 ng/l, LC/MS with 

solid-phase extraction; 0.1 μg/l, GC with nitrogen–phosphorus 

detection 

Metabolites: 5 ng/l, capillary GC with nitrogen thermionic specific 

detection and HPLC with photodiode array absorption detection 

following extraction with styrene-divinylbenzene sorbents and elution 

with acetone 

Treatment performance 0.1 μg/l can be achieved using GAC or PAC; also effective are 

bankside filtration and nanofiltration 

Guideline derivation 

• allocation to water 

• body weight 

• consumption 

20% of ADI 

60 kg adult 

2 litres/day 

Additional comments • JMPR considered that the NOAEL for atrazine is protective for 

the consequences of neuroendocrine and other adverse effects 

caused by prolonged exposure to atrazine and its chloro-s-triazine 

metabolites. 

• 20% allocation will be very conservative in most countries, as it is 

expected that exposure of the public will be primarily through 

drinking-water. 

Assessment date This assessment was conducted in 2009. 

Principal references FAO/WHO (2007) Atrazine. In: Pesticide residues in food—2007. 

Joint FAO/WHO Meeting on Pesticide Residues. Rome, Food and 

Agriculture Organization of the United Nations (FAO Plant Production 

and Protection Paper 191; 

http://www.fao.org/ag/AGP/AGPP/Pesticid/JMPR/DOWNLOAD/200

7_rep/report2007jmpr.pdf). 

FAO/WHO (2009) Atrazine. In: Pesticide residues in food—2007 

evaluations. Part II. Toxicological. Geneva, World Health 
Organization 

(http://whqlibdoc.who.int/publications/2009/9789241665230_eng.pdf). 

WHO (2009) Atrazine and its metabolites in drinking-water. 

Background document for development of WHO Guidelines for 

Drinking-water Quality. Geneva, World Health Organization 

(WHO/HSE/WSH/09.01/11). 

JMPR agreed that it is unlikely that atrazine is genotoxic and concluded that atrazine 

is not likely to pose a carcinogenic risk to humans, as the mode of carcinogenic action in 

certain susceptible rat strains is not relevant for human risk assessment. The weight of 

evidence from the epidemiological studies also did not support a causal association 

between exposure to atrazine and the occurrence of cancer in humans. 

In special studies of reproductive toxicity, exposure of rats during early pregnancy 

(i.e. the LH-dependent period) caused increased pre-implantation or post-implantation 

losses, including full-litter resorptions. Attenuation of the LH surge and subsequent 

disruption of the estrous cycle (characterized by an increase in days in estrus) were 

observed at and above 3.65 mg/kg body weight per day, with a NOAEL of 1.8 mg/kg 

body weight per day. The effects on the LH surge and disruption of the estrous cycle 

were further supported by a number of short-term mechanistic studies. Additional 

experiments suggested that the effects of atrazine on LH and prolactin secretion are 

mediated via a hypothalamic site of action. JMPR concluded that atrazine was not 

teratogenic. 

Studies using a variety of test systems in vitro and in vivo indicated that modulation 

of the immune system occurs after exposure to atrazine. However, effects suggestive of 

impaired function of the immune system were observed only at doses greater than those 

shown to affect neuroendocrine function, leading to disruption of the estrous cycle or 

developmental effects.

The toxicity profiles and mode of action of the chloro-s-triazine metabolites are 

similar to those of atrazine; the potency of these metabolites with regard to their 

neuroendocrine-disrupting properties appeared to be similar to that of the parent 

compound. 

The metabolite hydroxyatrazine does not have the same mode of action or toxicity 

profile as atrazine and its chlorometabolites. The main effect of hydroxyatrazine was 

kidney toxicity (owing to its low solubility in water, resulting in crystal formation and a 

subsequent inflammatory response), and there was no evidence that hydroxyatrazine has 

neuroendocrine-disrupting properties. There was no evidence of carcinogenicity, and 

hydroxyatrazine did not show genotoxicity in an adequate range of tests in vitro and in 

vivo.