WHO/HSE/WSH/10.01/11 

Atrazine and Its Metabolites in Drinking-water 

Background document for development of 

WHO Guidelines for Drinking-water Quality

Atrazine and Its Metabolites in Drinking-water 

Background document for development of WHO Guidelines for Drinking-water 

Quality

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Preface 

One of the primary goals of the World Health Organization (WHO) and its Member 

States is that “all people, whatever their stage of development and their social and 

economic conditions, have the right to have access to an adequate supply of safe 

drinking water.” A major WHO function to achieve such goals is the responsibility 

“to propose ... regulations, and to make recommendations with respect to international 

health matters ....” 

The first WHO document dealing specifically with public drinking-water quality was 

published in 1958 as International Standards for Drinking-water. It was subsequently 

revised in 1963 and in 1971 under the same title. In 1984–1985, the first edition of the 

WHO Guidelines for Drinking-water Quality (GDWQ) was published in three 

volumes: Volume 1, Recommendations; Volume 2, Health criteria and other 

supporting information; and Volume 3, Surveillance and control of community 

supplies. Second editions of these volumes were published in 1993, 1996 and 1997, 

respectively. Addenda to Volumes 1 and 2 of the second edition were published in 

1998, addressing selected chemicals. An addendum on microbiological aspects 

reviewing selected microorganisms was published in 2002. The third edition of the 

GDWQ was published in 2004, the first addendum to the third edition was published 

in 2006 and the second addendum to the third edition was published in 2008. The 

fourth edition will be published in 2011. 

The GDWQ are subject to a rolling revision process. Through this process, microbial, 

chemical and radiological aspects of drinking-water are subject to periodic review, 

and documentation related to aspects of protection and control of public drinkingwater quality is accordingly prepared and updated. 

Since the first edition of the GDWQ, WHO has published information on health 

criteria and other supporting information to the GDWQ, describing the approaches 

used in deriving guideline values and presenting critical reviews and evaluations of 

the effects on human health of the substances or contaminants of potential health 

concern in drinking-water. In the first and second editions, these constituted Volume 2 

of the GDWQ. Since publication of the third edition, they comprise a series of freestanding monographs, including this one. 

For each chemical contaminant or substance considered, a lead institution prepared a 

background document evaluating the risks for human health from exposure to the 

particular chemical in drinking-water. Institutions from Canada, Japan, the United 

Kingdom and the United States of America (USA) prepared the documents for the 

fourth edition. 

Under the oversight of a group of coordinators, each of whom was responsible for a 

group of chemicals considered in the GDWQ, the draft health criteria documents were 

submitted to a number of scientific institutions and selected experts for peer review. 

Comments were taken into consideration by the coordinators and authors. The draft 

documents were also released to the public domain for comment and submitted for 

final evaluation by expert meetings. 
During the preparation of background documents and at expert meetings, careful 

consideration was given to information available in previous risk assessments carried 

out by the International Programme on Chemical Safety, in its Environmental Health 

Criteria monographs and Concise International Chemical Assessment Documents, the 

International Agency for Research on Cancer, the Joint FAO/WHO Meetings on 

Pesticide Residues and the Joint FAO/WHO Expert Committee on Food Additives 

(which evaluates contaminants such as lead, cadmium, nitrate and nitrite, in addition 

to food additives). 

Further up-to-date information on the GDWQ and the process of their development is 

available on the WHO Internet site and in the current edition of the GDWQ. 
Acknowledgements 

The first draft of Atrazine and Its Metabolites in Drinking-water, Background 

document for development of WHO Guidelines for Drinking-water Quality (GDWQ),

was prepared by Mr J.K. Fawell, United Kingdom, to whom special thanks are due. 

This background document is an update of the background document published in the 

second edition of the GDWQ. 

The work of the following working group coordinators was crucial in the 

development of this document and others contributing to the fourth edition: 

Dr J. Cotruvo, J. Cotruvo Associates, USA (Materials and chemicals) 

Mr J.K. Fawell, United Kingdom (Naturally occurring and industrial 

contaminants and Pesticides) 

Ms M. Giddings, Health Canada (Disinfectants and disinfection by-products) 

Mr P. Jackson, WRc-NSF, United Kingdom (Chemicals – practical aspects) 

Professor Y. Magara, Hokkaido University, Japan (Analytical achievability) 

Dr Aiwerasia Vera Festo Ngowi, Muhimbili University of Health and Allied 

Sciences, United Republic of Tanzania (Pesticides) 

Dr E. Ohanian, Environmental Protection Agency, USA (Disinfectants and 

disinfection by-products) 

The draft text was discussed at the Expert Consultation for the fourth edition of the 

GDWQ, held on 9–13 November 2009. The final version of the document takes into 

consideration comments from both peer reviewers and the public. The input of those 

who provided comments and of participants at the meeting is gratefully 

acknowledged.

The WHO coordinators were Mr R. Bos and Mr B. Gordon, WHO Headquarters. Ms 

C. Vickers provided a liaison with the International Programme on Chemical Safety, 

WHO Headquarters. Mr M. Zaim, Public Health and the Environment Programme, 

WHO Headquarters, provided input on pesticides added to drinking-water for public 

health purposes. 

Ms P. Ward provided invaluable administrative support at the Expert Consultation 

and throughout the review and publication process. Ms M. Sheffer of Ottawa, Canada, 

was responsible for the scientific editing of the document. 

Many individuals from various countries contributed to the development of the 

GDWQ. The efforts of all who contributed to the preparation of this document and in 

particular those who provided peer or public domain review comments are greatly 

appreciated. 
Acronyms and abbreviations used in the text 

ADI acceptable daily intake 

DACT diaminochlorotriazine 

DEA deethyl-atrazine 

DIA deisopropyl-atrazine 

DWLOC Drinking Water Levels of Comparison (USA) 

FAO Food and Agriculture Organization of the United Nations 

GAC granular activated carbon 

JMPR Joint FAO/WHO Meeting on Pesticide Residues 

LC50 median lethal concentration 

LD50 median lethal dose 

LH luteinizing hormone 

LOAEL lowest-observed-adverse-effect level 

NOAEL no-observed-adverse-effect level 

PAC powdered activated carbon 

USA United States of America 

USEPA United States Environmental Protection Agency 

UV ultraviolet 

WHO World Health Organization 
Table of contents 

1. GENERAL DESCRIPTION......................................................................................1 

1.1 Identity .................................................................................................................1 

1.2 Physicochemical properties .................................................................................1 

1.3 Major uses and sources in drinking-water ...........................................................1 

1.4 Environmental fate...............................................................................................2 

2. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE..................................2 

3. KINETICS AND METABOLISM IN LABORATORY ANIMALS AND 

HUMANS ......................................................................................................................3 

4. TOXICOLOGICAL SUMMARY .............................................................................3 

4.1 Atrazine................................................................................................................3 

4.2 Metabolites of atrazine.........................................................................................7 

4.2.1 Chloro-s-triazine metabolites........................................................................7 

4.2.2 Hydroxyatrazine............................................................................................8 

5. PRACTICAL ASPECTS ...........................................................................................8 

5.1 Analytical methods and analytical achievability .................................................8 

5.2 Treatment and control methods and performance ...............................................9 

6. GUIDELINE VALUES ...........................................................................................11 

7. REFERENCES ........................................................................................................12 
1 

The atrazine drinking-water guideline prepared for the Third Edition of the WHO 

Guidelines for Drinking-water Quality has been revised following the recent Joint 

FAO/WHO Meeting on Pesticide Residues (JMPR) evaluation of atrazine and its 

environmental metabolites (FAO/WHO, 2007). 

This background document is based on and largely extracted from this recent 

JMPR evaluation. Except for the critical studies on which the guidelines are based, 

primary references are given only for text that has not been extracted from this 

report. The interested reader should refer to the toxicological monograph 

published by FAO/WHO (2009) for more detailed information and primary 

references. 

1. GENERAL DESCRIPTION 

1.1 Identity 

Chemical Abstracts Service Registry No.: 1912-24-9 

Molecular formula: C8H14ClN5

The International Union of Pure and Applied Chemistry name for atrazine is 6-chloroN2

-ethyl-N4-isopropyl-1,3,5-triazine-2,4-diamine. 

1.2 Physicochemical properties 

Some physical and chemical properties of atrazine that are relevant to its 

environmental fate are summarized in Table 1. 

Table 1: Physicochemical properties of atrazinea

Property Value 

Melting point 175–177 °C 

Density 1.187 g/cm3 at 20 °C 

Water solubility 30 mg/l at 20 °C 

Log octanol–water partition coefficient 2.3 

Vapour pressure 40 × 10−6

 Pa at 20 °C 

a

 From Meister (1989); Royal Society of Chemistry (1991); Worthing (1991). 

1.3 Major uses and sources in drinking-water 

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

control of annual broadleaf and grassy weeds (Worthing, 1991). Key crops in which 

atrazine-containing herbicides are used include maize, sorghum and sugarcane, with 

some other minor uses of local importance. Atrazine and its metabolites have been 

found in surface water and groundwater as a result of the use of atrazine as a preemergent or early post-emergent herbicide. The source of the residue should be 

considered when interpreting water monitoring data. Assessments should be based on 

whether diffuse sources (e.g. runoff from an agricultural field) or point sources (e.g. 

an accidental spill or inappropriate disposal) have contributed to a detection in water. 

The presence of atrazine and its metabolites in surface water is most likely to be 
ATRAZINE IN DRINKING-WATER 

2

intermittent, particularly in flowing water, but groundwater contamination will 

usually be relatively persistent. 

1.4 Environmental fate 

Atrazine can be degraded in surface water by photolysis and microorganisms via Ndealkylation and hydrolysis of the chloro substituent; the corresponding half-lives are 

greater than 100 days at 20 °C. Hydrolysis and microbial degradation also take place 

in soil, depending mainly on temperature, moisture and pH. Half-lives of 20–50 days 

at 20–25 °C have been found under laboratory conditions, increasing at lower 

temperatures (USEPA, 1988). These are similar to the half-lives found under natural 

conditions, but longer half-lives have been seen under special conditions (Schoen & 

Winterlin, 1987). Degradation rates normally decrease with increasing depth, and 

atrazine can be fairly stable in groundwater (Burnside, Fenster & Wicks, 1963). 

Atrazine’s degradation products in soil include several of the chloro-s-triazine 

metabolites commonly found in water (Keller, 1978) (see section 2). Unsubstituted 

amino metabolites and triazine are formed later and may be mineralized completely. 

Atrazine and its dealkylated metabolites are moderately to very mobile in sandy, silt 

and clay soils (Ciba-Geigy, 1986). Hydroxytriazines, however, are of low mobility 

(Helling, 1971) and persist for long periods in the soil (Kahn & Saidak, 1981). 

2. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE 

Atrazine and its chloro-s-triazine metabolites—deethyl-atrazine (DEA), deisopropylatrazine (DIA) and diaminochlorotriazine (DACT)—have been found in surface water 

and groundwater. The metabolite hydroxyatrazine is more commonly detected in 

groundwater than in surface water. 

A number of studies have monitored the concentrations of atrazine in groundwater 

and surface water over the last two decades. Recent monitoring data show declining 

levels and incidences of detection of atrazine and its chloro-s-triazine metabolites 

(DIA, DEA and DACT) compared with data collected in the early 1990s; this reflects 

restrictions on the use of atrazine that were introduced in the late 1990s and early 

2000s and the introduction of good agricultural practices in the European Union, the 

United States of America (USA) and other parts of the world. Therefore, older 

monitoring data generally represent an overestimate of environmental concentrations 

likely to arise from current use practices. 

In surface water, the concentrations of the chlorotriazine metabolites of atrazine are 

generally less than those of atrazine itself, whereas the concentrations of these 

metabolites in rural wells are more similar to those of atrazine. The relative order of 

concentrations in rural wells in the USA was generally as follows: atrazine ~ DEA ~ 

DACT > DIA > hydroxyatrazine. However, concentrations of DEA that are severalfold higher than those of the parent compound have been reported.

Monitoring carried out in a number of countries indicates that concentrations of 

atrazine and its chloro-s-triazine metabolites in groundwater and surface water rarely 

exceed 2 μg/l and are commonly well below 0.1 μg/l, although concentrations may be 

higher in agricultural areas where large amounts of atrazine are used. In the past, its 
ATRAZINE IN DRINKING-WATER 

3 

use for weed control on non-crop land, such as railway lines and paved areas, gave 

rise to contamination of groundwater in particular, although this use has largely 

disappeared worldwide. The concentration of atrazine in public water supplies in the 

USA does not exceed the United States Environmental Protection Agency’s (USEPA) 

Drinking Water Levels of Comparison (DWLOC)—the maximum concentrations in 

drinking-water that, when considered together with dietary exposure, do not exceed a 

level of concern—for any age group These DWLOCs, which account for atrazine plus 

its three chloro-s-triazine metabolites, range from 12.5 to 68 μg/l for intermediate 

(seasonal) or chronic (annual) exposure. Concentrations of atrazine in drinking-water 

in the United Kingdom are less than 0.1 μg/l, based on data measured when atrazine 

was registered and when good agricultural practices had been adopted. In Canada, 

concentrations of atrazine and its chloro-s-triazine metabolites did not exceed the 

interim guideline level (5 μg/l, includes metabolites) in any samples of drinking-water 

from 10 Canadian treatment plants in the cereal-growing regions of Ontario and 

Quebec (from groundwater and surface water). Levels of atrazine were below 0.83 

μg/l, concentrations of DEA were below 0.35 μg/l, and DIA and DACT were found 

less often and at lower levels in treated surface water. Total chloro-s-triazine 

concentrations from raw water were below 0.5 μg/l in groundwater and well below 

0.68 μg/l in surface water (Tauber, 2006). 

It is expected that exposure of the public will be primarily through drinking-water. 

3. KINETICS AND METABOLISM IN LABORATORY ANIMALS AND 

HUMANS 

After oral administration to rats, 14C-labelled atrazine was rapidly and almost 

completely absorbed, independent of dose and sex. Radioactivity was widely 

distributed throughout the body. Excretion was more than 93% of the administered 

dose within 7 days, primarily via the urine (approximately 73%) and to a lesser extent 

via the faeces (approximately 20%; approximately 7% via bile), with more than 50% 

being excreted within the first 24 h. The elimination half-life of radiolabel from the 

whole body was 31.3 h in rats; this prolonged half-life was caused by covalent 

binding of atrazine to cysteine sulfhydryl groups in the β-chain of rodent 

haemoglobin. Seven days after administration of a single low dose (1 mg/kg body 

weight), tissue residues represented 6.5–7.5% of the dose, with the highest 

concentrations in erythrocytes (≤0.63 mg/kg), liver (≤0.50 mg/kg) and kidneys (≤0.26 

mg/kg). 

Atrazine was extensively metabolized; more than 25 metabolites have been identified 

in rats. The major metabolic pathways were stepwise dealkylation via either DIA or 

DEA to DACT, the major metabolite. Dechlorination involving conjugation with 

glutathione was a minor pathway. The biotransformation of atrazine in rats and 

humans was qualitatively similar. 

4. TOXICOLOGICAL SUMMARY 

4.1 Atrazine 

Atrazine was of low acute toxicity in rats exposed orally (median lethal dose [LD50] 

1870–3090 mg/kg body weight), dermally (LD50 >2000 mg/kg body weight) or by 
ATRAZINE IN DRINKING-WATER 

4

inhalation (median lethal concentration [LC50] >5.8 mg/l). Atrazine was not a skin 

irritant or an eye irritant in rabbits. 

In short-term studies of toxicity in rats, dogs and rabbits, the consistent toxic effects 

noted across species included reduced body weight gain and food intake and a slight 

decrease in erythrocyte parameters. Also, liver weights and splenic haemosiderin 

deposition were increased in rats, whereas there was marked cardiac toxicity in dogs. 

Atrazine was tested for genotoxicity in a large number of studies covering an 

adequate range of end-points. JMPR agreed that it is unlikely that atrazine is 

genotoxic. 

Long-term studies of toxicity and carcinogenicity were conducted in mice and rats. As 

in short-term studies, reduced body weight gain and food intake and a decrease in 

erythrocyte parameters were noted consistently. Additionally, reduced survival of 

females and cardiovascular effects (atrial thrombi) in both sexes were observed in 

mice at high doses. 

In three studies of carcinogenicity in mice, no treatment-related carcinogenic effects 

were observed at dietary concentrations up to about 386 and 483 mg/kg body weight 

per day in males and females, respectively. Overall, the no-observed-adverse-effect 

level (NOAEL) was 1.2 mg/kg body weight per day, on the basis of lower body 

weight/body weight gain at 38.4 mg/kg body weight per day and greater. 

In one study of carcinogenicity in Fischer 344 rats fed diets containing atrazine at 

concentrations up to about 20 mg/kg body weight per day, there was no effect at any 

dose on the onset or incidence of tumours. The NOAEL was about 3.5 mg/kg body 

weight per day, on the basis of decreased body weight. 

In seven studies of carcinogenicity in Sprague-Dawley rats fed diets containing 

atrazine at concentrations up to about 42 and 65 mg/kg body weight per day in males 

and females, respectively, an increased incidence of mammary tumours (adenomas, 

carcinomas, fibroadenomas) with or without an earlier onset (relative to controls) was 

observed in four studies, whereas there was an earlier onset of mammary tumours 

without any increase in their overall lifetime incidence in two studies. An earlier onset 

of pituitary tumours was also observed in one study, with no increase in incidence at 

term. Overall, the NOAEL for mammary carcinogenicity was 1.5 mg/kg body weight 

per day, on the basis of a statistically significant increased incidence in mammary 

tumours at 3.1 mg/kg body weight per day. 

In a study of carcinogenicity in ovariectomized Sprague-Dawley rats, neither 

increases in mammary gland proliferative changes nor mammary tumours were seen 

at dietary concentrations up to about 21 mg/kg body weight per day, suggesting that 

the carcinogenic mode of action of atrazine in Sprague-Dawley rats is related to 

ovarian function. 

In a study designed to evaluate the effects of atrazine on the pre-ovulatory luteinizing 

hormone (LH) surge and on the estrous cycle, groups of 90 female Sprague-Dawley 

(Crl:CD BR) rats received diets containing atrazine (purity, 97.1%) at a concentration 

of 0, 25, 50 or 400 mg/kg (equal to 0, 1.8, 3.65 and 29.44 mg/kg bw per day) for 
ATRAZINE IN DRINKING-WATER 

5 

26 weeks. 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 

(Morseth, 1996). The NOAEL and lowest-observed-adverse-effect level (LOAEL) for 

these effects were comparable to those found in the studies of carcinogenicity. 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. 

The postulated mode of action for atrazine-induced mammary tumours in female 

Sprague-Dawley rats involved disruption of the hypothalamic–pituitary–ovary axis. 

Atrazine modifies catecholamine function and the regulation of gonadotropinreleasing hormone pulsatility in the rat hypothalamus, with the consequence that the 

pulse of LH released from the pituitary gland is of insufficient amplitude or duration 

to trigger ovulation. The failure to ovulate results in persistent secretion of estrogen, 

which provides a feedback to the pituitary, leading to increased secretion of prolactin. 

As a result, atrazine accelerates the normal reproductive ageing process in female 

Sprague-Dawley rats, whereby reproductive senescence is characterized by persistent 

exposure to estrogen and prolactin. In contrast, women respond to reduced levels of 

LH by reductions in levels of estrogen. Thus, JMPR considered that the mode of 

carcinogenic action in certain susceptible rat strains is not relevant for human risk 

assessment. 

Investigations of other modes of action did not provide any evidence that atrazine had 

intrinsic estrogenic activity or that it increased aromatase activity in vivo. 

JMPR concluded that atrazine is not likely to pose a carcinogenic risk to humans. 

Although carcinogenicity in humans was not a concern owing to the rat-specific mode 

of action, alterations in neurotransmitter and neuropeptide function regulating LH and 

secretion of prolactin may potentially induce adverse effects during critical periods of 

development (as found in special studies showing pregnancy loss, delayed puberty in 

males and females, and decreased suckling-induced prolactin release in lactating 

dams). Unlike the carcinogenic effects, the developmental effects do not appear to be 

specific to certain strains of rats, and JMPR therefore considered these effects to be 

relevant for risk assessment 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. Effects were seen at doses of ≥50 mg/kg body 

weight per day after treatment on days 6–10 of gestation, with a NOAEL of 25 mg/kg 

body weight per day. In contrast, exposure on days 11–15 of gestation (after the LHdependent period of pregnancy) at a dose of 200 mg/kg body weight per day did not 

induce full-litter resorptions. 

Suppression of the suckling-induced prolactin release in lactating rats was seen with 

atrazine at doses of ≥25 mg/kg body weight per day, with a NOAEL of 12.5 mg/kg 

body weight per day. Treatment of lactating rats on postnatal days 1–4 affected the 

development of tuberoinfundibular dopaminergic neurons in the pups (presumably 
ATRAZINE IN DRINKING-WATER 

6

due to the lack of prolactin derived from the dam’s milk), with the consequence of 

impaired regulation of prolactin secretion, hyperprolactinaemia prior to puberty and 

prostatitis in the adult male offspring. 

A delay in sexual development was observed in female rats after exposure on 

postnatal days 21–46 at doses of ≥30 mg/kg body weight per day, with a NOAEL of 

10 mg/kg body weight per day, and in male rats after exposure on postnatal days 23–

53 at doses of ≥12.5 mg/kg body weight per day, with a NOAEL of 6.25 mg/kg body 

weight per day. 

In a standard two-generation study of reproduction (conducted according to earlier 

guidelines, which did not include end-points such as estrous cyclicity and sexual 

development) in rats, there was no effect on fertility at 36.1 mg/kg body weight per 

day, the highest dose tested. The NOAEL for parental toxicity was 3.6 mg/kg body 

weight per day, on the basis of decreased body weight gains and food consumption. 

The NOAEL for reproductive toxicity was 3.6 mg/kg body weight per day, on the 

basis of decreased body weights of male pups at postnatal day 21. 

In two studies of prenatal developmental toxicity in rats given atrazine on days 6–15 

of gestation, the NOAELs for maternal toxicity were 10 or 25 mg/kg body weight per 

day on the basis of decreased body weight gain and food intake at 70 or 100 mg/kg 

body weight per day, respectively. The NOAELs for developmental toxicity were 10 

or 25 mg/kg body weight per day on the basis of incomplete ossification at several 

sites at 70 or 100 mg/kg body weight per day, respectively. In a study of prenatal 

developmental toxicity in rabbits given atrazine on days 7–19 gestation, the NOAEL 

for maternal toxicity was 5 mg/kg body weight per day on the basis of clinical signs, 

abortion and decreased food intake and body weight gain at 75 mg/kg body weight 

per day. The NOAEL for developmental toxicity was 5 mg/kg body weight per day on 

the basis of increased resorptions, reduced litter size and incomplete ossification at 75 

mg/kg body weight per day. In rats and rabbits, the developmental effects were 

observed only at maternally toxic doses. 

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. 

A range of epidemiological studies (including cohort studies, case–control studies, 

and ecological or correlational studies) assessed possible relationships between 

atrazine or other triazine herbicides and cancer in humans. For some cancer types, 

such as prostate or ovarian cancer and non-Hodgkin lymphoma, the increased risks 

reported in single studies either could be explained by the methodology used or had 

not been confirmed in more reliable studies. Thus, the weight of evidence from the 

epidemiological studies did not support a causal association between exposure to 

atrazine and the occurrence of cancer in humans. 
ATRAZINE IN DRINKING-WATER 

7 

4.2 Metabolites of atrazine 

4.2.1 Chloro-s-triazine metabolites 

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

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. 

Like atrazine, the chloro-s-triazine metabolites were of moderate or low acute oral 

toxicity in rats; LD50s were 1110, 1240 and 2310–5460 mg/kg body weight for DEA, 

DIA and DACT, respectively. 

Like atrazine, its chloro-s-triazine metabolites delayed sexual development of male 

rats exposed on postnatal days 23–53 at atrazine molar equivalent doses of ≥25 mg/kg 

body weight per day (DEA, DIA) and ≥12.5 mg/kg body weight per day (DACT), 

with NOAELs of 12.5 and 6.25 mg/kg body weight per day, respectively. Exposure of 

female rats to DACT on postnatal days 22–41 delayed sexual development at atrazine 

molar equivalent doses of ≥50 mg/kg body weight per day, and the NOAEL was 25 

mg/kg body weight per day. Doses at which these effects occurred were similar to 

those observed for parent atrazine. 

In short-term feeding studies in rats, the main effects of the chlorinated metabolites 

were similar to those of atrazine and included reduced body weight gain and 

decreased erythrocyte parameters and also, for DACT, disruption of the estrous cycle. 

The NOAELs were 3.2 mg/kg body weight per day for DEA and DIA and 7.6 mg/kg 

body weight per day for DACT. 

In a 29/52-week study with DACT in Sprague-Dawley rats, effects comparable to 

those observed with atrazine (attenuation of the LH surge, increased incidences of 

mammary tumours) were seen at 270 mg/kg diet; the NOAEL was 48 mg/kg diet, 

equal to 3.4 mg/kg body weight per day. No long-term studies were performed with 

DEA or DIA. 

In short-term feeding studies in dogs, the main effects of the chlorinated metabolites 

were similar to those of atrazine and included reduced body weight gain and 

decreased erythrocyte parameters, whereas DEA and DACT showed cardiac toxicity. 

The NOAELs were 3.7, 3.8 and 3.5 mg/kg body weight per day for DEA, DIA and 

DACT, respectively. 

DEA, DIA and DACT did not show genotoxicity in an adequate range of tests in vitro 

and in vivo. 

In studies of prenatal developmental toxicity in rats, the chlorinated metabolites 

induced increased incidences of fused sternebrae and/or incomplete ossification at 

doses of 25–100 mg/kg body weight per day; the NOAELs for developmental toxicity 

were 25, 5 and 2.5 mg/kg body weight per day for DEA, DIA and DACT, 

respectively. The effects were seen only at doses that also produced maternal toxicity. 
ATRAZINE IN DRINKING-WATER 

8

4.2.2 Hydroxyatrazine 

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. Also, the acute oral toxicity of 

hydroxyatrazine in rats (LD50 >5050 mg/kg body weight) was lower than that of 

atrazine or its chlorometabolites. 

In short-term feeding studies, the main effects of hydroxyatrazine in rats included 

reduced body weight gain, increased water consumption, changes in clinical 

chemistry and urine analysis parameters, and kidney lesions. The overall NOAEL was 

6.3 mg/kg body weight per day. In dogs, effects included reduced body weight gain 

and food consumption, changes in clinical chemistry and urine analysis parameters, 

and kidney lesions; the NOAEL was 5.8 mg/kg body weight per day. 

In a 2-year study of toxicity and carcinogenicity in rats, the effects of hydroxyatrazine 

included clinical signs and increased mortality, reduced body weight gain and food 

consumption, increased water consumption, changes in haematological, clinical 

chemistry and urine analysis parameters, and kidney lesions. The NOAEL was 1.0 

mg/kg body weight per day. There was no evidence of carcinogenicity (Chow & Hart, 

1995). 

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

in vivo. 

In a study of prenatal developmental toxicity in rats, the effects of hydroxyatrazine 

consisted of reduced food consumption and body weight gain in dams and increased 

incidences of incomplete and absent ossification in fetuses at 125 mg/kg body weight 

per day; the NOAEL was 25 mg/kg body weight per day for maternal and 

developmental toxicity. Exposure of female rats on postnatal days 22–41 at atrazine 

molar equivalent doses up to 200 mg/kg body weight per day did not delay sexual 

development. 

5. PRACTICAL ASPECTS 

5.1 Analytical methods and analytical achievability 

Atrazine is determined by gas chromatography with nitrogen–phosphorus detection 

following extraction with pentane or ethyl acetate. The detection limit in tap water 

and river water is about 0.1 μg/l (Yokley & Cheung, 2000). 

Atrazine is determined by gas chromatography/mass spectrometry with solid-phase 

extraction. The detection limit in raw water and drinking-water is 10 ng/l (Bruzzoniti 

et al., 2006). Extraction of the metabolites can be achieved using styrenedivinylbenzene sorbents. Detection limits for triazines determined by capillary gas 

chromatography with nitrogen thermionic specific detection and high-performance 

liquid chromatography with photodiode array absorption detection following 

extraction with styrene-divinylbenzene sorbents and elution with acetone were lower 
ATRAZINE IN DRINKING-WATER 

9 

than 5 ng/l (Drevenkar et al., 2002). Atrazine is also determined by isotope dilution 

gas chromatography/mass spectrometry with solid-phase extraction. The method 

detection limit in surface water is 1 ng/l (Planas et al., 2006). In the case of a largevolume injection approach using 50 μl of the 40-fold concentrated extract, the 

detection limit in river water is 2 ng/l (Schellin & Popp, 2007). Using a liquid 

chromatography/mass spectrometry method utilizing online solid-phase extraction 

(Koivunen et al., 2006) or ultra-performance liquid chromatography combined with 

tandem mass spectrometry (Gervais et al., 2008), the limit of quantification is 50 ng/l 

or 12 ng/l, respectively. 

Other methods are included in the USEPA’s (2009) document on Analytical Methods 

Approved for Drinking Water Compliance Monitoring of Organic Contaminants. 

5.2 Treatment and control methods and performance 

Coagulation and filtration are ineffective at removing atrazine. Only 7% removal was 

achieved with ferric chloride dosed with iron at at 14 mg/l, with an atrazine 

concentration of 0.84 μg/l (Normann, Haberer & Oehmichen, 1987). Aluminium 

sulfate (aluminium dose of 2 mg/l at pH 8) was also completely ineffective at 

reducing an atrazine concentration of 66 μg/l (Miltner et al., 1989). In laboratory tests, 

atrazine at 3 μg/l in river water was treated with aluminium sulfate (up to 10 mg/l as 

aluminium) or ferric sulfate (up 40 mg/l as iron), but no removal was observed (Jiang 

& Adams, 2006). Lime soda softening was also ineffective. Results from other studies 

also suggest that conventional coagulation-based water treatment processes are 

ineffective at reducing atrazine concentrations (Foster, Rachwal & White, 1991; Van 

Hoof, Ackermans & Celens, 1992). 

A full-scale granular activated carbon (GAC) plant treating river water with an 

atrazine concentration of 0.3–2 μg/l, with an empty bed contact time of 15–20 min, 

treated 20 000 bed volumes before 0.1 μg/l was reached in the effluent (Normann, 

Haberer & Oehmichen, 1987). Results from other treatment works incorporating GAC 

have shown that the atrazine concentration can be reduced to 0.1 μg/l (contact times 

19–20 min, bed lifetimes 20–24 months, initial atrazine concentrations 0.16–0.27 

μg/l) (Croll, Chadwick & Knight, 1991). One study found that the adsorption capacity 

of GAC varied between 0.04 and 0.22 mg/g carbon, depending on the type of GAC 

used (Duguet, 1994). The same study also found that the concentration of natural 

organic matter present greatly affected the capacity of the carbon to adsorb atrazine 

(e.g. 20 mg of atrazine per gram carbon for distilled water, reduced to 0.6–0.15 mg/g 

for dissolved organic carbon in range 2–8 mg/l as carbon). GAC has been applied 

successfully to pesticide removal (including atrazine) using slow sand filtration, as a 

layer 75–200 mm thick, sandwiched between conventional sand media. Contact times 

are 30–60 min (Anon, 1994). 

Powdered activated carbon (PAC) has been used to remove atrazine from surface 

waters, with only a seasonal requirement to reduce pesticide concentrations. A dose of 

5 mg/l with 40 min contact in a PAC reactor (coupled with coagulation) reduced the 

influent concentration of atrazine (0.53 μg/l) to 0.08 μg/l; there was a further 

reduction to <0.05 μg/l in the final water due to the remaining capacity in the PAC 

once it was separated at the filtration stage (Haist-Gulde, Baldauf & Brauch, 1993). 

Tests with a batch reactor showed that PAC (3.3 mg/l) reduced the initial 
ATRAZINE IN DRINKING-WATER 

10

concentration of atrazine (22.5 μg/l) by 60% after 75 min contact (Qi, 1994). Atrazine 

spiked into water at 5 μg/l was treated with two PACs at pH 7.5. At a PAC dose of 10 

mg/l in deionized water, both achieved ~100% removal. In river water, the removals 

were reduced to ~95% and ~90%, respectively (Jiang & Adams, 2006). In the same 

study, desethylatrazine was also ~100% removed from deionized water. In river 

water, the removals were reduced to ~85% and ~70%, respectively. 

At a waterworks, ozonation produced removals of 29% and 42% for concentrations of 

0.17 μg/l and 0.19 μg/l, respectively (Brauch & Kuhn, 1988). Ozonation conditions, 

such as dissolved ozone concentration, contact time and applied ozone dose, affect 

removal efficiency, as well as factors influencing the decomposition of ozone to form 

hydroxyl radicals (e.g. pH, temperature, organic matter content and bicarbonate 

concentration) (Duguet, 1994). A combination of ozone and either ultraviolet (UV) 

radiation or hydrogen peroxide improves removal efficiency and results in bed life 

extension if associated with GAC adsorption (Duguet, 1994). At full scale, one 

treatment works achieved a reduction of approximately 40% (initial concentration 

100–600 ng/l) with ozone alone (15 min contact, dose approximately 2.2 mg/l); for 

the same ozone dose, in combination with hydrogen peroxide (H2O2/O3 = 0.4 by 

mass), there was an 80% reduction in atrazine concentration (Duguet, 1992). For the 

treatment of atrazine at 1 mg/l to below 0.1 μg/l, the life of the GAC bed was doubled 

by ozonation alone and increased nearly 6-fold by the combination of oxidants. Other 

studies have found removals of 60% using ozone at 2.2 mg/l with a contact time of 5 

min on a solution containing atrazine at 3 μg/l (Meijers, Van der Veer & Kruithof, 

1993). Pilot plant trials have achieved removals of atrazine between 30% and 60% 

with ozone doses of 2–4 mg/l and 5–15 min contact time (Foster, Rachwal & White, 

1991). In a 9-month pilot study, raw water atrazine concentrations of 7–80 ng/l were 

hardly affected by aluminium sulfate coagulation treatment but were reduced by 66–

96% when ozonation (1.5–2 mg/l, 20 min contact) was applied (Hua, Bennett & 

Letcher, 2006). A combination of bankside storage, ozonation and finally GAC 

filtration reduced the concentration of atrazine in river water from 0.32 μg/l to 0.11, 

0.09 and <0.01 μg/l, respectively (Haist-Gulde, Baldauf & Brauch, 1993). 

Membrane filtration using ultrafiltration techniques does not remove atrazine, but 

nanofiltration is more successful; one study indicated that removals of between 66% 

and 98% were achieved for atrazine at an initial concentration of 3–5 μg/l (Hofman, 

1992). With nanofiltration, rejection rates varied between 75% and 100% for atrazine 

(influent atrazine 1 μg/l, combined with five other pesticides); the specific membrane 

type was an important factor in determining rejection rates. Pilot plant trials involving 

membrane filtration have achieved removals between 79% and 99% for atrazine 

(Hofman et al., 1993). Atrazine (10 μg/l) was 85–95% removed by a nanofiltration 

membrane (Chen et al., 2004). Atrazine (concentration not stated) was 80–85% 

removed by different nanofiltration membranes and 96% removed by a polyamide 

reverse osmosis membrane (Kosutic et al., 2005). A concentration of 0.5–1.5 mg/l 

was 98% and 68% removed by two polyvinyl alcohol/polyamide nanofiltration 

membranes, but only 15% and 11% removed by two polyethersulfone nanofiltration 

membranes (Kiso et al., 2000). Removals of 82%, 83% and 84% from a 150–300 μg/l 

solution were reported for three different nanofiltration membranes (Plakas et al., 

2006); fouling of the membrane by calcium and humic acid worsened the 

performance. A full-scale (140 000 m3/day) nanofiltration plant at Méry-sur-Oise, 

France, reduced a concentration of 850 ng/l to <50 ng/l (Cyna et al., 2002). In a pilot 
ATRAZINE IN DRINKING-WATER 

11 

plant study, DEA was spiked at 1 μg/l into distilled water, sand-filtered water and 

GAC-filtered water, then subjected to nanofiltration through composite polyamide 

membranes. Removals of 62–95% and 62–75% were obtained with two nanofiltration 

membranes (Boussahel, Baudu & Montiel, 2001). In another study (Boussahel et al., 

2000), one of the membranes gave ~90% removal from a 1 μg/l solution, and the 

other gave ~70% removal. With both membranes, adsorption onto the membrane 

accounted for about 35% removal. 

UV radiation was effective at reducing atrazine concentrations during laboratory 

studies. With an irrradiation time of 5 min, the atrazine concentration was reduced by 

almost 90%. With a longer duration of radiation, there was only a small further 

decrease in the atrazine concentration (Cermak & Cermakova, 1992). UV irradiation, 

at pilot plant scale, was found to be effective in decomposing atrazine in a chalk 

borehole water, up to 70% removal being achieved with UV doses of up to 700 

Wh/m3. Removal efficiency was constant over an influent concentration range of 0.1–

0.5 μg/l (Bourgine et al., 1995). UV irradiation causes substantial 

photodecomposition but not complete mineralization (Le Brun et al., 1993). 

A laboratory comparison of UV, hydrogen peroxide, ozone, ozone/UV, 

ozone/hydrogen peroxide, hydrogen peroxide/UV and ozone/hydrogen peroxide/UV 

demonstrated that all processes destroyed atrazine (hydrogen peroxide only at pH 

>10) and that UV/hydrogen peroxide gave the fastest degradation rate (Prado & 

Esplusgas, 1999). Treatment of 3 μg/l solutions of atrazine and DEA with 2 mg/l free 

chlorine and a 30 min contact time gave no removal (Jiang & Adams, 2006). 

A number of point-of-use and point-of-entry water treatment systems based on 

activated carbon are available and are suitable for treating water that may be 

contaminated with atrazine. These systems should be used only on microbially safe 

drinking-water, they should be well flushed before each use and the filters should be 

changed frequently. Point-of-use and point-of-entry reverse osmosis systems could 

also be used for removal of atrazine. 

Although specific published data on the removal of the atrazine metabolites are 

limited, what data there are suggest that these will behave in a manner similar to 

atrazine. 

6. GUIDELINE VALUES 

Drinking-water may contain metabolites of atrazine as well as atrazine itself. The 

chloro-s-triazine metabolites DEA, DIA and DACT share the same mode of action as 

atrazine and have a similar toxicological profile. Hence, JMPR decided to establish a 

group acceptable daily intake (ADI). Hydroxyatrazine, the plant and soil degradate, 

was not included because its mode of action and toxicological profile are different 

from those of atrazine and its chloro-s-triazine metabolites. 

JMPR established a group ADI of 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 LH 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 for interspecies 

and intraspecies variation. JMPR considered that this NOAEL is protective for the 
ATRAZINE IN DRINKING-WATER 

12

consequences of neuroendocrine and other adverse effects caused by prolonged 

exposure to atrazine and its chloro-s-triazine metabolites. 

Applying this group ADI to a 60 kg adult drinking 2 litres of water per day and 

allocating 20% of the total daily intake to drinking-water, as exposure to atrazine from 

other sources it expected to be low, a guideline value of 0.1 mg/l can be derived for 

atrazine and its chloro-s-triazine metabolites in drinking-water. This 20% allocation 

will be very conservative in most countries, as it is expected that exposure of the 

public will be primarily through drinking-water. 

For hydroxyatrazine, JMPR established an ADI of 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 (caused by low solubility in water, resulting in crystal formation and a 

subsequent inflammatory response) at 7.8 mg/kg body weight per day in a 24-month 

study in rats, and using a safety factor of 25. A modified safety factor on the basis of 

kinetic considerations was deemed appropriate, as the critical effect of 

hydroxyatrazine is dependent on its physicochemical properties, and the interspecies 

variability for such effects is lower than for effects dependent on the area under the 

curve. 

Applying this ADI to a 60 kg adult drinking 2 litres of water per day and allocating 

20% of the total daily intake to drinking-water, a guideline value of 0.2 mg/l can be 

derived for hydroxyatrazine in drinking-water. Again, this 20% allocation will be very 

conservative in most countries, as it is expected that exposure of the public will be 

primarily through drinking-water. 

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