Atrazine
(endorsed 2011)
Guideline
Based on human health concerns, atrazine in drinking water should not exceed 0.02 mg/L.
Related chemicals
Atrazine (CAS 1912-24-9) belongs to the triazine class of chemicals. There are a large number of herbicides in this class, including simazine, cyanazine, propazine, and ametryn (Tomlin 2006).
Human risk statement
With good water quality management practices, the exposure of the general population is expected to be well below levels that may cause health concerns.
If present in drinking water as a result of a spillage or through misuse, atrazine would not be a health concern unless the concentration exceeded 0.02 mg/L. Minor excursions above this level would need to occur over a significant period to be a health concern, as the health-based guideline value is based on long term effects.
With good water quality management practices, pesticides should not be detected in source waters used for drinking water supplies. Persistent detection of pesticides may indicate inappropriate use or accidental spillage, and investigation is required in line with established procedures in the risk management plan for the particular water source.
General description
Uses: Atrazine is a herbicide for the control of weeds and grasses in agricultural crops.
There are registered products that contain atrazine in Australia. These products are intended for professional use. Atrazine is available as concentrated solutions to be applied in diluted form using ground, aerial or hand-held sprays. Data on currently registered products are available from the Australian Pesticides and Veterinary Medicines Authority.
Exposure sources: The main source of public exposure to atrazine and its metabolites is residues in food and drinking water. Residue levels in food produced according to good agricultural practice are generally low. Maximum residue limits (MRLs) are at the level of detection.
Agricultural use of atrazine may potentially lead to contamination of source waters through processes such as run-off, spray drift or entry into groundwater.
Typical values in Australian drinking waters
Atrazine has been occasionally reported in Australian drinking waters, including in New South Wales, Queensland and Tasmania. It was detected at up to 0.0009 mg/L (0.9 µg/L) in surface waters in New South Wales (Tran et al. 2007) and 0.0013 mg/L (1.3 µg/L) in Queensland (Mitchell et al. 2005). In many countries, after application in agricultural areas, atrazine has been found in groundwater at levels of 0.00001–0.006 mg/L (0.01–6 µg/L) (WHO 2003). It has also been detected in drinking-water in several countries at levels of 0.00001–0.005 mg/L (0.01–5 µg/L) (WHO 2003) and as high as 0.0294 mg/L (29.4 µg/L) in Canada (Health Canada 1993). Regulation of atrazine use has become more stringent since the mid 1990s.
In cases where atrazine is present in drinking waters, there is a high likelihood that other closely related s-triazine metabolites with similar mammalian toxicity may also be present at similar concentrations.
Treatment of drinking water
Atrazine can be a relatively difficult pesticide to treat in drinking water. Oxidation by chlorine or ozone is only partially effective at typical doses, and adsorption to activated carbon can be incomplete (Ormad et al. 2008). Conventional clarification/chlorination has been shown to be unreliable for the removal of atrazine from water (CARAT 2000). However, a combination of ozone, activated carbon and coagulation-flocculation can be effective (Ormad et al. 2008).
Atrazine has been shown to be near-completely removed when water undergoes advanced oxidation with iron-catalysed ultraviolet (UV) irradiation and peroxide, i.e. Fenton reaction (Huston et al. 1999), with only moderate removal reported for UV-peroxide in the absence of added iron (Kruithof et al. 2002), although much lower removal rates have been obtained at full-scale plants (CARAT 2000). Photodegredation of the pesticide has been investigated (Azenha et al. 2003). Relatively high removal rates through powdered activated carbon adsorption have been reported (Bozkaya-Schrotter et al. 2008).
Measurement
Atrazine can be measured by routine gas chromatrography–mass spectrometry analysis, with a limit of reporting of 0.1 µg/L (Queensland Health 2007).
History of the health values
The current acceptable daily intake (ADI) for atrazine is 0.005 mg per kg of bodyweight (mg/kg bw), based on a no-observed-effect level (NOEL) of 0.5 mg/kg bw/day from a 2-year dietary rat study. The NOEL is based on an increased incidence of mammary tumours in female rats at the next highest dose (2.8 mg/kg bw/day). The ADI incorporates a safety factor of 100, and was established in 1990. Subsequently, in 1994, the Advisory Committee on Pesticides and Health concluded that the rat mammary tumours were not relevant to human health. However, it was considered that the NOEL of 0.5 mg/kg bw/day continued to be an appropriately conservative endpoint on which to base the ADI, as the tumours were considered to reflect a hormonal interaction considered relevant to humans (see ‘Long-term effects’).
The previous ADI for atrazine was set in 1985 at 0.0003 mg/kg bw/day, based on a NOEL of 0.6 mg/kg bw/day in a 2-year rat study and using a 2000-fold safety factor. This ADI was amended to its present level after submission of additional toxicity studies.
The previous health value was 0.04 mg/L (NHMRC and NRMMC 2004).
Health considerations
Metabolism: Atrazine is readily absorbed via the gastrointestinal tract in humans and rats. It is extensively metabolised, and is rapidly excreted in the urine and faeces, almost completely within 72 hours. Levels in tissues were low. The main metabolites were dealkylated forms that were of similar toxicity to atrazine.
Acute effects: Atrazine has low acute oral and dermal toxicity. It is not a skin sensitiser in humans, based on large-scale occupational studies, but is a sensitiser in guinea pigs.
Short-term effects: Four-week dietary studies in rats and dogs reported decreased food-use efficiency (rats only), and bodyweight gain at 21 mg/kg bw/day and above.
A 3-week oral study in female rats reported irregular ovarian cycles (but not persistent oestrus or diestrus) at 75 mg/kg bw/day.
Ninety-day dietary studies in rats and dogs reported reduced bodyweight gain and food consumption at 3.3 mg/kg bw/day in rats and at 5 mg/kg bw/day in dogs. Reduced testicular weights and anaemia were seen at 15 mg/kg bw/day in rats. In a 6-month dietary study in rats, there was suppression of the luteinising hormone surge (a process initiated in the pituitary that normally initiates ovulation), and disruption of the oestrous cycle at 3.6 mg/kg bw/day
Long-term effects: A 2-year dietary study in mice reported only decreased bodyweight gain at 36 mg/kg bw/day. One-year and 2-year dietary studies in rats reported decreased bodyweight gain, increased pituitary weight, pituitary adenomas, and mammary tumours (one strain only) at 4.2 mg/kg bw/day after 1-year. Behavioural effects, skeletal muscle degeneration, and mammary growths symptomatic of hormone perturbation were seen at 20 mg/kg bw/day and above in these studies. While the rat mammary tumours themselves are not considered relevant to humans, the increases in gonadotropin-releasing hormone and luteinising hormone from the pituitary, which are considered a precursor event to the development of rat mammary tumours, are considered relevant to humans. This is an area of ongoing research. In a long-term dog study, lethargy, increased heart rate, myocardial degeneration, and decreased heart weight were seen at 33 mg/kg bw/day. The lowest overall NOEL from these studies is 0.5 mg/kg bw/day, based on mammary tumours in rats. This NOEL is the basis for the current ADI.
Carcinogenicity: The weight of evidence from long-term studies in mice and rats indicates that atrazine is not carcinogenic in humans, since the rat mammary tumours are not considered relevant to humans.
Genotoxicity: Atrazine is not considered to be genotoxic, based on in vitro and in vivo short-term studies.
Reproductive and developmental effects: Two- and 3-generation reproductive studies in rats did not produce any evidence of effects on reproductive parameters. Developmental studies in rats produced some equivocal evidence of effects on foetal and post-natal development, but at doses much higher than those used in long-term studies.
Poisons Schedule: Atrazine is included in Schedule 5 of the Standard for the Uniform Scheduling of Medicines and Poisons No.1, 2010 (the Poisons Standard)(DoHA 2010). Current versions of the Poisons Standard should be consulted for further information.
Derivation of the health-based guideline
The health-based guideline of 0.02 mg/L for atrazine was determined as follows:
where:
0.5 mg/kg bw/day is the NOEL based on a long-term (2-year) study in rats.
70 kg is taken as the average weight of an adult.
0.1 is a proportionality factor based on the assumption that 10% of the ADI will arise from the consumption of drinking water.
2 L/day is the estimated maximum amount of water consumed by an adult.
100 is the safety factor applied to the NOEL derived from animal studies. This safety factor incorporates a factor of 10 for interspecies extrapolation and 10 for intraspecies variation.
The World Health Organization has established a health-based guideline value of 0.002 mg/L for atrazine in 1993 (WHO 2004). The WHO incorporated an additional 10-fold safety factor to reflect potential neoplasia; however, Australian authorities considered that the induction mechanism for the mammary tumours was not directly relevant to humans.
References
NOTE: The toxicological information used in developing this fact sheet is from reports and data held by the Department of Health, Office of Chemical Safety.
Azenha M, Burrows HD, Canle M, Coimbra R, Fernandez MI, Garcia MV, Peiteado MA, Santaballa JA (2003). Kinetic and mechanistic aspects of the direct photodegraclation of atrazine, atraton, ametryn and 2-hydroxyatrazine by 254 nm light in aqueous solution. Journal of Physical Organic Chemistry, 16(8):498-503.
Bozkaya-Schrotter B, Daines C, Lescourret A, Bignon A, Breant P, Schrotter J (2008). Treatment of trace organics in membrane concentrates I: pesticide elimination. Water Science and Technology: Water Supply, 8(2):223-230.
CARAT (Committee to Advise on Reassessment and Transition) (2000). Summary of Pesticide Removal/Transformation Efficiencies from Various Drinking Water Treatment Processes. United States Environmental Protection Agency & United States. Department of Agriculture Committee to Advise on Reassessment and Transition.
DoHA (2010) The Poisons Standard; Schedule 1-Standard for the Uniform Scheduling of Medicines and Poisons, Department of Health and Ageing, Commonwealth of Australia, Canberra.
Health Canada (1993). Guidelines for Canadian Drinking Water Quality: Technical documents – Atrazine.
Huston PL, Pignatello JJ (1999). Degradation of selected pesticide active ingredients and commercial formulations in water by the photo-assisted Fenton reaction. Water Research, 33(5):1238-1246.
Mitchell C, Brodie J, White I (2005). Sediments, nutrients and pesticide residues in event flow conditions in streams of the Mackay Whitsunday Region, Australia. Marine Pollution Bulletin, 51(1-4):23-36.
NHMRC (National Health and Medical Research Council), NRMMC (Natural Resources Management Ministerial Council) (2004). Australian Drinking Water Guidelines. National Water Quality Management Strategy, Paper 6. NHMRC and NRMMC.
Ormad MP, Miguel N, Claver A, Matesanz JM, Ovelleiro JL (2008). Pesticides removal in the process of drinking water production. Chemosphere, 71(1):97-106.
Queensland Health (2007). Organochlorine, organophosphorous and synthetic pyrethroid pesticide, urea and triazine herbicides and PCBs in water. QHFSS SOP 16315.
Tomlin CD (ed) (2006). The Pesticide Manual: a world compendium, 14th edition, British Crop Production Council, UK.
Tran AT, Hyne RV, Doble P (2007). Determination of commonly used polar herbicides in agricultural drainage waters in Australia by HPLC. Chemosphere, 67(5):944-53.
WHO (World Health Organization) (2003). Atrazine in Drinking-water. Background document for development of WHO Guidelines for Drinking-water Quality. WHO.
WHO (World Health Organization) (2004). Guidelines for Drinking-water Quality. 3rd Edition, WHO, Geneva, Switzerland.
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