Dimethoate
(endorsed 2011)
Guideline
Based on human health concerns, dimethoate in drinking water should not exceed 0.007 mg/L.
Related chemicals
Dimethoate (CAS 60-51-5) belongs to the organophosphate class of chemicals. There are many other pesticides in this class, which includes acephate, chlorpyrifos, diazinon, dichlorvos, fenitrothion, omethoate, profenofos and trichlorfon (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, dimethoate would not be a health concern unless the concentration exceeded 0.007 mg/L. Excursions above this level even for a short period are of concern, as the health-based guideline is based on short-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: Dimethoate is a broad use systemic insecticide and acaricide (miticide) for the control of insects and mites in the home garden and in agricultural crops.
There are registered products that contain dimethoate in Australia. These products are intended for professional and/or home garden use and are available in aerosol formulation or concentrated solutions. Agricultural products for professional use are intended for application as a dilute or concentrated spray using hand-held, ground boom, mist machine or aerial spray equipment, or application as a diluted seed dressing or concentrated pre-planting or post-harvest dip. Home garden products are intended for application as an aerosol spray or concentrated spray using hand-held equipment. Data on currently registered products are available from the Australian Pesticides and Veterinary Medicines Authority.
Exposure sources: The main sources of public exposure to dimethoate are the use of home garden products and residues in food. Omethoate is an environmental degradant of dimethoate and thus the residue definition for dimethoate is “sum of dimethoate and omethoate, expressed as dimethoate”. Residue levels of dimethoate and omethoate in food produced according to good agricultural practice are generally low.
Agricultural use of dimethoate 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 water
No data on the occurrence of dimethoate in Australian waters could be found. In Canadian waters, dimethoate was not detected in drinking water (<0.6 µg/L) or in surface waters (<0.5 µg/L) (Health Canada 1986). The United States Environmental Protection Agency predicted surface water concentration after application is 0.44 to 33.4 µg/L, depending on use pattern (USEPA 2008).
Treatment of drinking water
Dimethoate appears to be very well removed by chlorination but is likely to be transformed into omethoate in the process (Ormad et al. 2008). Activated carbon is partially effective for the removal of dimethoate (Ormad et al. 2008).
Measurement
Dimethoate can be measured by routine gas chromatography–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 dimethoate is 0.02 mg per kg of bodyweight (mg/kg bw), based on a no-observed-effect level (NOEL) of 0.2 mg/kg bw/day from a short-term (57-day) human volunteer study. The NOEL is based on cholinesterase inhibition. The ADI incorporates a safety factor of 10 and was established in 1988.
The previous health value was 0.05 mg/L (NHMRC and NRMMC 2004).
Health considerations
Since omethoate is an environmental degradant of dimethoate, the toxicity of omethoate needs to be considered in the context of the health impact of dimethoate in drinking water. A separate fact sheet is available for omethoate.
Metabolism: Dimethoate is well absorbed via the gastrointestinal tract and distributed rapidly to the tissues, accumulating in the liver and kidneys. It is slowly excreted as metabolites (85-91% of the dose within 5 days), primarily in the urine. The major metabolites were thiophosphate and phosphate esters, and omethoate (1-6%). The parent compound represented 1-2% of the excreted dose.
Acute effects: Dimethoate has moderate acute oral toxicity, and low acute dermal toxicity. It is not a skin sensitiser.
Short-term effects: Short-term dietary studies in rats and dogs reported the main effect to be on the nervous system, with reduced erythrocyte and brain cholinesterase activity from the lowest dose of 2.48 mg/kg bw/day (rats) and 2.2 mg/kg bw/day (dogs). From 40 mg/kg bw/day, severe clinical signs consistent with cholinesterase inhibition were observed. In addition, increased mortality occurred in dogs at high doses.
Short-term (57-day) volunteer studies in humans reported inhibition of cholinesterase in whole blood at doses of 0.4 mg/kg bw/day and above. The NOEL from this study was 0.2 mg/kg bw/day and is the basis for the current ADI.
Long-term effects: Long-term dietary studies in mice, rats and dogs showed the most sensitive effects to be on the nervous system. In mice, erythrocyte cholinesterase inhibition was reported at 3.6 mg/kg bw/day and above. In rats, erythrocyte and brain cholinesterase were inhibited at 0.23 mg/kg bw/day and above. In dogs, brain and erythrocyte cholinesterase were inhibited at 0.125 mg/kg bw/day and above. At higher dose levels, there were changes in haematological parameters and clinical chemistry, as well as organ weight changes. Clinical neurological signs consistent with cholinesterase inhibition were observed at 50 mg/kg bw/day.
Carcinogenicity: Based on long-term dietary studies in mice, rats and dogs, there was no evidence of carcinogenicity associated with dimethoate.
Genotoxicity: Dimethoate is not considered to be genotoxic, based on in vitro and in vivo short-term studies.
Reproductive and developmental effects: A two-generation reproduction study in rats and developmental toxicity studies in rats and rabbits did not produce evidence of effects on reproductive parameters or foetal development. A developmental neurotoxicity study in rats reported increased post-natal mortality and cholinesterase inhibition in pups dosed in utero and post-natally at 0.5 mg/kg bw/day and above, in the absence of maternal toxicity. The NOEL from this study is 0.1 mg/kg bw/day. The potential effects of dimethoate on foetal development are the subject of a current review.
Poisons Schedule: Dimethoate is included in Schedule 6 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 0.007 mg/L for dimethoate was determined as follows:
where:
0.2 mg/kg bw/day is the NOEL based on a short-term (57-day) human volunteer study.
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 human studies. This safety factor incorporates a factor of 10 for intraspecies (human) variation, with an additional safety factor of 10 to account for the uncertainty in the ADI (which is likely to be lower as a result of the current review).
The World Health Organization has a health-based guideline value of 0.006 mg/L for dimethoate (WHO 2004).
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.
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 (1986). Guidelines for Canadian Drinking Water Quality: Technical documents – Dimethoate. Available at https://www.canada.ca/en/health-canada/services/publications/healthy-living/guidelines-canadian-drinking-water-quality-guideline-technical-document-dimethoate.html
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, 71:97–106.
Queensland Health (2007). Organochlorine, organophosphorous and synthetic pyrethroid pesticide, urea and triazine herbicides and PCBs in water. QHFSS SOP 16315.
Department of Health and Ageing (Tomlin CD (ed) (2006). The Pesticide Manual: a world compendium, 14th edition, British Crop Production Council, UK.
USEPA (United States Environmental Protection Agency) (2008). Revised Interim Reregistration Eligibility Decision for Dimethoate. USEPA.
WHO (World Health Organization) (2006). Guidelines for Drinking-water Quality. 3rd Edition, WHO, Geneva, Switzerland.
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