Pirimiphos methyl
(endorsed 2011)
Guideline
Based on human health concerns, pirimiphos methyl in drinking water should not exceed 0.09 mg/L.
Related chemicals
Pirimiphos methyl (CAS 29232-93-7) belongs to the organophosphate class of chemicals. There are many other pesticides in this class including acephate, dichlorvos, fenthion, malathion, omethoate 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, pirimiphos methyl would not be a health concern unless the concentration exceeded 0.09 mg/L. Excursions above this level even for a relatively short period are of concern, as the health-based guideline is based on short- to medium-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: Pirimiphos methyl is an insecticide for the control of pests such as cockroaches, fleas, ants, mosquitoes and flies in domestic, public, commercial and industrial areas, and agricultural buildings. It is also used as a fumigant to treat stored grain and peanuts.
There are registered products that contain pirimiphos methyl in Australia. The products are intended for professional and domestic use and are available as concentrated solutions to be applied in diluted form using pressurised hand-held spray equipment. Data on currently registered products are available from the Australian Pesticides and Veterinary Medicines Authority.
Exposure sources: The possible sources of public exposure to pirimiphos methyl and its metabolites are the use of domestic products, residues found in publicly accessible areas, and residues in food. Residue levels in food produced according to good agricultural practice are generally low.
The use pattern of pirimiphos methyl for treatment of mosquito larvae involves direct application to water that may harbour larvae, and which may then enter source waters for drinking water. Other insecticidal uses of pirimiphos methyl 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 published reports on pirimiphos methyl occurrence in Australian drinking water supplies were found. Pirimiphos-methyl was considered by the World Health Organization (WHO) for addition to drinking water in containers as a mosquito larvicide treatment, particularly to control dengue fever. However, the WHO does not recommended their use for direct application to drinking water unless no other effective and safe treatment is available (WHO 2008).
Treatment of drinking water
Pirimiphos methyl can be completely mineralised by hydroxyl radicals (HO) generated by Electro-Fenton process (Guivarch et al. 2003) and it can be readily degraded in water by ozone-forming polar phenol derivatives (Chiron et al. 1998). Powdered activated carbon filtration and reverse osmosis have been demonstrated to be highly effective for the removal of organic chemicals including pesticides in water (Heijman and Hopman 1999).
Measurement
Pirimiphos methyl can be extracted from water by liquid/liquid extraction with dichloromethane. The extract is dried with sodium sulfate, concentrated, and analysed by gas chromatography–mass spectrometry in selected ion monitoring mode. The method can achieve a limit of quantitation (LOQ) of 0.06 µg/L. Solid-phase microextraction using ceramic/carbon materials followed by gas chromatography with a flame thermionic detector can achieve a LOQ of 15.6 ng/L (Zeng et al. 2008). Enzyme-linked immunosorbent assay can achieve pirimiphos detection limits of 0.01 µg/mL (Tang et al. 2008).
History of the health values
The current acceptable daily intake (ADI) for pirimiphos methyl is 0.02 mg per kg of bodyweight (mg/kg bw), based on a no-observed-effect level (NOEL) of 0.25 mg/kg bw/day from short-term studies on human volunteers. The NOEL is based on the absence of adverse effects at the highest dose tested. The ADI incorporates a safety factor of 10, and was established in 1991.
The previous health value was 0.05 mg/L (NHMRC and NRMMC 2004).
Health considerations
Metabolism: Pirimiphos methyl is readily absorbed via the gastrointestinal tract of rats and dogs, and is extensively metabolised to non-phosphorylated derivatives. In rats, pirimiphos methyl was excreted rapidly in both urine (85%) and faeces (15%), with 12 metabolites detected in urine but not identified.
Acute effects: Pirimiphos methyl has low acute oral and dermal toxicity. It methyl is not a skin sensitiser.
Short-term effects: Short-term dietary studies in rats reported decreased bodyweight gain and food consumption, and inhibition of brain and plasma cholinesterase, at doses of 4 mg/kg bw/day and above. Clinical signs of cholinesterase inhibition and haematological effects were reported at 200 mg/kg bw/day. A 13-week dietary study in dogs reported inhibition of erythrocyte cholinesterase at doses of 2 mg/kg bw/day. At doses of 10 mg/kg bw/day and above, clinical signs consistent with cholinesterase inhibition were observed, as well as decreased bodyweight gain and evidence of mild liver toxicity.
In two human volunteer studies (0.25 mg/kg bw/day for 28 or 56 days), there was no significant change in plasma and erythrocyte cholinesterase activity or liver function parameters. The NOEL from these studies was 0.25 mg/kg bw/day and is the basis of the current ADI.
Long-term effects: Long-term dietary studies in mice, rats and dogs reported cholinesterase inhibition to be the most sensitive toxicological effect. In mice, plasma and erythrocyte cholinesterase were inhibited at 25 mg/kg bw/day, with no associated clinical signs. In rats, plasma and brain cholinesterase were inhibited at 2.5 mg/kg bw/day, with slight anaemia at higher doses. In dogs, inhibition of plasma cholinesterase with associated clinical signs was reported at 2 mg/kg bw/day.
Carcinogenicity: Based on 2-year studies in dogs, mice and rats, there is no evidence of carcinogenicity for pirimiphos methyl.
Genotoxicity: Pirimiphos methyl is not considered to be genotoxic, based on in vitro and in vivo short-term studies.
Reproductive and developmental effects: A 3-generation study in rats and developmental studies in rats and rabbits did not indicate any adverse effects on reproductive parameters or foetal development.
Neurotoxicity: Special neurotoxicity studies in rats by dietary administration found no evidence of delayed neurotoxicity.
Poisons Schedule: Pirimiphos methyl 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 0.09 mg/L for pirimiphos methyl was determined as follows:
where:
0.25 mg/kg bw/day is the NOEL based on two short-term (28- and 56-day) studies involving human volunteers.
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.
10 is the safety factor applied to the NOEL derived from human studies, to allow for intraspecies variation.
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.
Chiron S, Rodriguez A, Fernandez-Alba A (1998). Application of gas and liquid chromatography-mass spectrometry to the evaluation of pirimiphos methyl degradation products in industrial water under ozone treatment. Journal of Chromatography A, 823(1-2):97-107.
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.
Guivarch E, Oturan N, Oturan MA (2003). Removal of organophosphorus pesticides from water by electrogenerated Fenton’s reagent. Environmental Chemistry Letters, 1(3):165-168.
Heijman SGJ, Hopman R (1999). Activated carbon filtration in drinking water production: model prediction and new concepts. Colloids and Surfaces A: Physicochemical and Engineering Aspects, 151:303–310.
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.
Tang J, Zhang M, Cheng G, Li A, Lu Y (2008). Development of IC-ELISA for detection of organophosphorus pesticides in water. Journal of Environmental Science and Health B, 43(8):707-12.
Tomlin CD (ed) (2006). The Pesticide Manual: a world compendium, 14th edition, British Crop Production Council, UK.
WHO (World Health Organization) (2008). Guidelines for Drinking-water Quality. 3rd Edition including 1st and 2nd addenda, WHO, Geneva, Switzerland.
Zeng J, Yu B, Chen W, Lin Z, Zhang L, Chen X, Wang X (2008). Application of ceramic/carbon composite as a novel coating for solid-phase microextraction. Journal of Chromatography A, 1188(1):26-33.
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