Propargite

(endorsed 2011)

Guideline

Based on human health concerns, propargite in drinking water should not exceed 0.007 mg/L.

Propargite (CAS 2312-35-8) is a sulfite ester acaricide. There are no other pesticides in this chemical class (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, propargite would not be a health concern unless the concentration exceeded 0.007 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 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: Propargite is an acaricide (miticide), used on a wide variety of food crops, ornamentals and cotton for the control of mites.

There are registered products that contain propargite in Australia. The products are for professional use. Some are emulsifiable concentrates used on cotton, to be diluted and typically applied by ground rig. Others are a water-dispersible granule formulation used on various fruits and vegetable crops and ornamentals. Data on currently registered products are available from the Australian Pesticides and Veterinary Medicines Authority.

Exposure sources: The main source of public exposure to propargite and its metabolites is residues in food. Residue levels in food produced according to good agricultural practice are generally low.

Agricultural use of propargite 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

Propargite was detected in 2000 at Carole Creek, at Mungindi Road bridge, New South Wales, at a concentration of 1.10 μg/L (Muschal 2001).

Treatment of drinking water

Measured removal of propargite by coagulation–flocculation during drinking water treatment ranged from less than 1% to 17% of the initial concentration (Ballard and Mackay 2005).

Measurement

Propargite can be extracted from water by liquid/liquid extraction with dichloromethane. The extract is then dried with sodium sulfate, concentrated, and analysed by gas chromatography–mass spectrometry (GC-MS) in selected ion monitoring mode (SIM). The method can achieve a limit of quantitation (LOQ) of 15 μg/L (Yu et al. 1997). Akhtar (1988) achieved a LOQ for propargite in groundwater of 0.1 μg/L using GC-MS-SIM. A multi-residue analysis of the pesticides involving extraction and clean-up using gel permeation chromatography and solid-phase extraction (SPE), and subsequent identification and quantification by GC-MS can achieve a LOQ of 2.5 μg/mL for propargite (Huang et al. 2007). SPE and gas chromatography ion-trap mass spectrometry can achieve a LOQ of 0.05 μg/L (Deger et al. 2000).

History of the health values

The current acceptable daily intake (ADI) for propargite is 0.002 mg per kg of bodyweight (mg/kg bw), based on a NOEL of 2 mg/kg bw/day from a long-term dietary study in rats. The NOEL is based on proliferation of cells in the small intestine (increased jejunal smooth muscle cells). The ADI was established in 1999 and incorporates a safety factor of 1000. The additional 10-fold safety factor was applied to address the uncertainty due to the narrow margin between the NOEL and the dose level at which jejunal tumours were observed (3 mg/kg bw/day).

The first ADI of 0.2 mg/kg bw was set in 1988 and was based on a NOEL of 22.5 mg/kg bw/day in a long-term (2-year) dietary study in dogs. This ADI was revised in 1992 to 0.02 mg/kg bw, based on a NOEL of 2 mg/kg bw/day in a rabbit developmental study.

The previous health value was 0.05 mg/L (NHMRC and NRMMC 2004).

Health considerations

Metabolism: Propargite is partially absorbed from the gastrointestinal tract, extensively metabolised, and distributed evenly in the tissues. Excretion is approximately equal between urine and faeces, with biliary excretion contributing to the faecal excretion. Little unchanged propargite was found in the bile or plasma.

Acute effects: Propargite has low to moderate acute oral toxicity and low dermal toxicity. It is a skin sensitiser in guinea pigs.

Short-term effects: A 90-day dietary study in rats reported clinical signs of toxicity, reduced bodyweight gain and haematological and clinical chemistry changes at 50 mg/kg bw and above.

A 13-week dietary study in dogs reported decreased food consumption, reduced bodyweight gain, increased pigmentation in the reticuloendothelial cells in the liver and increased haemosiderin deposits in the spleen at 50 mg/kg bw/day and above.

Long-term effects: A 2-year dietary study in rats reported a moderate decrease in bodyweight gain, clinical chemistry changes and relative liver and kidney weight changes at 19 mg/kg bw/day. There was also a dose-related increase in undifferentiated sarcomas of the jejunum, often associated with ulceration, at a dose level of 3 mg/kg bw/day and above in females and 19 mg/kg bw/day and above in males. In some animals, there were metastases to the mesentery and lungs. A more detailed long-term study examining the changes in the jejunum in rats showed significant cell proliferation and increased jejunal mass at 14 mg/kg bw/day in males and 21 mg/kg bw/day in females. The NOEL for cell proliferation was 2 mg/kg bw/day and this is the basis of the ADI.

An 18-month study in mice reported no increase in jejunal tumours at the highest dose level of 150 mg/kg bw/day.

Carcinogenicity: There was evidence of carcinogenicity in rats but not mice. In rats, sarcomas of the jejunum are likely to be the result of increased cell proliferation. This effect occurred at dose levels well in excess of the likely level of human exposure to propargite.

Genotoxicity: Propargite is not considered to be genotoxic, based on in vitro and in vivo short-term studies.

Reproductive and developmental effects: A 2-generation reproduction study in rats and developmental studies in rats and rabbits did not produce any evidence of effects on reproductive parameters or foetal development.

Poisons Schedule: Propargite 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 propargite was determined as follows:

 0.007 mg/L = 2.0 mg/kg bodyweight/day x 70 kg x 0.1  2 L/day x 1000 \text{ 0.007 mg/L } = \dfrac{\text{ 2.0 mg/kg bodyweight/day x 70 kg x 0.1 }}{\text{ 2 L/day x 1000 }}

where:

  • 2.0 mg/kg bw/day is the NOEL based on a long-term (20-month) dietary 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.

  • 1000 is the safety factor applied to the NOEL derived from animal studies. This safety factor incorporates a factor of 10 for interspecies extrapolation, 10 for intraspecies variation, and 10 for the narrow margin between the NOEL for cell proliferation (2 mg/kg bw/day) and the dose at which tumours occurred (3 mg/kg bw/day) in rats.

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.

Akhtar M (1988). Determination of Propargite and its Major Product Omite Glycol Ether in Ground Water. UNIROYAL: 8774, File No. OMIT- 83.

Ballard BD, MacKay AA (2005). Estimating the removal of anthropogenic organic chemicals from raw drinking water by coagulation flocculation. Journal of Environmental Engineering, 131(1):108-118.

Deger AB, Gremm TJ, Frimmel FH (2000). Problems and solutions in pesticide analysis using solid-phase extraction (SPE) and gas chromatography ion-trap mass spectrometry detection (GC-MS). Acta Hydrochimica et Hydrobiologica, 28(6):292-299.

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.

Huang Z, Li Y, Chen B, Yao S (2007). Simultaneous determination of 102 pesticide residues in Chinese teas by gas chromatography-mass spectrometry. Journal of Chromatography B, 853(1-2):154-62.

Muschal M (2001). Central and North West Regions’ Water Quality Program. 1999-2000 Report on pesticides monitoring. Parramatta, NSW Centre for Natural Resources , Department of Land and Concervation

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.

Tomlin CD (ed) (2006). The Pesticide Manual: a world compendium, 14th edition, British Crop Production Council, UK.

Yu L, Schoen R, Dunkin A, Firman M, Cushman H (1997). Rapid identification and quantitation of diphenylamine, o-phenylphenol, and propargite pesticide residues on apples by gas chromatography/mass spectrometry. Journal of Agricultural and FoodChemistry, 45(3): 748–752.

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