Disulfoton

(endorsed 2011)

Guideline

Based on human health concerns, disulfoton in drinking water should not exceed 0.004 mg/L.

Disulfoton (CAS 298-04-4) belongs to the organophosphate class of chemicals. There are many other pesticides in this class, including fenthion, parathion, profenofos and ethoprophos (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, disulfoton would not be a health concern unless the concentration exceeded 0.004 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: Disulfoton is an insecticide and acaricide (miticide) for the control of pest infestations in food crops.

There is at currently at least one registered product containing disulfoton in Australia. Disulfoton products are intended for use by professionals and are available as a granular formulation. The use pattern is to apply the granule at or below the soil level to lucerne, cotton, potato, pea, and bean crops in agricultural settings. Data on currently registered products are available from the Australian Pesticides and Veterinary Medicines Authority.

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

Agricultural use of disulfoton may potentially lead to contamination of source waters through processes such as run-off or entry into groundwater.

Typical values in Australian drinking water

Information of the presence of disulfoton in Australian waters was not found. In extensive surveys in the USA, disulfoton was not found in surface waters or groundwaters (US-NLM 2009).

Treatment of drinking water

Disulfoton has been shown to be completely removed when water undergoes advanced oxidation with iron-catalysed ultraviolet irradiation and peroxide (Fenton reaction) (Huston and Pignatello 1999).

Measurement

Disulfoton is commonly analysed in Australian laboratories after solvent extraction and gas chromatographic determination using a nitrogen-phosphorus detector or mass selective detector. Typical limits of quantitation (LOQ) are 1 µg/L. The use of solid phase microextraction can permit lower LOQs, down to 0.1 µg/L (Queiroz et al. 2001).

History of the health values

The current acceptable daily intake (ADI) for disulfoton is 0.001 mg per kg of bodyweight (mg/kg bw), based on a no-observed-effect level (NOEL) of 0.01 mg/kg bw/day from a 30-day dietary study in humans. This NOEL is based on inhibition of cholinesterase activity. The ADI incorporates a safety factor of 10, and was established in 1988.

The previous ADI set in 1969 was 0.002 mg/kg bw, based on studies reviewed by WHO.

The previous health value was 0.003 mg/L (NHMRC and NRMMC 2004).

Health considerations

Metabolism: Disulfoton is rapidly absorbed from the gastrointestinal tract, with wide, uniform tissue distribution. It is rapidly eliminated, mainly in the urine as sulfoxide and sulfone metabolites.

Acute effects: Disulfoton has high acute oral toxicity and low acute dermal toxicity. The potential for skin sensitisation is unknown.

Short-term and long-term effects: In a 30-day dietary study in humans, disulfoton administered at a dose of 0.01 mg/kg bw/day did not produce a reduction in cholinesterase activity. This NOEL is the basis for the ADI.

In short- and long-term studies in mice, rats and dogs, all reported reduced cholinesterase activity together with symptoms indicative of nervous system toxicity. In 3-month studies, these effects were observed at 0.65 mg/kg bw/day in mice and 0.12 mg/kg bw/day and above in rats.

In long-term studies in rats and dogs, these effects were observed at 0.12 mg/kg bw/day in rats and 0.06 mg/kg bw/day in dogs.

Carcinogenicity: Based on long-term studies in mice and rats, there is no evidence of carcinogenicity for disulfoton.

Genotoxicity: Disulfoton is not considered to be genotoxic, on the basis of in vitro and in vivo short-term studies.

Reproductive and developmental effects: A multigeneration reproduction study in rats and developmental studies in rats and rabbits did not produce any evidence of effects on reproductive parameters or on foetal development. The only effect noted was decreased cholinesterase activity in parental animals at dose levels above 0.1 mg/kg bw/day.

Poisons Schedule: Disulfoton is included in Schedule 6 and 7 of the Standard for the Uniform Scheduling of Medicines and Poisons No.1, 2010 (the Poisons Standard)(DoHA 2010), depending on its concentration. Current versions of the Poisons Standard should be consulted for further information.

Derivation of the health-based guideline

The health-based guideline value of 0.004 mg/L for disulfoton was determined as follows:

 0.004 mg/L = 0.01 mg/kg bodyweight/day x 70 kg x 0.1  2 L/day x 10 \text{ 0.004 mg/L } = \dfrac{\text{ 0.01 mg/kg bodyweight/day x 70 kg x 0.1 }}{\text{ 2 L/day x 10 }}

where:

  • 0.01 mg/kg bw/day is the NOEL from a short-term (30-day) dietary study in humans. No cholinesterase inhibition was observed at this dose.

  • 70 kg is taken as the average weight of an adult.

  • 0.1 is a proportionality factor based on the conservative 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 the human study. The safety factor incorporates a factor of 10 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.

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.

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.

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.

Queiroz M, Silva S, Carvalho D, Lancas F (2001). Comparison between solid-phase extraction methods for the chromatographic determination of organophosphorus pesticides in water. Journal of Environmental Science and Health Part B, 36(5):517-527.

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

US-NLM (United States National Library of Medicine (2019). Hazardous Substances Database. Available at https://www.nlm.nih.gov/databases/download/hsdb.html

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Australian Drinking Water Guidelines 6 2011, v3.9

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