Dicofol

(endorsed 2011)

Guideline

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

Dicofol (CAS 115-32-2) belongs to the organochlorine class of chemicals. Other previously used pesticides in this class include DDT, aldrin, dieldrin, chlordane and heptachlor (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, dicofol would not be a health concern unless the concentration exceeded 0.004 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: Dicofol is an acaricide for the control of mites in agricultural, veterinary, and household settings.

There are registered products containing dicofol in Australia. These are intended for professional and home garden use. Use patterns include ground spray onto plants and onto soil for professional use, and by hand-held spray for home garden use. Data on currently registered products are available from the Australian Pesticides and Veterinary Medicines Authority.

Exposure sources: The main sources of public exposure to dicofol are the use of home garden products, and residues in food. Residue levels in food produced according to good agricultural practice are generally low.

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

Reported values in Australian waters

No data were found on dicofol in Australian waters. Dicofol has low solubility and a very high sorption coefficient (Koc\text{K}_{oc}) and is expected to adsorb rapidly to sediments and suspended matters rather than be present in water, except in exceptional circumstances. For example, dicofol was found at concentrations up to 0.0025 mg/L at Orestimba Creek in the USA following agricultural spraying in the area (Domagalski et al. 1996).

Treatment of drinking water

Dicofol has been shown to be completely removed when water undergoes conventional clarification (with alum), powdered activated carbon dosing, followed by oxidation with ozone (Ormad et al. 2008). Adsorption onto powdered activated carbon has been performed with a relatively moderate-high level of removal. Chlorination/ozonation for dicofol removal has also been reported with moderate success.

Measurement

Dicofol 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 dicofol is 0.001 mg per kg of bodyweight (mg/kg bw), based on a no-observed-effect level (NOEL) of 0.12 mg/kg bw/day from a 1-year dietary study in dogs. This NOEL is based on evidence of toxicity in the pituitary and liver. The ADI incorporates a safety factor of 100 and was first established in 1990.

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

Health considerations

Metabolism: Dicofol is rapidly absorbed via the gastrointestinal tract with wide, uniform tissue distribution. It is slowly eliminated, mainly in the faeces, as benzophenone metabolites and de-chlorinated metabolites. Dicofol has a moderate potential for bioaccumulation in body fat.

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

Short-term and long-term effects: In short-term and long-term dietary studies in mice, rats and dogs, effects indicative of liver toxicity were reported in all species, and included changes in clinical chemistry parameters, enzyme levels and increased relative liver weight. Rats were the most sensitive species, with effects reported at dose levels of 0.7 mg/kg bw/day and above in a 3-month study and 2.5 mg/kg bw/day and above in a 2-year study. In dogs, pituitary toxicity in the form of cysts was noted at 0.72 mg/kg bw/day and above in a 1-year study. The lowest NOEL was 0.12 mg/kg bw/day and this is the basis of the ADI.

Carcinogenicity: Based on a long-term study in rats, there is no evidence of carcinogenicity for dicofol.

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

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

Poisons Schedule: Dicofol 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 0.004 mg/L for dicofol was determined as follows:

 0.004 mg/L = 0.12 mg/kg bodyweight/day x 70 kg x 0.1  2 L/day x 100 \text{ 0.004 mg/L } = \dfrac{\text{ 0.12 mg/kg bodyweight/day x 70 kg x 0.1 }}{\text{ 2 L/day x 100 }}

where:

  • 0.12 mg/kg bw/day is the NOEL based on a long-term (1-year) dietary study in dogs.

  • 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. The safety factor of 100 incorporates a factor of 10 for interspecies extrapolation and 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.

Domagalski J (1996). Occurrence of dicofol in the San Joaquin River, California. Bulletin of Environmental Contamination and Toxicology, 57(2):284-291.

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.

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

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Australian Drinking Water Guidelines 6 2011, v3.9

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