Carbofuran
(endorsed 2011)
Guideline
Based on human health concerns, carbofuran in drinking water should not exceed 0.01 mg/L.
Related chemicals
Carbofuran (CAS 1563-66-2) belongs to the carbamate class of chemicals. Other pesticides in this class include aldicarb, bendiocarb, carbaryl, methiocarb, methomyl, pirimicarb and propoxur (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, carbofuran would not be a health concern unless the concentration exceeded 0.01 mg/L. 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: Carbofuran is a broad-spectrum insecticide and nematicide used to control worms and other pests in a variety of crops.
There are registered products containing carbofuran in Australia. These are intended for professional use and are available in concentrated solutions or as granular formulations that are applied directly to crops and soil. Data on currently registered products are available from the Australian Pesticides and Veterinary Medicines Authority.
Exposure sources: The main source of public exposure to carbofuran is residues in food. Residue levels in food produced according to good agricultural practice are generally low.
Agricultural use of carbofuran 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 reports of this compound in Australian drinking water could be found and, given its physicochemical properties and rapid degradation, it is unlikely to persist in waters. Carbofuran was only detected in one sample of 678 samples in a survey of Canadian municipal and private water supplies (Health and Welfare Canada 1991). It has also been detected in streams in the USA (Kimbrough and Litke 1996).
Treatment of drinking water
Carbofuran has been shown to be nearly completely (99.9%) removed when water undergoes advanced oxidation with iron-catalysed ultraviolet irradiation and peroxide (Fenton reaction) (Huston and Pignatello 1999). Conventional clarification/chlorination has been demonstrated to be unreliable for the removal of carbofuran from water, although softening clarification improves removal through conventional plants substantially (CARAT 2000).
Measurement
Carbofuran in water is commonly analysed in Australian laboratories using high-performance liquid chromatography with pre-column derivitisation with orthophthalaldehyde and fluorescence detection of the derivative. The detection limit is usually around 1 µg/L.
History of the health values
The current acceptable daily intake (ADI) for carbofuran is 0.003 mg per kg of bodyweight (mg/kg bw), based on a no-observed-effect level (NOEL) of 0.33 mg/kg bw/day from a 1-year dietary study in dogs. This NOEL is based on inhibition of brain cholinesterase and histopathological effects. The ADI incorporates a safety factor of 100 and was established in 1987.
The previous health value was 0.01 mg/L (NHMRC and NRMMC 2004).
Health considerations
Metabolism: Carbofuran is rapidly absorbed via the gastrointestinal tract and undergoes rapid metabolism. The metabolites are formed by oxidative and hydrolytic pathways and are rapidly excreted, mainly in the urine.
Acute effects: Carbofuran has high acute oral and dermal toxicity. It is not a skin sensitiser.
Short-term effects: A 6-week intraperitoneal study in mice reported reduced cholinesterase activity.
Long-term effects: In long-term dietary studies in mice, rats and dogs, the most sensitive effect observed was inhibition of brain cholinesterase levels. The lowest dose at which this was observed was 0.66 mg/kg bw/day in dogs. Histopathological alterations in testicular tissue, lungs, liver and thyroid were also observed at this dose in dogs.
Carcinogenicity: Based on long-term studies in mice and rats, there is no evidence of carcinogenicity for carbofuran.
Genotoxicity: Carbofuran is not considered genotoxic, based on in vitro and in vivo short-term tests.
Reproductive and developmental effects: Two multigeneration reproduction studies in rats and developmental toxicity studies in mice, rats and rabbits reported no evidence of effects on reproductive parameters or on foetal development.
Poisons Schedule: Carbofuran is included in Schedule 7 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 0.01 mg/L for carbofuran was determined as follows:
where:
0.33 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.
The World Health Organization established a health-based guideline value of 0.007 mg/L for carbofuran in 1998 (WHO 2006).
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.
CARAT (Committee to Advise on Reassessment and Transition) (2000). Summary of Pesticide Removal/Transformation Efficiencies from Various Drinking Water Treatment Processes. United States Environmental Protection Agency & United States. Department of Agriculture Committee to Advise on Reassessment and Transition.
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 and Welfare Canada (1991). Guidelines for Canadian drinking water quality. Ottawa, Ontario.
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.
Kimbrough RA, Litke DW (1996). Pesticides in streams draining agricultural and urban areas in Colorado. Environmental Science and Technology, 30:908–916.
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.
WHO (World Health Organization) (2006). Guidelines for Drinking-water Quality. 3rd Edition, WHO, Geneva.
Last updated
