Thiobencarb
(endorsed 2011)
Guideline
Based on human health concerns, thiobencarb in drinking water should not exceed 0.04 mg/L.
Related chemicals
Thiobencarb (CAS 28249-77-6) belongs to the thiocarbamate class of chemicals. There are many other pesticides in this class, including EPTC, pebulate, and molinate (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, thiobencarb would not be a health concern unless the concentration exceeded 0.04 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: Thiobencarb is a selective herbicide for the control of grass weeds in rice crops.
There is at least one registered product containing thiobencarb in Australia. Thiobencarb products are intended for professional use, and are available as a concentrated solution to be diluted and applied to water via ground and aerial spray. Data on currently registered products are available from the Australian Pesticides and Veterinary Medicines Authority.
Exposure sources: The main source of public exposure to thiobencarb and its metabolites is residues in food and drinking water. Residue levels in food produced according to good agricultural practice are generally low, and maximum residue limits are at the level of detection.
The agricultural use of thiobencarb involves direct application into irrigation water, which may then enter source waters for drinking water.
Typical values in Australian drinking water
No reports of thiobencarb in Australian drinking waters have been identified. However, thiobencarb has been reported in run-off from Australian rice fields (Quayle et al. 2006), indicating the potential for drinking water contamination in rice-growing regions.
Treatment of drinking water
During chlorination of drinking water, thiobencarb has been shown to be quickly degraded, producing chlorobenzyl alcohol, chlorotoluene, chlorobenzyl chloride, chlorobenzoic acid and chlorobenzyl aldehyde as chlorination by-products (Magara et al. 1994).
Measurement
No suitable techniques for the analysis of thiobencarb in drinking water have been identified. However, thiobencarb has commonly been measured in soils and run-off from rice growing operations using high performance liquid chromatography–tandem mass spectrometry, and such methods could be adapted if required.
History of the health values
The current acceptable daily intake (ADI) for thiobencarb is 0.01 mg per kg of bodyweight (mg/kg bw), based on a no-observed-effect level (NOEL) of 1.0 mg/kg bw/day from long-term dietary studies in dogs (1-year) and rats (2-year). The NOEL is based on decreased plasma cholinesterase activity, reduced bodyweight gain, and evidence of anaemia at doses of 5 mg/kg bw/day and above. The ADI incorporates a safety factor of 100, and was established in 1989.
The previous ADI of 0.007 mg/kg bw was set in 1977, based on a NOEL of 0.75 mg/kg bw/day. The basis for this NOEL is not available.
The previous health value was 0.03 mg/L (NHMRC and NRMMC 2004).
Health considerations
Metabolism: Thiobencarb is readily and extensively absorbed via the gastrointestinal tract in rats. It is extensively metabolised by oxidation and hydrolysis to the major metabolites, 4-chlorohippuric acid and 4-chlorobenzoic acid. Excretion was via urine and to lesser extent faeces, and was almost complete within 72 hours.
Acute effects: Thiobencarb has moderate acute oral toxicity and low acute dermal toxicity. It is not a skin sensitiser.
Short-term effects: A three-month oral study in rats reported increased liver weight and serum alkaline phospatase activity at dose levels of 33 mg/kg bw/day and above.
Long-term effects: Long-term dietary studies in rats (2-year) and dogs (1-year) reported decreased plasma cholinesterase activity, reduced bodyweight gain, and evidence of anaemia at doses of 5 mg/kg bw/day and above. In a long-term dietary study in mice, liver discolouration was the only effect seen at high dose levels. The lowest overall NOEL was 1 mg/kg bw/day (in both rats and dogs). This NOEL is the basis for the current ADI.
Carcinogenicity: Based on 18-month studies in mice and a 2-year study in rats, there is no evidence of carcinogenicity for thiobencarb.
Genotoxicity: Thiobencarb 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: Thiobencarb 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 0.04 mg/L for thiobencarb was determined as follows:
where:
1.0 mg/kg bw/day is the NOEL based on a long-term dietary studies in dogs (1 year) and rats (2 years).
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. This safety factor 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.
Magara Y, Aizawa T, Matumoto N, Souna F (1994). Degradation of pesticides by chlorination during water-purification. Water Science and Technology, 30(7):119-128.
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.
Quayle WC, Oliver DP, Zrna S (2006). Field dissipation and environmental hazard assessment of clomazone, molinate, and thiobencarb in Australian rice culture. Journal of Agricultural and Food Chemistry, 54(19):7213-7220.
Tomlin CD (ed) (2006). The Pesticide Manual: a world compendium, 14th edition, British Crop Production Council, UK.
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