EPTC

(endorsed 2011)

Guideline

Based on human health concerns, EPTC in drinking water should not exceed 0.3 mg/L.

EPTC (S-ethyl-dipropylthiocarbamate)(CAS 759-94-4) belongs to the thiocarbamate class of chemicals. Other pesticides in this class include pebulate, thiobencarb, and butylate (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, EPTC would not be a health concern unless the concentration exceeded 0.3 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: EPTC is a pre-emergent herbicide for the control of certain grasses and broad-leaf weeds in agricultural vegetable crops.

There is at least one registered product containing EPTC in Australia. EPTC products are intended for professional use and are available as a concentrated solution to be diluted and applied directly onto the soil using ground, and hand-held sprays. Data on currently registered products are available from the Australian Pesticides and Veterinary Medicines Authority.

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

Agricultural use of EPTC 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 published reports on EPTC occurrence in Australian drinking water supplies were found. In the USA, EPTC was not detected at or above the limit of quantitation (1 μg/L) in any of the 3,873 public water systems sampled (serving a total population of 226 million) (USEPA 2008).

Treatment of drinking water

There is no evidence that EPTC is substantially removed by conventional treatments, such as coagulation/flocculation, sedimentation, and inert media filtration (USEPA 2008). Rapid degradation of EPTC has been reported with ultraviolet (UV) light at 254 nm. EPTC-sulfoxide, EPTC-sulfone, propylamine and dipropylamine were detected as photoproducts of EPTC at 254 nm There was negligible degradation of EPTC at 290 nm UV light (Abu-Qare et al. 2002). EPTC also shows high reactivity during the ozonation and ozone/hydrogen peroxide advanced oxidation process (Chen et al. 2008). Granular activated carbon is also considered a good option for the removal of EPTC from drinking water. Carbamate pesticides can be removed with 85.7% efficiency using a cellulose acetate membrane, 79.6–93% efficiency using a polyamide membrane, and greater than 92.9% efficiency using a thin-film composite membrane. These results indicate that reverse osmosis is effective in removing EPTC from drinking water (USEPA 2008).

Measurement

A solid-phase microextraction (SPME) method in water samples determined by gas chromatography coupled with flame thermionic detection for the measurement of EPTC can achieve a limit of quantitation (LOQ) of 0.01 μg/L. SPME, gas chromatography and mass spectrometric detection achieved a LOQ of 0.02 μg/L (Lambropoulou et al. 2002). EPTC can be detected in drinking water by United States Environmental Protection Agency (USEPA) Methods 507 and 525.2. USEPA Method 507 relies on solvent extraction of EPTC and separation by gas chromatography with a nitrogen-phosphorus detector. The method can achieve a LOQ of 0.08 μg/L. USEPA Method 525.2 uses liquid-solid extraction and capillary column gas chromatography/ mass spectrometry. The method can achieve a LOQ for EPTC in the range of 0.05 to 0.12 μg/L (USEPA 2008).

History of the health values

The current acceptable daily intake (ADI) for EPTC is 0.09 mg per kg of bodyweight (mg/kg bw), based on a no-observed-effect level (NOEL) of 9 mg/kg bw/day from a 2-year dietary study in rats. The NOEL is based on hindleg muscle atrophy and sciatic nerve demyelination at at 18 mg/kg bw/day. The ADI incorporates a safety factor of 100, and was established in 1995.

The previous ADI for EPTC of 0.01 mg/kg bw, based on a NOEL of 20 mg/kg bw/day from a long-term dietary study in mice with safety factor of 2000 to allow for the limited database, was set in 1970. The ADI was amended in 1995 after additional studies were submitted, including a long-term dietary study in rats demonstrating a lower overall NOEL.

The previous health value was 0.03 mg/L (NHMRC and NRMMC 2004).

Health considerations

Metabolism: EPTC is readily and extensively absorbed via the gastrointestinal tract in rats. It is extensively metabolised, mainly via sulfoxidation and ester hydrolysis. Excretion via the urine was essentially complete by 72 hours.

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

Short-term effects: In a 90-day dietary study in rats, there was decreased bodyweight gain and evidence of hepatocyte hypertrophy at the highest dose of 32 mg/kg bw/day. In a 16-week dietary study in dogs, there was hair loss at 22 mg/kg bw/day and decreased brain cholinesterase activity and changes to the gastric mucosa at 44 mg/kg bw/day.

Long-term effects: In a long-term (2-year) dietary study in rats, there was hindleg muscle atrophy, sciatic nerve demyelination, and increased serum AST at 18 mg/kg bw/day. Degenerative cardiomyopathy was seen at doses of 36 mg/kg bw/day and above. The NOEL was 9 mg/kg bw/day, and this is the basis for the current ADI.

Carcinogenicity: Based on a 2-year study in rats, there is no evidence of carcinogenicity for EPTC at doses up to 20 mg/kg/day.

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

Reproductive and developmental effects: A 3-generation reproduction study and a developmental toxicity study in rats did not produce any evidence of effects on reproductive parameters or foetal development.

Neurotoxicity: Hens dosed twice at a 21-day interval with oral doses of 7200 mg/kg bw EPTC did not exhibit any delayed neurotoxicity.

Poisons Schedule: EPTC 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 0.3 mg/L for EPTC was determined as follows:

 0.3 mg/L = 9 mg/kg bodyweight/day x 70 kg x 0.1  2 L/day x 100 \text{ 0.3 mg/L } = \dfrac{\text{ 9 mg/kg bodyweight/day x 70 kg x 0.1 }}{\text{ 2 L/day x 100 }}

where:

  • 9 mg/kg bw/day is the NOEL based on a long-term (2-year) 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.

  • 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.

Abu-Qare AW, Duncan HJ (2002). Photodegradation of the herbicide EPTC and the safener dichlormid, alone and in combination. Chemosphere, 46(8):1183-9.

Chen WR, Wu C, Elovitz MS, Linden KG, Mel Suffet IH (2008). Reactions of thiocarbamate, triazine and urea herbicides, RDX and benzenes on EPA Contaminant Candidate List with ozone and with hydroxyl radicals. Water Research, 42(1-2):137-44.

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.

Lambropoulou DA, Sakkas VA, Hela DG, Albanis TA (2002). Application of solid-phase microextraction in the monitoring of priority pesticides in the Kalamas River (N.W. Greece). Journal of Chromatography A, 963(1-2):107-16.

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.

USEPA (United States Environmental Protection Agency) (2008). Regulatory Determinations Support Document for Selected Contaminants from the Second Drinking Water Contaminant Candidate List (CCL 2). Office of Ground Water and Drinking Water, USEPA.

Last updated

Logo

Australian Drinking Water Guidelines 6 2011, v3.9

Go back to NHMRC website