Carbaryl
(endorsed 2011)
Guideline
Based on human health concerns, carbaryl in drinking water should not exceed 0.03 mg/L.
Related chemicals
Carbaryl (CAS 63-25-2) is in the carbamate class of chemicals. Other pesticides in this class include aldicarb, methomyl, oxamyl and pirimicarb (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, carbaryl would not be a health concern unless the concentration exceeded 0.03 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: Carbaryl is an insecticide effective against a broad range of insects, mites, lice, millipedes and other pests.
There are registered products containing carbaryl in Australia. These products are for professional and home garden use on lawns and turf; on horses, ponies and dogs; and other agricultural uses. They are applied as a wettable formulation spray domestically or by aerial spraying or boom spray in agriculture. Data on currently registered products are available from the Australian Pesticides and Veterinary Medicines Authority.
Exposure sources: The main sources of public exposure to carbaryl 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 carbaryl 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
Monitoring studies for carbaryl in raw and tap water are limited. No specific data from Australia were found. Carbaryl has been detected in water at µg/L concentrations but degradation is relatively rapid, with 1-naphthol identified as the major degradation product. Indirect and direct photolysis of carbaryl produces different naphthoquinones as well as some hydroxyl substituted naphthoquinones (Gunasekara et al. 2008).
Carbaryl is one of the three most frequently detected insecticides in surface water, according to US Geological Survey reports from 1991-2001. It is estimated that higher levels of carbaryl occur in surface water than in groundwater, based on available monitoring data and modeling. A 3-year monitoring study undertaken in the USA revealed that carbaryl was present in drinking water sources in the majority of the monitored sites (13 of 16 sites). The concentrations measured at these sites were low (0.002 to 0.031 µg/L) in raw water and generally lower in treated drinking water (USEPA 2004).
Treatment of drinking water
It is estimated that conventional drinking water treatment (i.e. coagulation, flocculation and settling) can reduce carbaryl concentration by 43% of the concentration prior to treatment. (USEPA 2004). Therefore, it is estimated that a carbaryl concentration below 0.05 mg/L should be achievable by conventional drinking-water treatment (WHO 2008). Ozone has been shown to be 99% effective in removing carbaryl from water. Similarly, granular activated carbon adsorption can effectively remove carbaryl during treatment. However, chlorine and hypochlorite may be ineffective at removing or degrading carbaryl. Softening of hard waters will reduce carbaryl concentrations (via alkaline hydrolysis), as softening raises the pH of the water (USEPA 2004).
High and stable removal efficiency of carbaryl can also be achieved using an anion exchange membrane anodic fenton treatment. This treatment oxidises carbaryl to 1-naphthol and 1,4-naphthoquinone (Wang et al. 2002, Kong et al. 2007).
Measurement
There are several methods for analysing carbaryl in drinking water. Its concentration in drinking-water may be determined by extraction, hydrolysis, derivatisation and separation by gas-liquid chromatography with electron capture detection or mass spectrometry. Detection limits vary according to the method, but typical limits of detection (LODs) of 0.2 µg/L are reported, and high-performance liquid chromatography (HPLC) with mass spectrometry is considered the conventional method of analysis.
HPLC using pre-concentration, elution, separation and ultraviolet determination can achieve a LOD in tap water between 0.03-0.2 µg/L (Driss et al. 1993). Another study using HPLC with fluorometric detection reported a LOD of 1.4 mg/mL for carbaryl (Massey et al. 1995). However, HPLC with fluorometric detection does not always provide the required specificity for determining carbaryl residues (Makihata et al. 2003). Solid-phase extraction followed by reversed-phase liquid chromatography can achieve LODs in the range 3-15 ng/L for the determination of nine N-methylcarbamate pesticides, including carbaryl, from drinking water (Morrica et al. 2005). Liquid chromatography electrospay ionisation tandem mass spectrometry, without a concentration procedure, has also been used for the measurement of carbaryl (LOD 2 µg/L) (Makihata et al. 2003).
Carbaryl can be analysed using the United States Environmental Protection Agency (USEPA) method 8270: Semivolatile Organic Compounds by Gas Chromatography/Mass Spectrometry (GC/MS): Capillary Column Technique, or the USEPA method 531: Direct Aqueous Injection high performance liquid chromatography (HPLC) with Post Column Derivatisation.
Other methods include immunoassay techniques, which achieve a LOD of 1.38 µg/L (Mauriz et al. 2006), or direct analysis by laser-induced fluorescence, which achieves a LOD in tap water of 20 ng/L (Burel-Deschamps et al. 2006).
History of the health values
The current acceptable daily intake (ADI) for carbaryl is 0.008 mg per kg of bodyweight (mg/kg bw) based on a lowest-observed-effect level (LOEL) of 16 mg/kg bw/day observed in a 2-year dietary study in mice. The ADI incorporates a safety factor of 2000 and was established in 2002. There is an additional factor of 5 is for the inadequate database and an additional factor of 4 for the seriousness of the carcinogenic response.
The acute reference dose (ARfD) of 0.01 mg/kg bw/day for carbaryl was established in 2002, based on a no-observed-effec leve (NOEL) of 1 mg/kg bw/day from a medium-term (13-week) and neurotoxicity study in rats, where there were behavioural indications of autonomic neurotoxicity and brain, plasma and erythrocyte cholinesterase depression. The ARfD incorporates a safety factor of 100.
The previous health value was 0.03 mg/L (NHMRC and NRMMC 2004).
Health considerations
Metabolism: Carbaryl is rapidly absorbed via the gastrointestinal tract in rodents and humans and is extensively metabolised. Excretion is predominantly via the urine, where ten metabolites have been identified. The potential for bioaccumulation is low.
Acute effects: Carbaryl has moderate oral toxicity and low dermal toxicity. Symptoms of acute poisoning include hyperexcitability, salivation, bronchoconstriction, headache, and vomiting. Carbaryl does not cause skin sensitisation.
Short-term: In a short-term dietary study in dogs, the major effect was depression of plasma cholinesterase at dose levels greater than 1.4 mg/kg bw/day.
Long-term effects: Long-term studies were conducted in rats and dogs. In a 2-year dietary study in rats, there was decreased bodyweight gain and cholinesterase inhibition at 70 mg/kg bw/day. A 1-year dietary study in dogs showed cholinesterase inhibition at 3.8 mg/kg bw/day and above,
Carcinogenicity: Studies in rodents reported renal and urinary bladder tumours in rats and liver tumours in mice at high dose levels only. These tumours are considered to develop via a non-genotoxic mechanism at dose levels greatly exceeding the likely human exposure level. In mice, vascular tumours were also observed at the lowest dose of 16 mg/kg bw/day. This LOEL is the basis for the ADI.
Genotoxicity: Carbaryl caused chromosome breakage in some in vitro studies, but overall, it was not considered to be genotoxic.
Reproductive and developmental effects: A 2-generation reproduction toxicity study in rats reported maternotoxicity and reduced pup survival at 4.7 mg/kg bw/day. Developmental studies in rats and rabbits reported maternotoxicity and foetotoxicity at 30 mg/kg bw/day and 150 mg/kg bw/day respectively. There was no evidence of teratogenicity.
Neurotoxicity: A 13-week oral neurotoxicity study in rats reported blood and brain cholinesterase depression and behavioural effects at 1 mg/kg bw/day and above. No pathological changes were noted.
Poisons Schedule: Carbaryl is included in Schedule 4, 5 or 6 in the Standard for the Uniform Scheduling of Medicines and Poisons (SUSMP) No.1 (2010), depending on the concentration and use of the product. Current versions of the Poisons Standard should be consulted for further information.
Derivation of health-based guideline
The health-based guideline of 0.03 mg/L for carbaryl was determined as follows:
where:
16.0 mg/kg body weight per day is the LOEL for the formation of vascular tumours observed in a long-term (2-year) dietary study in mice.
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 average maximum amount of water consumed by an adult.
2000 is the safety factor applied to the LOEL derived from animal studies. This safety factor incorporated a factor of 10 for interspecies extrapolation and 10 for intraspecies variation. There is an additional factor of 10 for the use of a LOEL and an additional factor of 2 for the uncertainty as to the mode/mechanism of vascular tumour formation and for the inability to dismiss the relevance of vascular tumours to humans.
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.
Burel-Deschamps L, Giamarchi P, Stephan L, Lijour Y, Le Bihan A (2006). Laser-induced fluorescence detection of carbamates traces in water. Journal of Fluorescence, 16(2):177-83.
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.
Driss MR, Hennion MC, Bouguerra ML (1993). Determination of carbaryl and some organophosphorus pesticides in drinking water using on-line liquid chromatographic preconcentration techniques. Journal of Chromatography, 639(2):352-8.
Gunasekara AS, Rubin AL, Goh KS, Spurlock FC, Tjeerdema RS (2008). Environmental fate and toxicology of carbaryl. Reviews of Environmental Contamination and Toxicology, 196: 95-121.
Kong L, Lemley AT (2007). Effect of nonionic surfactants on the oxidation of carbaryl by anodic Fenton treatment. Water Research, 41(12):2794-802.
Makihata N, Kawamoto T, Teranishi K (2003). Simultaneous analysis of carbamate pesticides in tap and raw water by LC/ESI/MS. Analytical Sciences, 19(4): 543-9.
Massey KA, Van Engelen DL, Warner IM (1995). Determination of carbaryl as its primary metabolite, 1-naphthol, by reversed-phase high-performance liquid chromatography with fluorometric detection. Talanta, 42(10):1457-63.
Mauriz E, Calle A, Abad A, Montoya A, Hildebrandt A, Barcelo D, Lechuga LM (2006). Determination of carbaryl in natural water samples by a surface plasmon resonance flow-through immunosensor. Biosensors and Bioelectronics, 21(11):2129-36.
Morrica P, Fidente P, Seccia S (2005). Liquid chromatographic determination of nine N-methylcarbamates in drinking water. Biomedical Chromatograpy, 19(1):107-10.
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) (2004). Carbaryl Interim Reregistration Eligibility Decision (IRED) Facts. Office of Prevention, Pesticides and Toxic Substances, Washington.
Wang Q, Lemley AT (2002). Oxidation of carbaryl in aqueous solution by membrane anodic fenton treatment. Journal of Agricultural and Food Chemistry, 50(8):2331-7.
WHO (World Health Organization) (2008). Carbaryl in Drinking-water. Background document for preparation of WHO Guidelines for Drinking-water quality. Geneva, World Health Organization (WHO/HSE/AMR/08.03/5).
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