Paraquat
(endorsed 2011)
Guideline
Based on human health concerns, paraquat in drinking water should not exceed 0.02 mg/L.
Related chemicals
Paraquat (CAS 4685-14-7 (paraquat); CAS 1910-42-5 (paraquat dichloride)) belongs to the bipyridinium class of compounds, which also includes the herbicide diquat (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, paraquat would not be a health concern unless the concentration exceeded 0.02 mg/L. Excursions above this level even for a short period are of concern, as the health-based guideline is based on an end-point that is common to both short-term and 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: Paraquat is a non-selective herbicide for the control of grasses and broad-leaf weeds in agricultural and horticultural crops.
There are registered products that contain paraquat (mainly as the dichloride) in Australia. These products are intended for professional use and are available as concentrated solutions to be applied in diluted form using ground, aerial or 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 paraquat is residues in food. Residue levels in food produced according to good agricultural practice are generally low.
Agricultural use of paraquat 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 occurrence data for paraquat in Australian water could be found. Paraquat dichloride binds so strongly to soil clay particles that it is extremely unlikely to be found in groundwater supplied as a drinking water source (Health Canada 1986, USEPA 1997).
Treatment of drinking water
Techniques effective in removing paraquat from water include adsorption by charcoal, ion exchange (66% and 70%) and modified peat (95% to 99%). Chlorine dioxide has been found to oxidize paraquat concentrations of 15 and 30 mg/L within minutes above pH 8.7. The use of bentonite, a clay adsorbent, for 10 minutes, followed by a 15-minute coagulation period, resulted in 90% removal of paraquat present at 1 mg/L (Health Canada, 1986).
Measurement
Paraquat can be measured by routine gas chromatography–mass spectrometry analysis, with a limit of reporting of 1 µg/L (Queensland Health 2007).
History of the health values
The current acceptable daily intake (ADI) for paraquat is 0.004 mg per kg of bodyweight (mg/kg bw), based on a no-observed-effect level (NOEL) of 0.45 mg/kg bw/day from a one-year dietary study in the dog. The NOEL is based on lung lesions at 0.93 to 1.0 mg/kg bw/day. The ADI incorporates a safety factor of 100 and was established in 1992.
The acute reference dose (ARfD) of 0.004 mg/kg bw/day for paraquat is based on the same NOEL as the ADI (0.45 mg/kg bw/day from a one-year dietary study in the dog). The NOEL is based on lung lesions at the next highest dose, 0.93 to 1.0 mg/kg bw/day. These lung lesions were evident also for shorter exposures. The ARfD incorporates a safety factor of 100, and was established in 2003.
The previous health value was 0.03 mg/L (NHMRC and NRMMC 2004).
Health considerations
Metabolism: Paraquat is poorly absorbed via the gastrointestinal tract, and is not extensively metabolised. Within 72 hours after administration, up to 80% appears unchanged in the faeces, up to 20% in urine, and less than 1% remains in the body. The small amount of urinary metabolites has not been identified. At 72 hours, there is no evidence of accumulation in most tissues, although paraquat may persist and accumulate in mouse brain.
Acute effects: Paraquat has moderate acute oral toxicity and low acute dermal toxicity. It is not a skin sensitiser.
Short-term effects: In 3-6 week dietary studies in mice, rats, rabbits and dogs, pathological changes in the lung, gastrointestinal tract and kidneys at dose levels above 2-4 mg/kg bw/day were reported. Significantly decreased food consumption and decreased bodyweight gain, and a dose-dependent increase in the mortality rate were also common observations. In a 13-week dietary study in dogs, there were macroscopic lung lesions and histopathological signs of alveolitis from 1.5 mg/kg bw/day. Alveolitis was detected in all dogs at 3 mg/kg bw/day.
In a one-year dietary study in dogs, there was an increased incidence of pulmonary lesions associated with chronic pneumonitis from 0.9 mg/kg bw/day. The NOEL was 0.45 mg/kg bw/day and this is the basis for the ADI and ARfD.
Long-term effects: A 2-year dietary study in mice reported clinical signs of toxicity at 1.9 mg/kg bw/day and an increased incidence of pulmonary adenomas at 15 mg/kg bw/day. A 2-year dietary study in rats reported cataracts and lenticular abnormalities of the eye from 2.5 mg/kg bw/day. At higher dose levels, lesions in the lungs included focal subpleural abnormalities, chronic pneumonitis, and proliferative lesions in the alveolar epithelium. Other effects included hydrocephalus, degeneration of the nerve fibres of the sciatic nerve and an increase in the numbers of cysts or cystic spaces in the spinal cord.
Carcinogenicity: There was evidence of proliferative lesions in the alveolar epithelium in a 2-year rat study, but only at dose levels well in excess of the likely level of human exposure. Long-term studies in mice showed no evidence of carcinogenicity.
Genotoxicity: Paraquat was clastogenic (causes chromosome breaks) in some in vitro short-term assays, but there was no evidence of genotoxicity in in vivo studies.
Reproductive and developmental effects: Two and three-generation dietary reproduction studies in rats and developmental toxicity studies in mice, rats and rabbits showed no evidence of effects on reproductive parameters or foetal development.
Neurotoxicity: In studies in mice and rats, paraquat produced evidence of neurodegeneration and induced changes in the brain similar to Parkinson’s disease. There is equivocal epidemiological evidence in some countries linking pesticide usage and the incidence of Parkinson’s disease.
Poisons Schedule: Paraquat is included in Schedule 7 of the Standard for the Uniform Scheduling of Medicines and Poisons No.1, 2010 (the Poisons Standard)(DoHA 2010). The Standard also indicates that aqueous solutions of paraquat must be coloured blue or green, and must contain a stenching agent. Current versions of the Poisons Standard should be consulted for further information.
Derivation of the health-based guideline
The health-based guideline of 0.02 mg/L for paraquat was determined as follows:
where:
0.45 mg/kg bw/day is the NOEL based on a long-term (1-year) 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. 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.
Health Canada (1986). Paraquat. Factsheet for the development of the Canadian Guidelines for Drinking Water Quality. Environmental and Workplace Health, Health Canada.
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.
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.
USEPA (United States Environmental Protection Agency) (1997). Reregistration eligibility decision (RED) – Paraquat dichloride. EPA 738-F-96-018. USEPA.
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