Napropamide
(endorsed 2011)
Guideline
Based on human health concerns, napropamide in drinking water should not exceed 0.4 mg/L.
Related chemicals
Napropamide (CAS 15299-99-7) belongs to the alkanamide class of chemicals. Another pesticide in this class is diphenamid (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, napropamide would not be a health concern unless the concentration exceeded 0.4 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: Napropamide is a pre-emergent herbicide for the control of grass weeds in tomato, almond, grape, and stone fruit crops and commercial farms.
There is at least one registered product that contains napropamide in Australia. Napropamide products are intended for agricultural use and are available as a concentrated water-soluble granule formulation to be diluted and sprayed onto soil and then incorporated mechanically or by irrigation. Data on currently registered products are available from the Australian Pesticides and Veterinary Medicines Authority.
Exposure sources: The main source of public exposure to napropamide and its metabolites is residues in food. Residue levels in food produced according to good agricultural practice are generally low.
Agricultural use of napropamide may potentially lead to contamination of source waters through processes such as run-off, spray drift or entry into groundwater.
Reported values in Australian waters
No data were found on the occurrence of napropamide in Australian waters. Napropamide is broken down very quickly in water, with a half-life as rapid as seven minutes (EXTOXNET 1993). In water, the breakdown is predominantly mediated by the action of sunlight (photolysis). Napropamide was not detected in groundwater in the USA in a national survey in 1988 (Williams et al. 1988).
Treatment of drinking water
No specific data on the treatment of napropamide in drinking water have been identified.
Measurement
Napropamide can be analysed by high-performance liquid chromatography with ultraviolet detection, with a limit of quantitation of 0.3 µg/L (USEPA Method 632.1).
History of the health values
The current acceptable daily intake (ADI) for napropamide is 0.1 mg per kg of bodyweight (mg/kg bw), based on a no-observed-effect level (NOEL) of 11 mg/kg bw/day from a long-term (2-year) dietary study in rats. The NOEL is based on liver spongiosis and decreased bodyweight gains. The ADI incorporates a safety factor of 100 and was established in 1994.
The previous ADI was 0.4 mg/kg bw based on a NOEL of 40 mg/kg bw/day in a long-term dietary study in rats and a medium-term dietary study in dogs. It was set in 1987.
The previous health value was 1 mg/L (NHMRC and NRMMC 2004).
Health considerations
Metabolism: Napropamide is readily absorbed from the gastrointestinal tract in rats. Over 80% of the dose is excreted in urine and faeces within 48 hours, and excretion is complete by 96 hours. There is no evidence of accumulation in blood or tissues.
Acute effects: Napropamide has low acute oral and dermal toxicity. It is not a skin sensitiser in guinea-pigs.
Short-term effects: Short-term (13-week) dietary studies were conducted in rats and dogs. In dogs, effects included increased absolute liver weights, and increased levels of glutamic transaminase and alkaline phosphatase enzymes in serum at 100 mg/kg bw/day. In rats, no toxic effects were seen up to the highest dose tested, 50 mg/kg bw/day.
Long-term effects: Long-term dietary studies were conducted in mice and rats and long-term dietary studies in dogs. The study in rats reported hepatic spongiosis and increased absolute liver and kidney weights at doses of 45 mg/kg bw/day and above. Effects in both mice and dogs were confined to decreased bodyweight gains at the highest doses tested (427 mg/kg bw/day for mice, 500 mg/kg bw/day for dogs). The lowest overall NOEL was 11 mg/kg bw/day (rat), based on liver spongiosis and decreased bodyweight gain.
Carcinogenicity: Based on a 2-year dietary study in rats and an 18-month dietary study in mice, there is no evidence of carcinogenicity for napropamide.
Genotoxicity: Napropamide 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 in rats and developmental studies in rats and rabbits did not produce any evidence of reproductive effects, delayed development or teratogenicity.
Poisons Schedule: Napropamide is considered not to require control by scheduling due to its low toxicity and is therefore included in Appendix B 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 0.4 mg/L for napropamide was determined as follows:
where:
11 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.
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.
EXTOXNET (1993). Pesticide Information Profile – Napropamide.
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 Method 632.1. The Determination of Carbamate and Amide Pesticides in Municipal and Industrial Wastewater. United States Environmental Protection Agency.
Williams WM, Holden PW, Parsons DW, Lorber MN (1988). Pesticides in Groundwater Data Base. 1988 Interim report. US Environmental Protection Agency. Office of Pesticide Programs. Environmental Fate and Effects Division. Environmental Fate and Ground Water Branch.
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