Bromoxynil
(endorsed 2011)
Guideline
Based on human health concerns, bromoxynil in drinking water should not exceed 0.01 mg/L.
Related chemicals
Bromoxynil (CAS 1689-84-5) is in the hydroxybenzonitrile class of chemicals. There are no other pesticides in this class (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, bromoxynil would not be a health concern unless the concentration exceeded 0.01 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: Bromoxynil is a post-emergent herbicide used to control broad-leaf weeds.
There are registered products containing bromoxynil in Australia. These products are intended for professional and home garden use and are applied by aircraft or boom spray by professional use, and by hand-held spray in the home garden. Data on currently registered products are available from the Australian Pesticides and Veterinary Medicines Authority.
Exposure sources: The main sources of public exposure to bromoxynil are use in the home garden and residues in food. Residue levels in food produced according to good agricultural practice are generally low.
Agricultural use of bromoxynil may potentially lead to the contamination of source waters through processes such as run-off, spray drift or entry into groundwater.
Typical values in Australian drinking water
No reports of bromoxynil in Australian drinking waters have been identified.
Treatment of drinking water
Current literature suggests that bromoxynil can be effectively removed by oxidation with ultraviolet (UV) radiation, UV and ultraviolet peroxide, chlorine and UV, ozonation, and by chlorination, with various levels of success depending on the water quality conditions (Guittonneau et al. 2005). Ozonation is considered the most effective, with chlorination the least effective (Guittonneau et al. 2005). Jar testing to identify the effectiveness of various oxidants in specific waters is recommended if bromoxynil is detected. Oxidation of any kind will result in the formation of by-products and therefore a by-product management plan is also recommended.
Photodegradation has shown to provide some removal of bromoxynil (Texier et al. 1998); however more research is required to determine the optimal conditions. Activated carbon has also been shown to remove bromoxynil effectively from water, but is dependant on the water quality and the application methods of the carbon (Yang et al. 2004).
Measurement
The practical limit of quantification for bromoxynil in water is 0.001 mg/L, using liquid chromatography–tandem mass spectrometry (Alder et al. 2006).
History of the health values
The current acceptable daily intake (ADI) for bromoxynil is 0.003 mg per kg of bodyweight (mg/kg bw), based on a no-observed-effect level (NOEL) of 0.3 mg/kg bw/day from a 12-month dietary study in dogs. The ADI incorporates a safety factor of 100 and was established in 1993.
The previous health value was 0.03 mg/L (NHMRC and NRMMC 2004)
Health considerations
Metabolism: Bromoxynil is readily absorbed via the gastrointestinal tract and widely distributed in the body in mammals. Virtually all absorbed bromoxynil is eliminated unchanged. It is slowly excreted mainly via the faeces, with some excretion in urine. Bromoxynil has a low potential for bioaccumulation.
Acute effects: Bromoxynil has a moderate acute oral toxicity and low dermal toxicity. There is no evidence of skin sensitisation.
Short-term effects: In medium-term dietary studies in dogs, there was decreased bodyweight gain, increased blood urea nitrogen, and kidney and liver weight changes at a dose of 12 mg/kg bw/day.
Long-term effects: Long-term dietary studies were conducted in rats and dogs. A 2-year rat study reported decreased bodyweight gain at 8.2 mg/kg bw/day and evidence of adverse effects in the liver, kidney and stomach at 26 mg/kg bw/day. A 1-year dog study reported reduced bodyweight gain at 1.5 mg/kg bw/day and evidence of anaemia at 7.5 mg/kg bw/day. The NOEL of 0.3 mg/kg bw/day in dogs is the basis of the ADI.
Carcinogenicity: Benign liver tumours were slightly increased in mice at 1.5 mg/kg bw/day and above, but these tumours were considered to be specific to mice and not of human relevance. Based on this and a 2-year study in rats, bromoxynil is not considered to have carcinogenic potential in humans.
Genotoxicity: Bromoxynil is not considered to be genotoxic, based on in vitro and in vivo short-term studies.
Reproductive and developmental effects: A reproduction study in rats and developmental studies in rats and rabbits did not produce any evidence of effects on reproductive parameters or on foetal development.
Poisons Schedule: Bromoxynil 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 0.01 mg/L for bromoxynil was determined as follows:
Where:
0.3 mg/kg bw/day is the NOEL based on a long-term (1-year) dietary 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 a 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.
Alder L, Greulich K, Kempe G, Vieth B (2006). Residue analysis of 500 high priority pesticides: better by GC-MS or LC-MS/MS? Mass Spectrometry Reviews, 25(6):838-65.
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.
Guittonneau S, Momege S, Schafmeier A, Viac P, Meallier P (2005). Dehalogenation of the herbicides bromoxynil (3,5-dibromo-4- hydroxybenzonitrile) and ioxynil (3,5-diiodino-4-hydroxybenzonitrile) by Desulfitobacterium chlororespirans. Applied and Environmental Microbiology, 71, 7, 3741-3746.
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.
Texier I, Giannotti C, Malato S, Richter C, Delaire J (1998). Solar photodegradation of pesticides water by sodium decatungstate. In: Proceedings of the 1998 9th SolarPaces International Symposium on Solar Thermal Concentrating Technologies. Editions de Physique Font-Romeu.
Tomlin CD (ed) (2006). The Pesticide Manual: a world compendium, 14th Edition, British Crop Production Council, UK.
Yang Y, Chun Y, Shang G, Huang M (2004). pH-dependence of pesticide adsorption by wheat-residue-derived black carbon. Langmuir, 20(16):6736-6741.
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