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Pesticide Fact Sheet

Diazinon

O,O-diethyl 0-[6-methyl-2-(1-methylethyl)-4-pyrimidinyl] phosphorothioate


General

Diazinon is an organophosphate insecticide. Trade names for the chemical include, Spectracide™, Knoxout™, and Basudin™. It is used as both a household lawn and agricultural pesticide targeting cockroaches, aphids, scales, mites, ants, crickets, fleas and ticks, flies, grubs and yellow jackets, among others.

How It Works

Diazinon has a mode of action similar to other organophosphates in that molecules of the pesticide attach themselves to the enzyme acetylcholinesterase (AChE) stopping the enzyme from destroying the neutrotransmitter acetylcholine. This causes a build up of the neurotransmitter in the body causing overstimulation causing death.[1] Diazinon itself is not a strong disruptor of the nervous system, but within living organisms, diazinon is metabolized to a more potent chemical, diazoxon.[2]
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Inert Ingredients

Pesticides are regulated based on the active ingredient, in this case diazinon. However, there exist numerous so-called inert ingredients within the commercial formulation of each pesticide that can pose serious health risks to applicators and other susceptible individuals.

Although research on these ingredients is somewhat limited, the following inert products have been identified in commercial diazinon; isobutene, a depressant of the central nervous system[3]; calcium silicate, shown to increase the frequency of abnormal chromosomes and sister chromatid exchanges[4]; and silica, a known human carcinogen[5], among others.

Health Effects

Acute toxicity effects to diazinon are similar to those of other organophosphates including, headache, nausea, salivation, abnormal heart rate, flu-like symptoms, seizures, muscle twitching and cardiac arrest.[6],[7],[8],[9] Seizures are more common in children than adults experiencing acute exposure. Children are also susceptible to inflammation of the pancreas.[10]

Diazinon is a common ingredient in pet flea collars. Studies of the effects of the collar on pets (both cats and dogs) showed inhibition of AChE for the entire length of time the collar remained on the pet.[11]

Children are particularly susceptible to diazinon poisoning, and the effects of a single exposure to the pesticide can have long lasting effects. A two-month old infant developed cerebral palsy symptoms as a result of a diazinon application in her home. The symptoms lasted for as long as they remained in the home, a total of seven months.[12] One explanation for this increased sensitivity is that infants have much lower levels of the enzyme that metabolizes the compound diaoxon.

Risks to Wildlife

Diazinon is acutely toxic to birds at doses less than 10mg/kg. Particularly sensitive species are the Canada goose, house sparrow, mallard duck and red-winged blackbird. In the United States, the Enivronmental Protection Agency stated that all its past efforts to mitigate risks to birds, “are not adequate to prevent mortality.” [13]

Behavioural development in young fish is impaired by diazinon, particularly the ability to develop a sense of smell to detect predators.[14] Genetic damage has occured in fish when diazinon concentrations are 1ppb or less[15], the reproductive capability of fish is reduced at concentrations of 300ppt.[16]

Earthworms, a commonly used indicator species, are extremely sensitive to diazinon applications on turf and lawns, where approximately 60% of the population is killed with application.[17]

Re-Evaluation

The Pest Management Regulatory Agency (PMRA) announced in 2000 that it would begin phasing out all indoor uses and non-agricultural uses of diazinon.[18] This includes both homeowner use and use by pest control operators. Agricultural uses however have not been affected by this re-evaluation. Therefore, wildlife is still at risk of exposure.

Conclusions

Diazinon is a potent pesticide and exposure puts our selves, pets and children at risk of serious health problems. It is known to effect the health and fitness of fish and birds, the latter of which cannot be mitigated through any precaution taken thus far. The Canadian government has taken the first steps to phase-out diazinon, yet these steps do not protect wildlife populations. We must change regulation to protect human, wildlife and ecosystem health.


Endnotes


[1] References
Seifert, J. and T. Pewnim. 1992. Alteration of mice L-tryptophan metabolism by the organophosphorus acid trimester diazinon. Biochem. Pharmacol. 44:2243-2250.

[2] U.S. Dept. of Health and Human Services. Public Health Service. Agency for Toxic Substances and Disease Registry. 1996. Toxicological profile for diazinon. Atlanta, GA, Aug. p.82.

[3] National Library of Medicine. Toxicology and Environmental Health Information Program. Hazardous Substance Database. 2000. Isobutane. www.toxnet.hlm.nih.gov, Feb.8.

[4] Aslam, M., Fatima, N. and Rahman, Q. 1993. Cytotoxic and genotoxic effects of calcium silicates on human lymphocytes in vitro. Mut. Res. 300(1):45-48.

[5] U.S. Dept. of Health and Human Services. Public Health Service. National Toxicology Program. 2000. Ninth Report on Carcinogens. http://ehis.niehs.nih.gov/roc/toc9.html.

[6] Reigart, J.R. and J.R. Roberts. 1999. Recognition and management of pesticide poisoning. Fifth edition. Washington, D.C.:U.S. EPA. Pp. 34-38.

[7] Murray, V.S. et al. 1992. Health effects of organophosphate sheep dips. Brit Med J. 305(6861):1090

[8] Wecker, L., R. Mrak, and W.-D. Dettbarn. 1985. Evidence of necrosis in human intercostal muscle following inhalation of an organophosphate insecticide. J. Environ. Pathol. Toxicol. Oncol. 6:171-175.

[9] Halle, A. and D.D. Sloas. 1987. Percultaneous organophosphate poisoning. South. Med. J. 80:1179-1181.

[10] Weizman, Z. and S. Sofer. 1992. Acute pancreatitis in children with anticholinesterase insecticide intoxication. Pediat. 81:121-126.

[11] U.S. EPA. Office of Pesticide Programs. Health Effects. Div. 1998. Tox Oneliner: Diazinon. Washington, DC, Aug. 10. Pp. 23.

[12] Wagner, S.L. and D.L. Orwick. 1994. Chronic organophosphate exposure associated with transient hypertonia in an infant. Pediat. 94:94-97.

[13] U.S. EPA. 2000. Environmental risk assessment for diazinon. (Prelminary.) Washington, DC. www.epa.gov/pesticides/op/diazinon.htm. Released May 19 2000. Pp. 75-78.

[14] Scholz, N.L. et al. 1999. Diazinon disrupts antipredator and homing behaviours in Chinook salmon: Implications for management of endangered and threatened fish species. Socieity of Environmental Toxicology and Chemistry. SETAC 20th Annual Meeting. Philadelphia PA, Nov. 14-18. Abstract Book. P.26.

[15] Vigfusson, N.V. et al. 1983. In vivo induction of sister chromatid exchange in Umbra limi by the insecticides endrin, chlordane, diazinon and guthion. Mut. Res. 118:61-68.

[16] Moore, A. and C.P. Waring. 1996. Sublethal effects of the pesticide diazinon on olfactory functions of mature male Atlantic parr. J. Fish. Biol. 48:758-775.

[17] Potter, D.A. et al. 1990. Toxicity of pesticides to earthworms (Oligochaeta: Lumbricidae) and effect on thatch degradation in Kentucky bluegrass turf. J. Econ. Entomol. 83:2362-2369.

[18] PMRA. 2000. Update on the Re-evaluation of Diazinon in Canada. http://www.hc-sc.gc.ca/pmra-arla/english/pdf/rev/rev2000-08-e.pdf

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