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Malathion - Background


Malathion Backgrounder  

(O,O-Dimethyl S- 1,2-(diethoxycarbamyl) ethyl phosphorodithioate)

General

Malathion is an organophosphate insecticide. The chemical structure of Malathion places it in the phosphorothionothiolate family, a subclass of organophosphates.[1] Malathion is one of the most commonly used organophosphates and has an wide range of uses including agriculture, stored grain and forests. The acute LD50 of Malathion ranges between 1522mg and 1945mg/kg of body weight. To apply that to humans, a dose of 5 oz. would be fatal to a chemically sensitive human of 70kg.

All organophosphates, including Malathion, are highly toxic to insects, animals and humans. Malathion works by attacking the nervous system, in laymen’s terms it is quite simply a nerve poison. It inhibits the action of a particular enzyme called acetylcholinesterase (AChE).[2] Acetylcholinesterase works to break down another chemical, acetylcholine, which is essential in communicating nerve impulses between nerves. When Malathion is used acetylcholine functions without AChE, causing incoordination, rapid twitching, incoordination, paralysis and death[3][4]. As the Malathion reacts in the organism or with its environment it creates other by-products such as Malaxon which is 40 times more toxic than Malathion.[5] Malaxon is a by-product formed by the oxidation of Malathion either in the body of the host organism or in sunlight.

Health Risks

Malathion is mutagenic, carcinogenic[6], has been implicated in vision loss, kidney damage[7], lung damage[8] shown to cause DNA abnormalities[9][10], and has been linked to child leukemia, aplastic anemia and adult leukopenia.[11] The acute (short term) effects of Malathion include headaches, nausea, dizziness, salivation, tearing, urination, diarrhea, convulsions, muscle weakness, incoordination, abdominal cramps, blurred vision, pupil constriction, abnormal eye movement, slowed heart beat, depressed respiratory system, skeletal muscle damage, paralysis and coma.[12][13][14] Quail and rabbit studies have indicated that the acute risk of Malathion exposure may be much higher if inhaled. Studies have shown that inhaled Malathion caused the inhibition of AChE equivalent to an oral dose 15 to 20 times greater.[15]

Pregnant woman who had been exposed to aerial spraying of Malathion during the second trimester of pregnancy gave birth to children with 2.5 times more gastrointestinal disorders.[16] Lab studies using rats has shown that a single exposure can severely impair the healthy functioning of the intentine.[17]

Risks to Wildlife

Malathion is an indiscriminate pesticide which kills a wide range of non-target species. It is extremely toxic to bees.[18] Malathion is of moderate toxicity to a variety of bird species and ranges from moderate to high toxicity to water organisms including fish.[19] Malathion can move through soil thus it can contaminate ground water.[20] The risk of Malathion contaminating groundwater is reduced due to its somewhat short half-life although it has been detected in groundwater. Malathion does not routinely biococentrate but some aquatic species have showed biococentration.[21]

Effectiveness

The effectiveness of Malathion decreases over time as mosquitoes build up resistance to the chemical. In the case of ultralow volume spraying by mist blowers, hydrqulic sprayers and adulticiding by aircraft, only about one drop in 1000 hit the target organism, in this case, the mosquito. It take three drops to kill a mosquito. Which means that in practical terms virtually all of the pesticide is ending up on non-target species.

Conclusions

When considering community mosquito control programs, even for West Nile Virus, Malathion is a very bad idea. It has been linked to a wide range of cancers, health risks and birth defects as well as effects to non-target species such as wildlife. The great irony is that it isn’t very effective. If communities are looking for ways to reduce mosquito numbers, the first line of defence needs to be prevention. If in an extreme case prevention is not effective larviciding with Bt is far more effective and far less harmful than Malathion.

 References

[1] Chamber, H.W. Organophosphorus Compounds: An Overview. Organophophates: Chemistry, Fate, and Effects; Chambers, J.E., Levi, P.E., Eds.: Academic: San Diego, CA, 1992; pp 3-17.

[2] US Environmental Protection Agency, Office of Pesticide Programs, Washington, DC. Malathion Preliminary Risk Assessments: Health Effects. http://www.epa.gov/pesticides/op/malathion.htm

[3] Tucker, J.W. and C.Q. Thompson. 1987. Dangers of using organophosphotus pesticides and diesel oil in fish ponds. Aquaculture Magazine 13 (3): 62-63.

[4] Gallo, M.A. ; Lawryk, N.J. Organic Phosphorus Residues. Handbook of Pesticide Toxicology; Hayes, W.J., Laws, E.R., Eds.; Academic: San Diego, CA; 1991; Vol. 2, pp 917-1123.

[5] Borwn, M.A. ; Petreas, M.X. ; Okamoto, H.S. ; Mischeke, T.M. ; Stephens, R.D. Monitoring of Malathion and its Impurities and Environmental Transformation Prodcuts on Surfaces and in Air Following Aerial Application. Environmental Science Technology. 1993, 27, 388-397.

[6] Cantor, K.P. et al. 1992. Pesticides and other risk factors for non-Hodgkin’s lymphoma among men in Iowa and Minnesota. Cancer Research. 52: 2447-2455.

[7] Albright, R.K., Kram, Barry W., White, Robert P.. 1983. Kidney Failure after man sprays Malathion in home. Journal of the American Association. 250 (18), Nov. 11, 1983.

[8] “Lung damage occurs from single oral dose of Malthion”. Division of Toxicology & Physiology, University of California. Toxicology. 26: 73-79, 1983.

[9] “Human genes ‘broken-off’ DNA molecule by Malathion”. Genetics Laboratory, University of Vermont. Cancer Research 56, 2393-2399, May 15, 1996.

[10] Balaji, M. & Sasikala, K. 1993. Chromosome damage occurs to human blood cells, Mutation Research , 301: 13-17.

[11] Reeves, Jerry D., Driggers, David A., Kiley, Vincent A.. 1981. Child leukemia and aplastic anemia after Malathion exposure. The Lancet. August 8, 1991.

[12] Rosembaum, E.A. et al. 1988. Early biochemical changes produced by Malathion in toad embryos. Archive Environmental Contamination Toxicology. 17: 831-835.

[13] Cabellero de Castro, A.C. et al. 1991. Effect of malathion on Bufo arenarum Hansel development. Biochemistry Pharmocology. 41 (4): 491-495.

[14] Abdel_Reheem, S., M.H. Belal, and G. Gupta. 1991. Photosynthesis inhibition of soybean leaves by insecticides. Environmental Pollution. 74:245-250.

[15] Weeks, M.H. et al. 1977. Preliminary assessment of the acute toxicology of malathion in animals. Archive Environmental Contamination Toxicology. 5:23-31.

[16] "Intestinal Disorders in Children Born After California Spraying." Department of Preventive Medicine, University of Southern California. Epidemiology 3(1):32-39, 1992.

[17] Wali, R.K., Singh, R., Dudeja, P.K., Sarkar, A.K. & Mahmood. 1984. Intestinal Problems in Test Animals Exposed to Malathion. Bulletin of Environmental Contamination Toxicology 33: 289-294.

[18] US Environmental Protection Agency, Office of Pesticide Programs, Washington, DC. Malathion Preliminary Risk Assessments: Environmental Fate and Effects. http://www.epa.gov/pesticides/op/malathion.htm.

[19] US Environmental Protection Agency, Office of Pesticide Programs, Washington, DC. Malathion Preliminary Risk Assessments: Environmental Fate and Effects. http://www.epa.gov/pesticides/op/malathion.htm.

[20] US Environmental Protection Agency, Office of Pesticide Programs, Washington, DC. Malathion Preliminary Risk Assessments: Environmental Fate and Effects. http://www.epa.gov/pesticides/op/malathion.htm.

[21] US Environmental Protection Agency, Office of Pesticide Programs, Washington, DC. Malathion Preliminary Risk Assessments: Environmental Fate and Effects. http://www.epa.gov/pesticides/op/malathion.htm.

 

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