Malathion Website

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MALATHION
Malathion belongs to the organophosphate family of chemicals that were originally developed as
nerve gas agents under the Nazi Third Reich. These agents are all toxic to the brain through
similar mechanisms of damage, although some at lower exposures than others.1 This chemical
class has been the cause of more toxic encephalopathy in the medical practice of Dr. Ziem than
any other single chemical class. Exposure to organophosphates has been recognized as capable
of inducing heightened sensitivity to chemicals for a quarter of a century2 and Malathion is the
fourth most common pesticide reported to the US EPA as associated with the onset of chemical
sensitivity.3 The first two most common agents are also organophosphates.3 Malathion by
products stored in the body inhibit prompt breakdown of malathion, increasing its toxicity.1
Permanent nerve damage can occur, with muscle, auditory and vestibular dysfunction, weakness
and easy fatigability.4 Vestibular dysfunction can impair balance and gait. Chronic brain damage
can result from organophosphate exposure.5,6,7 Organophosphates can also impair function of the
immune action of white blood cells, increasing recurrent infection rates of the upper and lower
respiratory system,5 and have other damaging immune effects.8 Malathion exposure is associated
with damage to multiple body organs, especially the brain and nervous system.9 Demyelination
(damage to nerve cell coating which impairs normal nerve function) of nerve cells can also
occur.10 Chronic neuropathy with weakness and other abnormalities of arms, legs, balance, gait,
etc. can also occur with organophosphate exposure.11 Prolonged persistent weakness, headaches,
respiratory, gastrointestinal, visual and other systemic changes as well as other Malathion effects
are substantially the same as for Chlorpyrifos, another oranophosphate. Organophosphates were
first developed in Germany during World War II by the I.G. Farben Company, which developed
them as nerve gas agents in warfare. Chlorpyrifos is closely related chemically to these chemical
warfare agents developed under the Third Reich and are in the same chemical family.
The first report of chemical sensitivity associated with organophosphate exposure was in 1966,
fairly soon after chlorpyrifos was introduced to the market. A review of 114 cases three years
after exposure showed chemical sensitivity present in 22 or 19%. An additional 18 or 16%
developed other persistent chronic health problems following exposure to organophosphate
including seven with persistent headaches, six with visual disturbances, and five with increased
nervousness. Because Tabershaw and Cooper, the authors of this study, were frequent
consultants to industry and widely published, and this article appeared in the mostly widely read
occupational journal of its day, industry should have been aware of this work (Tabershaw, I.R.
and Cooper, W.C. "Sequelae of acute organic phosphate pesticide poisoning." Journal of
Occupational Medicine 8:5-20, 1966).
Organophosphates interfere with the function of the nervous system by interfering with nerve
transmitters, including muscarinic, nicotine, and brain nerve transmitters. Muscarinic nerve
receptors, which are located in organs such as the heart, endocrine glands, blood vessels, and
other smooth muscle organs have altered function resulting in symptoms such as wheezing,
nausea, abdominal cramps, visual disturbance, and even vomiting.
Nicotinic nerve receptors are located in the nerves of skeletal muscles and the ganglia of the
autonomic nervous system and interference with their function causes symptoms such as muscle
twitching and cramping, fatigue, weakness, rapid or irregular heart rate, and changes in blood
pressure. Delayed effects can occur as well following acute or repeated chronic exposures.
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These can involve the peripheral nerves resulting in impaired balance and increased weakness.
The nerves controlling the intestinal and urinary tract can be interfered with causing reduced
control of bladder and bowel function.
Neurotransmitters in the brain can also be affected by organophosphate compounds resulting in
symptoms such as confusion, tremors, poor coordination, sleep disturbance, weakness, anxiety,
impaired coordination, mood alterations, etc. Persistent neurobehavioral alterations in brain
function can also result. There are also reports in the literature for both humans and animals of
disturbances of porphyrin metabolism which can be persistent following exposure to
organophosphates. Other changes with organophosphates includes increased susceptibility to
infectious diseases, possibly because of disturbances of immune function, impaired liver
function, loss of vigor and acceleration of the aging process as well as loss or decline in potency
and libido. Both chlorpyrifos and diazinon have been associated with alterations in brain
function in humans consistent with the general description for organophosphates above.
References:
Sherman, J. "Chlorpyrifos (Dursban)-associated birth defects: a proposed syndrome, report of four cases, and
discussion of the toxicology." Int J Ac Med Tox, 4:417-31, 1995.
Sherman, J. "Organophosphate pesticides/neurological and respiratory toxicity," Toxicology and Industrial Health
11:33-39, 1995.
Miller, C.S. and Mitzel, H.C. "Chemical sensitivity attributed to pesticide exposures vs remodeling," Archives of
Environmental Health 50:119-129, 1995.
Rosenthal, N.E. and Cameron, C.L. "Exaggerated sensitivity to an organophosphate pesticide," Amer J Psychiatry
148:1416, 1991.
The United Stated Environmental Protection Agency, Chlorpyrifos Science Chapters, June 1989. U.S. EPA
Document: 0002-EPAO-89-006.
California Morbidity Weekly Report, April 11, 1980.
Pattern, B. Journal of Allergy and Clinical Immunology, 1977. No. 597-603, 1986.
Broughton, A. Chronic health effects and immunologic alternations associated with pesticides. Toxicology, 4:5971, 1990.
Anderson, D. Environmental Science and Technology, 22:717-720, 1988.
Lotti, M. Inhibition of lymphocytic neuropathy target esterase predicts the development of organophosphateinduced delayed polyneuropathy. Archives of Toxicology, 59:176-179, 1986.
Amer, S. Cytogenetic effects of pesticides: I induction of micronuclei in mouth bone marrow by the insecticide
Dursban. Mutation Research, 101:247-255, 1982.
Berteau, P. Insecticide absorption from indoors surfaces. Biological Monitoring for Pesticide Exposure, American
Chemical Society, Washington, DC, Chapter 24, 1987.
Vaccaro, J. Risks associated with exposure to chlorpyrifos and chlorpyrifos formulation components. Chapter 25.
Pesticides in Urban Environments: Fate and Significance, American Chemical Society, 1993.
Aiuto, L. Life-threatening organophosphate-induced delayed polyneuropathy in a child after accidental chlorpyrifos
ingestion. Journal of Pediatrics, 22:658-660, 1993.
O'Brien, M. Chlorpyrifos. Journal of Pesticide Reform, 8:42-44, 1989.
Poisoning our Homes: Exposure to Pesticides Through Indoor Pest Extermination in Texas, Texas Center for Rural
Studies, Austin, Texas, 1987.
Stalberg, E. Effect of occupational exposure to organophosphorus insecticides on neuromuscular function.
Scandinavian Journal of Work Environment and Health, 4:255-261, 1978.
Rosenstock, L. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Lancet,
338:223-227, 1991.
Savage, B. Chronic neurological sequelae of an acute organophosphate pesticide poisoning. Archives of
Environmental Health, 43:38-45, 1988.
Senanayake, N. Neurotoxic effects of organophosphorus insecticides: intermediate syndrome. New England Journal
of Medicine, 316:761-763, 1987.
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Additional References:
1
Recognition and Management of Pesticide Poisonings, US Environmental Protection Agency, Fifth Edition, 1999.
Tabershaw, I.R., Cooper, W.C. "Sequelae of acute organic phosphate pesticide poisoning." Journal of
Occupational Medicine, 8:5-20, 1966.
3
Active Ingredients Mentioned in Calls to the National Pesticide Telecommunication Network Indicating Possible
Chemical.
4
D.J. Ecobichon and R.M. Joy, Editors, Pesticides and Neurologic Diseases, CRC Press, 1982.
5
L. Rosenstock etal., “Chronic central nervous system effects of acute organophosphates pesticide intoxication”,
Lancet 338:223-227, 1991.
6
F.H. Duffy etal, “Long term effects of an organophosphate upon the human electroencephalogram”, Toxicol and
Applied Pharm 47:161-176, 1979.
7
R. Repetto and S. Baliga, Pesticides and the Immune System, World Resources Institute, March 1996.
8
A. Broughton, “Chronic health effects and immunologic alterations associated with exposure to pesticides”
Comments Toxicol 1:59-71, 1990.
9
Criteria for a Recommended Standard: Malathion, NIOSH, DHEW, June 1976.
10
Neurotoxicity of Industrial and Commercial Chemicals, edited by Dr. J.L. O’Donoghue, CRC Press, 1985.
11
Neurotoxins in Clinical Practice, edited by Dr. C.G. Goetz, Medical and Scientific Books, Division of Spectrum
Publications, NY. 1985.
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