DIAZINON
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. Diazinon is closely related
chemically to these chemical warfare agents developed under the Third Reich and are in the same
chemical family. 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. 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 that 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.
Persistent human effects for diazinon include hypertonicity of the extremities and altered
neurocognitive function. Significant and/or persistent effects of diazinon in experimental animals
have included abnormal sperm, alteration of the epithelial layer, alterations of L-tryptophan
metabolism, behavioral changes, ultra structural changes in skeletal muscle, alterations of the
intestinal tract which could interfere with nutrition, protein alterations which could also alter
nutritional status, depletion of glycogen (necessary for brain function) in the brain, alteration of
brain neurotransmitters even at low dose levels (effecting aspartate, glutamate, GABA and
serotonin), porphyrin disturbance, delays in development and sexual maturity, and impaired tests of
neurologic and neuromuscular function. Immune abnormalities have been reported for exposure to
organophosphates such as chlorpyrifos and other pesticides, and include immune activation and
increased autoantibodies.
Sensitization can also develop from exposure to organophosphates such as diazinon. This
sensitization is a permanent process that involves alteration in brain function and has been described
in studies of animals as a phenomenon of time-dependent sensitization whereby intermittent, but
recurring exposures induced permanent sensitization in animals with low or modest exposures
which are recurrent or intermittent. This process can also occur in humans. After that, the animal
responds with illness to much smaller levels of petrochemicals (often synthetic pharmaceuticals).
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Of 114 persons suffering from organophosphate exposure in a 1966 study, 22 developed chemical
sensitivity. A 1995 study found that 14 of 36 patients exposed to chlorphyrifos developed multiple
chemical sensitivity. The National Pesticide Telecommunication Network has collected data on
incoming calls involving pesticide overexposure and has reviewed these for the presence of
chemical sensitivity. During the years between 1984 and 1991, 158 calls indicated symptoms of
chemical sensitivity following exposure to chlorphyrifos and 148 following exposure to diazinon,
both organophosphates.
Dr. Ziem has multiple patients whose chemical injury (involving chronic brain, neurologic,
respiratory and other damage) developed following exposure to diazinon. Thus, chronic health
effects involving multiple organ systems can arise following exposure to diazinon or chlorpyrifos.
One of these effects is chemical injury, but many other serious effects occur as well as described
above.
Patients with neurologic damage and neural sensitization have brain injury with neural sensitization,
heightened sensitivity to a wide variety of petrochemicals accompanied by chronic illness involving
multiple organ systems. There is typically impairment of brain function on neurocognitive testing,
altered immune function typically involving increased activation, increased autoantibodies, and/or
impaired T, B, and/or natural killer cell function, and the condition typically develops during and
following symptomatic pesticide or other petrochemical exposure.
The following are abnormalities seen in my chemically injured organophosphate poisoned patients.
Intestinal abnormalities are common and often involve impaired immunity of the gut (impaired
secretory IgA), impaired intestinal digestive enzymes, and increased pathogens probably due to
impaired immune function. Respiratory abnormalities are also common, due to the mechanism of
neurogenic inflammation in which neurologic abnormalities initiate and perpetuate a chronic
inflammatory state of heightened sensitivity of the respiratory tract resulting in chronic sinus, nasal,
and bronchial problems, and increased asthma. The alterations of the intestinal tract as well as
chemical injury to a wide number of body organs results in excessive utilization of nutrients and
impaired function of nutrients, resulting in a wide range of nutritional deficiencies which need to be
treated.
Liver function abnormalities also occur and often involve an imbalance between the Phase I and
Phase II steps of detoxification such that the unstable molecules produced by Phase I are not able to
be rapidly detoxified by Phase II, and these unstable molecules (free radicals) attack cell
membranes, body proteins, and cause a wide range of chemical injuries. These can result in
disturbed enzyme function as well as a wide range of other disturbances.
To attribute chemical injury to a particular exposure in our practice we require that symptoms
develop during the exposure or not longer than a few days following the exposure, that symptoms
improve when removed from exposure, that symptoms recur with return to exposure, and that
symptoms again are reduced with removal from exposure. Symptoms must also be present which
are consistent with those associated with the chemical or chemical family.
In theory, chemical sensitivity can also be diagnosed or confirmed by challenge testing. At this
time, the state of the science for challenge testing of chemically sensitive patients is such that this
type of testing cannot be guaranteed to be either sensitive or safe. We do not presently have
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sufficient information to know what levels of exposure for various chemicals are adequate to cause
response in a chemically sensitive person, but not in a non-sensitive person, nor what levels are safe
and will not result persisting or long-lasting aggravation of symptoms. In our practice, we utilize a
range of laboratory tests to confirm a pattern of chemical injury and we do not diagnose multiple
chemical sensitivity without laboratory testing, which in our experience is consistent in its results
with that which we see in other chemically sensitive patients.
I have been asked to explain the difference between my medical approach and that of clinical
ecologists. I am an occupational medicine physician and have developed my practice utilizing
conventional occupational medicine approaches evaluating exposures and conducting a
comprehensive history of exposure. While clinical ecologists often take some history of exposure,
their lack of training in the areas of occupational medicine, toxicology, and industrial hygiene lead
to less comprehensive exposure histories and less skill in identifying and correcting chemical
factors. This deficiency is widespread in main-stream medicine as well. With rare exceptions, I do
not read the clinically ecology literature and, even in the rare exceptions, I do not rely on this
literature unless I have independently verified the information.
Many clinical ecologists utilize a treatment known as provocation neutralization "therapy" in which
small doses of chemicals are administered to the patient at low doses, possibly homeopathic low
doses, as an ongoing form of "treatment." My understanding of toxicology suggests that this is
toxicologic nonsense when used as ongoing therapy. Clinical ecologists as a group seem to utilize
nutritional therapies too commonly when they have not documented deficiencies of the specific
nutrients in question. While they may have clinical experience with this approach, my approach is
to first document deficiencies and treat documented deficiencies. In my experience, patients with
chemical sensitivity can differ significantly between each other in terms of which specific nutrients
are effected. Many clinical ecologists currently lack sufficient epidemiologic expertise to recognize
limitations in their research and the research of others (a critique which also applies to most
mainstream physicians).
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Stockholm, Sweden, 1975.
Thrasher, J. etal. "Immunologic abnormalities in human exposed to chlorpyrifos: preliminary observations," Archives of
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Sherman, J. Toxicology and Industrial Health 11:33-39, 1995.
Sorg, B. etal. "Neuroanatomy and neurochemical mechanisms of time-dependent sensitization," Toxicology and
Industrial Health 10:369-386, 1994.
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Broughton, A. etal. "Chronic health effects and immunologic alterations associated with exposure to pesticides,"
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Veterinary and Human
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