Product Code Database
Diazinon (IUPAC name: O, O-Diethyl O-4-methyl-6-(propan-2-yl)pyrimidin-2-yl phosphorothioate, INN - Dimpylate), a colorless to dark brown liquid, is a thiophosphoric acid ester developed in 1952 by Ciba-Geigy, a Swiss chemical company (later Novartis and then Syngenta). It is a nonsystemic organophosphate insecticide formerly used to control , silverfish, , and in residential, non-food buildings. Diazinon was heavily used during the 1970s and early 1980s for general-purpose gardening use and indoor pest control. A bait form was used to control scavenger in the western U.S. Diazinon is used in flea collars for domestic pets in Australia and New Zealand. Diazinon is a major component in the "Golden Fleece" brand sheep dip. Residential uses of diazinon were outlawed in the U.S. in 2004 because of human health risks but it is still approved for agricultural uses. An emergency antidote is atropine.
Specific Health Risks: Routes of contact for diazinon include breathing it, consuming it, or contact with skin. The negative health effects when in contact with diazinon includes eye watering, drool or runny nose, not having any appetite, throwing up, intense coughing, abdominal pain, or even stiffness in various muscles/paralysis. Headaches can also be health risks. Some other physiological effects include pinpoint pupils, increased heart rate, seizures, or even coma. Larger exposure to diazinon is known to yield these risks. If it is a smaller exposure, the symptoms may be reduced such as just a runny nose or some eye watering. While diazinon has many different health risks, the US Agency for Toxic Substances and Disease Registry has not categorized it as a carcinogen.
However, as the decades following the award passed, DDT was found to be such an environmental danger that developed countries and eventually world-level organizations banned the insecticide for all purposes except for combating disease-vector insects, leading Ciba-Geigy to research alternatives.
Diazinon became available for mass use in 1955, while DDT production tapered. Before 1970, diazinon had issues with Impurity in its solution; but by the 1970s, alternative purification methods were used to reduce the residual, unwanted materials.
After this processing improvement, diazinon became an all-purpose, indoor-and-outdoor, commercial pest control product. In 2004, the US outlawed residential use of diazinon when the EPA determined that its ability to damage the nervous system posed a risk to human health (especially the health of children). The chemical is still used for industrial agricultural purposes.
When diazinon enters the body, it is oxidatively decomposed to diazoxon, an organophosphate compound that is much more poisonous than diazinon; it mainly causes the inhibition of AChE. The conversion of diazinon to diazoxon (Reaction 1) is performed by the liver Microsome enzyme system and requires O2 and NADPH. Diazinon can also be decomposed via oxidation in the liver (Reaction 2). Both reactions are possible, and likely are catalyzed nonspecifically by the same mixed function oxidase. Diazoxon is further broken down by in the microsomal and other subcellular functions within the liver (Reaction 3). Mammals metabolize diazoxon with a half-life of 2 to 6 weeks. Insects lack this hydrolysis step, which allows the toxic substance to accumulate rapidly; the detoxification of diazoxon is processed through the microsomal mixed function oxidase system. Although not fully understood, it is believed that this is the cause for the selectivity of diazinon against insects. After the hydrolysis or oxidation diazinon is broken down further (Reaction 4).
Banning of Diazinon
In the United States, President Clinton signed a tougher pesticide law in 1996. Diazinon was banned from use as an agricultural insecticide. At the time 80% of people in the United States could find Diazinon in their residential products. Despite the ban, it still may be in use in certain households, as it is still used and considered legal in 14 states, including California. Yet with the ban starting in 2004, having had 20 years pass, states which have accepted that ban have had hardware stores and other suppliers report that they have "ran out" of products with diazinon. These states which continue to use Diazinon is their products consider its risks low, yet its greatest effect is through inhalation and skin contact. Certain environmental groups continue to protest these states which still continue its use.
|
On the other hand, in regard to chronic toxicity, the WHO/FAO joint committee on pesticide residues gives the admissible daily intake (ADI) to be 0.005 mg/kg of body weight, while the Australian Pesticides and Veterinary Medicine authority gives the no-observed-adverse-effect-level (NOAEL) to be 0.02 mg/kg of body weight for adults.
Typically treatments will vary depending on exposure and method of administration of the toxin. Critical biomarkers such as urine samples, blood content and heart rates are measured while detoxifying the patient. Common treatments for patients with diazinon poisoning include:
Patients that continue to improve over the first 4 to 6 hours (after medical treatment) usually recover unscathed. Prolonged treatment often is needed to reverse the poisoning, including intensive care hospitalization and long-term therapy. Some toxicity may persist for weeks or months, or even longer.
Symptoms of acute diazinon exposure develop in minutes to hours following exposure, depending on the exposure pathway. The initial symptoms of humans are nausea, dizziness, salivation, headache, sweating, lacrimation, and rhinorrhea. The symptoms can progress to vomiting, abdominal cramps, diarrhea, muscle twitching, weakness, tremor, a lack of coordination and miosis. Furthermore, some studies have even reported some psychiatric side effects including memory loss, confusion, and depression.
Because diazinon is fat soluble, there is potential for delayed toxicity if significant amounts of diazinon are stored in fatty tissues. Intermediate syndrome generally occurs within 24–96 hours after exposure. Intermediate syndrome in humans is characterized by difficulty breathing and muscular weakness, often in the face, neck and proximal limb muscles. Cranial nerve palsies and depressed tendon reflexes have also been reported.
Studies have suggested that exposure to some organophosphate pesticides can result in long-term neurological problems including organophosphate-induced delayed neuropathy (weakness or paralysis as well as paresthesia in the extremities); however, reports of these symptoms following diazinon exposures are rare. Human who have been poisoned show increased levels of serum amylase and glucose as well as elevated urinary diastase levels accompanied by symptoms considered to be indicative of acute pancreatitis.
A study found that 10% of 21 typically developing show 2-isopropyl-6-methyl-4-pyrimidinol (IMPy, a metabolite of diazinon) in molars. Molars from the two oldest subjects contained the largest concentrations of IMPy. And this concentration in molars may be a biomarker of perinatal exposure and during molar formation.
|
|
