![]() For those males exposed to OP pesticides, poor semen and sperm quality have been seen, including reduced seminal volume and percentage motility, as well as a decrease in sperm count per ejaculate. ![]() Most of the research on reproductive effects has been conducted on farmers working with pesticides and insecticides in rural areas. The onset and severity of symptoms, whether acute or chronic, depends upon the specific chemical, the route of exposure (skin, lungs, or GI tract), the dose, and the individuals ability to degrade the compound, which the PON1 enzyme level will affect.Ĭertain reproductive effects in fertility, growth, and development for males and females have been linked specifically to OP pesticide exposure. The effects of organophosphate poisoning on muscarinic receptors are recalled using the mnemonic SLUDGEM ( salivation, lacrimation, urination, defecation, gastrointestinal motility, emesis, miosis) An additional mnemonic is MUDDLES: miosis, urination, diarrhea, diaphoresis, lacrimation, excitation, and salivation. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur. Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. Other symptoms include hypertension, and hypoglycemia. The symptoms of organophosphate poisoning include muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis. Organophosphate poisoning has been reported at least since 1962. Around 15% of people who are poisoned die as a result. There are nearly 3 million poisonings per year resulting in two hundred thousand deaths. OPs are one of the most common causes of poisoning worldwide. While there is a theoretical risk of health care workers taking care of a poisoned person becoming poisoned themselves, the degree of risk appears to be very small. Attempts to decontaminate the stomach, with activated charcoal or other means, have not been shown to be useful. General measures such as oxygen and intravenous fluids are also recommended. In those who have organophosphate poisoning the primary treatments are atropine, oximes such as pralidoxime, and diazepam. Among those who work with pesticides the use of protective clothing and showering before going home is also useful. Prevention efforts include banning very toxic types of organophosphates. Carbamate poisoning can present similarly. ![]() Diagnosis is typically based on the symptoms and can be confirmed by measuring butyrylcholinesterase activity in the blood. The underlying mechanism involves the inhibition of acetylcholinesterase (AChE), leading to the buildup of acetylcholine (ACh) in the body. Exposure can be from drinking, breathing in the vapors, or skin exposure. Organophosphate poisoning occurs most commonly as a suicide attempt in farming areas of the developing world and less commonly by accident. While onset of symptoms is often within minutes to hours, some symptoms can take weeks to appear. Symptoms include increased saliva and tear production, diarrhea, vomiting, small pupils, sweating, muscle tremors, and confusion. Organophosphates are used as insecticides, medications, and nerve agents. Organophosphate poisoning is poisoning due to organophosphates (OPs). Increased saliva, diarrhea, small pupils, muscle tremors, confusionīased on symptoms and confirmed by butyrylcholinesterase Organophosphate toxicity, organophosphate overdose, organophosphate intoxication Medical condition Organophosphate poisoning
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