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Health effects of pesticides may be acute or delayed in those who are exposed. [1] Acute effects can include pesticide poisoning, which may be a medical emergency. [2] Strong evidence exists for other, long-term negative health outcomes from pesticide exposure including birth defects, fetal death, [3] neurodevelopmental disorder, [4] cancer, and neurologic illness including Parkinson's disease ...
Small pesticide exposures have been shown to have an impact on young children's neurological and behavioral development. [47] Researchers have studied the effects of pesticides on children as opposed to adults, finding children's immature organs and bodies are more susceptible to health effects. [47]
Pesticides tracked into the home from family members increase the risk of exposure. Toxic residue in food may contribute to a child's exposure. [98] Epidemiological studies have reported adverse effects of certain pesticides at current levels of exposure on children's cognitive development. [99] The chemicals can bioaccumulate in the body over ...
Phytotoxicity describes any adverse effects on plant growth, physiology, or metabolism caused by a chemical substance, such as high levels of fertilizers, herbicides, heavy metals, or nanoparticles. [1] General phytotoxic effects include altered plant metabolism, growth inhibition, or plant death. [2]
Most cases of carbamate poisoning are due to exposure to pesticide products containing the chemical. The most common carbamate chemicals in use are captan, ferbam, carbofuran, carbaryl, and aldicarb. Suicidal and homicidal poisonings also occur, but are rare, due to the lower lethality of carbamates in humans compared to other toxic substances. [5]
After ingestion, toxic features usually develop within a few minutes. The major lethal consequence of aluminium phosphide ingestion is profound circulatory collapse, and is reportedly secondary to these toxins generated, which lead due to direct effects on cardiomyocytes, [3] fluid loss, and adrenal gland damage. [4]
In humans, cypermethrin is deactivated by enzymatic hydrolysis to several carboxylic acid metabolites, which are eliminated in the urine. Worker exposure to the chemical can be monitored by measurement of the urinary metabolites, while severe overdosage may be confirmed by quantitation of cypermethrin in blood or plasma.
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