[4] Symptoms include increased saliva and tear production, diarrhea, vomiting, small pupils, sweating, muscle tremors, and confusion.

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.

[12] 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.

Certain reproductive effects in fertility, growth, and development for males and females have been linked specifically to OP pesticide exposure.

In females menstrual cycle disturbances, longer pregnancies, spontaneous abortions, stillbirths, and some developmental effects in offspring have been linked to OP pesticide exposure.

Some of these effects include delayed mental development, Pervasive developmental disorder (PDD),[9] morphological abnormalities in the cerebral surface.

Cholinergic syndrome occurs in acute poisonings with OP pesticides and is directly related to levels of AChE activity.

For people affected by cholinergic syndrome, atropine sulfate combined with an oxime is used to combat the effects of the acute OP poisoning.

[16] Evidence of exposure to OP pesticides during gestation and early postnatal period have been linked to neurodevelopmental effects in animals, specifically rats.

OPs affect the cholinergic system of fetuses, so exposure to chlorpyrifos during critical periods of brain development potentially could cause cellular, synaptic, and neurobehavioral abnormalities in animals.

Organophosphates as whole have been linked to decreases in the length of limbs, head circumference, and slower rates of postnatal weight gain in mice.

The U.S. Environmental Protection Agency maintains an extensive list of commercially-sold organophosphate products for anyone worried about possible exposure.

[23] Exposure to any of the above-listed organophosphates may occur through inhalation, skin absorption, and ingestion, most commonly of food that has been treated with an OP herbicide or insecticide.

[24] The health effects associated with organophosphate poisoning are a result of excess acetylcholine (ACh) present at different nerve synapses and neuromuscular junctions across the body.

PON1 hydrolyzes the active metabolites in several OP insecticides such as chlorpyrifos oxon, and diazoxon, as well as nerve agents such as soman, sarin, and VX.

Animal experiments indicate that while PON1 plays a significant role in regulating the toxicity of OPs its degree of protection given depends on the compound (i.e. Chlorpyrifos oxon or diazoxon).

[27][29] However, for fast initial screening, determining AChE and BuChE activity in the blood are the most widely used procedures for confirming a diagnosis of OP poisoning.

Atropine can be used as an antidote in conjunction with pralidoxime or other pyridinium oximes (such as trimedoxime or obidoxime),[33][34] though the use of "-oximes" has been found to be of no benefit, or to be possibly harmful, in at least two meta-analyses.

HuBChe can offer a broad range of protection for nerve agents including soman, sarin, tabun, and VX.

[38] Currently there is potential for PON1 to be used to treat sarin exposure, but recombinant PON1 variants would need to first be generated to increase its catalytic efficiency.

Class III anti-arrhythmic agents block the potassium membrane currents in cardiac cells, which makes them a candidate for become a therapeutic of OP poisoning.

[42] A striking example of OPIDN occurred during the 1930s Prohibition Era when thousands of men in the American South and Midwest developed arm and leg weakness and pain after drinking a "medicinal" alcohol substitute.

[43][44] Research has linked the neurological abnormalities found in Persian Gulf War veterans who have chronic multisymptom illnesses to exposure to wartime combinations of organophosphate chemical nerve agents.

During the war veterans were exposed to combinations of organophosphate pesticides and nerve agents, which produced symptoms associated with chronic organophosphate-induced delayed polyneuropathy (OPIDP) syndrome.

No pesticide can be sold in the United States before the EPA has reviewed the manufacturer's application for registration and determined that the use of the product will not present an unreasonable risk to the public or the environment.

[49] In 1996, with the passage of the Food Quality Protection Act, Congress required the EPA to reassess all existing pesticide tolerances with specific consideration for children.

A group of leading EPA scientists sent a letter to the chief administrator, Stephen Johnson, decrying the lack of developmental neurotoxicity data in the review process.

EPA Letter EHP article New studies have shown toxicity to developing organisms during certain "critical periods" at doses much lower than those previously suspected to cause harm.

On February 8, 2013, the EPA requested comment on a preliminary evaluation of the potential risks to children and other bystanders from volatilization of chlorpyrifos from treated crops[55] Some populations are more vulnerable to pesticide poisoning.

"[6] This, coupled with the difficulty or uncertainty of recognizing and/or diagnosing chronic pesticide poisoning by the medical community,[58] makes it difficult for exposed workers to receive an effective remedy.