[5] When an organism is exposed to ethoprophos either via the oral, dermal or inhalation routes, it primarily inhibits carboxyl ester hydrolases, specifically acetylcholinesterase (AChE).

[7] In cases of exposure to ethoprophos, symptoms may include vomiting, nausea, diarrhea, miosis, abdominal cramps, dyspnoea, muscular weakness, bronchial hypersecretion, anxiety, confusion and convulsions.

[1] Additionally, ethoprophos is thought to be likely carcinogenic due to the occurrence of different types of tumors in rats after exposure to the compound.

[1] In tested animals, ethoprophos is widely distributed throughout the body, with the highest concentrations in the lungs, kidneys, and liver.

Short-term toxicity effects in rabbits and mice, exposed through different routes include inhibition of erythrocyte and brain cholinesterase.

[1] Acute toxicity studies on rats, in turn have resulted in more effects being observed, namely narcotic, cholinergic and respiratory.

[1] On the other hand, a long-term exposure experiment conducted on dogs found that the toxin led to mild liver toxicity.

On the other hand, offspring toxicity led to a decrease in body weight gain and rise in postnatal mortality.

[1] Finally, a study showed that ethoprophos, along with 4 other active substances, was responsible for 40% of the utilized pesticides in Costa Rica, yet they contributed to more than three quarters of the aquatic toxicity.

[1] When orally exposed to ethoprophos, absorption is fast and extensive: the time it takes to reach peak blood levels is below 1 hour and more than 90% of the substance is absorbed.

The dermal NOAEL was 0.1 mg/kg/day and the researchers found that there was acetylcholinesterase inhibition in plasma, erythrocytes and in the brain at a dose of 1.0 mg/kg/day.