Organophosphate and Carbamate Insecticides

Chemicals used to kill unwanted pests, including plants and animals.

A type of pesticide that targets insects.

A type of pesticide that targets rodents.

A type of pesticide that targets fungi.

A type of pesticide that targets unwanted plants (weeds).

A group of chemicals used as pesticides that can be absorbed by the body through ingestion, inhalation, or the skin.

A type of chemical that inhibits the enzyme acetylcholinesterase, leading to an accumulation of acetylcholine in the synapse.

Symptoms of organophosphate poisoning include: salivation, lacrimation, urination, defecation, gastrointestinal distress, bronchospasm, bradycardia, and muscle weakness.

Organophosphate (OP) and carbamate pesticides work by blocking the enzyme cholinesterase, which breaks down acetylcholine. This leads to a buildup of acetylcholine in the body, causing various symptoms.

Carbamates are pesticides that cause temporary blockage of cholinesterase, as the enzyme complex usually breaks down quickly.

The severity and speed of poisoning depend on factors such as how quickly the enzyme is phosphorylated, how fast the phosphorylated enzyme breaks down, and whether the enzyme undergoes aging.

One main difference between OPs and carbamates is that carbamates detach from the enzyme within 24 hours, while OPs can undergo aging, making the inactivation permanent.

The symptoms of OP and carbamate poisoning can be classified as muscarinic, nicotinic, or CNS effects, causing various bodily changes.

Mild poisoning from OPs and carbamates can lead to both CNS stimulant (nicotinic) and muscarinic effects.

Moderate poisoning is characterized by muscle twitches, tremors, and weakness, primarily due to nicotinic effects.

Severe poisoning is the most dangerous, leading to altered consciousness, paralysis, respiratory distress, and even convulsions.

A group of chemicals that can cause severe, potentially fatal, effects by interfering with the nervous system, primarily by inhibiting the enzyme acetylcholinesterase. This leads to an accumulation of acetylcholine, causing a range of symptoms like muscle weakness, paralysis, and respiratory failure.

A medication used to treat nerve agent poisoning. It acts by reversing the effects of the nerve agent on acetylcholinesterase, restoring normal nerve function.

A common herbicide used worldwide. When ingested, it is highly toxic to humans and can lead to serious respiratory problems, potentially leading to death.

A condition characterized by severe inflammation and fluid buildup in the lungs. This can occur due to exposure to certain substances like paraquat.

A substance that binds to and removes toxins from the body, often used in cases of poisoning.

A medical procedure involving the removal of the contents of the stomach through a tube inserted into the esophagus.

The enzyme responsible for breaking down acetylcholine, a neurotransmitter that plays a key role in nerve signaling.

A medication used to treat nerve agent poisoning. It acts by blocking the effects of acetylcholine, counteracting the overstimulation of the nervous system.

This stage begins within 1-5 days after exposure and involves local corrosive effects, characterized by coughing up blood (hemoptysis), ulceration of mucous membranes, nausea, diarrhea, and decreased urine output (oliguria).

This stage occurs 2-8 days post-exposure, marked by damage to the liver, kidneys, and heart. Symptoms include jaundice, fever, rapid heartbeat (tachycardia), inflammation of the heart muscle (myocarditis), respiratory distress with blue discoloration of the skin (cyanosis), elevated blood urea nitrogen (BUN), and high serum bilirubin levels.

This stage, happening 3-14 days after exposure, is marked by lung fibrosis, a scarring of the lungs. This leads to symptoms like coughing, shortness of breath (dyspnea), rapid breathing (tachypnea), fluid build-up (edema), fluid in the chest cavity (pleural effusion), collapsed lung sections (atelectasis), low oxygen levels in the blood (low arterial O2 tension), and a widened gap between lung and blood oxygen levels (increased alveolar O2 tension gradient), ultimately leading to respiratory failure.

This is a group of chemicals used to control unwanted plants, but some, like Paraquat, are highly toxic.

This process involves reducing the absorption of the poison into the body. It includes techniques like stomach pumping (gastric lavage), administering Fuller's earth (a clay-like substance that binds to the poison), using magnesium oxide (MOM) to prevent absorption in the gut, and washing the skin to remove the chemical.

This aims to cleanse the body of the poison by filtering the blood. Techniques include hemodialysis (using a machine to clean the blood) and hemoperfusion (passing the blood through a special filter to remove toxins).

This involves managing the harmful effects of the poison on the body. Examples include modulating inflammatory responses with medications like cyclophosphamide, dexamethasone, and chlorpheniramine, and preventing further oxidation with antioxidants like Vitamin C, Vitamin E, and N-acetylcysteine.