Parathion is an insecticide with the molecular formula C10H14NO5PS. At room temperature, parathion is a yellow-to-brown liquid with an odour of garlic. It is often dissolved in a hydrocarbon solvent before use. Parathion itself is not volatile. It is almost insoluble in water, slightly soluble in petroleum oils, and miscible with many organic solvents. 
Parathion is prepared by the reaction of diethyl phosphorothionchloridate with sodium p-nitrophenate. It is widely used as an agricultural insecticide. It has been used extensively by U.S. farmers on major crops such as wheat, fruit, vegetables, nuts, citrus fruits, alfalfa, corn, soybeans, and other field crops.
Sources & Routes of Exposure
Sources of Exposure 
- Humans are exposed to parathion primarily during field application and formulation; the general public may be exposed by dermal and inhalation exposure from spray drift in areas adjacent to agricultural fields.
- Exposure to parathion may occur in the workplace during its manufacture.
- Individuals may also be exposed by ingesting food containing parathion residues.
Routes of Exposure 
- Inhalation: Toxic inhalation of parathion vapour is unlikely at ordinary temperatures because of its low volatility, but toxic effects can occur after inhalation of parathion sprays or dusts. The hydrocarbon solvents (most commonly toluene and xylene) used to dissolve parathion are more volatile than parathion itself, and toxicity can result from inhalation of solvent vapour as well. The odour threshold of parathion is five times the OSHA PEL (0.1 mg/m³) and does not provide adequate warning of hazardous concentrations. Children exposed to the same levels of parathion as adults may receive a larger dose because they have greater lung surface area: body weight ratios and increased minute volumes: weight ratios.
- Skin/Eye Contact: Parathion is not irritating to the skin or eyes, but is rapidly absorbed through intact skin and eyes, contributing to systemic toxicity. Children are more vulnerable to toxicants absorbed through the skin because of their relatively larger surface area: body weight ratio.
- Ingestion: Acute toxic effects, including rapidly fatal systemic poisoning, can result from ingestion of parathion.
Health Effects 
Parathion, like all organophosphate pesticides, inhibits acetylcholinesterase and alters cholinergic synaptic transmission at neuroeffector junctions (muscarinic effects), at skeletal myoneural junctions and autonomic ganglia (nicotinic effects), and in the CNS. Inhibition occurs when a metabolite of parathion binds to acetylcholinesterase; thus, symptoms may be delayed after exposure. Signs and symptoms of poisoning vary according to age, dose, and concentration. Muscarinic effects include: pinpoint pupils; blurred vision; hypersecretion by salivary, lacrimal, sweat, and bronchial glands; narrowing of the bronchi; nausea, vomiting, diarrhoea, and crampy abdominal pains; urinary and faecal incontinence; and slow heart rate. Nicotinic effects include muscle twitching, cramping, and weakness. Nicotinic stimulation can obscure certain muscarinic effects and produce rapid heart rate and high blood pressure.
Central Nervous System
Central Nervous System (CNS) effects are often the earliest manifestations of poisoning in adults and constitute the major signs and symptoms in children. CNS effects include irritability, nervousness, giddiness, fatigue, lethargy, impairment of memory, confusion, slurred speech, visual disturbance, depression, impaired gait, convulsions, loss of consciousness, coma, and respiratory depression.
Peripheral neurologic effects include muscle twitching and weakness due to inhibition of acetylcholinesterase at neuromuscular junctions.
Respiratory failure is the most common cause of death due to parathion poisoning. Narrowing of the bronchi and markedly increased bronchial secretions can occur. Respiratory failure results from respiratory depression coupled with paralysis of the respiratory muscles and progressive airway obstruction from bronchorrhea. In addition, pulmonary aspiration of the hydrocarbon solvents found in many commercial preparations can cause inflammation of the lungs. Children may be more vulnerable because of relatively increased minute ventilation per kg and failure to evacuate as area promptly when exposed.
Most exposure victims experience bradycardia, but pulse rate may be increased initially and tachycardia is more common in very severe poisoning. Irregular heartbeat may occur.
Nausea, vomiting, abdominal cramps, diarrhoea, and faecal incontinence are common manifestations, regardless of the exposure route. These are generally the earliest symptoms to occur.
Profuse sweating is likely to occur and may lead to profound dehydration. This is somewhat less common in children.
Parathion is not generally irritating, but is readily absorbed through the skin. Skin contact can result in systemic poisoning. Because of their relatively larger surface area: body weight ratio, children are more vulnerable to toxicants absorbed through the skin.
Systemic poisoning typically causes pinpoint pupils and spasm of the muscle of visual accommodation (i.e., ciliary muscle) leading to blurred vision and aching pain in the eye. However, organophosphate poisoning may still be present without pinpoint pupils, and dilation of the pupils may even be noted occasionally. Eye irritation, if it occurs, is most likely caused by the hydrocarbon solvents used in commercial pesticide preparations.
Complete recovery generally occurs within 10 days unless severe lack of oxygen has caused residual brain damage. CNS effects such as confusion, fatigue, irritability, nervousness, and impairment of memory can occasionally last for several weeks. Six to twenty-one days after acute exposure to some organophosphate compounds, onset of nerve disorders of mixed sensory-motor type may occur; peripheral nerve recovery may never be complete. It is uncertain if parathion produces this delayed polyneuropathy.
Persistent weakness and impaired memory have been reported to occur from low-level exposures to organophosphates in the absence of acute cholinergic effects.
The International Agency for Research on Cancer has determined that parathion is not classifiable as to its carcinogenicity to humans. However, EPA lists parathion as a possible human carcinogen.
Reproductive and Developmental Effects
Studies have been reported in which parathion was embryo-toxic and fetotoxic in rodents. There are no studies addressing reproductive or developmental effects in humans exposed to parathion. Parathion is not included in Reproductive and Developmental Toxicants, a 1991 report published by the U.S. General Accounting Office (GAO) that lists 30 other chemicals of concern because of widely acknowledged reproductive and developmental consequences.
First Aid Measures
- If inhaled: If breathed in, move person into fresh air. If not breathing, give artificial respiration. Consult a physician.
- In case of skin contact: Wash off with soap and plenty of water. Take victim immediately to hospital. Consult a physician.
- In case of eye contact: Rinse thoroughly with plenty of water for at least 15 minutes and consult a physician.
- If swallowed: Never give anything by mouth to an unconscious person. Rinse mouth with water. Consult a physician.
Exposure Controls & Personal Protection
- Use appropriate engineering controls
- Avoid contact with skin, eyes and clothing.
- Wash hands before breaks and immediately after handling the product.
Personal Protective Equipment
The following personal protective equipment is recommended when handling parathion:
- Eye/face protection: Face shield and safety glasses Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).
- Skin protection: Handle with gloves. Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove’s outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands. The selected protective gloves have to satisfy the specifications of EU Directive 89/686/EEC and the standard EN 374 derived from it.
- Body Protection: Complete suit protecting against chemicals, the type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.
- Respiratory protection: Where risk assessment shows air-purifying respirators are appropriate use a full-face respirator with multi-purpose combination (US) or type ABEK (EN 14387) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).
OSHA: The United States Occupational Health & Safety Administration has established the following Permissible Exposure Limits (PEL):
- General Industry: 29 CFR 1910.1000 Z-1 Table — 0.1 mg/m3; Skin
- Construction Industry: 29 CFR 1926.55 Appendix A — 0.1 mg/m3; Skin
- Maritime: 29 CFR 1915.1000 Table Z-Shipyards — 0.1 mg/m3
ACGIH: The American Conference of Governmental Industrial Hygienists has set a Threshold Limit Value (TLV) for parathion of 0.05 mg/m3 TWA – Inhalable fraction, Vapour and aerosol; Skin; Appendix A4 – Not Classifiable as a Human Carcinogen; BEI
NIOSH: The National Institute for Occupational Safety and Health has set a Recommended Exposure Limit (REL) for parathion of 0.05 mg/m3 TWA; Skin
Safe Work Australia: Safe Work Australia has established a Time Weighted Average concentration for parathion of 0.1 mg/m3 for a 40-hour workweek.
Australia Drinking Water Guidelines specify an allowable concentration of 0.02 mg/L of parathion in drinking water.