CAS RN: 4685-14-7

Toxicity Summary

IDENTIFICATION AND USE: Paraquat is available as an odorless yellow solid, or off-white powder. The form marketed in the U.S. is a liquid with a blue dye added to keep it from being confused with beverages, a sharp odor to serve as a warning, and an agent to cause vomiting if someone drinks it. The U.S. Environmental Protection Agency classifies paraquat as "restricted use", so it can only be used by licensed applicators. It is used globally as a non-selective herbicide that kills all green plant tissue it contacts, especially grasses and weeds. It has been used for desiccation of seed crops; weed control in orchards; defoliation and desiccation of cotton; as a harvest aid in soybeans, sugarcane, guar, and sunflowers; and for killing dormant alfalfa and clover, potato vines, and marijuana plants. HUMAN EXPOSURE: Dermal exposure to paraquat usually results in minor skin or eye irritation. Rarely, with heavier exposures resulting from misuse, more serious effects may occur such as blistered or ulcerated skin, loss of fingernails, skin burns, and ulcers of the mouth, nosebleeds, and protracted or even permanent blindness. Several human deaths from ingestion or subcutaneous injection of paraquat have been reported, gradually developing lethal lung damage usually in 3 weeks (progressive fibrosis). It has been estimated that a lethal dose in man is about 14 mL of a 40% solution of paraquat. The symptoms of poisoning include burning of the mouth and throat, nausea and vomiting, respiratory distress, and transient effects on the kidneys, heart, and nervous system. In a study of 30 workers spraying paraquat over a 12 week period, approximately 50% of them had minor irritation of the eyes or nose; 1 worker had an episode of epistaxis. Of 296 spray operators with skin exposure described as gross and prolonged, 55 had damaged fingernails, the most common lesion was transverse white bands of discoloration, but loss of nail surface, transverse ridging, gross deformity of the nail plate, and loss of nails also occurred. Paraquat dichloride was weakly positive in human lymphocytes in culture cytogenetic assay, with and without metabolic activation. ANIMAL STUDIES: Two groups of rats were given a single ip dose of paraquat at 15 mg/kg. Three hr after injection, rats exhibited an uncoordinated gait and/or widely splayed limbs consistent with neurologic impairment. All paraquat-treated rats died within 42 to 96 hr. Toxicity included anorexia, adipsia, diarrhea, hyperpnea, dyspnea, and tachycardia, necrosis of liver, kidney, and GI tract with primary lesions in lungs. Paraquat provoked overt motor impairment (reduced home-cage activity and impaired vertical climbing) and signs of anxiety-like behavior (reduced open field exploration) in wild-type but not interferon-gamma (IFN-gamma) knockout mice. Correspondingly, paraquat promoted somewhat divergent variations in neurochemical activity among wild-type and IFN-gamma null mice at brain sites important for both motor (striatum) and co-morbid affective pathologies (dorsal hippocampus, medial prefrontal cortex, and locus coeruleus). In addition, the herbicide influenced serotonergic and noradrenergic activity within the dorsal hippocampus and medial prefrontal cortex; and elevated noradrenergic activity within the locus coeruleus. Paraquat has been found to have minimal to no genotoxic activity when evaluated in a variety of in vitro and in vivo test systems. In in vitro studies producing weakly positive results, paraquat genotoxicity was accompanied by high cytotoxicity. ECOTOXICITY STUDIES: Effects of the herbicide paraquat were assessed on the green freshwater alga Chlamydomonas reinhardtii. Paraquat concentrations above 0.25 uM induce toxic effects in C. reinhardtii, reflected in a significantly reduced growth rate and cell concentration with a corresponding median effective concentration (EC50) value of 0.26 uM. With increasing paraquat concentrations, an increase in cell volume was registered as well as an increase in reactive oxygen species. Several genes involved in oxidative stress defense mechanisms, such as L-ascorbate peroxidase, glutaredoxin, and a possible glutathione-S-transferase were differentially expressed. Signs of acute intoxication: Polydipsia, regurgitation, swallowing, ataxia, imbalance, wing-drop, hyporeactivity, slowness, asthenia, sitting, running and falling, and possible miosis occurred in birds exposed to paraquat. Polydipsia and regurgitation appeared as soon as 9 min and other signs of intoxication appeared 3 hr after treatment. Mortalities usually occurred between 3 and 20 hr after treatment. Remission took up to 12 days. Paraquat was found to provoke pseudo-feminization of the males during in vivo tests, where eggs were sprayed with 0.4-1.4% aqueous solution of paraquat, and in vitro tests were conducted on cultures prepared 8.5-9 days after the start of the incubation.
Find more information on this substance at: PubChem, PubMed