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The herbicide paraquat has claimed many fatalities due to accidental or deliberate ingestion of the concentrated form of the substance. Unlike most other poisons, the clinical course of paraquat intoxication is often protracted, and there is no known antidote for it. Treatment is often unsatisfactory. The principal target for the poison is the lung. Here, it causes destruction of the alveolar epithelium, followed by a progressive, inexorable, pulmonary fibrosis which causes death from respiratory failure. The pulmonary fibrosis starts with an infiltration into the alveolar spaces of primitive fibroblasts (profibroblasts) which differentiate into mature cells that completely occlude the alveolar spaces. Small quantities of collagen are also produced. The result is a cellular intra-alveolar fibrosis. Paraquat lung is not, therefore, a kind of diffuse interstitial pulmonary fibrosis as was once believed. The mechanism by which paraquat produces its toxic effects is obscure. It has a destructive action on epithelia, and in the lung, this may be enhanced by the high oxygen tension there. There is no satisfactory explanation for its fibrogenic action although this process may be aggravated by oxygen therapy. Even after 10 years, treatment for paraquat poisoning consists mainly of removing the paraquat from the stomach with colloidal material (bentonite) and from the blood with forced diuresis and/or hemodialysis. Steroid therapy has produced little success in halting the fibrosis, but better results are claimed from immunosuppressive and cytotoxic drugs. Recent research indicates that superoxide dismutase may be more successful as an antidote.

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