Pulmonary fibrosis paraquat

There is no evidence that inhalation exposures in occupational settings cause the rapid progressive pulmonary fibrosis and injury to the heart, liver, and kidneys that occur after ingestion. Because of the low vapor pressure, there is little inhalation hazard. Spray droplets are usually too large to reach the alveoli. If exposure is excessive, droplets may be inhaled into the upper respiratory tract and cause nosebleed, sore throat, headache, and coughing from local irritant action. Rarely, dermal exposure to paraquat has resulted in systemic poisonings and deaths with renal and pulmonary... 

Because of its widespread use as a herbicide, the possibility exists of substantial paraquat contamination of food. Drinking water contamination by paraquat has also been observed. The chronic effects of exposure to low levels of paraquat over extended periods of time are not well known. Acute exposure of animals to paraquat aerosols causes pulmonary fibrosis, and the lungs are affected even when exposure is through nonpulmonary routes. Paraquat affects enzyme activity. Acute exposure may cause variations in the levels of catecholamine, glucose, and insulin. 

Although paraquat can be corrosive at the point of contact, it is a systemic poison that is devastating to a number of organs. The most prominent initial symptom of poisoning is vomiting, sometimes followed by diarrhea. Within a few days, dyspnea, cyanosis, and evidence of impairment of the kidneys, liver, and heart become obvious. In fatal cases, the lungs develop pulmonary fibrosis, often with pulmonary edema and hemorrhaging. 

Selman, M., Montano, M., Ramos, C. et al. (1989). Experimental pulmonary fibrosis induced by paraquat plus oxygen in rats a morphologic and biochemical sequential study. Exp. Mol. Pathol. 50, 147-166. 

The next major class of widely used herbicides is made up of the bipyridi-um compounds, which include paraquat (l,l -dimethyl-4,4 -bipyridylium dichloride) and diquat (l,l -ethylene-2-2 -bipyridylium dibromide). Experimental exposure of animals, or accidental or deliberate exposure of humans to high doses of paraquat, produces respiratory toxicity after 10 to 14 days. Although this polar compound is poorly absorbed after oral delivery, it is actively concentrated in the lung. There it results in necrosis of pulmonary tissue followed by a proliferative phase that ultimately ends in pulmonary fibrosis and end-stage lung disease. The initial toxicity is directed at membranes and is a result of free radical oxidative damage secondary to generation of... 

There is no known antidote to paraquat or diquat poisoning. Some clinicians have used antioxidants such as vitamins C or E, N-acetyl cysteine, nitric oxide donors, and a combination of cyclophosphamide and corticosteroids to prevent inflammation and pulmonary fibrosis in severe cases. However, the effectiveness of these treatments appears to be marginal. If the chemical has been ingested, the main treatment is to prevent further absorption from the gastrointestinal tract. This is accomplished by the standard methods gastric lavage with safine solution to wash the substance from the stomach or ingestion of activated charcoal or Fuller s earth to act as absorbents. Since one of the effects of both paraquat and... 

Paraquat Oropharyngeal burning, headache, vomiting, delayed pulmonary fibrosis and death... 

Carbon monoxide Carboxyhemoglobinemia Cyanide Cytochrome oxidase inactivation Paraquat Pulmonary fibrosis Sodium nitrite Methemoglobinemia... 

In humans, cardiovascular collapse resulting from acute paraquat poisoning is associated with the distribution phase the late occurrence of death-related pulmonary fibrosis is associated with the elimination phase (Houze et al. 1990). Toxicokinetics studies conducted by these investigators in acute human poisoning cases indicated a concentration of paraquat in blood that had a mean... 

Paraquat is selectively taken up and concentrated by pulmonary alveolar cells, leading to cell necrosis followed by connective tissue proliferation and pulmonary fibrosis. 

IV. Diagnosis is based on a history of ingestion and the presence of gastroenteritis and oral burns. The oral mucosal burns may have the appearance of a pseudomembrane on the soft palate, sometimes confused with diphtheria. Rapidly progressive pulmonary fibrosis suggests paraquat poisoning. 

A. In paraquat poisoning, oxygen may contribute to lung injury. In fact, slightly hypox/c environments (10-12% oxygen) have been advocated to reduce the risk of pulmonary fibrosis from paraquat. 

Paraquat 75-150 34 300 (chronid Long-term exposure leads to chronic pulmonary fibrosis Narrow margin of safety for chronic effects... 

---