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ACUTE EXPOSURE INFORMATION

1. USES: Paraquat is used primarily as a herbicide. The solution is usually blue-green in color. Concentrates of the solution range from 20% to 40% with dilutions of 0.1% to 0.5% typically made for herbicidal use.

2. TOXICOLOGY: Contact with mucosus membranes may lead to caustic injury. Absorption of the toxin may lead to pulmonary, hepatic, renal, and myocardial injury. Paraquat is concentrated in type I and type II pneumocytes and leads to the generation of oxygen free radicals and subsequent pulmonary fibrosis.

3. EPIDEMIOLOGY: Paraquat is used in over 120 developed and developing countries in the world due to its efficacy as a herbicide, inactivation when in contact with soil, low toxicity when handled appropriately. Paraquat is a restricted-use pesticide in the United States, thus significant exposures are rare. Exposures are most common in areas with higher availability. Intentional ingestions pose the greatest risk of severe toxicity or death. Occupational exposures are primarily dermal and rarely result in systemic toxicity.

4. WITH POISONING/EXPOSURE
   1. MILD TO MODERATE TOXICITY: Ingestion of a 20% solution, the most commonly available concentrated solution, is expected to cause caustic injury to the oral mucosa and esophagus. Nausea and vomiting are common. The patient may develop transient renal, hepatic and respiratory impairment. Symptoms usually resolve in patients with a mild exposure. Patients with moderate toxicity can develop permanent pulmonary injury.
   2. SEVERE TOXICITY: Nearly all patients that develop severe paraquat toxicity have ingested concentrated forms of the herbicide. Patients may die in the first several days due to gastrointestinal perforations or multiorgan failure. Patients that survive the early phase of toxicity involving cardiovascular, hepatic, and renal systems develop pulmonary fibrosis and subsequent death over the following 2 to 4 weeks postingestion.
   3. EARLY FINDINGS may include:
      1. GASTROINTESTINAL: Nausea and vomiting are present almost immediately following ingestion. Corrosive injuries to the esophagus and stomach are common and perforations may occur.
      2. CARDIOVASCULAR: Patients may develop hypotension due to massive fluid losses and cardiac dysrhythmias.
      3. HEPATIC: Hepatic failure due to centrilobular necrosis progresses over the first 24 to 48 hours.
      4. RENAL: Renal failure due to acute tubular necrosis progresses rapidly over the ensuing 24 hours postingestion.
      5. NEUROLOGIC: Patients may develop CNS depression (eg, lethargy, coma) and seizures with severe toxicity.
   4. LATE FINDINGS may include:
      1. PULMONARY: The lungs are inordinately affected by paraquat toxicity due to transport of the toxin into pneumocytes. Patients develop progressive fibrosis and hypoxia over 2 to 4 weeks postingestion.
   5. DERMAL EXPOSURE: High concentrations may lead to corrosive injury to the dermis (blistering). Symptoms occur rapidly and may progress for 24 hours. Systemic toxicity due to dermal exposure through intact skin is uncommon. However, prolonged exposure to concentrated solutions can lead to skin damage and subsequent systemic absorption. INHALATION EXPOSURE: Significant pulmonary toxicity from inhalational exposures has not been reported. This is likely due to the large size of the paraquat droplets when sprayed. Patients may develop upper airway irritation or ulceration due to inhalational exposure. OCULAR EXPOSURE: Significant corrosive injury may progress for 24 hours. Corneal injury and protracted opacification of the cornea may result from exposure.

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