Over the last few years there has been an increasing incidence of admissions of Paraquat toxicity to the San Fernando General Hospital. We have done a detailed clinical and pathological study on thirteen (13) patients, ages 16 - 58, who died as a result of Paraquat toxicity. One patient was occupationally exposed to the Paraquat with percutaneous absorption of an unknown quantity. The remaining twelve (12) patients ingested the Paraquat for suicidal purposes. Vomiting occurred soon after the ingestion of Paraquat and was severe in eight patients. It was accompanied by weakness, lethargy, and semi stupor in four cases. Oral ulcers developed in all patients within two to three days following ingestion of the drug. Two patients developed respiratory distress within one to three days following ingestion. Four patients developed jaundice. Anuria was a complicating factor in two patients. The patient with tropical exposure developed skin ulcers at the site of exposure. This was followed by cough, repiratory difficulty and jaundice. The amounts of the chemical ingested range from 10 - 500 ml of the 40 percent solution. There was no direct correlation between the amount ingested and the length of survival. On histological examination, the pulmonary, hepatic and renal changes appeared to be progressive and related to survival time. On the first day, the predominant histological lesions in the lungs consisted of oedema; whereas, on the second day, oedema was associated with pulmonary haemorrhage. On subsequent days, and up to the seventieth day, the main changes were highlighted by progressive intersitial fibrosis. The main changes in the liver involved the bile excretory pathways and consisted mainly of cholestasis, usually localized in the centrilobular zone; and cholangiocellular injury involving the small and medium sized bile ducts in the portal areas. The sequence of hepatic lesions would suggest that Paraquat injury to the liver is biphasic. Ot is initially hepatocellular and becomes cholangiocellular after the first two days. The early renal changes were highlighted by interstitial oedema; whereas, after the second day, there was gradual progression from hydrophic degeneration of tubular cells to tubular necrosis. Renal biopsies done several days after ingestion in patients who survived, demonstrated findings consistent with interstitial nephritis. Our studies indicate that Paraquat is a highly toxic chemical agent and that ingestion of even small quantities of it is usually lethal. This study reveals that Paraquat causes significant pathological lesions in the lungs, liver, kidney, and upper gastrointestinal tract. The intensity of the pulmonary lesions appears to be the major pathological determinant in prognosis (AU)