Comments
Acute hemolytic anemia after occupational arsine exposure has been described in the smelting, refining, and chemical industries. In the reported cases, arsine was formed as a by-product of a chemical reaction between a base metal, an arsenic impurity, and an acid. After arsine exposure, symptoms may be delayed for several hours. Red or tea-colored urine (hemoglobinuria) is the characteristic clinical finding. The disease course may be complicated by acute renal failure. [ACGIH; LaDou, p. 264; EPA Pesticides, p. 132; Olson, p. 144-6] In some cases, methemoglobin-forming compounds cause denaturation of hemoglobin (Heinz bodies) followed by hemolytic anemia. It is not known why some individuals have methemoglobinemia and others experience hemolytic anemia after exposure to the same oxidants. [Sullivan, p. 376] Subacute hemolytic anemia has been described from arsine exposure in zinc smelting and gold extracting operations. Laboratory findings include hemoglobinuria, elevated unconjugated bilirubin, and a high reticulocyte count. [LaDou, p. 264] Hemolysis has been reported in cases of poisoning by ingestion of arsenic and copper. Hemolysis after high-dose lead exposure may occur in workers who remove lead paint. Many drugs can cause immune hemolysis; Trimellitic anhydride can cause immune hemolysis in the workplace. [Sullivan, p. 377] "Lead may produce anemia by shortening red blood cell survival and by inhibiting heme synthesis." [Ford, p. 729]
Diagnostic
Hemoglobinuria: earliest lab abnormality; Free hemoglobin very high; Falling haptoglobin; Initial CBC: poikilocytosis, basophilic stippling & polychromasia; Hemoglobin levels: 5-10 g/100ml within 12-36 hrs; Blood & urine arsenic levels confirm exposure;