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Occupationally related hematologic toxicity has occurred in a somewhat cyclical fashion, historically associated with the introduction of some new and untested chemicals into commerce. A common factor contributing to “epidemics” of toxicity has been the exposure of large numbers of workers without adequate protection. As the toxicities of these agents gradually became known, regulation of their use was instituted and exposure was reduced. Because hematologic toxicity, like other noncancer health effects, is known to exhibit a threshold for induction, subsequent reduction in exposure levels led to reduction in the frequency of these illnesses. In some cases, exposure to certain toxins such as radium has been eliminated. Hematologic toxins, such as lead, benzene, arsenic, and arsine gas, are still used; poisonings leading to hematotoxicity occasionally still occur in the workplace, and, in some settings, worker or consumer education is inadequate. The study of hematotoxicity has improved our understanding of hematologic pathophysiology, taught important pharmacologic lessons, and introduced the concept of individual susceptibility to specific toxic agents. Observation of individual variations in susceptibility to toxic agents was made by recognizing that chemicals with oxidative potential could cause cyanosis and a life-threatening hemolytic anemia in some individuals at exposure levels that had little effect on the population at large. The normal population will manifest similar toxicities but only when exposed to much higher levels. Consequently, it is important to identify workers with increased susceptibility to certain chemicals and place them in jobs with less risk of contact with these specific toxic substances, although elimination or reduction of exposure for all workers is a preferable strategy.

Exposure to hematotoxins may affect blood cell survival (denaturation of hemoglobin and hemolysis), porphyrin synthesis and metabolism (including some porphyrias), blood cell formation (aplasia), risk for hematopoietic ­neoplasms, or coagulation (through development of thrombocytopenia).



Methemoglobin is formed by the oxidation of ferrous (Fe2+) hemoglobin to ferric (Fe3+) hemoglobin. It was first recognized in the 1800s, when coal tars were converted into individual chemicals that served as precursors for many products ranging from explosives to synthetic dyes and perfumes. Overexposure to these chemicals—which included anilines, nitrobenzenes, and quinones—was common, and little was known about their potential toxicity. Workers in these plants came to be known as “blue workers” because they suffered from “blue lip” as a result of the chronic cyanosis from toxin-induced methemoglobinemia that developed in many of them. Gradually it was recognized that oxidation of hemoglobin was toxic to red blood cells and could be followed by an acute and life-threatening hemolysis known as Heinz body anemia. Heinz bodies are red blood cell inclusions that represent precipitated hemoglobin and are seen classically in individuals with a deficiency of glucose-6-phosphate dehydrogenase (G6PD) after exposure to an oxidant stress. Normal individuals exposed to large amounts of oxidant chemicals ...

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