Abstract
Chronic exposure to benzene leads to blood dyscrasias characterized by progressive depression in the levels of circulating leukocytes, thrombocytes, and/or erythrocytes, eventually leading to pancytopenia and aplastic anemia (1). The literature contains many descriptions of human benzene toxicity following chronic inhalation (2–4) and the process has been reproduced in several animal species either by exposing animals to atmospheric benzene (5,6) or by parenteral administration of benzene (7,8). The mechanism by which benzene produces bone marrow depression has been explored in a series of studies by Kissling and Speck (9,10) and by Boje et al. (11), who demonstrated that nucleic acid synthesis in bone marrow was inhibited in chronic benzene toxicity, but the molecular site of action is as yet unknown.
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Snyder, R., Andrews, L.S., Lee, E.W., Witmer, C.M., Reilly, M., Kocsis, J.J. (1977). Benzene Metabolism and Toxicity. In: Jollow, D.J., et al. Biological Reactive Intermediates. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-4124-6_31
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DOI: https://doi.org/10.1007/978-1-4613-4124-6_31
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