Hematotoxicity in Workers Exposed to Low Levels of Benzene

Author:

Lan Qing12345,Zhang Luoping12345,Li Guilan12345,Vermeulen Roel12345,Weinberg Rona S.12345,Dosemeci Mustafa12345,Rappaport Stephen M.12345,Shen Min12345,Alter Blanche P.12345,Wu Yongji12345,Kopp William12345,Waidyanatha Suramya12345,Rabkin Charles12345,Guo Weihong12345,Chanock Stephen12345,Hayes Richard B.12345,Linet Martha12345,Kim Sungkyoon12345,Yin Songnian12345,Rothman Nathaniel12345,Smith Martyn T.12345

Affiliation:

1. Division of Cancer Epidemiology and Genetics, National Cancer Institute (NCI), National Institutes of Health (NIH), Department of Health and Human Services (DHHS), Bethesda, MD 20892, USA.

2. School of Public Health, University of California, Berkeley, CA 94720, USA.

3. Chinese Center for Disease Control and Prevention, Beijing, China.

4. New York Blood Center, Clinical Services, White Plains, NY 10605, USA.

5. School of Public Health, University of North Carolina, Chapel Hill, NC 27599, USA.

Abstract

Benzene is known to have toxic effects on the blood and bone marrow, but its impact at levels below the U.S. occupational standard of 1 part per million (ppm) remains uncertain. In a study of 250 workers exposed to benzene, white blood cell and platelet counts were significantly lower than in 140 controls, even for exposure below 1 ppm in air. Progenitor cell colony formation significantly declined with increasing benzene exposure and was more sensitive to the effects of benzene than was the number of mature blood cells. Two genetic variants in key metabolizing enzymes, myeloperoxidase and NAD(P)H:quinone oxidoreductase, influenced susceptibility to benzene hematotoxicity. Thus, hematotoxicity from exposure to benzene occurred at air levels of 1 ppm or less and may be particularly evident among genetically susceptible subpopulations.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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4. B. I. Yoon et al., Exp. Hematol.29, 278 (2001).

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