- Full (HTML) - Full (PDF) - Related EHP Articles - PubMed:Related Articles - PubMed:Citation - Cited in PMC - Purchase This Issue

Jeffrey E. Korte,^1,* Irva Hertz-Picciotto,¹ Mark R. Schulz,¹ Louise M. Ball,² Eric J. Duell^1,**

¹Department of Epidemiology, ²Department of Environmental Sciences and Engineering, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA

Abstract

Cigarette smoking is associated with an increased risk of leukemia ; benzene, an established leukemogen, is present in cigarette smoke. By combining epidemiologic data on the health effects of smoking with risk assessment techniques for low-dose extrapolation, we assessed the proportion of smoking-induced total leukemia and acute myeloid leukemia (AML) attributable to the benzene in cigarette smoke. We fit both linear and quadratic models to data from two benzene-exposed occupational cohorts to estimate the leukemogenic potency of benzene. Using multiple-decrement life tables, we calculated lifetime risks of total leukemia and AML deaths for never, light, and heavy smokers. We repeated these calculations, removing the effect of benzene in cigarettes based on the estimated potencies. From these life tables we determined smoking-attributable risks and benzene-attributable risks. The ratio of the latter to the former constitutes the proportion of smoking-induced cases attributable to benzene. Based on linear potency models, the benzene in cigarette smoke contributed from 8 to 48% of smoking-induced total leukemia deaths [95% upper confidence limit (UCL) , 20-66%], and from 12 to 58% of smoking-induced AML deaths (95% UCL, 19-121%) . The inclusion of a quadratic term yielded results that were comparable ; however, potency models with only quadratic terms resulted in much lower attributable fractions--all < 1%. Thus, benzene is estimated to be responsible for approximately one-tenth to one-half of smoking-induced total leukemia mortality and up to three-fifths of smoking-related AML mortality. In contrast to theoretical arguments that linear models substantially overestimate low-dose risk, linear extrapolations from empirical data over a dose range of 10- to 100-fold resulted in plausible predictions. Key words: benzene, environmental exposure, epidemiology, leukemia, life tables, occupational exposure, risk assessment, smoking. Environ Health Perspect 108:333-339 (2000) . [Online 23 February 2000]

http://ehpnet1.niehs.nih.gov/docs/2000/108p333-339korte/ abstract.html

Address correspondence to I. Hertz-Picciotto, Department of Epidemiology, CB #7400, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7400 USA. Telephone: (919) 966-7445. Fax: (919) 966-2089. E-mail: ihp@unc.edu

*Current address: Unit of Environmental Cancer Epidemiology, IARC, 150 Cours Albert Thomas, 69008, Lyon, France.

**Current address: Department of Cancer Cell Biology, Harvard School of Public Health, Boston MA 02115 USA.

This research was supported by U.S. Environmental Protection Agency cooperative agreement CR822673 and by National Institute of Environmental Health Sciences grant P42-ES05948.

Received 27 May 1999 ; accepted 1 November 1999.