4.7 Article

Childhood Lymphohematopoietic Cancer Incidence and Hazardous Air Pollutants in Southeast Texas, 1995-2004

期刊

ENVIRONMENTAL HEALTH PERSPECTIVES
卷 116, 期 11, 页码 1576-1580

出版社

US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
DOI: 10.1289/ehp.11593

关键词

1,3-butadiene; air toxics; benzene; childhood cancer; epidemiology; hazardous air pollution

资金

  1. National Cancer Institute
  2. National Institutes of Health
  3. Department of Health and Human Services [1 R03 CA128106-01A1]
  4. Texas Department of State Health Services
  5. Texas Cancer Registry

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BACKGROUND: Cancer is the second leading cause of death among U.S. children with few known risk factors. There is increasing interest in the role of air pollutants, including benzene and 1,3-butadiene, in the etiology of childhood cancers. OBJECTIVE: Our goal was to assess whether census tracts with the highest benzene or 1,3-butadiene ambient air levels have increased childhood lymphohematopoietic cancer incidence. METHODS: Our ecologic analysis included 977 cases of childhood lymphohematopoietic cancer diagnosed from 1995-2004. We obtained the U.S. Environmental Protection Agency's 1999 modeled estimates of benzene and 1,3-butadiene for 886 census tracts surrounding Houston, Texas. We ran Poisson regression models by, pollutant to explore the associations between pollutant levels and census-tract cancer rates. We adjusted models for age, sex, race/ethnicity, and community-level socioeconomic status (cSES). RESULTS: Census tracts with the highest benzene levels had elevated rates of all leukemia [rate ratio (RR) = 1.37; 95% confidence interval (CI), 1.05, 1.781. This association was higher for acute myeloid leukemia (AML) (RR = 2.02; 95% CI, 1.03-3.96) than for acute lymphocytic leukemia (ALL) (RR = 1.24; 95% CI, 0.92-1.66). Among census tracts with the highest 1,3-butadiene levels, we observed RRs of 1.40 (95% CI, 1.07-1-81), 1.68 (95% CI, 0.84-3-35), and 1.32 (95% CI,, 0.98-1.77) for all leukemia, AML, and ALL, respectively. We detected no associations between benzene or 1,3-butadiene levels and lymphoma incidence. Results that examined joint exposure to benzene and 1,3-butadiene were similar to those that examined each pollutant separately. CONCLUSIONS: Our ecologic analysis suggests an association between childhood leukemia and hazardous air pollution; further research using more sophisticated methodology is warranted.

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