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Topic: RSS FeedChildhood cancer incidence rates and hazardous air pollutants in California: an exploratory analysis - Children's Health
Environmental Health Perspectives, April, 2003 by Peggy Reynolds, Julie Von Behren, Robert B. Gunier, Debbie E. Goldberg, Andrew Hertz, Daniel F. Smith
Hazardous air pollutants (HAPs) are compounds shown to cause cancer or other adverse health effects. We analyzed population-based childhood cancer incidence rates in California (USA) from 1988 to 1994, by HAP exposure scores, for all California census tracts. For each census tract, we calculated exposure scores by combining cancer potency factors with outdoor HAP concentrations modeled by the U.S. Environmental Protection Agency. We evaluated the relationship between childhood cancer rates and exposure scores for 25 potentially carcinogenic HAPs emitted from mobile, area, and point sources and from all sources combined. Our study period saw 7,143 newly diagnosed cancer cases in California; of these, 6,989 (97.8%) could be assigned to census tracts and included in our analysis. Using Poisson regression, we estimated rate ratios (RRs) adjusted for age, race/ethnicity, and sex. We found little evidence for elevated cancer RRs for all sites or for gliomas among children living in high-ranking combined-source exposure areas. We found elevated RRs and a significant trend with increasing exposure level for childhood leukemia in tracts ranked highest for exposure to the combined group of 25 HAPs (RR = 1.21; 95% confidence interval, 1.03, 1.42) and in tracts ranked highest for point-source HAP exposure (RR = 1.32; 95% confidence interval, 1.11, 1.57). Our findings suggest an association between increased childhood leukemia rates and high HAP exposure, but studies involving more comprehensive exposure assessment and individual-level exposure data will be important for elucidating this relationship. Key words: air pollution, brain cancer, childhood cancer, leukemia.
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Research to date has failed to firmly establish risk factors for childhood cancer other than ionizing radiation (Ross et al. 1994; Stewart et al. 1958), chemotherapy agents (Ross et al. 1994), and certain inherited genetic disorders (Cowell 1991; Li et al. 1988). The potential relationship between childhood cancer and air pollution from motor vehicle exhaust has been one of the more studied environmental factors. Many studies have shown an association between elevated childhood cancer risks and surrogate measures of exposure to vehicle exhaust, including traffic density, car density, and estimated nitrogen dioxide concentration in outdoor air (Feychting et al. 1998; Nordlinder and Jarvholm 1997; Pearson et al. 2000; Savitz and Feingold 1989). However, a study examining estimated nitrogen dioxide and benzene concentrations found no increase in childhood cancer risk (Raaschou-Nielsen et al. 2001). Two case-control studies conducted in urban areas of California (Langholz et al. 2002; Reynolds et al. 2001) and a statewide ecologic study in California (Reynolds et al. 2002) failed to show an association between increased rates and traffic density measures.
One British study identified childhood cancer excesses near industrial facilities considered major volatile organic compound emitters and near sources of exhaust from internal combustion engines (Knox and Gilman 1997). However, a similarly designed study, also in Britain, of lymphohematopoietic malignancies around oil refineries did not find an increased cancer risk among children (Wilkinson et al. 1999). Previous epidemiologic studies have also found associations between childhood cancer and parental occupational exposure to petroleum hydrocarbons (Colt and Blair 1998; Savitz and Chen 1990), but occupational exposure levels are generally much higher than those found in outdoor air. The risk of childhood cancer associated with exposure to ambient air pollution levels is unknown.
Limitations in available air monitoring data make it difficult to predict variations in the concentration of potentially carcinogenic pollutants at the neighborhood level (Kelly et al. 1994). Carcinogenic air pollutants have been measured routinely at only 20 sites throughout California, mostly urban areas where the highest concentrations would be expected (California ARB 1999). Amendments made to the U.S. Clean Air Act in 1990 (Clean Air Act 1990) identified 189 hazardous air pollutants (HAPs) (Stern 1992). HAPs are compounds found in ambient air known to cause cancer or other adverse health effects in laboratory animals or in occupational health studies. Because of the limited amount of air monitoring data available, the U.S. Environmental Protection Agency (U.S. EPA) developed a database with modeled outdoor concentrations of 148 HAPs, at the census tract level, for 1990. Comparison of these modeled HAP concentrations with available air monitoring data indicated good agreement (Rosenbaum et al. 1999).
The U.S. EPA's modeled HAP concentrations provide researchers the opportunity to study relationships between adverse health effects and estimated exposure to multiple chemicals emitted from various sources. Others have used the HAPs database to estimate excess lifetime cancer risk by census tract (EDF 1999; Morello-Frosch et al. 2002; Pratt et al. 2000; Woodruff et al. 1998, 2000). In this study, we analyzed population-based childhood cancer incidence rates in California census tracts by HAP exposure scores that were based on the estimated excess lifetime cancer risk. Our goal was to evaluate, at the census tract level, whether childhood cancer rates are elevated in areas estimated to have high exposure to potentially carcinogenic HAPs.
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