2 resultados para Hazardous geographic environments

em DigitalCommons@The Texas Medical Center


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In the United States, approximately 4,000 pregnancies each year are affected by the two most common birth defects, spina bifida and anencephaly. Studies have shown that exposure to environmental chemicals before and after conception may adversely affect reproduction by inducing cell death or dysfunction, which leads to infertility, fetal loss, lowered weight at birth, or birth anomalies in the offspring. The objective of the study was to evaluate the relationship between Neural Tube Defect births and residence at conception in proximity to hazardous waste sites in the Texas-Mexico border region between 1993 and 2000. ^ The study design was a nested matched case-control and utilized secondary data from a project, “The role of chemical and biological factors in the etiology of neural tube birth defects births along the Texas-Mexico Border” (Irina Cech, Principal Investigator). Geographic Information Systems (GIS) database methods were used to compare Neural Tube Defects cases to controls on status of conception residence occurring within a one-mile radius from hazardous waste sites, as compared to conception residence further away. Information on the exposures was obtained from the OnTarget Database and Environment Protection Agency website. Conditional logistic regression was used for the matched case-control study to investigate the relationship between an outcome of being a case or a control and proximity to hazardous waste sites. ^ The result of the study showed a 36 percent non-significant increased risk of having an NTD birth associated with maternal proximity to abandoned hazardous waste sites (95% CI = 0.62–3.02). In addition, there was a 24% non-significant elevated risk of having an NTD birth when living in proximity to air pollutant sites than when living further away (95% CI = 0.67–2.32). Although this study did not find statistically significant associations, it will expand on the existing knowledge of the relationship between NTD and proximity to hazardous waste sites. ^

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Southeast Texas, including Houston, has a large presence of industrial facilities and has been documented to have poorer air quality and significantly higher cancer rates than the remainder of Texas. Given citizens’ concerns in this 4th largest city in the U.S., Mayor Bill White recently partnered with the UT School of Public Health to determine methods to evaluate the health risks of hazardous air pollutants (HAPs). Sexton et al. (2007) published a report that strongly encouraged analytic studies linking these pollutants with health outcomes. In response, we set out to complete the following aims: 1. determine the optimal exposure assessment strategy to assess the association between childhood cancer rates and increased ambient levels of benzene and 1,3-butadiene (in an ecologic setting) and 2. evaluate whether census tracts with the highest levels of benzene or 1,3-butadiene have higher incidence of childhood lymphohematopoietic cancer compared with census tracts with the lowest levels of benzene or 1,3-butadiene, using Poisson regression. The first aim was achieved by evaluating the usefulness of four data sources: geographic information systems (GIS) to identify proximity to point sources of industrial air pollution, industrial emission data from the U.S. EPA’s Toxic Release Inventory (TRI), routine monitoring data from the U.S. EPA Air Quality System (AQS) from 1999-2000 and modeled ambient air levels from the U.S. EPA’s 1999 National Air Toxic Assessment Project (NATA) ASPEN model. Further, once these four data sources were evaluated, we narrowed them down to two: the routine monitoring data from the AQS for the years 1998-2000 and the 1999 U.S. EPA NATA ASPEN modeled data. We applied kriging (spatial interpolation) methodology to the monitoring data and compared the kriged values to the ASPEN modeled data. Our results indicated poor agreement between the two methods. Relative to the U.S. EPA ASPEN modeled estimates, relying on kriging to classify census tracts into exposure groups would have caused a great deal of misclassification. To address the second aim, we additionally obtained childhood lymphohematopoietic cancer data for 1995-2004 from the Texas Cancer Registry. The U.S. EPA ASPEN modeled data were used to estimate ambient levels of benzene and 1,3-butadiene in separate Poisson regression analyses. All data were analyzed at the census tract level. We found that census tracts with the highest benzene levels had elevated rates of all leukemia (rate ratio (RR) = 1.37; 95% confidence interval (CI), 1.05-1.78). Among census tracts with the highest 1,3-butadiene levels, we observed RRs of 1.40 (95% CI, 1.07-1.81) for all leukemia. We detected no associations between benzene or 1,3-butadiene levels and childhood lymphoma incidence. This study is the first to examine this association in Harris and surrounding counties in Texas and is among the first to correlate monitored levels of HAPs with childhood lymphohematopoietic cancer incidence, evaluating several analytic methods in an effort to determine the most appropriate approach to test this association. Despite recognized weakness of ecologic analyses, our analysis suggests an association between childhood leukemia and hazardous air pollution.^