Rationale: Recent U.S. data suggest an increased risk of work-related asthma among health care workers, yet only a few specific determinants have been elucidated. Objectives: To evaluate associations of asthma prevalence with occupational exposures in a cross-sectional survey of health care professionals. Methods: A detailed questionnaire was mailed to a random sample (n ϭ 5,600) of all Texas physicians, nurses, respiratory therapists, and occupational therapists with active licenses in 2003. Information on asthma symptoms and nonoccupational asthma risk factors obtained from the questionnaire was linked to occupational exposures derived through an industry-specific job-exposure matrix. Measurements: There were two a priori defined outcomes: (1 ) physiciandiagnosed asthma with onset after entry into health care ("reported asthma") and (2 ) "bronchial hyperresponsiveness-related symptoms," defined through an 8-item symptom-based predictor. Conclusions:The contribution of occupational exposures to asthma in health care professionals is not trivial, meriting both implementation of appropriate controls and further study.

Metabolic syndrome (MetS), Type 2 diabetes (T2D), and cardiovascular disease (CVD) share an inflammatory etiology and are known to be influenced by diet. We investigated associations of hypothesized prooxidative (Fe) and antioxidative (Zn, Mg, β-carotene, vitamin C, vitamin E) micronutrients with incident MetS, T2D, and CVD in the Multi-Ethnic Study of Atherosclerosis. Participants, 45-84 y at baseline (2000-2002), were followed through 2010. Diet was assessed by FFQ. After adjusting for demographics and behavioral confounders, including BMI, dietary vitamin E intake was inversely associated with incident MetS and CVD [HR for extreme quintiles: MetS = 0.78 (95% CI = 0.62, 0.97), P-trend = 0.01; CVD: HR = 0.69 (95% CI = 0.46, 1.03), P-trend = 0.04]. Intakes of heme iron and Zn from red meat, but not from other sources, were positively associated with risk of MetS [heme iron from red meat: HR = 1.25 (95% CI = 0.99,1.56), P-trend = 0.03; Zn from red meat: HR = 1.29 (95% CI = 1.03,1.61), P-trend = 0.04] and CVD [heme iron from red meat: HR = 1.65 (95% CI = 1.10,2.47), P-trend = 0.01; Zn from red meat: HR = 1.51 (95% CI = 1.02, 2.24), P-trend = 0.01]. Dietary intakes of nonheme iron, Mg, vitamin C, and β-carotene were not associated with risk of MetS, T2D, or CVD. Data provided little support for the associations between specific micronutrients and MetS, T2D, or CVD. However, nutrients consumed in red meat, or red meat as a whole, may increase risk of MetS and CVD.

BackgroundPrevious studies have reported positive associations between maternal exposure to air pollutants and several adverse birth outcomes. However, there have been no studies assessing the association between environmental levels of hazardous air pollutants, such as benzene, and neural tube defects (NTDs), a common and serious group of congenital malformations.ObjectiveOur goal was to conduct a case–control study assessing the association between ambient air levels of benzene, toluene, ethylbenzene, and xylene (BTEX) and the prevalence of NTDs among offspring.MethodsThe Texas Birth Defects Registry provided data on NTD cases (spina bifida and anencephaly) delivered between 1999 and 2004. The control group was a random sample of unaffected live births, frequency matched to cases on year of birth. Census tract–level estimates of annual BTEX levels were obtained from the U.S. Environmental Protection Agency 1999 Assessment System for Population Exposure Nationwide. Restricted cubic splines were used in mixed-effects logistic regression models to determine associations between each pollutant and NTD phenotype.ResultsMothers living in census tracts with the highest benzene levels were more likely to have offspring with spina bifida than were women living in census tracts with the lowest levels (odds ratio = 2.30; 95% confidence interval, 1.22–4.33). No significant associations were observed between anencephaly and benzene or between any of the NTD phenotypes and toluene, ethylbenzene, or xylene.ConclusionIn the first study to assess the relationship between environmental levels of BTEX and NTDs, we found an association between benzene and spina bifida. Our results contribute to the growing body of evidence regarding air pollutant exposure and adverse birth outcomes.

In studies of reproductive outcomes, maternal residence at delivery is often the only information available to characterise environmental exposures during pregnancy. The goal of this investigation was to describe residential mobility during pregnancy and to assess the extent to which change of residence may result in exposure misclassification when exposure is based on the address at delivery. Maternal residential mobility was compared between neural tube defect cases and unaffected controls from Texas participants in the National Birth Defects Prevention Study (NBDPS). Maternal residential information was obtained from the NBDPS interview. Data from the U.S. EPA National Air Toxics Assessment [Assessment System for Population Exposure Nationwide (ASPEN)], modelled at the census tract level, were used to estimate benzene exposure based on address at conception and address at delivery. Quartiles of exposure were assigned based on these estimates and the quartile assignments based on address at conception and address at delivery were compared using traditional methods (kappa statistics) and a novel application of mixed-effects ordinal logistic regression. Overall, 30% of case mothers and 24% of control mothers moved during pregnancy. Differences in maternal residential mobility were not significant between cases and controls, other than case mothers who moved did so earlier during pregnancy than control mothers (P = 0.01). There was good agreement between quartiles of estimated benzene exposure at both addresses (kappa = 0.78, P < 0.0001). Based on the mixed-effects regression model, address at delivery was not significantly different from using address at conception when assigning quartile of benzene exposure based on estimates from ASPEN (odds ratio 1.03, 95% confidence interval 0.85, 1.25). Our results indicate that, in this Texas population, maternal residential movement is generally within short distances, is typically not different between cases and controls, and does not significantly influence benzene exposure assessment.

BackgroundCancer 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.ObjectiveOur goal was to assess whether census tracts with the highest benzene or 1,3-butadiene ambient air levels have increased childhood lymphohematopoietic cancer incidence.MethodsOur 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).ResultsCensus 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]. 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.ConclusionsOur ecologic analysis suggests an association between childhood leukemia and hazardous air pollution; further research using more sophisticated methodology is warranted.