A peer-reviewed open access journal published by the National Institute of Environmental Health Sciences

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, 1.78]. 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. Conclusions: Our ecologic analysis suggests an association between childhood leukemia and hazardous air pollution; further research using more sophisticated methodology is warranted.

Pregnant women may be vulnerable to changes in ambient temperature and warming climates. Recent evidence suggests that temperature increases are associated with placental abruption, a risk factor for stillbirth. We investigated the effect of acute exposures to apparent temperature on stillbirths in Harris County, Texas, 2008-2013. We conducted a case-crossover study to investigate the association between temperature and stillbirth among 708 women. We used data from the National Climatic Data Center to estimate maternal exposure to daily average apparent temperature over the days (lag days 1 through 6) preceding the stillbirth event. We employed symmetric bidirectional sampling to select six control periods one to three weeks before and after each event and applied conditional logistic regression to examine associations between increases of apparent temperature and stillbirths during the warm season (May-September). We adjusted for fine particulate matter (PM_2.5), nitrogen dioxide (NO₂) and ozone (O₃) and used stratified analysis to examine differences in risk by maternal race/ethnicity. We also examined the association among stillbirths with and without placental abruptions. Independent of air pollutant exposures, a 10 °F increase in apparent temperature in the week preceding delivery (lag days 1 to 6) was positively associated with a 45% (adjusted OR = 1.45, 95% confidence interval (CI): 1.18, 1.77) increase in risk for stillbirth. Risks were elevated for stillbirths occurring in June through August, for Hispanic and non-Hispanic Black women, but not for non-Hispanic Whites. We also observed elevated risks associated with temperature increases in the few days preceding delivery among stillbirths caused by placental abruption, with the risk being highest on lag day 1 (OR = 1.93, 95% CI: 1.15, 3.23). Independent of maternal ambient air pollutant exposure, we found evidence of an association between apparent temperature increases in the week preceding an event and risk of stillbirth. Risks for stillbirth varied by race/ethnicity. Further, in the first study to evaluate the impact of temperature on a specific complication during pregnancy, the risks were higher among mothers with placental abruption.

Epidemiological studies have found that particulate matter is associated with increases in blood pressure. Yet, less is known about the effects of specific sources or constituents of particulate matter, such as diesel particulate matter or polycyclic aromatic hydrocarbons (PAHs). We evaluated associations between self-reported hypertension and residential air levels of diesel particulate matter and PAHs among individuals of Mexican origin living in a large inner city. The Mano a Mano cohort (established in 2001 by the University of Texas MD Anderson Cancer Center) is comprised of individuals of Mexican origin residing in Houston, Texas. Using geographical information systems, we linked modeled annual estimates of PAHs and diesel particulate matter at the census tract level from the 2002 and 2005 U.S. Environmental Protection Agency’s National-Scale Air Toxics Assessment to baseline residential addresses of cohort members who enrolled from 2001 to 2003 or 2004 to 2006, respectively. For each enrollment period, we applied mixed-effects logistic regression models to determine associations between diesel particulate matter and PAHs, separately, and self-reported hypertension while adjusting for confounders and the clustering of observations within census tracts and households. The study population consisted of 11218 participants of which 77 % were women. The mean participant age at baseline was 41 years. Following adjustment for age, there was a dose-dependent, positive association between PAHs and hypertension (medium exposure, adjusted odds ratio (OR) = 1.09, 95 % CI: 0.88-1.36; high exposure, OR = 1.40, 95 % CI: 1.01-1.94) for individuals enrolled during 2001–2003; associations were generally similar in magnitude, but less precise, following adjustment for age, gender, smoking, and BMI. No association was detected for the later period. There was no evidence of an association between residential levels of diesel particulate matter and hypertension. This study builds on a limited number of prior investigations of the association between ambient air levels of PAHs or diesel particulate matter and hypertension by focusing on a relatively young cohort of predominantly adult women of Mexican origin. Future analyses are warranted to explore associations in the cohort using incident hypertension when sufficient data become available and to further examine associations between specific chemical constituents of particulate matter and hypertension in this and other populations.