Estimating daily nitrogen dioxide level: Exploring traffic effects

Data used to assess acute health effects from air pollution typically have good temporal but poor spatial resolution or the opposite. A modified longitudinal model was developed that sought to improve resolution in both domains by bringing together data from three sources to estimate daily levels of nitrogen dioxide ($\mathrm {NO}_2$) at a geographic location. Monthly $\mathrm {NO}_2$ measurements at 316 sites were made available by the Study of Traffic, Air quality and Respiratory health (STAR). Four US Environmental Protection Agency monitoring stations have hourly measurements of $\mathrm {NO}_2$. Finally, the Connecticut Department of Transportation provides data on traffic density on major roadways, a primary contributor to $\mathrm {NO}_2$ pollution. Inclusion of a traffic variable improved performance of the model, and it provides a method for estimating exposure at points that do not have direct measurements of the outcome. This approach can be used to estimate daily variation in levels of $\mathrm {NO}_2$ over a region.Comment: Published in at http://dx.doi.org/10.1214/13-AOAS642 the Annals of Applied Statistics (http://www.imstat.org/aoas/) by the Institute of Mathematical Statistics (http://www.imstat.org

Spatiotemporal Calibration of Atmospheric Nitrogen Dioxide Concentration Estimates From an Air Quality Model for Connecticut

A spatiotemporal calibration and resolution refinement model was fitted to calibrate nitrogen dioxide (NO$_2$) concentration estimates from the Community Multiscale Air Quality (CMAQ) model, using two sources of observed data on NO$_2$ that differed in their spatial and temporal resolutions. To refine the spatial resolution of the CMAQ model estimates, we leveraged information using additional local covariates including total traffic volume within 2 km, population density, elevation, and land use characteristics. Predictions from this model greatly improved the bias in the CMAQ estimates, as observed by the much lower mean squared error (MSE) at the NO$_2$ monitor sites. The final model was used to predict the daily concentration of ambient NO$_2$ over the entire state of Connecticut on a grid with pixels of size 300 x 300 m. A comparison of the prediction map with a similar map for the CMAQ estimates showed marked improvement in the spatial resolution. The effect of local covariates was evident in the finer spatial resolution map, where the contribution of traffic on major highways to ambient NO$_2$ concentration stands out. An animation was also provided to show the change in the concentration of ambient NO$_2$ over space and time for 1994 and 1995.Comment: 23 pages, 8 figures, supplementary materia

Associations of PM2.5 Constituents and Sources with Hospital Admissions: Analysis of Four Counties in Connecticut and Massachusetts (USA) for Persons ≥ 65 Years of Age

Background: Epidemiological studies have demonstrated associations between short-term exposure to PM2.5 and hospital admissions. The chemical composition of particles varies across locations and time periods. Identifying the most harmful constituents and sources is an important health and regulatory concern. Objectives: We examined pollutant sources for associations with risk of hospital admissions for cardiovascular and respiratory causes. Methods: We obtained PM2.5 filter samples for four counties in Connecticut and Massachusetts and analyzed them for PM2.5 elements. Source apportionment was used to estimate daily PM2.5 contributions from sources (traffic, road dust, oil combustion, and sea salt as well as a regional source representing coal combustion and other sources). Associations between daily PM2.5 constituents and sources and risk of cardiovascular and respiratory hospitalizations for the Medicare population (> 333,000 persons ≥ 65 years of age) were estimated with time-series analyses (August 2000–February 2004). Results: PM2.5 total mass and PM2.5 road dust contribution were associated with cardiovascular hospitalizations, as were the PM2.5 constituents calcium, black carbon, vanadium, and zinc. For respiratory hospitalizations, associations were observed with PM2.5 road dust, and sea salt as well as aluminum, calcium, chlorine, black carbon, nickel, silicon, titanium, and vanadium. Effect estimates were generally robust to adjustment by co-pollutants of other constituents. An interquartile range increase in same-day PM2.5 road dust (1.71 μg/m3) was associated with a 2.11% (95% CI: 1.09, 3.15%) and 3.47% (95% CI: 2.03, 4.94%) increase in cardiovascular and respiratory admissions, respectively. Conclusions: Our results suggest some particle sources and constituents are more harmful than others and that in this Connecticut/Massachusetts region the most harmful particles include black carbon, calcium, and road dust PM2.5. Citation: Bell ML, Ebisu K, Leaderer BP, Gent JF, Lee HJ, Koutrakis P, Wang Y, Dominici F, Peng RD. 2014. Associations of PM2.5 constituents and sources with hospital admissions: analysis of four counties in Connecticut and Massachusetts (USA) for persons ≥ 65 years of age. Environ Health Perspect 122:138–144; http://dx.doi.org/10.1289/ehp.130665

Investigating the Impact of Maternal Residential Mobility on Identifying Critical Windows of Susceptibility to Ambient Air Pollution during Pregnancy

© 2018 The Author(s). Identifying periods of increased vulnerability to air pollution during pregnancy with respect to the development of adverse birth outcomes can improve understanding of possible mechanisms of disease development and provide guidelines for protection of the child. Exposure to air pollution during pregnancy is typically based on the mother's residence at delivery, potentially resulting in exposure misclassification and biasing the estimation of critical windows of pregnancy. In this study, we determined the impact of maternal residential mobility during pregnancy on defining weekly exposure to particulate matter less than or equal to 10 µm in aerodynamic diameter (PM 10) and estimating windows of susceptibility to term low birth weight. We utilized data sets from 4 Connecticut birth cohorts (1988-2008) that included information on all residential addresses between conception and delivery for each woman. We designed a simulation study to investigate the impact of increasing levels of mobility on identification of critical windows. Increased PM 10 exposure during pregnancy weeks 16-18 was associated with an increased probability of term low birth weight. Ignoring residential mobility when defining weekly exposure had only a minor impact on the identification of critical windows for PM 10 and term low birth weight in the data application and simulation study. Identification of critical pregnancy windows was robust to exposure misclassification caused by ignoring residential mobility in these Connecticut birth cohorts

Low-Level Ozone Exposure and Respiratory Symptoms in Infants

OBJECTIVE: Recent studies indicate that the U.S. Environmental Protection Agency (EPA) ozone standards may not protect sensitive individuals. In this study we examined respiratory effects of ozone in infants who may be vulnerable, particularly if they are children of asthmatic mothers. DESIGN: Women delivering babies at one of five hospitals in southwestern Virginia between 1994 and 1996 were invited to participate in a cohort study; 780 women enrolled. Ambient air quality data (ozone and particulate matter) were collected at a central monitoring site. PARTICIPANTS: This analysis is of 691 infants followed for approximately 83 days between 10 June and 31 August 1995 and/or 1996; they contributed a total of 52,421 infant-days of follow-up. Mothers were interviewed at enrollment and approximately biweekly to report infants’ daily symptoms. Repeated measures logistic regression models were run separately for wheeze, difficulty breathing, and cough. Ozone metrics included 24-hr average, peak 1-hr, and maximum 8-hr average. Analyses were repeated for the 61 infants whose mothers had asthma. RESULTS: For every interquartile-range increase in same-day 24-hr average ozone, likelihood of wheeze increased 37% [95% confidence interval (CI), 2–84%]. Among infants of asthmatic mothers, same-day 24-hr average ozone increased likelihood of wheeze 59% (95% CI, 1–154%) and of difficulty breathing 83% (95% CI, 42–136%). Maximum 8-hr ozone and peak 1-hr ozone were associated with difficulty breathing, but not wheeze, in infants of asthmatic mothers. Ozone was not associated with cough. CONCLUSIONS: At levels of ozone exposure near or below current U.S. EPA standards, infants are at increased risk of respiratory symptoms, particularly infants whose mothers have physician-diagnosed asthma

Effects of endotoxin exposure on childhood asthma risk are modified by a genetic polymorphism in ACAA1

<p>Abstract</p> <p>Background</p> <p>Polymorphisms in the endotoxin-mediated TLR4 pathway genes have been associated with asthma and atopy. We aimed to examine how genetic polymorphisms in innate immunity pathways interact with endotoxin to influence asthma risk in children.</p> <p>Methods</p> <p>In a previous analysis of 372 children from the Boston Home Allergens and the Connecticut Childhood Asthma studies, 7 SNPs in 6 genes (CARD15, TGFB1, LY96, ACAA1, DEFB1 and IFNG) involved in innate immune pathways were associated with asthma, and 5 SNPs in 3 genes (CD80, STAT4, IRAK2) were associated with eczema. We tested these SNPs for interaction with early life endotoxin exposure (n = 291), in models for asthma and eczema by age 6.</p> <p>Results</p> <p>We found a significant interaction between endotoxin and a SNP (rs156265) in ACAA1 (p = 0.0013 for interaction). Increased endotoxin exposure (by quartile) showed protective effects for asthma in individuals with at least one copy of the minor allele (OR = 0.39 per quartile increase in endotoxin, 95% CI 0.15 to 1.01). Endotoxin exposure did not reduce the risk of asthma in children homozygous for the major allele.</p> <p>Conclusion</p> <p>Our findings suggest that protective effects of endotoxin exposure on asthma may vary depending upon the presence or absence of a polymorphism in ACAA1.</p