58 research outputs found
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 () at a geographic location. Monthly
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 . Finally, the Connecticut Department of Transportation provides data on
traffic density on major roadways, a primary contributor to
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 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) concentration estimates from the Community
Multiscale Air Quality (CMAQ) model, using two sources of observed data on
NO 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 monitor sites. The final
model was used to predict the daily concentration of ambient NO 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 concentration
stands out. An animation was also provided to show the change in the
concentration of ambient NO over space and time for 1994 and 1995.Comment: 23 pages, 8 figures, supplementary materia
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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
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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
Symptoms and Medication Use in Children with Asthma and Traffic-Related Sources of Fine Particle Pollution
Association of surfactant protein A polymorphisms with otitis media in infants at risk for asthma
BACKGROUND: Otitis media is one of the most common infections of early childhood. Surfactant protein A functions as part of the innate immune response, which plays an important role in preventing infections early in life. This prospective study utilized a candidate gene approach to evaluate the association between polymorphisms in loci encoding SP-A and risk of otitis media during the first year of life among a cohort of infants at risk for developing asthma. METHODS: Between September 1996 and December 1998, women were invited to participate if they had at least one other child with physician-diagnosed asthma. Each mother was given a standardized questionnaire within 4 months of her infant's birth. Infant respiratory symptoms were collected during quarterly telephone interviews at 6, 9 and 12 months of age. Genotyping was done on 355 infants for whom whole blood and complete otitis media data were available. RESULTS: Polymorphisms at codons 19, 62, and 133 in SP-A1, and 223 in SP-A2 were associated with race/ethnicity. In logistic regression models incorporating estimates of uncertainty in haplotype assignment, the 6A(4)/1A(5)haplotype was protective for otitis media among white infants in our study population (OR 0.23; 95% CI 0.07,0.73). CONCLUSION: These results indicate that polymorphisms within SP-A loci may be associated with otitis media in white infants. Larger confirmatory studies in all ethnic groups are warranted
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