Dataset Information

Ultrafine and Fine Particle Number and Surface Area Concentrations and Daily Cause-Specific Mortality in the Ruhr Area, Germany, 2009-2014.

ABSTRACT: BACKGROUND:Although epidemiologic studies have shown associations between particle mass and daily mortality, evidence on other particle metrics is weak. OBJECTIVES:We investigated associations of size-specific particle number concentration (PNC) and lung-deposited particle surface area concentration (PSC) with cause-specific daily mortality in contrast to PM10. METHODS:We used time-series data (March 2009-December 2014) on daily natural, cardiovascular, and respiratory mortality (NM, CVM, RM) of three adjacent cities in the Ruhr Area, Germany. Size-specific PNC (electric mobility diameter of 13.3-750?nm), PSC, and PM10 were measured at an urban background monitoring site. In single- and multipollutant Poisson regression models, we estimated percentage change (95% confidence interval) [% (95% CI)] in mortality per interquartile range (IQR) in exposure at single-day (0-7) and aggregated lags (0-1, 2-3, 4-7), accounting for time trend, temperature, humidity, day of week, holidays, period of seasonal population decrease, and influenza. RESULTS:PNC100-750 and PSC were highly correlated and had similar immediate (lag0-1) and delayed (lag4-7) associations with NM and CVM, for example, 1.12% (95% CI: 0.09, 2.33) and 1.56% (95% CI: 0.22, 2.92) higher NM with IQR increases in PNC100-750 at lag0-1 and lag4-7, respectfully, which were slightly stronger then associations with IQR increases in PM10. Positive associations between PNC and NM were strongest for accumulation mode particles (PNC 100-500?nm), and for larger UFPs (PNC 50-100?nm). Associations between NM and PNC<100 changed little after adjustment for O3 or PM10, but were more sensitive to adjustment for NO2. CONCLUSION:Size-specific PNC (50-500?nm) and lung-deposited PSC were associated with natural and cardiovascular mortality in the Ruhr Area. Although associations were similar to those estimated for an IQR increase in PM10, particle number size distributions can be linked to emission sources, and thus may be more informative for potential public health interventions. Moreover, PSC could be used as an alternative metric that integrates particle size distribution as well as deposition efficiency. https://doi.org/10.1289/EHP2054.

SUBMITTER: Hennig F

PROVIDER: S-EPMC6066351 | biostudies-literature | 2018 Feb

REPOSITORIES: biostudies-literature

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Ultrafine and Fine Particle Number and Surface Area Concentrations and Daily Cause-Specific Mortality in the Ruhr Area, Germany, 2009-2014.

Hennig Frauke F Quass Ulrich U Hellack Bryan B Küpper Miriam M Kuhlbusch Thomas A J TAJ Stafoggia Massimo M Hoffmann Barbara B

Environmental health perspectives 20180215 2

<h4>Background</h4>Although epidemiologic studies have shown associations between particle mass and daily mortality, evidence on other particle metrics is weak.<h4>Objectives</h4>We investigated associations of size-specific particle number concentration (PNC) and lung-deposited particle surface area concentration (PSC) with cause-specific daily mortality in contrast to PM<sub>10</sub>.<h4>Methods</h4>We used time-series data (March 2009-December 2014) on daily natural, cardiovascular, and respi ...[more]

PMID: 29467106

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Project description:BACKGROUND:Epidemiological evidence on the health effects of ultrafine particles (UFP) remains insufficient to infer a causal relationship that is largely due to different size ranges and exposure metrics examined across studies. Moreover, evidence regarding the association between UFP and cardiovascular disease at a sub-daily timescale is lacking. OBJECTIVE:We investigated the relationship between different particle metrics, including particle number (PNC), length (PLC), and surface area (PSC) concentrations, and myocardial infarction (MI) at an hourly timescale. METHODS:We collected hourly air pollution and meteorological data from fixed urban background monitoring sites and hourly nonfatal MI cases from a MI registry in Augsburg, Germany, during 2005-2015. We conducted a time-stratified case-crossover analysis with conditional logistic regression to estimate the association between hourly particle metrics and MI cases, adjusted for air temperature and relative humidity. We also examined the independent effects of a certain particle metric in two-pollutant models by adjusting for copollutants, including particulate matter (PM) with an aerodynamic diameter of ?10?m or 2.5?m (PM10 and PM2.5, respectively), nitrogen dioxide, ozone, and black carbon. RESULTS:Overall, a total of 5,898 cases of nonfatal MI cases were recorded. Exploratory analyses showed similar associations across particle metrics in the first 6-12 h. For example, interquartile range increases in PNC within the size range of 10-100?nm, PLC, and PSC were associated with an increase of MI 6 h later by 3.27% [95% confidence interval (CI): 0.27, 6.37], 5.71% (95% CI: 1.79, 9.77), and 5.84% (95% CI: 1.04, 10.87), respectively. Positive, albeit imprecise, associations were observed for PNC within the size range of 10-30?nm and 100-500?nm. Effect estimates for PLC and PSC remained similar after adjustment for PM and gaseous pollutants. CONCLUSIONS:Transient exposure to particle number, length, and surface area concentrations or other potentially related exposures may trigger the onset of nonfatal myocardial infraction. https://doi.org/10.1289/EHP5478.

Project description:Epidemiology studies have linked exposure to pollutant particles to increased cardiovascular mortality and morbidity, however, the mechanism remains unknown. In this study, we hypothesized that the ultrafine fraction of ambient pollutant particles would cause endothelial cells dysfunction. We profiled gene expression of human pulmonary artery endothelial cells (HPAEC) exposed to ultrafine Chapel Hill particles (UFP) (100μg/ml) or vehicle for 4h with Affymetrix HG U133 Plus 2.0 chips (N = 4 each). Using an unpaired t-test (p <0.01, 5% false discovery rate) we found 426 unique genes to be differentially expressed with 320 upregulated genes and 106 downregulated genes. Among these genes, we noted upregulation of genes related to coagulation-inflammation circuitry including tissue factor (F3), coagulation factor II receptor-like 2 (F2RL2, PAR3), interleukin (IL)-6 and IL-8. Upregulation of these genes were independently confirmed by RT-PCR and/or protein release. Genes related to the CXC chemokine family that have been implicated in the pathogenesis of vascular disease were upregulated, including MCP-1 (2.60 fold), IL-8 (2.47 fold), CXCL1 (1.41 fold), CXCL2 (1.95 fold), CXCL3 (2.28 fold) and CXCR4 (1.30 fold). In addition, genes related to clotting independent signaling of F3 were also differentially expressed, including FOS, JUN and NFKBIA. Treatment of HPAEC with UFP for 16 hours increased the release of IL6 and IL8 by 1.9-fold and 1.8-fold respectively. Pretreatment of HPAEC with a blocking antibody against F3 attenuated IL6 and IL8 release by 30% and 70% respectively. Thus using gene profiling, we uncovered that UFP may induce vascular endothelial cells to express genes related to clotting and angiogenesis. These results provide a novel hypothesis that PM may cause cardiovascular adverse health effects via induction of tissue factor in vascular endothelial cells which then triggers clotting dependent and independent downstream signaling. Keywords: particle treatment

Project description:Ultrafine particles (UFP; aerodynamic diameter < 0.1 micrometers) are a ubiquitous exposure in the urban environment and are elevated near highways. Most epidemiological studies of UFP health effects use central site monitoring data, which may misclassify exposure. Our aims were to: (1) examine the relationship between distant and proximate monitoring sites and their ability to predict hourly UFP concentration measured at residences in an urban community with a major interstate highway and; (2) determine if meteorology and proximity to traffic improve explanatory power. Short-term (1 - 3 weeks) residential monitoring of UFP concentration was conducted at 18 homes. Long-term monitoring was conducted at two near-highway monitoring sites and a central site. We created models of outdoor residential UFP concentration based on concentrations at the near-highway site, at the central site, at both sites together and without fixed sites. UFP concentration at residential sites was more highly correlated with those at a near-highway site than a central site. In regression models of each site alone, a 10% increase in UFP concentration at a near-highway site was associated with a 6% (95% CI: 6%, 7%) increase at residences while a 10% increase in UFP concentration at the central site was associated with a 3% (95% CI: 2%, 3%) increase at residences. A model including both sites showed minimal change in the magnitude of the association between the near-highway site and the residences, but the estimated association with UFP concentration at the central site was substantially attenuated. These associations remained after adjustment for other significant predictors of residential UFP concentration, including distance from highway, wind speed, wind direction, highway traffic volume and precipitation. The use of a central site as an estimate of personal exposure for populations near local emissions of traffic-related air pollutants may result in exposure misclassification.

Dataset Information

Ultrafine and Fine Particle Number and Surface Area Concentrations and Daily Cause-Specific Mortality in the Ruhr Area, Germany, 2009-2014.

Publications

Ultrafine and Fine Particle Number and Surface Area Concentrations and Daily Cause-Specific Mortality in the Ruhr Area, Germany, 2009-2014.

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