Effect of air pollution controls on black smoke and sulfur dioxide concentrations across Ireland

During the 1980s Ireland experienced severe pollution episodes, principally because of domestic coal burning. In 1990, the Irish government introduced a ban on the marketing, sale, and distribution of coal in Dublin. They extended the ban to Cork in 1995 and to ten other communities in 1998 and 2000. We previously reported declines in particulate (black smoke [BS]) and sulfur dioxide (SO2) concentrations in Dublin following the 1990 coal ban. We now explore and compare the effectiveness of these sequential bans in 1990, 1995, 1998, and 2000. Daily BS and total gaseous acidity (502) measurements were compiled between 1980 and 2004. We calculated descriptive statistics for the pre-ban (5 yr before ban) and post-ban (5 yr after ban) periods for BS and SO2 concentrations and for season-specific periods. Mean BS levels fell in all centers post-ban compared with the pre-ban period, with decreases ranging; from 4 to 35 mu g.m(-3) (-45 to -70%). These reductions were smallest in the summer and largest in the winter. These BS, reductions were sustained in all centers until the end of the study period. We observed no clear pattern in SO2 changes associated with the coal bans. The 1990, 1995, 1998, and 2000 Irish coal sale bans resulted in immediate and sustained decreases in particulate levels in centers, with the largest declines in the winter. In contrast, we did not observe consistent declines in total acidity as a measure of SO2. It may be that coal was not the major source. of SO2. Simple legislation was very effective at improving ambient air quality in Irish cities with varying populations, geography/topography, and meteorological conditions

Suspected association of ventricular arrhythmia with air pollution in a motorbike rider: a case report

<p>Abstract</p> <p>Introduction</p> <p>Premature ventricular complexes are to some extent a normal finding in healthy individuals and the prevalence increases with age and is more common in men. Premature ventricular complexes can occur in association with a variety of stimuli, and a lesser known cause is the association between air pollution and ventricular arrhythmias.</p> <p>Case presentation</p> <p>A previously healthy man started to ride a lightweight motorbike in heavy traffic. A few weeks later he was admitted to hospital with premature ventricular complexes in bigeminy, which decreased after a few days when he was not exposed to exhaust fumes. A few weeks later he started using the motorbike again and the same symptoms developed once more, only to subside when he stopped riding in heavy traffic.</p> <p>Conclusion</p> <p>Studies have shown an association between air pollution and premature ventricular complexes and other kinds of arrhythmias. The mechanism may be changes in cardiac autonomic function, including heart rate and heart rate variability. Air pollution should be considered when patients present with arrhythmias and no other causes are found.</p

Particulate air pollution and survival in a COPD cohort

<p>Abstract</p> <p>Background</p> <p>Several studies have shown cross-sectional associations between long term exposure to particulate air pollution and survival in general population or convenience cohorts. Less is known about susceptibility, or year to year changes in exposure. We investigated whether particles were associated with survival in a cohort of persons with COPD in 34 US cities, eliminating the usual cross-sectional exposure and treating PM₁₀as a within city time varying exposure.</p> <p>Methods</p> <p>Using hospital discharge data, we constructed a cohort of persons discharged alive with chronic obstructive pulmonary disease using Medicare data between 1985 and 1999. 12-month averages of PM₁₀were merged to the individual annual follow up in each city. We applied Cox's proportional hazard regression model in each city, with adjustment for individual risk factors.</p> <p>Results</p> <p>We found significant associations in the survival analyses for single year and multiple lag exposures, with a hazard ratio for mortality for an increase of 10 μg/m³PM₁₀over the previous 4 years of 1.22 (95% CI: 1.17–1.27).</p> <p>Conclusion</p> <p>Persons discharged alive for COPD have substantial mortality risks associated with exposure to particles. The risk is evident for exposure in the previous year, and higher in a 4 year distributed lag model. These risks are significantly greater than seen in time series analyses.</p

The Influence of Living Near Roadways on Spirometry and Exhaled Nitric Oxide in Elementary Schoolchildren

BACKGROUND: Living near major roadways has been associated with an increase in respiratory symptoms, but little is known about how this relates to airway inflammation. OBJECTIVE: We assessed the effects of living near local residential roadways based on objective indicators of ventilatory function and airway inflammation. METHODS: We estimated ambient air pollution, resolved to the level of the child's neighborhood, using a land-use regression model for children 9-11 years of age. We also summed the length of roadways found within a 200-m radius of each child's neighborhood. We had measurements of both air pollution exposure and spirometry for 2,328 children, and also had measurements of exhaled nitric oxide (eNO) for 1,613 of these children. RESULTS: Each kilometer of local roadway within a 200-m radius of the home was associated with a 6.8% increase in eNO (p = 0.045). Each kilometer of any type of roadway (local, major, highway) was also associated with an increase in eNO of 10.1% (p = 0.002). Each microgram per cubic meter increase in PM2.5 was associated with a 3.9% increase in eNO (p = 0.058) and 0.70% decrease in forced vital capacity (FVC) expressed as a percentage of predicted (p = 0.39). Associations between roadway density and both forced expired volume in 1 sec and FVC were negative but not statistically significant at p < 0.05. CONCLUSION: Traffic from local neighborhood roadways may cause airway inflammation as indicated by eNO. This may be a more sensitive indicator of adverse air pollution effects than traditional measures of ventilatory function

Black Carbon Exposure, Oxidative Stress Genes, and Blood Pressure in a Repeated-Measures Study

BACKGROUND. Particulate matter (PM) air pollution has been associated with cardiovascular morbidity and mortality, and elevated blood pressure (BP) is a known risk factor for cardiovascular disease. A small number of studies have investigated the relationship between PM and BP and found mixed results. Evidence suggests that traffic-related air pollution contributes significantly to PM-related cardiovascular effects. OBJECTIVES. We hypothesized that black carbon (BC), a traffic-related combustion by-product, would be more strongly associated with BP than would fine PM [aerodynamic diameter ≤ 2.5 μm (PM2.5)], a heterogeneous PM mixture, and that these effects would be larger among participants with genetic variants associated with impaired antioxidative defense. METHODS. We performed a repeated-measures analysis in elderly men to analyze associations between PM2.5 and BC exposure and BP using mixed-effects models with random intercepts, adjusting for potential confounders. We also examined statistical interaction between BC and genetic variants related to oxidative stress defense: GSTM1, GSTP1, GSTT1, NQO1, catalase, and HMOX-1. RESULTS. A 1-SD increase in BC concentration was associated with a 1.5-mmHg increase in systolic BP [95% confidence interval (CI), 0.1-2.8] and a 0.9-mmHg increase in diastolic BP (95% CI, 0.2-1.6). We observed no evidence of statistical interaction between BC and any of the genetic variants examined and found no association between PM2.5 and BP. CONCLUSIONS. We observed positive associations between BP and BC, but not between BP and PM2.5, and found no evidence of effect modification of the association between BC and BP by gene variants related to antioxidative defense.National Institute of Environmental Health Sciences (ES015172, ES014663); National Cancer Institute (2-T32-CA009330); United States Environmental Protection Agency (R832416); United States Deparment of Veterans Affairs; Massachusetts Veterans Epidemiology Research and Information Cente

Opposing Effects of Particle Pollution, Ozone, and Ambient Temperature on Arterial Blood Pressure

Background: Diabetes increases the risk of hypertension and orthostatic hypotension and raises the risk of cardiovascular death during heat waves and high pollution episodes

Cumulative exposure to air pollution and long term outcomes after first acute myocardial infarction: A population-based cohort study. Objectives and methodology

<p>Abstract</p> <p>Background</p> <p>Cardiovascular disease is a leading cause of morbidity and mortality worldwide and epidemiological studies have consistently shown an increased risk for cardiovascular events in relation to exposure to air pollution. The Israel Study of First Acute Myocardial Infarction was designed to longitudinally assess clinical outcomes, psychosocial adjustment and quality of life in patients hospitalized with myocardial infarction. The current study, by introducing retrospective air pollution data, will examine the association between exposure to air pollution and outcome in myocardial infarction survivors. This report will describe the methods implemented and measures employed. The study specifically aims to examine the relationship between residential exposure to air pollution and long-term risk of recurrent coronary event, heart failure, stroke, cardiac and all-cause death in a geographically defined cohort of patients with myocardial infarction.</p> <p>Methods/Design</p> <p>All 1521 patients aged ≤65 years, admitted with first myocardial infarction between February 1992 and February 1993 to the 8 hospitals serving the population of central Israel, were followed for a median of 13 years. Data were collected on sociodemographic, clinical and environmental factors. Data from air quality monitoring stations will be incorporated retrospectively. Daily measures of air pollution will be summarised, allowing detailed maps to be developed in order to reflect chronic exposure for each participant.</p> <p>Discussion</p> <p>This study addresses some of the gaps in understanding of the prognostic importance of air pollution exposure after myocardial infarction, by allowing a sufficient follow-up period, using a well-defined community cohort, adequately controlling for multiple and multilevel confounding factors and providing extensive data on various outcomes.</p

Forecasting daily attendances at an emergency department to aid resource planning

<p>Abstract</p> <p>Background</p> <p>Accurate forecasting of emergency department (ED) attendances can be a valuable tool for micro and macro level planning.</p> <p>Methods</p> <p>Data for analysis was the counts of daily patient attendances at the ED of an acute care regional general hospital from July 2005 to Mar 2008. Patients were stratified into three acuity categories; i.e. P1, P2 and P3, with P1 being the most acute and P3 being the least acute. The autoregressive integrated moving average (ARIMA) method was separately applied to each of the three acuity categories and total patient attendances. Independent variables included in the model were public holiday (yes or no), ambient air quality measured by pollution standard index (PSI), daily ambient average temperature and daily relative humidity. The seasonal components of weekly and yearly periodicities in the time series of daily attendances were also studied. Univariate analysis by t-tests and multivariate time series analysis were carried out in SPSS version 15.</p> <p>Results</p> <p>By time series analyses, P1 attendances did not show any weekly or yearly periodicity and was only predicted by ambient air quality of PSI > 50. P2 and total attendances showed weekly periodicities, and were also significantly predicted by public holiday. P3 attendances were significantly correlated with day of the week, month of the year, public holiday, and ambient air quality of PSI > 50.</p> <p>After applying the developed models to validate the forecast, the MAPE of prediction by the models were 16.8%, 6.7%, 8.6% and 4.8% for P1, P2, P3 and total attendances, respectively. The models were able to account for most of the significant autocorrelations present in the data.</p> <p>Conclusion</p> <p>Time series analysis has been shown to provide a useful, readily available tool for predicting emergency department workload that can be used to plan staff roster and resource planning.</p

Genome-Wide Analysis of DNA Methylation and Fine Particulate Matter Air Pollution in Three Study Populations: KORA F3, KORA F4, and the Normative Aging Study

BACKGROUND: Epidemiological studies have reported associations between particulate matter (PM) concentrations and cancer and respiratory and cardiovascular diseases. DNA methylation has been identified as a possible link but so far it has only been analyzed in candidate sites. OBJECTIVES: We studied the association between DNA methylation and short-and mid-term air pollution exposure using genome-wide data and identified potential biological pathways for-additional investigation. METHODS: We collected whole blood samples from three independent studies-KORA F3 (2004-2005) and F4 (2006-2008) in Germany, and the Normative Aging Study (1999-2007) in the United States-and measured genome-wide DNA methylation proportions with the Illumina 450k BeadChip. PM concentration was measured daily at fixed monitoring stations and three different trailing averages were considered and regressed against DNA methylation: 2-day, 7-day and 28-day. Meta-analysis was performed to pool the study-specific results. RESULTS: Random-effect meta-analysis revealed 12 CpG (cytosine-guanine dinucleotide) sites as associated with PM concentration (1 for 2-day average, 1 for 7-day, and 10 for 28-day) at a genome-wide Bonferroni significance level (p 0.05 and I-2< 0.5: the site from the 7-day average results and 3 for the 28-day average. Applying false discovery rate, p-value < 0.05 was observed in 8 and 1,819 additional CpGs at 7- and 28-day average PM2.5 exposure respectively. CONCLUSION: The PM-related CpG sites found in our study suggest novel plausible systemic pathways linking ambient PM exposure to adverse health effect through variations in DNA methylation