The APHEA 2 project investigated short-term health effects of particles in eight European cities. In each city associations between particles with an aerodynamic diameter of less than 10 microm (PM(10)) and black smoke and daily counts of emergency hospital admissions for asthma (0-14 and 15-64 yr), chronic obstructive pulmonary disease (COPD), and all-respiratory disease (65+ yr) controlling for environmental factors and temporal patterns were investigated. Summary PM(10) effect estimates (percentage change in mean number of daily admissions per 10 microg/m(3) increase) were asthma (0-14 yr) 1.2% (95% CI: 0.2, 2.3), asthma (15-64 yr) 1.1% (0.3, 1.8), and COPD plus asthma and all-respiratory (65+ yr) 1.0% (0.4, 1.5) and 0.9% (0.6, 1.3). The combined estimates for Black Smoke tended to be smaller and less precisely estimated than for PM(10). Variability in the sizes of the PM(10) effect estimates between cities was also investigated. In the 65+ groups PM(10) estimates were positively associated with annual mean concentrations of ozone in the cities. For asthma admissions (0-14 yr) a number of city-specific factors, including smoking prevalence, explained some of their variability. This study confirms that particle concentrations in European cities are positively associated with increased numbers of admissions for respiratory diseases and that some of the variation in PM(10) effect estimates between cities can be explained by city characteristics.
This report provides the methodology and findings from the project: Air Pollution and Health: a European and North American Approach (APHENA). The principal purpose of the project was to provide an understanding of the degree of consistency among findings of multicity time-series studies on the effects of air pollution on mortality and hospitalization in several North American and European cities. The project included parallel and combined analyses of existing data. The investigators sought to understand how methodological differences might contribute to variation in effect estimates from different studies, to characterize the extent of heterogeneity in effect estimates, and to evaluate determinants of heterogeneity. The APHENA project was based on data collected by three groups of investigators for three earlier studies: (1) Air Pollution and Health: A European Approach (APHEA), which comprised two multicity projects in Europe. (Phase 1 [APHEA1] involving 15 cities, and Phase 2 [APHEA2] involving 32 cities); (2) the National Morbidity, Mortality, and Air Pollution Study (NMMAPS), conducted in the 90 largest U.S. cities; and (3) multicity research on the health effects of air pollution in 12 Canadian cities.
The project involved the initial development of analytic approaches for first-stage and second-stage analyses of the time-series data and the subsequent application of the resulting methods to the time-series data. With regard to the first-stage analysis, the various investigative groups had used conceptually similar approaches to the key issues of controlling for temporal confounding and temperature; however, specific methods differed. Consequently, the investigators needed to establish a standard protocol, but one that would be linked to prior approaches. Based on exploratory analyses and simulation studies, a first-stage analysis protocol was developed that used generalized linear models (GLM) with either penalized splines (PS) or natural splines (NS) to adjust for seasonality, with 3, 8, or 12 degrees of freedom (df) per year and also the number of degrees of freedom chosen by minimizing the partial autocorrelation function (PACF) of the model's residuals. For hospitalization data, the approach for model specification followed that used for mortality, accounting for seasonal patterns, but also, for weekend and vacation effects, and for epidemics of respiratory disease. The data were also analyzed to detect potential thresholds in the concentration-response relationships. The second-stage analysis used pooling approaches and assessed potential effect modification by sociodemographic characteristics and indicators of the pollution mixture across study regions. Specific quality control exercises were also undertaken. Risks were estimated for two pollutants: particulate matter - 10 pm in aerodynamic diameter (PM10) and ozone (O3).
The first-stage analysis yielded estimates that were relatively robust to the underlying smoothing approach and to the number of degrees of freedom. The first-stage APHENA results generally replicated the previous independent analyses performed by the three groups of investigators. PM10 effects on mortality risk estimates from the APHEA2 and NMMAPS databases were quite close, while estimates from the Canadian studies were substantially higher. For hospitalization, results were more variable without discernable patterns of variation among the three data sets. PM10 effect-modification patterns, explored only for cities with daily pollution data (i.e., 22 in Europe and 15 in the U.S.), were not entirely consistent across centers. Thus, the levels of pollutants modified the effects differently in Europe than in the United States. Climatic variables were important only in Europe. In both Europe and the United States, a higher proportion of older persons in the study population was associated with increased PM10 risk estimates, as was a higher rate of unemployment - the sole indicator of socioeconomic status uniformly available across the data sets. APHENA study results on the effects of O3 on mortality were less comprehensive than for PM10 because the studies from the three regions varied in whether they analyzed data for the full year or only for the summer months. The effects tended to be larger for summer in Europe and the United States. In the United States they were lower when controlled for PM10. The estimated effect of O3 varied by degrees of freedom and across the three geographic regions. The effects of O3 on mortality were larger in Canada, and there was little consistent indication of effect modification in any location.
APHENA has shown that mortality findings obtained with the new standardized analysis were generally comparable to those obtained in the earlier studies, and that they were relatively robust to the data analysis method used. For PM10, the effect-modification patterns observed were not entirely consistent between Europe and the United States. For O3, there was no indication of strong effect modification in any of the three data sets.
Sudden infant death syndrome (SIDS) affects approximately 1 in 1000 live births and is the most common cause of infant death after the perinatal period.
To determine the influence of air pollution on the incidence of SIDS.
Time-series analyses were performed to compare the daily mortality rates for SIDS and the daily air pollution concentrations in each of 12 Canadian cities during the period of 1984-1999. Serial autocorrelation was controlled for by city, and then the city-specific estimates were pooled. Increased daily rates of SIDS were associated with increases, on the previous day, in the levels of sulfur dioxide (SO2), nitrogen dioxide (NO2), and carbon monoxide but not ozone or fine particles measured every sixth day. Effects persisted despite adjustments for season alone or the combination of daily mean temperature, relative humidity, and changes in barometric pressure for NO2 and SO2 but not carbon monoxide.
Increases in both SO2 and NO2, equivalent to their interquartile ranges, were associated with a 17.72% increase in SIDS incidence.
Ambient SO2 and NO2 may be important risk factors for SIDS.
Atmospheric pollution has been proposed as one of the possible factors responsible for increases in asthma mortality and morbidity.
We sought to examine whether we could demonstrate a relationship between emergency room visits for asthma and alterations in environmental conditions.
Over a 1-year period, the frequency of emergency room visits for asthma in a large urban hospital were documented and compared to outdoor concentrations of SO2, NO2, and ozone in addition to two overall measures of air quality (air pollution index and air quality index).
A total of 854 emergency room visits were noted with the highest number of visits occurring in May and between September and December. Significant variations in the frequency of visits as well as environmental conditions could be seen on a daily basis. Despite comparisons of results on a daily, weekly, and monthly basis, no significant relationships could be found between any of the pollution indices and emergency room visits. Staggering visits by 1 and 7 days, however, revealed a relationship between emergency room visits and air pollution index and air quality index. An association between emergency room visits and NO2 and ozone was seen when visits were staggered by 7 but not by 1 day.
We conclude the fluctuations in overall air quality are associated with increased frequency of emergency room visits but only when data are lagged by a predefined period.
Natural areas are important interfaces between air quality, the public, science and regulation. In the United States and Canada, national parks received over 315million visits during 2004. Many natural areas have been experiencing decreased visibility, increased ozone (O(3)) levels and elevated nitrogen deposition. Ozone is the most pervasive air pollutant in North American natural areas. There is an extensive scientific literature on O(3) exposure-tree response in chambered environments and, lately, free-air exposure systems. Yet, less is known about O(3) impacts on natural terrestrial ecosystems. To advance scientifically defensible O(3) risk assessment for natural forest areas, species-level measurement endpoints must be socially, economically and ecologically relevant. Exposure-based indices, based on appropriate final endpoints, present an underused opportunity to meet this need. Exposure-plant indices should have a high degree of statistical significance, have high goodness of fit, be biologically plausible and include confidence intervals to define uncertainty. They must be supported by exposure-response functions and be easy to use within an air quality regulation context. Ozone exposure-response indices developed within an ambient air context have great potential for improving risk assessment in natural forest areas and enhancing scientific literacy.
BACKGROUND: Ambient air pollution has been associated with increases in acute morbidity and mortality. The objective of this study was to evaluate the short-term effects of urban air pollution on cardiac hospital readmissions in survivors of myocardial infarction, a potentially susceptible subpopulation. METHODS AND RESULTS: In this European multicenter cohort study, 22,006 survivors of a first myocardial infarction were recruited in Augsburg, Germany; Barcelona, Spain; Helsinki, Finland; Rome, Italy; and Stockholm, Sweden, from 1992 to 2000. Hospital readmissions were recorded in 1992 to 2001. Ambient nitrogen dioxide, carbon monoxide, ozone, and mass of particles
The authors investigated the association between daily variations in ozone and cause-specific mortality. Fixed-site air pollution monitors in Montreal, Quebec, provided daily mean levels of ozone, particles, and other gaseous pollutants. Information on the date and underlying cause of death was obtained for residents of Montreal who died in the city between 1984 and 1993. The authors regressed the logarithm of daily counts of cause-specific mortality on mean levels of ozone, after accounting for seasonal and subseasonal fluctuations in the mortality time series, non-Poisson dispersion, and weather variables. The effect of ozone on mortality was generally higher in the warm season and among persons aged 65 years or over. For an increase in the 3-day running mean concentration of ozone of 21.3 microg/m(3), the percentage of increase in daily deaths in the warm season was the following: nonaccidental deaths, 3.3% (95% confidence interval (CI): 1.7, 5.0); cancer, 3.9% (95% CI: 1.0, 6.91); cardiovascular diseases, 2.5% (95% CI: 0.2, 5.0); and respiratory diseases, 6.6% (95% CI: 1.8, 11.8). These results were independent of the effects of other pollutants and were consistent with a log-linear response function.
The effects of low levels of air pollution and weather conditions on the number of patients admitted to hospitals for exacerbation of chronic bronchitis or emphysema (n = 2807) was studied in Helsinki during a 3-year period, 1987-1989. The daily number of admissions via the emergency room was significantly associated with prevailing levels of sulfur dioxide (SO2) and nitrogen dioxide (NO2) in Poisson regressions controlled for weather, season, time trends, and day of the week, whereas the total number of admissions (via the emergency room and otherwise) was not significantly associated with these pollutants. The effect of SO2 was observed only among those under 65 years old; a significant peak of admissions was seen during the same day (RR, 1.31 for a 2.7-fold increase in SO2; 95% CI, 1.01-1.70; P = 0.039), and another after a 3-day lag (RR, 1.39; 95% CI, 1.05-1.86; P = 0.021). The effect of NO2 was strongest after a 6-day lag and was significant only among those over 64 years old (RR, 1.31; 95% CI, 1.03-1.66; P = 0.022). The average of mean 24-hr concentrations of NO2 was 39 micrograms/m3 (0.021 ppm) and that for SO2 was 19 micrograms/m3 (0.0067 ppm). No relationship was found between admissions and the concentrations of total suspended particulates (TSP) or ozone (O3), the temperature, or the relative humidity. However, the number of admissions among those over 64 years of age was significantly lower, irrespective of temperature, during the summer than during other seasons. The mean daily concentration of O3 was fairly low (22 micrograms/m3 or 0.011 ppm), but that of TSP was high, 76 micrograms/m3. the mean temperature was low, +4.7 degrees C. These results suggest that SO2 and NO2 concentrations lower than those given as guidelines in many countries, and lower than previously shown, may increase the incidence of symptoms in some patients with chronic bronchitis or emphysema.
Assessment of the global burden of disease is based on epidemiological cohort studies that connect premature mortality to a wide range of causes, including the long-term health impacts of ozone and fine particulate matter with a diameter smaller than 2.5 micrometres (PM2.5). It has proved difficult to quantify premature mortality related to air pollution, notably in regions where air quality is not monitored, and also because the toxicity of particles from various sources may vary. Here we use a global atmospheric chemistry model to investigate the link between premature mortality and seven emission source categories in urban and rural environments. In accord with the global burden of disease for 2010 (ref. 5), we calculate that outdoor air pollution, mostly by PM2.5, leads to 3.3 (95 per cent confidence interval 1.61-4.81) million premature deaths per year worldwide, predominantly in Asia. We primarily assume that all particles are equally toxic, but also include a sensitivity study that accounts for differential toxicity. We find that emissions from residential energy use such as heating and cooking, prevalent in India and China, have the largest impact on premature mortality globally, being even more dominant if carbonaceous particles are assumed to be most toxic. Whereas in much of the USA and in a few other countries emissions from traffic and power generation are important, in eastern USA, Europe, Russia and East Asia agricultural emissions make the largest relative contribution to PM2.5, with the estimate of overall health impact depending on assumptions regarding particle toxicity. Model projections based on a business-as-usual emission scenario indicate that the contribution of outdoor air pollution to premature mortality could double by 2050.
A retrospective study using ambient ozone, temperature, and other environmental variables and their effect on the frequency of hospital visits for asthma was conducted in New Jersey, an area that often exceeds the allowable national standard for ozone. Data on emergency department visits for asthma, bronchitis, and finger wounds (a nonrespiratory control) were analyzed for the period May through August for 1988 and 1989. Asthma visits were correlated with temperature while the correlation between asthma visits and ozone concentration was nonsignificant. However, when temperature was controlled for in a multiple regression analysis, a highly significant relationship between asthma visits and ozone concentration was identified. Between 13 and 15% of the variability of the asthma visits was explained in the regression model by temperature and ambient ozone levels. This association, when compared to similar studies in Canada, shows the contribution of ozone to asthma admissions to be stronger in areas with higher ozone concentrations. Thus, among regions with periodic accumulations of ozone in the ambient atmosphere, an exposure-response relationship may be discernible. This supports the need to attain air quality standards for ozone to protect individuals in the general population from the adverse health effects caused by ambient ozone exposure.