Search

BACKGROUND: Concentrations of outdoor nitrogen dioxide (NO2) have been associated with increased mortality. Hazard ratios (HRs) from cohort studies are used to assess population health impact and burden. We undertook meta-analyses to derive concentration-response functions suitable for such evaluations and assessed their sensitivity to study selection based upon cohort characteristics. METHODS: We searched online databases and existing reviews for cohort studies published to October 2016 reporting HRs for NO2 and mortality. We calculated meta-analytic summary estimates using fixed/random effects models. RESULTS: We identified 48 articles analyzing 28 cohorts. Meta-analysis of HRs found positive associations between NO2 and all-cause (1.02 (95% CI: 1.01, 1.03); prediction interval (PI): (0.99, 1.06) per 10µg/m increment in NO2), cardiovascular (1.03 (95% CI: 1.02,1.05); PI: (0.98, 1.08)) , respiratory (1.03 (95% CI: 1.01,1.05); PI: (0.97, 1.10)) and lung cancer mortality (1.05 (95% CI: 1.02,1.08); PI: (0.94, 1.17)) with evidence of substantial heterogeneity between studies. In subgroup analysis, summary HRs varied by age at cohort entry, spatial resolution of pollution estimates, and adjustment for smoking and body mass index at the individual level; for some sub-groups the HR was close to unity, with lower confidence limits below 1. CONCLUSIONS: Given the many uncertainties inherent in the assessment of this evidence base and the sensitivity of health impact calculations to small changes in the magnitude of the HRs, calculation of the impact on health of policies to reduce long-term exposure to NO2 should use prediction intervals and report ranges of impact rather than focusing upon point estimates.This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.

Objective To investigate the relation between exposure to both air and noise pollution from road traffic and birth weight outcomes.Design Retrospective population based cohort study.Setting Greater London and surrounding counties up to the M25 motorway (2317 km2), UK, from 2006 to 2010.Participants 540 365 singleton term live births.Main outcome measures Term low birth weight (LBW), small for gestational age (SGA) at term, and term birth weight.Results Average air pollutant exposures across pregnancy were 41 μg/m3 nitrogen dioxide (NO2), 73 μg/m3 nitrogen oxides (NOx), 14 μg/m3 particulate matter with aerodynamic diameter 13.8 μg/m3during pregnancy.Conclusions The findings suggest that air pollution from road traffic in London is adversely affecting fetal growth. The results suggest little evidence for an independent exposure-response effect of traffic related noise on birth weight outcomes.

Background\ud \ud Exposure to ambient air pollution increases morbidity and mortality, and is a leading contributor to global disease burden. We explored spatial and temporal trends in mortality and burden of disease attributable to ambient air pollution from 1990 to 2015 at global, regional, and country levels.\ud Methods\ud \ud We estimated global population-weighted mean concentrations of particle mass with aerodynamic diameter less than 2·5 μm (PM2·5) and ozone at an approximate 11 km × 11 km resolution with satellite-based estimates, chemical transport models, and ground-level measurements. Using integrated exposure–response functions for each cause of death, we estimated the relative risk of mortality from ischaemic heart disease, cerebrovascular disease, chronic obstructive pulmonary disease, lung cancer, and lower respiratory infections from epidemiological studies using non-linear exposure–response functions spanning the global range of exposure.\ud Findings\ud \ud Ambient PM2·5 was the fifth-ranking mortality risk factor in 2015. Exposure to PM2·5 caused 4·2 million (95% uncertainty interval [UI] 3·7 million to 4·8 million) deaths and 103·1 million (90·8 million 115·1 million) disability-adjusted life-years (DALYs) in 2015, representing 7·6% of total global deaths and 4·2% of global DALYs, 59% of these in east and south Asia. Deaths attributable to ambient PM2·5 increased from 3·5 million (95% UI 3·0 million to 4·0 million) in 1990 to 4·2 million (3·7 million to 4·8 million) in 2015. Exposure to ozone caused an additional 254 000 (95% UI 97 000–422 000) deaths and a loss of 4·1 million (1·6 million to 6·8 million) DALYs from chronic obstructive pulmonary disease in 2015.\ud Interpretation\ud \ud Ambient air pollution contributed substantially to the global burden of disease in 2015, which increased over the past 25 years, due to population ageing, changes in non-communicable disease rates, and increasing air pollution in low-income and middle-income countries. Modest reductions in burden will occur in the most polluted countries unless PM2·5 values are decreased substantially, but there is potential for substantial health benefits from exposure reduction.

Summary Background Up-to-date evidence about levels and trends in disease and injury incidence, prevalence, and years lived with disability (YLDs) is an essential input into global, regional, and national health policies. In the Global Burden of Disease Study 2013 (GBD 2013), we estimated these quantities for acute and chronic diseases and injuries for 188 countries between 1990 and 2013. Methods Estimates were calculated for disease and injury incidence, prevalence, and YLDs using GBD 2010 methods with some important refinements. Results for incidence of acute disorders and prevalence of chronic disorders are new additions to the analysis. Key improvements include expansion to the cause and sequelae list, updated systematic reviews, use of detailed injury codes, improvements to the Bayesian meta-regression method (DisMod-MR), and use of severity splits for various causes. An index of data representativeness, showing data availability, was calculated for each cause and impairment during three periods globally and at the country level for 2013. In total, 35 620 distinct sources of data were used and documented to calculated estimates for 301 diseases and injuries and 2337 sequelae. The comorbidity simulation provides estimates for the number of sequelae, concurrently, by individuals by country, year, age, and sex. Disability weights were updated with the addition of new population-based survey data from four countries. Findings Disease and injury were highly prevalent; only a small fraction of individuals had no sequelae. Comorbidity rose substantially with age and in absolute terms from 1990 to 2013. Incidence of acute sequelae were predominantly infectious diseases and short-term injuries, with over 2 billion cases of upper respiratory infections and diarrhoeal disease episodes in 2013, with the notable exception of tooth pain due to permanent caries with more than 200 million incident cases in 2013. Conversely, leading chronic sequelae were largely attributable to non-communicable diseases, with prevalence estimates for asymptomatic permanent caries and tension-type headache of 2·4 billion and 1·6 billion, respectively. The distribution of the number of sequelae in populations varied widely across regions, with an expected relation between age and disease prevalence. YLDs for both sexes increased from 537·6 million in 1990 to 764·8 million in 2013 due to population growth and ageing, whereas the age-standardised rate decreased little from 114·87 per 1000 people to 110·31 per 1000 people between 1990 and 2013. Leading causes of YLDs included low back pain and major depressive disorder among the top ten causes of YLDs in every country. YLD rates per person, by major cause groups, indicated the main drivers of increases were due to musculoskeletal, mental, and substance use disorders, neurological disorders, and chronic respiratory diseases; however HIV/AIDS was a notable driver of increasing YLDs in sub-Saharan Africa. Also, the proportion of disability-adjusted life years due to YLDs increased globally from 21·1% in 1990 to 31·2% in 2013. Interpretation Ageing of the world's population is leading to a substantial increase in the numbers of individuals with sequelae of diseases and injuries. Rates of YLDs are declining much more slowly than mortality rates. The non-fatal dimensions of disease and injury will require more and more attention from health systems. The transition to non-fatal outcomes as the dominant source of burden of disease is occurring rapidly outside of sub-Saharan Africa. Our results can guide future health initiatives through examination of epidemiological trends and a better understanding of variation across countries. Funding Bill & Melinda Gates Foundation. Background Up-to-date evidence about levels and trends in disease and injury incidence, prevalence, and years lived with disability (YLDs) is an essential input into global, regional, and national health policies. In the Global Burden of Disease Study 2013 (GBD 2013), we estimated these quantities for acute and chronic diseases and injuries for 188 countries between 1990 and 2013. Methods Estimates were calculated for disease and injury incidence, prevalence, and YLDs using GBD 2010 methods with some important refinements. Results for incidence of acute disorders and prevalence of chronic disorders are new additions to the analysis. Key improvements include expansion to the cause and sequelae list, updated systematic reviews, use of detailed injury codes, improvements to the Bayesian meta-regression method (DisMod-MR), and use of severity splits for various causes. An index of data representativeness, showing data availability, was calculated for each cause and impairment during three periods globally and at the country level for 2013. In total, 35 620 distinct sources of data were used and documented to calculated estimates for 301 diseases and injuries and 2337 sequelae. The comorbidity simulation provides estimates for the number of sequelae, concurrently, by individuals by country, year, age, and sex. Disability weights were updated with the addition of new population-based survey data from four countries. Findings Disease and injury were highly prevalent; only a small fraction of individuals had no sequelae. Comorbidity rose substantially with age and in absolute terms from 1990 to 2013. Incidence of acute sequelae were predominantly infectious diseases and short-term injuries, with over 2 billion cases of upper respiratory infections and diarrhoeal disease episodes in 2013, with the notable exception of tooth pain due to permanent caries with more than 200 million incident cases in 2013. Conversely, leading chronic sequelae were largely attributable to non-communicable diseases, with prevalence estimates for asymptomatic permanent caries and tension-type headache of 2·4 billion and 1·6 billion, respectively. The distribution of the number of sequelae in populations varied widely across regions, with an expected relation between age and disease prevalence. YLDs for both sexes increased from 537·6 million in 1990 to 764·8 million in 2013 due to population growth and ageing, whereas the age-standardised rate decreased little from 114·87 per 1000 people to 110·31 per 1000 people between 1990 and 2013. Leading causes of YLDs included low back pain and major depressive disorder among the top ten causes of YLDs in every country. YLD rates per person, by major cause groups, indicated the main drivers of increases were due to musculoskeletal, mental, and substance use disorders, neurological disorders, and chronic respiratory diseases; however HIV/AIDS was a notable driver of increasing YLDs in sub-Saharan Africa. Also, the proportion of disability-adjusted life years due to YLDs increased globally from 21·1% in 1990 to 31·2% in 2013. Interpretation Ageing of the world's population is leading to a substantial increase in the numbers of individuals with sequelae of diseases and injuries. Rates of YLDs are declining much more slowly than mortality rates. The non-fatal dimensions of disease and injury will require more and more attention from health systems. The transition to non-fatal outcomes as the dominant source of burden of disease is occurring rapidly outside of sub-Saharan Africa. Our results can guide future health initiatives through examination of epidemiological trends and a better understanding of variation across countries. Funding Bill & Melinda Gates Foundation.

Here we describe the development of the London Hybrid Exposure Model (LHEM), which calculates exposure of the Greater London population to outdoor air pollution sources, in-buildings, in-vehicles, and outdoors, using survey data of when and where people spend their time. For comparison and to estimate exposure misclassification we compared Londoners LHEM exposure with exposure at the residential address, a commonly used exposure metric in epidemiological research. In 2011, the mean annual LHEM exposure to outdoor sources was estimated to be 37% lower for PM2.5 and 63% lower for NO2 than at the residential address. These decreased estimates reflect the effects of reduced exposure indoors, the amount of time spent indoors (∼95%), and the mode and duration of travel in London. We find that an individual's exposure to PM2.5 and NO2 outside their residential address is highly correlated (Pearson's R of 0.9). In contrast, LHEM exposure estimates for PM2.5 and NO2 suggest that the degree of correlation is influenced by their exposure in different transport modes. Further development of the LHEM has the potential to increase the understanding of exposure error and bias in time-series and cohort studies and thus better distinguish the independent effects of NO2 and PM2.5.

© 2016 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY license Background The Global Burden of Diseases, Injuries, and Risk Factors Study 2015 provides an up-to-date synthesis of the evidence for risk factor exposure and the attributable burden of disease. By providing national and subnational assessments spanning the past 25 years, this study can inform debates on the importance of addressing risks in context. Methods We used the comparative risk assessment framework developed for previous iterations of the Global Burden of Disease Study to estimate attributable deaths, disability-adjusted life-years (DALYs), and trends in exposure by age group, sex, year, and geography for 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks from 1990 to 2015. This study included 388 risk-outcome pairs that met World Cancer Research Fund-defined criteria for convincing or probable evidence. We extracted relative risk and exposure estimates from randomised controlled trials, cohorts, pooled cohorts, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. We developed a metric that allows comparisons of exposure across risk factors—the summary exposure value. Using the counterfactual scenario of theoretical minimum risk level, we estimated the portion of deaths and DALYs that could be attributed to a given risk. We decomposed trends in attributable burden into contributions from population growth, population age structure, risk exposure, and risk-deleted cause-specific DALY rates. We characterised risk exposure in relation to a Socio-demographic Index (SDI). Findings Between 1990 and 2015, global exposure to unsafe sanitation, household air pollution, childhood underweight, childhood stunting, and smoking each decreased by more than 25%. Global exposure for several occupational risks, high body-mass index (BMI), and drug use increased by more than 25% over the same period. All risks jointly evaluated in 2015 accounted for 57·8% (95% CI 56·6–58·8) of global deaths and 41·2% (39·8–42·8) of DALYs. In 2015, the ten largest contributors to global DALYs among Level 3 risks were high systolic blood pressure (211·8 million [192·7 million to 231·1 million] global DALYs), smoking (148·6 million [134·2 million to 163·1 million]), high fasting plasma glucose (143·1 million [125·1 million to 163·5 million]), high BMI (120·1 million [83·8 million to 158·4 million]), childhood undernutrition (113·3 million [103·9 million to 123·4 million]), ambient particulate matter (103·1 million [90·8 million to 115·1 million]), high total cholesterol (88·7 million [74·6 million to 105·7 million]), household air pollution (85·6 million [66·7 million to 106·1 million]), alcohol use (85·0 million [77·2 million to 93·0 million]), and diets high in sodium (83·0 million [49·3 million to 127·5 million]). From 1990 to 2015, attributable DALYs declined for micronutrient deficiencies, childhood undernutrition, unsafe sanitation and water, and household air pollution; reductions in risk-deleted DALY rates rather than reductions in exposure drove these declines. Rising exposure contributed to notable increases in attributable DALYs from high BMI, high fasting plasma glucose, occupational carcinogens, and drug use. Environmental risks and childhood undernutrition declined steadily with SDI; low physical activity, high BMI, and high fasting plasma glucose increased with SDI. In 119 countries, metabolic risks, such as high BMI and fasting plasma glucose, contributed the most attributable DALYs in 2015. Regionally, smoking still ranked among the leading five risk factors for attributable DALYs in 109 countries; childhood underweight and unsafe sex remained primary drivers of early death and disability in much of sub-Saharan Africa. Interpretation Declines in some key environmental risks have contributed to declines in critical infectious diseases. Some risks appear to be invariant to SDI. Increasing risks, including high BMI, high fasting plasma glucose, drug use, and some occupational exposures, contribute to rising burden from some conditions, but also provide opportunities for intervention. Some highly preventable risks, such as smoking, remain major causes of attributable DALYs, even as exposure is declining. Public policy makers need to pay attention to the risks that are increasingly major contributors to global burden. Funding Bill & Melinda Gates Foundation.

Evidence on the effects of long-term exposure to traffic pollution on health is inconsistent. In Greater London we examined associations between traffic pollution and emergency hospital admissions for cardio-respiratory diseases by applying linear and piecewise linear Poisson regression models in a small-area analysis. For both models the results for children and adults were close to unity. In the elderly, linear models found negative associations whereas piecewise models found non-linear associations characterized by positive risks in the lowest and negative risks in the highest exposure category. An increased risk was observed among those living in areas with the highest socioeconomic deprivation. Estimates were not affected by adjustment for traffic noise. The lack of convincing positive linear associations between primary traffic pollution and hospital admissions agrees with a number of other reports, but may reflect residual confounding. The relatively greater vulnerability of the most deprived populations has important implications for public health.

There is considerable concern about possible links between ambient air pollution and the upward trend in asthma. This chapter reviews the mechanistic and epidemiological evidence concerning air pollution and asthma and examines the hypothesis that trends in asthma could be explained by air pollution. It is concluded that existing evidence is not sufficient to link air pollution with the initiation of asthma in healthy subjects. Although there is better evidence that air pollution can provoke or aggravate asthma, it probably plays a minor role at a public health level, in comparison with other factors. It is therefore unlikely that trends in asthma could be explained by air pollution. Furthermore, correlations between some air pollutants and asthma over time are not consistent with the hypothesis. The possibility of a specific effect of motor vehicle pollution needs further investigation but this factor is unlikely to be the main cause of the worldwide increase in asthma.

Background: Particulate air pollution is associated with increased mortality. There is a need for European results from multicountry databases concerning cause-specific mortality to obtain more accurate effect estimates. Methods: We report the estimated effects of ambient particle concentrations (black smoke and particulate matter less than 10 Am [PM10]) on cardiovascular and respiratory mortality, from 29 European cities, within the Air Pollution and Health: a European Approach (APHEA2) project. We applied a 2-stage hierarchical modeling approach assessing city-specific effects first and then overall effects. City characteristics were considered as potential effect modifiers. Results: An increase in PM10 by 10 mu g/m(3) (lag 0 + 1) was associated with increases of 0.76% (95% confidence interval = 0.47 to 1.05%) in cardiovascular deaths and 0.58% (0.21 to 0.95%) in respiratory deaths. The same increase in black smoke was associated with increases of 0.62% (0.35 to 0.90%) and 0.84% (0.11 to 1.57%), respectively. Conclusions: These effect estimates are appropriate for health impact assessment and standard-setting procedures.

Within the framework of the APHEA2 (Air Pollution on Health: a European Approach) project, the effects of ambient particles on mortality among persons greater than or equal to65 yrs were investigated. Daily measurements for particles with a 50%, cut-off aerodynamic diameter of 10 pm (PM10) and black smoke (BS), as well as the daily number of deaths among persons 65 yrs of age, from 29 European cities, have been collected. Data on other pollutants and meteorological variables, to adjust for confounding effects and data on city characteristics, to investigate potential effect modification, were also recorded. For individual city analysis, generalised additive models extending Poisson regression, using a locally weighted regression (LOESS) smoother to control for seasonal effects, were applied. To combine individual city results and explore effect modification, second stage regression models were applied. The per cent increase (95% confidence intervals), associated with a 10 mug.m(-3) increase in PM10, in the elderly daily number of deaths was 0.8%, (0.7-0.9%) and the corresponding number for BS was 0.6%, (0.5-0.8%). The effect size was modified by the long-term average levels of nitrogen dioxide (higher levels were associated with larger effects), temperature (larger effects were observed in warmer countries), and by the proportion of the elderly in each city (a larger proportion was associated with higher effects). These results indicate that ambient particles have effects on mortality among the elderly, with relative risks comparable or slightly higher than those observed for total mortality and similar effect modification patterns. The effects among the older persons are of particular importance, since the attributable number of events will be much larger, compared to the number of deaths among the younger population.

Short-term effects of air pollution on daily mortality in eight western and five central-eastern European countries have been reported previously, as part of the APHEA project. One intriguing finding was that the effects were lower in central-eastern European cities. The analysis used sinusoidal terms for seasonal control and polynomial terms for meteorologic variables, but chi is a more rigid approach than the currently accepted method, which uses generalized additive models (GAM). We therefore reanalyzed the original data to examine the sensitivity of the results to the statistical model. The data were identical to those used in the earlier analyses. The outcome was the daily total number of deaths, and the pollutants analyzed were black smoke (BS) and sulfur dioxide (SO2). The analyses were restricted to days with pollutant concentration < 200 g/m(3) and < 150 g/m(3) alternately. We used Poisson regression in a GAM model, and combined individual city regression coefficients using fixed and random-effect models. An increase in BS by 50 mug/m(3) was associated with a 2.2% and 3.1% increase in mortality when analysis was restricted to days < 200 g/m(3) and < 150 g/m(3), respectively. The corresponding figures were 5.0% and 5.6% for a similar increase in SO2. These estimates are larger than the ones published previously: by 69% for BS and 55% for SO2. The increase occurred only in central-eastern European cities. The ratio of western to central-eastern cities for estimates was reduced to 1.3 for BS (previously 4.8) and 2.6 for SO2 (previously 4.4). We conclude that part of the heterogeneity in the estimates of air pollution effects between western and central-eastern cities reported in previous publications was caused by the statistical approach used and the inclusion of days with pollutant levels above 150 mug/m(3). However, these results must be investigated further.

We present the results of the Air Pollution and Health: A European Approach (APHEA-2,) project on short-term effects of ambient particles on mortality with emphasis on effect modification. We used daily measurements for particulate matter less than 10 mum in aerodynamic diameter (PM10) and/or black smoke from 29 European cities. We considered confounding from other pollutants as well as meteorologic and chronologic variables. We investigated several variables describing the cities’ pollution, climate, population, and geography as potential effect modifiers. For the individual city analysis, generalized additive models extending Poisson regression, using a smoother to control for seasonal patterns, were applied. To provide quantitative summaries of the results and explain remaining heterogeneity, we applied second-stage regression models. The estimated increase in the daily number of deaths for all ages for a 10 mug/m(3) increase in daily PM10 or black smoke concentrations was 0.6% [95% confidence interval (CI) = 0.4-0.8%], whereas for the elderly it was slightly higher. We found important effect modification for several of the variables studied. Thus, in a city with low average NO2, the estimated increase in daily mortality for an increase of 10 mug/m(3) in PM10 was 0.19 (95% CI = 0.00-0.41), whereas in a city with high average NO2 it was 0.80% (95% CI = 0.67-0.93%); in a relatively cold climate the corresponding effect was 0.29% (95% CI = 0.16-0.42), whereas in a warm climate it was 0.82% (95% CI = 0.69-0.96); in a city with low standardized mortality rate it was 0.80% (95% CI = 0.65-0.95%), and in one with a high rate it was 0.43% (95% CI = 0.24-0.62). Our results confirm those previously reported on the effects of ambient particles on mortality. Furthermore, they show that the heterogeneity found in the effect parameters among cities reflects real effect modification, which is explained by specific city characteristics.

The Air Pollution and Health: a European Approach (APHEA) project is a coordinated study of the short-term effects of air pollution on mortality and hospital admissions. Five West European cities (i.e., London, Amsterdam, Rotterdam, Paris, Milano) contributed several years of hospital admissions data for all respiratory causes. In the current study, the authors describe the results obtained from the quantitative pooling (meta-analysis) of local analyses. The diagnostic group was defined by ICD 460-519. The age groups studied were 15-64 y (i.e., adults) and 65 + y (elderly). The air pollutants studied were sulfur dioxide; particles (i.e., Black Smoke or total suspended particles); ozone; and nitrogen dioxide. The pollutants were obtained from existing fixed-site monitors in a standardized manner. We used Poisson models and standardized confounder models to examine the associations between daily hospital admissions and air pollution. We conducted quantitative pooling by calculating the weighted means of local regression coefficients. We used a fixed-effects model when no heterogeneity could be detected; otherwise, we used a random-effects model. When possible, the authors investigated the factors correlated with heterogeneity. The most consistent and strong finding was a significant increase of daily admissions for respiratory diseases (adults and elderly) with elevated levels of ozone. This finding was stronger in the elderly, had a rather immediate effect (same or next day), and was homogeneous over cities. The elderly were affected more during the warm season. The Sulfur dioxide daily mean was available in all cities, and it was not associated consistently with an adverse effect. Effects were present in areas in which more than one station was used in the assessment of daily exposure. Some significant associations were observed, although no conclusion that related to an overall particle effect could be drawn. The effect of Black Smoke was significantly stronger with high nitrogen dioxide levels on the same day, but nitrogen dioxide itself was not associated with admissions. The ozone results were in good agreement with the results of similar U.S. studies. The coherence of the results of this study and other results gained under different conditions strengthens the argument for causality.

In this study, the position bound shape, spreading, detachment and migration of adhering HUVEC endothelial cells on dichlorodimethylsilane (DDS) chemical gradient surfaces was investigated during exposure to flow in a parallel plate flow chamber in the presence of` serum proteins. Gradient surfaces were prepared by the diffusion method and characterized by the Wilhelmy plate technique for their wettability. Ln order to measure the possible influence of wettability steepness on the position bound cellular response. shallow and steep wettability gradients were prepared by applying two different diffusion times and DDS-concentrations. Quantitative analyses of the cellular response on the gradient surfaces showed that the position bound spread area and,shape Factor of adhering cells increased when going from the hydrophobic to the hydrophilic end, concurrent with the steepness of the gradient. After exposure to Row, cells detached immediately from the hydrophobic side and maintained their positions more easily on the hydrophilic side. Furthermore, it was shown that the pc:,position bound detachment and migration of cells depended on the steepness of` the wettability gradient and the direction of the flow. When the Row was to the hydrophilic end, migration velocity did not vary along the length of the gradients, and was lower on the steep (approximately 2 mu m/min) than on the shallow (approximately ly 3 mu m/min) gradients. However, when flow was to the hydropbobic end, migration velocities appeared position bound and were higher on the hydrophobic ends of both gradients.

We investigated the short-term effects of air pollution on hospital admissions for chronic obstructive pulmonary disease (COPD) in Europe. As part of a European project (Air Pollution and Health, a European Approach (APHEA)), we analysed data from the cities of Amsterdam, Barcelona, London, Milan, Paris and Rotterdam, using a standardized approach to data eligibility and statistical analysis. Relative risks for daily COPD admissions were obtained using Poisson regression, controlling for: seasonal and other cycles; influenza epidemics; day of the week; temperature; humidity and autocorrelation. Summary effects for each pollutant were estimated as the mean of each city’s regression coefficients weighted by the inverse of the variance, allowing for additional between-cities variance, as necessary. For all ages, the relative risks (95% confidence limits (95% CL)) for a 50 mu g.m(-3) increase in daily mean level of pollutant (lagged 1-3 days) were (95% CL): sulphur dioxide 1.02 (0.98, 1.06); black smoke 1.04 (1.01, 1.06); total suspended particulates 1.02 (1.00, 1.05), nitrogen dioxide 1.02 (1.00, 1.05) and ozone (8 h) 1.04 (1.02, 1.07). The results confirm that air pollution is associated with daily admissions for chronic obstructive pulmonary disease in European cities with widely varying climates. The results for particles and ozone are broadly consistent with those from North America, though the coefficients for particles are substantially smaller. Overall, the evidence points to a causal relationship but the mechanisms of action, exposure response relationships and pollutant interactions remain unclear.

Objectives: To carry out a prospective combined quantitative analysis of the associations between all cause mortality and ambient particulate matter and sulphur dioxide. . Design: Analysis of time series data on daily number of deaths from all causes and concentrations of sulphur dioxide and particulate matter (measured as black smoke or particles smaller than 10 mu m in diameter (PM10)) and potential confounders. Setting: 12 European cities in the APHEA project (Air Pollution and Health: a European Approach). Main outcome measure: Relative risk of death. Results: In western European cities it was found that an increase of 50 mu g/m(3) in sulphur dioxide or black smoke was associated with a 3% (95% confidence interval 2% to 4%) increase in daily mortality and the corresponding figure for PM10 was 2% (1% to 3%). In central eastern European cities the increases in mortality associated with a 50 mu/m(3) change in sulphur dioxide was 0.8% (-0.1% to 2.4%) and in black smoke 0.6% (0.2% to 1.1%). Cumulative effects of prolonged (two to four days) exposure to air pollutants resulted to estimates comparable with the one day effects. The effects of both pollutants were stronger during the summer and were mutually independent Conclusions: The internal consistency of the results in western European cities with wide differences in climate and environmental conditions suggest that these associations may be causal. The long term health impact of these effects is uncertain, but today’s relatively low levels of sulphur dioxide and particles still have detectable short term effects on health and further reductions in air pollution are advisable.

Background and objectives - Results from several studies over the past five years have shown that the current levels of pollutants in Europe and North America have adverse shortterm effects on health. The APHEA project aims to quantifying these in Europe, using standardised methodology. The project protocol and analytical methodology are presented here. Design - Daily time series data were gathered for several air pollutants (sulphur dioxide; particulate matter, measured as total particles or as the particle fraction with an aerodynamic diameter smaller than a certain cut off, or as black smoke; nitrogen dioxide; and ozone) and health outcomes (the total and cause specific number of deaths and emergency hospital admissions). The data included fulfilled the quality criteria set by the APHEA protocol. Setting - Fifteen European cities from 10 different countries with a total population over 25 million. Methodology - The APHEA collaborative group decided on a specific methodological procedure to control for confounding effects and evaluate the hypothesis. At the same time there was sufficient flexibility to allow local characteristics to be taken into account. The procedure included modelling of all potential confounding factors (that is, seasonal and long term patterns, meteorological factors, day of the week, holidays, and other unusual events), choosing the ‘’best” air pollution models, and applying diagnostic tools to check the adequacy of the models. The final analysis used autoregressive Poisson models allowing for overdispersion. Effects were reported as relative risks contrasting defined increases in the corresponding pollutant levels. Each participating group applied the analyses to their own data. Conclusions - This methodology enabled results from many different European settings to be considered collectively. It represented the best available compromise between feasibility, comparability, and local adaptibility when using aggregated time series data not originally collected for the purpose of epidemiological studies.

Recent studies investigating the adverse health effects of air pollution indicate that effects exist around and below the current national and international air quality guidelines and standards, However, the difficult methodological issues involved, and the diversity of analytical techniques so far applied, hinder direct between-study comparability and the drawing of clear conclusions. The APHEA (Air Pollution on Health: European Approach) project is an attempt to provide quantitative estimates of the short-term health effects of air pollution, using an extensive data base from 10 different European countries, which represent various social, environmental and air pollution situations. Within the framework of the project, the methodology of analysing epidemiological time series data, as well as that of performing meta-analysis, are further developed and standardized. Data have been collected from 15 European cities with a total population exceeding 25 million. The exposure data consist of daily measurements of black smoke, sulphur dioxide, suspended particles, nitrogen dioxide and ozone (each available in several, though not all, cities) from already existing monitoring networks. There is substantial variability in air pollution mixtures and air pollutant levels in participating cities. The mean (24 h) levels of SO2 range 27-327 mu g . m(3) in the winter season, and those of black smoke range 15-292 mu g . m(3). The mean (1 h) levels of ozone in the summer season range 32-166 mu g . m(3). The outcome data are daily counts of total and cause-specific deaths and hospital emergency admissions. Data on potential confounders (mainly meteorological and chronological variables) are also used. There is large diversity in the climatic conditions in the different cities. Thus, the mean winter temperature ranges -4 to 10 degrees C (minimum -1 to -37 degrees C) and the mean summer temperature 16 degrees to 26 degrees C (maximum 26 degrees to 35 degrees C). Poisson regression allowing for autocorrelation and overdispersion is used in the analysis, after careful control of seasonality and other periodic patterns, and other confounding effects. The protocol and procedures followed are described, and the advantages and expectations from such an extensive European collaborative effort are presented and discussed.

In this paper a number of techniques are investigated for predicting the performance of a digital system in fading channels. A method is presented which combines both bit error rate simulation and site-specific channel characterisation using ray tracing techniques. Probability density functions are developed for the resulting signal variations which show instantaneous bit error rate versus fade depth. Using this approach, the irreducible error rate for both random FM and RMS delay spread have been determined for π/4DQPSK. It is shown that RMS delay spread alone cannot fully represent the distorting effect of the wideband channel. However, if combined with narrowband fading statistics, it becomes possible to estimate the average bit error rate for a given propagation environment. To increase the speed of our fading simulations, an importance sampling approach has also been developed which yields results that are comparable to those generated from full simulations