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Background: Long-term exposure to particulate air pollution has been associated with mortality in urban cohort studies. Few studies have investigated the association between emission contributions from different particle sources and mortality in large-scale population registries, including non-urban populations., Objectives: The aim of the study was to evaluate the associations between long-term exposure to particulate air pollution from different source categories and non-accidental mortality in the Netherlands based on existing national databases., Methods: We used existing Dutch national databases on mortality, individual characteristics, residence history, neighbourhood characteristics and modelled air pollution concentrations from different sources and air pollution components: particulate matter PM10, primary particulate matter PM10 (PPM10), particulate matter PM2.5, primary particulate matter PM2.5 (PPM2.5), elemental carbon (EC), nitrogen dioxide (NO 2 ) and secondary inorganic aerosol (SIA) in PM10 (SIA10) or in PM2.5 (SIA2.5). We established a cohort of 7.5 million individuals 30 years or older. We followed the cohort for eight years (2008-2015). We applied Cox proportional hazard regression models adjusting for potential individual and area-specific confounders., Results: We found statistically significant associations between total and primary particulate matter (PM10 and PM2.5), elemental carbon and mortality. Adjustment for nitrogen dioxide did not change the associations. Secondary inorganic aerosol showed less consistent associations. All primary PM sources were associated with mortality, except agricultural emissions and, depending on the statistical model, industrial PM emissions., Conclusions: We could not identify one or more specific source categories of particulate air pollution as main determinants of the mortality effects found in this and in a previous study. This suggests that present policy measures should be focussed on the wider spectrum of air pollution sources instead of on specific sources., (Copyright © 2018 The Authors. Published by Elsevier B.V. All rights reserved.)

Background: Although the health effects of long term exposure to air pollution are well established, it is difficult to effectively communicate the health risks of this (largely invisible) risk factor to the public and policy makers. The purpose of this study is to develop a method that expresses the health effects of air pollution in an equivalent number of daily passively smoked cigarettes., Methods: Defined changes in PM2.5, nitrogen dioxide (NO2) and Black Carbon (BC) concentration were expressed into number of passively smoked cigarettes, based on equivalent health risks for four outcome measures: Low Birth Weight (<2500g at term), decreased lung function (FEV1), cardiovascular mortality and lung cancer. To describe the strength of the relationship with ETS and air pollutants, we summarized the epidemiological literature using published or new meta-analyses., Results: Realistic increments of 10µg/m(3) in PM2.5 and NO2 concentration and a 1µg/m(3) increment in BC concentration correspond to on average (standard error in parentheses) 5.5 (1.6), 2.5 (0.6) and 4.0 (1.2) passively smoked cigarettes per day across the four health endpoints, respectively. The uncertainty reflects differences in equivalence between the health endpoints and uncertainty in the concentration response functions. The health risk of living along a major freeway in Amsterdam is, compared to a counterfactual situation with 'clean' air, equivalent to 10 daily passively smoked cigarettes.., Conclusions: We developed a method that expresses the health risks of air pollution and the health benefits of better air quality in a simple, appealing manner. The method can be used both at the national/regional and the local level. Evaluation of the usefulness of the method as a communication tool is needed., (Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Evaluations of the effectiveness of air pollution policy interventions are scarce. This study investigated air pollution at street level before and after implementation of local traffic policies including low emission zones (LEZ) directed at heavy duty vehicles (trucks) in five Dutch cities., Methods: Measurements of PM(10), PM(2.5), 'soot', NO(2), NO(x), and elemental composition of PM(10) and PM(2.5) were conducted simultaneously at eight streets, six urban background locations and four suburban background locations before (2008) and two years after implementation of the policies (2010). The four suburban locations were selected as control locations to account for generic air pollution trends and weather differences., Results: All pollutant concentrations were lower in 2010 than in 2008. For traffic-related pollutants including 'soot' and NO(x) and elemental composition (Cr, Cu, Fe) the decrease did not differ significantly between the intervention locations and the suburban control locations. Only for PM(2.5) reductions were considerably larger at urban streets (30%) and urban background locations (27%) than at the matching suburban control locations (20%). In one urban street where traffic intensity was reduced with 50%, 'soot', NO(x) and NO(2) concentrations were reduced substantially more (41, 36 and 25%) than at the corresponding suburban control location (22, 14 and 7%)., Conclusion: With the exception of one urban street where traffic flows were drastically reduced, the local traffic policies including LEZ were too modest to produce significant decreases in traffic-related air pollution concentrations., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Background: Daily variations in the levels of air pollution are well known to be associated with daily variations in mortality counts. Given the large number of time-series studies, there is little need for simple replication of these results in additional locations. However, additional analyses of time-series data might be useful in elucidating remaining questions on the role of air pollution on mortality., Objectives: Because of ongoing issues related to causality, changing toxicity, the difficulty in isolating the independent effects of individual pollutants, the availability of new methods to detect effect thresholds, and questions about the extent to which effects are restricted to frail members of the population, additional analyses of time-series data might be helpful in addressing these issues. We show an example where additional time-series analyses can be helpful in elucidating specific questions in the field of air pollution epidemiology., Methods: We analysed daily mortality and air pollution data using Poisson regression in generalised additive models. Air pollution data for the overall period 1992-2006 and for four different periods were analysed to assess the overall risk estimates for the whole period and to assess variability over time for the different effect estimates., Results and Conclusion: We found some statistically significant upward trends, but this was only the case for a few associations without a consistent pattern over the cause-specific deaths. Whether these findings are consistent over time or whether our findings are merely the result of statistical chance can only be elucidated by continuation of monitoring of the relative risks over time in the future. Although these results may indicate that both photochemical and particulate matter air pollution might have become more toxic, the lack of a clear pattern in the results makes these conclusions speculative., (Copyright © 2010 Elsevier Inc. All rights reserved.)

Levels of exhaled nitric oxide (NO) were determined in well-characterized atopic and nonatopic subjects on 4 days with a different level of outdoor air pollution. The two groups matched well regarding spirometric values, i.e., no difference with regard to FEV(1), FVC, and peak flow. On the 4 test days asymptomatic atopic subjects exhaled 1.5- to 2.4-fold higher levels of NO compared with nonatopic subjects. In both groups the increase in exhaled NO in response to air pollution was similar (2.5 times maximal increase, P < 0.01). In conclusion, atopic subjects exhale higher levels of NO compared with nonatopic subjects, but respond to a similar degree to increased levels of air pollution., (Copyright 1999 Academic Press.)

Short-term ozone exposure causes lung function decrements, increased airway reactivity, airway inflammation, increased respiratory symptoms and hospital admissions. Exposure to long-term elevated ozone levels seems to be associated with reduced lung function (aging), increase of respiratory symptoms, exacerbation of asthma, and airway cell and tissue changes. Health risk caused by exposure to ozone has been evaluated mainly in a qualitative way by comparing ozone air quality data with health-based guidelines or standards. A preliminary approach to quantifying health risk from short-term exposure to oxidant air pollution has been taken by expert judgement, describing known or expected effects at specific levels of ozone. For quantitative assessment of the health impact of distinct ozone exposure conditions (acute, repeated daily, chronic) specific exposure-dose-response models are being developed which can be linked to human exposure data. Exposure-(dose-)response models using data from epidemiological, human-clinical and animal toxicity studies are presented.