Abstract  Numerous reports have shown that fine particulates threaten human health. Since their health impact is associated with both mass and number concentrations, it is necessary to evaluate the emission standards for particulate mass accordingly. This study examined the particulate matter characteristics of diesel locomotive engine exhaust at various engine ratings. Diesel engine exhaust was collected via a dilution tunnel and the concentration and size distribution of fine particles were measured by a scanning mobility particle sizer. Exhaust gasses were measured simultaneously by a stack sampler. The maximum carbon monoxide emission was reached at 59% of the maximum rating, after which emissions decreased. The particle count median diameter increased with the engine rating, until a maximum was reached at 40% of the maximum rating. Most exhaust particles were nanoparticles with the nuclei mode range, a particle diameter (D(P))<50 nm. The increase in particles with the accumulation mode range, 50<D(P)<1000 nm, led to a mass concentration increase and number concentration reduction. The count median diameter was within the nuclei mode range at lower engine ratings, and within the accumulation mode range at higher engine ratings. Since diesel engines mainly generate fine particles, exhaust particle mass and size distribution should be considered in emission regulations.

Abstract  OBJECTIVE: This article reviews panel studies of air pollution on children's respiratory health and proposes future research directions.

METHODS: The PubMed electronic database was used to search published original epidemiological studies in peer-reviewed journals from 2000 to November 2011. Children's age was limited to ≤18 years old. A total of 33 relevant articles were obtained, with 20 articles relating to lung function, 21 articles relating to respiratory symptoms, and 8 articles examining both.

RESULTS: Most studies suggested the adverse effects of air pollution on children's lung function and respiratory symptoms. Particles and NO(2) showed more significant results, whereas effects of SO(2) were not consistent. A few studies indicated that O(3) interacted with temperature and sometimes seemed to be a protective factor for children's respiratory health. Negative associations between air pollutants and pulmonary health were more serious in asthmatic children than in healthy subjects. However, many outcomes depended on the number of lag days. Peak expiratory flow (PEF) was the most usual measurement for children's lung function, followed by forced expiratory volume in 1 second (FEV(1)).

CONCLUSIONS: There are significant adverse effects of air pollution on children's pulmonary health, especially for asthmatics. Future studies need to examine the lag effects of air pollution on children's lung function and respiratory symptoms. Ambient temperature is predicted to change worldwide due to climate change, which will threaten population health. Further research is needed to examine the effects of ambient temperature and the interactive effects between air pollution and ambient temperature on children's lung function and respiratory symptoms.

Abstract  Acute periods of pulmonary exacerbation are the single most important cause of morbidity in cystic fibrosis patients, and may be associated with a loss of lung function. Intervening prior to the onset of a substantially increased inflammatory response may limit the associated damage to the airways. While a number of biomarker assays based on inflammatory markers have been developed, providing useful and important measures of disease during these periods, such factors are typically only elevated once the process of exacerbation has been initiated. Identifying biomarkers that can predict the onset of pulmonary exacerbation at an early stage would provide an opportunity to intervene before the establishment of a substantial immune response, with major implications for the advancement of cystic fibrosis care. The precise triggers of pulmonary exacerbation remain to be determined; however, the majority of models relate to the activity of microbes present in the patient's lower airways of cystic fibrosis. Advances in diagnostic microbiology now allow for the examination of these complex systems at a level likely to identify factors on which biomarker assays can be based. In this article, we discuss key considerations in the design and testing of assays that could predict pulmonary exacerbations.

Abstract  BACKGROUND: Asthma has its origins in early childhood, but different patterns of childhood wheezing vary in their associations with subsequent asthma, atopy, and bronchial hyperresponsiveness (BHR). Novel wheezing phenotypes have been identified on the basis of analyses of longitudinal data from the Avon Longitudinal Study of Parents And Children (ALSPAC). It is unclear whether these phenotypes can be replicated in other birth cohorts.

OBJECTIVE: To compare wheezing phenotypes identified in the first 8 years of life in the ALSPAC study and the Prevention and Incidence of Asthma and Mite Allergy (PIAMA) study.

METHODS: We used longitudinal latent class analysis to identify phenotypes on the basis of repeated reports of wheezing from 0 to 8 years in 5760 children from the ALSPAC study and 2810 children from the PIAMA study. Phenotypes were compared between cohorts. Associations with asthma, atopy, BHR, and lung function were analyzed by using weighted regression analyses.

RESULTS: The model with the best fit to PIAMA data in the first 8 years of life was a 5-class model. Phenotypes identified in the PIAMA study had wheezing patterns that were similar to those previously reported in ALSPAC, adding further evidence to the existence of an intermediate-onset phenotype with onset of wheeze after 2 years of age. Associations with asthma, atopy, BHR, and lung function were remarkably similar in the 2 cohorts.

CONCLUSION: Wheezing phenotypes identified by using longitudinal latent class analysis were comparable in 2 large birth cohorts. Study of genetic and environmental factors associated with different phenotypes may help elucidate the origins of asthma.

Abstract  The aim of this study was to investigate the influence of the vertical position of a motorway on the pollutant concentrations in the vicinity of the motorway. Therefore, a near-road monitoring campaign was performed along two adjoining motorway stretches: one motorway at ground level and a motorway flyover. PM2.5 and nitrogen oxides (NO, NO2 and NOx) were measured at both sides of the motorway on a 30-min resolution. In addition, EC (elemental carbon) was measured on both sides of the road on a daily basis using low volume samplers and thermal–optical transmission (TOT) analysis of filters. PNC (particle number concentration) was measured at one side. The measurement locations on each side of the road were located at 29 m and 102 m from the motorway at ground level and at 60 m and 120 m from the motorway flyover. Pollution roses, showed increased average concentrations in the direction of the road for nitrogen oxides and PM2.5. The impact of road traffic appeared to be higher at ground level compared to the flyover. The difference in concentration between both sides of the road for PM2.5, NO, NO2 and NOx was analysed using linear mixed models. The concentration difference, which can be seen as the contribution of road traffic to the pollutant concentration, was calculated taking into account prevailing wind directions. The results indicate that taking into account confounding parameters (time of day, day of the week, distance to the road and wind speed), the contribution of the motorway traffic to pollutant concentrations is significantly higher when the motorway is at ground level. Furthermore, time of day and day of the week also have a significant effect on the concentration difference. The linear mixed model estimated a reduced road increment at the motorway flyover compared to the ground level motorway of 119 ppb for NO, 29 ppb for NO2 and 3.5 μg m−3 for PM2.5. taking into account confounding parameters. The highest EC and PNC concentrations were measured downwind of the motorway at ground level.

Abstract  INTRODUCTION: The Aphekom project aimed to provide new, clear, and meaningful information on the health effects of air pollution in Europe. Among others, it assessed the health and monetary benefits of reducing short and long-term exposure to particulate matter (PM) and ozone in 25 European cities.

METHOD: Health impact assessments were performed using routine health and air quality data, and a common methodology. Two scenarios were considered: a decrease of the air pollutant levels by a fixed amount and a decrease to the World Health Organization (WHO) air quality guidelines. Results were economically valued by using a willingness to pay approach for mortality and a cost of illness approach for morbidity.

RESULTS: In the 25 cities, the largest health burden was attributable to the impacts of chronic exposure to PM2.5. Complying with the WHO guideline of 10 μg/m(3) in annual mean would add up to 22 months of life expectancy at age 30, depending on the city, corresponding to a total of 19,000 deaths delayed. The associated monetary gain would total some €31 billion annually, including savings on health expenditures, absenteeism and intangible costs such as well-being, life expectancy and quality of life.

CONCLUSION: European citizens are still exposed to concentrations exceeding the WHO recommendations. Aphekom provided robust estimates confirming that reducing urban air pollution would result in significant health and monetary gains in Europe. This work is particularly relevant now when the current EU legislation is being revised for an update in 2013.

Abstract  BACKGROUND: Emergency department (ED) visit and hospital admissions (HA) data have been an indispensible resource for assessing acute morbidity impacts of air pollution. ED visits and HAs are types of health care visits with similarities, but also potentially important differences. Little previous information is available regarding the impact of health care visit type on observed acute air pollution-health associations from studies conducted for the same location, time period, outcome definitions and model specifications.

METHODS: As part of a broader study of air pollution and health in St. Louis, individual-level ED and HA data were obtained for a 6.5 year period for acute care hospitals in the eight Missouri counties of the St. Louis metropolitan area. Patient demographic characteristics and diagnostic code distributions were compared for four visit types including ED visits, HAs, HAs that came through the ED, and non-elective HAs. Time-series analyses of the relationship between daily ambient ozone and PM₂.₅ and selected cardiorespiratory outcomes were conducted for each visit type.

RESULTS: Our results indicate that, compared with ED patients, HA patients tended to be older, had evidence of greater severity for some outcomes, and had a different mix of specific outcomes. Consideration of 'HA through ED' appeared to more effectively select acute visits than consideration of 'non-elective HA'. While outcomes with the strongest observed temporal associations with air pollutants tended to show strong associations for all visit types, we found some differences in observed associations for ED visits and HAs. For example, risk ratios for the respiratory disease-ozone association were 1.020 for ED visits and 1.004 for 'HA through ED'; risk ratios for the asthma/wheeze-ozone association were 1.069 for ED visits and 1.106 for 'HA through ED'. Several factors (e.g. age) were identified that may be responsible, in part, for the differences in observed associations.

CONCLUSIONS: Demographic and diagnostic differences between visit types may lead to preference for one visit type over another for some questions and populations. The strengths of observed associations with air pollutants sometimes varied between different health care visit types, but the relative strengths of association generally were specific to the pollutant-outcome combination.

Abstract  BACKGROUND: Asthma is a chronic inflammatory disease characterized by airways hyperresponsiveness (AHR), reversible airflow obstruction, airway remodeling, and episodic exacerbations caused by air pollutants, such as particulate matter (PM; PM <2.5 μm in diameter [PM(2.5)]) and ozone (O(3)). Spleen tyrosine kinase (Syk), an immunoregulatory kinase, has been implicated in the pathogenesis of asthma.

OBJECTIVE: We sought to evaluate the effect of Syk inhibition on AHR in a chronic mouse model of allergic airways inflammation and pollutant exposure.

METHODS: We used a 12-week chronic ovalbumin (OVA) sensitization and challenge mouse model of airways inflammation followed by exposure to PM(2.5) plus O(3). Respiratory mechanics and methacholine (MCh) responsiveness were assessed by using the flexiVent system. The Syk inhibitor NVP-QAB-205 was nebulized intratracheally by using a treatment-based protocol 15 minutes before assessment of MCh responsiveness.

RESULTS: Syk expression increased significantly in the airway epithelia of OVA-sensitized and OVA-challenged (OVA/OVA) mice compared with OVA-sensitized but PBS-challenged (OVA/PBS) control mice. OVA/OVA mice exhibited AHR to MCh, which was attenuated by a single administration of NVP-QAB-205 (0.3 and 3 mg/kg). PM(2.5) plus O(3) significantly augmented AHR to MCh in the OVA/OVA mice, which was abrogated by NVP-QAB-205. Total inflammatory cell counts were significantly higher in the bronchoalveolar lavage fluid from OVA/OVA than OVA/PBS mice and were unaffected by PM(2.5) plus O(3) or NVP-QAB-205.

CONCLUSION: NVP-QAB-205 reduced AHR and the enhanced response to PM(2.5) plus O(3) to normal levels in an established model of chronic allergic airways inflammation, suggesting that Syk inhibitors have promise as a therapy for asthma.

Abstract  We conducted a multicity time-series study using monitoring data to assess seasonal patterns of short-term ozone-mortality association among elderly aged 65 years and over in Japan. Daily exposure to ambient ozone was computed using hourly measurements of photochemical oxidants available at multiple monitoring stations in each city. Effects of ozone on daily all-cause non-accidental, cardiovascular, and respiratory mortality were estimated using distributed lag linear models, controlling for confounding by temporal, day of the week, temperature, and flu epidemics. City-level effect estimates were combined using inverse variance meta-analysis. In spring and autumn, a 10-ppbv increase of daily maximum 8-h average ozone concentration in the previous 3 days was associated with 0.69 % (95 % confidence interval (CI): 0.27-1.10), 1.07 % (0.34-1.82), and 1.77 % (0.78-2.77) increases in daily all-cause, cardiovascular, and respiratory mortality, respectively. Forward displacement of respiratory mortality was large during the cold season despite lower ozone concentration. Results were generally independent of fine particulate matter and nitrogen dioxide. Findings suggest significant mortality effects of short-term ozone exposure among the elderly during the moderate season. Those with underlying respiratory diseases were susceptible, even during winter.

Abstract  Rationale: Cohort evidence linking long-term exposure to outdoor particulate air pollution and mortality has come largely from the United States. There is relatively little evidence from nationally representative cohorts in other countries. Objectives: To investigate the relationship between long-term exposure to a range of pollutants and causes of death in a national English cohort. Methods: A total of 835,607 patients aged 40-89 years registered with 205 general practices were followed from 2003-2007. Annual average concentrations in 2002 for particulate matter with a median aerodynamic diameter less than 10 (PM10) and less than 2.5 μm (PM2.5), nitrogen dioxide (NO2), ozone, and sulfur dioxide (SO2) at 1 km(2) resolution, estimated from emission-based models, were linked to residential postcode. Deaths (n = 83,103) were ascertained from linkage to death certificates, and hazard ratios (HRs) for all- and cause-specific mortality for pollutants were estimated for interquartile pollutant changes from Cox models adjusting for age, sex, smoking, body mass index, and area-level socioeconomic status markers. Measurements and Main Results: Residential concentrations of all pollutants except ozone were positively associated with all-cause mortality (HR, 1.02, 1.03, and 1.04 for PM2.5, NO2, and SO2, respectively). Associations for PM2.5, NO2, and SO2 were larger for respiratory deaths (HR, 1.09 each) and lung cancer (HR, 1.02, 1.06, and 1.05) but nearer unity for cardiovascular deaths (1.00, 1.00, and 1.04). Conclusions: These results strengthen the evidence linking long-term ambient air pollution exposure to increased all-cause mortality. However, the stronger associations with respiratory mortality are not consistent with most US studies in which associations with cardiovascular causes of death tend to predominate.

Abstract  Accumulating evidence suggests that outdoor air pollution may have a significant impact on central nervous system (CNS) health and disease. To address this issue, the National Institute of Environmental Health Sciences/National Institute of Health convened a panel of research scientists that was assigned the task of identifying research gaps and priority goals essential for advancing this growing field and addressing an emerging human health concern. Here, we review recent findings that have established the effects of inhaled air pollutants in the brain, explore the potential mechanisms driving these phenomena, and discuss the recommended research priorities/approaches that were identified by the panel. (c) 2012 Elsevier Inc. All rights reserved.

Abstract  This review explores the recent epidemiological literature to identify possible risk factors for childhood asthma development, as well as the proportion of cases that might be attributable to each factor. Tobacco smoke and house-dust-mite allergy are the only environmental risk factors with firmly established roles in asthma development. Together with genetics, these risk factors probably account for much of childhood asthma development. Suggestive risk factors include cockroach, pet, and mold allergens; low birth weight; small family size; and viral infection. More theoretical risk factors include insufficient breastfeeding, obesity/inactivity, ambient ozone, and living in non-farm settings.

National/international trends suggest several risk factors that could play major roles in the rising prevalence of asthma. The "tighter" building construction of modern housing and the increasing time that children spend indoors has undoubtedly increased indoor allergen exposures. Children also spend more time in sedentary activities, with a concomitant decrease in physical activity and increase in obesity. Modern "hygiene" and the changing nature of childhood infection may have also increased asthma prevalence. Mechanisms have been suggested implicating ambient air pollution in asthma development, and there is limited epidemiological evidence supporting this hypothesis. However, this evidence does not resolve why pollution levels have been decreasing throughout the period that asthma rates have risen.

Abstract  In Brazil, very little experimental work on measurements of indoor air pollutant levels has been done. Nowadays, increasing attention is being given to indoor air quality and the health problems associated with buildings and the indoor work environment. The scope of this paper is to review the major pollutants found in indoor environments and their sources. Subsequently, exposure to indoor air pollutants and health effects are considered. The review concludes by briefly addressing assessment of indoor air quality in Brazil and research needs.

Abstract  PURPOSE OF REVIEW: This overview highlights recent experimental and epidemiological evidence for the programming effects of outdoor air pollution exposures during early development on lung function and chronic respiratory disorders, such as asthma and related allergic disorders.

RECENT FINDINGS: Air pollutants may impact anatomy and/or physiological functioning of the lung and interrelated systems. Programming effects may result from pollutant-induced shifts in a number of molecular, cellular, and physiological states and their interacting systems. Specific key regulatory systems susceptible to programming may influence lung development and vulnerability to respiratory diseases, including both central and peripheral components of neuroendocrine pathways and autonomic nervous system (ANS) functioning which, in turn, influence the immune system. Starting in utero, environmental factors, including air pollutants, may permanently organize these systems toward trajectories of enhanced pediatric (e.g., asthma, allergy) as well as adult disease risk (e.g., chronic obstructive pulmonary disease). Evidence supports a central role of oxidative stress in the toxic effects of air pollution. Additional research suggests xenobiotic metabolism and subcellular components, such as mitochondria are targets of ambient air pollution and play a role in asthma and allergy programming. Mechanisms operating at the level of the placenta are being elucidated. Epigenetic mechanisms may be at the roots of adaptive developmental programming.

SUMMARY: Optimal coordinated functioning of many complex processes and their networks of interaction are necessary for normal lung development and the maintenance of respiratory health. Outdoor air pollution may play an important role in early programming of respiratory health and is potentially amenable to intervention.

Abstract  BACKGROUND: Previous epidemiological studies have shown acute effects of ambient air pollutants in children with respiratory disorders.

METHODS: The chronic effects of air pollution in Bangkok children were investigated. Children aged 10-15 years were examined for lung functions using spirometry tests and for respiratory symptoms by the American Thoracic Society's Division of Lung Diseases (ATS-DLD-78-C) questionnaire during May-August 2004. Effects of residential area were estimated by multiple logistic regression analysis. Of the 878 children, 722 (82%) had completed lung function test and ATS-DLD questionnaire.

RESULTS: In children, who live in roadside (R) and general (G) areas with high (H) pollution, the prevalence of respiratory symptoms increased significantly [odds ratios (95% confidence interval) in HR and HG are 2.44 (1.21-4.93) and 2.60 (1.38-4.91), respectively]. Children with normal lung function were less observed in H- and M-polluted roadside and general area [HR, OR = 1.41 (95% CI 0.89-2.22); HG, 1.08 (0.71-1.64); and MR, 0.99 (0.63-1.57)]. Residential locations and family members were associated with the prevalence of respiratory symptoms, whereas factors such as the responder of ATS-DLD, gender, age, residential years, home size, parental smoking habits, use of air conditioners, and domestic pets were not associated. Age was associated with the impaired lung function, whereas others factors were not associated.

CONCLUSION: The prevalence of respiratory symptoms and impaired lung function were higher among children living in areas with high pollution than those in areas with low pollution.

Abstract  Background: In recent years (2000-2007), ambient levels of fine particulate matter (PM2.5) have continued to decline as a result of interventions, but the decline has been at a slower rate than previous years (1980-2000). Whether these more recent and slower declines of PM2.5 levels continue to improve life expectancy and whether they benefit all populations equally is unknown. METHODS: We assembled a data set for 545 U.S. counties consisting of yearly county-specific average PM2.5, yearly county-specific life expectancy, and several potentially confounding variables measuring socioeconomic status, smoking prevalence, and demographic characteristics for the years 2000 and 2007. We used regression models to estimate the association between reductions in PM2.5 and changes in life expectancy for the period from 2000 to 2007. RESULTS: A decrease of 10 μg/m in the concentration of PM2.5 was associated with an increase in mean life expectancy of 0.35 years (SD = 0.16 years, P = 0.033). This association was stronger in more urban and densely populated counties. CONCLUSIONS: Reductions in PM2.5 were associated with improvements in life expectancy for the period from 2000 to 2007. Air pollution control in the last decade has continued to have a positive impact on public health.

Abstract  UNLABELLED: Ambient air pollution has been associated with decreased growth in lung function among children; but little is known about the impact of indoor air pollution. We examined relationships between indoor air pollution metrics and lung function growth, among children (n = 3273) aged 6-13 years living in four Chinese cities. Lung function parameters (FVC and FEV(1) ) were measured twice a year. Questionnaires were used to determine home coal burning and ventilation practices. Generalized estimating equations were used to examine associations. Use of coal as a household fuel was associated with 16.5 ml/year lower (33%, P < 0.001) and 20.5 ml/year lower (39%, P < 0.001) growth in children's FEV(1) and FVC, respectively. FEV(1) growth was 10.2 ml/year higher (20%, P = 0.009), and FVC growth was 17.0 ml/year higher (33%, P < 0.001) among children who lived in houses with the presence of a ventilation device. Among children living in houses where coal was used as a fuel and no ventilation devices were present, adjusted FVC and FEV(1) growth, respectively, were 37% and 61% that of the average growth per year in the full cohort. This suggests that household coal use may cause deficits in lung function growth, while using ventilation devices may be protective of lung development.

PRACTICAL IMPLICATIONS: Nearly 3.4 billion people use solid fuels in homes for cooking and/or heating. We report the following findings from a longitudinal study: (i) household coal use is significantly associated with reduction in children's lung function growth and (ii) the use of household ventilation devices is significantly associated with higher lung function growth, particularly among children living in households where coal is used as a fuel. These findings not only provide evidence that indoor coal use impairs children's lung development but also point to the importance of improving ventilation conditions in reducing harmful effects of indoor air pollution sources.

Abstract  Epidemiological research to identify subpopulations with enhanced susceptibility to air pollution is still at an early stage. From the available studies, there is evidence that both "endogenous" and "exogenous" factors contribute to individual susceptibility. Females and the elderly are at an increased risk of pollution-related diseases. Moreover, some chronic clinical conditions seem to be good candidates for identifying the "frail" populations: chronic obstructive pulmonary disease including asthma, coronary heart diseases, congestive heart failure, and heart rhythm disorders. It seems clear that epidemiological research on susceptibility in the future should investigate the underlying biological and physiological mechanisms, in addition to the environmental and toxicological effects.

Abstract  Multiple environmental factors including hormones, dietary factors, infections, and exposure to tobacco smoke, as well as gene-environment interactions, have been associated with increased risk for rheumatoid arthritis (RA). The growing understanding of the prolonged period before the first onset of symptoms of RA suggests that these environmental and genetic factors are likely acting to drive the development of RA-related autoimmunity long before the appearance of the first joint symptoms and clinical findings that are characteristic of RA. This article reviews these factors and interactions, especially those that have been investigated in a prospective fashion before the symptomatic onset of RA.

Abstract  In response to the World Health Organization Children's Environment and Health Action Plan for Europe (CEHAPE), a town near Vienna initiated a health survey of schoolchildren. To create recommendations for the community's decision makers, the health survey tried to identify the environmental factors influencing the respiratory health of children. The survey consisted of a questionnaire and spirometry. For 186 of 207 children of first and second grade, parents consented to include their children and answered a questionnaire. Spirometry was performed in 177 children. Results of lung function testing revealed that lung function was significantly reduced in children with visible mould infestation at home and living on a street with frequent lorry traffic. Larger family size and living in a rural area had positive effects on lung function. Our study provides an example for a feasible strategy to provide local decision makers with recommendations based on scientific evidence and actual observations and to help them implement measures in accordance with CEHAPE. Journal of Public Health Policy (2009) 30, 144-157. doi:10.1057/jphp.2009.5

Abstract  Outdoor air pollution poses risks to human health in communities around the world, and research on populations who are most susceptible continues to reveal new insights. Human susceptibility to adverse health effects from exposure to air pollution can be related to underlying disease; demographic or anthropometric characteristics; genetic profile; race and ethnicity; lifestyle, behaviors, and socioeconomic position; and location of residence or daily activities. In health research, an individual or group may have an enhanced responsiveness to a given, identical level of pollution exposure compared to those who are less susceptible. Or, people in these different groups may experience varying levels of exposure (for example, a theoretically homogeneous population whose members differ only by proximity to a road). Often the information available for health research may relate to both exposure and enhanced response to a given dose of pollution. This paper discusses the general direction of research on susceptibility to air pollution, with a general though not an exclusive focus on particulate matter, with specific examples of research on susceptibility related to cardiovascular disease, diabetes, asthma, and genetic and epigenetic features. We conclude by commenting how emerging knowledge of susceptibility can inform policy for controlling pollution sources and exposures to yield maximal health benefit and discuss two areas of emerging interest: studying air pollution and its connection to perinatal health, as well as land use and urban infrastructure design.

Abstract  Ambient air pollution has been associated with increased mortality and morbidity; however, few studies have examined the short-term effect of air pollution specifically on chronic obstructive pulmonary disease (COPD), which is an important cause of mortality and morbidity world wide. In this analysis, we examined the associations between daily air pollution levels [particulate matter less than 10 microns in aerodynamic diameter (PM10), sulfur dioxide (SO2) and nitrogen dioxide (NO2)] and COPD mortality in four Chinese cities. We used Poisson regression models with natural spline smoothing functions to adjust for long-term and seasonal trends of COPD mortality, as well as other time-varying covariates. We did a meta-analysis to obtain the 4-city average estimates. Air pollution (PM10, SO2, and NO2) was found to be associated with increased risk of COPD mortality in these four cities. Using the random-effects model, an increase of 10 mu g m(-3) of 2-day moving average concentrations of PM10, SO2 and NO2 corresponded to a 0.78% (95% CI, 0.13-1.42), 1.30% (95% CI, 0.61-1.99), and 1.78% (95% CI, 1.10-2.46) increase of COPD mortality, respectively. The concentration response curves indicated linear associations without threshold. Only NO2 remained significant in the multi-pollutant models. To our knowledge, this is the first multi-city study in Asian developing region to report the short-term effect of air pollution on COPD mortality. Our results contribute to very limited data on the effects of air pollution on COPD mortality for high exposure settings typical in developing countries. (C) 2013 Elsevier Ltd. All rights reserved.

Abstract  Exacerbations of chronic obstructive pulmonary disease (COPD) are episodes of worsening of symptoms, leading to substantial morbidity and mortality. COPD exacerbations are associated with increased airway and systemic inflammation and physiological changes, especially the development of hyperinflation. They are triggered mainly by respiratory viruses and bacteria, which infect the lower airway and increase airway inflammation. Some patients are particularly susceptible to exacerbations, and show worse health status and faster disease progression than those who have infrequent exacerbations. Several pharmacological interventions are effective for the reduction of exacerbation frequency and severity in COPD such as inhaled steroids, long-acting bronchodilators, and their combinations. Non-pharmacological therapies such as pulmonary rehabilitation, self-management, and home ventilatory support are becoming increasingly important, but still need to be studied in controlled trials. The future of exacerbation prevention is in assessment of optimum combinations of pharmacological and non-pharmacological therapies that will result in improvement of health status, and reduction of hospital admission and mortality associated with COPD.