Suchergebnisse

The breathing of polluted air is associated with the development and exacerbation of various health conditions, and the cost of treating such conditions is substantial. However, while the correlation with respiratory-related health conditions is well documented, less is known about this relationship from a longitudinal perspective and how pollution affects other health problems, such as neurodegenerative diseases (e.g. dementia) or diseases of the endocrine system (e.g. diabetes). More research is therefore needed to better identify the health risks and costs of pollution.
The aim of this study is to investigate the relationship between exposure to ambient air pollution and health outcomes at the individual level. The analysis is based on data from the Northern Ireland Longitudinal Study (NILS) - a representative 28% sample of the Northern Ireland population drawn from an administrative health database and linked to Census returns and other administrative databases - linked with routinely collected prescriptions data. Exposure to air pollution is assessed by linking modelled background pollution data at a 1x1 km grid square resolution to residential address. Annual measures of eight separate pollutants will allow us to examine cumulative exposure between 2001 and 2016.
Regression analysis will be used to estimate the health effects of exposure to air pollution. Preliminary analysis currently underway will focus on outcomes such as self-reported health at the 2011 Census (e.g. the presence of breathing difficulties and memory loss) and all-cause and respiratory-related mortality since 2001. Stage two of the analysis will utilise the prescriptions linkage to define illness-specific health outcomes using receipt of medicines prescribed by General Practitioners (GPs) to treat cardiovascular- and respiratory-related health conditions as well as diabetes, dementia and Parkinsonism. Longitudinal analysis will enable us to assess whether these relationships are affected by unobserved confounders. Preliminary results for both stages of the analysis are expected by autumn 2019.

AbstractThere is growing evidence that air pollutants might affect human behavior. This study assesses the associations between air pollution concentrations and emergency department (ED) visits for abuse of psychoactive substances. 28,745 such ED visits were identified and retrieved from a health database containing diagnosed visits from five hospitals in Edmonton (Canada) over 10 years. The ED visits were analyzed as daily counts. Conditional Poisson regression models were used to estimate the associations between the number of ED visits and concentration levels of gaseous air pollutants (carbon monoxide (CO), nitrogen dioxide (NO2), sulphur dioxide (SO2), ozone (O3)) and particulate matters (PM2.5 and PM10, fine and coarse, respectively). Air pollutants and weather factors in the realized statistical models were lagged by the same number of days, from 0 to 5 days. The associations were estimated in the form of concentration-response functions. The results show relative risks and their 95% confidence intervals. Positive and statistically significant associations were obtained for CO for all patients (lags from 0 to 5), males (lags 1 and 3–5), and females (lag 4). For NO2, exposure lagged by 1 and 2 days has a positive statistically significant association for all and male patients. PM10 shows the same type of associations lagged by 2 and 3 days. PM2.5 (lag 2) is associated only in females. The results indicate that urban air pollution may have an impact on the abuse of psychoactive substances.

According to the World Health Organisation (WHO), environmental air pollution is among the leading risks for noncommunicable diseases worldwide in terms of the global disease burden and the leading environmental cause of disease and death particularly in low- and middle-income countries. Air pollution is a highly complex mixture of various organic and inorganic components from natural and anthropogenic sources, occurring locally or being introduced by longrange transport of pollutants. Moreover, air pollution is modified by regional meteorological conditions. Accordingly, levels and composition of air pollution can vary substantially at a site, nevertheless typically showing a diurnal, weekly and annual cycle. Regulatory limits, as defined by the Air Quality Guidelines of the European Union, are enforced to minimize air pollution associated health hazards for the population. However, legal limits of the European Union clearly exceed the guideline values of the WHO, especially with regard to particulate matter. The burden of ambient air pollution is monitored by means of different indicator pollutants, especially particulate matter up to 2.5m (PM2.5) or 10m (PM10) in aerodynamic diameter, and gases such as nitrogen dioxide (NO2) or ozone (O3). In recent decades, in the western world, decreasing levels of air pollution have been achieved so that the main focus is nowadays on health hazards caused by low concentrations of pollutants. However, in Germany, especially urban areas are still suffering under higher levels of air pollution. In recent decades, a large number of studies have highlighted the harmful effects of air pollution on public health. Primarily, the respiratory and the cardiovascular system are targeted with exposure to higher levels of air pollution being associated with reduced lung function, unspecific respiratory symptoms, increased use of medication and acute exacerbations of lung diseases, myocardial infarction, stroke and even death. Further negative health outcomes such as atherosclerosis, reduced fetal growth, diabetes and limitations of cognitive function and neuronal development are supported by recent studies. Moreover, these studies have substantially improved our understanding of the underlying pathophysiological mechanisms. The 2015 Global Burden of Disease Study underlined the significance of air pollution for public health, particularly in relation to increased morbidity and mortality resulting from chronic diseases. As causal factor for premature death, particularly cardiovascular death, ambient PM2.5 is the number 5 risk factor, well behind the commonly known risk factors elevated blood pressure, smoking, and increased blood levels of glucose and cholesterol. Ambient air pollution is the number 10 risk factor for the disease burden and also the leading environmental risk factor in Germany. Different studies have estimated that ambient air pollution increases mortality and may decrease life expectancy on average by about one year in the European Union. State of the art knowledge on the negative health effects of ambient air pollution and recommendations for environmental safety and health are introduced by this statement of the German Respiratory Society (Deutsche Gesellschaft fur Pneumologie und Beatmungsmedizin). General concepts and health effects concerning the respiratory system are described in the first part of this statement.

AbstractTo investigate the acute impact of various air pollutants on various disease groups in the urban area of the city of Toronto, Canada. Statistical models were developed to estimate the relative risk of an emergency department visit associated with ambient air pollution concentration levels. These models were generated for 8 air pollutants (lagged from 0 to 14 days) and for 18 strata (based on sex, age group, and season). Twelve disease groups extracted from the International Classification of Diseases 10th Revision (ICD-10) were used as health classifications in the models. The qualitative results were collected in matrices composed of 18 rows (strata) and 15 columns (lags) for each air pollutant and the 12 health classifications. The matrix cells were assigned a value of 1 if the association was positively statistically significant; otherwise, they were assigned to a value of 0. The constructed matrices were totalized separately for each air pollutant. The resulting matrices show qualitative associations for grouped diseases, air pollutants, and their corresponding lagged concentrations and indicate the frequency of statistically significant positive associations. The results are presented in colour-gradient matrices with the number of associations for every combination of patient strata, pollutant, and lag in corresponding cells. The highest number of the associations was 8 (of 12 possible) obtained for the same day exposure to carbon monoxide, nitrogen dioxide, and days with elevated air quality health index (AQHI) values. For carbon monoxide, the number of the associations decreases with the increasing lags. For this air pollutant, there were almost no associations after 8 days of lag. In the case of nitrogen dioxide, the associations persist even for longer lags. The numerical values obtained from the models are provided for every pollutant. The constructed matrices are a useful tool to analyze the impact of ambient air pollution concentrations on public health.

Abstract

Objectives
Some studies have shown that environmental risk factors, including air pollution, might be related to the incidence or recurrence of multiple sclerosis (MS). This systematic review was conducted to investigate the relation between air pollution and MS.


Methods
A systematic search was conducted in PubMed, Scopus, Science Direct, Embase, and Web of Science; until January 2020 with no restrictions. The search strategy was conducted with air pollution key words such as CO, PM2.5, PM10, SO2, and NO2, for exposure and the key word "Multiple sclerosis" as the outcome.


Results
Eventually, after applying the inclusion and exclusion criteria, 17 articles were included. The methodologies and outcomes reported were heterogeneous and different metrics had been used in the results; therefore conducting a meta-analysis was not possible. Eight studies had analyzed the relation between particulate matter (PM) and the prevalence or relapse of MS and had observed a significant relation. NO2 and NOx were associated with recurrence or prevalence of MS in three studies. But, in three cohort studies, no association was observed between air pollution and recurrence or occurrence of MS.


Conclusions
The results of this systematic review show that outdoor air pollution, especially PM and nitrogen oxides might be related to the prevalence or relapse of MS.

Designing air quality policies that improve public health can benefit from information about air pollution health risks and impacts, which include respiratory and cardiovascular diseases and premature death. Several computer‐based tools help automate air pollution health impact assessments and are being used for a variety of contexts. Expanding information gathered for a May 2014 World Health Organization expert meeting, we survey 12 multinational air pollution health impact assessment tools, categorize them according to key technical and operational characteristics, and identify limitations and challenges. Key characteristics include spatial resolution, pollutants and health effect outcomes evaluated, and method for characterizing population exposure, as well as tool format, accessibility, complexity, and degree of peer review and application in policy contexts. While many of the tools use common data sources for concentration‐response associations, population, and baseline mortality rates, they vary in the exposure information source, format, and degree of technical complexity. We find that there is an important tradeoff between technical refinement and accessibility for a broad range of applications. Analysts should apply tools that provide the appropriate geographic scope, resolution, and maximum degree of technical rigor for the intended assessment, within resources constraints. A systematic intercomparison of the tools' inputs, assumptions, calculations, and results would be helpful to determine the appropriateness of each for different types of assessment. Future work would benefit from accounting for multiple uncertainty sources and integrating ambient air pollution health impact assessment tools with those addressing other related health risks (e.g., smoking, indoor pollution, climate change, vehicle accidents, physical activity).

Ambient air pollution (AAP) is recognized a cardiovascular risk factor and lipid profile dysregulation seems to be one of the potential mediators involved. However, results from epidemiologic research on the association between exposure to AAP and altered lipid profile have been inconsistent. This study aims to systematically review and meta-analyse epidemiologic evidence on the association between exposure to ambient air pollutants (particulate matter, nitrogen oxides, sulphur dioxide, ozone, carbon monoxide, back carbon) and lipid profile parameters (Total cholesterol; High-Density Lipoprotein Cholesterol; Low-Density Lipoprotein Cholesterol; TG-Triglycerides) or dyslipidaemia. Systematic electronic literature search was performed in PubMed, Web of Science and Scopus databases (last search on 24th May 2019) using keywords related to the exposure (ambient air pollutants) and to the outcomes (lipid profile parameters/dyslipidaemia). Qualitative and quantitative information of the studies were extracted and fixed or random-effects models were used to obtain a pooled effect estimate per each pollutant/outcome combination. 22 studies were qualitatively analysed and, from those, 3 studies were quantitatively analysed. Particulate matters were the most studied pollutants and a considerable heterogeneity in air pollution assessment methods and outcomes definitions was detected. Age, obesity related measures, tobacco consumption, sex and socioeconomic factors were the most frequent considered variables for confounding adjustment in the models. In a long-term exposure scenario, we found a 3.14% (1.36%-4.95%) increase in TG levels per 10 μg/m3 PM10 increment and a 4.24% (1.37%-7.19%) increase in TG levels per 10 μg/m3 NO2 increment. No significant associations were detected for the remaining pollutant/outcome combinations. Despite the few studies included in the meta-analysis, our study suggests some epidemiologic evidence supporting the association between PM10 and NO2 exposures and increased TG levels. Due to the very low level of evidence, more studies are needed to clarify the role of lipid profile dysregulation as a mediator on the AAP adverse cardiovascular effects. ; Highlights: Ambient air pollution (AAP) is recognized as a risk factor for cardiovascular diseases; First systematic review and meta-analysis on the association between ambient air pollutants exposure and lipid profile; Some epidemiologic evidence supporting the association between PM10 and NO2 exposures and increased Triglycerides levels; More studies are needed to clarify the association between ambient air pollutants exposure and lipid profile. ; The authors are grateful to all the professionals and participants involved in the INSEF. INSEF was developed as part of the Predefined project financed under the Public Health Initiatives Program, ''Improvement of epidemiological health information to support public health decision and management in Portugal. Towards reduced inequalities, improved health, and bilateral cooperation", with a 1.500.000V Grant from Iceland, Liechtenstein and Norway from EEA Grants and the Portuguese Government. The present study was also funded by the Portuguese Foundation for Science and Technology (FCT) (PhD Scholarship Reference: SFRH/BD/129426/2017). ; info:eu-repo/semantics/publishedVersion

Abstract Background Air pollution is a major health challenge worldwide and has previously been strongly associated with adverse reproductive health. This study aimed to examine the association between spontaneous abortion and seasonal variation of air pollutants in Ulaanbaatar, Mongolia. Methods Monthly average O 3 , SO 2 , NO 2 , CO, PM 10 and PM 2.5 levels were measured at Mongolian Government Air Quality Monitoring stations. The medical records of 1219 women admitted to the hospital due to spontaneous abortion between 2009–2011 were examined retrospectively. Fetal deaths per calendar month from January-December, 2011 were counted and correlated with mean monthly levels of various air pollutants by means of regression analysis. Results Regression of ambient pollutants against fetal death as a dose–response toxicity curve revealed very strong dose–response correlations for SO 2 r > 0.9 (p 0.8), CO (r > 0.9), PM 10 (r > 0.9) and PM 2.5 (r > 0.8), (p < 0.001), indicating a strong correlation between air pollution and decreased fetal wellbeing. Conclusion The present study identified alarmingly strong statistical correlations between ambient air pollutants and spontaneous abortion. Further studies need to be done to examine possible correlations between personal exposure to air pollutants and pregnancy loss.

Meta-Analysis ; Ambient air pollution (AAP) is recognized a cardiovascular risk factor and lipid profile dysregulation seems to be one of the potential mediators involved. However, results from epidemiologic research on the association between exposure to AAP and altered lipid profile have been inconsistent. This study aims to systematically review and meta-analyse epidemiologic evidence on the association between exposure to ambient air pollutants (particulate matter, nitrogen oxides, sulphur dioxide, ozone, carbon monoxide, back carbon) and lipid profile parameters (Total cholesterol; High-Density Lipoprotein Cholesterol; Low-Density Lipoprotein Cholesterol; TG-Triglycerides) or dyslipidaemia. Systematic electronic literature search was performed in PubMed, Web of Science and Scopus databases (last search on 24th May 2019) using keywords related to the exposure (ambient air pollutants) and to the outcomes (lipid profile parameters/dyslipidaemia). Qualitative and quantitative information of the studies were extracted and fixed or random-effects models were used to obtain a pooled effect estimate per each pollutant/outcome combination. 22 studies were qualitatively analysed and, from those, 3 studies were quantitatively analysed. Particulate matters were the most studied pollutants and a considerable heterogeneity in air pollution assessment methods and outcomes definitions was detected. Age, obesity related measures, tobacco consumption, sex and socioeconomic factors were the most frequent considered variables for confounding adjustment in the models. In a long-term exposure scenario, we found a 3.14% (1.36%-4.95%) increase in TG levels per 10 μg/m3 PM10 increment and a 4.24% (1.37%-7.19%) increase in TG levels per 10 μg/m3 NO2 increment. No significant associations were detected for the remaining pollutant/outcome combinations. Despite the few studies included in the meta-analysis, our study suggests some epidemiologic evidence supporting the association between PM10 and NO2 exposures and increased TG levels. Due to the very low level of evidence, more studies are needed to clarify the role of lipid profile dysregulation as a mediator on the AAP adverse cardiovascular effects. ; INSEF was developed as part of the Predefined project financed under the Public Health Initiatives Program, ''Improvement of epidemiological health information to support public health decision and management in Portugal. Towards reduced inequalities, improved health, and bilateral cooperation", with a 1.500.000V Grant from Iceland, Liechtenstein and Norway from EEA Grants and the Portuguese Government. The present study was also funded by the Portuguese Foundation for Science and Technology (FCT) (PhD Scholarship Reference: SFRH/ BD/129426/2017). ; info:eu-repo/semantics/publishedVersion

Long-term exposure to air pollution has been associated with several adverse health effects including cardiovascular, respiratory diseases and cancers. However, underlying molecular alterations remain to be further investigated. The aim of this study is to investigate the effects of long-term exposure to air pollutants on (a) average DNA methylation at functional regions and, (b) individual differentially methylated CpG sites. An assumption is that omic measurements, including the methylome, are more sensitive to low doses than hard health outcomes. This study included blood-derived DNA methylation (Illumina-HM450 methylation) for 454 Italian and 159 Dutch participants from the European Prospective Investigation into Cancer and Nutrition (EPIC). Long-term air pollution exposure levels, including NO2, NOx, PM2.5, PMcoarse, PM10, PM2.5 absorbance (soot) were estimated using models developed within the ESCAPE project, and back-extrapolated to the time of sampling when possible. We meta-analysed the associations between the air pollutants and global DNA methylation, methylation in functional regions and epigenome-wide methylation. CpG sites found differentially methylated with air pollution were further investigated for functional interpretation in an independent population (EnviroGenoMarkers project), where (N=613) participants had both methylation and gene expression data available. Exposure to NO2 was associated with a significant global somatic hypomethylation (p-value=0.014). Hypomethylation of CpG island's shores and shelves and gene bodies was significantly associated with higher exposures to NO2 and NOx. Meta-analysing the epigenome-wide findings of the 2 cohorts did not show genome-wide significant associations at single CpG site level. However, several significant CpG were found if the analyses were separated by countries. By regressing gene expression levels against methylation levels of the exposure-related CpG sites, we identified several significant CpG-transcript pairs and highlighted 5 enriched pathways for NO2 and 9 for NOx mainly related to the immune system and its regulation. Our findings support results on global hypomethylation associated with air pollution, and suggest that the shores and shelves of CpG islands and gene bodies are mostly affected by higher exposure to NO2 and NOx. Functional differences in the immune system were suggested by transcriptome analyses. ; EPIC-Italy was financially supported by the Italian Association for Cancer Research (AIRC). Genome-wide DNA methylation profiling of EPIC-Italy samples was financially supported by the Human Genetics Foundation (HuGeF) and Compagnia di San Paolo. EPIC-Netherlands was financially supported by the Dutch Ministry of Public Health, Welfare, and Sports (VWS), by the Netherlands Cancer Registry, by LK Research Funds, by Dutch Prevention Funds, by the Netherlands Organisation for Health Research and Development (ZON), and by the World Cancer Research Fund (WCRF). Genome-wide DNA methylation profiling of EPIC-Netherlands samples was financially supported by internal Imperial College funds. The REGICOR study was supported by the Spanish Ministry of Economy and Innovation through the Carlos III Health Institute [Red HERACLES RD12/0042, PI12/00232, PI09/90506], European Funds for Development (ERDF-FEDER), and by the Catalan Research and Technology Innovation Interdepartmental Commission [SGR 1195]. Michelle Plusquin was supported by the People Program (Marie Curie Actions) of the European Union's Seventh Framework Program FP7/2007-2013/ under REA grant agreement n [628858]. Florence Guida was supported by the COLT foundation. Support for this work was also provided by the project EXPOSOMICS, grant agreement 308610-FP7European Commission. Sergi Sayols-Baixeras was funded by a contract from Instituto de Salud Carlos III FEDER [IFI14/00007].