Levels Of Particulate Air Pollution Research Articles

Molecular-Level Insights into the Relationship between Volatility of Organic Aerosol Constituents and PM2.5 Air Pollution Levels: A Study with Ultrahigh-Resolution Mass Spectrometry.

Volatility of organic aerosols (OAs) significantly influences new particle formation and the occurrence of particulate air pollution. However, the relationship between the volatility of OA and the level of particulate air pollution (i.e., particulate matter concentration) is not well understood. In this study, we compared the chemical composition (identified by an ultrahigh-resolution Orbitrap mass spectrometer) and volatility (estimated based on a predeveloped parametrization method) of OAs in urban PM2.5 (particulate matter with aerodynamic diameter ≤ 2.5 μm) samples from seven German and Chinese cities, where the PM2.5 concentration ranged from a light (14 μg m-3) to heavy (319 μg m-3) pollution level. A large fraction (71-98%) of compounds in PM2.5 samples were attributable to intermediate-volatility organic compounds (IVOCs) and semivolatile organic compounds (SVOCs). The fraction of low-volatility organic compounds (LVOCs) and extremely low-volatility organic compounds (ELVOCs) decreased from clean (28%) to heavily polluted urban regions (2%), while that of IVOCs increased from 34 to 62%. We found that the average peak area-weighted volatility of organic compounds in different cities showed a logarithmic correlation with the average PM2.5 concentration, indicating that the volatility of urban OAs increases with the increase of air pollution level. Our results provide new insights into the relationship between OA volatility and PM pollution levels and deepen the understanding of urban air pollutant evolution.

Low-grade malt lymphoma of the nasopharynx in young adults: Successful treatment of a rare diagnosis at a rare site by radiotherapy.

Mucosa Associated Lymphoid Tissue (MALT) lymphoma is the third most common subgroup of Non-Hodgkin's lymphoma and is the most common type of primary extranodal lymphoma. They are rarely found in the nasopharyngeal region and their mean age at presentation is the sixth decade of life. We present the clinical, pathological, treatment and 5-year follow-up data of 5 cases of nasopharyngeal MALT lymphoma treated with definitive radiotherapy at our hospital, between 2009 and 2011. The average age of diagnosis was 27 years which is more than a decade earlier than what has been reported previously. Clinical symptoms included nasal obstruction, tinnitus and hearing loss. All five patients had locoregional disease. They were treated by definitive radiotherapy to a dose between 30 to 40 Gy. At 5 years of follow-up, 4 patients were in complete remission while one had disease relapse. The younger age of presentation compared to older reports in this rare subsite was an interesting finding in our study. The authors speculate that rising levels of particulate air pollution may have played a part in the etiology in this younger population. Our series shows that despite the younger age, the disease displays an indolent course and responds well to radiotherapy alone as the primary treatment. Recurrence or disseminated disease is also highly treatable with systemic chemotherapy.

Air pollution and biomarkers of cardiovascular disease and inflammation in the Malm\xf6 Diet and Cancer cohort

IntroductionAir pollution is associated with increased risk of cardiovascular disease, possibly through chronic systemic inflammation that promotes the progression of atherosclerosis and the risk of cardiovascular events. This study aimed to investigate the associations between air pollution and established biomarkers of inflammation and cardiovascular disease.MethodsThe Cardiovascular Subcohort of the Malmö Diet and Cancer cohort includes 6103 participants from the general population of Malmö, Sweden. The participants were recruited 1991–1994. Annual mean residential exposure to particulate matter < 2.5 and < 10 μm (PM2.5 and PM10), and nitrogen oxides (NOx) at year of recruitment were assigned from dispersion models. Blood samples collected at recruitment, including blood cell counts, and biomarkers (lymphocyte- and neutrophil counts, C-reactive protein (CRP), soluble urokinase-type plasminogen activator receptor (suPAR), lipoprotein-associated phospholipase A2 (Lp-PLA2), ceruloplasmin, orosomucoid, haptoglobin, complement-C3, and alpha-1-antitrypsin) were analyzed. Multiple linear regression models were used to investigate the cross-sectional associations between air pollutants and biomarkers.ResultsThe mean annual exposure levels in the cohort were only slightly or moderately above the new WHO guidelines of 5 μg/m3 PM2.5 (10.5 μg/m3 PM2.5). Residential PM2.5 exposure was associated with increased levels of ceruloplasmin, orosomucoid, C3, alpha-1-antitrypsin, haptoglobin, Lp-PLA2 and the neutrophil-lymphocyte ratio. Ceruloplasmin, orosomucoid, C3 and alpha-1-antitrypsin were also positively associated with PM10. There were no associations between air pollutants and suPAR, leukocyte counts or CRP. The associations between particles and biomarkers were still significant after removing outliers and adjustment for CRP levels. The associations were more prominent in smokers.ConclusionLong-term residential exposure to moderate levels of particulate air pollution was associated with several biomarkers of inflammation and cardiovascular disease. This supports inflammation as a mechanism behind the association between air pollution and cardiovascular disease.

Association of Air Pollutant Exposure and Sinonasal Histopathology Findings in Chronic Rhinosinusitis.

Ambient air pollution is well known to cause inflammatory change in respiratory epithelium and is associated with exacerbations of inflammatory conditions such as asthma and chronic obstructive pulmonary disease. However, limited work has been done on the impact of air pollution on pathogenesis of chronic rhinosinusitis and there are no reports in the literature of how pollutant exposure may impact sinonasal histopathology in patients with chronic rhinosinusitis. This study aims to identify associations between certain histopathologic characteristics seen in sinus tissue of patients with chronic rhinosinusitis (CRS) and levels of particulate air pollution (PM2.5) and ground-level ozone in their place of residence. A structured histopathology report was created to characterize the tissues of CRS patients undergoing sinus surgery. An estimate for each patient's exposure to air pollutants including small particulate matter (PM2.5) and ground-level ozone was obtained using the Environmental Protection Agency's (EPA) Environmental Justice Screening and Mapping Tool (EJSCREEN). Mean pollutant exposures for patients whose tissues exhibited varying histopathologic features were compared using logistic regression models. Data from 291 CRS patients were analyzed. Higher degree of inflammation was significantly associated with increased ozone exposure (p = 0.031). Amongst the patients with CRSwNP (n=131), presence of eosinophilic aggregates (p = 0.018) and Charcot-Leyden crystals (p = 0.036) was associated with increased ozone exposure. Exposure to ambient air pollutants may contribute to pathogenesis of CRS. Increasing ozone exposure was linked to both higher tissue inflammation and presence of eosinophilic aggregates and Charcot-Leyden crystals in CRSwNP patients.

Reduced repressive epigenetic marks, increased DNA damage and Alzheimer's disease hallmarks in the brain of humans and mice exposed to particulate urban air pollution

Exposure to air pollutants is associated with an increased risk of developing Alzheimer's disease (AD). AD pathological hallmarks and cognitive deficits are documented in children and young adults in polluted cities (e.g. Metropolitan Mexico City, MMC). Iron-rich combustion- and friction-derived nanoparticles (CFDNPs) that are abundantly present in airborne particulate matter pollution have been detected in abundance in the brains of young urbanites. Epigenetic gene regulation has emerged as a candidate mechanism linking exposure to air pollution and brain diseases. A global decrease of the repressive histone post-translational modifications (HPTMs) H3K9me2 and H3K9me3 (H3K9me2/me3) has been described both in AD patients and animal models. Here, we evaluated nuclear levels of H3K9me2/me3 and the DNA double-strand-break marker γ-H2AX by immunostaining in post-mortem prefrontal white matter samples from 23 young adults (age 29 ± 6 years) who resided in MMC (n = 13) versus low-pollution areas (n = 10). Lower H3K9me2/me3 and higher γ-H2A.X staining were present in MMC urbanites, who also displayed the presence of hyperphosphorylated tau and amyloid-β (Aβ) plaques. Transmission electron microscopy revealed abundant CFDNPs in neuronal, glial and endothelial nuclei in MMC residents' frontal samples. In addition, mice exposed to particulate air pollution (for 7 months) in urban Santiago (Chile) displayed similar brain impacts; reduced H3K9me2/me3 and increased γ-H2A.X staining, together with increased levels of AD-related tau phosphorylation. Together, these findings suggest that particulate air pollution, including metal-rich CFDNPs, impairs brain chromatin silencing and reduces DNA integrity, increasing the risk of developing AD in young individuals exposed to high levels of particulate air pollution.

Traffic-Related Air Pollution as a Risk Factor for Dementia: No Clear Modifying Effects of APOEɛ4 in the Betula Cohort.

It is widely known that the apolipoprotein E (APOE) ɛ4 allele imposes a higher risk for Alzheimer's disease (AD). Recent evidence suggests that exposure to air pollution is also a risk factor for AD, and results from a few studies indicate that the effect of air pollution on cognitive function and dementia is stronger in APOEɛ4 carriers than in non-carriers. Air pollution and interaction with APOEɛ4 on AD risk thus merits further attention. We studied dementia incidence over a 15-year period from the longitudinal Betula study in Northern Sweden. As a marker for long-term exposure to traffic-related air pollution, we used modelled annual mean nitrogen oxide levels at the residential address of the participants at start of follow-up. Nitrogen oxide correlate well with fine particulate air pollution levels in the study area. We had full data on air pollution, incidence of AD and vascular dementia (VaD), APOEɛ4 carrier status, and relevant confounding factors for 1,567 participants. As expected, air pollution was rather clearly associated with dementia incidence. However, there was no evidence for a modifying effect by APOEɛ4 on the association (p-value for interaction > 0.30 for both total dementia (AD+VaD) and AD). The results from this study do not imply that adverse effects of air pollution on dementia incidence is limited to, or stronger in, APOEɛ4 carriers than in the total population.

Association between short-term exposure to particulate matter air pollution and cause-specific mortality in Changzhou, China

BackgroundExtensive studies have linked ambient particulate matter (PM) to an increased mortality burden from a wide range of causes. However, the effects of PM on mortality rates from specific causes were unclear. This study aimed to estimate the detrimental effects of PM on cause specific deaths in Changzhou, China. MethodData representing daily mortality rates, weather conditions and particulate air pollution levels were obtained from government-controlled agencies of Changzhou, from January 1, 2015 to December 31, 2016. An inverse distance weighting method was used to assess the population exposure to PM and a time-series was performed to detect the detrimental effects of PM. ResultsPositive associations were identified between PMs and daily mortality rates from non-accidental, circulatory, hypertensive, respiratory and chronic lower respiratory causes at a lag of 0–3 days. The effects of PMs were strongest on hypertensive mortality, with an increase of 5.27% (95% confidence interval (CI): 2.43–8.19%) and 3.52% (95% CI: 1.55–5.53%), per 10 μg/m3 increment in PM2.5 and PM10 respectively. The elderly exhibited a higher mortality risk with PMs exposure. Females were more vulnerable to circulatory, hypertensive and respiratory death while males were more sensitive to chronic lower respiratory and neurodegenerative mortality. The effects were stronger in warm seasons for circulatory mortality and stronger in cold seasons for respiratory mortality. ConclusionThese findings indicate that PM could exert adverse influences on the outcomes of several pathological processes, especially for women and the elderly with hypertension disease.

A Citizen Science and Government Collaboration: Developing Tools to Facilitate Community Air Monitoring.

The U.S. Environmental Protection Agency (EPA) is actively involved in supporting citizen science projects and providing communities with information and assistance for conducting their own air pollution monitoring. As part of a Regional Applied Research Effort (RARE) project, EPA's Office of Research and Development (ORD) worked collaboratively with EPA Region 2 and the Ironbound Community Corporation (ICC) in Newark, New Jersey, to develop and test the "Air Sensor Toolbox for Citizen Scientists." In this collaboration, citizen scientists measured local gaseous and particulate air pollution levels by using a customized low-cost sensor pod designed and fabricated by EPA. This citizen science air quality measurement project provided an excellent opportunity for EPA to evaluate and improve the Toolbox resources available to communities. The Air Sensor Toolbox, developed in coordination with the ICC, can serve as a template for communities across the country to use in developing their own air pollution monitoring programs in areas where air pollution is a concern. This pilot project provided an opportunity for a highly motivated citizen science organization and the EPA to work together directly to address environmental concerns within the community. Useful lessons were learned about how to improve coordination between the government and communities and the types of tools and technologies needed for conducting an effective citizen science project that can be applied to future efforts.

Mortality and emergency hospitalizations associated with atmospheric particulate matter episodes across the UK in spring 2014

Exposure to particulate air pollution is known to have negative impacts on human health. Long-term exposure to anthropogenic particulate matter is associated with the equivalent of around 29,000 deaths a year in the UK. However, short-lived air pollution episodes on the order of a few days are also associated with increased daily mortality and emergency hospital admissions for respiratory and cardiovascular conditions. The UK experienced widespread high levels of particulate air pollution in March–April 2014; observations of hourly mean PM2.5 concentrations reached up to 83μgm−3 at urban background sites. We performed an exposure and health impact assessment of the spring air pollution, focusing on two episodes with the highest concentrations of PM2.5 (12–14 March and 28 March–3 April 2014). Across these two episodes of elevated air pollution, totalling 10days, around 600 deaths were brought forward from short-term exposure to PM2.5, representing 3.9% of total all-cause (excluding external) mortality during these days. Using observed levels of PM2.5 from other years, we estimate that this is 2.0 to 2.7 times the mortality burden associated with typical urban background levels of PM2.5 at this time of year. Our results highlight the potential public health impacts and may aid planning for health care resources when such an episode is forecast.

Exposure to airborne particulate matter during pregnancy is associated with preterm birth: a population-based cohort study.

BackgroundTest the hypothesis that exposure to fine particulate matter in the air (PM2.5) is associated with increased risk of preterm birth (PTB).MethodsGeo-spatial population-based cohort study using live birth records from Ohio (2007–2010) linked to average daily measures of PM2.5, recorded by 57 EPA network monitoring stations across the state. Geographic coordinates of the home residence for births were linked to the nearest monitoring station using ArcGIS. Association between PTB and high PM2.5 levels (above the EPA annual standard of 15 μg/m3) was estimated using GEE, with adjustment for age, race, education, parity, insurance, tobacco, birth season and year, and infant gender. An exchangeable correlation matrix for the monitor stations was used in the models. Analyses were limited to non-anomalous singleton births at 20-42weeks with no known chromosome abnormality occurring within 10 km of a monitor station.ResultsThe frequency of PTB was 8.5 % in the study cohort of 224,921 singleton live births. High PM2.5 exposure (>EPA recommended maximum) occurred frequently during the study period, with 24,662 women (11 %) having high exposure in all three trimesters. Pregnancies with high PM2.5 exposure through pregnancy had increased PTB risk even after adjustment for coexisting risk factors, adjOR 1.19 (95 % CI 1.09–1.30). Assessed per trimester, high 3rd trimester PM2.5 exposure resulted in the highest PTB risk, adjOR 1.28 (95 % CI 1.20–1.37).ConclusionsExposure to high levels of particulate air pollution, PM2.5, in pregnancy is associated with a 19 % increased risk of PTB; with greatest risk with high 3rd trimester exposure. Although the risk increase associated with high PM2.5 levels is modest, the potential impact on overall PTB rates is robust as all pregnant women are potentially at risk. This exposure may in part contribute to the higher preterm birth rates in Ohio compared to other states in the US, especially in urban areas.

Upgrading the Estimation of Daily PM10 Concentrations Utilizing Prediction Variables Reflecting Atmospheric Processes

ABSTRACTThis paper formulates a Multiple Linear Regression Model (MLRM), for the estimation of daily PM10 concentrations in background urban areas. 24-hour backward air mass trajectories, NO2 concentrations and gridded (1° × 1° resolution) Aerosol Optical Depth (AOD) observations from MODIS were used in order to compose the model’s predictor variables. As a supplement to local combustion/non-combustion contributions, the suggested method intends to comprise and quantify the effect that transboundary PM sources and wind dispersion have, on particulate air pollution levels. The proposed technique was implemented at a background sampling site in Birmingham (United Kingdom) and the results were compared with the outcome of a Simple Linear Regression Model (SLRM) which contained only one predictor variable expressing local combustion. Various statistical indices signified the upgraded performance of the MLRM, in comparison with SLRM, thus the participation of long range transport and wind dispersion variables in the MLRM was successful. According to the MLRM’s findings, anthropogenic combustion (traffic, heating) is the strongest source of PM10 in the selected background urban area, followed by local non-combustion emissions and long range transport. Extreme PM2.5 intrusions from continental Europe also emerged.

Dynamics of Particle Size on Inhalation of Environmental Aerosol and Impact on Deposition Fraction.

Inhalation of elevated levels of particulate air pollution has been shown to elicit the onset of adverse health effects in humans, where the magnitude of the response is a product of where in the lung the particulate dose is delivered. At any point in time during inhalation the depositional flux of the aerosol is a function of the radius of the droplet, thus a detailed understanding of the rate and magnitude of the mass flux of water to the droplet during inhalation is crucial. In this study, we assess the impact of aerosol hygroscopicity on deposited dose through the inclusion of a detailed treatment of the mass flux of water to account for the dynamics of particle size in a modified version of the standard International Commission on Radiological Protection (ICRP) whole lung deposition model. The ability to account for the role of the relative humidity (RH) of the aerosol prior to, and during, inhalation on the deposition pattern is explored, and found to have a significant effect on the deposition pattern. The model is verified by comparison to previously published measurements, and used to demonstrate that ambient RH affects where in the lung indoor particulate air pollution is delivered.

Acute Effect Of Particulate Air Pollution On Myocardial Infarction Incidence In Shanghai, China

Introduction: Evidence based on ecological studies in China suggests that short-term exposure to particulate matter is associated with cardiovascular mortality. However, there is less evidence for myocardial infarction (MI) morbidity. This study aims to investigate the relation between ambient particulate matter and MI incidence in people aged above 40 in Shanghai. Methods: Daily MI events during 2005-2012 were identified from outpatients and hospital admissions. Daily average concentrations for particulate matter with aerodynamic diameter less than 10 microns (PM10) were collected over the 8-year period. Particulate matter with aerodynamic diameter less than 2.5 microns (PM2.5) were measured from 2009 to 2012. Analyses were performed using quasi-poisson regression models adjusting for confounders, including long-term trend, seasonality, day of the week, public holiday and meteorological factors. The effects were also examined by gender and age group (40-64 years, 65-84 years, and above 85). Results: There were 619928 MI outpatient visits and 21703 admitted. The average concentrations of PM10 and PM2.5 were 81.7μg/m3 and 38.6μg/m3, respectively. While evidence was weak for relationship with hospital admissions, particulate air pollution (PM10, PM2.5) was consistently associated with increased risk of MI outpatients visits. An interquartile range increase in PM10 (IQR: 46.0-102.0μg/m3) and in PM2.5 (IQR: 20.0-50.2μg/m3) of the current day produced a 1.22% (95% CI: 0.46%, 1.98%) and a 1.65% (95% CI: 0.25%, 3.06%) increase of MI outpatients, respectively. The associations appeared to be more evident in male and the elderly (65-84 years). Discussion: Short-term exposure to particulate air pollution (PM10 and PM2.5) was associated with increased risk of MI outpatient visits in Shanghai. However, similar associations for hospital admissions were not found. It provides evidence that the current high level of particulate air pollution in Shanghai has an adverse health effect.

Indoor air quality due to secondhand smoke: Signals from selected hospitality locations in rural and urban areas of Bangalore and Dharwad districts in Karnataka, India.

Tobacco smoke has compounds that are known as human carcinogens. With every breath of secondhand smoke we inhale thousands of chemicals. The Government of India in the interest of public health has enacted the Cigarette and Other Tobacco Products Act (COTPA), 2003, which bans smoking in all the public places including hotels and restaurants. The purpose of this study was to observe and record air pollution in smoke free and smoke observed locations and thereby find out whether the owners/managers of hotels, restaurants, and bars comply with rules of COTPA. The objectives of the study were to measure and compare the level of particulate air pollution from secondhand smoke (PM2.5) in smoking and nonsmoking venues. The study was conducted from September 2009 to March 2010 in Karnataka, India following a nonrandom sample of 79 locations, which included restaurants, bars, cafes, hotels, and tea stalls in two districts. The concentration of PM2.5 was measured using a TSI SidePak AM510 Personal Aerosol Monitor. In Karnataka out of the 79 hospitality locations, smoking was observed in 58% places and only 28% had displayed the required "No Smoking" signage. Places where indoor smoking was observed had high levels of air pollution with average 135 PM2.5, which were 3.1 times higher than the average 43 PM2.5 in smoke-free locations and 14 times higher than the World Health Organization (WHO) target air quality guideline for PM2.5. The average PM2.5 levels in different locations ranged from 11 to 417 μg/m(3) and was lower in the case of apparently compliant designated smoking area (DSR). The patrons and the workers in the hospitality sector continue to be exposed to secondhand smoke despite the enactment of COTPA, which bans smoking in public places. This situation demands stringent measures for effective implementation of the Smoke Free Act and negative response to smoking among civil society.

Carbon Black Particle Exhibits Size Dependent Toxicity in Human Monocytes

Increased levels of particulate air pollution are associated with increased respiratory and cardiovascular mortality and morbidity. Some epidemiologic and toxicological researches suggest ultrafine particles (<100 nm) to be more harmful per unit mass than larger particles. In the present study, the effect of particle size (nano and micro) of carbon black (CB) particle on viability, phagocytosis, cytokine induction, and DNA damage in human monocytes, THP-1 cells, was analysed. The cells were incubated with nanosize (~50 nm) and micron (~500 nm) size of CB particles in a concentration range of 50–800 µg/mL. The parameters like MTT assay, phagocytosis assay, ELISA, gene expression, and DNA analysis were studied. Exposure to nano- and micron-sized CB particles showed size- and concentration dependent decrease in cell viability and significant increase in proinflammatory cytokines IL-1β, TNF-α and IL-6 as well as chemokine IL-8 release. Gene expression study showed upregulation of monocyte chemoattractant protein-1 gene while cyclooxygenase-2 gene remained unaffected. Nano CB particles altered the phagocytic capacity of monocytes although micron CB had no significant effect. CB particles did not show any significant effect on DNA of monocytes. The investigations indicate that CB particles in nanosize exhibit higher propensity of inducing cytotoxicity, inflammation, and altered phagocytosis in human monocytes than their micron size.

Particulate air pollution and cardiovascular disease – it is time to take it seriously

Worldwide, there were over 3 million deaths attributable to exposure to excessive levels of particulate air pollution in 2010. This is similar to the number of deaths attributable to high blood sugar (3.4 million) but less than the number of deaths attributed to smoking (5.7 million) and excessive alcohol consumption (5.0 million). Globally, ambient particulate air pollution was the ninth leading cause of premature deaths, and most of the disease attributable to exposure to ambient particulate air pollution is cardiovascular disease. Short-term and long-term exposures to outdoor particulate matter pollution are associated with a range of adverse cardiovascular health effects such as heart rate variability, development of atherosclerosis, myocardial ischemia, myocardial infarction, stroke, and deaths. Despite this, there is not the same recognition of particulate air pollution as an important risk factor for cardiovascular disease morbidity and mortality compared to the more established risk factors such as cigarette smoking and hypertension. It is now time to reevaluate the contribution of particulate air pollution to cardiovascular disease.

Long-term exposure to high particulate matter pollution and cardiovascular mortality: A 12-year cohort study in four cities in northern China

Epidemiologic studies have demonstrated that long-term exposure to relatively low levels of particulate air pollution is associated with adverse cardiovascular outcomes in Europe and North America. However, few studies have assessed the association with high level air pollutants. We aimed to assess the cardiovascular effects of long-term exposure to high level concentrations of inhalable particulate and to identify the characteristics of the Chinese population that are susceptible to the health effects. A retrospective cohort, containing 39,054 subjects from four cities in northern China, was followed for mortality of all cause and specific cardiovascular diseases from 1998 to 2009. Information on concentrations of PM10 (particulate matter<10μm in aerodynamic diameter) was collected from the local Environmental Monitoring Centers. The estimated exposure for the study participants was the mean concentration of PM10 over their surviving years during the cohort period. Relative risk values were obtained using Cox proportional hazards regression models after adjusting for potential confounding factors. For each 10μg/m3 increase in PM10, the relative risk ratios (RRs) of all-cause mortality, cardiovascular disease mortality, ischemic heart disease mortality, heart failure disease mortality, and cerebrovascular disease mortality were 1.24 (95% CI, 1.22–1.27), 1.23 (95% CI, 1.19–1.26), 1.37 (95% CI, 1.28–1.47), 1.11(95% CI, 1.05–1.17), and 1.23(95% CI:1.18–1.28), respectively. Results from stratified analyses suggest that the effects of PM10 on cardiovascular mortality were more pronounced in males, smokers and people with a higher socioeconomic status. Long-term exposure to PM10 increases mortality from cardiovascular disease, especially from ischemic heart disease and this association seemed to be modified by other factors. Further research that focuses on exploring dose–response relationship and inter-population comparisons is warranted.

Particulate air pollution and health inequalities: a Europe-wide ecological analysis

BackgroundEnvironmental disparities may underlie the unequal distribution of health across socioeconomic groups. However, this assertion has not been tested across a range of countries: an important knowledge gap for a transboundary health issue such as air pollution. We consider whether populations of low-income European regions were a) exposed to disproportionately high levels of particulate air pollution (PM10) and/or b) disproportionately susceptible to pollution-related mortality effects.MethodsEurope-wide gridded PM10 and population distribution data were used to calculate population-weighted average PM10 concentrations for 268 sub-national regions (NUTS level 2 regions) for the period 2004–2008. The data were mapped, and patterning by mean household income was assessed statistically. Ordinary least squares regression was used to model the association between PM10 and cause-specific mortality, after adjusting for regional-level household income and smoking rates.ResultsAir quality improved for most regions between 2004 and 2008, although large differences between Eastern and Western regions persisted. Across Europe, PM10 was correlated with low household income but this association primarily reflected East–West inequalities and was not found when Eastern or Western Europe regions were considered separately. Notably, some of the most polluted regions in Western Europe were also among the richest. PM10 was more strongly associated with plausibly-related mortality outcomes in Eastern than Western Europe, presumably because of higher ambient concentrations. Populations of lower-income regions appeared more susceptible to the effects of PM10, but only for circulatory disease mortality in Eastern Europe and male respiratory mortality in Western Europe.ConclusionsIncome-related inequalities in exposure to ambient PM10 may contribute to Europe-wide mortality inequalities, and to those in Eastern but not Western European regions. We found some evidence that lower-income regions were more susceptible to the health effects of PM10.

Low-level exposure to ambient particulate matter is associated with systemic inflammation in ischemic heart disease patients

Short-term exposure to ambient air pollution is associated with increased cardiovascular mortality and morbidity. This adverse health effect is suggested to be mediated by inflammatory processes. The purpose of this study was to determine if low levels of particulate matter, typical for smaller cities, are associated with acute systemic inflammation.Fifty-two elderly individuals with ischemic heart disease were followed for six months with biweekly clinical visits in the city of Kotka, Finland. Blood samples were collected for the determination of inflammatory markers interleukin (IL)-1β, IL-6, IL-8, IL-12, interferon (IFN)γ, C-reactive protein (CRP), fibrinogen, myeloperoxidase and white blood cell count. Particle number concentration and fine particle (particles with aerodynamic diameters <2.5μm (PM2.5)) as well as thoracic particle (particles with aerodynamic diameters <10μm (PM10)) mass concentration were measured daily at a fixed outdoor measurement site. Light-absorbance of PM2.5 filter samples, an indicator of combustion derived particles, was measured with a smoke-stain reflectometer. In addition, personal exposure to PM2.5 was measured with portable photometers. During the study period, wildfires in Eastern Europe led to a 12-day air pollution episode, which was excluded from the main analyses.Average ambient PM2.5 concentration was 8.7μg/m3. Of the studied pollutants, PM2.5 and absorbance were most strongly associated with increased levels of inflammatory markers; most notably with C-reactive protein and IL-12 within a few days of exposure. There was also some evidence of an effect of particulate air pollution on fibrinogen and myeloperoxidase. The concentration of IL-12 was considerably (227%) higher during than before the forest fire episode. These findings show that even low levels of particulate air pollution from urban sources are associated with acute systemic inflammation. Also particles from wildfires may exhibit pro-inflammatory effects.

Add Depression to Ills Linked to Air Pollution

Back to table of contents Previous article Next article Clinical & Research NewsFull AccessAdd Depression to Ills Linked to Air PollutionJoan Arehart-TreichelJoan Arehart-TreichelSearch for more papers by this authorPublished Online:4 Nov 2011https://doi.org/10.1176/pn.46.21.psychnews_46_21_16_1AbstractNot long ago, scientists linked suicides with air pollutants such as particulate matter, sulfur dioxide, and ozone (Psychiatric News, June 17). A growing body of literature is implicating secondhand smoke exposure in depression. And now scientists report that long-term exposure to airborne particulate matter leads, in mice at least, to depression-like behavior, learning and memory problems, and neuroinflammation in the hippocampus.The lead investigator of the new study was Laura Fonken, a neuroscience graduate student at Ohio State University. The results appeared in the October Molecular Psychiatry. Fonken and her colleagues exposed one group of four-month-old male mice for 10 months to particulate air pollution and another group of four-month-old male mice for 10 months to filtered air. At the end of that time, both groups underwent a battery of behavioral tests to evaluate affective responses and learning and memory. Following behavioral testing, the mice were re-exposed to their respective air conditions for one month. Source: Laura Fonken et. al, Molecular Psychiatry, October 2011The researchers found that the mice that had been exposed to the particulate pollutants demonstrated more depressive-like symptoms and learning and memory problems than the control mice. And the hippocampi of the group that had been exposed to the pollutants showed both proinflammatory cytokines and neuronal damage compared with the hippocampi from the control group. Thus it looked as if air particulates caused depression-like and learning and memory problems in the mice that had been exposed to them long term and that the particulates might have done so by damaging the hippocampus, since that brain region is highly vulnerable to injury and inflammation and hippocampal changes in both humans and rodents have been linked with depression and cognitive impairment.The researchers also speculated on how particulates might have damaged the mice's hippocampi. Since particulates have been heavily implicated in heart and lung illnesses, it's possible that immune reactions in the mice's hearts and lungs to particulates led to the formation of inflammatory substances such as cytokines. These substances might then have crossed the blood-brain barrier into the mice's brains and damaged neurons in the hippocampus. "Taken together, these data suggest that long-term exposure to particulate air pollution levels typical of exposure in major cities around the globe can alter affective responses and impair cognition," they concluded. And if that is indeed the case, then the public-health implications could be profound since "in many regions of the world, individuals are exposed to particulate air pollution over their entire lives." The study was funded by the National Institutes of Health.An abstract of "Air Pollution Impairs Cognition, Provokes Depressive-like Behaviors, and Alters Hippocampal Cytokine Expression and Morphology" is posted at <www.nature.com/mp/journal/v16/n10/abs/mp201176a.html>. ISSUES NewArchived