Short-Term Fluctuations in Air Pollution and Asthma in Scania, Sweden. Is the Association Modified by Long-Term Concentrations?
ABSTRACT: Asthma is one of the most common respiratory diseases in the world. Research has shown that temporal increases in air pollution concentrations can aggravate asthma symptoms. The aim of this study was to assess whether individuals living in areas with higher air pollution concentrations responded differently to short-term temporal exposure to air pollution than those living in lower air pollution areas.The study was designed as a case-crossover study in Scania, Sweden. Outcome data was visits to primary health care clinics with asthma as the main complaint during the years 2007 to 2010. Nitrogen dioxide levels were obtained from 21 different air pollution monitoring stations. Short-term exposure was defined as the average concentration four days prior to the visit. Data was pooled for areas above and below a two-year average NO2 concentration of 10 ?g/m3, dispersion modelled with an emission database.The short-term association between NO2 and asthma visits seemed stronger in areas with NO2 levels below 10 ?g/m3, with an odds ratio (OR) of 1.15 (95% confidence interval (CI): 1.08-1.23) associated with a 10 ?g/m3 increase in NO2 compared to areas above 10 ?g/m3 NO2 levels, where corresponding OR of 1.09 (95% CI: 1.02-1.17). However, this difference was not statistically significant. (p = 0.13).The study provided some evidence, although not statistically significant, that short-term associations between air pollution and asthma may depend on background air pollution levels. However, we cannot rule out that the association is due to other spatially dependent factors in Scania. The study should be reproduced in other study areas.
Project description:INTRODUCTION:There is some evidence that exam results are worse when students are acutely exposed to air pollution. Studies investigating the association between air pollution and academic attainment have been constrained by small sample sizes. METHODS:Cross sectional educational attainment data (2009-2015) from students aged 15-16 years in Cardiff, Wales were linked to primary health care data, modelled air pollution and measured pollen data, and analysed using multilevel linear regression models. Annual cohort, school and individual level confounders were adjusted for in single and multi-pollutant/pollen models. We stratified by treatment of asthma and/or Seasonal Allergic Rhinitis (SAR). RESULTS:A unit (10?g/m3) increase of short-term exposure to NO2 was associated with 0.044 (95% CI: -0.079, -0.008) reduction of standardised Capped Point Score (CPS) after adjusting for individual and household risk factors for 18,241 students. This association remained statistically significant after controlling for other pollutants and pollen. There was no association of PM2.5, O3, or Pollen with standardised CPS remaining after adjustment. We found no evidence that treatment for asthma or SAR modified the observed NO2 effect on educational attainment. CONCLUSION:Our study showed that short-term exposure to traffic-related air pollution, specifically NO2, was associated with detrimental educational attainment for students aged 15-16. Longitudinal investigations in different settings are required to confirm this possible impact and further work may uncover the long-term economic implications, and degree to which impacts are cumulative and permanent.
Project description:<h4>Background</h4>The impact of nitrogen dioxide (NO2) and particulate matter with an aerodynamic diameter of less than or equal to 2.5. microns (PM2.5) exposures on lung function has been investigated mainly in children and less in adults. Furthermore, it is unclear whether short-term deviations of air pollutant concentration need to be considered in long-term exposure models.<h4>Objectives</h4>The aims of this study were to investigate the association between short-term air pollution exposure and lung function and to assess whether short-term deviations of air pollutant concentration should be integrated into long-term exposure models.<h4>Methods</h4>Short-term (daily averages 0-7 d prior) and long-term (1- and 4-y means) NO2 and PM2.5 concentrations were modeled using satellite, land use, and meteorological data calibrated on ground measurements. Forced expiratory volume within the first second (FEV1) of forced exhalation and forced vital capacity (FVC) were measured during a LuftiBus assessment (2003-2012) and linked to exposure information from the Swiss National Cohort for 36,085 adults (ages 18-95 y). We used multiple linear regression to estimate adjusted associations, and additionally adjusted models of long-term exposures for short-term deviations in air pollutant concentrations.<h4>Results</h4>A 10?g/m3 increase in NO2 and PM2.5 on the day of the pulmonary function test was associated with lower FEV1 and FVC (NO2: FEV1 -8.0?ml [95% confidence interval: -13.4, -2.7], FVC -16.7?ml [-23.4, -10.0]; PM2.5: FEV1 -15.3?ml [-21.9, -8.7], FVC -18.5?ml [-26.5, -10.5]). A 10?g/m3 increase in 1-y mean NO2 was also associated with lower FEV1 (-7.7?ml; -15.9, 0.5) and FVC (-21.6?ml; -31.9, -11.4), as was a 10?g/m3 increase in 1-y mean PM2.5 (FEV1: -42.2?ml; -56.9, -27.5; FVC: -82.0?ml; -100.1, -63.9). These associations were robust to adjustment for short-term deviations in the concentration of each air pollutant.<h4>Conclusions</h4>Short- and long-term air pollution exposures were negatively associated with lung function, in particular long-term PM2.5 exposure with FVC. Our findings contribute substantially to the evidence of adverse associations between air pollution and lung function in adults. https://doi.org/10.1289/EHP7529.
Project description:BACKGROUND:Short-term exposure to ambient air pollution triggers acute cardiovascular events. Here, we evaluate the association of exposure to ambient air pollution with two intermediate cardiovascular endpoints: blood pressure and carotid stiffness. METHODS:In a one-year panel study, we included 20 healthy volunteers (10 male-female couples aged 59-75?years) with air pollution and health parameters measured every two months at their region of residence (Leuven, Belgium) and twice during two ten-day periods in two locations, one with higher (Milan, Italy) and one with lower (Vindeln, Sweden) air pollution levels (220 observations). We measured blood pressure, carotid arterial stiffness, personal exposure to NO2, and ambient concentrations of PM10, PM2.5, and NO2. We used linear mixed models to evaluate the associations between the health outcomes and the air pollutants. RESULTS:Compared with Leuven, exposure to pollutants was higher in Milan and lower in Vindeln, with the highest contrast for NO2 (median 20.7??g/m3 (IQR:7.4) vs 65.1??g/m3 (9.0) and 4.5?mg/m3 (0.8), respectively). We did not observe significant associations between either systolic or diastolic blood pressure and variations in air pollution. However, we found significant associations between arterial stiffness and 5?day average exposure to the studied pollutants. The strongest associations were observed for PM10 with carotid distensibility (DC) and compliance (CC) coefficients, and the young elastic modulus (YEM): 4.3% (95%CI:7.0;1.5) increase in DC, 4.7% (95%CI:7.1;2.3) increase in CC and 4.2% (95%CI:1.1;7.3) decrease in YEM for each 10??g/m3 decreases in PM10. CONCLUSIONS:Our study suggests that short-term exposure to air pollution results in reductions in carotid elasticity among elderly population.
Project description:BACKGROUND: Pooled estimates of air pollution health effects are important drivers of environmental risk communications and political willingness. In China, there is a lack of review studies to provide such estimates for health impact assessments. METHODS: We systematically searched the MEDLINE database using keywords of 80 major Chinese cities in Mainland China, Hong Kong and Taiwan on 30 June 2012, yielding 350 abstracts with 48 non-duplicated reports either in English or Chinese after screening. We pooled the relative risks (RR) per 10 ?g/m3 of particulate matter (PM10), nitrogen dioxide (NO2), sulphur dioxide (SO2) and ozone (O3). RESULTS: For short-term effects, the pooled RR (p<0.05) ranges were: 1.0031 (PM10) to 1.0140 (NO2) for all-cause mortality, 1.0034 (cardiopulmonary, PM10) to 1.0235 (influenza and pneumonia, SO2) for 9 specific-causes mortality, 1.0021 (cardiovascular, PM10) to 1.0162 (asthma, O3) for 5 specific-causes hospital admissions. For birth outcomes, the RR (p<0.05) ranged from 1.0051 (stillbirth, O3) to 1.1189 (preterm-birth, SO2) and for long-term effect on mortality from 1.0150 (respiratory, SO2) to 1.0297 (respiratory, NO2). Publication bias was absent (Egger test: p=0.326 to 0.624). Annual PM10 and NO2 concentrations were inversely associated with RR of mortality (p=0.017-0.028). CONCLUSIONS: Evidence on short-term effects of air pollution is consistent and sufficient for health impact assessment but that on long-term effects is still insufficient.
Project description:While a great number of papers have been published on the short-term effects of air pollution on mortality, few have tried to assess whether this association varies according to the neighbourhood socioeconomic level and long-term ambient air concentrations measured at the place of residence. We explored the effect modification of 1) socioeconomic status, 2) long-term NO2 ambient air concentrations, and 3) both combined, on the association between short-term exposure to NO2 and all-cause mortality in Paris (France).A time-stratified case-crossover analysis was performed to evaluate the effect of short-term NO2 variations on mortality, based on 79,107 deaths having occurred among subjects aged over 35 years, from 2004 to 2009, in the city of Paris. Simple and double interactions were statistically tested in order to analyse effect modification by neighbourhood characteristics on the association between mortality and short-term NO2 exposure. The data was estimated at the census block scale (n=866).The mean of the NO2 concentrations during the five days prior to deaths were associated with an increased risk of all-cause mortality: overall Excess Risk (ER) was 0.94% (95%CI=[0.08;1.80]. A higher risk was revealed for subjects living in the most deprived census blocks in comparison with higher socioeconomic level areas (ER=3.14% (95%CI=[1.41-4.90], p<0.001). Among these deprived census blocks, excess risk was even higher where long-term average NO2 concentrations were above 55.8 ?g/m3 (the top tercile of distribution): ER=4.84% (95%CI=[1.56;8.24], p for interaction=0.02).Our results show that people living in census blocks characterized by low socioeconomic status are more vulnerable to air pollution episodes. There is also an indication that people living in these disadvantaged census blocks might experience even higher risk following short-term air pollution episodes, when they are also chronically exposed to higher NO2 levels.
Project description:Associations between long-term exposure to air pollution and carotid intima-media thickness (CIMT) have inconsistent findings.In this study we aimed to evaluate association between 1-year average exposure to traffic-related air pollution and CIMT in middle-aged adults in Asia.CIMT was measured in Taipei, Taiwan, between 2009 and 2011 in 689 volunteers 35-65 years of age who were recruited as the control subjects of an acute coronary heart disease cohort study. We applied land-use regression models developed by the European Study of Cohorts for Air Pollution Effects (ESCAPE) to estimate each subject's 1-year average exposure to traffic-related air pollutants with particulate matter diameters ? 10 ?m (PM10) and ? 2.5 ?m (PM2.5) and the absorbance levels of PM2.5 (PM2.5abs), nitrogen dioxide (NO2), and nitrogen oxides (NOx) in the urban environment.One-year average air pollution exposures were 44.21 ± 4.19 ?g/m3 for PM10, 27.34 ± 5.12 ?g/m3 for PM2.5, and (1.97 ± 0.36) × 10-5/m for PM2.5abs. Multivariate regression analyses showed average percentage increases in maximum left CIMT of 4.23% (95% CI: 0.32, 8.13) per 1.0 × 10-5/m increase in PM2.5abs; 3.72% (95% CI: 0.32, 7.11) per 10-?g/m3 increase in PM10; 2.81% (95% CI: 0.32, 5.31) per 20-?g/m3 increase in NO2; and 0.74% (95% CI: 0.08, 1.41) per 10-?g/m3 increase in NOx. The associations were not evident for right CIMT, and PM2.5 mass concentration was not associated with the outcomes.Long-term exposures to traffic-related air pollution of PM2.5abs, PM10, NO2, and NOx were positively associated with subclinical atherosclerosis in middle-aged adults.
Project description:BACKGROUND: Air pollution is associated with asthma exacerbations. We examined the associations of exposure to ambient particulate matter (PM10) and nitrogen dioxide (NO2) with the risk of wheezing in preschool children, and assessed whether these associations were modified by tobacco smoke exposure. METHODS: This study was embedded in the Generation R Study, a population-based prospective cohort study among 4,634 children. PM10 and NO2 levels were estimated for the home addresses using dispersion modeling. Annual parental reports of wheezing until the age of 3 years and fetal and infant tobacco smoke exposure was obtained by questionnaires. RESULTS: Average annual PM10 or NO2 exposure levels per year were not associated with wheezing in the same year. Longitudinal analyses revealed non-significant tendencies towards positive associations of PM10 or NO2 exposure levels with wheezing during the first 3 years of life (overall odds ratios (95% confidence interval): 1.21 (0.79, 1.87) and 1.06 (0.92, 1.22)) per 10 ?g/m3 increase PM10 and NO2, respectively). Stratified analyses showed that the associations were stronger and only significant among children who were exposed to both fetal and infant tobacco smoke (overall odds ratios 4.54 (1.17, 17.65) and 1.85 (1.15, 2.96)) per 10 ?g/m3 increase PM10 and NO2, respectively (p-value for interactions <0.05). CONCLUSIONS: Our results suggest that long term exposure to traffic-related air pollutants is associated with increased risks of wheezing in children exposed to tobacco smoke in fetal life and infancy. Smoke exposure in early life might lead to increased vulnerability of the lungs to air pollution.
Project description:OBJECTIVE:To investigate the association between ambient air pollution and stroke morbidity in different subgroups and seasons. METHODS:We performed a time-series analysis based on generalised linear models to study the short-term exposure-response relationships between air pollution and stroke hospitalisations, and conducted subgroup analyses to identify possible sensitive populations. RESULTS:For every 10?µg/m3 increase in the concentration of air pollutants, across lag 0-3 days, the relative risk of stroke hospitalisation was 1.029 (95% CI 1.013 to 1.045) for PM2.5, 1.054 (95% CI 1.031 to 1.077) for NO2 and 1.012 (95% CI 1.002 to 1.022) for O3. Subgroup analyses showed that statistically significant associations were found in both men and women, middle-aged and older populations, and both cerebral infarction and intracerebral haemorrhage. The seasonal analyses showed that statistically significant associations were found only in the winter. CONCLUSIONS:Our study indicates that short-term exposure to PM2.5, NO2 and O3 may induce stroke morbidity, and the government should take actions to mitigate air pollution and protect sensitive populations.
Project description:BACKGROUND: Genetics may partially explain observed heterogeneity in associations between traffic-related air pollution and incident asthma. OBJECTIVE: Our aim was to investigate the impact of gene variants associated with oxidative stress and inflammation on associations between air pollution and incident childhood asthma. METHODS: Traffic-related air pollution, asthma, wheeze, gene variant, and potential confounder data were pooled across six birth cohorts. Parents reported physician-diagnosed asthma and wheeze from birth to 7-8 years of age (confirmed by pediatric allergist in two cohorts). Individual estimates of annual average air pollution [nitrogen dioxide (NO2), particulate matter ? 2.5 ?m (PM2.5), PM2.5 absorbance, ozone] were assigned to each child's birth address using land use regression, atmospheric modeling, and ambient monitoring data. Effect modification by variants in GSTP1 (rs1138272/Ala114Val and rs1695/IIe105Val) and TNF (rs1800629/G-308A) was investigated. RESULTS: Data on asthma, wheeze, potential confounders, at least one SNP of interest, and NO2 were available for 5,115 children. GSTP1 rs1138272 and TNF rs1800629 SNPs were associated with asthma and wheeze, respectively. In relation to air pollution exposure, children with one or more GSTP1 rs1138272 minor allele were at increased risk of current asthma [odds ratio (OR) = 2.59; 95% CI: 1.43, 4.68 per 10 ?g/m3 NO2] and ever asthma (OR = 1.64; 95% CI: 1.06, 2.53) compared with homozygous major allele carriers (OR = 0.95; 95% CI: 0.68, 1.32 for current and OR = 1.20; 95% CI: 0.98, 1.48 for ever asthma; Bonferroni-corrected interaction p = 0.04 and 0.01, respectively). Similarly, for GSTP1 rs1695, associations between NO2 and current and ever asthma had ORs of 1.43 (95% CI: 1.03, 1.98) and 1.36 (95% CI: 1.08, 1.70), respectively, for minor allele carriers compared with ORs of 0.82 (95% CI: 0.52, 1.32) and 1.12 (95% CI: 0.84, 1.49) for homozygous major allele carriers (Bonferroni-corrected interaction p-values 0.48 and 0.09). There were no clear differences by TNF genotype. CONCLUSIONS: Children carrying GSTP1 rs1138272 or rs1695 minor alleles may constitute a susceptible population at increased risk of asthma associated with air pollution.
Project description:BACKGROUND AND PURPOSE:The data concerning the association between environmental pollution and epilepsy attacks are limited. The aim of this study was to explore the association between acute air pollution exposure and epilepsy attack. METHODS:A hospital record-based study was carried out in Xi'an, a heavily-polluted metropolis in China. Daily baseline data were obtained. Time-series Poisson regression models were applied to analyze the association between air pollution and epilepsy. RESULTS:A 10 ?g/m3 increase of NO2, SO2, and O3 concentrations corresponded to 3.17% (95%Cl: 1.41%, 4.93%), 3.55% (95%Cl: 1.93%, 5.18%), and -0.84% (95%Cl: -1.58%, 0.09%) increase in outpatient-visits for epilepsy on the concurrent days, which were significantly influenced by sex and age. The effects of NO2 and SO2 would be stronger when adjusted for PM2.5. As for O3, a -1.14% (95%Cl: -1.90%, -0.39%) decrease was evidenced when adjusted for NO2. The lag models showed that the most significant effects were evidenced on concurrent days. CONCLUSIONS:We discovered previously undocumented relationships between short-term air pollution exposure and epilepsy: while NO2 and SO2 were positively associated with outpatient-visits of epilepsy, O3 might be associated with reduced risk.