Bayesian spatiotemporal modelling for the assessment of short-term exposure to particle pollution in urban areas.
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ABSTRACT:
SUBMITTER: Pirani M
PROVIDER: S-EPMC3994509 | biostudies-other | 2014 May-Jun
REPOSITORIES: biostudies-other
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Project description:Exposure to air pollution is associated with increased cardio- and cerebrovascular diseases. However, the evidence regarding the short-term effect of air pollution on cardio- and cerebrovascular hospitalisations in areas with relatively low air pollution levels is limited. This study aims to examine the effect of short-term exposure to different air pollutants on hospital admissions due to cardio- and cerebrovascular diseases in rural and regional Australia with low air pollution. The study was conducted in five local Government areas of Hunter New England Local Health District (HNE-LHD). Hospitalisation data from January 2018 to February 2020 (820 days) were accessed from the HNE-LHD admitted patients' dataset. Poisson regression model was used to examine the association between the exposure (air pollutants) and outcome variables (hospitalisation due to cardio- and cerebrovascular disease). The concentrations of gaseous air pollutants, Sulphur Dioxide (SO2), Nitrogen Dioxide (NO2), Ozone (O3), Carbon Monoxide (CO), and Ammonia (NH3) were below national benchmark concentrations for every day of the study period. In single pollutant models, SO2 and NO2 significantly increased the daily number of cardio- and cerebrovascular hospitalisations. The highest cumulative effect for SO2 was observed across lag 0-3 days (Incidence Rate Ratio, IRR: 1.77; 95% Confidence Interval, CI: 1.18-2.65; p-value: 0.01), and for NO2, it was across lag 0-2 days (IRR: 1.13; 95% CI: 1.02-1.25; p-value: 0.02). In contrast, higher O3 was associated with decreased cardio- and cerebrovascular hospitalisations, with the largest effect observed at lag 0 (IRR: 0.94; 95% CI: 0.89-0.98; p-value: 0.02). In the multi-pollutant model, the effect of NO2 remained significant at lag 0 and corresponded to a 21% increase in cardio- and cerebrovascular hospitalisation (95% CI: 1-44%; p-value = 0.04). Thus, the study revealed that gaseous air pollutants, specifically NO2, were positively related to increased cardio- and cerebrovascular hospitalisations, even at concentrations below the national standards.
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Project description:To evaluate the effectiveness of alternative policies and measures to reduce air pollution effects on urban citizen's health, population exposure assessments are needed. Due to road traffic emissions being a major source of emissions and exposure in European cities, it is necessary to account for differentiated transport environments in population dynamics for exposure studies. In this study, we applied a modelling system to evaluate population exposure in the urban area of Hamburg in 2016. The modeling system consists of an urban-scale chemistry transport model to account for ambient air pollutant concentrations and a dynamic time-microenvironment-activity (TMA) approach, which accounts for population dynamics in different environments as well as for infiltration of outdoor to indoor air pollution. We integrated different modes of transport in the TMA approach to improve population exposure assessments in transport environments. The newly developed approach reports 12% more total exposure to NO2 and 19% more to PM2.5 compared with exposure estimates based on residential addresses. During the time people spend in different transport environments, the in-car environment contributes with 40% and 33% to the annual sum of exposure to NO2 and PM2.5, in the walking environment with 26% and 30%, in the cycling environment with 15% and 17% and other environments (buses, subway, suburban, and regional trains) with less than 10% respectively. The relative contribution of road traffic emissions to population exposure is highest in the in-car environment (57% for NO2 and 15% for PM2.5). Results for population-weighted exposure revealed exposure to PM2.5 concentrations above the WHO AQG limit value in the cycling environment. Uncertainties for the exposure contributions arising from emissions and infiltration from outdoor to indoor pollutant concentrations range from -12% to +7% for NO2 and PM2.5. The developed "dynamic transport approach" is integrated in a computationally efficient exposure model, which is generally applicable in European urban areas. The presented methodology is promoted for use in urban mobility planning, e.g., to investigate on policy-driven changes in modal split and their combined effect on emissions, population activity and population exposure.
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Project description:We investigated associations between ambient air pollution and microvessel function measured by peripheral arterial tonometry between 2003 and 2008 in the Framingham Heart Study Offspring and Third Generation Cohorts. We measured particulate matter with aerodynamic diameter ≤2.5 µm (PM2.5), black carbon, sulfates, particle number, nitrogen oxides, and ozone by using fixed monitors, and we determined moving averages for 1-7 days preceding vascular testing. We examined associations between these exposures and hyperemic response to ischemia and baseline pulse amplitude, a measure of arterial tone (n = 2,369). Higher short-term exposure to air pollutants, including PM2.5, black carbon, and particle number was associated with higher baseline pulse amplitude. For example, higher 3-day average PM2.5 exposure was associated with 6.3% higher baseline pulse amplitude (95% confidence interval: 2.0, 10.9). However, there were no consistent associations between the air pollution exposures assessed and hyperemic response. Our findings in a community-based sample exposed to relatively low pollution levels suggest that short-term exposure to ambient particulate pollution is not associated with vasodilator response, but that particulate air pollution is associated with baseline pulse amplitude, suggesting potentially adverse alterations in baseline vascular tone or compliance.
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Project description:PurposeLong-term exposure to ambient fine particle (PM2.5) concentrations has been associated with an increased rate or risk of neurodegenerative conditions, but individual PM sources have not been previously examined in relation to neurodegenerative diseases.MethodsUsing the Statewide Planning and Research Cooperative System database, we studied 63,287 hospital admissions with a primary diagnosis of either Alzheimer's disease, dementia, or Parkinson's disease for New York State residents living within 15 miles from six PM2.5 monitoring sites. In addition to PM2.5 concentrations, we studied seven specific PM2.5 sources: secondary sulfate, secondary nitrate, biomass burning, diesel, spark-ignition emissions, pyrolyzed organic rich, and road dust. We estimated the rate of neurodegenerative hospital admissions associated with increased concentration of PM2.5 and individual PM2.5 sources average concentrations in the previous 0-29, 0-179, and 0-364 days.ResultsIncreases in ambient PM2.5 concentrations were not consistently associated with increased hospital admissions rates. Increased source-specific PM2.5 concentrations were associated with both increased (e.g., secondary sulfates and diesel emissions) and decreased rates (e.g., secondary nitrate and spark-ignition vehicular emissions) of neurodegenerative admissions.ConclusionsWe did not observe clear associations between overall ambient PM2.5 concentrations or source-apportioned ambient PM2.5 contributions and rates of neurologic disease hospitalizations.
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Project description:ImportancePsoriasis is a chronic inflammatory disease with a relapsing-remitting course. Selected environmental factors such as infections, stressful life events, or drugs may trigger disease flares. Whether air pollution could trigger psoriasis flares is still unknown.ObjectiveTo investigate whether short-term exposure to environmental air pollution is associated with psoriasis flares.Design, setting, and participantsThis observational study with both case-crossover and cross-sectional design retrospectively analyzed longitudinal data from September 2013 to January 2020 from patients with chronic plaque psoriasis consecutively attending the outpatient dermatologic clinic of the University Hospital of Verona. For the case-crossover analysis, patients were included who had at least 1 disease flare, defined as Psoriasis Area and Severity Index (PASI) increase of 5 or greater between 2 consecutive assessments in a time frame of 3 to 4 months. For the cross-sectional analysis, patients were included who received any systemic treatment for 6 or more months, with grade 2 or higher consecutive PASI assessment.Main outcomes and measuresWe compared the mean and cumulative (area under the curve) concentrations of several air pollutants (carbon monoxide, nitrogen dioxide, other nitrogen oxides, benzene, coarse particulate matter [PM; 2.5-10.0 μm in diameter, PM10] and fine PM [<2.5 μm in diameter, PM2.5]) in the 60 days preceding the psoriasis flare and the control visits.ResultsA total of 957 patients with plaque psoriasis with 4398 follow-up visits were included in the study. Patients had a mean (SD) age of 61 (15) years and 602 (62.9%) were men. More than 15 000 measurements of air pollutant concentration from the official, open-source bulletin of the Italian Institute for Environmental Protection and Research (ISPRA) were retrieved. Among the overall cohort, 369 (38.6%) patients with psoriasis flare were included in the case-crossover study. We found that concentrations of all pollutants were significantly higher in the 60 days before psoriasis flare (median PASI at the flare 12; IQR, 9-18) compared with the control visit (median PASI 1; IQR, 1-3, P < .001). In the cross-sectional analysis, exposure to mean PM10 over 20 μg/m3 and mean PM2.5 over 15 μg/m3 in the 60 days before assessment were associated with a higher risk of PASI 5 or greater point worsening (adjusted odds ratio [aOR], 1.55; 95% CI, 1.21-1.99; and aOR, 1.25; 95% CI, 1.0-1.57, respectively). Sensitivity analyses that stratified for trimester of evaluation, with various lag of exposure and adjusting for type of treatment, yielded similar results.Conclusions and relevanceThe findings of this case-crossover and cross-sectional study suggest that air pollution may be a trigger factor for psoriasis flare.
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Project description:The US Environmental Protection Agency is required to reexamine its National Ambient Air Quality Standards (NAAQS) every 5 years, but evidence of mortality risk is lacking at air pollution levels below the current daily NAAQS in unmonitored areas and for sensitive subgroups.To estimate the association between short-term exposures to ambient fine particulate matter (PM2.5) and ozone, and at levels below the current daily NAAQS, and mortality in the continental United States.Case-crossover design and conditional logistic regression to estimate the association between short-term exposures to PM2.5 and ozone (mean of daily exposure on the same day of death and 1 day prior) and mortality in 2-pollutant models. The study included the entire Medicare population from January 1, 2000, to December 31, 2012, residing in 39?182 zip codes.Daily PM2.5 and ozone levels in a 1-km × 1-km grid were estimated using published and validated air pollution prediction models based on land use, chemical transport modeling, and satellite remote sensing data. From these gridded exposures, daily exposures were calculated for every zip code in the United States. Warm-season ozone was defined as ozone levels for the months April to September of each year.All-cause mortality in the entire Medicare population from 2000 to 2012.During the study period, there were 22?433?862 million case days and 76?143?209 control days. Of all case and control days, 93.6% had PM2.5 levels below 25 ?g/m3, during which 95.2% of deaths occurred (21?353?817 of 22?433?862), and 91.1% of days had ozone levels below 60 parts per billion, during which 93.4% of deaths occurred (20?955?387 of 22?433?862). The baseline daily mortality rates were 137.33 and 129.44 (per 1 million persons at risk per day) for the entire year and for the warm season, respectively. Each short-term increase of 10 ?g/m3 in PM2.5 (adjusted by ozone) and 10 parts per billion (10-9) in warm-season ozone (adjusted by PM2.5) were statistically significantly associated with a relative increase of 1.05% (95% CI, 0.95%-1.15%) and 0.51% (95% CI, 0.41%-0.61%) in daily mortality rate, respectively. Absolute risk differences in daily mortality rate were 1.42 (95% CI, 1.29-1.56) and 0.66 (95% CI, 0.53-0.78) per 1 million persons at risk per day. There was no evidence of a threshold in the exposure-response relationship.In the US Medicare population from 2000 to 2012, short-term exposures to PM2.5 and warm-season ozone were significantly associated with increased risk of mortality. This risk occurred at levels below current national air quality standards, suggesting that these standards may need to be reevaluated.
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Project description:Increasing experimental evidence has suggested air pollution as new risk factor for neurological disease. Although long-term exposure is reportedly related to neurological disease, information on association with short-term exposure is scarce. We examined the association of short-term exposure to particles <2.5 μm (PM2.5), nitrogen dioxide (NO2), sulfur dioxide (SO2), ozone (O3), and carbon monoxide (CO) with PD aggravation in Seoul from the National Health Insurance Service-National Sample Cohort, Korea during 2002-2013. PD aggravation cases were defined as emergency hospital admissions for primarily diagnosed PD and analyzed with a case-crossover analysis, designed for rare acute outcomes. Pollutants concentrations on case and control days were compared and effect modifications were explored. A unit increase in 8-day moving average of concentrations was significantly associated with PD aggravation. The association was consistent for PM2.5 (odds ratio [95% confidence interval]: 1.61 [1.14-2.29] per 10 μg/m3), NO2 (2.35 [1.39-3.97] per 10 ppb), SO2 (1.54 [1.11-2.14] per 1 ppb), and CO (1.46 [1.05-2.04] per 0.1 ppm). The associations were stronger in women, patients aged 65-74 years, and cold season, but not significant. In conclusion, short-term air pollution exposure increased risk of PD aggravation, and may cause neurological disease progression in humans.
| S-EPMC5353743 | biostudies-literature
Project description:ObjectiveTo review the evidence for the short term association between air pollution and stroke.DesignSystematic review and meta-analysis of observational studiesData sourcesMedline, Embase, Global Health, Cumulative Index to Nursing and Allied Health Literature (CINAHL), and Web of Science searched to January 2014 with no language restrictions.Eligibility criteriaStudies investigating the short term associations (up to lag of seven days) between daily increases in gaseous pollutants (carbon monoxide, sulphur dioxide, nitrogen dioxide, ozone) and particulate matter (<2.5 µm or <10 µm diameter (PM2.5 and PM10)), and admission to hospital for stroke or mortality.Main outcome measuresAdmission to hospital and mortality from stroke.ResultsFrom 2748 articles, 238 were reviewed in depth with 103 satisfying our inclusion criteria and 94 contributing to our meta-estimates. This provided a total of 6.2 million events across 28 countries. Admission to hospital for stroke or mortality from stroke was associated with an increase in concentrations of carbon monoxide (relative risk 1.015 per 1 ppm, 95% confidence interval 1.004 to 1.026), sulphur dioxide (1.019 per 10 ppb, 1.011 to 1.027), and nitrogen dioxide (1.014 per 10 ppb, 1.009 to 1.019). Increases in PM2.5 and PM10 concentration were also associated with admission and mortality (1.011 per 10 μg/m(3) (1.011 to 1.012) and 1.003 per 10 µg/m(3) (1.002 to 1.004), respectively). The weakest association was seen with ozone (1.001 per 10 ppb, 1.000 to 1.002). Strongest associations were observed on the day of exposure with more persistent effects observed for PM(2·5).ConclusionGaseous and particulate air pollutants have a marked and close temporal association with admissions to hospital for stroke or mortality from stroke. Public and environmental health policies to reduce air pollution could reduce the burden of stroke.Systematic review registrationPROSPERO-CRD42014009225.
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