Dataset Information

Short-term exposure to traffic-related air pollution and daily mortality in London, UK.

ABSTRACT: Epidemiological studies have linked daily concentrations of urban air pollution to mortality, but few have investigated specific traffic sources that can inform abatement policies. We assembled a database of >100 daily, measured and modelled pollutant concentrations characterizing air pollution in London between 2011 and 2012. Based on the analyses of temporal patterns and correlations between the metrics, knowledge of local emission sources and reference to the existing literature, we selected, a priori, markers of traffic pollution: oxides of nitrogen (general traffic); elemental and black carbon (EC/BC) (diesel exhaust); carbon monoxide (petrol exhaust); copper (tyre), zinc (brake) and aluminium (mineral dust). Poisson regression accounting for seasonality and meteorology was used to estimate the percentage change in risk of death associated with an interquartile increment of each pollutant. Associations were generally small with confidence intervals that spanned 0% and tended to be negative for cardiovascular mortality and positive for respiratory mortality. The strongest positive associations were for EC and BC adjusted for particle mass and respiratory mortality, 2.66% (95% confidence interval: 0.11, 5.28) and 2.72% (0.09, 5.42) per 0.8 and 1.0 μg/m(3), respectively. These associations were robust to adjustment for other traffic metrics and regional pollutants, suggesting a degree of specificity with respiratory mortality and diesel exhaust containing EC/BC.

SUBMITTER: Atkinson RW

PROVIDER: S-EPMC4756269 | biostudies-literature | 2016 Mar-Apr

REPOSITORIES: biostudies-literature

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Short-term exposure to traffic-related air pollution and daily mortality in London, UK.

Atkinson Richard W RW Analitis Antonis A Samoli Evangelia E Fuller Gary W GW Green David C DC Mudway Ian S IS Anderson Hugh R HR Kelly Frank J FJ

Journal of exposure science & environmental epidemiology 20151014 2

Epidemiological studies have linked daily concentrations of urban air pollution to mortality, but few have investigated specific traffic sources that can inform abatement policies. We assembled a database of >100 daily, measured and modelled pollutant concentrations characterizing air pollution in London between 2011 and 2012. Based on the analyses of temporal patterns and correlations between the metrics, knowledge of local emission sources and reference to the existing literature, we selected, ...[more]

PMID: 26464095

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Project description:Deprived communities in many cities are exposed to higher levels of outdoor air pollution, and there is increasing evidence of similar disparities for indoor air pollution exposure. There is a need to understand the drivers for this exposure disparity in order to develop effective interventions aimed at improving population health and reducing health inequities. With a focus on London, UK, this paper assembles evidence to examine why indoor exposure to PM2.5, NOx and CO may disproportionately impact low-income groups. In particular, five factors are explored, namely: housing location and ambient outdoor levels of pollution; housing characteristics, including ventilation properties and internal sources of pollution; occupant behaviours; time spent indoors; and underlying health conditions. Evidence is drawn from various sources, including building physics models, modelled outdoor air pollution levels, time-activity surveys, housing stock surveys, geographical data, and peer-reviewed research. A systems framework is then proposed to integrate these factors, highlighting how exposure to high levels of indoor air pollution in low-income homes is in large part due to factors beyond the control of occupants, and is therefore an area of systemic inequality.Policy relevanceThere is increasing public and political awareness of the impact of air pollution on public health. Strong scientific evidence links exposure to air pollution with morbidity and mortality. Deprived communities may be more affected, however, with limited evidence on how deprivation may influence their personal exposure to air pollution, both outdoors and indoors. This paper describes different factors that may lead to low-income households being exposed to higher levels of indoor air pollution than the general population, using available data and models for London (i.e. living in areas of higher outdoor air pollution, in poor-quality housing, undertaking more pollution-generating activities indoors and spending more time indoors). A systems approach is used to show how these factors lead to systemic exposure inequalities, with low-income households having limited opportunities to improve their indoor air quality. This paper can inform actions and public policies to reduce environmental health inequalities, considering both indoor and outdoor air.

Project description:ImportanceThe 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.ObjectiveTo 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.Design, setting, and participantsCase-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.ExposuresDaily 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.Main outcomes and measuresAll-cause mortality in the entire Medicare population from 2000 to 2012.ResultsDuring 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 μg/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 μg/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.Conclusions and relevanceIn 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:Background and aimInfant mortality is a widely reported indicator of population health and a leading public health concern. In this systematic review and meta-analysis, we review the available literature for epidemiologic evidence of the association between short-term air pollution exposure and infant mortality.MethodsRelevant publications were identified through PubMed and Web of Science databases using comprehensive search terms and screened using predefined inclusion/exclusion criteria. We extracted data from included studies and applied a systematic rubric for evaluating study quality across domains including participant selection, outcome, exposure, confounding, analysis, selective reporting, sensitivity, and overall quality. We performed meta-analyses, using both fixed and random-effect methods, and estimated pooled odds ratios (ORs) and 95 % confidence intervals (95%CI) for pollutants (nitrogen dioxide (NO2), sulfur dioxide (SO2), coarse particulate matter (PM10), fine particulate matter (PM2.5), ozone (O3), carbon monoxide (CO)) and infant mortality, neonatal mortality, or postneonatal mortality.ResultsOur search returned 549 studies. We excluded 490 studies in the abstract screening phase and an additional 37 studies in the full text screening phase, leaving 22 studies for inclusion. Among these 22 studies, 14 included effect estimates for PM10, 13 for O3, 11 for both NO2 and CO, 8 for SO2, and 3 for PM2.5. We did not calculate a pooled OR for PM2.5 due to the limited number of studies available and demonstrated heterogeneity in the effect estimates. The pooled ORs (95%CI) with the greatest magnitudes were for a 10-ppb increase in SO2 or NO2 concentration in the days before death (1.07 [95%CI: 1.02, 1.12], 1.04 [95%CI: 1.01, 1.08], respectively). The pooled OR for PM10 was 1.02 (95%CI: 1.00, 1.03), and the pooled ORs for CO and O3 were 1.01 (95%CI: 1.00, 1.02) and 0.99 (95%CI: 0.97, 1.01).ConclusionsIncreased exposure to SO2, NO2, PM10, or CO is associated with infant mortality across studies.

Dataset Information

Short-term exposure to traffic-related air pollution and daily mortality in London, UK.

Publications

Short-term exposure to traffic-related air pollution and daily mortality in London, UK.

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