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

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. © 2016 Macmillan Publishers Limited

Differential health effects of short-term exposure to source-specific particles in London, U.K.

Background There is ample evidence of adverse associations between short-term exposure to ambient particle mass concentrations and health but little is known about the relative contribution from various sources. Methods We used air particle composition and number networks in London between 2011 and 2012 to derive six source-related factors for PM10 and four factors for size distributions of ultrafine particles (NSD). We assessed the associations of these factors, at pre-specified lags, with daily total, cardiovascular (CVD) and respiratory mortality and hospitalizations using Poisson regression. Relative risks and 95% confidence intervals (CI) were expressed as percentage change per interquartile range increment in source-factor mass or number concentration. We evaluated the sensitivity of associations to adjustment for multiple other factors and by season. Results We found no evidence of associations between PM10 or NSD source-related factors and daily mortality, as the direction of the estimates were variable with 95% CI spanning 0%. Traffic-related PM10 and NSD displayed consistent associations with CVD admissions aged 15–64 years (1.01% (95%CI: 0.03%, 2.00%) and 1.04% (95%CI: − 0.62%, 2.72%) respectively) as did particles from background urban sources (0.36% for PM10 and 0.81% for NSD). Most sources were positively associated with pediatric (0–14 years) respiratory hospitalizations, with stronger evidence for fuel oil PM10 (3.43%, 95%CI: 1.26%, 5.65%). Our results did not suggest associations with cardiovascular admissions in 65 + or respiratory admissions in 15 + age groups. Effect estimates were generally robust to adjustment for other factors and by season. Conclusions Our findings are broadly consistent with the growing evidence of the toxicity of traffic and combustion particles, particularly in relation to respiratory morbidity in children and cardiovascular morbidity in younger adults. © 2016 The Author

Short-term associations between particle oxidative potential and daily mortality and hospital admissions in London

Background: Particulate matter (PM) from traffic and other sources has been associated with adverse health effects. One unifying theory is that PM, whatever its source, acts on the human body via its capacity to cause damaging oxidation reactions related to its content of pro-oxidants components. Few epidemiological studies have investigated particle oxidative potential (OP) and health. We conducted a time series analysis to assess associations between daily particle OP measures and numbers of deaths and hospital admissions for cardiovascular and respiratory diseases. Methods: During 2011 and 2012 particles with an aerodynamic diameter less than 2.5 and 10 μm (PM2.5 and PM10 respectively) were collected daily on Partisol filters located at an urban background monitoring station in Central London. Particulate OP was assessed based on the capacity of the particles to oxidize ascorbate (OPAA) and glutathione (OPGSH) from a simple chemical model reflecting the antioxidant composition of human respiratory tract lining fluid. Particulate OP, expressed as % loss of antioxidant per μg of PM, was then multiplied by the daily concentrations of PM to derive the daily OP of PM mass concentrations (% loss per m3). Daily numbers of deaths and age- and cause-specific hospital admissions in London were obtained from national registries. Poisson regression accounting for seasonality and meteorology was used to estimate the percentage change in risk of death or admission associated with an interquartile increment in particle OP. Results: We found little evidence for adverse associations between OPAA and OPGSH and mortality. Associations with cardiovascular admissions were generally positive in younger adults and negative in older adults with confidence intervals including 0%. For respiratory admissions there was a trend, from positive to negative associations, with increasing age although confidence intervals generally included 0%. Conclusions: Our study, the first to analyse daily particle OP measures and mortality and admissions in a large population over two years, found little evidence to support the hypothesis that short-term exposure to particle OP is associated with adverse health effects. Further studies with improved exposure assessment and longer time series are required to confirm or reject the role of particle OP in triggering exacerbations of disease. © 2016 The Author

In vitro screening of biomass combustion aerosol toxicity : Part 1: Oxidative potential

Godkänd; 2011; 20111022 (esbpet