Ross Anderson

Chronic Exposure to Outdoor Air Pollution and Markers of Systemic Inflammation

Background: Cohort studies suggest that long-term exposure to higher levels of outdoor air pollution increases risk of developing cardiovascular disease. One suggested mechanism is that air pollution, especially particulate matter, induces systemic inflammation, thereby increasing the risk of developing long-term pathologic changes in the cardiovascular system, We aimed to examine the association between long-term exposure to higher levels of air pollution and chronic systemic inflammation. Methods: We examined the relationship between 2 markers of systemic inflammation (fibrinogen and C-reactive protein) and measures of outdoor air pollution estimated for each postcode sector of residence, using models incorporating information on pollutant emissions from multiple sources, and atmospheric dispersion and processing, in 3 representative cross-sectional studies of the English population in 1994, 1998, and 2003. These included about 25,000 adults with fibrinogen measurements and 17,000 adults with C-reactive protein measurements. We used multilevel linear regression modeling and pooled the results from the 3 surveys using meta-analysis. Results: We found no associations between concentrations of fibrinogen or C-reactive protein and measures of outdoor air pollution (particulate matter <10 &mgr;m in diameter (PM10), nitrogen dioxide, sulfur dioxide, and ozone). Specifically, we found, for each 1-&mgr;g/m3 increase in PM10 concentration, a change in fibrinogen concentrations of −0.08% (95% confidence interval = 0.25–0.10) and in C-reactive protein concentrations of 0.14% (95% confidence interval = 1.00–1.30). Conclusions: Our findings do not support the hypothesis that the association between outdoor air pollution exposure and later cardiovascular disease is mediated by chronic systemic inflammation.

Short-term effects of air pollution on total and cardiovascular mortality: the confounding effect of influenza epidemics.

Background: Air pollution is associated with total mortality. This association may be confounded by uncontrolled time-varying risk factors such as influenza epidemics. Methods: We analyzed independent data on influenza epidemics from 7 European cities that also had data on mortality associated with particulates (PM10). We used 10 methods to control for epidemics (5 derived from influenza data and 5 from respiratory mortality series) and compared those results with analyses that did not control for these epidemics. Results: Adjustment for influenza epidemics increased the PM10 effect estimate in most cases (% change in the pooled regression coefficient: −1.9 to 38.9 for total mortality and 1.3 to 25.5 for cardiovascular mortality). A 10-μg/m3 increase in PM10 concentrations (lag 0–1) was associated with a 0.48% (95% confidence interval = 0.27–0.70%) increase in daily mortality unadjusted for influenza epidemics, whereas under the various methods to control for epidemics the increase ranged from 0.45% (0.26–0.69%) to 0.67% (0.46–0.89%). The corresponding figures for cardiovascular mortality were 0.85% (0.53–1.18%) with no adjustment and from 0.86% (0.53–1.19%) to 1.06% (0.74–1.39%) with the methods of control. Conclusions: The association between air pollution and mortality is not weakened by control for influenza epidemic irrespective of the method used. To adjust for influenza epidemics, one can use methods based on respiratory mortality counts instead of counts of influenza cases if the latter are not available. However, adjustment for influenza by any method tested did not markedly alter the air pollution effect estimate.

Epidemiological time series studies of PM2.5 and daily mortality and hospital admissions

Background Short-term exposure to outdoor fine particulate matter (particles with a median aerodynamic diameter <2.5 μm (PM2.5)) air pollution has been associated with adverse health effects. Existing literature reviews have been limited in size and scope. Methods We conducted a comprehensive, systematic review and meta-analysis of 110 peer-reviewed time series studies indexed in medical databases to May 2011 to assess the evidence for associations between PM2.5 and daily mortality and hospital admissions for a range of diseases and ages. We stratified our analyses by geographical region to determine the consistency of the evidence worldwide and investigated small study bias. Results Based upon 23 estimates for all-cause mortality, a 10 µg/m3 increment in PM2.5 was associated with a 1.04% (95% CI 0.52% to 1.56%) increase in the risk of death. Worldwide, there was substantial regional variation (0.25% to 2.08%). Associations for respiratory causes of death were larger than for cardiovascular causes, 1.51% (1.01% to 2.01%) vs 0.84% (0.41% to 1.28%). Positive associations with mortality for most other causes of death and for cardiovascular and respiratory hospital admissions were also observed. We found evidence for small study bias in single-city mortality studies and in multicity studies of cardiovascular disease. Conclusions The consistency of the evidence for adverse health effects of short-term exposure to PM2.5 across a range of important health outcomes and diseases supports policy measures to control PM2.5 concentrations. However, reasons for heterogeneity in effect estimates in different regions of the world require further investigation. Small study bias should also be considered in assessing and quantifying health risks from PM2.5.