A simple method for correcting for the loading effects of aethalometer data is presented. The formula BC CORRECTED = (1 + k ATN)∙BC NONCORRECTED, where ATN is the attenuation and BC is black carbon...

Air pollution has been associated with cardiovascular mortality, but it remains unclear as to whether specific pollutants are related to specific cardiovascular causes of death. Within the multicenter European Study of Cohorts for Air Pollution Effects (ESCAPE), we investigated the associations of long-term exposure to several air pollutants with all cardiovascular disease (CVD) mortality, as well as with specific cardiovascular causes of death. Data from 22 European cohort studies were used. Using a standardized protocol, study area-specific air pollution exposure at the residential address was characterized as annual average concentrations of the following: nitrogen oxides (NO2 and NOx); particles with diameters of less than 2.5 μm (PM2.5), less than 10 μm (PM10), and 10 μm to 2.5 μm (PMcoarse); PM2.5 absorbance estimated by land-use regression models; and traffic indicators. We applied cohort-specific Cox proportional hazards models using a standardized protocol. Random-effects meta-analysis was used to obtain pooled effect estimates. The total study population consisted of 367,383 participants, with 9994 deaths from CVD (including 4,992 from ischemic heart disease, 2264 from myocardial infarction, and 2484 from cerebrovascular disease). All hazard ratios were approximately 1.0, except for particle mass and cerebrovascular disease mortality; for PM2.5, the hazard ratio was 1.21 (95% confidence interval = 0.87-1.69) per 5 μg/m and for PM10, 1.22 (0.91-1.63) per 10 μg/m. In a joint analysis of data from 22 European cohorts, most hazard ratios for the association of air pollutants with mortality from overall CVD and with specific CVDs were approximately 1.0, with the exception of particulate mass and cerebrovascular disease mortality for which there was suggestive evidence for an association.

Background: It is known that particulate air pollution affects cardiorespiratory health; however, it is unclear which particle size fractions and sources of particles are responsible for the health effects. Methods: Daily levels of nucleation (<0.03 μm), Aitken (0.03–0.1 μm), accumulation (0.1–0.29 μm), and coarse mode (2.5–10 μm) particles, particles with diameter <2.5 μm (PM_2.5), and gaseous pollutants were measured at central outdoor measurement sites in Helsinki, Finland between 1998 and 2004. We determined the associations of particles with daily cardiorespiratory mortality and acute hospital admissions among the elderly (≥65 years). For the analyses we used Poisson generalized additive models and for the source apportionment of PM_2.5 we used the EPA positive matrix factorization method. Results: There was a suggestion of an association of hospital admissions for arrhythmia with Aitken mode particles and PM_2.5 from traffic. Otherwise few associations were observed between various sizes and types of particles and either cardiovascular admissions or mortality. In contrast, most particle fractions had positive associations with admissions for pneumonia and asthma-chronic obstructive pulmonary disease (COPD). The strongest and most consistent associations were found for accumulation mode particles (3.1%; 95% confidence interval = 0.43–5.8 for pneumonia over the 5-day mean, and 3.8%; 1.3–6.3 for asthma-COPD at lag 0, for an interquartile increase in particles). We also found a positive association of respiratory mortality mainly with accumulation mode particles (5.1%; 1.2–9.0 at lag 0). Conclusions: All particle fractions including Aitken, accumulation, and coarse mode had especially adverse respiratory health effects among the elderly. Overall associations were stronger for respiratory than for cardiovascular outcomes.