摘要：Background: Epidemiological evidence on the health effects of ultrafine particles (UFP) remains insufficient to infer a causal relationship that is largely due to different size ranges and exposure metrics examined across studies. Moreover, evidence regarding the association between UFP and cardiovascular disease at a sub-daily timescale is lacking. Objective: We investigated the relationship between different particle metrics, including particle number (PNC), length (PLC), and surface area (PSC) concentrations, and myocardial infarction (MI) at an hourly timescale. Methods: We collected hourly air pollution and meteorological data from fixed urban background monitoring sites and hourly nonfatal MI cases from a MI registry in Augsburg, Germany, during 2005–2015. We conducted a time-stratified case-crossover analysis with conditional logistic regression to estimate the association between hourly particle metrics and MI cases, adjusted for air temperature and relative humidity. We also examined the independent effects of a certain particle metric in two-pollutant models by adjusting for copollutants, including particulate matter (PM) with an aerodynamic diameter of ≤ 10 μ m or 2.5 μ m ( PM 10 and PM 2.5 , respectively), nitrogen dioxide, ozone, and black carbon. Results: Overall, a total of 5,898 cases of nonfatal MI cases were recorded. Exploratory analyses showed similar associations across particle metrics in the first 6–12 h. For example, interquartile range increases in PNC within the size range of 10 – 100 nm , PLC, and PSC were associated with an increase of MI 6 h later by 3.27% [95% confidence interval (CI): 0.27, 6.37], 5.71% (95% CI: 1.79, 9.77), and 5.84% (95% CI: 1.04, 10.87), respectively. Positive, albeit imprecise, associations were observed for PNC within the size range of 10 – 30 nm and 100 – 500 nm . Effect estimates for PLC and PSC remained similar after adjustment for PM and gaseous pollutants. Conclusions: Transient exposure to particle number, length, and surface area concentrations or other potentially related exposures may trigger the onset of nonfatal myocardial infraction.
