OPS 56: Ultrafine particles exposure and health effects, Beatrix Theater, August 27, 2019, 4:30 PM - 5:30 PM Background: Epidemiological evidence on the health effects of ultrafine particles (UFP) remains insufficient to infer a causal relationship, which is largely due to the 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: To investigate 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 the MONICA/KORA 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 co-pollutants, including particulate matter with an aerodynamic diameter ≤10 µm or 2.5 µm (PM10, PM2.5), nitrogen dioxide, ozone, and black carbon. Results: Overall, a total of 5,898 cases of nonfatal MI cases were recorded. Interquartile range increases in PNC within the size range of 10-100 nm (UFP), PLC, and PSC were associated with an increase of MI six hours later by 3.27% (95% confidence interval [CI]: 0.27%, 6.37%), 5.71% (95% CI: 1.79%, 9.77%), and 5.56% (95% CI: 1.11%, 10.20%), respectively. No association was observed for PNC within the size range of 100-500 nm. The effect estimates for PLC and PSC remained similar after adjustment for PM and gaseous pollutants. The associations were not modified by individual characteristics, co-pollutants, or air temperature. Conclusions: Transient exposure to particle length and surface area concentrations may trigger the onset of myocardial infraction.