Background/Objectives: Ambient air pollution is a significant public health concern, known to affect cardiovascular health adversely. Research has identified both long-term and short-term cardiovascular risks associated with various air pollutants, including those linked to acute coronary syndromes. However, the observed effects are rather small, with most data sourced from highly polluted regions. Methods: This study utilized a prospective registry database, documenting 12,581 myocardial infarction (MI) events in Styria, Austria from January 2007 to December 2015. Pollutants analyzed included particulate matter (PM2.5, PM10) and gases, such as NO2, CO, SO2, O3 and NOx. We employed generalized linear models to examine the interaction of each of these pollutants on the daily incidence of MI. Additionally, we conducted separate analyses for patients with specific comorbidities: diabetes mellitus (DM), arterial hypertension (HTN), heart failure with reduced ejection fraction (HFrEF), chronic obstructive pulmonary disease (COPD) and current smokers. Results: No significant associations were identified between any of the pollutants and MI incidence, both in the overall cohort and in patient subgroups with DM, HTN, HFrEF or COPD. However, among active smokers, we observed a decreased relative risk of MI associated with elevated levels of NO2, CO, SO2 and NOx on the day of MI (p < 0.01 for all pollutants). Conversely, an increased MI risk was associated with rising ozone levels (p = 0.0027). This counterintuitive finding aligns with previously published data and may suggest a new dimension to the “smoker’s paradox”. Conclusions: In regions with low pollution levels, air pollutants pose only minor or insignificant short-term risks for myocardial infarction. Active smokers exhibit an altered response to ambient air pollution.
