We conducted a systematic review and meta-analysis of global epidemiological studies of air pollution and angina pectoris, aiming to explore the deleterious air pollutant(s) and vulnerable sub-populations. PubMed and Web of Science databases were searched for eligible articles published between database inception and October 2021. Meta-analysis weighted by inverse-variance was utilized to pool effect estimates based on the type of air pollutant, including particulate matters (PM2.5 and PM10: particulate matter with an aerodynamic diameter ≤ 2.5 µm and ≤ 10 µm), gaseous pollutants (NO2: nitrogen dioxide; CO: carbon monoxide; SO2: sulfur dioxide, and O3: ozone). Study-specific effect estimates were standardized and calculated with percentage change of angina pectoris for each 10 µg/m3 increase in air pollutant concentration. Twelve studies involving 663,276 angina events from Asia, America, Oceania, and Europe were finally included. Meta-analysis showed that each 10 µg/m3 increase in PM2.5 and PM10 concentration was associated with an increase of 0.66% (95%CI: 0.58%, 0.73%; p < 0.001) and 0.57% (95%CI: 0.20%, 0.94%; p = 0.003) in the risk of angina pectoris on the second day of exposure. Adverse effects were also observed for NO2 (0.67%, 95%CI: 0.33%, 1.02%; p < v0.001) on the second day, CO (0.010%, 95%CI: 0.006%, 0.014%; p < 0.001). The elderly and patients with coronary artery disease (CAD) appeared to be at higher risk of angina pectoris. Our findings suggest that short-term exposure to PM2.5, PM10, NO2, and CO was associated with an increased risk of angina pectoris, which may have implications for cardiologists and patients to prevent negative cardiovascular outcomes.