PP-29-173 Background/Aims: Traffic-related environmental exposures are described as noise and nitrogen dioxide air pollution. Recent studies related to the impact on myocardial infarction show a slight increased risk. The aim of our study was to assess the association between urban traffic noise at the residential area and myocardial infarction risk, controlling traffic-related air pollutant—nitrogen dioxide. Methods: We conducted a population-based case-control study among men aged 25–64 years in a general population of Kaunas city. The study comprised 1042 cases—patients survived after first myocardial infarction. Control group included 2341 patients without ischemic heart disease signs. We measured traffic-related noise levels at the 117 electoral districts and linked these levels with residential addresses using Geographical Information System techniques. In daytime period (10–12 hours, 10 min), traffic-related noise emission fluctuated between 58 dB(A) and 82 dB(A), and about 18% of citizens were exposed to noise level exceeding 65 dB(A) in their residential district. We used SPSS version 13.0 for data analysis. Results: The study results showed that after adjustment for age, smoking, blood pressure, body mass index, stress status, and subjective noise annoyance, the risk of myocardial infarction was higher for the men exposed to 70–75 dBA (odds ratio [OR] = 1.17, 95% confidence interval [CI]: 0.99–1.39) and to >75 dBA (OR = 1.30, 95% CI: 0.88–1.92) noise levels in the residential areas. OR for continuous exposure parameter was 1.16, 95% CI: 1.00–1.39. Among subgroup aged 55–64 years, the excess risk to myocardial infarction was found to be higher (OR = 1.28, 95% CI: 0.98–1.65) and 1.70, 95% CI: 1.01–2.93 in moderate and high noise exposure area, respectively. After additional adjustment to nitrogen dioxide, OR for men aged 25–64 years was 1.05 and 1.16, and for men aged 55–64 years it was 1.05 and 1.39, correspondingly. Conclusion: Our results indicate a relationship between traffic noise exposure and risk of myocardial infarction. Exposure to nitrogen dioxide shows mediating effect.