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to examine the relations between personal exposure to PM2.5 and inflammatory and oxidation markers.We conducted a panel study with three sampling time points (baseline, two months follow-up, and four months follow-up) among 68 healthy non-smoking young adults from 3 different areas (Area A [residential and commercial area], Area B [industrial area] and Area C [scientific park]).the average PM2.5 concentrations was 37.3 µg/m3 for personal sampling and 31.6 µg/m3 for nearest air quality monitoring station. Among them, the personal PM2.5 concentrations in B zone was significant highest than A and C zone. For the longitudinal study, we used linear Mixed-model was as follows: Yit =α0 + α1Timeit + β0Zkm + β1ZkmTimeit +γXi0 + εkm + εi + εit, where Zkm used four PM2.5 counting methods: (1) personal PM2.5 concentrations; (2) average personal PM2.5 concentrations at three sampling times; (3) average personal PM2.5 concentrations with area under the curve during 120 days; (4) average personal PM2.5 concentrations during 120 days (>35 µg/m3 vs.≤35µg/m3 ). After adjustment for age, gender, smoking habits, sampling zones, height, weight, temperature, and relative humidity, we found that the Urinary N7-MeG/creatinine was significantly decreased with PM2.5 exposure concentrations, and Urinary HEL/creatinine was significantly increased with PM2.5 exposure concentrations by time, regardless of which PM2.5 exposure models were used. While we only used average personal PM2.5 concentrations at three sampling times, we found that SDNN and GPx were significantly increased with PM2.5 exposure concentrations by time.