Introduction: The specific relationship between long-term exposure to air pollutants and the risk of HTN requires further investigation. This study aims to assess the association between AP and HTN occurrence and examine whether the effects differ between individuals with and without HTN in a long-term perspective. Hypothesis: Based on the previous research linking AP to cardiovascular diseases, we hypothesize that long-term exposure to air pollutants is associated with an increased risk of developing HTN. Methods: This study used modeled AP data linked with Korean Genome Epidemiologic Survey (KoGES) cohort data based on participant addresses. Among the 77,048 participants who completed the follow-up, 23,935 subjects had HTN at the baseline, while 53,113 subjects were non-hypertensive. AP exposure concentrations were evaluated using the 1-year and 3-year averages prior to the follow-up date and the average of the entire follow-up period. Logistic regression models were employed to analyze the relationship between HTN and air pollutants in the non-hypertensive group. Results: The analysis revealed that non-hypertensive subjects exposed to air pollutants had an increased risk of developing HTN, with the exception of O 3 . Notably, particulate matter 2.5 (PM 2.5 ) exposure demonstrated a gradual increase in HTN risk based on the duration of exposure (Odds Ratio [OR] 1.024, 1-year; OR 1.030, 3-year; OR 1.041, average survey period.) These findings suggest that prolonged exposure to high concentrations of PM 2.5 is associated with an elevated risk of HTN. Chronic exposure to other gaseous AP components were also similarly associated with higher risk of development of HTN. Conclusions: This study highlights the detrimental association of long-term exposure to air pollutants on the risk of HTN. Managing blood pressure in those exposed to high AP levels, even if not hypertensive is important also with a perspective of public health and environmental policies.