BACKGROUND: Although particulate matter (PM) has been implicated in various systemic and cutaneous diseases, large-scale evidence on whether PM exposure affects the risk of alopecia areata (AA) remains limited. OBJECTIVES: To assess the epidemiological association between long-term PM exposure and incident AA risk with exploration of potential biological mechanisms. METHODS: In the epidemiological study, annual average concentrations of fine (PM2.5) and coarse (PM10) PM were linked to individuals who underwent national health screening between 2006 and 2022, and the risk of incident AA, defined as ≥ 3 outpatient claims with relevant diagnostic codes within a 1-year period, was evaluated. In the preliminary in vitro experiment, human hair outer root sheath (ORS) cells were exposed to varying concentrations of PM10-like fine dust for 24 h. The expression of inflammatory cytokines was evaluated using quantitative real-time polymerase chain reaction, Western blotting and immunofluorescence analyses. RESULTS: Higher long-term PM2.5 and PM10 exposures were associated with increased risk of incident AA [per 10 μg m-3 increase: adjusted hazard ratio (aHR) 1.45, 95% confidence interval (CI) 1.39-1.52 for PM2.5 and aHR 1.32, 95% CI 1.28-1.36 for PM10] with the strongest association for alopecia universalis (per 10 μg m-3 increase: aHR 2.23, 95% CI 1.83-2.63 for PM2.5 and adjusted HR 1.82, 95% CI 1.58-2.07 for PM10). PM10 exposure increased reactive oxygen species generation, the expression of interleukin (IL)-1β, IL-6, IL-8 and IL-15RA, and phosphorylation of p38 and signal transducer and activator of transcription 3 in ORS cells. CONCLUSIONS: This study suggests that ambient PM may be a modifiable environmental risk factor for AA through the activation of selective inflammatory pathways, underscoring the need for public health efforts to reduce PM exposure and potentially mitigate AA risk.