Background <p>Although air pollution has been recognized as a risk factor for chronic obstructive pulmonary disease (COPD), little is known regarding the role of air pollutant exposure, specifically particulate matter (PM), in the dynamic transitions among normal spirometry (lung function), pre-COPD status, and COPD status.</p> Methods <p>Pulmonary function observations from the UK Biobank cohort were categorized as normal spirometry, preserved ratio impaired spirometry (PRISm), defined as forced expiratory volume in one second (FEV₁) &lt; 80% predicted and FEV₁/ forced vital capacity (FVC) &gt; 0.70, or spirometry-defined COPD. Multi-state Markov models were used to characterize the association between air pollution exposure (PM_2.5, PM coarse, PM₁₀, NO₂, and NO_x) and transitional pathways among three COPD statuses.</p> Results <p>We include 33,217 participants (71,287 visits) and find that each interquartile range increase in exposure of PM_2.5, NO₂, and NO_x is associated with a lower probability of reverting from PRISm to normal spirometry [HR (95% CI): 0.88 (0.81, 0.96) for PM_2.5; 0.86 (0.79, 0.93) for NO₂ and 0.89 (0.83, 0.96) for NO_x]. Progression from PRISm to COPD shows PM₁₀ exposure is positively associated with a significant risk increase [1.16 (1.02, 1.31)]. In a counterfactual scenario where we reduce the exposure level of PM_2.5 from 9.92 μg/m³ to 5 μg/m³, the study participants could have been 4.42% less likely to progress from PRISm to COPD.</p> Conclusions <p>Findings reveal that higher levels of PM₁₀ exposure are linked to an increased risk of PRISm progression, while exposure to PM_2.5, NO₂, and NO_x is associated with a reduced likelihood of spirometry recovery to normal levels. These findings offer new insights into potential health benefits resulting from interventions targeting air pollution.</p>