N6‐methyladenosine (m6A) is a prevalent mRNA modifier, yet its role in chronic obstructive pulmonary disease (COPD) remains unexplored. We sourced expression levels of m6A methylation regulators from the GSE76925 dataset. These regulators' differential expression (DEMs) predicted COPD risk via random forest and support vector machine models. Additionally, a nomogram model using DEMs estimated COPD prevalence. We employed consistent cluster analysis of m6A methylation regulators to categorise COPD samples into distinct subtypes. Analyses of immune cell infiltration in these subtypes and differential gene expression (DEGs) across m6A methylation subtypes were conducted. A cell model validated several m6A regulators and their associated pathways. Fifteen m6A methylation regulators showed differential expression and were used in random forest and support vector machine models. Eleven were selected for a nomogram model, which decision curve analysis suggested could benefit patients. Consensus cluster analysis divided the COPD samples into two subtypes: Cluster A and Cluster B. Cluster B was associated with neutrophil and eosinophil‐dominated immunity, while Cluster A was linked with monocyte‐dominated immunity. Validation of some research findings was achieved through cell experiments. m6A methylation regulators appear instrumental in diagnosing and classifying subtypes of COPD.