PM2.5 exposure not only activated oxidative stress pathways but also significantly altered cancer metabolism and tumour microenvironment formation, as evidenced by the upregulation of SLC16A6, a member of the monocarboxylate transporter (MCT) family involved in the export of lactate, pyruvate, and ketone bodies, all of which play crucial roles in cancer metabolism and microenvironment regulation [34,35]. Here, SLC16A6 is linked to neoplasm.