Continuous exposure to fine particulate matter (of less than 2.5 μm diameter, known as PM2.5), both in vivo in mice and in vitro in a human lung cancer cell line, led to increased expression of genes involved in EMT, including those in the PI3K–AKT and JAK–STAT pathways, both of which are downstream effectors of epidermal growth factor receptor (EGFR)68. Here, EGFR is linked to lung carcinoma.