Consistent with cells that had accumulated intracellular lipids, we also found that transcript levels for the lipid scavenger receptor CD36 and the intracellular lipid receptor PPAR-γ were significantly increased in BAL cells from silicosis patients (Fig. 3A,B) (P < 0.05), supporting the notion that lipid homeostasis is altered in pulmonary silicosis. Here, PPARG is linked to silicosis.