Chronic ethanol exposure in mice lengthens the circadian period by approximately 2 h (p < 0.05) and induces an approximately 7% phase shift in PER2 rhythms in lung slices. Ethanol alters the oscillatory patterns of clock genes such as Bmal1, Clock, Rorα, and Rev-erbα, as well as the profibrotic markers Tgfβ, α-SMA, and Fn1 in the lung. In primary mouse lung fibroblasts (PLFs), ethanol suppresses the expression of BMAL1 and RORα. Activation of RORα by the agonist SR1078 reverses ethanol-induced increased expression of TGFβ and α-SMA, whereas the inverse agonist SR3335 mimics the effects of ethanol. RORα gene silencing by siRNA significantly increases TGFβ and α-SMA expression with a trend toward increased Fn1. Ethanol thus disrupts circadian signaling and increases profibrotic gene expression in lung fibroblasts in part by suppressing RORα, while activation of RORα moderates these effects.