Obstructive sleep apnea (OSA) and idiopathic pulmonary fibrosis (IPF) are serious diseases with growing relevance in modern medicine. OSA affects around 300 individuals per 100,000 in the U.S. and IPF affects between 43-63 individuals per 100,000. Recent evidence has shown a strong and thus far unexplored correlation between IPF and OSA. Of patients diagnosed with IPF, 77-88% had OSA, and treatment of OSA in individuals suffering from both IPF and OSA decreases mortality rates. We hypothesized that increased oxidative stress from chronic intermittent hypoxia (CIH), a common complication of OSA, underlies this correlation and amplifies IPF. To test this, we chemically induced IPF in rats by instilling their lungs with bleomycin and subjected them to a regimen of repeating episodes of hypoxia to mimic CIH. After termination, we measured lipid peroxidation of lung tissue to determine levels of oxidative stress. Our results were inconclusive in determining whether oxidative stress from CIH was directly responsible for exacerbation of IPF. However, trends in our data indicated that lipid peroxidation may increase with CIH treatment, as lipid peroxidation was elevated in rats with both chemically-induced IPF and CIH. Furthermore, qualitative and quantitative data showed a possible anatomical shift of fibrosis within the lung itself as a result of CIH treatment. Performing the experiment with a longer period of CIH is recommended as this would better imitate the condition experienced by patients and would likely result in significant differences of lipid peroxidation between treatment groups.