Delta 9 tetrahydrocannabinol (Δ-9-THC or THC), the primary psychoactive constituent of marijuana, has been found to affect the human body in a variety of ways. According to the Substance Abuse and Mental Health Services Administration (SAMHSA) of the U.S. Department of Health and Human Services, the amount of THC in marijuana has steadily climbed over the past few decades, with today's marijuana having three times the concentration of THC compared to 25 years ago. Inhalation is a major route of exposure, allowing substances to enter the body via the respiratory tract. Therefore, it is imperative to understand the molecular underpinning of THC exposure in the lung epithelium, as lung cells receive significant amounts of THC during marijuana smoking. In this study, the transcriptional alterations caused by various concentrations of THC in non-cancerous human bronchial epithelial cell line (BEAS-2B) were studied. THC exposure (0, 800, 1000, 1200, and 1500 ng/mL) caused a significant dose-dependent decrease in cell viability after 24-hour exposure. Transcriptome analysis showed a distinct dose-dependent response. HIF-1 signaling, ferroptosis, AMPK signaling, and immunogenic pathways were activated by upregulated genes associated with dosing concentration of THC. Glutathione and fatty acid metabolic pathways were significantly altered by THC-dependent downregulated genes. and downregulated genes and their associated pathways in BEAS-2B cells. Ingenuity Pathway Analysis revealed several top canonical pathways altered by THC exposure, among which ferroptosis, NRF-2 mediated oxidative stress response, caveolar mediated endocytosis (loss of cell adhesion to the substrate), tumor microenvironment, HIF1alpha signaling, and the unfolded protein response pathways were the major pathways affected. The top genes that were significantly altered as a result of THC exposure were HMOX1, CDK7, HLA-C, and SLC39A4. Present results suggested that THC exposure can induce a variety of effects, including cell death, which may involve ferroptosis and the NRF-2 signaling pathway. Moreover, the Δ-9-THC-induced cell death was ameliorated by inhibiting the ferroptosis pathway. In contrast, the ferroptosis agonist exacerbated the cell death process, suggesting that Δ-9-THC utilizes the ferroptosis pathway to induce cell death in bronchial epithelial cells.