Polycyclic aromatic hydrocarbons (PAHs) are widespread environmental pollutants with established carcinogenic properties traditionally linked to genotoxicity, oxidative stress, and DNA adduct formation. Emerging evidence indicates that PAHs also function as chronotoxic agents, disrupting circadian homeostasis through transcriptional and epigenetic reprogramming of core clock genes. This review critically examines the molecular interplay between PAH exposure, circadian clock dysregulation, and the initiation and progression of lung and breast cancers. Central to this interaction is the activation of the aryl hydrocarbon receptor (AhR), which exhibits bidirectional crosstalk with core circadian regulators including CLOCK and BMAL1. Sustained AhR activation, coupled with oxidative stress, inflammatory signaling, and epigenetic modifications including DNA methylation, histone remodeling, and non-coding RNA dysregulation, alters rhythmic expression of key circadian genes (PER, CRY, BMAL1, and CLOCK). These molecular alterations impair DNA repair, cell-cycle regulation, apoptosis, xenobiotic metabolism and metabolic homeostasis, thereby creating a permissive environment for tumorigenesis. The review synthesizes current evidence on tissue-specific mechanisms underlying PAH-induced chronodisruption in lung and breast tissues, highlighting how organ-specific physiology influences carcinogenic susceptibility and discussing the translational relevance of circadian biomarkers in cancer prognosis and therapy. Finally, emerging therapeutic and translational strategies including chronotherapy, circadian-targeted interventions, epigenetic modulation and integrative multi-omics systems biology are explored as potential approaches for refining precision oncology and mitigating environmentally induced carcinogenesis. Collectively, this review establishes environmental chronotoxicology as a critical framework for understanding the temporal dimension of cancer development associated with PAHs exposure.