Abstract
Lymphoma therapeutics research revealed an unsettling parallel: the plastic we consume daily might contribute to the very disease we're trying to cure. Microplastics-and particularly nanoplastics with their superior ability to enter the bloodstream-are now detected in human blood, lungs, and placentas. While direct evidence linking them to lymphoma remains absent, our recent comprehensive mechanistic review hypothesized biological plausibility through five convergent pathways-inflammation, oxidative stress, immune dysregulation, genotoxicity, and endocrine disruption. Nanoplastics, with their enhanced bioavailability and cellular penetration, may represent the primary etiological agents, though microplastics serve as the persistent environmental reservoir from which nanoplastics continuously fragment. Unlike therapeutic compounds that kill cancer cells through acute pathway activation, chronic low-dose plastic exposure may promote cancer through the same mechanisms. Critical evidence gaps exist-no studies have measured plastic particles in lymph nodes or compared exposures between lymphoma patients and controls-making urgent investigation necessary. This hypothesis, while mechanistically plausible based on our recent comprehensive review, requires rigorous testing through epidemiological studies, lymph node tissue analysis, and animal carcinogenesis bioassays before any causal claims can be made.