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Assessing Inflammatory Risks of Manufactured Polyacrylonitrile Nano- and Microplastics in Monocyte-Derived Systems in vitro
- Snyder, Dylan Matthew
- Advisor(s): Bui, Jack
Abstract
Plastics are highly inert and environmentally persistent petroleum derivatives employed in commercial, industrial, and residential applications. Disintegration via mechanical and chemical means generates plastic fragments of micro (≤ 1 mm) or nanoscopic (≤ 1 μm) sizes. Such particles are highly heterogeneous in size, morphology, structural chemistry, and surface topography. With a vast and often indiscernible environmental burden, the biochemical and biophysical influences of plastics on mammalian physiology are of concern, especially regarding chronic inflammation. Utilizing three monocyte-derived model systems, a mouse cell line, bone marrow-derived macrophages (BMDMs), and patient-derived, monocyte-enriched PBMCs, morphologically heterogeneous microplastics, such as polystyrene (PS) and polyacrylonitrile (PAN), at low, medium, and high dosages were imaged for topographical variety via scanning electron microscopy (SEM), size characterized by dynamic light scattering (DLS), analyzed for chemical composition by MALDI-TOF and FTIR, and screened in a TNF-ɑ ELISA. The primary thrusts are to observe hallmark inflammatory responses to microplastic exposure, profile the physicochemical structure of polymers, and reproducibly and sterilely generate and characterize microplastics from larger fragments through sonication, microwaving, and mechanical degradation. All three cell types responded positively to PAN at sizes <1 μm and at high concentrations, with the dual upregulation of TNF-ɑ and M2-like transcriptional programs in murine cells. Two PAN vendors differed in diameter, average molecular weight, sonication receptivity, fibrousness, porosity, and FTIR-derived chemical composition, with time-dependent aggregation tendencies. These data suggest that a microplastic derived from PAN can have biological effects on macrophages, promoting a tissue remodeling signature with preserved, antithetical mechanisms along the TNF-ɑ axis. Future directions will include performing a mechanistic evaluation, incubating size-enriched PAN subpopulations, and screening for unknown soluble contaminants with inflammatory potential.