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56 Combined microplastic and indoor or urban dust exposure potentiates inflammatory responses in a human alveolar model in vitro

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Researchers exposed a three-cell alveolar model — including type I and type II pneumocytes alongside macrophages — at the air-liquid interface to polyamide, PET, or polystyrene particles followed by urban or indoor dust, finding that while single plastic exposures produced minimal cytokine release, combined exposures significantly elevated IL-8, indicating synergistic pulmonary inflammation.

Models
Study Type In vitro

Abstract The potential health effects posed by inhaled micro/nanoplastics (MNPs) is an area of increasing concern. There is therefore a requirement to assess environmentally relevant MNP samples using methods that accurately mirror real human exposures, whilst considering potential concomitant effects of the ambient air pollution mixture. Here, an in vitro alveolar model at the air-liquid interface, comprising anatomically appropriate densities of type I pneumocytes (hAELVi), type II pneumocytes (NCI-H441) and macrophages (differentiated THP-1), was exposed to MNPs using an aerosol exposure system (VITROCELL® Cloud12). Polyamide (PA), polyethylene terephthalate (PET) or polystyrene (PS) were deposited onto cultures by nebulising 200 μL MNP suspension (1 mg/mL) three times, followed by sequential urban dust (SRM 1649b) or indoor dust (SRM 2583) (780 ng/cm2) (NIST) exposure. Twenty-four hours post-exposure, there were no significant changes to cell viability (Erythrosin B assay) or barrier integrity (blue dextran assay). As single pollutants, PET and PS, but not PA non-significantly increased IL-6 and IL-8 release (ELISA). Co-exposure of all MNPs with SRM 1649b or SRM 2583 increased IL-6 and IL-8 release compared to respective single pollutant exposures, however significance was only reached for IL-8 release when PS was co-exposed with either SRM 1649b or SRM 2583 (P < 0.05). It is shown here that MNPs may be able to act synergistically with other ambient air pollution samples to induce pulmonary inflammation whereas a single pollutant does not induce this effect, further emphasising the requirements to consider the toxicological profile of realistic air pollutant mixtures on human health.

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