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99 The Relative Toxicity and Bioreactivity of Ambient Microplastic Pollution to Human Alveolar Lung Epithelial Cells with and Without Urban PM2.5
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This lab study exposed human lung cells to microplastic particles (polypropylene and polyamide) at sizes found in real-world air pollution, finding that both types caused cell death while urban air pollution particles (PM2.5) triggered inflammatory responses instead. The two types of harm worked through different mechanisms and didn't reliably combine when mixed, suggesting that microplastics in inhaled air pose a distinct and understudied risk to the respiratory system beyond conventional air pollution.
Abstract Plastic has unique properties with multiple applications. Microsized plastic fragments (0.1−1000µm; secondary microplastics) are generated throughout the lifespan of plastic materials; primary microplastics are manufactured. Microplastics are present in PM2.5. With increased use of electric cars and reduction in tail pipe emissions, the amount and proportion of microplastics in airborne PM2.5 could increase. We know little about the effects of microplastic inhalation on human health. Hypothesis: Inhaled plastic microparticles will have adverse effects on the respiratory epithelium, both independently and in combination with PM2.5. Two atmospheric plastics, polypropylene (PP) and polyamide (PA), were generated and characterized prior to study. They had a similar size distribution (1-3µm), polydispersity (PA: 0.9002; PP: 0.9037) and charge (PA: -9.66; PP: -5.79) in culture medium. Human alveolar epithelial type 1-like cells (TT1) were exposed for 24h to 1.25-80µg/ml of PP, PA, and PM2.5; viability fell after PA exposure to 10µg/ml (~10%), reaching ~30% at 80µg/ml (p<0.0001); only 40 and 80µg/ml of PP caused a 15 and 20% drop in viability, respectively (p<0.01). PM2.5 had no effect on viability. Although plastics had no effect on IL-6 or IL-8 release, PM2.5 stimulated release at 20-80µg/ml, reaching 10-fold (p<0.001) and 2.5-fold (p<0.05) for IL6 and IL8 respectively. Exposure to plastic/PM2.5 ratios from 0.0001:1 to 1:1 had no consistent effect. TEM suggests internalization of PA, PP and PM2.5 by TT1 cells. Thus, microplastics exhibit different responses (increased cell death) to PM2.5 (increased mediator production). The inconsistent response to particle mixtures is likely dependent upon the proportion of microplastics.
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