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Size- and oxidative potential-dependent toxicity of environmentally relevant expanded polystyrene styrofoam microplastics to macrophages
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Researchers tested how Styrofoam microplastics of different sizes and weathering conditions affect human immune cells and found that smaller particles, UV-weathered particles, and those from real-world sources were all more toxic. The microplastics triggered inflammation through a pathway called the NLRP3 inflammasome, which is linked to many chronic diseases. This is concerning because most Styrofoam in the environment has been weathered by sunlight, meaning the real-world health risks may be worse than lab studies using fresh materials suggest.
Expanded polystyrene (EPS), also known as Styrofoam, is a widespread global pollutant, and its lightweight floating property increases its chances of weathering by abrasion and ultraviolet (UV) irradiation, resulting in microplastics. Herein, we investigated the effects of particle size ((1 µm versus 10 µm), UV irradiation (pristine versus UV oxidation), and origin (secondary versus primary) on the toxicity of Styrofoam microplastics. The target cells used in this study were selected based on human exposure-relevant cell lines: differentiated THP-1 cells for macrophages, Caco-2 for enterocytes, HepG2 for hepatocytes, and A549 for alveolar epithelial cells. In the differentiated THP-1 cells, the levels of cytotoxicity and inflammatory cytokines showed size- (1 µm > 10 µm), UV oxidation- (UV > pristine), and origin- (secondary > primary) dependency. Furthermore, the intrinsic oxidative potential of the test particles was positively correlated with cellular oxidative levels and toxicity endpoints, suggesting that the toxicity of Styrofoam microplastics also follows the oxidative stress paradigm. Additionally, all microplastics induced the activation of the pyrin domain-containing protein 3 (NLRP3) inflammasome and the release of interleukin-1β (IL-1β). These results imply that weathering process can aggravate the toxicity of Styrofoam microplastics due to the increased oxidative potential and decreased particle size.
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Researchers found that polystyrene microplastics aged by sunlight exposure for just three hours triggered stronger inflammatory responses and DNA damage in immune cells than fresh microplastics, even at very low concentrations. The aging process changed the particles' surface properties, making them more biologically reactive. Since most microplastics in the real world have been weathered by sunlight, this study suggests their actual health impact may be greater than lab studies using pristine particles indicate.
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Researchers exposed human lung and immune cells to polystyrene micro and nanoparticles and found they triggered a type of inflammation that does not require infection, called sterile inflammation. Aged (oxidized) particles and those that interacted with immune cells were especially potent at activating inflammatory pathways including the NLRP3 inflammasome. This suggests that breathing in airborne microplastics could cause chronic lung inflammation over time.
35 Comparative evaluation of ROS–NLRP3 inflammasome-mediated pulmonary toxicity induced by primary and secondary microplastics
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Researchers compared UV-aged secondary polystyrene microplastics against virgin primary particles and found that environmental weathering amplifies toxicity — secondary particles caused greater cytotoxicity, stronger NLRP3 inflammasome activation, and higher pulmonary inflammatory markers in mice — implicating intrinsic reactive oxygen species generated during UV degradation as the key driver.
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Researchers studied how virgin and environmentally aged polystyrene nano- and microplastics affect human immune cells (monocytes and macrophages). The study found that oxidized particles, which simulate environmental aging, caused significantly greater DNA damage and oxidative stress than virgin particles, suggesting that weathered plastics in the environment may pose higher health risks.
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