Polylactic acid nanoplastics (PLA-NPLs) induce adverse effects on an in vitro model of the human lung epithelium: The Calu-3 air-liquid interface (ALI) barrier.

The expected increments in the production/use of bioplastics, as an alternative to petroleum-based plastics, require a deep understanding of their potential environmental and health hazards, mainly as nanoplastics (NPLs). Since one important exposure route to NPLs is through inhalation, this study aims to determine the fate and effects of true-to-life polylactic acid nanoplastics (PLA-NPLs), using the in vitro Calu-3 model of bronchial epithelium, under air-liquid interphase exposure conditions. To determine the harmful effects of PLA-NPLs in a more realistic scenario, both acute (24 h) and long-term (1 and 2 weeks) exposures were used. Flow cytometry results indicated that PLA-NPLs internalized easily in the barrier (∼10 % at 24 h and ∼40 % after 2 weeks), which affected the expression of tight-junctions formation (∼50 % less vs control) and the mucus secretion (∼50 % more vs control), both measured by immunostaining. Interestingly, significant genotoxic effects (DNA breaks) were detected by using the comet assay, with long-term effects being more marked than acute ones (7.01 vs 4.54 % of DNA damage). When an array of cellular proteins including cytokines, chemokines, and growth factors were used, a significant over-expression was mainly found in long-term exposures (∼20 proteins vs 5 proteins after acute exposure). Overall, these results described the potential hazards posed by PLA-NPLs, under relevant long-term exposure scenarios, highlighting the advantages of the model used to study bronchial epithelium tissue damage, and signaling endpoints related to inflammation.

Impact of diesel exhaust particles on infections with Mycobacterium bovis BCG in in vitro human macrophages and an in vivo Galleria mellonella model.

There are strong suggestions for a link between pulmonary tuberculosis (TB) and air quality. Diesel exhaust is one of the main contributors to pollution and it is reported to be able to modify susceptibility to lung infections. In this study we exposed THP-1 human macrophages and Mycobacterium bovis BCG to diesel exhaust particles (DEPs). High cytotoxicity and activation of apoptosis was found in THP-1 cells at 3 and 6 days, but no effect was found on the growth of M. bovis BCG. Infection of THP-1 cells exposed to a non-cytotoxic DEP concentration showed a limited capacity to engulf latex beads. However, M. bovis BCG infection of macrophages did not result in an increase in the bacterial burden, but it did result in an increase in the bacteria recovered from the extracellular media, suggesting a poor contention of M. bovis BCG. We also observed that DEP exposure limited the production of cytokines. Using the Galleria mellonella model of infection, we observed that larvae exposed to low levels of DEPs were less able to survive after infection with M. bovis BCG and had a higher internal bacterial load after 4 days of infection. Unraveling the links between air pollution and impairment of human antimycobacterial immunity is vital, because pollution is rapidly increasing in areas where TB incidence is extremely high.