Abstract
ObjectivesAccumulating studies have investigated the PM2.5‐induced pulmonary toxicity, while gaps still remain in understanding its toxic mechanism. Due to its high specific surface area and adsorption capacity similar to nanoparticles, PM2.5 acts as a significant carrier of metals in air and then leads to altered toxic effects. In this study, we aimed to use CBs and Ni as model materials to investigate the autophagy changes and pulmonary toxic effects at 30 days following intratracheal instillation of CBs‐Ni mixture.Materials and methodsGroups of mice were instilled with 100 µL normal saline (NS), 20 µg CBs, and 4 µg Ni or CBs‐Ni mixture, respectively. At 7 and 30 days post‐instillation, all the mice were weighed and then sacrificed. The evaluation system was composed of the following: (a) autophagy and lysosomal function assessment, (b) trace element biodistribution observation in lungs, (c) pulmonary lavage biomedical analysis, (d) lung histopathological evaluation, (e) coefficient analysis of major organs and (f) CBs‐Ni interaction and cell proliferation assessment.ResultsWe found that after CBs‐Ni co‐exposure, no obvious autophagy and lysosomal dysfunction or pulmonary toxicity was detected, along with complete clearance of Ni from lung tissues as well as recovery of biochemical indexes to normal range.ConclusionsWe conclude that the damaged autophagy and lysosomal function, as well as physiological function, was repaired at 30 days after exposure of CBs‐Ni. Our findings provide a new idea for scientific assessment of the impact of fine particles on environment and human health, and useful information for the comprehensive treatment of air pollution.
Highlights
Exposure to PM2.5 has been found to be associated with adverse health effects, including cardiovascular disease, respiratory irritation and pulmonary dysfunction,[1,2,3,4] yet gaps still remain in understanding the comprehensive mechanisms of PM2.5-induced pulmonary toxicity
We found co-exposure to CBs and metals caused a synergistic pulmonary toxic effect attributed to autophagy and lysosomal dysfunction at 1 and 7 days post-instillation in mice
The results show that there were no significant differences in Bronchoalveolar lavage fluid (BALF) biomedical indexes, including Lactate dehydrogenase (LDH), alkaline phosphatase (ALP) and acid phosphatase (ACP) activity in normal saline (NS), CBs, Ni- or CBs-Ni mixture-treated groups compared with that in normal groups (Figure 4A), suggesting no lung cell toxicity.[34]
Summary
Exposure to PM2.5 has been found to be associated with adverse health effects, including cardiovascular disease, respiratory irritation and pulmonary dysfunction,[1,2,3,4] yet gaps still remain in understanding the comprehensive mechanisms of PM2.5-induced pulmonary toxicity. Further study of autophagy changes as well as long-term systematic biocompatibility assessment following exposure of PM2.5 is essential. We used CBs and metal ions as mimicking model materials to investigate the synergistic pulmonary effects and its mechanism.[10] We found co-exposure to CBs and metals caused a synergistic pulmonary toxic effect attributed to autophagy and lysosomal dysfunction at 1 and 7 days post-instillation in mice. An improved understanding of the long-term changes in autophagy and toxicity after co-exposure to CBs and metals is essential. Autophagy and lysosomal function assessment, as well as toxicological investigations, will be needed for evaluating the comprehensive lung function following exposure of CBs-metal ions
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