Label-free biocompatible detection and quantification of airborne particulate matter (PM2.5) and chronic tissue injury in heart and lung of mouse

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Abstract While it is known that air borne particulate matter (PM2.5) may pass through the pulmonary circulation of blood at the alveolar level between lung and heart and cross the air-blood barrier, the mechanism and effects are not completely clear. In this study the imaging method fluorescence lifetime imaging microscopy (FLIM) is adopted for visualization with high spatial resolution and quantification of PM particles in mouse lung and heart tissues. The results showed that the median numbers of particles in lung of mice exposed to particulate matter of diameter less than 2.5 µm (PM2.5) was about 2.0 times more than that in the filtered air (FA)-treated mice, and about 1.3 times more in heart of PM2.5-treated mice than in FA-treated mice. Interestingly, PM2.5 particles were more abundant in heart than lung, likely due to how PM particles are cleared by phagocytosis and transport via circulation from lungs. It is proposed that the powerful flow of blood through the heart may contribute to invasion of PM2.5 particles into heart muscles. The histopathological evaluations revealed that exposure of PM2.5 to lungs dilated air spaces and showed signs of inflammation. Moreover, heart tissues showed inflammation and amyloid deposition. The component analysis of concentrated airborne PM2.5 particles suggested traffic exhausts and industrial emissions as predominant sources. Our results strongly suggest association of PM2.5 exposure to chronic lung and heart tissue injuries. The current study supports the contention that industrial air pollution is one of the causative factors for rising levels of chronic pulmonary and cardiac diseases.

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