The effects of ambient particulate matter on human adipose tissue.

J Toxicol Environ Health A

a Environmental Health Research Institute, Soroka University Medical Center and Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva , Israel.

Published: May 2020

AI Article Synopsis

  • The study investigates how particulate matter (PM) air pollution affects human adipose tissue by examining 25 cellular markers in both omental and subcutaneous fat.
  • The researchers utilized a new satellite-based model to assess PM exposure over different time frames (acute, intermediate, and chronic) before tissue collection.
  • Findings revealed that PM exposure increases inflammatory markers and stress signals in fat tissue, decreases adipocyte size, and correlates with immune cell activity, suggesting air pollution may lead to inflammation and metabolic issues in fat tissue.

Article Abstract

The effects of particulate matter (PM) air pollution on adipose tissue have mainly been studied in animal models. The aim of this study was to examine the potential associations between PM exposure and 25 cellular markers in human omental (OM) and subcutaneous (SC) adipose tissue. The PM exposure assessments for both PM (PM <2.5 μm in diameter) and PM (<10 μm) were based upon a novel hybrid satellite-based spatio-temporally resolved model. We calculated the PM exposure above the background threshold for 1 week (acute phase), 3 and 6 months (intermediate phase), and 1 year (chronic phase) prior to tissue harvesting and tested the associations with adipose cell metabolic effects using multiple linear regressions and heat maps strategy. Chemokine levels were found to increase after acute and intermediate exposure duration to PM. The levels of stress signaling biomarkers in the SC and OM tissues rose after acute exposure to PM and PM. Macrophage and leucocyte counts were associated with severity of PM exposure in all three duration groups. Adipocyte diameter decreased in all exposure periods. Our results provide evidence for significant contribution of air pollutants exposure to adipose tissue inflammation as well as for pathophysiological mechanisms of metabolic dysregulation that may be involved in the observed responses.

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http://dx.doi.org/10.1080/15287394.2019.1634381DOI Listing

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