Kidney damage induced by repeated fine particulate matter exposure: Effects of different components

Chung Shin Yuan, Ching Shu Lai, Guo Ping Chang-Chien, Yu Lun Tseng, Fu Jen Cheng*

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

12 Scopus citations

Abstract

Background: Exposure to fine particulate matter with an aerodynamic diameter of ≤2.5 μm (PM2.5) is associated with adverse health effects. This study aimed to evaluate the toxic effects of the constituents of PM2.5 on mouse kidneys. Methods: We collected PM2.5 near an industrial complex located in southern Kaohsiung, Taiwan, that was divided into water extract and insoluble particles. Male C57BL/6 mice were divided into five groups: control, low- and high-dose insoluble particle exposure, and low- and high-dose water extract exposure. Biochemical analysis, Western blot analysis, histological examination, and immunohistochemistry were performed to evaluate the impact of PM2.5 constituents on mice kidneys. Results: PM2.5 was collected from January 1, 2021, to February 8, 2021, from an industrial complex in Kaohsiung, Taiwan. Metallic element analysis showed that Pb, Ni, V, and Ti were non-essential metals with enrichment factors >10. Polycyclic aromatic hydrocarbon and nitrate polycyclic aromatic hydrocarbon analyses revealed that the toxic equivalents are, in the order, benzo(a)pyrene (BaP), indeno(1,2,3-cd) pyrene (IP), dibenzo(a,h)anthracene (DBA), and benzo(b)fluoranthene (BbF), which are potential carcinogens. Both water extract and insoluble particle exposure induced inflammatory cytokine upregulation, inflammatory cell infiltration, antioxidant activity downregulation, and elevation of kidney injury molecule 1 (KIM-1) level in mouse kidneys. A dose-dependent effect of PM2.5 water extract and insoluble particle exposure on angiotensin converter enzyme 2 downregulation in mouse kidneys was observed. Conclusion: We found that water-soluble extract and insoluble particles of PM2.5 could induce oxidative stress and inflammatory reactions, influence the regulation of renin-angiotensin system (RAS), and lead to kidney injury marker level elevation in mouse kidneys. The lowest-observed-adverse-effect level for renal toxicity in mice was 40 μg water-soluble extract/insoluble particle inhalation per week, which was approximately equal to the ambient PM2.5 concentration of 44 μg/m3 for mice.

Original languageEnglish
Article number157528
JournalScience of the Total Environment
Volume847
DOIs
StatePublished - 15 11 2022

Bibliographical note

Publisher Copyright:
© 2022 The Authors

Keywords

  • ACE
  • Air pollution
  • Angiotensin converter enzyme
  • Apoptosis
  • Fine particulate matter
  • Inflammatory
  • Mice kidney
  • Oxidative stress
  • PM

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