Abstract

Air pollution is known to increase the risk of pneumonia. However, the effects of air pollution on the pleural effusion of patients with pneumonia are unclear. The objective of this study was to investigate alterations in inflammatory–immune biomarkers by air pollution in patients with pneumonia by analyzing their pleural effusion. Patients who had undergone thoracentesis to drain their pleural effusion in a hospital were recruited for this study. Patients with pneumonia and those with congestive heart failure respectively served as the case and control groups. We observed that an increase of 1 ppb in one-year NO2 was associated with a decrease of 0.105 ng/mL in cluster of differentiation 62 (CD62) (95% confidence interval (CI) = -0.085, -0.004, p < 0.05) in the pleural effusion. Furthermore, we observed that an increase in one-year 1 ppb of NO2 was associated with a decrease of 0.026 ng/mL in molybdenum (Mo) (95% CI = -0.138, -0.020, p < 0.05). An increase in one-year 1 ppb of SO2 was associated with a decrease of 0.531 ng/mL in zinc (95% CI = -0.164, -0.006, p < 0.05). Also, an increase in one-year 1 ppb of O3 was associated with a decrease of 0.025 ng/mL in Mo (95% CI = -0.372, -0.053, p < 0.05). In conclusion, air pollution exposure, especially gaseous pollution, may be associated with the regulation of immune responses and changes in metal levels in the pleural effusion of pneumonia patients.

Original languageEnglish
Article number705
JournalInternational Journal of Environmental Research and Public Health
Volume16
Issue number5
DOIs
Publication statusPublished - Mar 1 2019

Keywords

  • Air pollution
  • Heart failure
  • Immune function
  • Infection
  • Metal
  • Environmental Monitoring
  • Inflammation/chemically induced
  • Humans
  • Middle Aged
  • Male
  • Pleural Effusion/chemically induced
  • Pneumonia/physiopathology
  • Air Pollution/adverse effects
  • Heart Failure/physiopathology
  • Metals/adverse effects
  • Aged, 80 and over
  • Biomarkers/blood
  • Female
  • Aged

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health
  • Health, Toxicology and Mutagenesis

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