Early age exposure to moisture damage and systemic inflammation at the age of 6 years

Indoor Air. 2018 May;28(3):450-458. doi: 10.1111/ina.12454. Epub 2018 Mar 24.

Abstract

Cross-sectional studies have shown that exposure to indoor moisture damage and mold may be associated with subclinical inflammation. Our aim was to determine whether early age exposure to moisture damage or mold is prospectively associated with subclinical systemic inflammation or with immune responsiveness in later childhood. Home inspections were performed in children's homes in the first year of life. At age 6 years, subclinical systemic inflammation was measured by serum C-reactive protein (CRP) and blood leukocytes and immune responsiveness by ex vivo production of interleukin 1-beta (IL-1β), IL-6, and tumor necrosis factor alpha (TNF-α) in whole blood cultures without stimulation or after 24 hours stimulation with phorbol 12-myristate 13-acetate and ionomycin (PI), lipopolysaccharide (LPS), or peptidoglycan (PPG) in 251-270 children. Moisture damage in child's main living areas in infancy was not significantly associated with elevated levels of CRP or leukocytes at 6 years. In contrast, there was some suggestion for an effect on immune responsiveness, as moisture damage with visible mold was positively associated with LPS-stimulated production of TNF-α and minor moisture damage was inversely associated with PI-stimulated IL-1β. While early life exposure to mold damage may have some influence on later immune responsiveness, it does not seem to increase subclinical systemic inflammation in later life.

Keywords: children; cytokines; indoor; inflammation; moisture damage; mold.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Air Pollutants / analysis
  • Air Pollutants / toxicity*
  • Air Pollution, Indoor / adverse effects*
  • Air Pollution, Indoor / analysis
  • C-Reactive Protein / analysis
  • Child
  • Cytokines / blood
  • Environmental Exposure / adverse effects*
  • Environmental Exposure / analysis
  • Female
  • Fungi*
  • Humans
  • Infant
  • Inflammation / blood*
  • Inflammation / etiology
  • Interleukin-1beta / blood
  • Interleukin-6 / blood
  • Ionomycin
  • Leukocyte Count
  • Leukocytes
  • Lipopolysaccharides
  • Male
  • Peptidoglycan
  • Prospective Studies
  • Tetradecanoylphorbol Acetate / analogs & derivatives
  • Tumor Necrosis Factor-alpha / blood

Substances

  • Air Pollutants
  • Cytokines
  • IL6 protein, human
  • Interleukin-1beta
  • Interleukin-6
  • Lipopolysaccharides
  • Peptidoglycan
  • Tumor Necrosis Factor-alpha
  • Ionomycin
  • phorbolol myristate acetate
  • C-Reactive Protein
  • Tetradecanoylphorbol Acetate