Early age exposure to moisture damage and systemic inflammation at the age of 6 years. (24th March 2018)

• Record Type: Journal Article
• Authors: Karvonen, A. M.; Tischer, C.; Kirjavainen, P. V.; Roponen, M.; Hyvärinen, A.; Illi, S.; Mustonen, K.; Pfefferle, P. I.; Renz, H.; Remes, S.; Schaub, B.; von Mutius, E.; Pekkanen, J.
• Is Part Of: Indoor air. Volume 28:Number 3(2018)
• Page Start: 450
• Page End: 458
• Publication Date: 2018-03-24
• Subjects: children -- cytokines -- indoor -- inflammation -- moisture damage -- mold; Indoor air pollution -- Periodicals; Sick building syndrome -- Periodicals; Ventilation -- Periodicals; 613.5
• DOI: 10.1111/ina.12454
• Languages: English
• ISSNs: 0905-6947

Abstract

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.