Bioaerosols and sick building syndrome: particles, inflammation, and allergy

Robert J Laumbach1, Howard M Kipen

  • 1Environmental and Occupational Health Sciences Institute, UMDNJ-Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, USA. laumbach@eohsi.rutgers.edu

Abstract

Insights

Indoor bioaerosols, like mold, may link to sick building syndrome (SBS). While allergy plays a role, nonallergic inflammation and stress likely contribute to SBS symptoms.

Area of Science:

  • Environmental Health
  • Occupational Medicine
  • Toxicology

Background:

  • Sick building syndrome (SBS) symptoms are often nonspecific and challenging to diagnose.
  • Concerns are shifting towards indoor bioaerosols, particularly mold, as a potential cause of SBS.
  • Allergies may contribute, but are unlikely to fully explain the diverse symptoms of SBS.

Purpose of the Study:

  • To review recent literature on the role of bioaerosols in sick building syndrome.
  • To examine the contributions of both allergic and nonallergic mechanisms in SBS.
  • To contextualize the current understanding of bioaerosols and building-related illnesses.

Main Methods:

  • Review of epidemiological studies investigating associations between bioaerosols and SBS symptoms.
  • Analysis of toxicological research on the health effects of inhaled bioaerosols.
  • Evaluation of challenges in exposure assessment and biomonitoring for indoor bioaerosols.

Main Results:

  • Epidemiological studies show possible links between bioaerosols and SBS, but face methodological limitations.
  • Cross-sectional studies associate indoor bioaerosols with SBS symptoms, yet definitions and exposure assessments are problematic.
  • Toxicological studies suggest bioaerosol toxicity, but often at doses higher than typical indoor exposures.

Conclusions:

  • Evidence suggests an association between bioaerosols and SBS, with some toxicological support.
  • The precise contribution of bioaerosol exposure to nonspecific SBS symptoms remains unclear.
  • Nonspecific inflammatory responses, potentially modulated by psychosocial factors like stress, warrant further research.

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