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0191 Are indoor concentrations of airborne mould spores in non-industrial environments sufficiently high to cause hypersensitivity pneumonitis?
  1. Henrik A Kolstad1,
  2. Simon Skov2,
  3. Tine Birgitte Halsen Malling3,
  4. Elisabeth Bendstrup4,
  5. Vivi Schlünssen1,5
  1. 1Department of Occupational Medicine, Danish Ramazzini Centre, Aarhus University Hospital, Aarhus, Denmark
  2. 2Forest and Landscape, Faculty of Life Sciences, University of Copenhagen, Copenhagen, Denmark
  3. 3Department of Occupational Medicine, Danish Ramazzini Centre, Aalborg University Hospital, Aalborg, Denmark
  4. 4Department of Respiratory Medicine and Allergology, Aarhus University Hospital, Aarhus, Denmark
  5. 5Department of Public Health, Section for Environment, Work, and Health, Danish Ramazzini Centre, Aarhus University, Aarhus, Denmark

Abstract

Objectives Antigen exposure is the only diagnostic criteria specific for hypersensitivity pneumonitis (HP) compared with other interstitial lung diseases. Indoor mould exposure in non-industrial environments has been claimed to cause HP, but little is known about exposure levels. Our objective was to compare indoor concentrations of airborne mould spores for patients diagnosed with indoor HP with background levels and levels measured for patients diagnosed with farmers’ lung and suberosis.

Method We included 8 patients diagnosed with HP based on characteristic clinical findings, signs of indoor mould growth at home or at their non-industrial work place, and increased levels of precipitating antibodies for moulds. We collected 110 air samples from all affected rooms, adjacent rooms, and outdoor.

Results The average total spore concentrations varied between 22 000 and 36 000 spores per m3, and the average viable concentrations between 35 CFU/m3 and 457 CFU/m3, with no clear association between spore concentration and affected rooms, adjacent rooms and outdoor.

Conclusions The observed levels did not exceed usual indoor and outdoor levels and were orders of magnitude below levels measured for patients diagnosed with farmers’ lung and suberosis, and we question if indoor mould levels in non-industrial environments are sufficient to cause HP. Relying solely on signs of moulds or presence of precipitating antibodies when diagnosing HP may cause other interstitial lung diseases to be overseen and patients may take initiatives such as quitting the job or leaving their homes that will not alleviate their disease but have significant social consequences.

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