OBJECTIVES: Organic dust is associated with adverse effects on human airways. This study was done to investigate whether the addition of beta-(1,3)-D glucan or aldehydes to office dust causes enhanced inflammation in human airways. METHODS:Thirty-six volunteers were exposed randomly to clean air, office dust, dust spiked with glucan, and dust spiked with aldehydes. The three dust exposures contained between 332 and 379 microg dust/m(3). Spiking with 1 gram of dust was done with 10 milligrams of glucan or 0.1 microliters of aldehydes. Acoustic rhinometry, rhinostereometry, nasal lavage, and lung function tests were applied. RESULTS: After the exposures to dust spiked with the glucan and aldehydes, the nasal volume decreased (-1.33 and -1.39 cm(3) (mean), respectively) when compared with the -0.9 cm(3) after clean air or office dust (P=0.036 for a difference in decrease between exposures). After 2-3 hours the aldehyde-spiked dust caused a 0.6-mm swelling of the inferior turbinate, and glucan-spiked dust produced a 0.7-mm swelling (P=0.039 for a difference in the swelling between the four exposures). The preexposure nasal lavage cleaned off the mucosa, and lower cytokine concentrations were found after all of the exposures. For interleukin-8, this decrease in concentration was smaller after the dust exposures spiked with glucan and aldehydes (-2.9 and -25.8 pg/ml, respectively) than after office dust or clean air (-65.9 and -74.1 pg/ml, respectively) (P=0.042). The nasal eosinophil cell concentration increased after exposure to dust spiked with glucan (P=0.045). CONCLUSIONS: beta-(1,3)-D glucan and aldehydes in office dust enhance the inflammatory effects of dust on the upper airways.
RCT Entities:
OBJECTIVES: Organic dust is associated with adverse effects on human airways. This study was done to investigate whether the addition of beta-(1,3)-D glucan or aldehydes to office dust causes enhanced inflammation in human airways. METHODS: Thirty-six volunteers were exposed randomly to clean air, office dust, dust spiked with glucan, and dust spiked with aldehydes. The three dust exposures contained between 332 and 379 microg dust/m(3). Spiking with 1 gram of dust was done with 10 milligrams of glucan or 0.1 microliters of aldehydes. Acoustic rhinometry, rhinostereometry, nasal lavage, and lung function tests were applied. RESULTS: After the exposures to dust spiked with the glucan and aldehydes, the nasal volume decreased (-1.33 and -1.39 cm(3) (mean), respectively) when compared with the -0.9 cm(3) after clean air or office dust (P=0.036 for a difference in decrease between exposures). After 2-3 hours the aldehyde-spiked dust caused a 0.6-mm swelling of the inferior turbinate, and glucan-spiked dust produced a 0.7-mm swelling (P=0.039 for a difference in the swelling between the four exposures). The preexposure nasal lavage cleaned off the mucosa, and lower cytokine concentrations were found after all of the exposures. For interleukin-8, this decrease in concentration was smaller after the dust exposures spiked with glucan and aldehydes (-2.9 and -25.8 pg/ml, respectively) than after office dust or clean air (-65.9 and -74.1 pg/ml, respectively) (P=0.042). The nasal eosinophil cell concentration increased after exposure to dust spiked with glucan (P=0.045). CONCLUSIONS:beta-(1,3)-D glucan and aldehydes in office dust enhance the inflammatory effects of dust on the upper airways.
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