Abstract:
INTRODUCTION:Air pollution causes respiratory symptoms and pulmonary disease. Airway inflammation may be involved in the mechanism also for cardiovascular disease. Wood smoke is a significant contributor to air pollution, with complex and varying composition. We examined airway effects of two kinds of wood smoke in a chamber study. MATERIALS AND METHODS:Thirteen subjects were exposed to filtered air and to wood smoke from the start-up phase and the burn-out phase of the wood-burning cycle. Levels of PM(2.5) were 295 µg/m(3) and 146 µg/m(3), number concentrations 140 000/cm(3) and 100 000/cm(3). Biomarkers in blood, breath and urine were measured before and on several occasions after exposure. Effects of wood smoke exposure were assessed adjusting for results with filtered air. RESULTS:After exposure to wood smoke from the start-up, but not the burn-out session, Clara cell protein 16 (CC16) increased in serum after 4 hours, and in urine the next morning. CC16 showed a clear diurnal variation. Fraction of exhaled nitric oxide (FENO) increased after wood smoke exposure from the burn-out phase, but partly due to a decrease after exposure to filtered air. No other airway markers increased. CONCLUSIONS:The results indicate that relatively low levels of wood smoke exposure induce effects on airways. Effects on airway epithelial permeability was shown for the start-up phase of wood burning, while FENO increased after the burn-out session. CC16 seems to be a sensitive marker of effects of air pollution both in serum and urine, but its function and the significance need to be clarified.
journal_name
Inhal Toxicoljournal_title
Inhalation toxicologyauthors
Stockfelt L,Sallsten G,Olin AC,Almerud P,Samuelsson L,Johannesson S,Molnar P,Strandberg B,Almstrand AC,Bergemalm-Rynell K,Barregard Ldoi
10.3109/08958378.2011.633281subject
Has Abstractpub_date
2012-01-01 00:00:00pages
47-59issue
1eissn
0895-8378issn
1091-7691journal_volume
24pub_type
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