Effects on airways of short-term exposure to two kinds of wood smoke in a chamber study of healthy humans.
BACKGROUND
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.


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.
Department of Occupational and Environmental Medicine, Sahlgrenska University Hospital and Academy, University of Gothenburg, Gothenburg, Sweden. Leo.stockfelt@amm.gu.se
Leo
L
Stockfelt
Gerd
G
Sallsten
Anna-Carin
AC
Olin
Pernilla
P
Almerud
Lena
L
Samuelsson
Sandra
S
Johannesson
Peter
P
Molnar
Bo
B
Strandberg
Ann-Charlotte
AC
Almstrand
Kerstin
K
Bergemalm-Rynell
Lars
L
Barregard
D000328:Adult; D015415:Biomarkers; D001944:Breath Tests; D005260:Female; D006801:Humans; D019570:Inhalation Exposure / Q000009:adverse effects*; D008168:Lung / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008875:Middle Aged; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress; D010316:Particle Size; D011084:Polycyclic Aromatic Hydrocarbons / Q000032:analysis / Q000633:toxicity*; D037662:Pulmonary Surfactant-Associated Protein A / Q000378:metabolism; D037663:Pulmonary Surfactant-Associated Protein D / Q000378:metabolism; D012906:Smoke / Q000009:adverse effects* / Q000032:analysis; D011795:Surveys and Questionnaires; D014598:Uteroglobin / Q000097:blood / Q000652:urine; D055549:Volatile Organic Compounds / Q000032:analysis / Q000633:toxicity*; D014934:Wood; D055815:Young Adult
D015415:Biomarkers; D011084:Polycyclic Aromatic Hydrocarbons; D037662:Pulmonary Surfactant-Associated Protein A; D037663:Pulmonary Surfactant-Associated Protein D; C556389:SCGB1A1 protein, human; D012906:Smoke; D055549:Volatile Organic Compounds; D009569:Nitric Oxide; D008315:Malondialdehyde; D014598:Uteroglobin