Experimental exposure to wood-smoke particles in healthy humans: effects on markers of inflammation, coagulation, and lipid peroxidation.
Particulate air pollution is known to increase cardiovascular morbidity and mortality. Proposed mechanisms underlying this increase include effects on inflammation, coagulation factors, and oxidative stress, which could increase the risk of coronary events and atherosclerosis. The aim of this study was to examine whether short-term exposure to wood smoke affects markers of inflammation, blood hemostasis, and lipid peroxidation in healthy humans. Thirteen subjects were exposed to wood smoke and clean air in a chamber during two 4-h sessions, 1 wk apart. The mass concentrations of fine particles at wood smoke exposure were 240-280 mug/m3, and number concentrations were 95,000-180,000/cm3. About half of the particles were ultrafine (< 100 nm). Blood and urine samples were taken before and after the experiment. Exposure to wood smoke increased the levels of serum amyloid A, a cardiovascular risk factor, as well as factor VIII in plasma and the factor VIII/von Willebrand factor ratio, indicating a slight effect on the balance of coagulation factors. Moreover, there was an increased urinary excretion of free 8-iso-prostaglandin2alpha, a major F2-isoprostane, though this was based on nine subjects only, indicating a temporary increase in free radical-mediated lipid peroxidation. Thus, wood-smoke particles at levels that can be found in smoky indoor environments seem to affect inflammation, coagulation, and possibly lipid peroxidation. These factors may be involved in the mechanisms whereby particulate air pollution affects cardiovascular morbidity and mortality. The exposure setup could be used to establish which particle characteristics are critical for the effects.
Barregard
Lars
L
Department of Occupational and Environmental Medicine, Sahlgrenska University Hospital and Academy, Goteborg University, Goteborg, Sweden. lars.barregard@amm.gu.se
Sällsten
Gerd
G
Gustafson
Pernilla
P
Andersson
Lena
L
Johansson
Linda
L
Basu
Samar
S
Stigendal
Lennart
L
D000210:Acute-Phase Reaction / Q000139:chemically induced* / Q000378:metabolism; D000328:Adult; D000393:Air Pollutants / Q000009:adverse effects*; D015415:Biomarkers / Q000378:metabolism; D001777:Blood Coagulation / Q000187:drug effects*; D015237:Dinoprost / Q000031:analogs & derivatives / Q000652:urine; D005169:Factor VIII / Q000032:analysis; D005260:Female; D006403:Hematologic Tests; D006801:Humans; D019570:Inhalation Exposure; D015227:Lipid Peroxidation / Q000187:drug effects*; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D010316:Particle Size; D000685:Serum Amyloid A Protein / Q000378:metabolism; D012906:Smoke / Q000009:adverse effects*; D015208:Smoke Inhalation Injury / Q000139:chemically induced* / Q000378:metabolism; D011795:Surveys and Questionnaires; D014934:Wood; D014841:von Willebrand Factor / Q000032:analysis
D000393:Air Pollutants; D015415:Biomarkers; D000685:Serum Amyloid A Protein; D012906:Smoke; D014841:von Willebrand Factor; C075750:8-epi-prostaglandin F2alpha; D005169:Factor VIII; D015237:Dinoprost