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Source category-specific PM2.5 and urinary levels of Clara cell protein CC16. The ULTRA study.
Inhal. Toxicol. 21, 1068-1076 (2009)
We have previously reported that outdoor levels of fine particles (PM(2.5), diameter <2.5 microm) are associated with urinary CC16, a marker for lung damage, in Helsinki, Finland, but not in the other two ULTRA cities (Amsterdam, The Netherlands, and Erfurt, Germany). We here evaluated whether PM(2.5) from specific source categories would be more strongly associated with CC16 than (total) PM(2.5). In addition, we compared two source apportionment methods. METHODS: We collected biweekly spot urinary samples over 6 months from 121 subjects with coronary heart disease for the determination of CC16 (n = 1251). Principal component analysis (PCA) was used to apportion daily outdoor PM(2.5) between different source categories. In addition, the multilinear engine (ME) was used for the source apportionment in Amsterdam and Helsinki. We analyzed associations of source category-specific PM(2.5) and PM(2.5) absorbance, an indicator for combustion originating particles, with logarithmized values of CC16 adjusting for urinary creatinine using multivariate mixed models in STATA. RESULTS: In the pooled analyses, CC16 was increased by 0.6% (standard error 0.3%) per 1 x 10(-5) m(-1) increase in the same-day levels of PM(2.5) absorbance. Source category-specific PM(2.5) concentrations were not consistently associated with the levels of CC16 in the three cities. Correlations between source category-specific PM(2.5) determined using either PCA or ME were in general high. Associations of source category-specific PM(2.5) with CC16 in Amsterdam and Helsinki were statistically less significant when ME was used. CONCLUSIONS: The present results suggest that PM(2.5) from combustion sources increases epithelial barrier permeability in lungs.
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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
Absorbance ; Cc16 ; Source Specific Pm2.5
ISSN (print) / ISBN
0895-8378
e-ISSN
1091-7691
Zeitschrift
Inhalation Toxicology
Quellenangaben
Band: 21,
Heft: 13,
Seiten: 1068-1076
Verlag
Informa Healthcare
Verlagsort
England
Nichtpatentliteratur
Publikationen
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute of Epidemiology (EPI)