Associations of primary and secondary organic aerosols with airway and systemic inflammation in an elderly panel cohort.
BACKGROUND
Exposure-response information about particulate air-pollution constituents is needed to protect sensitive populations. Particulate matter <2.5 mm (PM2.5) components may induce oxidative stress through reactive-oxygen-species generation, including primary organics from combustion sources and secondary organics from photochemically oxidized volatile organic compounds. We evaluated differences in airway versus systemic inflammatory responses to primary versus secondary organic particle components, particle size fractions, and the potential of particles to induce cellular production of reactive oxygen species.


METHODS
A total of 60 elderly subjects contributed up to 12 weekly measurements of fractional exhaled nitric oxide (NO; airway inflammation biomarker), and plasma interleukin-6 (IL-6; systemic inflammation biomarker). PM2.5 mass fractions were PM0.25 (<0.25 μm) and PM0.25-2.5 (0.25-2.5 μm). Primary organic markers included PM2.5 primary organic carbon, and PM0.25 polycyclic aromatic hydrocarbons and hopanes. Secondary organic markers included PM2.5 secondary organic carbon, and PM0.25 water soluble organic carbon and n-alkanoic acids. Gaseous pollutants included carbon monoxide (CO) and nitrogen oxides (NOx; combustion emissions markers), and ozone (O3; photochemistry marker). To assess PM oxidative potential, we exposed rat alveolar macrophages in vitro to aqueous extracts of PM0.25 filters and measured reactive-oxygen-species production. Biomarker associations with exposures were evaluated with mixed-effects models.


RESULTS
Secondary organic markers, PM0.25-2.5, and O3 were positively associated with exhaled NO. Primary organic markers, PM0.25, CO, and NOx were positively associated with IL-6. Reactive oxygen species were associated with both outcomes.


CONCLUSIONS
Particle effects on airway versus systemic inflammation differ by composition, but overall particle potential to induce generation of cellular reactive oxygen species is related to both outcomes.
Delfino
Ralph J
RJ
Department of Epidemiology, School of Medicine, University of California, Irvine, CA 92617-7555, USA. rdelfino@uci.edu
Staimer
Norbert
N
Tjoa
Thomas
T
Arhami
Mohammad
M
Polidori
Andrea
A
Gillen
Daniel L
DL
George
Steven C
SC
Shafer
Martin M
MM
Schauer
James J
JJ
Sioutas
Constantinos
C
D000336:Aerosols; D000368:Aged; D000369:Aged, 80 and over; D000393:Air Pollutants / Q000633:toxicity*; D001980:Bronchi / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D015331:Cohort Studies; D005260:Female; D006801:Humans; D007249:Inflammation / Q000139:chemically induced*; D008137:Longitudinal Studies; D008297:Male; D009930:Organic Chemicals / Q000633:toxicity*; D017382:Reactive Oxygen Species / Q000378:metabolism; D018746:Systemic Inflammatory Response Syndrome / Q000139:chemically induced*; D014132:Trachea / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology
D000336:Aerosols; D000393:Air Pollutants; D009930:Organic Chemicals; D017382:Reactive Oxygen Species
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