Association of biomarkers of systemic inflammation with organic components and source tracers in quasi-ultrafine particles

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From: Environmental Health Perspectives(Vol. 118, Issue 6)
Publisher: National Institute of Environmental Health Sciences
Document Type: Report
Length: 6,384 words
Lexile Measure: 1550L

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BACKGROUND: Evidence is needed regarding the air pollutant components and their sources responsible for associations between particle mass concentrations and human cardiovascular out-comes. We previously found associations between circulating biomarkers of inflammation and mass concentrations of quasi-ultrafine particles [less than or equal to] 0.25 [micro]m in aerodynamic diameter ([PM.sub.0.25]) in a panel cohort study of. 60 elderly subjects with coronary artery disease living in the Los Angeles Basin.

OBJECTIVES: We reassessed biomarker associations with [PM.sub.0.25] using new particle composition data.

METHODS: Weekly biomarkers of inflammation were plasma interleukin-6 (IL-6) and soluble tumor necrosis factor-[alpha] receptor II (sTNF-RII) (n = 578). Exposures included indoor and outdoor community organic [PM.sub.0.25] constituents [polycyclic aromatic hydrocarbons (PAHs), hopanes, n-alkanes, organic acids, water-soluble organic carbon, and transition metals]. We analyzed the relation between biomarkers and exposures with mixed-effects models adjusted for potential confounders.

RESULTS: Indoor and outdoor PAHs (low-, medium-, and high-molecular-weight PAHs), followed by hopanes (vehicle emissions tracer), were positively associated with biomarkers, but other organic components and transition metals were not. sTNF-RII increased by 135 pg/mL [95% confidence interval (CI), 45-225 pg/mL], and IL-6 increased by 0.27 pg/mL (95% CI, 0.10-0.44 pg/mL) per interquartile range increase of 0.56 ng/[m.sup.3] outdoor total PAHs. Two-pollutant models of [PM.sub.0.25] with PAHs showed that nominal associations of IL-6 and sTNF-RII with [PM.sub.0.25] mass were completely confounded by PAHs. Vehicular emission sources estimated from chemical mass balance models were strongly correlated with PAHs (R = 0.71).

CONCLUSIONS: Traffic emission sources of organic chemicals represented by PAHs are associated with increased systemic inflammation and explain associations with quasi-ultrafine particle mass.

KEY WORDS: air toxics, biomarkers of effect, cytokines, epidemiology, longitudinal data analysis. Environ Health Perspect 118:756-762 (2010). doi:10.1289/ehp.090l407 [Online 2 February 2010]

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Cardiovascular hospital admissions and mortality have been associated with ambient mass concentrations of fine particulate matter (PM) air pollution [less than or equal to] 2.5 [micro]m in aerodynamic diameter ([PM.sub.2.5]) (Pope and Dockery 2006). Questions remain regarding the underlying causal chemical components and sources responsible for these associations. A recent time-series study of 106 U.S. counties showed stronger associations of cardiovascular hospital admissions with countywide averages of [PM.sub.2.5] when there were higher fractions of elemental carbon (EC), nickel (Ni), and vanadium (V), suggesting that important sources included fossil fuel combustion, biomass burning, and oil combustion (Bell et al. 2009).

Unlike [PM.sub.2.5], ultrafine particles (UFPs; generally defined as < 0.1 [micro]m in diameter) are not regulated by the U.S. Environmental Protection Agency (EPA), yet this is the size fraction that may have the highest toxic potential because it has magnitudes greater number concentrations and surface area than the larger particles that dominate [PM.sub.2.5] mass (Oberdorster et al. 2005). On that large surface area, UFPs carry and deliver redoxactive organic chemicals, including polycyclic aromatic hydrocarbons (PAHs), to the respiratory tract in disproportionately higher concentrations than do larger particles (Ntziachristos et al. 2007), possibly leading to a cascade of effects related to oxidative stress and inflammation in the lungs and at extrapulmonary sites (Delfino et al. 2005). These and other...

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Gale Document Number: GALE|A229861076