UC Irvine

BACKGROUND: Cardiovascular disease is the leading cause of death in the United States. Short-term exposures to air pollution have been associated with acute increases in cardiovascular hospitalization and mortality. However, the causative chemical components and underlying pathophysiological mechanisms remain to be clarified.

METHODS: We conducted a cohort panel study involving 97 elderly subjects living in the Los Angeles metropolitan area. Weekly, we measured microvascular function, represented by reactive hyperemia index (RHI), and airway and circulating biomarkers of oxidative stress and inflammation, including exhaled breath condensate malondialdehyde (EBC MDA), fractional exhaled nitric oxide, oxidized low-density lipoprotein, and plasma interleukin-6 (IL-6) over 12 weeks. Exposures included 7-day personal nitrogen oxides (NOX), daily ambient pollutants, including particulate matter size <0.25 µm in aerodynamic diameter (PM2.5), ozone, carbon monoxide (CO), black carbon (BC), and NOx, five-day average PM measured in three size-fractions and characterized by chemical components including transition metals, PM oxidative potential, and electrophilic potential. CAlifornia LINE Source Dispersion Model, version 4 (CALINE4) was used to estimate individual exposure to local traffic-generated NOx. Associations between clinical outcomes and pollutants were assessed using linear mixed effects regression models. Potential effect modification by demographic characteristics and CALINE4-modeled NOx was assessed by adding interaction terms to these models.

RESULTS: RHI was inversely associated with daily ambient traffic-related air pollutants (BC, NOX, and CO), other mobile-source components/tracers (polycyclic aromatic hydrocarbons, elemental carbon, and hopanes), PM oxidative potential, and transition metals, and was positively associated electrophilic potential. We found significant positive associations of airway oxidative stress (EBC MDA), and inflammation (IL-6) with traffic-related air pollutants, ultrafine particles, and transition metals. The observed associations were generally stronger among subjects at higher local traffic-generated NOx (estimated by CALINE4). Associations between systemic oxidative stress and inflammation biomarkers and air pollutants were mostly non-significant, expect for positive associations that observed for IL-6 and traffic-related air pollutants at 1-day averages.

CONCLUSIONS: Short-term exposure to pollutants with high oxidative potential (traffic-related pollutants, ultrafine particles, and transition metals) was associated with impaired microvascular function and increased airway oxidative stress and inflammation in elderly adults. Chronic exposure to residential NOx may further strengthen the observed associations.