Air Pollution Exposures and Circulating Biomarkers of Effect in a Susceptible Population: Clues to Potential Causal Component mixtures and mechanisms

Abstract

BackgroundMechanisms involving oxidative stress and inflammation have been proposed to explain associations of ambient air pollution with cardiovascular morbidity and mortality. Experimental evidence suggests that organic components and ultrafine particles (UFP) are important.MethodsWe conducted a panel study of 60 elderly subjects with coronary artery disease living in retirement communities within the Los Angeles, California, air basin. Weekly biomarkers of inflammation included plasma interleukin-6, tumor necrosis factor-α soluble receptor II (sTNF-RII), soluble platelet selectin (sP-selectin), and C-reactive protein (CRP). Biomarkers of erythrocyte antioxidant activity included glutathione peroxidase-1 and superoxide dismutase. Exposures included outdoor home daily particle mass [particulate matter < 0.25, 0.25–2.5, and 2.5–10 μm in aerodynamic diameter (PM0.25, PM0.25–2.5, PM2.5–10)], and hourly elemental and black carbon (EC–BC), estimated primary and secondary organic carbon (OCpri, SOC), particle number (PN), carbon monoxide (CO), and nitrogen oxides–nitrogen dioxide (NOx–NO2). We analyzed the relation of biomarkers to exposures with mixed effects models adjusted for potential confounders.ResultsPrimary combustion markers (EC–BC, OCpri, CO, NOx–NO2), but not SOC, were positively associated with inflammatory biomarkers and inversely associated with erythrocyte anti-oxidant enzymes (n = 578). PN and PM0.25 were more strongly associated with biomarkers than PM0.25–2.5. Associations for all exposures were stronger during cooler periods when only OCpri, PN, and NOx were higher. We found weaker associations with statin (sTNF-RII, CRP) and clopidogrel use (sP-selectin).ConclusionsTraffic-related air pollutants are associated with increased systemic inflammation, increased platelet activation, and decreased erythrocyte antioxidant enzyme activity, which may be partly behind air pollutant–related increases in systemic inflammation. Differences in association by particle size, OC fraction, and seasonal period suggest components carried by UFP are important.

Public health and components of particulate matter: The changing assessment of black carbon

“…Monitors inside and outside homes of retirees (Delfino et al, 2008(Delfino et al, , 2009. Mobile monitors that travelled with retirees (Adar et al, 2007).…”

“…All of these biological changes are factors in development of cardiovascular diseases. Delfino et al (2008Delfino et al ( , 2009 found elevated platelet P-selectin expression and depletion of erythrocyte superoxide dismutase (SOD) in a panel study of elderly residents of retirement centers in Los Angeles, in association with higher concentrations of BC, EC, and primary organic carbon (POC), suggesting commonality of effects from different sources of similar emissions. Increased ROS has been found in association with exposure to diesel emissions in workplaces (e.g., Sauvain et al, 2009, bus maintenance workers; Lee et al, 2011, diesel exhaust inspectors).…”

Interaction of Amorphous Silica Nanoparticles with Erythrocytesin Vitro: Role of Oxidative Stress

“…It has been reported that exposure to particulate air pollution causes a decrease in erythrocyte antioxidant enzyme activity [8]. A decrease in erythrocytes in association with exposure to either particulate air pollution or nanoparticles in humans and experimental animals has been reported [9,10,11].…”

Polycyclic aromatic hydrocarbon exposure and wheeze in a cohort of children with asthma in Fresno, CA

“…Air pollution has been linked to a variety of health outcomes, but the strongest evidence for pathways from exposure to disease exists for traffic-related air pollution and cardiovascular disease (Rosenlund, Berglind, Pershagen, Hallqvist, Jonson and Bellander, 2006; Tonne, Melly, Mittleman, Coull, Goldberg and Schwartz, 2007), all cause mortality (Jerrett, et al, 2009a; Jerrett, et al, 2009b), and asthma exacerbations (Kunzli, et al, 2000). Recently, exposure to PAHs, which are a major component of primary traffic emissions (HEI Panel on the Health Effects of Traffic-Related Air Pollution 2010), has been associated with relevant biomarkers (Delfino, et al, 2009) and implicated as a contributor to the onset of asthma (Burton, 2009; McConnell, et al, 2010). …”