Abstract
BackgroundAmbient air pollution has been associated with activation of systemic inflammation and hypercoagulability and increased plasma homocysteine, but the chemical constituents behind the association are not well understood. We examined the relations of various chemical constituents of fine particles (PM2.5) and biomarkers of inflammation, coagulation and homocysteine in the context of traffic-related air pollution.MethodsA panel of 40 healthy college students underwent biweekly blood collection for 12 times before and after their relocation from a suburban campus to an urban campus with changing air pollution contents in Beijing. Blood samples were measured for circulatory biomarkers of high-sensitivity C reactive protein (hs-CRP), tumor necrosis factor alpha (TNF-α), fibrinogen, plasminogen activator inhibitor type 1 (PAI-1), tissue-type plasminogen activator (t-PA), von Willebrand factor (vWF), soluble platelet selectin (sP-selectin), and total homocysteine (tHcy). Various air pollutants were measured in a central air-monitoring station in each campus and 32 PM2.5 chemical constituents were determined in the laboratory. We used three different mixed-effects models (single-constituent model, constituent-PM2.5 joint model and constituent residual model) controlling for potential confounders to estimate the effects of PM2.5 chemical constituents on circulatory biomarkers.ResultsWe found consistent positive associations between the following biomarkers and PM2.5 chemical constituents across different models: TNF-α with secondary organic carbon, chloride, zinc, molybdenum and stannum; fibrinogen with magnesium, iron, titanium, cobalt and cadmium; PAI-1 with titanium, cobalt and manganese; t-PA with cadmium and selenium; vWF with aluminum. We also found consistent inverse associations of vWF with nitrate, chloride and sodium, and sP-selectin with manganese. Two positive associations of zinc with TNF-α and of cobalt with fibrinogen, and two inverse associations of nitrate with vWF, and of manganese with sP-selectin, were independent of the other constituents in two-constituent models using constituent residual data. We only found weak air pollution effects on hs-CRP and tHcy.ConclusionsOur results provide clues for the potential roles that PM2.5 chemical constituents may play in the biological mechanisms through which air pollution may influence the cardiovascular system.
Highlights
Ambient air pollution has been associated with activation of systemic inflammation and hypercoagulability and increased plasma homocysteine, but the chemical constituents behind the association are not well understood
A previous panel study under urban exposure setting found significant positive effects of particles on high-sensitivity C reactive protein (hs-CRP), fibrinogen and plasminogen activator inhibitor type 1 (PAI-1) but not on type plasminogen activator (t-PA) in young adults [13]; a crossover study did not find any significant differences in inflammatory biomarkers (CRP, fibrinogen and TNF-α) after exposure to particle rich air in young healthy individuals [29]; a population-based survey found a positive association between von Willebrand factor (vWF) and shortterm particulate matter with aerodynamic diameter≤10 μm (PM10) exposure [30] whereas a panel study in patients with chronic pulmonary disease found inverse associations between vWF and various air pollutants including particles and gases [31]; panel studies by Delfino et al [14,15] found significant positive associations between sP-selectin and particles and its carbonaceous contents whereas ours did not (Figure 1)
In summary, we found that PM2.5 chemical constituents may be the major air pollution components that contribute to the observed short-term cardiovascular effects in healthy adults in the context of traffic-related air pollution
Summary
Ambient air pollution has been associated with activation of systemic inflammation and hypercoagulability and increased plasma homocysteine, but the chemical constituents behind the association are not well understood. It has been proposed that air pollutants especially the PM may enter the circulation to induce systemic inflammation and hypercoagulability [4,5], alter cardiac autonomic nervous system [6], elevate peripheral blood pressure [7], and promote the development of atherosclerosis through oxidation pathway [8]. Other epidemiologic studies found that air pollution exposure was associated with activation of systemic inflammation and hypercoagulability [12,13,14,15], increased peripheral blood pressure [16], and elevated plasma homocysteine (a risk factor for atherosclerosis) [8,17]
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