Original articleResponse of biomarkers of inflammation and coagulation to short-term changes in central site, local, and predicted particle number concentrations
Introduction
Air pollution is widespread in the urban environment and there is substantial evidence of associations with cardiovascular (CV) morbidity and mortality [1], [2], [3], [4]. Three principal pathways have been proposed to explain the adverse CV effects of inhalation of particulate matter: oxidative stress and inflammation, stimulation of the autonomic nervous system, and direct interaction between particles or their components and the CV system [1]. The first pathway, which begins with pulmonary inflammation, progresses to a systemic inflammatory state of oxidative stress, acute phase response, and endothelial dysfunction. Supporting this pathway are observations of associations between particulate matter and markers of systemic inflammation [5], [6], [7], [8], [9] and blood pressure [10], [11], [12].
The specific components responsible for associations between air pollution and adverse outcomes are yet to be fully defined; however, there is evidence from human, animal, and in vitro studies that ultrafine particles (UFP; diameter <0.1 μm) have causal effects [5], [13], [14], [15], [16], [17]. UFP have the ability to deposit deep into the lungs, where large surface areas are available for the adsorption of harmful chemicals [14], [18], [19]. In the urban environment, regional levels of UFP are augmented by contributions from motor vehicle exhaust resulting in both substantial temporal and spatial variability, particularly near busy roadways [20], [21], [22].
Our goal was to examine the effect of short-term exposure to UFP on biomarkers of inflammation and coagulation in a predominately near-highway population. UFP can be reasonably approximated by particle number concentration (PNC) because 80% to 90% of PNC is in the ultrafine range in urban areas [23], [24]. We hypothesized that short-term changes in ambient PNC would be related to increases in interleukin-6 (IL-6), high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor-α receptor II (TNF-RII), and fibrinogen. In most published studies, a single metric is used for PNC exposure, typically from a central site [8], [9], [25], [26], [27], [28]. However, central sites may not represent PNC variation (and therefore exposures) near highways and a neighborhood monitor or predicted residential concentrations [29]. In other studies in which residential measurements have provided the data for exposure, associations of residential PNC and quasi-UFP (diameter <0.25 μm) with blood pressure and inflammatory markers have been identified [6], [30]. We evaluated potential associations of PNC measured at a central site, a near-highway monitor, and modeled values with biomarkers of inflammation and coagulation.
Section snippets
Study area and population
This analysis used data from the Community Assessment of Freeway Exposure and Health (CAFEH) study, a cross-sectional, community-based participatory research study of near-highway air pollution and CV health [31]. The study enrolled residents from three near-highway neighborhoods in Boston, Massachusetts (United States), metropolitan area.
We used data from the Somerville, Massachusetts subsample of CAFEH for this analysis. A detailed description of the study is provided elsewhere [32].
Results
Characteristics of the study participants from both random and convenience samples are summarized in Table 1. A total of 145 participants attended the clinic at least once. After removal of ineligible participants, valid blood samples were obtained one or more times from 142 individuals, for a total of 250 separate samples. Thirty-six participants provided one blood sample, 104 provided two blood samples, and two provided three blood samples. Only samples taken on or after November 14, 2009
Discussion
To our knowledge, we are one of the first to test relationships of acute changes of near-highway, central site, and predicted residential PNC with biomarkers. PNC measured at a central site was associated with IL-6, TNF-RII, and fibrinogen for our predominantly near-highway population. Effect estimates generally increased with longer averaging times for IL-6, hs-CRP, and fibrinogen, and CIs were highly skewed, although most associations did not reach statistical significance. However, neither
Conclusion
Our finding that central site PNC data were associated with blood markers of inflammation whereas similar data from a near-highway site near the residences and predicted residential values based on mobile monitoring were not associated is not easy to explain. But it does not appear to be due to error in the near-highway data to the extent we could assess that possibility or significant error in the residential model. There is a need for additional studies with larger sample sizes to test the
Acknowledgments
We thank the members of the CAFEH Steering Committee and field team for their valuable contributions including Ellin Reisner, Baolian Kuang, Michelle Liang, Mario Davila, David Arond, Don Meglio, Kevin Stone, Marie Manis, Consuelo Perez, Marjorie Alexander, Maria Crispin, Reva Levin, Helene Sroat, Carmen Rodriguez, Migdalia Tracy, and Sidia Escobar. We are also grateful to José Vallarino for his assistance in field work and Steve Melly for field planning, GIS, and database management. We thank
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