Kevin J Lane1, Jonathan I Levy2, Madeleine K Scammell2, Junenette L Peters2, Allison P Patton3, Ellin Reisner4, Lydia Lowe5, Wig Zamore4, John L Durant6, Doug Brugge7. 1. Department of Environmental Health, Boston University School of Public Health, Boston, MA, United States; Yale University School of Forestry & Environmental Studies, 195 Prospect Street, New Haven, CT, United States. Electronic address: kevin.lane@yale.edu. 2. Department of Environmental Health, Boston University School of Public Health, Boston, MA, United States. 3. Department of Civil and Environmental Engineering, Tufts University, Medford, MA, United States; Environmental and Occupational Health Sciences Institute, Rutgers University, Piscataway, NJ, United States. 4. Somerville Transportation Equity Partnership, Somerville, MA, United States. 5. Chinese Progressive Association, Boston, MA, United States. 6. Department of Civil and Environmental Engineering, Tufts University, Medford, MA, United States. 7. Department of Civil and Environmental Engineering, Tufts University, Medford, MA, United States; Department of Public Health and Community Medicine, Tufts University School of Medicine, Boston, MA, United States; Jonathan M. Tisch College of Citizenship and Public Service.
Abstract
BACKGROUND: Long-term exposure to fine particulate matter has been linked to cardiovascular disease and systemic inflammatory responses; however, evidence is limited regarding the effects of long-term exposure to ultrafine particulate matter (UFP, <100nm). We used a cross-sectional study design to examine the association of long-term exposure to near-highway UFP with measures of systemic inflammation and coagulation. METHODS: We analyzed blood samples from 408 individuals aged 40-91years living in three near-highway and three urban background areas in and near Boston, Massachusetts. We conducted mobile monitoring of particle number concentration (PNC) in each area, and used the data to develop and validate highly resolved spatiotemporal (hourly, 20m) PNC regression models. These models were linked with participant time-activity data to determine individual time-activity adjusted (TAA) annual average PNC exposures. Multivariable regression modeling and stratification were used to assess the association between TAA-PNC and single peripheral blood measures of high-sensitivity C-reactive protein (hsCRP), interleukin-6 (IL-6), tumor-necrosis factor alpha receptor II (TNFRII) and fibrinogen. RESULTS: After adjusting for age, sex, education, body mass index, smoking and race/ethnicity, an interquartile-range (10,000particles/cm(3)) increase in TAA-PNC had a positive non-significant association with a 14.0% (95% CI: -4.6%, 36.2%) positive difference in hsCRP, an 8.9% (95% CI: -0.4%, 10.9%) positive difference in IL-6, and a 5.1% (95% CI: -0.4%, 10.9%) positive difference in TNFRII. Stratification by race/ethnicity revealed that TAA-PNC had larger effect estimates for all three inflammatory markers and was significantly associated with hsCRP and TNFRII in white non-Hispanic, but not East Asian participants. Fibrinogen had a negative non-significant association with TAA-PNC. CONCLUSIONS: Our findings suggest an association between annual average near-highway TAA-PNC and subclinical inflammatory markers of CVD risk.
BACKGROUND: Long-term exposure to fine particulate matter has been linked to cardiovascular disease and systemic inflammatory responses; however, evidence is limited regarding the effects of long-term exposure to ultrafine particulate matter (UFP, <100nm). We used a cross-sectional study design to examine the association of long-term exposure to near-highway UFP with measures of systemic inflammation and coagulation. METHODS: We analyzed blood samples from 408 individuals aged 40-91years living in three near-highway and three urban background areas in and near Boston, Massachusetts. We conducted mobile monitoring of particle number concentration (PNC) in each area, and used the data to develop and validate highly resolved spatiotemporal (hourly, 20m) PNC regression models. These models were linked with participant time-activity data to determine individual time-activity adjusted (TAA) annual average PNC exposures. Multivariable regression modeling and stratification were used to assess the association between TAA-PNC and single peripheral blood measures of high-sensitivity C-reactive protein (hsCRP), interleukin-6 (IL-6), tumor-necrosis factor alpha receptor II (TNFRII) and fibrinogen. RESULTS: After adjusting for age, sex, education, body mass index, smoking and race/ethnicity, an interquartile-range (10,000particles/cm(3)) increase in TAA-PNC had a positive non-significant association with a 14.0% (95% CI: -4.6%, 36.2%) positive difference in hsCRP, an 8.9% (95% CI: -0.4%, 10.9%) positive difference in IL-6, and a 5.1% (95% CI: -0.4%, 10.9%) positive difference in TNFRII. Stratification by race/ethnicity revealed that TAA-PNC had larger effect estimates for all three inflammatory markers and was significantly associated with hsCRP and TNFRII in white non-Hispanic, but not East Asian participants. Fibrinogen had a negative non-significant association with TAA-PNC. CONCLUSIONS: Our findings suggest an association between annual average near-highway TAA-PNC and subclinical inflammatory markers of CVD risk.
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