TY - JOUR
T1 - Coarse Particulate Matter and Markers of Inflammation and Coagulation in the Multi-Ethnic Study of Atherosclerosis (MESA) Population
T2 - A Repeat Measures Analysis
AU - Pedde, Meredith
AU - Larson, Timothy V.
AU - D’Souza, Jennifer
AU - Szpiro, Adam A.
AU - Kloog, Itai
AU - Lisabeth, Lynda D.
AU - Jacobs, David
AU - Sheppard, Lianne
AU - Allison, Matthew
AU - Kaufman, Joel D.
AU - Adar, Sara D.
N1 - Publisher Copyright:
© 2024, Public Health Services, US Dept of Health and Human Services. All rights reserved.
PY - 2024/2/1
Y1 - 2024/2/1
N2 - Background: In contrast to fine particles, less is known of the inflammatory and coagulation impacts of coarse particulate matter (PM10-2:5, particulate matter with aerodynamic diameter <10 im and >2.5 im). Toxicological research suggests that these pathways might be important processes by which PM10-2:5 impacts health, but there are relatively few epidemiological studies due to a lack of a national PM10-2.5 monitoring network. Objectives: We used new spatiotemporal exposure models to examine associations of both 1-y and 1-month average PM10-2.5 concentrations with markers of inflammation and coagulation. Methods: We leveraged data from 7,071 Multi-Ethnic Study of Atherosclerosis and ancillary study participants 45-84 y of age who had repeated plasma measures of inflammatory and coagulation biomarkers. We estimated PM10-2.5 at participant addresses 1 y and 1 month before each of up to four exams (2000-2012) using spatiotemporal models that incorporated satellite, regulatory monitoring, and local geographic data and accounted for spatial correlation. We used random effects models to estimate associations with interleukin-6 (IL-6), C-reactive protein (CRP), fibrinogen, and D-dimer, controlling for potential confounders. Results: Increases in PM10-2.5 were not associated with greater levels of inflammation or coagulation. A 10-μg/m3 increase in annual average PM10-2.5 was associated with a 2.5% decrease in CRP [95% confidence interval (CI): -5.5, 0.6]. We saw no association between annual average PM10-2.5 and the other markers (IL-6: -0.7%, 95% CI: -2.6, 1.2; fibrinogen: -0.3%, 95% CI: -0.9, 0.3; D-dimer: -0.2%, 95% CI: -2.6, 2.4). Associations consistently showed that a 10-μg/m3 increase in 1-month average PM10-2.5 was associated with reduced inflammation and coagulation, though none were distinguishable from no association (IL-6: -1.2%, 95% CI: -3.0 , 0.5; CRP: -2.5%, 95% CI: -5.3, 0.4; fibrinogen: -0.4%, 95% CI: -1.0, 0.1; D-dimer: -2.0%, 95% CI: -4.3, 0.3). Discussion: We found no evidence that PM10-2.5 is associated with higher inflammation or coagulation levels. More research is needed to determine whether the inflammation and coagulation pathways are as important in explaining observed PM10-2.5 health impacts in humans as they have been shown tobe in toxicology studies or whether PM10-2.5 might impact human health through alternative biological mechanisms.
AB - Background: In contrast to fine particles, less is known of the inflammatory and coagulation impacts of coarse particulate matter (PM10-2:5, particulate matter with aerodynamic diameter <10 im and >2.5 im). Toxicological research suggests that these pathways might be important processes by which PM10-2:5 impacts health, but there are relatively few epidemiological studies due to a lack of a national PM10-2.5 monitoring network. Objectives: We used new spatiotemporal exposure models to examine associations of both 1-y and 1-month average PM10-2.5 concentrations with markers of inflammation and coagulation. Methods: We leveraged data from 7,071 Multi-Ethnic Study of Atherosclerosis and ancillary study participants 45-84 y of age who had repeated plasma measures of inflammatory and coagulation biomarkers. We estimated PM10-2.5 at participant addresses 1 y and 1 month before each of up to four exams (2000-2012) using spatiotemporal models that incorporated satellite, regulatory monitoring, and local geographic data and accounted for spatial correlation. We used random effects models to estimate associations with interleukin-6 (IL-6), C-reactive protein (CRP), fibrinogen, and D-dimer, controlling for potential confounders. Results: Increases in PM10-2.5 were not associated with greater levels of inflammation or coagulation. A 10-μg/m3 increase in annual average PM10-2.5 was associated with a 2.5% decrease in CRP [95% confidence interval (CI): -5.5, 0.6]. We saw no association between annual average PM10-2.5 and the other markers (IL-6: -0.7%, 95% CI: -2.6, 1.2; fibrinogen: -0.3%, 95% CI: -0.9, 0.3; D-dimer: -0.2%, 95% CI: -2.6, 2.4). Associations consistently showed that a 10-μg/m3 increase in 1-month average PM10-2.5 was associated with reduced inflammation and coagulation, though none were distinguishable from no association (IL-6: -1.2%, 95% CI: -3.0 , 0.5; CRP: -2.5%, 95% CI: -5.3, 0.4; fibrinogen: -0.4%, 95% CI: -1.0, 0.1; D-dimer: -2.0%, 95% CI: -4.3, 0.3). Discussion: We found no evidence that PM10-2.5 is associated with higher inflammation or coagulation levels. More research is needed to determine whether the inflammation and coagulation pathways are as important in explaining observed PM10-2.5 health impacts in humans as they have been shown tobe in toxicology studies or whether PM10-2.5 might impact human health through alternative biological mechanisms.
UR - http://www.scopus.com/inward/record.url?scp=85185618121&partnerID=8YFLogxK
U2 - 10.1289/EHP12972
DO - 10.1289/EHP12972
M3 - Article
C2 - 38381480
AN - SCOPUS:85185618121
SN - 0091-6765
VL - 132
JO - Environmental Health Perspectives
JF - Environmental Health Perspectives
IS - 2
M1 - 027009
ER -