TY - JOUR
T1 - Exposure to ambient air pollution and autoantibody status in rheumatoid arthritis
AU - Alex, Asha M.
AU - Kunkel, Gary
AU - Sayles, Harlan
AU - Flautero Arcos, Jorge D.
AU - Mikuls, Ted R.
AU - Kerr, Gail S.
N1 - Funding Information:
The Veterans Affairs Rheumatoid Arthritis Registry (VARA) has received funding from: Nebraska Arthritis Outcomes Research Center at the University of Nebraska Medical Center; Veterans Affairs Health Services Research and Development Program of the Veterans Health Administration (HSR&D), Veterans Health Administration (Veterans Affairs Merit award); HSR&D Career Development Award, Grant Number: CDA 07-221. No financial or non-financial conflicts of interest exist for any of the authors.
PY - 2020/3/1
Y1 - 2020/3/1
N2 - Objective: To evaluate the relationship between air pollutant (AP) exposure and rheumatoid arthritis (RA) autoantibody status Methods: We performed a cross sectional study utilizing enrollment data from participants in the Veterans Affairs rheumatoid arthritis registry. HLA-DRB1 shared epitope (SE), smoking, rheumatoid factor (RF), and anti-cyclic citrullinated peptide antibody (ACPA) status were collected. Mean exposure levels were obtained for AP (NO2, SO2, particulate matter [PM2.5, PM10], and ozone) from air quality monitoring stations at patients’ residential zip codes in the year prior to enrollment. Multivariable logistic and ordinary least squares regression models were used to determine independent associations of AP with RA seropositivity and autoantibody concentration. Results: The cohort included 557 veterans (90% male, 76% Caucasian), with mean age of 70 years and mean disease duration of 13 years. The majority were HLA-DRB1 SE, RF, and ACPA positive (73%, 79%, and 76%, respectively). In univariate models, PM2.5 exposure was associated with higher ACPA concentration (p = 0.009). Similarly, in multivariable regression models, PM2.5 exposure was independently associated with higher ACPA concentration (p = 0.037). Current smoking independently predicted RF and ACPA positivity and titers, while HLA-DRB1 SE alleles were associated with RF positivity and ACPA positivity and titers. Conclusions: In an elderly cohort of RA patients, fine particulate matter (PM2.5) exposure independently predicted higher ACPA concentration. Further study of fine particulate matter in the pathogenesis of RA is warranted.
AB - Objective: To evaluate the relationship between air pollutant (AP) exposure and rheumatoid arthritis (RA) autoantibody status Methods: We performed a cross sectional study utilizing enrollment data from participants in the Veterans Affairs rheumatoid arthritis registry. HLA-DRB1 shared epitope (SE), smoking, rheumatoid factor (RF), and anti-cyclic citrullinated peptide antibody (ACPA) status were collected. Mean exposure levels were obtained for AP (NO2, SO2, particulate matter [PM2.5, PM10], and ozone) from air quality monitoring stations at patients’ residential zip codes in the year prior to enrollment. Multivariable logistic and ordinary least squares regression models were used to determine independent associations of AP with RA seropositivity and autoantibody concentration. Results: The cohort included 557 veterans (90% male, 76% Caucasian), with mean age of 70 years and mean disease duration of 13 years. The majority were HLA-DRB1 SE, RF, and ACPA positive (73%, 79%, and 76%, respectively). In univariate models, PM2.5 exposure was associated with higher ACPA concentration (p = 0.009). Similarly, in multivariable regression models, PM2.5 exposure was independently associated with higher ACPA concentration (p = 0.037). Current smoking independently predicted RF and ACPA positivity and titers, while HLA-DRB1 SE alleles were associated with RF positivity and ACPA positivity and titers. Conclusions: In an elderly cohort of RA patients, fine particulate matter (PM2.5) exposure independently predicted higher ACPA concentration. Further study of fine particulate matter in the pathogenesis of RA is warranted.
KW - Air pollution
KW - Autoantibodies
KW - Environment
KW - Rheumatoid arthritis
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U2 - 10.1007/s10067-019-04813-w
DO - 10.1007/s10067-019-04813-w
M3 - Article
C2 - 31729679
AN - SCOPUS:85075258828
VL - 39
SP - 761
EP - 768
JO - Clinical Rheumatology
JF - Clinical Rheumatology
SN - 0770-3198
IS - 3
ER -