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Abstract Number: 2654

Exposure to Air Pollution and the Onset and Progression of Systemic Lupus Erythematosus

Gaurav Gulati1, Cole Brokamp2, Patrick Ryan2 and Hermine I. Brunner3, 1Division of Immunology, Allergy and Rheumatology, University of Cincinnati College of Medicine, Cincinnati, OH, 2Department of Biostatistics and Epidemiology, Cincinnati Childrens Hospital and Medical Center, Cincinnati, OH, 3Pediatric Rheumatology Collaborative Study Group (PRCSG), Cincinnati Children’s Hospital Medical Center, Cincinnati, OH

Meeting: 2018 ACR/ARHP Annual Meeting

Keywords: Environmental factors and systemic lupus erythematosus (SLE), Lupus

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Session Information

Date: Tuesday, October 23, 2018

Title: Systemic Lupus Erythematosus – Clinical Poster III: Treatment

Session Type: ACR Poster Session C

Session Time: 9:00AM-11:00AM

Background/Purpose: Air pollution may contribute to many autoimmune diseases including systemic lupus erythematosus (SLE), but limited information is available on its role in the onset and progression of SLE. The objective of the current study was to determine the relationship between air pollution exposure and characteristics associated with expression and severity of SLE.

Methods: In this retrospective cohort study, we identified patients with childhood onset SLE (cSLE) residing in the greater Cincinnati, OH region at the time of their SLE diagnosis and being followed for their care at Cincinnati Children’s Hospital Medical Center (CCHMC). Demographic and clinical information at the time of diagnosis were extracted from our cSLE cohort, and included phenotypic information on SLE (1997 American College of Rheumatology classification criteria) and SLE disease activity index (SLEDAI). Patients’ home address at the time of diagnosis was geocoded. Exposure to traffic-related pollutants was estimated for each participant by calculating the distance to the nearest major road. In addition, a previously developed and validated land-use regression model for the study region was applied to estimate the concentrations of elemental carbon attributable to traffic (ECAT), a surrogate marker for traffic related air pollution and specifically attributable to diesel exhaust. SLEDAI scores were categorized as high (> 8) or low to moderate activity (≤8). ECAT concentrations were log transformed and logistic regression was used to estimate the association between air pollution exposures and SLEDAI (high/low) and ACR classification criteria for phenotypic expression of disease.

Results: The cSLE patients’ (n = 158) mean age at diagnosis was 16.9 (SD 4.2) years. The majority (76.7%) were female with nearly equal representation of Caucasians and African Americans (42.1% and 41.5%, respectively). ECAT exposures were not associated with overall disease activity (SLEDAI) (Odds Ratio (OR) 1.4 (95% CI 0.3 – 7.1). However, as shown in Table 1with higher ECAT exposures there was a significantly increased risk for renal involvement (OR = 3 (95% CI 1.0- 8.7)) also a trend towards experience more commonly serositis (OR = 3.8 (95% CI 0.8 – 18.2)).

Conclusion: Our preliminary study suggests that environmental exposure to air pollution is associated with increased risk for certain manifestations of cSLE. Further work is needed to establish longitudinal effect of air pollution on the disease activity and cumulative damage and cSLE phenotypes over time.

TABLE 1: Logistic Regression Analysis of log (ECAT) values versus presence of phenotypic features of cSLE at disease onset

Dependent Variable

(ACR classification Criteria)

log (ECAT)

OR

95% CI

P value

Malar rash

0.631

0.223 – 1.784

0.3852

Discoid rash

1.972

0.485 – 8.019

0.3425

Photosensitivity

1.184

0.419 – 3.347

0.7505

Mucosal ulcers

0.540

0.185 – 1.578

0.2602

Arthritis

0.785

0.241 – 2.556

0.6880

Serositis

3.806

0.795 – 18.224

0.0944

Renal

2.991

1.026 – 8.720

0.0448

Neurologic

1.159

0.290 – 4.631

0.8341

Hematologic

1.082

0.348 – 3.366

0.8920

Immunologic

0.653

0.198 – 2.154

0.4837

ANA

1.071

0.127 – 9.070

0.9495

ECAT = elemental carbon attributable to traffic; ACR = American College of Rheumatology; ANA = Antinuclear antibody


Disclosure: G. Gulati, None; C. Brokamp, None; P. Ryan, None; H. I. Brunner, Novartis, Genentech, Pfizer, UCB, Lilly, Janssen, Ablynx, AbbVie, Bristol-Myers Squibb, EMD Serono, Astrazeneca, 5,Genentech and Novartis, 8.

To cite this abstract in AMA style:

Gulati G, Brokamp C, Ryan P, Brunner HI. Exposure to Air Pollution and the Onset and Progression of Systemic Lupus Erythematosus [abstract]. Arthritis Rheumatol. 2018; 70 (suppl 9). https://acrabstracts.org/abstract/exposure-to-air-pollution-and-the-onset-and-progression-of-systemic-lupus-erythematosus/. Accessed .
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