It's well known that cigarette smoking can increase one's risk of getting rheumatoid arthritis (RA). Researchers now are learning other environmental contaminants also may increase the risk.
UNMC researchers set out to determine the association between inhalant exposures with rheumatoid arthritis-related autoantibodies and severity in U.S. veterans. The results were recently published in Arthritis & Rheumatology.
Other UNMC research collaborators, who also are affiliated with the VA Nebraska-Western Iowa Health Care System, include:
- Ted Mikuls, MD;
- Geoffrey Thiele, PhD;
- Jill Poole, MD; and
- Ariadne Ebel, DO, rheumatology fellow and manuscript first author.
Other participating institutions were:
- The University of Nebraska-Lincoln;
- Philadelphia VA and the University of Pennsylvania;
- Salt Lake City VA and the University of Utah in Salt Lake City;
- Birmingham VA and the University of Alabama at Birmingham;
- Washington, D.C. VA and Georgetown and Howard University in Washington, D.C.;
- Dallas VA and University of Texas Southwestern in Dallas;
- Portland VA and Oregon Health Science University in Portland;
- the University of Washington in Seattle; and
- Pittsburgh VA and the University of Pittsburgh.
One of the study's main conclusions found that military burn pit and military waste disposal exposures were associated with rheumatoid arthritis autoantibody expression, thus, may affect the risk of developing rheumatoid arthritis.
"What we inhale from our environment may affect our risk of developing rheumatoid arthritis by stimulating our immune system to produce pathogenic antibodies," said Bryant England, MD, PhD, assistant professor in the UNMC Department of Internal Medicine-Division of Rheumatology & Immunology and Omaha VA Medical Center. "Among the most important findings was the association between military burn pits and waste disposal exposures with rheumatoid arthritis. Autoantibodies were strongest in individuals who also had a genetic background that predisposes them to rheumatoid arthritis-related autoimmunity."
Dr. England, who is senior author of the paper, said the study's conclusion supports the concept that both genetic and environmental factors drive rheumatoid arthritis-autoimmunity and rheumatoid arthritis risk. He said the findings are consistent with emerging evidence that various inhalant exposures influence autoantibody expression and rheumatoid arthritis risk.
Data for the study came from surveys mailed to participants in the Veterans Affairs Rheumatoid Arthritis Registry as well as clinical data in the registry of the 797 study participants. Researchers assessed occupational, agricultural and military inhalant exposures with rheumatoid arthritis-related factors.
Study participants who responded were older, more often white or male, less frequent smokers, and had lower disease activity.
The study was funded by the Central States Center for Agricultural Safety and Health headquartered at UNMC.
Dr. England said there is emerging evidence that rheumatoid arthritis-related autoimmunity may start outside of the joints at mucosal surfaces, including in the lungs.
"While smoking has been recognized as the strongest environmental risk factor for rheumatoid arthritis, it is little understood about how other inhalant exposures may affect rheumatoid arthritis risk," Dr. England said.
He hopes the study findings will encourage other researchers to continue to study various inhalants as risk factors for the development of rheumatoid arthritis.
"Ultimately, we hope to uncover mechanisms that may help us treat rheumatoid arthritis and rheumatoid arthritis-related lung disease better and pursue a long-term goal of preventing rheumatoid arthritis and rheumatoid arthritis-related lung disease," Dr. England said.