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This
publication is made possible by an educational grant from Amgen Inc.
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Volume 51, Number 10
The Role of
Environmental Factors in Rheumatic Diseases
Daniel J. Wallace, MD
Michael H. Weisman, MD
Division of Rheumatology
Cedars-Sinai Medical Center/UCLA School of Medicine
Los Angeles, CA
Summary Points
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It
is difficult to know if there is any causal relationship between
environmental factors and rheumatic diseases because of the difficulty in
obtaining sufficient numbers of patients and adequate controls and defining
the exposure.
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There
are some examples of environmental agents inducing rheumatic diseases,
including contaminated rapeseed oil causing a scleroderma-like disease and
contaminated L-tryptophan causing eosinophilic myalgia syndrome.
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Ultraviolet
light may trigger lupus, and smoking may aggravate or worsen a number of
rheumatic diseases.
Introduction
Rheumatic
and autoimmune disorders stem from a combination of factors. The current
accepted hypothesis is that in the presence of certain susceptibility genes,
drugs, chemicals, and other agents in the environment are thought to play
inciting roles.
Over the last 30 years, progress has been
made in defining the epidemiology
of rheumatoid arthritis, systemic lupus erythematosus, scleroderma, inflammatory
myopathy, the
vasculitides, polymyalgia rheumatica, and the seronegative
spondyloarthropathies. Investigators have
been able to elucidate incidence, prevalence,
mortality rates, as well as age, sex, racial, and comorbid associations. Candidate
genes or putative genetic associations have
been identified for nearly all of these diseases.
Our
understanding of the role
of the environment has been less successful (1).
In place of scientific evidence, unsubstantiated theories of the role of certain
non-infectious environmental agents (eg, contaminated ground water causes lupus
and scleroderma) has led to costly litigation and an industry that has been
called “junk science” (2).
The lack of substantiated work in this area has resulted in confusion among
organizations that advocate for
patients with rheumatic diseases. In an Arthritis & Rheumatism
editorial, Rose concluded that “establishing a cause-and-effect relationship
between an agent and a disease…requires a valid statistical association
between the putative agent and the disease, and a feasible biologic mechanism to
account for the association” (3).

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