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Mold-Exposure and Sarcoidosis Risk

Sarcoidosis is an immune lung condition involving the formation of granulomas, clusters of inflammation surrounded by immune cells and other tissues.

Immune Dysfunction and Environmental Risk

At heart, sarcoidosis is an immune condition triggered by a breakdown in regulatory T cells, also known as Tregs. The granuloma forms when a particle irritates the lungs and stimulates a walling off process. An aberrant inflammatory cascade causes macrophages around the particle to transform into a barrier.

According to environmental specialist Dr. Scott McMahon, Chronic Inflammatory Response Syndrome, an immune disorder triggered by damp building exposure, causes low levels of Tregs—the necessary precondition for granuloma formation. By its effect on Tregs, Dr. McMahon reasons that since Chronic Inflammatory Response Syndrome can be linked to the development of any granulomatous disease.

One study found a link between environmental factors and sarcoidosis risk.(1) The authors noted “the prevailing view suggests that sarcoidosis occurs as the consequence of exposure to one or more environmental agents interacting with genetic factors.” In 706 newly diagnosed sarcoidosis subjects across ten medical centers, study participants answered questions regarding work and nonoccupational exposure.

Compared with healthy controls, the subjects showed significant increases in agricultural employment (46% risk increase), insecticide exposure at work (61% risk increase), and exposure to musty odors (62% risk increase).

The authors noted the significance of musty odors which indicate fungal contamination and increased volatile organic compounds, noxious gasses exuded during the mold’s active growth state. Moreover, sarcoidosis risks increased in subjects reporting central air conditioner use. The authors concluded:

“Our results, in context with several previous studies, add to mounting evidence linking microbial bioaerosols to sarcoidosis risk.”

The HLA Gene — A Key Genetic Risk Factor

A group of genetic factors, known as HLA, showed significantly elevated risk of sarcoidosis.(2)

In a study of 58 patients, researchers found an increased frequency of an HLA subtype (HLA-DRw52). Subjects with this gene exhibited a higher prevalence of sarcoidosis—but they also showed high levels of spontaneous disease resolution. This finding led the Japanese research team to conclude that the gene affected the sarcoidosis onset, but not its persistence.

Another research group found various HLA subtypes to be associated with sarcoidosis presentation. (3) Acute disease onset was observed in patients with HLA DRB1*3 or HLA DQB1*0201. A chronic form of sarcoidosis was associated with HLA DRB1*15 and HLA DQB1*0601. Certain HLA makers predicted disease progression while others conferred disease protection. The study author’s posited:

“It is conceivable that both resolving and persistent sarcoidosis arise due to a unique combination of a specific genetic background and exposure to one or several environmental triggers.”


1. Newman, Lee S., et al. “A case control etiologic study of sarcoidosis: environmental and occupational risk factors.” American journal of respiratory and critical care medicine170.12 (2004): 1324-1330.

2. Abe, Shosaku, et al. “Association of HLA-DR with sarcoidosis: correlation with clinical course.” Chest 92.3 (1987): 488-490.

3. Broos, Caroline E., et al. “Granuloma formation in pulmonary sarcoidosis.” Frontiers in immunology 4 (2013): 437.