Occupational silica exposure could trigger MPA in some cases: Report
Kidney problems seen in man with genetic predisposition exposed at work
Occupational exposure to silica, one of the most common minerals in the earth’s crust, may lead to microscopic polyangiitis (MPA) — a type of ANCA-associated vasculitis — particularly in individuals with a genetic predisposition to autoimmune diseases, a case report suggests.
Silica, found in sand and rocks, is known to stimulate inflammatory reactions. In fact, silicosis is an occupational lung disease common among those exposed to the mineral that can cause kidney injury and lead to more autoimmune conditions.
In a recent report, a team of researchers in Turkey detailed the case of a 29-year-old man with kidney dysfunction linked to silica exposure who was diagnosed with MPA associated with silicosis.
“Considering that the use and therefore frequency of exposure to silica is increasing with industrial development, awareness should be raised of not only the pulmonary effects of silicosis but also the renal [kidney] damage,” the researchers wrote.
The case report, “Occupational Silica Exposure as a Potential Risk for Microscopic Polyangiitis,” was published in the journal Wilderness & Environmental Medicine.
Man in Turkey diagnosed with MPA after silica exposure at mine job
ANCA-associated vasculitis (AAV) is a group of autoimmune diseases characterized by inflammation and damage to small blood vessels, typically caused by ANCAs, self-reactive antibodies that bind to and activate neutrophils — a type of immune cell.
This is thought to occur due to a combination of genetics and environmental factors, such as the inhalation of silica.
Most people with MPA, the most common AAV type, carry antibodies targeting the protein myeloperoxidase, typically found close to and inside the cell nucleus. Patients usually don’t have granulomas, or masses of immune cells at sites of inflammation.
In this case, a man who had worked in a quartz mine for eight years was found to have kidney dysfunction associated with silica exposure. The researchers noted that the man did not use a silica dust protective mask for the first 3.5 years.
His family history included a sister and a niece with lupus, also an autoimmune disorder.
Silica exposure should be avoided, especially in patients with a familial history of autoimmune diseases, as in our patient.
The man was admitted to the emergency department with complaints of weakness, cough, a cough with blood on one occasion, and dark urine. A physical examination revealed coarse breath sounds, or crackles, and a fast heart rate.
Laboratory work detected high blood levels of creatinine, and high urine levels of protein and albumin, all indicative of kidney damage. The patient also had a high red blood cell sedimentation rate, a marker of inflammation.
A biopsy of lung tissue detected sites of inflammation and scarring, or fibrosis. Pneumoconiosis, a lung disease caused by the inhalation of dust, initially was considered as a potential diagnosis.
However, a thorax CT scan revealed a nodular and fibrotic appearance in both lungs, as well as enlarged lymph nodes. A further biopsy of the kidney showed inflammation and marked thickening of blood vessels, but no granulomas.
With all of these findings considered, the patient was diagnosed with MPA associated with silicosis.
The man started treatment with rituximab, a therapy that reduces the number of immune B-cells that produce ANCAs, along with steroids to reduce inflammation. After four cycles of rituximab, at day 82 of follow-up — nearly three months after beginning treatment — the patient’s blood creatinine lowered to normal levels.
According to the researchers, “silica exposure should be avoided, especially in patients with a familial history of autoimmune diseases, as in our patient.”
Exposed individuals should undergo routine screenings, the team added.
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