Environmental dust inhalation in the European badger (Meles meles): Systemic distribution of silica-laden macrophages, pathological changes, and association with Mycobacterium bovis infection status

Chronic inhalation of crystalline silica and silicates may lead to severe lung disease in humans, termed silicosis. The disease is an occupational health concern in miners and related professions worldwide. Silicosis is also a strong risk factor for tuberculosis in humans. Due to its subterranean lifestyle, the European badger (Meles meles) is continuously exposed to environmental dust, while this species is also susceptible to tuberculosis, caused by Mycobacterium bovis. To date, a thorough investigation of mineral dust retention and its possible implication as a risk factor for mycobacterial infection in badgers has not been performed. The aims of this retrospective histological study were (1) to describe the systemic tissue distribution of silica-laden macrophages (SLMs) in badgers; (2) to compare the amount of SLMs in tissues of badgers of differing M. bovis infection status, pulmonary SLM burden and age; and (3) to assess whether inflammation was associated with SLMs. We assessed lung, lymph nodes, liver and spleen of 60 wild-caught badgers of known M. bovis infection status for the presence of SLMs using polarizing light microscopy. SLMs were consistently present within the lungs and were widely distributed throughout the lymphatic system. No inflammatory reaction to SLMs, as occurs in human silicosis, was observed in any tissue. Distribution and amount of SLMs were similar between M. bovis positive and negative badgers, and we were not able to show an association between the amount of SLMs and M. bovis infection status. The amount of SLMs within intra- and extrathoracic lymph nodes was positively associated with the amount of pulmonary SLMs, and with age. This is the first report of substantial and systemic tissue retention of mineral dust particles in a mammalian species lacking associated chronic inflammation (i.e. silicosis). We further highlight different pathogenetic mechanisms underlying silicosis and benign SLM accumulations following siliceous dust inhalation.