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

Janne M Schoening,Alan Wolfe,Joseph P Cassidy,Leigh A L Corner,Locksley L Mcv Messam,Philip J Hogarth

doi:10.1371/journal.pone.0190230

Abstract

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.

Highlights

Silicon dioxide (SiO2), in its crystalline form alone or in combination with various trace elements, e.g. Al, Fe, Mg and others, constitutes a wide variety of rocks and sands worldwide, and is a major component of inorganic dusts [1].Finely ground and aerosolized silica and silicates pose an occupational health hazard to mine workers, sandblasters and related professions, where persistent inhalation leads to silicosis, a chronic-progressive fibrosing lung disease [2, 3]
silica-laden macrophages (SLMs) were widely distributed throughout the lungs and lymphatic system
No inflammatory response or excess fibrous tissue associated with the presence of SLMs was microscopically detectable in any of these routinely stained sections (Fig 2A and 2B)

Summary

Introduction

Ground and aerosolized silica and silicates pose an occupational health hazard to mine workers, sandblasters and related professions, where persistent inhalation leads to silicosis, a chronic-progressive fibrosing lung disease [2, 3]. Crystalline silica is toxic to alveolar macrophages, leading to the formation of reactive oxygen species among other cytotoxic effects [8,9,10,11]. Silica inhalation in the absence of chronic disease, are strong risk factors for tuberculosis in miners [14,15,16,17]. While the exact underlying pathogenesis of this relationship remains unclear, modulatory effects of silica on pulmonary immune function, including macrophage activity, have been suggested [18, 19]

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Discussion

Conclusion