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1.
Radiologie (Heidelb) ; 64(8): 636-642, 2024 Aug.
Artículo en Alemán | MEDLINE | ID: mdl-39012478

RESUMEN

A variety of workplace exposures (organic or inorganic dusts as well as gases, fumes, or vapors) can cause diffuse interstitial lung disease. The latency period until onset of the disease can exceed 30 years. The disease course varies greatly and depends on the quantity of the inhaled substance and its fibrogenic effect. Pulmonary high-resolution computed tomography (HRCT) patterns do not differ significantly from those of interstitial lung diseases (ILD) of other etiologies. Therefore, without knowledge of the occupational history, work-related ILDs are often classified as idiopathic. In addition, there is increasing evidence in the recent literature that high exposure to silica dust can trigger autoimmune diseases (also involving the lungs). For this reason, a qualified occupational history is now an indispensable part of the interdisciplinary diagnosis of ILDs.


Asunto(s)
Enfermedades Pulmonares Intersticiales , Enfermedades Profesionales , Humanos , Enfermedades Pulmonares Intersticiales/etiología , Enfermedades Pulmonares Intersticiales/diagnóstico , Enfermedades Pulmonares Intersticiales/epidemiología , Enfermedades Profesionales/etiología , Enfermedades Profesionales/diagnóstico , Tomografía Computarizada por Rayos X , Exposición Profesional/efectos adversos
2.
Biomedicines ; 10(10)2022 Oct 21.
Artículo en Inglés | MEDLINE | ID: mdl-36289927

RESUMEN

Alumina nanoparticles (Al2O3 NPs) can be released in occupational environments in different contexts such as industry, defense, and aerospace. Workers can be exposed by inhalation to these NPs, for instance, through welding fumes or aerosolized propellant combustion residues. Several clinical and epidemiological studies have reported that inhalation of Al2O3 NPs could trigger aluminosis, inflammation in the lung parenchyma, respiratory symptoms such as cough or shortness of breath, and probably long-term pulmonary fibrosis. The present review is a critical update of the current knowledge on underlying toxicological, molecular, and cellular mechanisms induced by exposure to Al2O3 NPs in the lungs. A major part of animal studies also points out inflammatory cells and secreted biomarkers in broncho-alveolar lavage fluid (BALF) and blood serum, while in vitro studies on lung cells indicate contradictory results regarding the toxicity of these NPs.

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