Silicotic lesions of the bone marrow: histopathology and microanalysis

Eide, Johan; Gylseth, B; Skaug, Vidar

doi:10.1111/j.1365-2559.1984.tb02381.x

Cited by 21 publications

(11 citation statements)

References 12 publications

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“…Thus, effects such as inflammation, oxidative stress and molecular cell activation are likely to occur not only in the primary organ of entry, but also in secondary target organs. Such effects are unlikely to occur with larger particles, except under lung particle overload conditions (silicosis of the liver, spleen, bone marrow [Eide et al ., 1984; Slavin et al ., 1985]) and in the case of asbestos-induced mesothelioma and associated lympho-hematogenic spread of asbestos fibers (Brown, 1974). An important caveat to keep in mind is that Table 1 refers to the particles themselves and not to any soluble fractions, either of the particle or of adsorbed materials.…”

Section: Concepts Of Inhalation Nanotoxicologymentioning

confidence: 99%

Nanoparticles and the Brain: Cause for Concern?

Oberdörster¹,

Elder²,

Rinderknecht³

2009

j nanosci nanotechnol

302

179

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Engineered nanoparticles (NPs) are in the same size category as atmospheric ultrafine particles, <100 nm. Per given volume, both have high numbers and surface areas compared to larger particles. The high proportion of surface atoms/molecules can give rise to a greater chemical as well as biological activity, for example the induction of reactive oxygen species in cell-free medium as well as in cells. When inhaled as singlet particles, NPs of different sizes deposit efficiently in all regions of the respiratory tract by diffusion. A major difference to larger size particles is the propensity of NPs to translocate across cell barriers from the portal of entry (e.g., the respiratory tract) to secondary organs and to enter cells by various mechanisms and associate with subcellular structures. This makes NPs uniquely suitable for therapeutic and diagnostic uses, but it also leaves target organs such as the central nervous system (CNS) vulnerable to potential adverse effects (e.g., oxidative stress). Neuronal transport of NPs has been described, involving retrograde and anterograde movement in axons and dendrites as well as perineural translocation. This is of importance for access of inhaled NPs to the central nervous system (CNS) via sensory nerves existing in the nasopharyngeal and tracheobronchial regions of the respiratory tract. The neuronal pathway circumvents the very tight blood brain barrier. In general, translocation rates of NP from the portal of entry into the blood compartment or the CNS are very low. Important modifiers of translocation are the physicochemical characteristics of NPs, most notably their size and surface properties, particularly surface chemistry. Primary surface coating (when NPs are manufactured) and secondary surface coating (adsorption of lipids/proteins occurring at the portal of entry and during subsequent translocation) can significantly alter NP biokinetics and their effects. Implications of species differences in respiratory tract anatomy, breathing pattern and brain anatomy for extrapolation to humans of NP effects observed in rodents need to be considered. Although there are anecdotal data indicating a causal relationship between long-term ultrafine particle exposures in ambient air (e.g., traffic related) or at the workplace (e.g., metal fumes) and resultant neurotoxic effects in humans, more studies are needed to test the hypothesis that inhaled nanoparticles cause neurodegenerative effects. Some, but probably not the majority of NPs, will have a significant toxicity (hazard) potential, and this will pose a significant risk if there is a sufficient exposure. The challenge is to identify such hazardous NPs and take appropriate measures to prevent exposure.

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Section: Concepts Of Inhalation Nanotoxicologymentioning

confidence: 99%

Nanoparticles and the Brain: Cause for Concern?

Oberdörster¹,

Elder²,

Rinderknecht³

2009

j nanosci nanotechnol

302

179

View full text Add to dashboard Cite

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“…Once in the circulation, it may be phagocytosed by the reticuloendothelial system of the spleen, liver, and bone marrow [2,3].…”

Section: Discussionmentioning

confidence: 99%

“…Extrapulmonary silicosis [1,2], with hepatosplenic silicosis as a special subcategory, is far less documented in the radiological literature [3,4], and to the best our knowledge, there is only one previous case report on splenic calcifications disclosed on CT scan [4].…”

Section: Discussionmentioning

confidence: 99%

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Hepatosplenic antracosilicosis: a rare cause of splenic calcifications

Vanhoenacker

Brande²,

Schepper

2001

Eur Radiol

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A case of a 62-year-old man with known longstanding pulmonary antracosilicosis, with associated hepatosplenic antracosilicosis, is presented. A CT scan of the upper abdomen revealed multiple calcifications within the spleen, and to a lesser degree within the subcapsular region of the liver, as well as "egg-shell" calcifications of abdominal lymph nodes, most noticeable at the splenic hilum. Although histopathologically not proven, the similar appearance of the calcified hepatosplenic nodules to the small round calcifications scattered throughout the lungs, as well as the typical "egg-shell" morphology of the calcified abdominal lymph nodes, should raise the suspicion of hepatosplenic antracosilicosis.

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“…Thus silica is not deposited only in the lungs; cells with phagocytic activity belonging to the mononuclear phagocyte system ofthe liver, spleen, and bone marrow may contain silica. 35 We do not know whether type A synoviocyte-that is, cells with the characteristics of phagocytising fixed tissue macrophages-eposit silica-within joint cavities. Interestingly, in addition to the secretion of a factor that-stimulates proliferation of lymphocytes and fibroblasts (interleukin 1),36 macrophages exposed to silica also secrete a factor(s) that stimulates deoxyribonucleic acid synthesis of human synovial cells in vitro.37…”

Section: Discussionmentioning

confidence: 99%

Silica exposure and rheumatoid arthritis: a follow up study of granite workers 1940-81.

Klockars

Koskela

Järvinen

et al. 1987

BMJ

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The incidence and prevalence of subjects awarded disability pensions and the prevalence of subjects receiving free medicines because of rheumatoid arthritis were studied in a Finnish cohort of 1026 granite workers hired between 1940 and 1971 and followed up until 31 December 1981. The incidence of awards of disability pensions because of rheumatoid arthritis during 1969-81, the prevalence of rheumatoid arthritis on 31 December 1981, and the prevalence of subjects receiving free medicines for rheumatoid arthritis at the end of 1981 were significantly higher among the granite workers than in the general male population of the same age. Retrospective analysis ofthe records ofall patients with rheumatoid arthritis in the cohort showed a predominance of a severe, serologically positive and erosive form ofrheumatoid arthritis, usually with an age at onset of 50 or over.The possible aetiological or pathophysiological role ofgranite dust in rheumatoid arthritis may be based on the effects of quartz on the immune system.

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Silicotic lesions of the bone marrow: histopathology and microanalysis

Cited by 21 publications

References 12 publications

Nanoparticles and the Brain: Cause for Concern?

Nanoparticles and the Brain: Cause for Concern?

Hepatosplenic antracosilicosis: a rare cause of splenic calcifications

Silica exposure and rheumatoid arthritis: a follow up study of granite workers 1940-81.

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