Simple Siliceous Pneumoconiosis in Negev Bedouins

Bar‐Ziv, Jacob; Goldberg, Gil M.

doi:10.1080/00039896.1974.10666548

Cited by 65 publications

(20 citation statements)

References 1 publication

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“…This circumstance together with the statistically significant connection between the presence of dustladen macrophage aggregates and such fibrotic conditions that are not related to echinococcosis and chronic pneumonia in our material, warrants the diagnosis of silicosis. Siliceous pneumoconiosis in people living in the North Saharan deserts has not been considered as a clinically significant condition, partly since the classic silicotic type of fibrosis was not present (POLICARD and COLLET, 1952;BAR-ZIV and GOLDBERG, 1974). The clinical significance of silicosis in camels, however, cannot be assessed from the present material.…”

Section: Discussionmentioning

confidence: 73%

Silicate Pneumoconiosis in Camels (Camelus Dromedarius L.)

Hansen

Jama

Nilsson

et al. 1989

Journal of Veterinary Medicine Series A

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Summary In a random screening of camel diseases in Somalia dust‐laden macrophages in lungs and/or bronchial lymph nodes were discovered in 94 of 134 animals. In 44 cases the dust‐laden macrophages occurred in a number of small or large aggregates. There was a significant positive correlation between dust‐laden macrophage aggregates in the lungs and pulmonary fibrosis not related to other chronic lung diseases, such as echinococcosis and chronic pneumonia. Six cases showed a cellular reaction and hyalinized nodules of the classic silicotic type. Energy dispersive X‐ray analysis of the dust particles revealed presence of silica, aluminium, potassium and iron in that order. The possible clinical significance as well as the comparative pathology of the observations is discussed. Zusammenfassung Silikat‐Pneumokoniose bei Kamelen (Camelus dromedarius L.) Bei einer randomisierten Erhebung über Kamel‐Krankheiten in Somalia wurden bei 94 von 134 Tieren staubbeladene Makrophagen in der Lunge und/oder in den bronchialen Lymphknoten gefunden. In 44 Fällen kamen die staubbeladenen Makrophagen teilweise als kleine oder große Ansammlungen vor. Zwischen den Ansammlungen von staubbeladenen Makrophagen in der Lunge und der nicht mit anderen chronischen Lungenerkrankungen, wie z. B. Echinokokkose und chronischer Pneumonie, in Zusammenhang stehenden Fibrose ergab sich eine signifikante positive Korrelation. Sechs Fälle zeigten eine zelluläre Reaktion und hyaline Knötchen vom klassischen silikotischen Typ. Die Röntgenstrahl‐Dispersions‐Analyse der Staubpartikel ergab in abfallender Reihenfolge die Anwesenheit von Siliziumoxyd, Aluminium, Kalium und Eisen. Die Beobachtungen werden bezüglich der möglichen klinischen Bedeutung sowie hinsichtlich der vergleichenden Pathologie diskutiert.

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Section: Discussionmentioning

confidence: 73%

Silicate Pneumoconiosis in Camels (Camelus Dromedarius L.)

Hansen

Jama

Nilsson

et al. 1989

Journal of Veterinary Medicine Series A

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“…In some of them, a fibrotic reaction of the lung parenchyma in terms of silicosis has been reported [16]. These observations have been interpreted as typical morphological findings of silica containing dust deposits due to sand dust inhalation during desert storms, a characteristic observation in recent populations of the Sahara and Negev deserts [2,13]. The latter study [13] also clearly demonstrated the presence of silica crystals in the affected lung tissue by radiodiffraction analysis, so that it seems fair to assume that our historic patient suffered from the same condition, although we could not prove the presence of silica crystals in our patient by chemical or radiodiffraction methods.…”

Section: Discussionmentioning

confidence: 87%

Extensive pulmonary haemorrhage in an Egyptian mummy

Nerlich

Parsche²,

Wiest

et al. 1995

Vichows Archiv A Pathol Anat

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We report on the morphological and trace element findings of several internal organs from an Egyptian mummy approximately dating from the year 950 B.C. according to 14C-analysis. By use of a multidisciplinary approach we succeeded in discovering evidence for severe and presumably recurrent pulmonary bleeding during life. This was suggested by the finding of massive haemosiderin deposits in the lung and a selectively and markedly elevated level of iron in trace element analysis of the lung tissue. Furthermore, we observed an enhanced deposition of birefringent particles in the lung tissue, without significant fibrosis. The histological analysis of liver, stomach and intestine confirmed the macroscopic organ diagnoses without evidence of any major pathological processes. In addition, analysis for various drugs revealed a significant deposition of tetrahydrocannabinol (THC), nicotine and cocaine in several organs of the mummy. The concentration profiles additionally provide evidence for a preferential inhalation of THC, while nicotine and cocaine containing drugs seem to have been consumed orally.

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“…Increased collagen is frequently observed in the lungs of cigarette smokers,53–55 and irregular opacities reflecting this fibrosis can be observed on their chest X-rays comparable to those in pneumoconioses 23,56–58. Collagen deposition and fibrosis in the human lung have been described following exposure to ambient air pollution particles,59 environmental exposure to crustal particles (eg, windstorms),60,61 and inhalation of emission source particles 62. This fibrogenic property of particles is exploited therapeutically with the instillation of gram quantities of a mineral oxide (ie, talc) particle into the pleural space to provide sclerosis 63…”

Section: Particle-related Lung Injurymentioning

confidence: 99%

Lung injury after cigarette smoking is particle related

Sangani¹,

Ghio

2011

COPD

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The specific component responsible and the mechanistic pathway for increased human morbidity and mortality after cigarette smoking are yet to be delineated. We propose that 1) injury and disease following cigarette smoking are associated with exposure to and retention of particles produced during smoking and 2) the biological effects of particles associated with cigarette smoking share a single mechanism of injury with all particles. Smoking one cigarette exposes the human respiratory tract to between 15,000 and 40,000 μg particulate matter; this is a carbonaceous product of an incomplete combustion. There are numerous human exposures to other particles, and these vary widely in composition, absolute magnitude, and size of the particle. Individuals exposed to all these particles share a common clinical presentation with a loss of pulmonary function, increased bronchial hyperresponsiveness, pathologic changes of emphysema and fibrosis, and comorbidities, including cardiovascular disease, cerebrovascular disease, peripheral vascular disease, and cancers. Mechanistically, all particle exposures produce an oxidative stress, which is associated with a series of reactions, including an activation of kinase cascades and transcription factors, release of inflammatory mediators, and apoptosis. If disease associated with cigarette smoking is recognized to be particle related, then certain aspects of the clinical presentation can be predicted; this would include worsening of pulmonary function and progression of pathological changes and comorbidity (eg, emphysema and carcinogenesis) after smoking cessation since the particle is retained in the lung and the exposure continues.

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Simple Siliceous Pneumoconiosis in Negev Bedouins

Cited by 65 publications

References 1 publication

Silicate Pneumoconiosis in Camels (Camelus Dromedarius L.)

Silicate Pneumoconiosis in Camels (Camelus Dromedarius L.)

Extensive pulmonary haemorrhage in an Egyptian mummy

Lung injury after cigarette smoking is particle related

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