Acute Silicosis

Acute Silicosis

A complication of intense exposure to respirable crystalline silica, associated with sandblasting, coal mining, or any other job in which there is heavy exposure to fine particulate silica. Unlike classic silicosis, acute silicosis appears within a few weeks to 5 years of initial exposure. 
Occupations Abrasive (sand) blasting, mining, quarrying, manufacture of abrasives—including abrasive soaps, tunnelling, foundry work, glass manufacture, ceramic and pottery production, and cement and concrete production.
Clinical findings Rapid onset of severe respiratory impairment, dyspnoea, cough, weakness, weight loss, often leading to death.
Imaging, chest Multifocal ground glass appearance and air space consolidation.
DiffDx Pneumonia, pulmonary oedema, alveolar haemorrhage, bronchioloalveolar cell cancer.
References in periodicals archive ?
Accelerated silicosis occurs after 5-10 years of exposure to higher silica levels, and acute silicosis can occur after only weeks or months of exposure to extremely high silica concentrations.
The onset of symptoms takes longer than in acute silicosis.
Acute silicosis occurs after a few months or as long as two years following exposures to extremely high concentrations of respirable crystalline silica.
4 It occurs in three ways chronic silicosis which is progressive lung disease characterized by development of scar in response to inhalation of silicates bearing dusts; acute silicosis is the destruction of airways in order for the lungs to become heavy and rigid as air spaces are filled with granular silicate particles and accelerated silicosis which is exposure to silica dusts of almost pure quartz in which the victims show no clinical abnormalities until the condition becomes acute resulting in a decrease of lung function.
Acute silicosis responding to corticosteroid therapy.
Because apoptosis is believed to play an essential role in the inflammation associated with one pneumoconiosis, acute silicosis, and because inflammation increased as CYP1A1 activity decreased in the rat model of coal workers' pneumoconiosis (Ghanem et al.
Apoptosis underlies immunopathogenic mechanisms in acute silicosis.
But acute silicosis can occur after only a few months of extremely high concentrations of respirable silica.
Sand blasters, rock drillers, and silica-flour millers all face a high risk of acute silicosis, a life-threatening inflammatory disease that disables its victims--sometimes in as little as 5 years--by killing lung cells and letting their liquids leak out.
Cherniak estimates that acute silicosis killed several hundred of the 5,000 men employed on the project and sickened or disabled as many as 1,500 more.
This would be consistent with the decedent developing acute silicosis after an extremely high exposure to respirable crystalline silica.
Shorter induction periods are associated with heavy exposures, and acute silicosis might develop within months after massive silica exposure.

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