Find information on thousands of medical conditions and prescription drugs.

Silicosis

Silicosis (also known as Grinder's disease) is a form of pneumoconiosis caused by inhalation of crystalline silica dust, and is marked by inflammation and scarring in forms of nodular lesions in the upper lobes of the lungs. more...

Home
Diseases
A
B
C
D
E
F
G
H
I
J
K
L
M
N
O
P
Q
R
S
Sabinas brittle hair...
Saccharopinuria
Sacral agenesis
Saethre-Chotzen syndrome
Salla disease
Salmonellosis
Sandhoff disease
Sanfilippo syndrome
Sarcoidosis
Say Meyer syndrome
Scabies
Scabiophobia
Scarlet fever
Schamberg disease...
Schistosomiasis
Schizencephaly
Schizophrenia
Schmitt Gillenwater Kelly...
Sciatica
Scimitar syndrome
Sciophobia
Scleroderma
Scrapie
Scurvy
Selachophobia
Selective mutism
Seminoma
Sensorineural hearing loss
Seplophobia
Sepsis
Septo-optic dysplasia
Serum sickness
Severe acute respiratory...
Severe combined...
Sezary syndrome
Sheehan syndrome
Shigellosis
Shingles
Shock
Short bowel syndrome
Short QT syndrome
Shprintzen syndrome
Shulman-Upshaw syndrome
Shwachman syndrome
Shwachman-Diamond syndrome
Shy-Drager syndrome
Sialidosis
Sickle-cell disease
Sickle-cell disease
Sickle-cell disease
Siderosis
Silicosis
Silver-Russell dwarfism
Sipple syndrome
Sirenomelia
Sjogren's syndrome
Sly syndrome
Smallpox
Smith-Magenis Syndrome
Sociophobia
Soft tissue sarcoma
Somniphobia
Sotos syndrome
Spasmodic dysphonia
Spasmodic torticollis
Spherocytosis
Sphingolipidosis
Spinal cord injury
Spinal muscular atrophy
Spinal shock
Spinal stenosis
Spinocerebellar ataxia
Splenic-flexure syndrome
Splenomegaly
Spondylitis
Spondyloepiphyseal...
Spondylometaphyseal...
Sporotrichosis
Squamous cell carcinoma
St. Anthony's fire
Stein-Leventhal syndrome
Stevens-Johnson syndrome
Stickler syndrome
Stiff man syndrome
Still's disease
Stomach cancer
Stomatitis
Strabismus
Strep throat
Strongyloidiasis
Strumpell-lorrain disease
Sturge-Weber syndrome
Subacute sclerosing...
Sudden infant death syndrome
Sugarman syndrome
Sweet syndrome
Swimmer's ear
Swyer syndrome
Sydenham's chorea
Syncope
Syndactyly
Syndrome X
Synovial osteochondromatosis
Synovial sarcoma
Synovitis
Syphilis
Syringomas
Syringomyelia
Systemic carnitine...
Systemic lupus erythematosus
Systemic mastocytosis
Systemic sclerosis
T
U
V
W
X
Y
Z
Medicines

Silicosis (especially the acute form) is characterized by shortness of breath, fever, and cyanosis (bluish skin). It may often be misdiagnosed as pulmonary edema (fluid in the lungs), pneumonia, or tuberculosis.

This respiratory disease was first recognized in 1705 by Ramazzini who noticed sand-like substances in the lungs of stonecutters. The name silicosis (from the latin silex or flint) was attributed to Visconti in 1870.

Silica

Silica is the second most common mineral on earth. It is found in concrete, masonry, sandstone, rock, paint, and other abrasives. The cutting, breaking, crushing, drilling, grinding, or abrasive blasting of these materials may produce fine silica dust. It can also be in soil, mortar, plaster, and shingles. Silicosis is due to deposition of fine dust (less than 1μm in diameter) containing crystalline alpha-quartz silica or silicon dioxide.

The induction period between initial silica exposure and development of radiographically detectable nodular silicosis is usually 10 years. Shorter induction periods are associated with heavy exposures, and acute silicosis may develop within 6 months to 2 years following massive silica exposure.

Pathology

When the small silica dust particles are breathed into the lungs, they can embed themselves deeply into the tiny alveolar sacs and ducts where oxygen and carbon dioxide gases are exchanged. There, the lungs cannot clear out the dust by mucous or coughing.

When fine particles of silica dust are deposited in the lungs, macrophages that ingest the dust particles will set off an inflammation response by releasing tumor necrosis factor, interleukin-1, leukotriene B4 and other cytokines. In turn, these stimulate fibroblasts to proliferate and produce collagen around the silica particle, thus resulting in fibrosis and the formation of the nodular lesions.

Furthermore, the surface of silicon dust can generate silicon-based radicals that lead to the production of hydroxyl and oxygen radicals, as well as hydrogen peroxide, which can inflict damage to the surrounding cells.

Characteristic lung tissue pathology in nodular silicosis consists of fibrotic nodules with concentric "onion-skinned" arrangement of collagen fibers, central hyalinization, and a cellular peripheral zone, with lightly birefringent particles seen under polarized light. In acute silicosis, microscopic pathology shows a periodic acid-Schiff positive alveolar exudate (alveolar lipoproteinosis) and a cellular infiltrate of the alveolar walls.

Prevalence

Although silicosis has been known for centuries, the industrialization of mining has lead to an increase in silicosis cases. In the United States, a 1930 epidemic of silicosis due to the construction of the Hawk's Nest Tunnel near Gauley Bridge, West Virginia caused the death of more than 400 workers.

Read more at Wikipedia.org


[List your site here Free!]


From silicosis to 'litigosis'
From Risk & Insurance, 7/1/05 by Joseph A. Ziemianski

Like swirling dust, growing numbers of silica claims are stirring up the concern of businesses and their insurers, and raising the specter of fraud. Congress and many state legislatures, already poised to act on asbestos lawsuits, are now taking notice of silica litigation as well.

Sen. Aden Specter, chairman of the Senate Judiciary Committee, is supporting legislation to create an alternative claims processing system for workers injured by exposure to asbestos and silica. Florida's legislature approved a bill on May 5, that would require claimants alleging asbestos- or silica-related injury to meet specific medical criteria before pursuing their claims. Similar legislation passed or is pending in Ohio, Georgia and Texas.

Meanwhile, insurers and insure& must still address silica claims as they arise. So what steps should insurers take to evaluate such claims?

Here are some caveats to consider.

* Watch for fraud or "litigosis."

Silica claims frequently are presented en masse by hundreds or thousands of plaintiffs. Diagnoses often are made in an assembly-line process by one or two physicians or screeners chosen by attorneys. The potential for fraud in this environment is obvious. Motions for sanctions are pending against plaintiffs' attorneys in a Corpus Christi, Texas, federal district court based on allegations that the attorneys presented approximately 10,000 bogus silicosis (the respiratory disease caused by inhaling silica dust) claims. Dr. Gary Friedman of the Texas Lung Institute testified in the case that the only explanation was misdiagnosis--or, as he called it, "litigosis."

* Challenge the due diligence.

This potential for fraud makes it incumbent upon insurers and insureds with large self-insured retentions or fronting policies to act reasonably when handling silica claims. Facing a suit with thousands of plaintiffs, the tendency often is to avoid review of individual medical records and reach a settlement. The insureds and carriers will then turn to excess insurers for the settlement's funding. The excess insurers, however, can challenge the reasonableness of the settlement where it appears that an appropriate investigation was not conducted.

* Take advantage of timing.

Another problem with the "quick global settlement" approach is that it generally overlooks or downplays the timing of each claimant's exposure and diagnosis. Courts generally rely on exposure dates, diagnosis dates, or both, to determine which insurance policies are implicated or "triggered." Where this information is lacking, an insurer may deny coverage for claims.

* Use silica timing.

Many courts have ruled that, due to the harmful nature of asbestos, bodily injury takes place upon exposure and triggers all policies in effect during the exposure. With silica, there is often a tendency to follow asbestos cases. The inhalation of silica particles, however, does not necessarily mean that injury to lung tissue will occur. There is no evidence of adverse health effects from brief or casual exposure to silica dust. Insurers and insureds, therefore, can argue that policies should be triggered based on "manifestation" or diagnosis rather than on exposure. At a minimum, an exposure, to trigger a policy, should be of a type, degree and duration scientifically recognized as harmful.

When handling silica claims, it is critical for insurance adjusters and risk managers to keep an eye on the claims' demonstrated potential for fraud, the significant differences between silica and asbestos in both liability and coverage, and the importance of medical evidence at all stages of claims processing.

JOSEPH A. ZIEMIANSKI is a member of Cozen O'Connor's insurance litigation department and managing partner of its Houston office.

COPYRIGHT 2005 Axon Group
COPYRIGHT 2005 Gale Group

Return to Silicosis
Home Contact Resources Exchange Links ebay