Pneumoconioses

"Occupational mineral dust exposures can be broadly categorized as strongly fibrogenic dusts (silica, asbestos, and coal) and other mineral dusts (emery, graphite, gypsum, marble, mica, perlite, plaster of Paris, Portland cement, silicon, silicon carbide, soapstone, and talc) that may also be associated with adverse lung effects." [Asthma in the Workplace, p. 685]

"Proper mineralogic analysis of samples of an ore body taken from different locations and ongoing analysis of environmental samples from the workplace are crucial in the recognition, evaluation, and control of potential pulmonary health risks." [Rosenstock, p. 408]

"The development of pneumoconiosis typically requires 5 or more years of exposure to the causative agent(s) with a latency between exposure and diagnosis of 10 or more years." [Hendrick, p. 164]

"Upper airway filter mechanisms are usually highly efficient at preventing any particle larger than 10 um in diameter from reaching the tracheobronchial tree." [Hendrick, p. 166]

"It is suspected that this lung airway defense system can be overcome by several different mechanisms: by the physical characteristics of the particle that prevent phagocytosis or cell movement, as seen in asbestosis; by direct cytotoxicity, as in the case of silica dust or cytoxic metals and compounds; or by simply overloading the clearance capacity of the system, which is most likely the mechanism of injury from normally non-fibrogenic 'nuisance' dusts." [Hendrick, p. 167]

"The authors of a 1990 review concluded that (1) there is little evidence that occupational exposure to pure kaolin, talc, mica, or vermiculite carries any important risk for health; (2) long and heavy exposure to kaolin and mica may result in low-grade radiographic changes, but clinically important pneumoconioses in work forces exposed to these phyllosilicates are likely to be the result of contamination by silica or asbestos fiber;" [Murray, p. 1773-1774]

"Compared with asbestos, silica, and coal there is only limited toxicologic or epidemiological evidence linking the other minerals considered here with diffuse parenchymal lung diseases." [Hendrick, p. 169]

Table 3--Pneumoconioses Caused by Silicates and Other Dusts  

Pneumoconioses, Other

Pneumoconioses, Benign

Ores May Be Asbestos Contaminated

Ores May Be Silica Contaminated

Alumina (Al2O3)

 

 

 

MD

Antimony*

MAD

D

 

DS

Baritosis*

 

MDS

 

MAD

Bentonite

 

A

 

AS

Chromite

MAS

 

 

 

Dental technician

A

 

 

 

Diatomaceous

AS

 

 

A

Flock

A

 

 

 

Fuller's earth

M

 

A

S

Graphite

ADS

 

 

DS

Gypsum

S

 

 

 

Kaolin

M

 

 

DS

Mica

MADS

 

 

D

Oil shale

ADS

 

 

ADS

Perlite

 

S

 

M

Phosphate

S

 

 

 

Polyvinyl chloride

A

 

 

 

Potash

 

S

 

 

Refractory ceramic fibers

D

 

 

 

Siderosis*

M

MADS

 

M

Silicon carbide

A

 

 

 

Stannosis*

 

MADS

 

MAD

Talc

M

 

MADS

MADS

Titanium dioxide

M

A

 

 

Trona

 

AS

 

 

Vermiculite

 

 

D

D

Wollastonite

A

 

 

 

*Highly opaque to x-rays, relative to other minerals;

M Mapel (Hendrick, 2002)      A Antou (Rom, 2006)      D Donovan (Rosenstock, 2005)      S Short (Harber, 1996)

Examples of mixed dust pneumoconioses include:

  1. Labrador lung (iron ore miners exposed to silica);

  2. Anthrasilicosis (coal miners);

  3. Silicoaluminosis (alumina abrasive workers);

  4. Argyriasiderosis (silver finishers); [Rom, p. 525]

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Revised: March 14, 2013

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