"Occupational inorganic and coal dust exposures can be broadly categorized as strongly fibrogenic dusts (silica, asbestos, and coal) and other inorganic dusts and metal fumes that may also be associated with adverse respiratory effects (e.g., iron, emery, graphite, gypsum, marble, mica, perlite, plaster of Paris, Portland cement, silicon, silicon carbide, soapstone, talc, and welding fume particles." [Asthma in the Workplace, p. 378]

"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]

Revised: May 30, 2018

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