Background Information on Silica

Appendix A: Background Information on Silica

This appendix provides an overview of the following silica-related topics: the forms and sources of silica;
common industrial uses of silica and workplaces with silica exposure; history of silicosis; and health
effects associated with exposure. The reference list at the end of this appendix, as well as the expanded
bibliography in Appendix J, provide many sources that may prove useful to those interested in a more in depth treatment of these topics.

Introduction

“Silica,” is a term which refers broadly to the mineral compound silicon dioxide (SiO2). Silica can be
crystalline or amorphous. Crystalline silica is significantly more hazardous to employees than amorphous
silica. In addition to causing the disabling and irreversible lung disease known as silicosis, crystalline
silica has been classified as a human carcinogen by the International Agency for Research on Cancer
(IARC) [IARC, 1997]. As it is typically used in this document, “silica” refers specifically to crystalline silica.
Crystalline silica is characterized by a large scale, repeating pattern of silicon and oxygen atoms, as
distinguished from the more random arrangement found in amorphous silica. Abundant in the earth’s
crust, crystalline silica is a basic component of most classes of rock. Naturally-occurring forms of
amorphous silica include diatomaceous earth (the skeletal remains of marine organisms) and vitreous
silica or volcanic glass [Markowitz and Rosner, 1995; Davis, 1996].

Forms and Sources of Crystalline Silica

Crystalline silica occurs in three primary mineralogical forms, or polymorphs–quartz, cristobalite, and
tridymite. Silica is also called “free silica,” to distinguish it from the silicates, which are minerals containing
silicon dioxide bound to one or more cations [Beckett et al., 1997].
Quartz is by far the most common form of naturally-occurring silica [Davis, 1996; IARC, 1997].
Cristobalite and tridymite, which are molecularly identical to quartz, are distinguishable by their unique
crystalline structures. They are less stable than quartz, thus accounting for the dominance of the quartz
form. Quartz itself exists as either of two sub-polymorphs, alpha-quartz (also known as low quartz), and
beta-quartz (high quartz). Alpha-quartz is the thermodynamically stable form of crystalline silica and
accounts for the overwhelming portion of naturally-occurring crystalline silica [IARC, 1997].
Quartz is a major component of soils and is readily found in both sedimentary and igneous rocks,
although the quartz content varies greatly from one rock type to another. For instance, granite contains on
average about 30 percent quartz, and shales contain about 20 percent quartz. Natural stone, such as
beach sand or sandstone, may be nearly pure quartz [IARC, 1997; Davis, 1996].
Cristobalite and tridymite are natural constituents of some volcanic rock, and man-made forms result from
direct conversion of quartz or amorphous silica that has been subjected to high temperature or pressure.
Diatomaceous earth, composed of amorphous silica, crystallizes during heating (calcining), yielding a
calcined product that contains as much as 75 percent cristobalite.
Cristobalite is also found in the superficial layers of refractory brick that has been repeatedly subjected to
contact with molten metal [Markowitz and Rosner, 1995; Ganter, 1986; Cheng et al., 1992; Bergen et al.,
1994].

Major Industrial Sources of Crystalline Silica Exposure

Crystalline silica is an important industrial material and occupational exposure occurs across a broad
range of industries, including mining, manufacturing, construction, maritime, and agriculture (see
A-2
Appendix B for a listing of industries and Standard Industrial Classifications with potential for significant
occupational exposure). Processes associated historically with high rates of silicosis include sandblasting,
sand-casting foundry operations, mining, tunneling, and granite cutting.
Crystalline silica, in the form of finely ground quartz sand as an abrasive blasting agent, is used to
remove surface coatings prior to repainting or treating, a process that typically generates extremely high
levels of airborne respirable crystalline silica. A 1992 report published by the National Institute for
Occupational Safety and Health (NIOSH) estimates that there are more than one million U.S. employees
who are at risk for developing silicosis, and of these employees, more than 100,000 are employed as
sandblasters. Abrasive blasting is performed in a wide variety of different industries; the construction
industry employs the largest number of employees as abrasive blasters, concentrated in the special
trades [NIOSH 92-102; CDC, 1997].
In addition to abrasive blasting, construction employees perform numerous other activities that may result
in significant silica exposure, including tunnel and road construction, excavation and earth moving,
masonry and concrete work, and demolition [IARC, 1997]. Foundry employees, primarily in iron and steel
foundries, may be exposed to crystalline silica throughout the metalcasting process, including the
production of sand-based molds and cores, shakeout and knockout, and finishing and grinding
operations.
Crystalline silica, primarily as quartz, is a major component of the sand, clay, and stone raw materials
used to manufacture a variety of products, including concrete, brick, tile, porcelain, pottery, glass, and
abrasives. The powdered form of quartz, also called silica flour, is used in the manufacture of fine china
and porcelain. Finely ground crystalline silica is also used as a functional filler in the manufacture of
paints, plastics, and other materials. The rock crystal form of quartz is of great value to the electronics
industry.
Agricultural employees perform activities, including plowing and harvesting, that may generate elevated
silica levels. However, OSHA does not regulate crystalline silica exposure on farms with fewer than ten
employees and exposure data for this population is lacking [Linch et al., 1998]. On the other hand, OSHA
does regulate crystalline silica exposure in the agricultural services sector, and crystalline silica
exposures have been documented in the sorting, grading, and washing areas of food processing
operations for crops such as potatoes and beans.
Cristobalite, as calcined diatomaceous earth, is used as a filler in materials such as paints and as a
filtering media in food and beverage processing. Maintenance and trades personnel who repair and
replace refractory brick linings of rotary kilns and cupola furnaces may be exposed to significant levels of
quartz, as well as cristobalite and tridymite. These kilns and furnaces are found in glass, ceramics, and
paper manufacturing facilities as well as foundries [Markowitz and Rosner, 1995].
The industries described above, (see Appendix B) represent the major industrial sources of crystalline
silica exposure. However, there are numerous other operations in which silica may be used or otherwise
encountered, and it is important to be aware of the risk of silicosis in industries not previously recognized
to be at risk.

History of Silicosis

Silicosis is one of the world’s oldest known occupational diseases; reports of employees with the disease
date back to ancient Greece. By 1800, there were numerous common names for the lung disease now
known as silicosis. The names frequently referred to the affected laborers’ trade, such as grinders’
asthma, grinders’ rot, masons’ disease, miners’ asthma, miners’ phthisis, potters’ rot, sewer disease, and
stonemasons’ disease. Despite its different names through the centuries, silicosis is a single disease with
a single cause–exposure to respirable crystalline silica dust.
During the 1920s, the health risks of the “dusty” trades, in particular the granite industry, emerged as a
significant public health concern, and by 1930 silicosis was considered the most serious occupational
A-3
disease in the United States. During the 1930s and 1940s, the granite industry was the focus of a major
effort to alleviate dusty conditions and create a safer working environment [Rosner and Markowitz, 1994].
However, as the more extreme silica hazards were brought under control, attention shifted away from
silica to other occupational health hazards. Nonetheless, as the studies described below indicate, in
recent decades silicosis has continued to pose a significant health threat to employees in a variety of
occupations, including but not limited to construction, foundries, and sandblasting. It is important to be
aware of the possible risk of silicosis in workplaces not previously recognized to be at risk.
• Silicosis was listed as the underlying cause of death in 6,322 fatalities in the United States from
1968 through 1990, according to a study reviewing multiple-cause-of-death data from the
National Center for Health Statistics. The total number of U.S. deaths with mention of silicosis for
that period was 13,744. The study found that 69 percent of the deaths due to silicosis were
concentrated in 12 states: California, Colorado, Florida, Illinois, Michigan, New Jersey, New York,
Ohio, Pennsylvania, Virginia, West Virginia, and Wisconsin. The construction industry accounted
for more than 10 percent of the total silicosis-related deaths, and iron and steel foundries
accounted for another 5.4 percent [Bang et al., 1995].
• Death certificates for approximately 868 men and 46 women listed silicosis as the underlying
cause of death in non-mining occupations, according to a study that reviewed death certificates
for the period 1985 to 1992. The researchers focused on death certificates that provided an entry
for indicating the potential for substantial silica exposure, reviewing a total of 411,404 death
certificates for men and 30,563 for women [Walsh, 1999].
• A ten-year study (1985 to 1995) of Michigan employees found that nearly 80 percent of the 577
confirmed cases of silicosis occurred in industries in the Standard Industrial Classification (SIC)
3300, Primary Metals, which encompasses iron and steel foundries [Rosenman et al., 1997]. In
another study, foundry employees whose lungs exhibited radiographic changes consistent with
silicosis were concentrated in four primary job assignments: core making, mold making, core
knockout, and cleaning/finishing. The study was conducted at a Midwestern gray iron foundry that
has produced automotive engine blocks since 1949; the researchers analyzed medical records
and silica exposure data for 1,072 current and retired employees with at least five years of
employment as of June 1991. Radiographic readings consistent with silicosis were also
correlated with the number of years at the foundry, smoking habits, and silica exposure levels
[Rosenman et al., 1996].
• In the mid-1990s, there were two cases of accelerated silicosis in relatively young sandblasters
following short periods of extremely high crystalline silica exposures. In 1995, a 36-year-old man
who had sandblasted oil field tanks in Western Texas for 36 months died from respiratory failure,
eleven years after his initial exposure to crystalline silica. A second sandblaster at the same
facility, a 30-year-old man who had worked as a sandblaster from 1986 to 1990, died in 1996, ten
years after his initial exposure [CDC, 1998]. Both of these sandblasters died from progressive
massive fibrosis, an advanced stage of silicosis.

Adverse Health Effects of Crystalline Silica Exposure

Pulmonary silicosis has historically been the disease most well-known as being caused by the inhalation
of respirable crystalline silica particles. Additionally, there is evidence that exposure to crystalline silicacontaining
dusts causes or is associated with the following conditions: lung cancer, tuberculosis, chronic
obstructive pulmonary disease (including emphysema and bronchitis), autoimmune diseases or
immunologic disorders, chronic renal disease, and subclinical renal changes [NIOSH, 2002].

Silicosis

Silicosis is a fibrotic disease of the lungs caused by the inhalation of crystalline silica dust. It is a type of
pneumoconiosis, which is a general term for chronic lung disease that occurs when certain particles are
inhaled and deposited deep in the lung. There are two main types of silicosis, chronic silicosis (also
A-4
called “classical” or “nodular” silicosis) and acute silicosis, medically referred to as silico-proteinosis or
alveolar lipoproteinosis-like silicosis. Chronic silicosis, by far the most common form of the occupational
disease, typically appears 20 to 40 years after initial exposure and tends to progress even after exposure
ceases. Accelerated silicosis is a variant of chronic silicosis but develops after more intense exposure to
crystalline silica; it is characterized by earlier onset (within 5 to 15 years of initial exposure) and more
rapid progression of disease than chronic silicosis [Weill et al., 1994].
Acute silicosis results from an overwhelming exposure to silica and the symptoms become manifest in as
little time as a few weeks after exposure. Acute silicosis appears to be distinct from the other forms of
silicosis, possibly involving an immune mechanism not associated with either accelerated or chronic
silicosis. This disease, though rare, is invariably fatal. Outbreaks of acute silicosis have occurred among
sandblasters and silica flour mill employees [Peters, 1986].
The development of silicosis is dependent on the size of the crystalline silica dust particle, the dust
concentration, and the duration of exposure. Crystalline silica particles smaller than 10 micrometers (µm)
in diameter, so-called respirable particles, are particularly hazardous, because they easily pass through
the tracheobronchial tree and are deposited in the deepest recesses of the lungs, the alveolar structures.
Particles larger than 10 µm in diameter are trapped in the nose or the mucous lining of the airway and are
removed by the mucociliary escalator. Chronic silicosis has an early manifestation of a dry or nonproductive
cough when there is continued exposure to the inhaled irritant. The cough then becomes
prolonged and distressing, with sputum production as the disease advances. Initially, breathlessness
occurs while exercising, but progresses to shortness of breath during normal activity [Porth, 1994].
Wheezing typically only occurs when conditions such as chronic obstructive bronchitis or asthma are also
present. Advanced states of silicosis include pneumothorax and respiratory failure. Respiratory symptoms
increase with the progression of silicosis [Wang, 1999].
A rapid increase in the rate of synthesis and deposition of lung collagen has also been seen with the
inhalation of crystalline silica particles. The collagen formed is unique to silica-induced lung disease and
is biochemically different from normal lung collagen [Olishifski and Plog, 1988]. Silicosis in all its forms is
incurable and causes significant impairment or death. Therefore, eliminating or controlling occupational
exposure to respirable crystalline silica is critical to prevention of the disease.

Lung Cancer

The International Agency for Research on Cancer [IARC, 1997] classifies crystalline silica inhaled in the
form of quartz or cristobalite from occupational source as “carcinogenic to humans (Group 1).” However,
in making the overall evaluation, the IARC Working Group noted “that carcinogenicity in humans was not
detected in all industrial circumstances studied.” The Working Group also stated: “Carcinogenicity may be
dependent on inherent characteristics of the crystalline silica or on external factors affecting its biological
activity or distribution of its polymorphs.”
The IARC analysis included studies of U.S. gold miners, Danish stone industry employees, U.S. granite
shed and quarry employees, U.S. crushed stone industry employees, U.S. diatomaceous earth
employees, Chinese refractory brick makers, Italian refractory brick makers, U.K. pottery makers, Chinese
pottery makers and cohorts of registered silicotics from North Carolina and Finland. Most of these studies
found a statistically significant association between occupational exposure to crystalline silica and lung
cancer.

Tuberculosis

Epidemiologic studies have firmly established the association between TB and silicosis. Some studies
have indicated that employees who do not have silicosis but who have had long exposures to silica dust
may also be at increased risk of developing TB [NIOSH, 2002].
A-5
Individuals with chronic silicosis are more susceptible to developing active tuberculosis than the general
population. However, it is not clear whether low-level exposure to silica, in cases where silicosis has not
developed, also predisposes employees to tuberculosis [Davis, 1996].
Chronic Obstructive Pulmonary Disorder
Epidemiologic studies have shown that occupational exposure to respirable crystalline silica is associated
with chronic obstructive pulmonary disease, including bronchitis and emphysema. The findings from
some of these studies suggest that emphysema and bronchitis may occur less frequently or not all in
nonsmokers. Epidemiologic studies have also found significant increases in mortality from nonmalignant
respiratory disease, a category that includes silicosis, emphysema, and bronchitis, as well as some other
related pulmonary diseases [NIOSH, 2002].

Immunologic Disorders and Autoimmune Diseases

Several epidemiologic studies have found statistically significant increases in mortality from or cases of
immunologic disorders and autoimmune diseases in employees exposed to silica. These disorders and
diseases include scleroderma (a rare multisystem disorder characterized by inflammatory, vascular, and
fibrotic changes usually involving the skin, blood vessels, joints, and skeletal muscle), rheumatoid
arthritis, systemic lupus erythematosus (lupus), and sarcoidosis (a rare multisystem granulomatous
disease characterized by alterations in the immune system) [NIOSH, 2002].
Renal Disease
Epidemiological studies report statistically significant associations between occupational exposure to
silica dust and several renal diseases or effects, including end-stage renal disease morbidity (including
that caused by glomerular nephritis, chronic renal disease mortality, and Wegener’s granulomatosis
(systemic vasculitis often accompanied by glomerulonephritis) [NIOSH, 2002].

Stomach and Other Cancers

There is some evidence from studies of various occupational groups exposed to crystalline silica of
statistically significant excesses of mortality from stomach or gastric cancer. However, most of these
studies did not adjust for confounding factors and possible exposure-response relationships were not
assessed. Similar issues with confounding and lack of exposure-response assessment exist for the
infrequent reports of statistically significant numbers of excess deaths or cases in silica-exposed
employees of other nonlung cancers such as nasopharygeal or pharyngeal, salivary gland, liver, bone,
pancreatic, skin, esophageal, digestive system, intestinal or peritoneal, lymphopoietic or hematopoietic,
brain, and bladder [NIOSH, 2002].

Summary

As these health findings indicate, crystalline silica exposure is associated with a number of diseases, in
addition to silicosis. Silica exposure continues to pose substantial risks to employees, centuries after it
was first identified as an occupational hazard. The only way to prevent disease is to eliminate exposure to
crystalline silica or reduce crystalline silica exposure to safe levels.


http://hpd.zurichna.com/media/08_2164_silica_control_kit_fin/docs/Appendix%20A.pdf

References

ACGIH (2000) 2000 TLVs® and BEIs®. Threshold Limit Values for Chemical Substances and Physical
Agents and Biological Exposure Indices. American Conference of Governmental Industrial Hygienists.
Cincinnati, OH.
Archer, C., Gordon, D.A. (1996) Silica and Progressive Systemic Sclerosis (Scleroderma): Evidence for
Workers’ Compensation Policy. American Journal of Industrial Medicine. 29:533- 538.
A-6
Bang, K.M., Althouse, R.B., Kim, J.H., et al. (1995) Silicosis Mortality Surveillance in the United States,
1968-1990. Appl. Occup. Environ. Hyg. 10(12):1070-1074.
Beckett, W., et al. (1997) Adverse Effects of Crystalline Silica Exposure. Statement of the American
Thoracic Society, Medical Section of the American Lung Association. American Journal of Respiratory
and Critical Care Medicine. 155:761-765.
Bergen, E.A.V.D., Rocchi, P.S.J., Boogaard, P.J. (1994) Ceramic Fibers and other Respiratory Hazards
during the Renewal of the Refractory Lining in a Large Industrial Furnace. Appl.Occup. Environ. Hyg.
9(1):32-35.
Boujemaa, W., Lauwerys, R., Bernard, A. (1994) Early Indicators of Renal Dysfunction in Silicotic
Workers. Scand J Work Environ Health. 20:180-3.
Centers for Disease Control and Prevention. (1998) Silicosis Deaths Among Young Adults - United
States, 1968-1994. MMWR 47(16):331-335.
Centers for Disease Control and Prevention. (1997) Silicosis Among Workers Involved in Abrasive
Blasting - Cleveland, Ohio, 1995. MMWR 46(32):744-747.
Checkoway, H., Heyer, N.J., Demers, P.A., et al. (1993) Mortality among workers in the diatomaceous
earth industry. Brit. Jour. Ind. Med. 50:586-597.
Cheng, R.T., McDermott, H.J., Gia, G.M., et al. (June 1992) Exposure to Refractory Ceramic Fiber in
Refineries and Chemical Plants. Appl. Occup. Environ. Hyg. 7(6):361-367.
Davis, G.S. (1996) “Silica,” in Occupational and Environmental Respiratory Disease, Mosby–Yearbook
Inc., St. Louis, MO, eds. Harber, P., Schencker, M. B., Balmes, J.R.
Gantner, B.A. (1986) Respiratory Hazard from Removal of Ceramic Fiber Insulation from High
Temperature Industrial Furnaces. Am. Ind. Hyg. Assoc. J. 47(8):530-534.
Goldsmith, D.F. (1994) Silica exposure and pulmonary cancer. In: Epidemiology of Lung Cancer, 245-
298, Samet, J.M. ed. New York: Marcel Dekker, Inc.
IARC. (1997) IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Silica, Some
Silicates, Coal Dust and para-Aramid Fibrils. Vol. 68. Lyon, France. International Agency for Research on
Cancer, World Health Organization.
Linch, K.D., Miller, W.E., Althouse, R.B., Groce, D.W., Hale, J.M. (1998) Surveillance of Respirable
Crystalline Silica Dust using OSHA Compliance Data (1979-1995). American Journal of Industrial
Medicine. 34:547-558.
Lippmann, M. (1995) Exposure Assessment Strategies for Crystalline Silica Health Effects. Appl. Occup.
Environ. Hyg. 10(12):981-990.
National Institute for Occupational Safety and Health, Publication No. 92-102 (1992) Hazard Alert:
Preventing Silicosis and Deaths from Sandblasting.
Olishifski, L.B.; Plog, B.A. (1988) Overview of Industrial Hygiene, Fundamentals of Industrial Hygiene 3rd
ed. Chicago, National Safety Council.
Peters, J.M. (1986) Silicosis. Occupational Respiratory Diseases. Division of Respiratory Disease
Studies, Appalachian Laboratory for Occupational Safety and Health, ed. J.A. Merchant, published by the
National Institute for Occupational Safety and Health.
A-7
Porth, C.M. (1994) Pathophysiology: Concepts of Altered Health States, 4th ed. Unit V, Ch. 26 & 27, J.B.
Lippincott Co., Philadelphia.
Proctor, N.H., Hughes, J.P., Fischman, M.L. (1988) Chemical Hazards of the Workplace. 2nd ed.
J.B. Lippincott Co. Philadelphia. Rapiti, E., Speranti, A., Miceli, M., et al. (1999) End Stage Renal Disease
Among Ceramic Workers Exposed to Silica. Occup. Environ. Med. 56:559-561.
Rosenman, K.D., Reilly, M.J., Kalinowski, D.J., Watt, F.C. (1997) Silicosis in the 1990s. Chest.
111(3):779-782.
Rosenman, K.D., Reilly, M.J., Rice, C., et al. (1996) Silicosis Among Foundry Workers: Implications for
the Need to Revise the OSHA Standard. Am. J. Epidemiol. 144(9):890-900.
Rosner, D., Markowitz, G. (1994) Deadly Dust: Silicosis and the Politics of Occupational Disease in
Twentieth-Century America. Princeton: Princeton University Press.
Schluter, D.P. (1994) Silicosis and Coal Worker’s Pneumoconiosis. Occupational Medicine. eds. Zens C.,
et al. 3rd ed. St Louis, Mosby-Year Book, Inc.
Starzynski, Z., Marek, K., Kujawska, A., Szymczak, W. (1996) Mortality Among Different Occupational
Groups of Workers with Pneumoconiosis: Results From a Register-Based Cohort Study. Am. J. of Ind.
Med. 30:718-725.
Steenland, K., Mannetje, A., Boffetta, P., Stayner,L., Attfield, M., Chen, J., Dosemeci, M., DeKlerk, N.,
Hnizdo, E., Koskela, R., and Checkoway, H. (2001). Pooled exposure-response analyses and risk
assessment for lung cancer in 10 cohorts of silica-exposed workers: an IARC multicentre study. Cancer
Causes and Control 12:773-784.
Walsh, S.J. (1999) Effects of Non-mining Occupational Silica Exposures on Proportional Mortality from
Silicosis and Systemic Sclerosis. The Journal of Rheumatology. 26(10):2179-2185.
Wang, X., Yano, E., Nonaka, K., et al. (1997) Respiratory Impairments Due to Dust Exposure: A
Comparative Study Among Workers Exposed to Silica, Asbestos, and Coal Mine Dust. Am. J. of
Ind. Med. 31:495-502.
Wang, X., Yano, E. (1999) Pulmonary Dysfunction in Silica-Exposed Workers: A Relationship to
Radiographic Signs of Silicosis and Emphysema. Am. J. of Ind. Med. 36:299-306.
Weill, H., Jones, R.N., Parkes, W.R. (1994) Silicosis and Related Diseases, in Occupational Lung
Disorders, 3rd ed., Butterworth-Heinemann Ltd., Oxford, England.
Weill, H., McDonald, J.C. (1996) Exposure to Crystalline Silica and Risk of Lung Cancer: The
Epidemiological Evidence. Thorax. 51:97-102.
Winter, P.D., Gardner, M.J., Fletcher, A.C., Jones, R.D. (1990) A mortality follow-up study of pottery
workers: Preliminary findings of lung cancer. In: Occupational Exposure to Silica and Cancer Risk (IARC
Scientific Publications, No. 97), 83-94, Simonato, L., et al. eds. International Agency for Research on
Cancer. Lyon.