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FEATURE

A brief overview of crystallinesilica

Silicon, and its oxide silica, are naturally abundant. Exposure to crystalline silica has long been known tocause silicosis and other lung disorders. Crystalline silica exposures are also associated with development ofactive tuberculosis, lung cancer, and certain autoimmune and renal disorders.

Silicosis may occur in acute, accelerated and chronic forms with latency periods ranging from weeks to40+ years, respectively.

Silica exposure is controlled by the same methods that apply to any other dust inhalation hazard. Nospecific OSHA standard applies, beyond the PELs published in 29 CFR. These PELs depend on determina-tion of the percent silica in a sample. This analysis should be performed in accordance with NIOSHanalytical methods.

By Eileen Mason,Sophie K. Thompson

INTRODUCTION

Silicon is the second-most abundantelement in the world.1 Silica, the com-mon oxide, (SiO2) occurs naturally andis widespread. Crystalline formsof silicainclude alpha- and beta-quartz, cristo-balite and tridymite. Because, alpha-quartz is the most thermodynamicallystable form, most naturally occurringcrystalline silica is found in this mor-phology.2 Alpha-quartz has the greatesthealth impact because it is encounteredmost often. Cristobalite and tridymiteare formed by exposure to high tem-perature, such as volcanic processes,or by calcining diatomaceous earth. Tri-dymite tends to be less hazardous thanother crystalline forms, and amorphoussilica is of lesser toxicological interestthan crystalline silica.

Because silica, especially in the formof quartz, is so ubiquitous, exposuresmay occur in any dusty location, and

may be both occupational and non-occupational. Common beach sand isalmost pure silica, as is volcanic glass.Topsoil, dust, and sedimentary andmetamorphic rocks all contain silicain varying amounts. Granites containin the neighborhood of 30% quartz,while shales are comprised of about20% quartz. Some igneous rock maycontain silica. Diatoms and radiolar-ians extract silica from water to formshells. Deposits of these shells aremined as diatomaceous earth, a non-crystalline form of silica. Opal, perliteand pumice are composed of amor-phous hydrated silica.

Historical Background

Reports of adverse health effects ofexposure to silica date back to theancient Greeks.3 Agricola’s 1556 Trea-tise on Mining describes pulmonaryeffects of silica exposure, and the topicis again discussed by Ramazzini in1713. Today, we realize that it is pri-marily the crystalline form of silica thatpresents the health hazard. Such infor-mation was not available historically.

Silicosis, a type of pneumoconiosis,occurs when crystalline silica particlesare deposited in the lung tissue, leadingto fibrotic changes. This accumulationof crystalline silica dust in the lungs hasbeen known historically as ‘‘miners’asthma’’, ‘‘potters rot’’, ‘‘phthisis’’,‘‘stonemason’s disease’’ and ‘‘sewerdisease’’.4 By the 1920s, dust inhala-tion, especially in the granite industry,was recognized as a serious healthproblem.

During the 1930s, after the HaNest disaster gained national attion, silicosis was considered the mserious occupational disease incountry. The Hawks Nest disaoccurred during the period 191931, when approximately 5,workers were employed to bore a tnel through Gauley Mountain in WVirginia.5 About half of these empees worked inside the tunnel, excaing sandstone which was estimatecontain over 90% silica. Respiraprotection was supplied only to magement, and wet drilling methwere used infrequently, since dry dling was faster.

A historical marker on the site doments a total of 109 deaths, but ssequent studies determined thatleast 764 workers died due to silicand other silica-related conditionsthis time, safety laws were promgated at the state level. Although o11 states regulated silica exposprior to Hawks Nest, congressiohearings held in 1937 were followby passage of laws in an additionastates.

TOXICOLOGY

Silicosis may be acute, chronic,accelerated. In all its forms, silicis incurable and symptoms are diffito manage. The disease may progeven if there is no further exposursilica. Inevitably, silicosis leads toious loss of function and often dea

Eileen Mason is affiliated with MurrayState University, Occupational Safety& Health, 157 IT Center, Murray, KY420071, United States(e-mail: eileenmason@lycos.com).

Sophie K. Thompson is affiliated withOld Dominion University, UnitedStates(e-mail: sxthomps@odu.edu).

6 � Division of Chemical Health and Safety of the American Chemical Society 1871-5532/$36.00

Elsevier Inc. All rights reserved. doi:10.1016/j.jchas.2009.09.001

Overwhelming exposure to silicaresults in acute silicosis. Symptomsmay become apparent within a fewweeks. Employees at the Hawks Nestproject were hired for periods aver-aging only 15 weeks – so that theycould ‘‘leave the area and die some-place far from the source of their ill-ness’’.6 Although relatively rare, acutesilicosis still occurs among sandbla-sters and silica flour mill employees.7

Acute silicosis seems to involve animmune mechanism distinct fromthose associated with chronic andaccelerated silicosis.

Chronic silicosis, also known assilico-proteinosis oralveolar lipoprotei-nosis-like silicosis, is the most commonpresentation and typically appears 20–40 years after initial exposure. Symp-toms may be mild or absent forextended periods, with subsequentdevelopment of a dry cough and short-ness of breath during exertion. Even-tually, the cough becomes persistentand productive, with shortness ofbreath during normal activity. Exami-nation of chest X-rays shows develop-ment of characteristic, extremely hardsilica nodules, primarily located in themid- and upper zones of the lung. Thesenodules proliferate and may coalesce asthe disease progresses to massive pul-monary fibrosis. Eventually, pneu-mothorax and respiratory failure result.

Accelerated silicosis is similar tochronic silicosis, but the latency periodis reduced to 5–15 years from initialexposure, and the disease progressesmore rapidly than does chronic silico-sis.

Exposure to crystalline silica is asso-ciated with a variety of respiratory dis-eases in addition to silicosis. There is aclear association between silica expo-sure and development of active tuber-culosis, not only among silicoticindividuals, but even in those whohave long-term exposure to silica dustbut do not have silicosis.

Epidemiological studies have alsoshown an association between silicaexposure and chronic bronchitis,emphysema and other forms of chronicobstructive pulmonary disease.

Initial reports from Sweden8 andOntario9 and additional studies duringthe 1980s confirmed a probable rela-tionship between crystalline silica and

Journal of Chemical Health & Safety, March

lung cancer. In 1987, IARC classifiedcrystalline silica as Group 2A, Prob-ably Carcinogenic to Humans.10 In1996, with additional information,IARC revised the classification of thequartz and cristobalite polymorphs ofcrystalline silica upward to Group I,Carcinogenic to Humans.2 There isonly limited evidence from animal stu-dies that tridymite is carcinogenic,even though it is still a crystalline poly-morph.

In addition, exposure to inhaledsilica can lead to diseases which donot involve the lungs.4 Employeesexposed to silica have statistically sig-nificant increased rates of developingimmunologic and autoimmune dis-eases, such as rheumatoid arthritis,systemic lupus erythematosus and sar-coidosis. Increased prevalence of renaldisease, including end-stage renal fail-ure, stomach and other cancers, hasalso been noted.

EXPOSURE CONTROL ANDREGULATION

Exposure to crystalline silica can becontrolled by the same methods asexposure to any other airborne dust.Engineering controls include ventila-tion, enclosure or isolation of the dust-producing activity. Silica-containingabrasives used in ‘‘sandblasting’’ canbe replaced with less harmful alterna-tives. Job rotation and wet methods areadministrative and work practice con-trols useful in minimizing dust expo-sure. Personal protective equipment,primarily respirators, is the final resortif engineering and work practice con-trols cannot reduce ambient concen-trations to a safe level.

Despite the known hazards and vari-ety of health effects of exposure tocrystalline silica, OSHA has no sub-stance-specific standards as are pro-vided for asbestos, lead, cadmium,and 22 other materials, in addition to13 select carcinogens.11 None of thesesubstances is found as widely as crys-talline silica. Federal statutory controlof crystalline silica is limited to com-pliance with the published permissibleexposure limits (PELs).

Meaningful control requires stan-dards against which ambient expo-

/April 2010

sures can be measured. The currentOSHA crystalline quartz PEL for theConstruction industry12 is

250 mppcf

ð%SiO2 þ 5Þ :

mppcf : millions of particles per cubicfoot of air; based on impinger samplescounted by light-field techniques.

Per a foot note to the table, ‘‘Thepercentage of crystalline silica in theformula is the amount determinedfrom airborne samples, except in thoseinstances in which other methods havebeen shown to be applicable.’’

The General Industry standardsinclude a PEL for total quartz:13

ð30 mg=m3Þð%SiO2 þ 2Þ

The current PEL for respirable crystal-line quartz for General Industry iseither

250 mppcf

ð%SiO2 þ 5Þ orð10 mg=m3Þð%SiO2 þ 2Þ

The two PELS (mppcf and mg/m3)cannot be interconverted with mathe-matical exactitude.

The actual measurement of crystal-line silica exposure remains proble-matic because of the need to identifythe proportion of crystalline silica in asample. This information is necessaryto calculate the PEL of a particularsilica-containing material. The deter-mination of actual silica content iscrucial for regulatory compliance aswell as health protection: HazardCommunication, for example, requiresidentification of crystalline silica at anylevel in excess of 0.1%.

ANALYTICAL METHODS

Determination of the percent silicacontent of a sample is not straightfor-ward. While chemical tests for ele-mental silicon are readily availableand accurate to the level of 0.1%, ele-mental analysis does not identify theform in which silicon is present. Meth-ods of isolating the silica componentmay be less than satisfactory, becauseof incomplete separation or removalof some of the silica content alongwith the non-silica components.

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Additionally, analytical methods mayeither change or fail to distinguishamong the various polymorphs ofsilica.

Analytical methods for crystallinesilica may be either chemical, physical,or a combination of the two.14 Chemi-cal methods typically cannot identifythe specific polymorph present in asample. Fusion of a sample withsodium pyrosulfate removes non-silicacontent, leaving an insoluble residuecontaining quartz, cristobalite, tridy-mite and opal.15 This method doesnot distinguish between the specificcrystalline forms, or between crystal-line silica and amorphous opal. Strongacids may be used to remove othercomponents of a mixture or matrix,leaving behind the relatively insolublecrystalline silica. Unfortunately, someof the contaminant material may notdissolve unless digestion times areextended, even to several days. Suchextended digestion may proceed to dis-solve some of the crystalline silica pre-sent,16 especially if the particles aresmall. Rate of dissolution may alsobe modified by the presence of amor-phous layers that may form on thecrystalline surfaces. This loss of mate-rial is especially significant in mixtureswhere the crystalline silica is present inlow concentrations.

NIOSH has provided standardmethods of analysis.

NIOSH Method 7601,17 whichrelies on digestion in phosphoric acid,is primarily intended for characteriza-tion of respirable dusts, and is oftenused in industrial settings to determinequantatively the crystalline silica levelsin samples that do not include amor-phous silicas and other silicas whichmight be resistant to digestion. Themethod is used to concentrate samplesbefore analysis by X-ray diffraction,such as NIOSH Method 7500.18

NIOSH 7500 is a nondestructivemethod and can identify individualcrystalline silica polymorphs and evenquantify the amount of quartz andcristobalite above threshold levels of10 mg and 30 mg respectively. In anyquantitative X-ray diffraction method,spectral overlap may complicate inter-pretation of the diffraction pattern,

and the technique is useful primawhen silica is a major phase. Whensample involves thicker films,NIOSH absorption correction facis ‘‘not always appropriate’’.14

NIOSH Method 760219 describemethods of identifying crystalline siin bulk samples, and NIOSH 760refines the method when the samis mixed with coal dust. Samples shobe concentrated before analysis. Sptral overlap with other forms of silicmay confound analysis unless thmaterials are removed. It is also diffito distinguish among polymorphscrystalline silica using IR methods.

Observation and identificationcrystalline silica particles is possusing microscopic techniques. Thiespecially appropriate if the mpPEL is used. However, microscoanalysis is exceedingly time consumand requires a highly skilled analy

CONCLUSIONS

Silicosis and other conditions relato exposure to crystalline silica hhistorically been significant puhealth and occupational health issDespite better control of exposuthe hazards still remain. Regulatcontrol of exposure is hamperedthe lack of a specific standard, anfurther complicated by the difficultaccurately determining the crystalsilica content of samples used for exsure monitoring.

REFERENCES1. Crystalline Silica Primer, US Dep

Interior, Special Publication, 1992.2. IARC, Silica, Some Silicates, Coal D

and para-Aramid Fibrils, vol. 68, LInternational Agency for ResearchCancer, 1997.

3. Rosen, G. The History of MinDisease: A Medical and Social Inpretation; Schuman; NY, 1943,459–76.

4. PL 03-00-007 – National EmphProgram – Crystalline Silica. Acceon 7/13/2009 at http://www.osha.gpls/oshaweb.

5. ‘‘Silicosis Mortality, PreventionControl — United States, 1968–20

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on

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asisssedov/

and02’’.

Accessed on 8/2/2009 at http://wcdc.gov/mmw r/preview/mmwrhmm5416a2.htm.

6. ‘‘Hawks Nest worker graves lay forten for decades’’ from the CharleGazette, Charleston, WV, February2008. Quoted by the Greater Soeastern Massachusetts Labor CouAccessed on 8/2/2009 at http://wgsmlaborcouncil.org/node/2427.

7. Peters, J. M. In J. A. Merchant (ESilicosis, Occupational RespiraDiseases, Division of Respiratoryease Studies, Appalachian Laborafor Occupational Safety and HeNational Institute for OccupatiSafety and Health, 1986.

8. Westerholm, P. Silicosis observationa case register. Scand. J. Work EnvHealth, 1980, 6(Suppl. 2), 1–86.

9. Finkelstein, M.; Kusiak, R.; SuranyMortaility among miners receiworkmen’s compensation for silicin Ontario: 1940–1975. J. Occup. M1982, 24, 663–667.

10. IARC, Supplement 7 of IARC Mographs. Lyon, International AgencyResearch on Cancer, vol. 42, 1987

11. 29 CFR 1910.1001-1018; 291910.1025-1029, 29 CFR 1919.11050.

12. 29 CFR 1926.55, Appendix A, mindusts.

13. 29 CFR 1910.1000, Table Z-3: mindusts.

14. Miles William, J. Issues and conversy: the measurement of crystasilica; Review papers on analymethods. AIHA J. 1999, 60(MJune), 396–402.

15. Chapman, S. L.; Syers, J. K.; JacksM. L. Quantatitive determinationquartz in soils, sediemtns and rockpyrosulfate fusion and hydorfluosiacid treatment. Soil Sci. 1969,348–355.

16. Knopf, A. The Quantitative Determtion of Quartz (free silica) in dustsPublic Health Report, No. 48,shington, DC. 1933, pp. 183–90.

17. NIOSH 7601. Accessed on 8/18/0http://www.cdc.gov/niosh/nmapdfs/7601.pdf.

18. NIOSH 7500. Accessed on 8/18/0http://www.cdc.gov/niosh/nmapdfs/7500.pdf.

19. NIOSH 7602. Accessed on 8/18/0http://www.cdc.gov/niosh/nmapdfs/7602.pdf.

20. NIOSH 7603. Accessed on 8/18/0http://www.cdc.gov/niosh/nmapdfs/7603.pdf.

Journal of C

hemical Health & Safety, March/April 2010