AMERICAN COLLEGE OF OCCUPATIONAL AND ENVIRONMENTAL MEDICINEACOEM is the pre-eminent organization of physicians who champion the health and safety of workers, workplaces, and environments
MEMBER LOGIN

Medical Surveillance of Workers Exposed to Crystalline Silica

 I. Introduction

Silica is a major component of sand, rock, and mineral ores and is the second most common mineral in the earth’s crust, next to feldspar. The generic term refers to the chemical compound silicon dioxide (SiO 2) which occurs naturally in crystalline, amorphous, and glassy states. It is crystalline silica which poses the occupational respiratory hazard. Structurally, crystalline silica is composed of a three-dimensional network of silicon/oxygen tetrahedrons (SiO 4) cross-linked at each of the four corners. Variations in the molecular arrangement of the silicon tetrahedron result in different polymorphs of silica.

The three major industrial types of crystalline silica include quartz, cristobalite, and tridymite, with other types being less important. Crystalline silica is essentially insoluble in water, but its solubility is increased with heating or increasing pH. It also reacts with most metallic oxides. Amorphous, non crystalline, or glassy varieties of silica result from the completely random orientation of the silicon dioxide structural units, occurring in nature as diatomaceous earth, vitreous silica, or volcanic glass. These are classified as nuisance dusts, whose exposures are relatively harmless. However, amorphous silica can transform into crystalline structures (e.g., cristobalite) when exposed to high temperatures and pressures.

More than one million workers in the United States are exposed to crystalline silica, with more than 100,000 of these workers involved in activities associated with a high risk for silica exposure.(1) These high-risk activities include mining, rock drilling, construction activities, steel rolling and finishing mills, foundry work, and abrasive blasting with silica-containing material. The current Occupational Safety and Health Administration (OSHA) Permissible Exposure Limit (PEL) for respirable crystalline silica is a respirable dust concentration of 10 mg/m 3 divided by (% SiO 2 + 2), averaged over an 8 hour shift.(2) For example, dust composed of 98% crystalline silica has a PEL of 10/(98 + 2) = 0.1 mg/m 3. However, convincing data indicate that the current OSHA PEL does not provide sufficient protection from the development of silicosis.(3-6) Moreover, OSHA found that 48% of industry sites inspected during 1980-1992 had exposures to respirable silica in excess of the PEL.(7)

Despite some optimistic views on the decline of silicosis, its persistence is a matter of record (8) and some students of the disease believe its incidence is on the increase. OSHA has found that overexposure to silica remains widespread; the U.S. estimated death rate from silicosis in recent years is up to 200 to 300 per year.(9)

The purpose of this American College of Occupational and Environmental Medicine (ACOEM) position statement is to recommend objectives, key elements, and implementation strategies for a medical surveillance program for workers exposed to silica. The program would blend with recent increased efforts to prevent and eventually eliminate silicosis at both the national and international levels.(10-14)

II. Overview of Health Effects of Silica

The major adverse effects of exposure to crystalline silica include silicosis, chronic bronchitis, certain connective tissue disorders, and lung cancer. The limited value of treatment for these conditions lends urgency to their prevention. In addition, mycobacterial disease has long been associated with silicosis. Recently, an important comprehensive review of the literature on the adverse effects of silica exposure was published as a position paper of the American Thoracic Society.(3)

Silicosis is an irreversible, often disabling and sometimes fatal fibrotic lung disease that can present in three very different forms.(13) Chronic silicosis is the most common and typically occurs after 10 or more years at a relatively lower-level exposure to crystalline silica than the other two forms. Accelerated silicosis can occur within 5 to 10 years of initial exposure and is caused by high levels of exposure, often to freshly fragmented silica which is felt to be more toxic than “aged” silica.(2) Accelerated silicosis tends to progress more rapidly into complicated silicosis (progressive massive fibrosis), and is more likely to be complicated by mycobacterial disease than chronic silicosis. Acute silicosis (silicoproteinosis) is much less common, may develop within a few weeks to 4-5 years of exposure to extremely high levels of crystalline silica, and is often fatal. Approximately 200-300 Americans die each year from silicosis.(15,16) Although most deaths involve workers age 65 or older, (16) silicosis can also result in increased mortality in young workers as well.(17) Clinically, neither significant decrements in lung function nor respiratory symptoms are likely in the early stages of simple silicosis. In complicated disease, both obstructive and restrictive ventilatory defects, as well as decreases in diffusing capacity, are common;(18) at this stage, exertional dyspnea is the predominant symptom.

An increased risk of tuberculosis (TB) among workers with silicosis has long been recognized.(19,20) Thus, individuals with chronic silicosis have a three fold higher risk of tuberculosis than similar individuals without silicosis, and the risk appears higher with increasing profusion of radiographic abnormalities.(21) In addition to Mycobacterium tuberculosis, non-tuberculosis mycobacteria, such as M. kansasii and M. avium complex, have been found in high frequency in individuals with silicosis.(22) A cluster of Acinetobacter pneumonia in foundry workers heavily exposed to silica has also been reported, with two deaths related to this organism, rarely a pathogen to healthy persons.(23)

Symptoms of chronic bronchitis, with or without accompanying obstructive ventilatory defects in spirometry, have also been described in some epidemiological studies of silica-exposed workers, even in the absence of silicosis.(24-29) Scleroderma and rheumatoid arthritis, both connective tissue diseases, have been associated with silicosis, especially the accelerated type.(30-32) Evidence of both glomerular and tubular nephropathy has also been reported,(32,33) sometimes after less than two years of exposure to silica with no evidence of silicosis.(34)

In 1996, the International Agency for Research on Cancer (IARC) re-classified silica as a Class I human lung carcinogen, based on sufficient animal and human data.(35) Although the degree of increased risk varies (with relative risks ranging from 1.3 to 6.9), the risk appears to be greatest in workers with silicosis who smoke. The cancer risk to silica-exposed workers without silicosis (especially if they are not smokers) is less clear despite continuing research, some of which has yielded disparate results.(36-40)

Unfortunately, there is no cure for silicosis, nor has any pharmacologic prophylaxis been adequately validated. Aggressive courses of antimycobacterial agents can cure tuberculosis, but there is no cure for the other diseases associated with silica exposures, with the rare exception of a cancer that could be removed surgically. Thus, it is important to stress that the single most important aspect of prevention of silicosis and other silica-associated diseases is limitation of exposure to respirable crystalline silica. While a review of measures to limit such exposure is beyond the scope of this document, experience has shown that dust suppression techniques are not difficult or expensive to implement. Appropriate use of personal protective equipment (PPE), as a supplement to engineering controls, is very important.

III. Principles of Medical Surveillance

The primary purpose of any medical surveillance program is the early detection of an adverse health effect, at a time when intervention can lead to disease reversal or cessation of progression. The medical tests used for surveillance should be reasonably reliable detectors of early disease with good sensitivity and specificity. They should be simple and cost-effective to administer, and present little risk or inconvenience to workers. Additional benefits of a surveillance program include the opportunity to educate workers about risks they face and the opportunity to do research into early predictors of disease. Finally, a surveillance program can even stimulate employers to add engineering or administrative controls to the workplace (e.g., audiometry in hearing conservation programs).

Recommended Surveillance Program

  1. Target Population
    The pool of workers to be included consists of those individuals exposed to levels of crystalline silica that place them at risk for silicosis. Since the exact exposure-response relationship remains unclear,(2) it is appropriate to make the inclusion criteria for this program conservative. Thus, inclusion of any workers exposed to a crystalline silica concentration > 0.05 mg/m 3 is recommended. This level is both the National Institute for Occupational Safety and Health’s (NIOSH’s) Recommended Exposure Limit (REL) and essentially one half of the current OSHA PEL for pure crystalline silica.
  1. Components of the Evaluation
    As specified in the OSHA Special Emphasis Program,(14) components of the surveillance evaluation should include the following:
  1. Occupational and medical history (questionnaire)
  2. Physical examination
  3. Purified protein derivative (PPD) tuberculin skin test
  4. Chest radiography
  5. Spirometry

The history can be obtained using a directed questionnaire focusing on characterization of risk and identification of symptoms related to silicosis, tuberculosis, obstructive pulmonary disease, connective tissue disease, and lung cancer. Important items regarding risk characterization include identification of likely onset and duration of silica exposure, intensity of silica exposure, description of all job titles associated with silica exposure, a review of types of respirators used and the quality of the respiratory protection program, and presence of other risk factors associated with the various silica-related adverse health effects (e.g., smoking, non-occupational risk factors for tuberculosis, etc.). If possible, exposure data from the worker should be supplemented by exposure data obtained by an industrial hygienist. Whenever possible, questions relating to symptoms should be validated questions (41,42) and in as complete and concise a format as possible.

In addition to risk characterization, this questionnaire can be useful for the early detection of chronic obstructive pulmonary disease, active mycobacterial disease, and connective tissue disorders. The OSHA Asbestos Questionnaire (43) could be used as a model for a silica questionnaire, but it would need significant revision and supplementation to make it useful to identify those risks and symptoms of particular concern for silica. For example, Question 22 of the Initial Questionnaire and Question 12 of the Periodic Questionnaire would need to be expanded to address silica-exposing work. Questions aimed at identifying extra-pulmonary aspects of silica exposure would need to be added.

The physical examination should be focused on the general condition and respiratory status of the worker. Depending on the questionnaire responses, additional parts of the examination, such as the musculoskeletal, can be added.

The baseline tuberculin skin test reactivity status of all silica-exposed workers should be established at job entry, by intradermal administration of purified protein derivative (PPD), using the Mantoux technique.(44) The two-step technique for PPD skin test administration and interpretation of results (positive = > 10 mm induration) should be followed for this baseline determination, following current Centers for Disease Control and Prevention (CDC) guidelines for the detection and evaluation of tuberculosis.(45) Periodic monitoring of PPD skin test reactivity is useful for the detection of both latent tuberculosis infection and active tuberculosis.

The chest radiograph has long been a cornerstone in the diagnosis of silicosis, and radiographic manifestations of this disease often precede the development of symptoms and clinically significant pulmonary function loss. It is felt that detection of simple silicosis, followed by removal from silica exposure, can decrease the risk of progression of the disease.(46) Chest radiography is also useful for monitoring the progression of silicosis, as well as for identifying the appearance of treatable complications, such as mycobacterial disease. Consequently, a chest radiograph should be considered a fundamental tool in the medical surveillance of silica-exposed workers. It is essential that interpretations be based on films meeting high-quality standards. The interpretation should be performed by a physician knowledgeable about the radiographic manifestations of occupational lung diseases, and in accordance with the 2000 International Labor Office (ILO) International Classification of Radiographs and Pneumoconioses.(47,48)

Although clinically significant decrements in spirometry are not typically observed in the early stages of simple silicosis, previous studies have shown that the prevalence of obstructive ventilatory defects is higher in silica-exposed workers, even in the absence of silicosis and after accounting for smoking.(25,26) Therefore, spirometry is useful in this worker population. Spirometry should be performed in accordance with accepted standards for quality assurance and interpretation.(49,50) ACOEM has authored position statements on Spirometry in the Occupational Setting (51) and Evaluating Pulmonary Function Change over Time in the Occupational Setting (52) to provide additional practical guidance in these areas. Forced vital capacity (FVC), forced expiratory volume in one second (FEV 1) and FEV 1/FVC ratio should be evaluated cross-sectionally relative to predicted values.(51) FVC and FEV 1 can also be evaluated longitudinally, to determine whether a worker’s change over time is excessive.(52-54) Although measurement of diffusing capacity has been suggested for inclusion in medical surveillance,(12) at present it is not practical because of limited availability near the worksite, cost, and inter-laboratory variability in results and reference ranges.(55,56) Several other tests were considered as part of this surveillance evaluation but not included because of lack of value as screening tools. A high-resolution chest CT scan may be more sensitive in identifying the parenchymal opacities of silicosis than a plain chest radiograph. However, the increased radiation dose, as well as the added expense and time involved, do not justify its use as a surveillance tool. In addition, the standard method of diagnosing silicosis is by history and chest X-ray.

Serum immunological markers for connective tissue diseases, such as ANA (57) and rheumatoid factor,(31) have not been included, because of their low predictive value for these diseases in the absence of compatible symptoms or signs. More recent techniques such as studies of silica-induced DNA changes in lymphocytes,(58,59) in serum and urine levels of neopterin,(60) and in the release of reactive oxygen and nitrogen species, cytokines and specific transforming factors (61-63) by alveolar macrophages have been studied only in small groups or in silica-exposed animal models thus far. Their place in medical surveillance remains to be established. The feasibility of using induced sputum rather than bronchoalveolar lavage to assess the effects of silica exposure has been reported by some investigators.(64,65) The role of urinary screening to detect renal injury (32-34) is yet to be determined. The cost-effectiveness of these new approaches also needs to be investigated.

Aggressive techniques to look for lung cancer, such as chest CT, cytology, and bronchoscopy, are not indicated in medical surveillance for silica-related diseases, although they may play a role in individual clinical evaluations, when guided by history, physical examination, and radiographic abnormalities.

  1. Frequency of Surveillance Evaluations
  1. Baseline Evaluation
    An evaluation should be done on each worker, when he/she accepts a position involving exposure to a work site where silica is present and the concentration is either unknown or above 0.05 mg/m 3.Such an evaluation would both establish baseline lung function and TB skin status plus identify the presence of pre-existing lung disease. All findings should be discussed and explained to the worker promptly. Copies of pertinent results should be provided to the worker. Information provided to the employer should be limited to whether the worker is medically fit to perform the job and whether work restrictions are indicated. Such an evaluation may be combined with an employer’s standard post-offer evaluation. Ideally, the same provider would perform the baseline evaluation and follow-up surveillance evaluations to maximize continuity in the surveillance program. The ACOEM longitudinal spirometry statement, Evaluating Pulmonary Function Change over Time in the Occupational Setting, addresses the pitfalls to be avoided when serial measurements of spirometry are considered.(52)

  2. Follow-up Evaluations
    The initial follow-up examination should be performed within 12 months since acute silicosis and tuberculosis can occur in a relatively short period of time. The one-year follow-up evaluation allows the health care providers performing the medical surveillance evaluations to estimate the actual exposure the worker faces at a time when intervention might have significant benefits. It also provides an opportunity to reinforce to the worker the importance of preventive measures. Repeating the chest radiograph after one year should be at the discretion of the health care provider, but under most circumstances would not be needed unless local circumstances so indicate.

For workers with exposures < 0.05 mg/m 3, the frequency of follow-up can be reduced, based on questionnaire responses and documented exposure data. For workers with < 10 years of work experience with silica, frequency of follow-up evaluation should be every three years. For workers with > 10 years work experience with silica, follow-up evaluation should be every two years since workers with longer duration of exposure and time from initial exposure are at higher risk for silica-related abnormalities. Those workers who are more heavily exposed may warrant closer medical supervision. When a worker changes from one job involving exposure to silica to another, the health care provider should re-evaluate the need for an additional medical surveillance evaluation for that worker based on the new job tasks and level of silica exposure.

If a worker is suspected as having silicosis during the surveillance evaluation, he/she should be immediately removed from further exposure and promptly referred to a physician knowledgeable in the diagnosis and management of silicosis. If the diagnosis is confirmed, further management should be provided promptly. The management plan will necessarily depend on the specifics of each case.

  1. Exit Evaluation
    A worker leaving a job with potential for silica exposure should be offered an exit medical evaluation. The components of the evaluation should be based on the results of the previous evaluations, time from initial exposure and duration and level of silica exposure, and change in symptoms from previous evaluations. For those workers with > 10 years of work experience with silica, a complete medical surveillance evaluation is indicated if the last evaluation occurred more than 12 months previously. If the worker is moving into a different job working with silica, the exit evaluation can also serve as the baseline evaluation for the next job.
  1. Education Component
    An informed workforce is vital to the success of a program that intends to minimize exposure to crystalline silica and thus prevent the diseases it can cause. Specific information should therefore be clearly provided and its importance to worker health be emphasized to every employee who undergoes a surveillance evaluation. The information provided should include the following:
  1. Adverse health defects with crystalline silica exposure.
    This would include information on silicosis, tuberculosis, connective tissue and renal disorders, and lung cancer.
  1. Methods of Prevention
    This would include information emphasizing the role of primary prevention, which includes engineering controls, personal protective equipment and methods to avoid home contamination with work place dusts.
  1. Exposure Limits
    This would include information on the OSHA PEL for crystalline silica, the NIOSH REL,the significance of these limits and the fact that the texture, type, and size of silica particles play a role in the development of health effects.

  1. Purpose of the Evaluation
    The emphasis of the evaluation on screening for silicosis, tuberculosis, and obstructive pulmonary disease should be noted. It should also be noted that the evaluation is not specifically designed to screen for connective tissue diseases or lung cancer, although the risks of these conditions should be incorporated in worker training sessions.

  1. Associated Risk
    The associated risk of silica exposure with cigarette smoking and tuberculosis should be discussed.
  1. Supervision
    The program must be under the direction of a physician with thorough knowledge of surveillance principles, health effects of silica, tuberculosis, interpretation of pulmonary function tests (both individual and group data), and the ILO classification of radiographs.
  1. Reporting
    All the results of the surveillance evaluation should be reported and explained to the worker in prompt fashion. Copies of the pulmonary function results and chest X-ray results should be provided to the worker. If the worker identifies a primary care provider and gives permission for notification of the primary care provider, a copy of the surveillance evaluation results should be sent to that provider. If the data from the surveillance evaluation are suggestive, but not diagnostic of silicosis, the worker should be referred to a physician knowledgeable in the evaluation and management of silicosis, in consultation with the worker’s primary care provider. A summary of results, limited specifically to silica-related surveillance data without individual identifiers, should be reported to the employer. The employer should be notified if a worker has a silica-related health problem. When a specific disease is identified, certain specific steps are to be followed:
  1. Silicosis
    The specific type of silicosis (chronic, accelerated, or acute) must be identified. The diagnosis should then be reported to the applicable local, state, and/or federal agency. The various past and present job tasks of the affected worker should be reviewed and, when applicable, environmental control measures reviewed and revised. When appropriate, medical restrictions in relationship to job tasks should be documented, and reasonable job accommodations should be made. The worker should be referred to a physician knowledgeable in the management of silicosis, in consultation with the worker’s primary care provider.
  1. Positive PPD Skin Test
    A worker with a positive PPD should be evaluated promptly for the presence of active tuberculosis. Until tuberculosis is ruled out, precautions should be taken to decrease the risk of transmission. Once tuberculosis has been ruled out, the worker should be counseled regarding the risks and benefits of treatment of latent tuberculosis infection and such treatment offered, if appropriate.(66) If the worker has active tuberculosis, appropriate treatment should be started immediately and the appropriate public health authorities notified. The above steps should be carried out in consultation with the worker’s primary care provider.
  1. Tobacco (Cigarette) Use
    A worker identified as a cigarette smoker should be encouraged to stop smoking and that worker should be educated as to currently available methodologies for aiding smoking cessation. The worker should be encouraged to discuss smoking cessation methods with his/her primary care provider.
  1. Recordkeeping
    Medical records of surveillance program data, including spirometry graphs and spirometer calibration records, are to be kept for 30 years after the last known date of employment of the worker in a job involving silica exposure. These records are to be maintained in a confidential fashion, and access to records should conform to the OSHA Standard on Access to Employee Exposure and Medical Records (29 CFR 1910.1020).
  1. Responsibility
    Responsibility for the medical surveillance program is multi-faceted and will need the cooperation of all parties involved in order to be successful. The employer’s responsibility involves facilitating worker participation in the medical surveillance program by allowing employees time off from work with pay for the medical evaluation and by covering the costs of the medical surveillance evaluations. The employee’s responsibility is to participate in the medical surveillance program and to provide accurate and truthful information in the evaluation process. Finally, it is the responsibility of the physician to follow the surveillance guidelines described in this document. It is incumbent upon the physician to report silica-related diseases when diagnosed and report these findings to individual workers. It is also the responsibility of the physician to maintain confidentiality of non-work-related medical findings.

IV. Conclusion
While silicosis is irreversible and sometimes fatal, it is preventable if a proper medical surveillance program is implemented. Limitation of exposure to respirable crystalline silica is the single most important aspect of prevention of silicosis and other silica-associated diseases. Only when employers, workers, and physicians and other health professionals take the team approach to medical surveillance can exposures to silica be reduced or eliminated. ACOEM strongly supports any and all efforts to reduce occupational silica exposure.

Acknowledgement
This ACOEM guideline was developed by Lawrence Raymond, MD, and members of the ACOEM Occupational and Environmental Lung Disorder Committee under the auspices of the Council on Scientific Affairs. The guideline was peer reviewed by the Committee and Council and was approved by the ACOEM Board of Directors on February 6, 2005.

References

1. NIOSH/Department of Labor Fact Sheet. Preventing Silicosis. October 31, 1996.

2. Office of the Federal Register. 1994. 29 CFR 1910.1000. US Government Printing Office. Washington, DC.

3. American Thoracic Society. Adverse effects of crystalline silica exposure. Amer J Respir Crit Care Med. 1997;155(2):761-8.

4. Steenland K, Brown D. Silicosis among gold miners: exposure-response analyses and assessment. Am J Public Health.1995;85(10):1372-77.

5. Hnizdo E, Sluis-Cremer GK. Risk of silicosis in a cohort of white South African gold miners. Am J Ind Med. 1993;24(4):447-57.

6. Rosenman KD, Reilly MJ, Rice C, Hertzberg V, Tseng CY, Anderson HA. Silicosis among foundry workers. Implications for the need to revise the OSHA standard. Am J Epidemiol. 1996;144(9):890-900.

7. Freeman CS, Grossman EA. Silica exposures in the United States between 1980 and 1992. Scand J Work Environ Health. 1995;21 (suppl 2):47-49.

8. Wagner GR. The inexcusable persistence of silicosis. Am J Public Health. 1995;85(10):1346-7.

9. OSHA. Questions for Stakeholders on the Development of a Comprehensive Crystalline Silica Standard. June, 1999. www.osha.gov/dhs/stakeholdermeetings/Chic-sf.html.

10. Fedotov IA. Global elimination of silicosis: The ILO/WHO programme. Asian-Pacific Newsletter Occup Health Safety. 1997;pp.34-35.

11. NIOSH. Hazard Alert: Prevention of Silicosis and Deaths from Silicosis from Sandblasting. DHHS (NIOSH) Publ. No. 92-102. 1992.

12. NIOSH. Hazard Alert: Prevention of Silicosis and Deaths from Silicosis in Rock Drillers. DHHS (NIOSH) Publ. No. 92-107. 1992.

13. NIOSH. Hazard Alert: Prevention of Silicosis and Deaths in Construction Workers. DHHS (NIOSH) Publ. No. 96-112. 1992.

14. OSHA. Special Emphasis Program on Silicosis. (Web Page) Available at www.osha-slc.gov/Silica/SpecialEmphasis.html.

15. American Lung Association/Department of Labor. Press Releases of Joint Campaign on Silicosis Prevention. October 31, 1996.

16. NIOSH. The Work-Related Lung Disease Surveillance Report, 2002. DHHS (NIOSH) Publ. No. 2003-111. 2003.

17. CDC. Silicosis deaths among young adults. MMWR. 1998;47:331-335.

18. Ziskind M, Jones RN, Weill H. Silicosis. Am Rev Respir Dis. 1976;113(5):643-65.

19. Watkins-Pitchford W. The silicosis of the South African gold mines and the changes produced by it in legislative and administrative effort. J Ind Hyg. 1927;9:109-39.

20. Althouse RB, Bang KM, Castellan RM. Tuberculosis comortality with silicosis – United States, 1979-1991. Appl Occup Environ Hyg. 1995;10(12):1037-41.

21. Cowie RL. The epidemiology of tuberculosis in coal miners with silicosis. Amer J Respir Crit Care Med. 1994;150(5 Pt 1):1460-2.

22. Bailey WC, Brown M, Buechner HA, Weill H, Ichinose H, Ziskind M. Silico-mycobacterial disease in sandblasters. Amer Rev of Respir Dis. 1974;110(2):115-25.

23. Cordes LG, Brink EW, Checko PJ, et al. A cluster of Acinetobacter Pneumonia in foundry workers. Ann Intern Med. 1981;95(6):688-93.

24. Becklake MR. Occupational exposures: evidence for a causal association with chronic obstructive pulmonary disease. Amer Rev Respir Dis. 1989;140(3 Pt 2):S85-91.

25. Ng TP, Chan SL. Lung function in relation to silicosis and silica exposure in granite workers. Eur Respir J. 1992;5(8):986-91.

26. Cowie RL, Mabena SK. Silicosis, chronic airflow limitation, and chronic bronchitis in South African gold miners. Amer Rev Respir Dis. 1991;143(1):80-4.

27. Morgan WK. Industrial bronchitis. Br J Ind Med. 1978;35(4):285-91.

28. Holman CD, Psaila-Savona P, Roberts M, McNulty JC. Determinants of chronic bronchitis and lung dysfunction in Western Australian gold miners. Br J Ind Med. 1987;44(12):810-8.

29. Becklake MR, Irwig L, Kielkowski D, Webster I, de Beer M, Landau S. The predictors of emphysema in South African gold miners. Am Rev Respir Dis. 1987;135(16):1234-41.

30. Cowie RL. Silica-dust-exposed mine workers with scleroderma (systemic sclerosis). Chest. 1987;92(2):260-2.

31. Calvert GM, Rice FL, Boiano JM, Sheehy JW, Sanderson WT. Occupational silica exposure and risk of various diseases: an analysis using death certificates from 27 states of the United States. Occup Environ Med. 2003;60(2):122-9.

32. Stratta P, Canavese C, Messuerotti A, Fenoglio I, Fubini B. Silica and renal diseases: no longer a problem in the 21 st century? J Nephrol. 2001;14(4):228-47.

33. EL-Safty IA , Gadallah M, Shjouman AE. Effect of silica exposure on urinary excretion of copper and zinc. Amer J Med Sci. 2003;326(3):122-7.

34. Hotz P, Gonzalez-Lorenzo J, Siles E, Trujillano G, Lauwerys R, Bernard A. Subclinical signs of kidney dysfunction following short exposure to silica in the absence of silicosis. Nephron. 1995;70(4):438-42.

35. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans: Silica, some silicates, coal dust and para-aramid fibrils. Lyon , 15-22 October 1996. IARC Monogr Eval Carcinog Risks Hum. 1997;68:1-475.

36. Amandus H, Costello J. Silicosis and lung cancer in US metal workers. Arch Environ Health. 1991;46(2):82-9.

37. Steenland K, Stayner L. Silica, asbestos, man-made mineral fibers, and cancer. Cancer Causes Control. 1997;8(3):491-503.

38. Checkoway H, Franzblau A. Is silicosis required for silica-associated lung cancer? Am J Ind Med. 2000;37(3):252-9.

39. Attfield MD, Costello J. Quantitative exposure-response for silica dust and lung cancer in Vermont granite workers. Am J Ind Med. 2004;45(2):129-38

40. Graham WG, Costello J, Vacek PM. Vermont granite mortality study: an update with an emphasis on lung cancer. J Occup Environ Med. 2004;46(5):459-66.

41. Ferris BG. Epidemiology Standardization Project (American Thoracic Society). Am Rev Respir Dis. 1978;118(6 Pt 2):1-120.

42. Ruof J, Bruhlmann P, Michel BA, Stucki G. Development and validation of a self-administered systemic sclerosis questionnaire (SysSQ). Rheumatology ( Oxford ) 1999;38(6):535-42.

43. Office of the Federal Register. 1994. 29 CFR 1910.1001. US Government Printing Office. Washington, DC.

44. Huebner RE, Schein MF, Bass JB Jr. The tuberculin skin test. Clin Infect Dis. 1993; 17(6):968-75.

45. Centers for Disease Control and Prevention. Screening for Tuberculosis and Tuberculosis Infection in High-Risk Populations. Recommendations of the Advisory Council for the Elimination of Tuberculosis. MMWR. 1995;44(RR-11):19-34.

46. Wagner GR. Asbestosis and silicosis. Lancet. 1997;349(9061):1311-5.

47. ILO (International Labor Office). Classification of Radiographs of the Pneumoconiosis. Med Radiogr Photogr. 1981;57(1):2-17.

48. International Labor Office. Guidelines for the use of the ILO International Classification of radiographs of pneumoconiosis. Revised Edition 2000. International Labor Organization. Geneva .

49. American Thoracic Society. Standardization of spirometry, 1994 update. Am J Respir Crit Care Med. 1995;152(3):1107-36.

50. American Thoracic Society. Lung function testing: selection of reference values and interpretative strategies. Am Rev Respir Dis. 1991;144(5):1202-18.

51. Townsend M. ACOEM position statement. Spirometry in the occupational setting. J Occup Environ Med. 2000;42(3):228-45.

52. ACOEM Position Statement. Evaluating pulmonary function change over time in the occupational setting. J Occup Environ Med in publication. (Also available on-line)

53. NIOSH: Criteria for a Recommended Standard: Occupational Exposure to Respirable Coal Mine Dust. September, 1995

54. Wang ML, Petsonk EL. Repeated measures of FEV1 over six to twelve months: what change is abnormal? J Occup Environ Med. 2004;46(6):591-5.

55. Crapo RO, Forster RE 2nd. Carbon monoxide diffusing capacity. Clin Chest Med. 1989;10(2):187-98.

56. American Thoracic Society. Single-breath carbon monoxide diffusing capacity (transfer factor). Recommendations for a standard technique - 1995 update. Am J Respir Crit Care Med. 1995;152(6 Pt 1):2185-98.

57. Conrad K, Mehlhom J, Luthe K, Dorner T, Frank KH. Systemic lupus erythematosus after heavy exposure to quartz dust in uranium mines: clinical and serological characteristics. Lupus. 1996;5(1):62-9.

58. Basaran N, Shubair M, Undeger U, Kars A. Monitoring of DNA damage in foundry and pottery workers exposed to silica by the alkaline comet assay. Am J Ind Med. 2003;43(6):602-10.

59. Kopinski P. Use of flow cytometry in evaluation of cellular changes in interstitial lung diseases [in Polish; English abstract]. Folia Med Cracov. 1997;38(3-4):69-115.

60. Altindag ZZ, Baydar T, Isimer A, Sahin G. Neopterin as a new biomarker for the evaluation of occupational exposure to silica. Int Arch Occup Environ Health. 2003;76(4):318-22.

61. Chen F, Shi X. NF-kappaB, a pivotal transcription factor in silica-induced diseases. Mol Cell Biochem. 2002;234-235(1-2):169-76.

62. Castranova V, Porter D, Millecchia L, Ma JY, Hubbs AF, Teass A. Effect of inhaled crystalline silica in a rat model: time course of pulmonary reactions. Mol Cell Biochem. 2002;234-235(1-2):177-84.

63. Fubini B, Hubbard A. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) generation by silica in inflammation and fibrosis. Free Radic Biol Med. 2003;34(12):1507-16.

64. Fireman E, Greif J, Schwarz Y, et al. Assessment of hazardous dust exposure by BAL and induced sputum. Chest. 1999;115(6):1720-8.

65. Lerman Y, Schwarz Y, Kaufman G, Ganor E, Fireman E. Case series: use of induced sputum in the evaluation of occupational lung diseases. Arch Environ Health. 2003;58(5):284-9.

66. American Thoracic Society/Centers for Disease Control and Prevention. Targeted tuberculin testing and treatment of latent tuberculosis infection. Am J Respir Crit Care Med. 2000;161(4 Pt 2):S221-47.

 

Return to Policies and Position Statements

Home | Join Today | Contact Us | Privacy | Site Map 

American College of Occupational and Environmental Medicine
25 Northwest Point Blvd., Suite 700
Elk Grove Village, Illinois, 60007-1030
Telephone: 847/818-1800, Fax: 847/818-9266

© 2010 ACOEM. All Rights Reserved.