Open Access

Do bullae and emphysema increase risk of pneumothorax in silicosis?

  • Iraj Mohebbi1Email author,
  • Ebrahim Hassani2,
  • Shaker Salarilak3 and
  • Abdul Rahman Bahrami4
Journal of Occupational Medicine and Toxicology20072:8

DOI: 10.1186/1745-6673-2-8

Received: 22 April 2007

Accepted: 15 September 2007

Published: 15 September 2007

Abstract

Background

The occurrence of occupational lung diseases is decreasing due to improvements in occupational health in recent years; however, silicosis and its complications remain important occupational health problems. We have studied the role of emphysema and bullae as predictive factors of secondary spontaneous pneumothorax in acute and accelerated silicosis.

Methods

This study was carried out using questionnaire items on occupational history and conventional computed tomography of lungs. Differences between two groups (silicosis with and without secondary spontaneous pneumothorax) in terms of age, interval of exposure-diagnosis and therefore silica exposure duration were assessed by independent t-test. Fisher's exact test was used to determine the association between secondary spontaneous pneumothorax and both emphysema and bullae.

Results

We found a significant association between secondary spontaneous pneumothorax and bullae in acute and accelerated silicosis.

Conclusion

Pneumothorax in silicosis could be attributed to previous bullae.

Background

Pneumothorax is the presence of air in the pleural cavity [1]. The spontaneous form is generally due to the rupture of subpleural blebs. Clinical diagnosis of pneumothorax is established by history, physical examination and where possible, by radiological investigations [24]. Secondary spontaneous pneumothorax (SSP) occurs as a complication of an underlying lung disease, which can be identified. Chronic obstructive pulmonary disease (COPD) and Pneumocystis carinii pneumonia are the most common conditions associated with SSP [1, 5]. Pleural involvement in silicosis is rare and SSP is the only recognised pleural complication of silicosis [611]. SSP is usually unilateral, when it occurs in the course of silicosis. There are only a few reports in which patients with silicosis had bilateral SSP [9, 11]. Some investigators have reported that emphysema and bullae formation may lead to the occurrence of SSP [3, 12]. Emphysema is defined as enlargement of airspaces distal to the terminal bronchiole, accompanied by destructive changes of alveolar walls [13]. It is usually classified into the following three main subtypes: centrilobular emphysema; panlobular emphysema; and paraseptal emphysema [14]. Bullae can develop in association with any type of emphysema. A bulla is a sharply demarcated area with a diameter greater than 1 cm and possessing a wall less than 1 mm in thickness [15].

This case-control study was performed to evaluate the association between SSP and both emphysema and bullae on the basis of lung conventional computerized tomography (CCT) scan in the non-smoker silicotic patients.

Methods

We studied all of registered silicotic patients who had immigrated as seasonal temporary workers from West Azarbaijan province to the stone grinding factories of Azandarian area. Pneumothorax was defined by detection of the thin, visceral line in the expiratory postero-anterior chest radiographs that was displaced from the chest wall. Those who suffered pneumothorax selected as case group and others as control.

Characteristics of the factories and study population

From September 2000 to March 2006, 21 subjects with silicosis had been registered in the Urmia Occupational Medical Center of West Azarbaijan province in Iran. They had immigrated as seasonal workers from West Azarbaijan province (in the west of Iran) to the Azandarian area, a suburb of Hamadan province in the center of Iran. This area located 750 Km far away from West Azarbaijan province, and also is a base for stone-cutting and stone-grinding factories in Hamadan province. Each factory usually employs 5 to 10 seasonal temporary workers from various districts. We studied only workers who were resident in the West Azarbaijan province with history of employment in aforementioned factories. We did not have accesses to other workers, because they were scattered in other provinces. All of the workers who are included in this study had previously worked in the same stone-grinding factories in the Azandarian area. They did not have any reported silica exposure before working at those workplaces. They described the working environment as being very dusty, with no provision of engineering control or exhaust ventilation.

Diagnostic methods

Diagnosis of silicosis was made on the basis of clinical findings, chest radiological criteria in accordance with the ILO International Classification of Radiographs of Pneumoconiosis, an unequivocal history of substantial silica dust exposure and an appropriate interval of time after exposure. We defined acute and accelerated silicosis according to NIOSH definition [16]. Patients with silicosis were entered into the study if the high voltage posterior-anterior radiograph of the chest with acceptable quality showed reticular-nodular shadowing at least 1/1 profusion grade according to the ILO system. Expiratory postero-anterior chest radiography was reviewed for detection of pneumothorax and also SSP was defined by identification of the thin, visceral line that was displaced from the chest wall. In each subject, CCT of lung was reviewed for recognition of emphysema and bullae. For each subject, a detailed history of work occupations was recorded as follows: (a) the age of onset of exposure to silica dust; (b) the age when the exposure to silica dust ended; (c) the age when the initial diagnosis was made.

CCT procedures

The scanners of GE 4000 SYTEC (GE Medical Systems, Milwaukee, WI, USA) and X VISION-EX CT (Toshiba; Tokyo, Japan) were used for recognition of emphysema and bullae. For each subject, CCT scans had been obtained with 10 mm collimation at 1 cm intervals from the upper to the lower thorax in the supine position. Emphysema was defined as well-delineated focal peripheral areas surrounded by a thin wall and less than 10 mm in diameter. If an area of emphysema was greater than 1 cm in diameter, this was defined as a bulla.

Stone grinding process

There was the same process in the 20 stone grinding factories as follows: The quartz stone is first put into a jaw crusher where large stone is broken into smaller pieces, which are then taken through a conveyor belt to disintegrator, which makes powder out of these small pieces. It is then separated according to its fineness through a vibrating screen. The quartz powder is also passed through a magnetic separator in order to remove the extraneous ferrous material from the product raw material.

Characteristics of the occupational exposure

In the Azandarian area where the patients had been employed, all of the stone-grinding factories were selected for the assessment of environmental exposure of silica particles. The determination of quartz was carried out according to the NIOSH method number 7500. A rotameter was used to adjust the flow. The respirable dust samples were collected on 25 mm cellulose acetate filters (pore size 0.8 μm) placed in a 25 mm conductive plastic cyclone. The cyclone was attached to the worker's overalls as closely as possible to the face in order to determine respirable dust in the breathing zone. The filters were conditioned in desiccator environmental chamber for 24 hours at 25°C and weighed before and after testing to determine total penetrating weights. The analysis was done by X-ray diffraction (XRD) using a Siemens Model D5000 diffractometer equipped with variable slit in research laboratory of X-ray at the Faculty of Science, Tehran University.

Statistical analysis

Statistical analysis was performed using commercially available software (SPSS 10.0 for Windows; SPSS; Chicago, IL, USA). Differences between the two groups (silicosis with SSP and silicosis without SSP) in age, interval between the onset of exposure to silica dust and clinical diagnosis of silicosis, and silica exposure duration were assessed by independent t-test. We used Fisher's exact test to determine the association between SSP and predictive factors that included emphysema and bullae.

Results

The total working period was 12 to 14 h a day for 1 to 5 consecutive years. All of the subjects were male and non-smokers with the youngest being 20 and the oldest 79, of whom 18 (86%) were younger than 40. The acute and accelerated silicosis were found in 43% and 57%, respectively. Latency periods of the acute and accelerated forms were 3.2 ± 0.83 (mean ± SD) and 6.4 ± 1.6 (mean ± SD) years, respectively. In the chest radiographs, 3(14.3%) had radiological profusion category 1, and8(38.1%) category 2. 10 (47.7%) showed category3. The most common subcategories of small opacities profusion was 3/3 (42.9%).

In patients who experienced SSP, the interval between the onset of exposure to silica dust and clinical diagnosis of silicosis was 3.2 ± 1.1 (mean ± SD) years and in those without SSP, it was 5.42 ± 1.60 years. The mean of exposure duration in patients with SSP was 2.14 ± 1 years and in those without SSP, it was 2.86 ± 1.2 years. The difference in age between the two groups at the end of exposure was not significant. There was a significant difference between the two groups in the interval from first silica exposure to diagnosis of SSP and no significant differences in exposure duration (Table 1).
Table 1

Comparison of age, interval between onset of exposure and clinical diagnosis, and exposure duration between the two groups

Variable

Silicosis with SSP(mean ± SD)

Silicosis without SSP (mean ± SD)

T

p value

Age at the end of exposure (years)

26.43 ± 5.85

34.50 ± 17.7

1.22

0.073

Interval between the onset of exposure and clinical diagnosis (years)

3.2 ± 1.1

5.42 ± 1.6

3.5

0.002

Exposure duration (years)

2.14 ± 1

2.86 ± 1.2

1.3

0.19

In our study, SSP was identified in 34% of subjects (Figure 1) of which 19% was bilateral. Emphysema and bullae were found in 49% and 52%, respectively (Figure 2). There was a high odds ratio between SSP and emphysema (odds ratio = 10.8 CI; 0.997–117). We found that the probabilities of SSP were higher in those with bullae (odds ratio = 15 CI; 1.3–168), as shown in Table 2.
Figure 1

CT. 1: Large localized pneumothorax in right lung. 2: Mixed alveolar and interstitial fibrosis. 3: Pleural thickening in right lung. 4: Several bullae in right lung. 5: Alveolar and interstitial shadowing. 6: Paraseptal emphysema in anterior segment of left upper lobe.

Figure 2

CT. 1: Hydropneumothorax in right lung. 2: Multiple bullae in both lungs. 3: Paraseptal emphysema in left lung. 4: Mixed alveolar and interstitial pattern as silicoproteinosis and fibrosis. 5: Air bronchogram

Table 2

Odds ratio and comparison of risk factors between the two groups

Risk Factor

 

Pneumothorax

Odds ratio

95% Confidence Interval

  

No

Yes

  

Bullae

No

10

1

15

1.3–168

 

Yes

4

6

  

Emphysema

No

9

1

10.8

.997–117

 

Yes

5

6

  
The silica particles in the ambient air at all of the factories were higher than OSHA level, as shown in Table 3.
Table 3

Exposure assessment in each industrial unit (mg/m 3)

Industrial unit

Total dust

Total Respirable dust

Respirable quartz

1

1355.37

66.70

17.35

2

1438.21

78.34

19.60

3

1442.21

79.45

17.89

4

1472.73

83.87

20.34

5

1542.32

88.45

22.87

6

1618.71

94.45

26.00

7

1624.45

83.45

23.90

8

1641.34

105.54

31.89

9

1645.13

104.79

32.90

10

1725.75

109.86

31.00

11

1747.00

111.27

39.90

12

1747.00

121.32

42.27

13

1747.45

121.30

42.80

14

1836.73

126.97

44.90

15

1845.37

127.12

44.89

16

1924.14

134.12

45.89

17

1995.34

134.78

50.90

18

2032.80

159.45

56.90

19

2058.81

141.00

48.50

20

2067.83

134.60

44.80

Discussion

The results of the present study demonstrate that in individuals with advanced silicosis, SSP is significantly associated with the presence of bullae. The results also indicate that advanced silicosis causes distal airspace enlargement independent of smoking.

To the best of our knowledge, predictive factors of SSP as a complication of silicosis have not been extensively described in the literature [1, 5]. Choi et al. studied 458 patients who underwent transthoracic needle biopsy (TTNB). They found a significantly higher (p < 0.001) risk of pneumothorax in patients with emphysema and concluded that development of pneumothorax may be prevented by the elastic recoil of the normal lung parenchyma and pleura [17]. Mitlehner et al. suggested that the presence of bullae in patients with primary spontaneous pneumothorax has no predictive value for the future development of recurrences [18]. Conversely, bullae rupture in SSP appears to be due to local airway obstruction, emphysema susceptibility, and the presence of bronchial abnormalities [3]. Functionally, massive fibrosis results in stiff nondistensible lungs with increased elastic recoil [19]. In advanced silicosis, coalescence of perinodular emphysematous regions may lead to formation of macroscopic blebs, which can rupture causing a pneumothorax [12]. Our findings were consistent with these findings and indicate that the occurrence of SSP could be attributed to the presence of bullae.

In the absence of smoking, coal pneumoconiosis and confluent silicosis are associated with emphysematous changes in the lungs [20]. Some investigators have reported that emphysema with silicosis has also been observed to occur independently of smoking [21, 22]. Emphysema is common in silicosis and has been attributed as the major cause of corpulmonale and disability rather than fibrosis by some investigators [23].

In this study, all of the subjects were non-smokers and the results confirmed that emphysematous changes are common in non-smoker silicotic patients.

In a case series study, Kawano et al. suggested that there was no correlation between the onset of SSP and duration of occupational exposure to silica [24]. Our findings support this hypothesis as shown in Table 1. According to an investigation by Bahrami and Mahjub in the stone-grinding factories where the study subjects had been employed, the concentration of silica compounds in the ambient air had been 25–50 times higher than Occupational Safety and Health Administration (OSHA) levels [25]. Our findings were consistent with these findings. Our study also showed that the interval between the onset of exposure and clinical diagnosis of silicosis was statistically different for both groups, but both of them were exposed to extremely high levels of respirable silica. In summary, development of SSP may be enhanced by increased elastic recoil of the lung parenchyma, and bullae rupture. There is a high probability of SSP occurring in acute and accelerated silicosis.

Historically, people employed in stone-grinding factories are from lower income backgrounds and have not had the advantage of regular medical surveillance or specialized care until their conditions become very advanced. A significant difference between the two groups in the interval from first silica dust exposure to clinical diagnosis of silicosis might possibly be a confounding issue that silicosis may be misdiagnosed due to lack of appropriate health surveillance. We concluded that a brief, but intensive exposure to silica dust could cause SSP after a short latency period. It is recommended that an effective hygiene program be implemented to monitor the health of these workers.

Our methodology for assessing odds ratios and the association between pneumothorax and both bullae and emphysema in silicosis has both strengths and weaknesses. Its strengths are as follows. All subjects had worked in the same unregulated stone-grinding workplaces and had no history of smoking, underlying disease of COPD and/or other mineral dust exposure. Information was available on the specific occupational exposure to silica powder in the stone-grinding factories. Although the sample size in our study was only 21, to the best of our knowledge, it is larger than any previous study of pneumothorax in silicosis worldwide, so its major strength is due to the number of cases. A final strength is that information was available on possible confounding factors such as tobacco use.

The main limitation of our study also concerns the number of subjects; however, we attempted to find all of scattered workers. We used the opportunity and discussed the implications for enforcement of regulations on a national level to prevent the occurrence of silicosis (especially in Hamadan province where this outbreak had occurred). Due to the rarity of acute and accelerated silicosis and also SSP in silicosis, statistical analysis of binary outcomes is almost always based on odds ratios and it is the same as the risk ratio [26]. Therefore, we believe this study might be a good estimation of odds ratio or relative risk of SSP in acute and accelerated silicosis.

Conclusion

Our study findings reemphasize the clinical importance of SSP and its association with bullae. The results also indicate that advanced silicosis causes distal airspace enlargement independently of smoking.

Abbreviations

CCT: 

Conventional computerized tomography

COPD: 

Chronic obstructive pulmonary disease

ILO: 

International Labour Office

NIOSH: 

National Institute for Occupational Safety and Health

OSHA: 

Occupational Safety and Health Administration

SSP: 

Secondary spontaneous pneumothorax

TTNB: 

Transthoracic needle biopsy

Declarations

Acknowledgements

This work was performed at the Urmia Medical Sciences University, Urmia, Iran. None of the authors has any financial interest in any of the products mentioned in this article. We would like to thank Dr Mehrdad Arjomandi for his distinguished recommendations and review of the manuscript. The authors are grateful to Dr Zubeyri, Dr Mohammadi, and Dr Jalili in the CT imaging suite of Urmia Medical Sciences University for their assistance. Thanks also to Alpha Science Editors for English editing services and to all West Azerbaijan Healthcare staff for their help.

Authors’ Affiliations

(1)
Department of Occupational Medicine, Urmia University of Medical Sciences
(2)
Department of Anesthesiology, Urmia University of Medical Sciences
(3)
Department of Community Medicine, Urmia University of Medical Sciences
(4)
Department of Occupational Health, Hamadan University of Medical Sciences

References

  1. Sahn SA, Heffner JE: Spontaneous pneumothorax. N Engl J Med 2000, 342: 868–874. 10.1056/NEJM200003233421207View ArticlePubMedGoogle Scholar
  2. Strobel SL: Pathologic quiz case: Recurrent spontaneous pneumothorax in an industrial worker. Arch Pathol Lab Med 2002, 126: 749–750.PubMedGoogle Scholar
  3. Al-Qudah A: Treatment options of spontaneous pneumothorax. Indian J Chest Dis Allied Sci 2006, 48: 191–200.PubMedGoogle Scholar
  4. Weill H, Jones RN, Parkes WR: Silicosis and related diseases. In Occupational Lung Disorders. 3rd edition. Edited by: Parkes WR. Oxford, UK: Butterworth-Heinemann; 1994:285–339.Google Scholar
  5. Gupta D, Hansell A, Nichols T, Duong T, Ayres JG, Strachan D: Epidemiology of pneumothorax in England. Thorax 2000, 55: 666–671. 10.1136/thorax.55.8.666PubMed CentralView ArticlePubMedGoogle Scholar
  6. Light RW: Disease of the pleura, mediastinum, chest wall, and diaphragm. In Chest Medicine, Essentials of Pulmonary and Critical Care Medicine. 4th edition. Edited by: George RB, Light RW, Matthay MA, Matthay RA. Philadelphia, PA: Lippincott, Williams & Wilkins; 2000:441–477.Google Scholar
  7. Kobashi Y, Manabe T, Hara H, Nakashima T, Matsushima T: A case of silicoproteinosis with pneumothorax. Nihon Kokyuki Gakkai Zasshi 2003, 41: 117–122.PubMedGoogle Scholar
  8. Suratt PM, Winn WC, Brody AR, Bolton WK, Giles RD: Acute silicosis in tombstone sandblasters. Am Rev Respir Dis 1977, 115: 521–529.PubMedGoogle Scholar
  9. Rao S, Rau PV: Bilateral spontaneous pneumothorax in silicosis. Indian J Chest Dis Allied Sci 1993, 35: 47–49.PubMedGoogle Scholar
  10. Gupta KB, Manchanda M, Kaur P: Bilateral spontaneous pneumothorax in silicosis. Indian J Chest Dis Allied Sci 2006, 48: 201–203.PubMedGoogle Scholar
  11. Arora VK, Seetharaman ML, Veliath AJ: Silicotic alveolar proteinosis with bilateral spontaneous pneumothorax. J Assoc Physicians India 1992, 40: 760–762.PubMedGoogle Scholar
  12. Davis SG: Silicosis. In Occupational Disorders of the Lung. 1st edition. Edited by: Hendrick DJ, Burge PS, Becket WS, Churg A. WB Saunders; 2002:105–127.Google Scholar
  13. American Thoracic Society: Chronic bronchitis, asthma, and pulmonary emphysema: statement by the Committee on Diagnostic Standards for Nontuberculous Respiratory Disease. Am Rev Respir Dis 1962, 85: 762–768. [ISI]Google Scholar
  14. Thurlbeck WM, Müller NL: Emphysema: definition, imaging, and quantification. AJR Am J Roentgenol 1995, 163: 1017–1025.View ArticleGoogle Scholar
  15. Tuddenham WJ: Glossary of terms for thoracic radiology: recommendations of the Nomenclature Committee of the Fleishner Society. AJR Am J Roentgenol 1984, 143: 509–517.View ArticlePubMedGoogle Scholar
  16. NIOSH: NIOSH Case Study in Occupational Epidemiology. SILICOSIS IN SANDBLASTERS. DHHS (NIOSH) Publication; 2002:1–21.Google Scholar
  17. Choi CM, Um SW, Yoo CG, Kim YW, Han SK, Shim YS, Lee CT: Incidence and risk factors of delayed pneumothorax after transthoracic needle biopsy of the lung. Chest 2004, 126: 1516–1521. 10.1378/chest.126.5.1516View ArticlePubMedGoogle Scholar
  18. Mitlehner W, Friedrich M, Dissmann W: Value of computer tomography in the detection of bullae and blebs in patients with primary spontaneous pneumothorax. Respiration 1992, 59: 221–227.View ArticlePubMedGoogle Scholar
  19. Redlich CA: Pulmonary fibrosis and interstitial lung diseases. In Occupational and Environmental Respiratory Disease. 1st edition. Edited by: Harber P, Schenker MB, Balmes JR. Mosby; 1996:216–227.Google Scholar
  20. Begin R, Filion R, Ostiguy G: Emphysema in silica- and asbestos-exposed workers seeking compensation. A CT scan study. Chest 1995, 108: 647–655.View ArticlePubMedGoogle Scholar
  21. American Thoracic Society Committee of the Scientific Assembly of Environmental and Occupational Health: Adverse effects of crystalline silica exposure. Am J Respir Crit Care Med 1997, 155: 761–765.View ArticleGoogle Scholar
  22. Oxman AD, Muir DCF, Shannon HS, Stock SR, Hnizdo E, Lange HJ: Occupational dust exposure and chronic obstructive pulmonary disease. Am Rev Respir Dis 1993, 148: 38–48.View ArticlePubMedGoogle Scholar
  23. Murray J, Reid G, Kielkowski D, de Beer M: Cor pulmonale and silicosis: a necropsy based case control study. Br J Ind Med 1993, 50: 544–548.PubMed CentralPubMedGoogle Scholar
  24. Kawano M, Miura H, Anan H, Shimizu M: Treatment of secondary spontaneous pneumothorax complicating silicosis and progressive massive fibrosis. Kurume Med J 2002, 49: 35–40.View ArticlePubMedGoogle Scholar
  25. Bahrami AR, Mahjub H: Comparative study of lung function in Iranian factory workers exposed to silica dust. East Mediterr Health J 2003, 9: 390–398.PubMedGoogle Scholar
  26. Kirkwood BR, Stern JAC: Comparing two proportions. In Essential Medical Statistics. 2nd edition. Edited by: Kirkwood BR, Stern JAC. Blackwell Science; 2003:148–164.Google Scholar

Copyright

© Mohebbi et al; licensee BioMed Central Ltd. 2007

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Advertisement