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CASE REPORT |
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Year : 2019 | Volume
: 23
| Issue : 2 | Page : 90-92 |
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Blowing balloons and pulmonary talcosis: An uncommon hazard
Mahismita Patro1, Dipti Gothi1, Umesh Ojha2, Ram B Sah1, Sameer Vaidya1
1 Department of Pulmonary Medicine, ESI-PGIMSR, New Delhi, India 2 Department of Pulmonary Medicine, ESI-PGIMSR; Institute of Occupational Health and Environmental Research, ESIC Hospital, Basaidarapur, New Delhi, India
Date of Submission | 17-Oct-2018 |
Date of Acceptance | 19-Mar-2019 |
Date of Web Publication | 25-Sep-2019 |
Correspondence Address: Dr. Dipti Gothi Department of Pulmonary Medicine, ESI-PGIMSR, Basaidarapur, New Delhi – 110 015 India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/ijoem.IJOEM_222_18
A 65-year-old nonsmoker man presented with bilateral upper lobe conglomerated calcific opacities with basal reticulations. The patient denied any significant occupational exposure. Repeated and persistent enquiry revealed an intense exposure to talc 20 years back, from blowing balloons stained with talc powder for a period of 1 year. To the best of our knowledge, only one case has been reported in the past with talcosis due to balloon blowing.
Keywords: Balloons, interstitial lung disease, talcosis
How to cite this article: Patro M, Gothi D, Ojha U, Sah RB, Vaidya S. Blowing balloons and pulmonary talcosis: An uncommon hazard. Indian J Occup Environ Med 2019;23:90-2 |
How to cite this URL: Patro M, Gothi D, Ojha U, Sah RB, Vaidya S. Blowing balloons and pulmonary talcosis: An uncommon hazard. Indian J Occup Environ Med [serial online] 2019 [cited 2023 Feb 7];23:90-2. Available from: https://www.ijoem.com/text.asp?2019/23/2/90/267758 |
Introduction | |  |
Talc is a hydrated magnesium silicate [Mg3 Si4O10(OH)2] that has been widely used for many purposes in daily life and various industries such as chemical, ceramic, cosmetic, leather, paper, and building. It is known to be fibrogenic due to an immunological response. Exposure to talc by inhalation or intravenous use has been associated with many forms of lung disease. The diagnosis of talc-induced interstitial lung disease is based on radiological findings, histological findings, and a consistent history of exposure. We present an uncommon case of pulmonary talcosis in a 65-year-old man who had relatively short but intense exposure to talc due to blowing of talc-stained balloons, in the remote past.
Case Report | |  |
A 65-year-old man presented with complaints of cough and exertional dyspnea for 2 months. He was a former smoker with smoking index of 30 pack-years and had quit smoking since the last 10 years. He was a vendor by occupation, making and selling fast-food items. He denied exposure to biomass fuels or any other occupational exposure to dust and fumes. There was no history of tuberculosis or any medical illness in the past. On examination, his pulse rate was 104/min, blood pressure 110/70 mmHg, and oxygen saturation 98% on room air. On respiratory system examination, he had bilateral rhonchi with occasional basal fine crepitations. The other system examinations were normal. Routine investigations showed hemoglobin of 15.5 g/dL, total leucocyte count of 7300/μL, blood sugar level of 105 mg/dL, and urea of 25 mg/dL. The chest radiograph showed large fibrocalcific opacities in bilateral upper zones [Figure 1]. High-resolution computed tomography (HRCT) of chest showed presence of conglomerated masses of high attenuation in bilateral upper lobes along with bilateral basal intralobular and interlobular septal thickening with architectural distortion [Figure 2] and [Figure 3]. Bronchoscopy did not reveal any endobronchial abnormalities. Bronchoalveolar lavage was negative for mycobacteria and other infectious agents, and no neoplastic cells were found. Transbronchial biopsy from right lower lobe showed lung tissue with mild focal septal thickening, exfoliated respiratory epithelial cells, and focal lymphocytes with anthracotic pigment. Iron stain was negative and macrophages did not show any conspicuous particles or asbestos bodies. Spirometry was normal with an Forced expiratory volume in first second (FEV1) of 70% of predicted, forced vital capacity (FVC) of 75% of predicted, and FEV1/FVC ratio of 0.73. Further enquiry into his occupational history revealed that he had worked in a factory, where his job was to blow balloons 20 years ago. He worked there for 2 years and had to blow balloons throughout the day during which he had an intense exposure to dust containing talc. The balloons were coated with a thin layer of talc from inside to prevent sticking among themselves. There were no dust control measures. He denied having any other exposures to dust except for this period. He also confirmed that two of his coworkers had similar lung disease. | Figure 1: Chest radiograph in posteroanterior projection showing bilateral upper zone fibrocalcific opacities
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 | Figure 2: Computed tomography scan showing bilateral upper lobe conglomerated fibrocalcific masses similar to progressive massive fibrosis
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 | Figure 3: Computed tomography scan showing bilateral basal reticulation and septal thickening
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Discussion | |  |
Talc is known to cause lung disease due to its inflammatory and fibrogenic properties. The patterns of pulmonary disease related to talc exposure can be of four types: (1) talco-silicosis, caused due to inhalation of talc contaminated with silica, (2) talco-asbestosis due to inhalation of talc contaminated with asbestos, (3) pure talcosis due to inhalation of talc in the absence of other minerals, and (4) pulmonary talcosis in intravenous drug abusers. Talco-asbestosis and talco-silicosis related to inhalational exposure of talc closely resemble pure asbestosis and silicosis, respectively. Talco-asbestosis can also be associated with lung cancer as with pure asbestosis. Pure talcosis may cause acute or chronic bronchitis and interstitial inflammation.[1],[2] Talcosis in intravenous drug users is due to injection of talc containing oral medications such as methylphenidate, methadone, diazepam, promethazine, cocaine, acetaminophen, meperidone, pentazocine, oxymorphone, and heroin. These medications contain talc as a bulking and lubricating agent. The drug abusers use these medications parenterally by crushing the oral tablets and reconstituting them in saline or sterile water. This leads to intravascular dissemination of talc particles, entrapment in the pulmonary vasculature, and granulomatous reaction in the pulmonary interstitium.[3]
The radiological manifestations of talcosis include small centrilobular nodules, ground-glass opacities, reticulations, hilar adenopathy, foreign body granulomas, and emphysema. They can be either diffuse or predominantly in the lower zones. With progressive disease, the nodule confluence leads to large opacities especially in the upper zones. They are seen on CT as large confluent masses with internal foci of high attenuation and resemble that of progressive massive fibrosis. The pattern of involvement in inhalational and intravenous exposures differs. In inhalational exposure, apical involvement is seen and emphysema is centrilobular type. Whereas in intravenous drug users the lung apices and costophrenic sulci are generally spared and emphysema is panlobular type with a basal predominance.[4],[5]
The diagnosis of occupational lung disease requires the presence of following criteria: (1) the clinical presentation and workup to be consistent with the diagnosis, (2) previously established causal relationship between exposure and diagnosis, (3) history of sufficient exposure, (4) temporal relationship between exposure and disease, and (5) absence of other likely diagnosis.[6] Our patient was diagnosed with talcosis on the basis of the diagnostic criteria for occupational lung disease, presence of talc exposure, HRCT pattern, pathological finding of interstitial fibrosis without any specific pattern, and history of coworkers having similar disease.
Talcosis has a slowly progressive course. It can occur even after exposure to the dust has ceased.[7] The first case of talc pneumoconiosis was reported by Thorel in 1896, following which there have been many reports of talcosis in intravenous drug abusers and those with inhalational exposure due to heavy use of talcum powder for cosmetic purposes.[8] But to the best of our knowledge, there is only one case report of talcosis secondary to blowing of talc stained balloons, in an accountant engaged in recreational activity of blowing balloons.[9] Usually fresh-from-the-factory balloons have a thin layer of talc powder from inside to keep them from sticking to themselves. While blowing them up, the subjects inhale heavy amount leading to progressive deposition in the lungs.
There are various ways by which inhalation of talc during blowing of balloons can be avoided. Breathing through nose rather than mouth helps in avoidance of direct inhalation of talc. Use of electronic blowing devices to inflate the balloons is also a safe alternative.[10] However, these safety measures were not followed at workplace in our patient. With proper implementation of such safe practices, this occupational hazard of talc pneumoconiosis can be avoided. This case is possibly a tip of the iceberg of balloon blowing industry in India.
To conclude, for appropriate diagnosis, a detailed history of exposure including those in the remote past, which might sometimes be forgotten, is important in every case of interstitial lung disease. Also, safety measures in balloon blowing industry should be standardized to prevent this irreversible disease.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References | |  |
1. | Gysbrechts C, Michiels E, Verbeken E, Verschakelen J, Dinsdale D, Nemery B, et al. Interstitial lung disease more than 40 years after a 5 year occupational exposure to talc. Eur Respir J 1998;11:1412-5. |
2. | Frank C, Jorge L. An uncommon hazard: Pulmonary talcosis as a result of recurrent aspiration of baby powder. Respir Med CME 2011;4:109-11. |
3. | Siddiqui MF, Saleem S, Badireddi S. Pulmonary talcosis with intravenous drug abuse. Respir Care 2013;58:e126-8. |
4. | Tukiainen P, Nickels J, Taskinen E, Nyberg M. Pulmonary granulomatous reaction: Talc pneumoconiosis or chronic sarcoidosis? Br J Ind Med 1984;41:84-7. |
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6. | Gulati M, Redlich CA. Occupational lung disorders: General principles and approaches. In: Fishman AP, editor. Fishman's Pulmonary Diseases and Disorders. 4 th ed. New York: McGraw-Hill Education; 2008. p. 936. |
7. | Jones RN, Weill H, Parkes WR. Disease related to non-asbestos silicates. “Talc” pneumoconiosis. In: Parkes WN, editor. Occupational Lung Disorders. 3 rd ed. Oxford: Butterworth-Heinemann; 1994. p. 536-50. |
8. | Thorel C. Talc lung: A contribution to the pathological anatomy of pneumoconiosis. Beitr Pathol Anat Allgem Pathol 1896;20:85-101. |
9. | Thomeer M, Van Bleyenbergh P, Nemery B, Demedts M. A breathless accountant who blew up balloons. Lancet 1999;354:124. |
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[Figure 1], [Figure 2], [Figure 3]
This article has been cited by | 1 |
Accidental Acute Talcum Powder Inhalation in an Adult: A Rare Case with a Short Review of Literature
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| Sadananda B. Naik, Mamatha Guruprasad | | Indian Journal of Critical Care Medicine. 2020; 24(6): 490 | | [Pubmed] | [DOI] | |
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