From the Departments of *Forensic Medicine and †Pathology (Cardiovascular and Thoracic Division), Seth GS Medical College, Mumbai, India.
Manuscript received August 20, 2012; accepted April 21, 2013.
The authors report no conflicts of interest.
Reprints: Pradeep Vaideeswar, MD, Department of Pathology (Cardiovascular and Thoracic Division), Seth GS Medical College, Parel, Mumbai 400 012, India. E-mail: email@example.com.
Talcosis is a rare form of pneumoconiosis caused by long-term exposure to talc (hydrous magnesium silicate) through inhalation or intravenous exposures. Although it occurs commonly as an occupational hazard or is due to abuse/overuse of talc, talcosis in the course of food adulteration is seldom or hardly reported. We present a case of talcosis in a worker who had considerable exposure to talc during the initial preparation of “samosa,” a triangular fried Indian savory. There were typical pulmonary histological findings of talcosis with extensive deposition of birefringent crystals in histiocytes. On account of this unusual pathogenesis, we have coined a new terminology “samosa pneumoconiosis” to describe this condition.
Pneumoconiosis is a disease of the lungs caused by inhalation of dust. Of all the different types of pneumoconiosis known, silicosis (caused by silica or silicon dioxide) is the most common and oldest, being documented since the era of Hippocrates and ancient Egypt.1 On the other hand, talcosis is a rare form of pneumoconiosis caused by long-term exposure to talc (hydrous magnesium silicate, often mixed with other contaminants) through inhalational or intravenous exposure and was first reported by Thorel2 in 1896. Although workers in various industries and intravenous drug abusers can present with this condition, pneumoconiosis developing during use of talc as a food adulterant is hitherto unheard of and unreported. We present a case of talcosis in a worker who had considerable exposure to talc during the initial preparation of “samosa,” a triangular fried Indian savory; he was brought dead in our hospital, and a medicolegal autopsy had been performed.
A 35-year-old man developed an acute episode of breathlessness while he was at work. He was immediately brought to the emergency services department where he was declared dead on arrival. As per the history obtained, he used to work as a cook for the last 5 years. He had no history of any illness at the time of recruitment. For the last 3 years, he had developed recurrent episodes of incessant cough with occasional spells of shortness of breath and gradual loss of weight. He frequented a nearby family physician, who provided him symptomatic treatment every now and then. For the last year, he was drained of much of his physical strength and used to tire out even on minimal labor.
A medicolegal autopsy was performed. On examination, nonspecific signs such as peripheral cyanosis and congestion of visceral organs were present. The lungs exhibited remarkable findings. The pleurae on both sides were mildly to moderately opacified with foci of puckering. The lungs were firm with congested and dark reddish-brown cut surfaces (Fig. 1). Fibrocavitatory lesions and large foci of caseation necroses were seen in the anterior segment of left upper lobe and right lower lobe, respectively (Fig. 1). Scrapings from zones of caseation were positive for acid-fast bacilli. Multiple, small, firm, glistening gray-white nodules, some with central cavitation (Fig. 1), were scattered all over, especially prominent in the lower lobes. On histology, the normal lung parenchyma was distorted because of large and small stellate foci of fibrosis around the bronchovascular bundles with collection of spindle-shaped to polygonal histiocytes and giant cells within the interstitium; they were responsible for the nodules seen on gross examination. Interestingly, the cytoplasm was packed with coarse needle-shaped to wafer-shaped yellowish crystals (Fig. 2). The zones of caseation also contained crystalline material and were bordered by granulation tissue with lymphocytes and crystal-laden macrophages (Fig. 3). Needle-shaped morphology was better appreciated on polarization (Fig. 4). The alveolar spaces were filled with macrophages containing similar crystals and exfoliated plump hyperplastic pneumocytes. The hilar and mediastinal lymph nodes were focally anthracotic.
Because of these extraordinary findings in the lung, one of the authors (D.N.) visited the deceased’s place of work. Contrary to the authors’ perception that the deceased was employed in an eatery or restaurant, the place was actually a small store room of size not more than 6 feet in all dimensions with no ventilation. The walls were lined by huge sacks of wheat flour and another white powder (locally called as “sang jira” powder), heaped on top of each other. The air inside the room was heavily laden with dust. The floor was covered with a thick layer of white dust. There were 4 workers in that room. On enquiring, they had confided that they (including the deceased) used to work in that dust-polluted room for 10 to 12 hours every day. Their job was to mix flour with sang jira and add water to make dough to prepare the ready-made outer covering (“patti”) of the samosas (this variety is designated as “patti samosa”). They refused to specify the quantitative proportion of each ingredient in the mixture. No protective gear was used. A wet preparation of a sample of sang jira (translated in English as powdered stone) and talcum powder was made and compared under microscope; they appeared identical. The sang jira powder was unperfumed talcum powder. To substantiate our diagnosis, mineralogical analysis of a lung tissue sample was done; the result showed presence of magnesium. Thus, the deceased had overwhelming pulmonary talcosis along with active tuberculosis.
Four variants of talc-induced pneumoconiosis have been described: talc asbestosis, talc silicosis, inhalational talcosis, and intravenous talcosis.3 The first 2 variants have radiological and pathological features almost identical to that of asbestosis and silicosis, respectively.3 Inhalational talcosis is generally encountered in workers engaged in mining and crushing industries; manufacture of ceramic, plastics, rubber, cosmetics, paint and confectioneries; and even pharmaceutical preparations.4 There are also studies on record to underline that talcosis can be caused by abundant use of cosmetic talcum powder.5 The subject of our study was exposed to pure talc for about 5 years through food adulteration, ultimately manifesting as talcosis. The samosa is an indigenous delicacy of India, cooked and savored by people all over the country. It is prepared by mashing boiled potatoes and creating a coat over it with a layer of flour, which is then fried in oil. Considering the rather rampant and flourishing adulterated food market in India, it comes as no surprise that flour was adulterated with unperfumed talc to make ready-made strips of dough. The talc was used to increase the volume of flour and was also supposed to increase the crispness of samosas.
Inhalational talcosis, on histology, may present as diffuse fibrosis of interstitium with dust-laden macrophages or irregular/stellate nodular collections of dust-laden macrophages and fibroblasts or as noncaseating granulomatous reaction.4,5 The size of the particles is mostly less than 5 µm.6 Larger particles are usually detected on intravenous exposure, which occur following intravenous injection of drugs or prescription medication. Here, the pathological picture exhibits consolidation, large nodules, and masses along with intravascular and perivascular granulomas.7 The distinctive pathological picture (classic involvement of the pulmonary interstitium with formation of irregular and stellate nodules), apparent size of the particles, and absence of intravascular granulomas enable us to conclude that the mode of entry of talc in the body of the deceased was via inhalation rather than parenteral. The cytoplasm of the macrophages and giant cells were packed with colorless to pale yellow, clear, needle-shaped or flat, single or clustered, birefringent crystals. Scanning electron microscopy or energy dispersive x-ray analysis would have provided conclusive results. However, we do not have such facilities, and we relied on the characteristic histopathologic findings and mineralogical analysis of the samples to confirm our diagnosis of talcosis. Depending on the duration of exposure, the patients present with symptoms ranging from mild cough and exertional dyspnea to severe debilitating illness with respiratory failure and night sweats, weight loss, and progressive dyspnoea.6 Similarly, radiological findings would range from interstitial fibrosis with nodular or ground opacities to massive fibrosis.8 Treatment with corticosteroids has shown favorable results with alleviation of signs and symptoms, although the possibility of relapse after cessation of treatment cannot be ruled out.4 Shlomi et al9 advocate lung transplantation as a viable option in its management. In general, pneumoconioses, especially silicosis and even talcosis, increase the risk of development of tuberculosis (as seen in our case), often with major morbidity and mortality attributed to macrophage dysfunction.10 Besides Mycobacterium tuberculosis, atypical mycobacteria also produce disease.11 In the index case, granulomatous reaction was seen as a reaction to concomitant tuberculosis, and even the caseation necrosis was full of crystals. In such cases, antituberculous therapy should also be instituted.
Talcosis, to date, has not yet been designated as a notifiable disease in India, and consequently, most of the cases go unreported. Considering that this is the first hitherto reported case of talcosis due to preparation of samosas, we have coined a new term “samosa pneumoconiosis” to describe this condition. The report also further reiterates the importance of a proper and relevant history with due emphasis on occupational, environmental, and recreational exposure.
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