Acute respiratory distress in a silversmith.

A 25-year-old young male patient presented in casualty department with severe respiratory distress on the fourth day from onset of symptoms. The patient was nonsmoker and had no antecedent medical or drug history. Prior to admission, patient had dry cough and bilateral pleuritic chest pain for the last three days. He was in severe respiratory distress with use of accessory muscles of respiration. On examination, he had heart rate of 120 beats/min, blood pressure (BP) of 150/80, respiratory rate of 48-52/min and central cyanosis present. On systemic examination, reduced intensity of breath sounds with extensive rhonchi and crepitation was found in both lung fields, with other examination being within normal limits. On pulse oximetry, oxygen saturation was 28% on room air, which increased up to 36% with the help of 4 L oxygen via nasal prongs. PaO2/FiO2 ratio was 100. Chest X-ray analysis was suggestive of non-cardiac pulmonary edema in view of bilateral fluffy opacity without cardiomegaly. In view of 2/3 positive criteria, his provisional diagnosis was Acute Respiratory Distress Syndrome (ARDS). He required mechanical ventilatory support and was gradually weaned over a period of 10 days. The patient was treated with broad spectrum antibiotics and other supportive measures. On re-evaluation of history, we found that he was a goldsmith by occupation, smelting silver and gold for the past 8-10 years. On the day of onset of symptoms, while smelting silver he was exposed to golden yellow fumes for around 15 minutes, with the quantum of exposure more than any other day earlier. From previous experience and analysis of similar silver metals, he was able to tell us that the silver was adulterated with large amount of cadmium on that day than before. Serum level of cadmium was 2.9 μg/L 6 days after initial exposure. At the time of discharge, he had residual opacities in the chest radiograph and resting oxygen saturation was 94% on room air.

A 25-year-old man, a silversmith by profession, was admitted with rapidly progressive dyspnea. He was a nonsmoker and was in good health prior to the present illness. He related that while smelting silver, he had inhaled golden yellow fumes three days prior to admission. He developed a dry cough and bilateral pleuritic chest pain; dyspnea followed and worsened rapidly, prompting admission. He was acutely breathless with tachycardia (120/min), respiratory rate of 48-50/min, was diaphoretic and cyanosed. Chest auscultation revealed extensive bilateral crepitations and rhonchi. His oxygen saturation on room air was 30% and increased only to 38% on 4 L of oxygen via nasal prongs. Arterial blood gases on room air showed severe hypoxia (PaO2-40 mmHg), hypocapnia (pCO2-2 5 mmHg and metabolic acidosis, pH 7.24). The PaO2/FiO2 ratio was 100, denoting acute respiratory distress syndrome. His hemoglobin, routine blood counts, renal and liver parameters were all within normal limits. The chest [Figure 1] showed extensive bilateral opacities consistent with Acute Respiratory Distress Syndrome (ARDS).

Figure 1

Chest radiograph showing extensive bilateral opacities

He was placed on a volume ventilator and on broad spectrum antibiotics as well as other supportive measures. He needed the assisted ventilation for 10 days, and thereafter, he was “weaned” from the respiratory support. At the time of discharge, he had residual opacities in the chest radiograph and resting oxygen saturation was 94% on room air. Serum level of cadmium was 2.9 μg/L 6 days after initial exposure. The upper limit of normal is 2.6 μg/L.

Silver is often contaminated with cadmium—the so called fake silver—and our patient stated that this was by far the most intense exposure he has had. Cadmium fumes are bright yellowish-brown as compared to the white-grayish fumes of silver. Cadmium (Cd) is a soft, silvery white metal with a low melting point. It was discovered in Germany by Stromeyer in 1917. It is present in the earth's crust. Cadmium is a common impurity in zinc and is released while smelting. It is used in a variety of industries like batteries, pigments, plating solutions, polymer stabilizers, and metal alloys. It has long been known that cadmium can cause health consequences both on an acute basis and long-term exposure. Cadmium can be ingested or inhaled as particulate matter. Cadmium fumes are particularly dangerous because they have a very high vapor pressure and may reach up to 50,000 times over the safe limit when molten. Mild exposures can result in upper airway irritation, which subsides; more intense exposure, as in our patient, can result in a rapidly progressive ARDS. Long-term exposure can cause a condition akin to chronic obstructive pulmonary disease (COPD), and carcinogenesis.[1] Renal tubular damage is also well-documented.[2]

A large number of goldsmiths and silversmiths in our country work in poorly ventilated workplaces. It is only to be expected that exposures over the safe limits of noxious fumes is commonplace. Comprehensive and critical study of these subjects with lung functions, etc., may indeed reveal subclinical illnesses. As suggested by Singh et al.[3], prevention of further exposure may be of great benefit. Substitution with cadmium-free alloys has been recommended. Finally, affected workers can claim compensation as legislation is being established with regards to human exposure limits.