Arc welder's lung - (a case report)KC Patel, SM Sheth, SR Kamat
Department of Chest Medicine, K. E. M. Hospital and Seth G. S. Medical College, Parel, Bombay-400012., India
Correspondence Address: Source of Support: None, Conflict of Interest: None PMID: 615258
Source of Support: None, Conflict of Interest: None
A patient working for 18 years at arc welding and complaining of cough and dyspnoea was diagnosed by open lung biopsy as lung fibrosis suggestive of arc welder's lung. The salient features o f this case and the relevant literature are presented.
It is known that pulmonary fibrosis occurs following inhalation of several types of dusts such as asbestos, silica. coal, tin, aluminium oxide etc. Whether iron oxide used in arc welding produces such a reaction is controversial and it is believed by some that the metal particles of substances being welded may be responsible where as others do not agree with this. ,,,,,,, Arc welding has been described to produce interstitial fibrosis. , We are reporting a case with such a picture.
A 45 year old male, working as arc welder in the naval dockyard for 18 years, attended this hospital on 3-2-1976. He complained of exertional dyspnoea and productive cough of seven years' duration.
Clinically he had tachypnoea, a blood pressure of 130/90 mm. Hg. and slight pedal oedema. Chest examination revealed prolonged expiration with multiple rales and a few rhonchi. There was evidence of congestive cardiac failure.
Investigations: Haemoglobin 13.1 gm%; Haematocrit 41%; ESR 40 mm, total leukocyte count 11300/cu mm; polymorphs 56%, Lymphocytes 35%, Eosinophils 9%, stool-cysts of Giardia Lamblia and ankylostoma deodenale. Sputum negative for tubercle bacilli, Routine culture of sputum grew Klebsiella pneumoniae. Sputum did not show asbestos bodies.
Routine liver and renal functions were normal.
An electrocardiogram showed right ventricular hypertrophy.
Pulmonary Function Tests: showed moderate restrictive disability with some reversible obstruction as evident from [Table 1].
Arterial gases: study with exercise, 70 steps in 5minutes showed the following results presented in [Table 2]
This indicated anoxia at rest which worsened a little with exercise indicating V: P imbalance.
Radiograph of chest revealed diffuse fine reticular opacities more on the right side see [Figure 1] on page 34 b.
Lung biospy showed acute bronchitis and discrete areas of interstitial pneumonitis with fibrosis see [Figure 2] on page 34 b. Increased perivascular fibrous tissue and deposition of anthracotic pigment were seen. The tissue did not stain with prussian blue.
In the process of welding, metals are joined by melting their contact surfaces. During the process of arc welding, oxides of various metals like iron, calcium. sodium, lead, aluminium, manganese, silicon, magnesium, tin, cadmium, copper and titanium are produced together with nitrogen peroxide and ozone.  Radiological changes are many times attributed to inhalation of these fumes . 
After inhalation of these tiny particles, 1 µ in size, into the lung alveoli they are arrested into the peribronchial and perivascular lymphatics and lymph nodes. Fine mottling in the lungs of welders with no symptoms has also been described. Doig et al  and Enzer et al  described pathological studies of the lungs including photomicrographs of a welder who died after an accident and who during the life had shown characteristic radiological changes. Harding  and Harding et al  introduced iron oxide into the lungs of rats both by intratracheal injections and inhalation and obtained radiographs comparable with those in human siderosis. Titus et al  have shown after series of animal experiments that pulmonary oedema associated with welding in confined spaces is caused by the gases, nitrogen peroxide and ozone, generated at electric arc and not by the fine particles of iron oxide found in the fumes.
Charr  reported various cases of lung disease in arc welders and of these, two were submitted to lung biopsy. Their clinical picture showed evidence of fibrosis and pulmonary emphysema with decrease in oxygen saturation of blood. These patients became incapacitated after exposure to arc welding fumes. Doig and McLaughlin  gave an excellent follow up of 15 welders for over 9 years. At the end of 7 years, 7 were normal, 2 had suspicious lesions and 6 developed well defined radiological lesions. At the end of another 2 years a second follow up was recorded. Out of 7 who were normal initially, 5 still remained normal while one developed suspicious and the other developed definite lesions Out of two who had suspicious lesions at the end of 7 years both developed definite radiological lesions whereas out of 6 who had well developed radiological changes at the end of 7 years, 4 maintained status quo. Out of 2 one gave up job and abnormal shadows disappeared. One spent less time at work and the lesions became less intense.
Some people attribute X-ray changes to the inhalation of iron particles only  where as others believe them to be due to more than one factor. , There is a controversy regarding the harmful nature of the fumes. Doig and McLaughlin , and Pendergrass and Leopold  believe that the fumes are harmless and change: are reversible. Harding,  Harding et al,  Enzer et al  and Morgan et al  believe that siderosis is harmless and iron oxide is not fibrogenic. In contrast to this, then have been several reports describing both respiratory symptoms and severe impairment of lung functions in welders. ,
However a composite postulation was put forward by Friede et al  and Anderson.  They believe that even if fibrosing activity of iron may be minimal it might be modified by the presence of silica to produce diffuse interstitial fibrosis rather than a localized nodular fibrosis typical of silica alone.
Our patient did exhibit pulmonary function abnormality together with iron oxide deposits and fibrosis. We agree totally with Charr,  Friede et al  and Anderson  in that the pulmonary parenchymatous damage occurs in welders, that iron oxide is fibrogenic and that fibrosis might be enhanced by asbestos to which they are simultaneously exposed.
We thank Dr. Kinare, Dr. Raval and Dr. A. P. Desai from the Department of Pathology as well as the technical staff of Pulmonary function and Blood gas laboratories for their help. We also thank Dr. C. K. Deshpande, Dean, K.E.M. Hospital, for allowing us to publish the hospital data.
[Figure 1], [Figure 2]
[Table 1], [Table 2]