"Horse play and the Lung“ a possible cobalt effect?

Correct answer is E. Choice D is also plausible but was considered to be less likely – see the discussion below.

A. Work-exacerbated asthma or Reactive Airways Dysfunction Syndrome are possible causes for her immediate symptoms. She had a history of mild asthma and symptoms on the first day of exposure could have suggested asthma. She may have had an irritant-related airway response from the physical properties of the dust in the feed. She was also exposed to other asthma triggers such as horse allergens, dust, fungi, and bird allergens but was not atopic on allergy skin testing at this time. Work-exacerbated asthma would not have explained her subsequent clinical course, the normal airflows and decreased diffusing capacity on pulmonary function testing, and the radiologic abnormalities. Exposure to inhaled cobalt has been linked to the development of occupational asthma in industrial workers^3-6 but similarly would not explain her clinical findings.

B. Acute inhalation injury from a high level inhaled irritant is not likely because she was exposed to the recommended dosage of the supplement, at which no similar lung symptoms had been reported, and she was in a well-ventilated environment when the exposure occurred. In addition, there were no obstructive changes observed on the pulmonary function tests.

C. The patient’s acute symptoms were not typical for organic dust toxic syndrome. Reported manifestations of this syndrome after unloading silos⁷ included fever (79%), myalgia (76%), chest tightness (72%), cough (66%), headache (59%), starting an average of 5.3 hours (SD 3.3 h) after exposure with leukocytosis (mean WBC count = 13.2 X 10⁹/L). However, these cases were associated with normal chest radiographs and arterial oxygen saturation, and had a more rapid resolution than the present case.

D. Hypersensitivity pneumonitis (HP) is a possible consideration. The patient’s clinical course is consistent with acute/subacute HP and she was exposed to several known precipitants for this condition (avian proteins, thermophilic actinomycetes, mycobacterium avian intracellulare, rat proteins). However, precipitating serum antibodies were negative to common causes of HP and she continued to be exposed to these antigens after this episode with no ill effect, suggesting that there was another explanation for this patient’s presentation.

E. Interstitial lung disease from cobalt exposure. The only change in the patient’s environment that was temporally associated with development of her acute symptoms was the introduction of a new horse-feed supplement, which included iron, cobalt and copper. Cobalt-induced lung disease has been well-described in workers engaged in the manufacture, utilization, or maintenance of tools composed of hard metal [a material composed mainly of tungsten carbide and cobalt] or diamond-cobalt^8,9. Better known as “hard metal disease” or “cobalt lung”, this entity is associated with giant cell interstitial lung disease which is considered to be a hypersensitivity response to cobalt. It can have a subacute presentation of fever, weight-loss, non-productive cough and dyspnea¹⁰, with a possible evolution to pulmonary fibrosis. Although most often reported with exposure to tungsten carbide, it has also been reported with exposure to cobalt without concurrent tungsten exposure. Experimental studies demonstrate that cobalt metal and metallic carbides can also induce lung toxicity possibly due to the production of activated oxygen species¹¹. Although manufacturing of animal feed has been listed as a cause of cobalt-related dermatitis¹², we were unable to find any reports of cobalt-related lung disease in manufacturers or farmers using these supplements.  We hypothesize that this patient may have had previous cobalt exposure in horse-feed supplements, perhaps causing sensitization, but the fine dust in the new supplement may have resulted in greater cobalt inhalation and subsequent alveolitis. The more classical histologic finding of interstitial lung disease related to cobalt is that of giant cell interstitial pneumonitis. No giant cells were apparent on the biopsy from this patient and therefore the histology was not diagnostic but remains consistent with a hypersensitivity response, which in this case appeared likely to be due to exposure to cobalt.

Hard metal lung disease remains a disease that is not fully understood¹³. While chronic fibrosis is the better known form of hard metal disease, there have been a few cases reported in the literature of a more acute alveolitis from cobalt exposure.  Four hard metal workers from a factory in Sweden were exposed to cobalt in the course of their occupation and developed respiratory illnesses⁶. Three of these patients developed a nonproductive cough, dyspnea with exertion and minimal or no abnormal findings on auscultation. Chest radiographs at the time of the initial presentation showed basilar infiltrates similar to this case. Pulmonary function testing during their initial presentations showed decreased lung volumes without a primary obstructive disease. All of the patients improved with removal of exposure to further cobalt (+/- addition of systemic corticosteroids), and each recurred when they were re-introduced to environments with cobalt. In this patient, further challenge/exposure to the horse-feed supplement was not considered to be justified due to the severity of her previous episode.

Question 4

Which one of the following has NOT been described about for an initial episode of acute alveolitis from cobalt? (Review the answer to question 4 before going to question 5.)

	A.	Long term disability after cessation of exposure Correct!
	B.	Recurrence with further exposures Incorrect!
	C.	Complete or near-complete recovery without relapse after permanent removal from the offending environment. Incorrect!
	D.	Occurrence in a minority of exposed workers Incorrect!
	E.	Occurrence at exposure levels which are not considered to be irritant to the lungs Incorrect!