Occupational Asthma

The air we breathe may contain allergens of natural origin or generated as a consequence of industrial or environmental processes. In addition, chemicals in the air may irritate the airways and lower the threshold for airway responsiveness. These same irritants may in addition be allergens for susceptible individuals. Besides industrially related exposure, modern life generates pollutants that linger in the air, generally in or around cities, which may damage the lungs. Thus, everyone is at risk of breathing potentially harmful substances, but asthmatics are at much greater risk to react adversely to them. Certain pollutants such as ozone increase airway reactivity even in normal subjects, and asthma may be exacerbated during pollution with either industrial or photochemical smog. Approximately 2-15% of all cases of adult-onset asthma in men are of occupational origin (depending on the level of airway irritants and allergens in any working area).

Suspicion of occupational lung disease should be raised by the history of cough or chest tightness in relationship to the workplace. In asthmatics, worsening of symptoms every week, especially early in the week, may be noted. Such suspicions can be strengthened by evidence of wheezing or abnormal pulmonary function after occupational exposure. Only a few appropriate antigens are available for skin testing, so provocation with

Table 6

Some Agents Capable of Causing Occupational Asthma


Active substance

Metal salts Wood dusts Vegetable dusts

Industrial chemicals

Pharmaceutical agents Biological enzymes

Salts of platinum, nickel, chrome

Oak, western red cedar (plicatic acid),redwood, mahogany Grain (mite, weevil), flour, castor bean, green coffee, gums, cottonseed, cotton dust Toluene diisocyanate, polyvinyl chloride, phthalic and trimelletic anhydrides, ethylenediamine Penicillin, phenylglycine acid chloride, ethylenediamine Bacillus subtilis, pancreatic enzymes Animal and insect materials Rodent urine protein, canine or feline saliva or secretions the suspected airborne chemical or particulate may be the only confirmatory test available. Some of the more common occupational exposures leading to asthma are listed on Table 6.

The prevalence of occupational asthma varies with the exposure and the provocative agent. Although only about 5% of workers regularly exposed to toluene diisocyanate develop asthma, 10-45% of workers exposed to relatively high concentrations of proteolytic enzymes in laundry detergent in the past were affected. The pattern of response may be immediate, late, or both. The underlying mechanism involves direct irritation and/or the induction of immunological processes, including IgE- or IgG-type responses. Removal of the worker from the workplace may reduce or reverse the airways disease, although there are many exceptions.

Chemical or Drug Exposure

Aspirin and Nonsteroidal Anti-Inflammatory Drugs

It is estimated that 3-5% of asthmatics will reliably worsen after the ingestion of aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs). Ingestion of aspirin or other NSAIDs may provoke either of two responses: respiratory responses, including bronchorrhea, rhinorrhea, bronchospasm, conjunctivitis, lacrimation, and flushing; or urticaria and angioedema. Rarely, combinations of the two patterns are seen. Aspirinsensitive patients may be recognized by the presence of nasal polyps, nonallergic rhinitis, persistent sinusitis, and asthma associated with moderate eosinophilia (>1000/mm3). The frequency of NSAID sensitivity increases with age, although children and families have been described with clear-cut reactivity. There may be a wide range of associated allergies, but many subjects (about 50%) are not allergic.

The mechanism responsible for NSAID sensitivity appears to involve an abnormal modulation of eicosanoid production (increased production of leukotrienes C and D). NSAIDs inhibit the cyclooxygenase (COX) enzyme system responsible for prostaglandin formation, thereby reducing prostaglandin production and leading to increased production of lipoxygenase products. It has been suggested that NSAIDs cause asthma by reducing the formation of prostaglandins such as PGE, that help maintain normal airway function while increasing the formation of asthma-provoking eicosanoids, including hydroxyeicosatetraenoic acids (HETEs) and leukotrienes C and D. Recent work in humans has confirmed this suspicion, demonstrating that sensitive subjects exposed to NSAIDs secrete excessive quantities in leukotrienes in their respiratory tract and develop both rhinitis and asthma.

Aspirin sensitivity should be suspected in any asthmatic with nasal polyposis, chronic sinusitis, and eosinophilia. The polyposis and sinusitis may precede the onset of recognized NSAID sensitivity by years. Under some circumstances, selected patients with this syndrome can be "desensitized" to NSAIDs by repeated oral challenges with aspirin and may remain unresponsive to subsequent NSAID exposure if oral NSAIDs are given daily. Many asthma investigators believe that leukotriene antagonists are indicated in these patients. Generally, aspirin-sensitive patients can safely take COX-2 inhibitors without developing asthma.

Sulfiting Agents

Sulfiting agents include sulfur dioxide (SO2) and any of its five sulfite salts, which are added to foods to prevent nonenzymatic browning, to inhibit growth of microorganisms, to inhibit enzymatic activity, and to act as antioxidants and reducing agents, as bleaching agents, as processing aids, as pH controls, and for stabilization. In 1986, in response to the recognition that sulfites could precipitate asthma, the US Food and Drug Administration (FDA) banned their use on fruits and vegetables served fresh. Other products, like beer and wine, are now labeled as containing sulfites. Sulfites are generally converted under acid conditions to sulfur dioxide and are largely liberated during the processing and cooking of foods. It is thought that ingestion of sulfites leads to the liberation of SO2in the mouth and stomach, which is then inspired. In very sensitive asthmatics, inhalation of SO2, even in small amounts, provokes asthmatic attacks. It may be anticipated that only the most hyperresponsive asthmatics will react to ingested sulfites.

Sulfite sensitivity should be suspected in asthmatics who worsen in relationship to eating processed foods containing sulfites (e.g., dried fruit, fruit juices, or processed potatoes) or wine and beer. Sulfite-sensitive asthmatics should be advised to have a MediAlert bracelet and to carry a bronchodilator metered-dose inhaler (MDI) and injectable epinephrine.

p -Adrenergic Antagonists

The p-adrenergic blocking agent propranolol hydrochloride was introduced in 1964, and it was immediately recognized that asthmatics were adversely affected by this drug. p-Adrenergic blocking agents are being used in diverse diseases such as glaucoma, migraine, hypertension, myocardial infarction, and tremor. The underlying mechanism by which p blockade induces asthma is thought to involve prevention of the normal p-adrenergic inhibitory influences on the parasympathetic ganglia in the airways. The reduction in p -adrenergic inhibitory influences at this level thereby allows relatively unimpaired cholinergic constrictor influences to develop. In the opinion of most specialists, asthmatics should not take p -adrenergic blocking agents in most situations. Of note, worsening of the status of a previously stable asthmatic should provoke inquiries as to other medications given by practitioners, in search of possible p -adrenergic blocking agent administration. There is an ever-widening use of p -blockers, and some p -blockers are now "hidden" in combination tablets, along with diuretics.


In 1951, Churg and Strauss described a vasculitic process that had pathological findings and clinical features warranting the designation of a separate disease entity, allergic angiitis and granulomatosis. The disease is characterized pathologically by necrotizing vasculitis, tissue infiltration by eosinophils, and extravascular granulomas. The disease has three phases, beginning with a prodrome of allergic asthma and allergic rhinitis that may exist for many years. The second phase includes eosinophilia along with the development of pulmonary eosinophilic infiltrates resembling Loffler's syndrome, eosino-philic pneumonia, or eosinophilic gastroenteritis. The third phase is the vasculitic phase involving pulmonary vessels (96%), skin (67%), peripheral nerves (63%), the gastrointestinal tract (42%), heart (38%), and kidney (38%).

The syndrome affects males and females equally; the onset of first stage involving allergic rhinitis and asthma occurs around the age of 30 yr, while the vasculitis becomes apparent by the age of 38 and is suggested by the development of eosinophilia greater than 1500/mm3, infiltrates in chest roentgenogram, hypertension, abdominal pain, purpura, urticaria, subcutaneous nodules, mononeuritis multiplex, general malaise, persistent low-grade fever, and weight loss. Many patients have an increased IgE level and the presence of rheumatoid factor. The prognosis in untreated patients is poor. Treatment generally consists of CCSs alone or combined with cytotoxic therapy.

Although this is a rare disease (approx 1:30,000-50,000 asthmatics has Churg-Strauss syndrome), the recent introduction of leukotriene antagonists has led to an increased recognition of this disease. Thus, asthmatics who are weaned off oral CCSs and develop a flu-like syndrome with eosinophilia should be suspected of having Churg-Strauss syndrome. In that circumstance, a chest X-ray is indicated to search for pulmonary infiltrates.

Idiopathic or Intrinsic Asthma

Up to 30% of asthmatic patients, particularly those over 30 yr of age, have no apparent cause for their asthma. Often their disease begins with a severe upper or lower respiratory tract infection or sinusitis and progresses to asthma in short order. Such patients often have coexistent sinusitis and nasal polyposis, as well as vasomotor rhinitis. It has been thought that such patients have a worse prognosis than other types of asthmatics, but this is certainly not predictable. In such patients it is necessary to search for factors that might worsen asthma. Many patients with idiopathic asthma regularly produce mucus and have a history of tobacco smoking; such patients may have an asthmatic form of bronchitis. In some patients a trial of antibiotics for low-grade infectious bronchitis might be appropriate.

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