Asthma is the most common occupational lung disease. It replaces mineral dust associated lung diseases in postindustrial countries. Of these dust-associated diseases, only silicosis remains prevalent. This review summarizes etiology, basic pathophysiology, and diagnosis of occupational respiratory diseases in postindustrial countries. Newer aspects of occupational respiratory lung disease discussed are: 1) individual differences in susceptibility and metabolism, 2) latent periods between exposure and disease onset, and 3) the possibility of contracting lung disease in office buildings and hospitals. The role of lung anatomy in particle and gas deposition is omitted from this summary in the interest of brevity. Diseases are discussed below by anatomical region and category followed by important points of diagnosis and treatment. Etiologic agents are summarized in 3 tables organized by region of the lung.

Rhinitis and Laryngitis:

A variety of substances cause rhinitis and laryngitis. There are two primary responses of the nose, larynx, and pharynx depending upon the compound inhaled. Irritants cause congestion or burning. Allergens cause itching, rhinorrhea, congestion, and sneezing. Examples of compounds involved are listed in Table 1 below. Genetic susceptibility and previous allergic disease are risk factors considered when investigating disease etiology in the nasopharyngeal region.

The larynx is particularly susceptible to irritation because its small diameter allows increased deposition of particulate matter relative to anterior regions of the nasopharynx. Vocal cords may become inflamed and irritated from this direct deposition of substances. Vocal cords may also be damaged by drainage of inflammatory mediators from the nasal passages.

Tracheitis, Bronchitis, and Bronchiolitis:

Occupations such as welding, mining, cotton-textile milling, and chemical, grain, feed, or food processing may cause industrial bronchitis. Specific compounds involved are listed in Table 2 below. Acute bronchitis is due to post-exposure mucosal inflammation. Asthma may develop after bronchitis resolves. Chronic bronchitis is defined by a cough productive of mucus on most days for three months in a year for two consecutive years. Histology confirms mucous cell and mucous gland hyperplasia resulting in excess mucus secretion in chronic bronchitis.

Exposure to high concentrations of gases and chemical fumes causes bronchiolitis obliterans that is a narrowing and filling of bronchioles resulting in irreversible airflow obstruction. Examples of causative agents are listed in Table 2. Bronchiolitis obliterans must be differentiated from asthma. Both diseases present with wheezing and a clear chest X-ray. High-resolution CT shows a patchy interstitial pattern in bronchiolitis obliterans.

Asthma:

Occupational exposure to over 250 substances (Table 2) may cause asthma. Occupational asthma includes several classes:

Isocyanates often cause asthma. HLA-DQB1*0501 and HLA–DQA1*0501, DR1 haplotypes appear to protect against isocyanate-induced asthma. HLA-DQB1*0503 and the allelic component HLA-DQB1*0201/0301 seem to make isocyanate workers more sensitive to asthma development.

Chronic Obstructive Pulmonary Disease or Chronic Airflow Limitation:

Emphysema or chronic airflow limitation is also caused by occupational exposure to dusts some of which are listed in Table 2. The disease may progress for years after cessation of exposure to coal and silica dust in particular. Pneumoconiosis may develop with emphysema from exposure to beryllium or silica dust.

Lung Cancer:

Five percent of lung cancer cases in the US are thought to be occupational in nature. Most are caused by asbestos, radon, silica, chromium, cadmium, nickel, arsenic, beryllium, bis(chloromethyl)ether and chloromethyl methyl ether. The risk of lung cancer increases when there is multiple exposure to both asbestos and cigarette smoke. Occupations historically associated with asbestos exposure include pipe insulation, shipyard working, and building construction.

A genetic component was shown in asbestos-related cancer. Homozygous deletion of the glutathione S-transferase M1 (GSTM1) gene or an N-acetyltransferase 2 (NAT2) slow acetylator genotype may increase risk of asbestos-induced lung cancer.

Interstitial Lung Disease:

Alveolar and interstitial inflammation may result when dusts are small enough to bypass the defense systems of the upper respiratory tract. Occupational causes of these diseases are listed in Table 3.

 Fibrotic Disease:

Twenty years ago this class of diseases surpassed asthma in incidence. Coal worker’s pneumoconiosis has decreased over the last 25 years while silicosis is still prevalent. Other mineral dusts including talc, kaolin, coal, and cobalt are also causes of pneumoconiosis. Dusts such as silica may also result in diffuse alveolar-filling disease caused by excess Type II cell surfactant production.

Granulomatous Disease:

Stimulation of the immune response after inhalation of some substances may cause hypersensitivity pneumonitis. This is acute pneumonitis with fever and elevated peripheral blood leukocytes. Occupational agents known to cause this are listed in Table 3 under hypersensitivity pneumonia. Cigarette smoke may exacerbate sensitization to some substances. Permanent damage in the form of interstitial fibrosis may be averted by early treatment with corticosteroids.

Inhalation Fever:

Inhalation fever is defined by a transient fever with elevated white count and little or no pulmonary inflammation after a single inhalation exposure. Molds, bacteria, and organic dusts may cause inhalation fever.

DIAGNOSIS:

History, physical, chest x-ray and pulmonary function tests are used to diagnose most occupational lung disease. Diagnosis is also helped by finding 1) a temporal association of work with symptoms and 2) known etiologic agents in the workplace. Perhaps one of the most vexing problems to employers is why one person develops an occupational lung disease and another does not. As explained by the author:

"Polymorphisms in genes produce variation in the rate and pathway of metabolism, which results in marked differences in susceptibility to occupational substances among workers, just as polymorphisms affect responses to some medications. Interactions among occupational exposure, atopic predisposition, nutrition, home or avocational exposure, and host factors (such as gastroesophageal reflux, cigarette smoking, and viral infections) are common, and they help to explain the occurrence of disease in certain persons."

There may be a latent period of 10 or more years between initial exposure to the appearance of pulmonary symptoms of diseases such as berylliosis, silicosis, and asbestosis. Therefore definitive recognition of some exposures requires a lifetime occupational history.

TREATMENT:

Occupational lung diseases are treated identically to other lung diseases. Twenty-three states require physicians to report occupational lung disease to state health departments. The physician must initiate a change in the patient’s work environment and restrict aggravating activities. Patients are encouraged to continue with work by the scope of the Americans with Disabilities Act. The physician may be instrumental in guiding the patient to a transfer in the workplace or to job retraining in the interest of maintaining the livelihood and health of the patient.