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Harrison’s Manual of Medicine



Occupational Exposures and Pulmonary Disease
General Environmental Exposures
Principles of Management

Approach to the Patient

Ask about workplace and work history in detail: Specific contaminants? Availability and use of protective devices? Ventilation? Do co-workers have similar complaints? Ask about every job; short-term exposures may be significant. CXR is very valuable but may over- or underestimate functional impact of pneumoconioses. PFTs may both quantify impairment and suggest the nature of exposure.
An individual’s dose of an environmental agent is influenced by intensity as well as by physiologic factors (ventilation rate and depth).

Occupational Exposures and Pulmonary Disease
INORGANIC DUSTS   Asbestosis   Exposures may occur in mining, milling, and manufacture of asbestos products; construction trades (pipefitting, boilermaking); and manufacture of safety garments, filler for plastic material, and friction materials (brake and clutch linings). Major health effects of asbestos include pulmonary fibrosis (asbestosis) and cancers of the respiratory tract, pleura, and peritoneum.
Asbestosis is a diffuse interstitial fibrosing disease of the lung that is directly related to intensity and duration of exposure, usually requiring ³10 years of moderate to severe exposure. PFTs show a restrictive pattern. CXR reveals irregular or linear opacities, greatest in lower lung fields. High-resolution CT may show distinct changes of subpleural curvilinear line 5–10 cm in length. Pleural plaques indicate past exposure. Excess frequency of lung cancer occurs 15 to 20 years after first asbestos exposure. Smoking substantially increases risk of lung cancer after asbestos exposure but does not alter risk of mesotheliomas, which peaks 30 to 50 years after (an often brief) initial exposure.
Silicosis   Exposure to free silica (crystalline quartz) occurs in mining, stone cutting, abrasive industries, blasting, quarrying. Short-term, high-intensity exposures (as brief as 10 months) may produce acute silicosis—rapidly fatal pulmonary fibrosis with radiographic picture of profuse miliary infiltration or consolidation. Longer-term, less-intense exposures are associated with upper lobe fibrosis and hilar adenopathy ³15 years after exposure. Fibrosis is nodular and may lead to pulmonary restriction and airflow obstruction. Pts with silicosis are at higher than normal risk for tuberculosis, and pts with chronic silicosis and a positive PPD warrant antituberculous treatment.
Coal Worker’s Pneumoconiosis (CWP)   Symptoms of simple CWP are additive to the effects of cigarette smoking on chronic bronchitis and obstructive lung disease. X-ray signs of simple CWP are small, irregular opacities (reticular pattern) that may progress to small, rounded opacities (nodular pattern). Complicated CWP is indicated by roentgenographic appearance of nodules >1 cm in diameter in upper lung fields; DLCO is reduced.
Berylliosis   Beryllium exposure may produce acute pneumonitis or chronic interstitial pneumonitis. Histology is indistinguishable from sarcoidosis (non- caseating granulomas).
ORGANIC DUSTS   Cotton Dust (Byssinosis)   Exposures occur in production of yarns for cotton, linen, and rope making. (Flax, hemp, and jute produce a similar syndrome.) Chest tightness occurs typically on first day of work week. In 10–25% of workers, disease may be progressive with chest tightness persisting throughout the work week. After 10 years, recurrent symptoms are associated with irreversible airflow obstruction. Therapy includes bronchodilators, antihistamines, and elimination of exposure.
Grain Dust   Farmers and grain elevator operators are at risk. Symptoms are those of cigarette smokers—cough, mucus production, wheezing, and airflow obstruction.
Farmer’s Lung   Persons exposed to mold hay with spores of thermophilic actinomycetes may develop a hypersensitivity pneumonitis. Acute farmer’s lung causes fever, chills, malaise, cough, and dyspnea 4–8 h after exposure. Chronic low-intensity exposure causes interstitial fibrosis.
TOXIC CHEMICALS   Many toxic chemicals can affect the lung in the form of vapor and gases.
Smoke inhalation kills more fire victims than does thermal injury. Severe cases may develop pulmonary edema. CO poisoning causing O2 desaturation may be fatal. Early endoscopy may distinguish thermal upper airway injury from diffuse lower airway damage due to toxic constituents of inhaled smoke.
Agents used in the manufacture of synthetic materials may produce sensitizaton to isocyanates, aromatic amines, and aldehydes. Repeated exposure causes some workers to develop productive cough, asthma, or low-grade fever and malaise.
Fluorocarbons, transmitted from a worker’s hands to cigarettes, may be volatilized. The inhaled agent causes fever, chills, malaise, and sometimes wheezing. Occurring in plastic workers, the syndrome is termed polymer fume fever.

Treatment of environment lung diseases almost invariably involves avoidance of toxic substance. Inorganic dust inhalation produces fibrosis without inflammation, unresponsive to pharmacologic treatment. Acute organic dust exposures may respond to glucocorticoids.

General Environmental Exposures
Air Pollution   Difficult to relate specific health effects to any single pollutant. Symptoms and diseases of air pollution are also the nononcogenic conditions associated with cigarette smoking (respiratory infections, airway irritation).
Passive Cigarette Smoking   Increased respiratory illness and reduced lung function have been found in children of smoking parents. Lung cancer risk is elevated in adults exposed to passive smoke.
Radon   Risk factor for lung cancer, exacerbated by cigarette smoke.
Principles of Management
With many environmental agents, lung disease occurs years after exposure. If exposure continues, inciting agent must be eliminated, usually by removing pt from workplace. Pulmonary fibrosis (e.g., asbestosis, CWP) is not responsive to glucocorticoids. Therapy of occupational asthma follows usual guidelines (Chap. 128 ). Lung cancer screening has not yet proven effective, even in high- risk occupations.

For a more detailed discussion, see Speizer FE: Environmental Lung Diseases, Chap. 254, p. 1467, in HPIM-15.


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