Environmental Lung Diseases th Dr. Carabeo + Harrison’s 17 Ed.

July 20, 2011
ENVIRONMENTAL LUNG DISEASES    Particle size is an important determinant of the impact of environmental exposures on the respiratory system. Particles >10 μm in diameter typically are captured by the upper airway. Particles 2.5–10 μm in diameter will likely deposit in the upper tracheobronchial tree, while smaller particles will reach the alveoli. APPROACH TO THE PATIENT WITH ENVIRONMENTAL LUNG DISEASES   Obtaining careful occupational history is essential Types of occupation performed by the patient, the specific environmental exposures, use of protective respiratory devices, and ventilation of the work environment can provide key information. Assessing the temporal development of symptoms relative to the pt’s work schedule also can be very useful. . Pulmonary function tests should be used to assess the severity of impairment. Some radiologic patterns are distinctive for certain occupational lung diseases  chest x-rays are widely used  Chest CT scans can provide more detailed evaluation. OCCUPATIONAL EXPOSURES AND PULMONARY DISEASE Categories of Occupational Exposure and Associated Respiratory Conditions Occupational Exposures Nature of Respiratory Responses Inorganic Dusts Fibrosis (asbestosis), pleural disease, cancer, mesothelioma Fibrosis (silicosis), PMF, cancer, silicotuberculosis, COPD Fibrosis (coal workers' pneumoconiosis), PMF, COPD Acute pneumonitis, chronic granulomatous disease, lung cancer Wide variety of conditions from acute pneumonitis to lung cancer and asthma Organic Dusts Cotton dust: milling, processing Byssinosis (an asthma-like syndrome), chronic bronchitis, COPD Increasing risk in developing countries with drop in United States as jobs shift overseas Comment Grain dust: elevator agents, dock workers, milling, bakers Other agricultural dusts: fungal spores, vegetable products, insect fragments, animal dander, bird and rodent feces, endotoxins, microorganisms, pollens Asthma, chronic bronchitis, COPD

I-9B
Risk shifting more to migrant labor pool

Hypersensitivity pneumonitis (farmers' lung), asthma, chronic bronchitis

Important in migrant labor pool but also resulting from in-home exposures Reduced risk with recognized hazards; increasing risk for developing countries where controlled labor practices are less stringent

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Toxic chemicals: wide variety of industries

Chronic bronchitis, COPD, hypersensitivity pneumonitis, pneumoconiosis, and cancer

Other respiratory environmental agents (proven or highly suspect): uranium and radon daughters, environmental tobacco smoke, polycyclic hydrocarbons, biomass fuels, diesel exhaust, welding fumes, woods or wood finishing products

Estimates vary from ~3 to 10% of all lung cancers; in addition chronic bronchitis, COPD, and fibrosis

In-home exposures important, in developing countries disease rates as high or higher in females compared to males

Asbestos: mining, processing, construction, ship repair Silica: mining, stone cutting, sandblasting, quarrying Coal dust: mining Beryllium: processing alloys for high-tech industries Other metals: aluminum, chromium, cobalt, nickel, titanium, tungsten carbide, or "hard metal"

Virtually all new mining and construction with asbestos done in developing countries Improved protection in United States, persistent risk in developing countries Risk dropping in United States, increasing where new mines open Risk in high-tech industries persists New diseases appear with new process development

INORGANIC DUSTS Asbestos-Related Diseases   Exposures to asbestos may occur during the production of asbestos products (from mining to manufacturing) Common occupational asbestos exposures also occur in o shipbuilding and other construction trades (e.g., pipefitting, boilermaking) o manufacture of safety garments and friction materials (e.g., brake and clutch linings) Pleural plaques indicate that asbestos exposure has occurred, but they are typically not symptomatic. Interstitial lung disease o often referred to as asbestosis o pathologically and radiologically similar to idiopathic pulmonary fibrosis o Typically accompanied by a restrictive ventilatory defect on pulmonary function testing. Asbestosis can develop after 10 years of exposure, and no specific therapy is available. Benign pleural effusions can also occur from asbestos exposure. Lung cancer is clearly associated with asbestos exposure but does not typically present for at least 15 years after initial exposure. Lung cancer risk increases multiplicatively with cigarette smoking.

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Mesotheliomas (both pleural and peritoneal) are strongly associated with asbestos exposure, but are not related to smoking Brief asbestos exposures may lead to mesotheliomas, which typically do not develop for decades after the initial exposure. Biopsy of pleural tissue by thoracoscopic surgery, is required for diagnosing mesothelioma.

ORGANIC DUSTS Cotton Dust (Byssinosis)      Dust exposures occur in the production of yarns for cotton, linen, and ropemaking. Flax, hemp, and jute produce a similar syndrome. At the early stages of byssinosis, chest tightness occurs near the end of the first day of the work week. In progressive cases, symptoms are present throughout the work week. After at least 10 years of exposure, chronic airflow obstruction can develop. In symptomatic individuals, limiting further exposure is essential.

Silicosis  Results from exposure to free silica (crystalline quartz) o occurs in mining, stone cutting, abrasive industries (e.g., stone, clay, glass, and cement manufacturing), foundry work, and quarrying. Heavy exposures over relatively brief time periods (as little as 10 months) can cause acute silicosis o pathologically similar to pulmonary alveolar proteinosis and associated with a characteristic chest CT pattern known as “crazy paving.” Acute silicosis can be severe and progressive o whole lung lavage may be of some therapeutic benefit. Longer-term exposures can result in simple silicosis, with small rounded pacities in the upper lobes of the lungs. Calcification of hilar lymph nodes can give a characteristic “eggshell” appearance. Progressive nodular fibrosis can result in masses >1 cm in diameter in complicated silicosis o When such masses become very large, the term progressive massive fibrosis is used to describe the condition. Silicosis patients are at increased risk of tuberculosis, atypical mycobacterial infections, and fungal infections due to impaired cell-mediated immunity Silica may also be a lung carcinogen.

Grain Dust    Farmers and grain elevator operators are at risk for grain dust– related lung disease, which is similar to COPD. Symptoms include cough, wheezing, and dyspnea. Pulmonary function tests show airflow obstruction.

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Farmer’s Lung    Exposure to moldy hay containing thermophilic actinomycetes can lead to the development of hypersensitivity pneumonitis. Acute presentation of farmer’s lung includes fever, cough, and dyspnea within 8hrs after exposure. Chronic and patchy interstitial lung disease can develop with repeated exposures TOXIC CHEMICALS

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Coal Worker’s Pneumoconiosis   Occupational exposure to coal dust predisposes to coal worker’s pneumoconiosis (CWP) 1. Simple CWP o Defined radiologically by small nodular opacities and is not typically symptomatic. Complicated CWP o Characterized by the development of larger nodules (>1 cm in diameter), usually in the upper lobes o Often symptomatic and is associated with reduced pulmonary function and increased mortality. Many toxic chemicals can affect the lung in the form of vapors and gases.  Carbon monoxide poisoning can cause life-threatening hypoxemia.  Combustion of plastics and polyurethanes can release toxic agents including cyanide.  Occupational asthma can result from exposure to diisocyanates in polyurethanes and acid anhydrides in epoxides.

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Selected Common Toxic Chemical Agents Affecting the Lung Acute Effects from High or Accidental Exposure Mucous membrane irritation, followed by chemical pneumonitis 2–3 days later Chronic Effects from Relatively Low Exposure Bronchitis and suggestion of mildly reduced pulmonary function in children with lifelong residential exposure to high levels; clinical significance unknown Mutagen in animals, no human data Chronic bronchitis

Agent(s)

Selected Exposures Manufacture of fertilizers, chlorinated organic compounds, dyes, explosives, rubber products, metal etching, plastics

Berylliosis     Beryllium exposure may occur in the manufacturing of alloys, ceramics, and electronic devices. acute beryllium exposure can rarely produce acute pneumonitis a chronic granulomatous disease very similar to sarcoidosis is much more common. Chronic beryllium disease  characterized radiologically by pulmonary nodules along septal lines.  either a restrictive or obstructive ventilatory pattern on pulmonary function testing can be seen.  Bronchoscopy with transbronchial biopsy is typically required to diagnose. The most effective way to distinguish chronic beryllium disease from sarcoidosis is to perform a beryllium lymphocyte proliferation test using blood or bronchoalveolar lavage lymphocytes. Removal from further beryllium exposure is required, and corticosteroids may be beneficial.

Acid fumes: H2SO4, HNO3

Acrolein and other aldehydes

Ammonia

By-product of burning plastics, woods, tobacco smoke Refrigeration; petroleum refining; manufacture of fertilizers, explosives, plastics, and other chemicals

Mucous membrane irritant, decrease in lung function Mucous membrane irritation, followed by chemical pneumonitis 2–3 days later

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Anhydrides

Manufacture of resin esters, polyester resins, thermoactivated adhesives Smelting, soldering, battery production

Nasal irritation, cough

Asthma, chronic bronchitis, hypersensitivity pneumonitis COPD Organic compound, metallurgy, volatilization of chlorine-containing compounds Manufacture of sulfuric acid, bleaches, coating of nonferrous metals, food processing, refrigerant, burning of fossil fuels, wood pulp industry

Cadmium fumes

Formaldehyde

Halides and acid salts (Cl, Br, F)

Hydrogen sulfide

Manufacture of resins, leathers, rubber, metals, and woods; laboratory workers, embalmers; emission from urethane foam insulation Bleaching in pulp, paper, textile industry; manufacture of chemical compounds; synthetic rubber, plastics, disinfectant, rocket fuel, gasoline By-product of many industrial processes, oil, other petroleum processes and storage

Mucous membrane irritant, acute respiratory distress syndrome (ARDS) Mucous membrane irritation, followed by chemical pneumonitis 2–3 days later

Phosgene Cancers in one species; no data on humans

transiently in children and adults, and increased hospitalization with exposure to summer haze Delayed onset of bronchiolitis and pulmonary edema

Chronic bronchitis

Mucous membrane irritant, epistaxis

?Chronic bronchitis

Sulfur dioxide

Mucous membrane irritation, pulmonary edema; possible reduced FVC 1– 2 yrs after exposure

Dryness of mucous membrane, epistaxis, dental fluorosis, tracheobronchitis

PRINCIPLES OF MANAGEMENT  Treatment involves limiting or avoiding exposures to the toxic substance. Chronic interstitial lung diseases (e.g., asbestosis, CWP) are not responsive to glucocorticoids Acute organic dust exposures may respond to corticosteroids. Therapy of occupational asthma (e.g., diisocyanates) follows usual asthma guideline Therapy of occupationalCOPD (e.g., byssinosis) follows usual COPD guidelines

  Conjunctival irritation, chronic bronchitis, recurrent pneumonitis 

Isocyanates (TDI, HDI, MDI)

Production of polyurethane foams, plastics, adhesives, surface coatings

Nitrogen dioxide

Silage, metal etching, explosives, rocket fuels, welding, byproduct of burning fossil fuels

Increase in respiratory rate followed by respiratory arrest, lactic acidosis, pulmonary edema, death Mucous membrane irritation, dyspnea, cough, wheeze, pulmonary edema Cough, dyspnea, pulmonary edema may be delayed 4–12 h; possible result from acute exposure: bronchiolitis obliterans in 2–6 wks Mucous membrane irritant, pulmonary hemorrhage and edema, reduced pulmonary function

MNEMONICS of Differential Diagnosis For DYSPNEA Upper respiratory tract irritation, cough, asthma, allergic alveolitis “Acute DYSPNEA”
A – Asthma/Airway obstruction C – COPD U – UMN Lesion T – Tracheal Obstruction E – Endocrine/Environmental D – Deformed Chest Wall Y – hYperventilation Syndrome (labooo..) S – Sarcoid/Shock P – 5 P’s of pleuritic Pain (pericarditis, pulmonary Embolism, pneumomediastinum, pleurisy/pneumonia, pneumothorax N – Neoplasm E – Edema A – Anemia/Acidosis

Ozone

Arc welding, flour bleaching, deodorizing, emissions from copying equipment, photochemical air pollutant

Emphysema in animals, ?chronic bronchitis, associated with reduced lung function in children with lifelong residential exposure, clinical significance unknown Chronic eye irritation and slight excess in cardiopulmonary mortality in susceptible individuals

For Cough “HACKING”
H – Hilar adenopathy A – Aneurysm, Asthma, Aspiration C – CHF K – Killer Neoplasms I – Infections N – Nasal Drip G – Growth on vocal cord

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