Occupational Lung Disease



Occupational Lung Disease


Peter G. Tuteur

Barbara Lutey



Introduction



  • The workplace contains a wide range of materials and conditions that can potentially aggravate pre-existing conditions or cause pulmonary disease in susceptible hosts. Table 26-1 lists a number of some relatively common potentially hazardous agents.


  • Diagnosis of workplace-related pulmonary disease requires a high index of suspicion because there may be no clear temporal relationship between an exposure and the subsequent development of signs and symptoms, which may be nonspecific and fleeting.


  • Obtaining a detailed occupational history from a patient with a possible workplace-related pulmonary disease is an essential part of the diagnostic evaluation.1



    • The occupational history is a comprehensive list of the activities and environments of all remunerative or volunteer work the patient has ever performed, including short-term/temporary/military jobs and hobbies, which is compiled to identify all exposures (Table 26-2).


    • Assessment of the home environment, especially during childhood, emphasizing biomass fuel exhaust, radon, and mineral dust exposures may also be important.


  • General management principles



    • The patient should avoid further exposure to the offending agent. This intervention may involve a change in job responsibilities and patients should be made aware of the fact.


    • Supportive care measures which will depend upon individual patient requirements:



      • Supplemental oxygen


      • Pulmonary rehabilitation


      • Tobacco cessation


      • Bronchodilators


      • Influenza/pneumonia vaccinations


    • Because disease can progress even after exposure has ended, serial imaging and pulmonary function tests (PFTs) are recommended in the first years after retirement.


  • Issues of impairment, disability, and workers’ compensation frequently arise with a diagnosis of workplace-related pulmonary disease.



    • Impairment means objectively determined abnormality of functional assessment.


    • Disability implies inability to perform certain tasks owing to impairment.


    • The disability certification process often involves multiple agencies and procedures that vary from state to state.


    • For assistance with definitions and criteria, the American Medical Association Guides to the Evaluation of Permanent Impairment is a valuable resource.2


Asbestos-Associated Lung Disease


General Principles



  • Asbestos is composed of hydrated silicates with varying combinations of other elements such as sodium, magnesium, and iron.


  • Asbestos can be classified according to the shape of its fibers: amphibolites which are linear fibers or serpentines which are curly fibers.









    TABLE 26-1 POTENTIALLY HAZARDOUS AGENTS IN THE WORKPLACE




    Gases/vapors
      Carbon monoxide
      Formaldehyde
      Hydrochloric acid
      Sulfuric acid
      Sodium hydroxide
      Bleach
      Hydrogen sulfide
      Ethylene oxide
      Nitrogen dioxide
      Ozone
      Phosgene
      Smoke
      Sulfur dioxide
      Fumes from welding and metal processing
      Acids/alkalis
      Ammonia
      Chlorine
    Biologic agents
      Bacteria
      Fungi
      Molds
      Rickettsia
      Spores
    Inorganic dusts
      Asbestos
      Silica
      Coal mine dust
      Nickel
      Talc
      Beryllium
    Organic dusts
      Cotton dust
      Wood dust
    Solvents
      Benzene
      Carbon tetrachloride
      Methanol
      Chloroform
      Trichloroethylene
      Xylene
    Metals
      Aluminum
      Arsenic
      Cadmium
      Cobalt
      Iron
      Lead
      Mercury
      Chromium
    Other
      Plastics
        Vinyl chloride
        Acrylonitrile
        Styrene
      Dyes
      Petrochemicals
        Creosote
        Asphalt and tar
      Poisons
        Insecticides
        Herbicides
      Products of combustion
        Biomass fuel
        Diesel exhaust


  • Asbestos fibers can damage lung parenchyma and pleura, causing both benign and malignant disease by complex processes that are incompletely understood.3,4



    • Fibers can be suspended in air and inhaled.


    • Inhaled fibers penetrate deeply into the lungs and cellular structures.


    • Fibers are incompletely cleared.


  • All asbestos-containing materials, whether made from amosite, crocidolite, tremolite, or chrysotile, can cause fibrosis, lung cancer, and diffuse malignant mesothelioma.


  • Clinical and radiographic manifestations of disease may be delayed for decades.


  • Asbestos was widely used in construction and manufactured products until 1975. Routes for exposure include:



    • The manufacture of asbestos-containing products.









      TABLE 26-2 SAMPLE OCCUPATIONAL HISTORY






      1. List all jobs you have ever held and the dates of employment beginning with the very first one.
      2. 2. For each job identify:

        1. Chemicals/dusts or other substances you may have been exposed to? Nature of exposure risk: contact/inhalation/ingestion?
        2. Protective equipment:

          1. Was equipment available? Did you use it? Describe
          2. Was the equipment fit tested?
          3. Did you use the equipment as instructed? When? What percentage of the time? Under what circumstances did you not use it?

        3. Air quality:

          1. What kind of active ventilation was provided? What was the maintenance schedule?
          2. Were there strong odors/taste in the air?
          3. Could you see haze/dust in the air?
          4. Did your eyes burn/water?

        4. Facilities for washing/showering present?
        5. Were uniforms provided? Did you wear them? Were they washed at home? By whom?
        6. Did you eat, drink, or smoke in the workplace?
        7. Procedures for accidental exposure?
        8. Your symptoms:

          1. Date of onset?
          2. Relationship to exposure: Worse at beginning/end of shift/week? Better after weekend off/vacation?
          3. Do you blow dust from your nose or cough it up?

        9. Coworkers with similar symptoms? Other problems?
        10. Were there animals/insects in the workplace?
        11. Is the workplace damp? Is there standing water?
        12. Any usual event such as spills, excessive exposure, or fires?

      3. Other exposures:

        1. Smoking history?
        2. Alcohol history?
        3. Chemicals used at home in housekeeping/hobbies/lawn care/automobile maintenance?
        4. Animals at home: pets, livestock, birds?


    • Removal of floor tiles, insulated pipes, roofing materials, brake linings, and other asbestos-containing materials currently in place.


    • Employment in the construction, maintenance, textile, or roofing industries.


Diagnosis



  • The exposure history may be essential to making the diagnosis. The patient should have a history of exposure to asbestos fibers and a suitable latency period before development of symptoms or radiographic findings.



    • Pleural effusions >1 year


    • Pleural plaques >10 years


    • Asbestosis, lung cancer, diffuse malignant mesothelioma (DMM) >20 years


  • The presentation, examination, PFTs, and radiologic findings can be nonspecific.3




    • Patients may complain of cough, persistent progressive dyspnea, and sometimes chest discomfort.


    • Late inspiratory crackles may be heard on auscultation and clubbing may be seen in some cases.


    • PFTs show decreased lung volumes, especially total lung capacity (TLC) and decreased forced vital capacity (FVC), along with decreased diffusing capacity of the lung for carbon monoxide (DLCO).


    • Impairment of gas exchange is most sensitively determined by arterial blood gas (ABG) analysis conducted at rest and during exercise.


    • CT is more sensitive than CXR for detecting subtle findings as well as for characterizing pleural processes.5,6,7


    • Special studies such as bronchoalveolar lavage, tissue biopsy, and sputum evaluations may be necessary to find asbestos fibers if exposure requires documentation.


  • Asbestosis



    • The presence of asbestos fibers may result in a persistent inflammatory process culminating in diffuse interstitial fibrosis, with distortion of the lung parenchyma. Diffuse interstitial fibrosis usually develops no sooner than 20 years after the first and heavy exposure.


    • CT scan shows multiple abnormalities: curving subpleural lines, parenchymal banding, short peripheral lines, and honeycombing in advanced disease.


    • Both bilateral pleural plaques and parenchymal processes must be present to make the diagnosis.


  • Pleural disease5,6,7



    • Pleural disease may result from translocation of fibers into the pleural space to stimulate an inflammatory and fibrotic response.


    • Pleural thickening



      • Fibrosis of the visceral pleural with adhesions to the parietal pleura occurs, obliterating the pleural space and extending into lung parenchyma.


      • CXR shows widely distributed plaques that do not spare the apices or the costophrenic angles.


      • Plaques are invariably asymptomatic.


    • Rounded atelectasis



      • Pleural thickening may entrap a section of lung, causing atelectasis and associated volume loss.


      • CXR shows thickened pleura surrounding a section of atelectatic lung with a so-called comet tail extending in the direction of the hilum.


    • Pleural effusion



      • This is the earliest clinical phenomenon, occurring as early as 1 year, but more typically, longer than 10 years after exposure.


      • Patients may complain of chest pain and breathlessness.


      • CXR usually shows a unilateral effusion but it may be bilateral, either synchronous or metachronous.


      • Thoracentesis yields an exudative, sometimes bloody effusion. Fibers are not often found in pleural fluid.


  • DMM



    • DMM is a malignant process of the parietal surface of the thoracic and/or abdominal cavities that invades heart and lung by direct extension.


    • Almost all DMM in the United States is due to asbestos exposure. Exposure may have been apparently minimal, indirect, and not occupational. For example, helping a parent to clean work clothes as a child or being present during a ship refitting.


    • Exposure almost always occurred >20 years before clinical manifestations.


    • Radiographic findings include lobulated growth over the parietal pleural surface.5



    • The diagnosis is usually established by the surgeon’s description and confirmed by tumor biopsy.


    • There is no curative treatment. The prognosis for this malignancy is very grim but new combined surgical and chemotherapeutic regimens show some therapeutic promise.


  • There is an association of asbestos-related lung disease and lung cancer.3,4,6,7,8,9



    • Asbestos has been classified by the International Agency for Research on Cancer (IARC) as group 1, carcinogenic to humans.10 Exposure to asbestos, both in amphibole or serpentine forms, clearly is associated with increased lung cancer risk.


    • Tobacco smoking additively, and possibly synergistically, increases lung cancer risk in persons who have even short-term exposure to asbestos. Therefore, tobacco cessation is imperative.


    • Because asbestos exposure has been associated with a substantial increased risk for lung cancer and early diagnosis may improve outcome, CT surveillance may be employed with expected outcome benefit.


Coal Dust–Associated Pulmonary Disease


General Principles



  • Coal is ranked according to its carbon content, which is determined by the geologic setting in which it was formed.


  • Coal dust is primarily carbon but silica, kaolin, mica, metal dusts, and other potentially harmful contaminants may also be present.


  • The amount and nature of exposure during coal mining depends upon the rank of coal, quality of dust control measures, and the individual’s work responsibilities.



    • Exposure is greatest working underground at the coal face.


    • Above-ground workers who operate drills or transport coal may also have sufficient exposure to produce disease in a susceptible host.


  • The National Institute for Occupational Safety and Health (NIOSH) estimated that 4% of coal workers develop a coal dust-associated pulmonary disease for the period 1995–1999. However, the prevalence increased to 9% during 2005–2006.11


Diagnosis



  • The spectrum of clinical manifestations is wide. Patients may be asymptomatic with mild radiographic abnormalities or severely disabled with obvious and advanced radiographic abnormalities.


  • Coal workers’ pneumoconiosis



    • The hallmark symptom is shortness of breath.


    • Persistent late inspiratory crackles are heard on examination.


    • PFTs may show a restrictive ventilatory defect, with impaired O2 exchange seen first during exercise. Obstructive ventilatory defects are rarely due to coal mine dust and difficult to distinguish from the more common tobacco-associated disease in smoking miners.


    • CXR shows small nodular opacities in the upper lobes in the early stages, which become more numerous and confluent as disease progresses.


  • Progressive massive fibrosis



    • Patients complain of shortness of breath and cough.


    • PFTs may show both obstructive and restrictive ventilatory defects.


    • CXR shows coalescence of nodules >12 mm in size.


  • Chronic obstructive pulmonary disease (COPD) phenotype12,13

Nov 20, 2018 | Posted by in RESPIRATORY | Comments Off on Occupational Lung Disease
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