Practice Essentials
Occupational lung diseases refers to the development of lung diseases from inhalational exposure that occurs at the work place. However, these lung diseases may also occur in environments other than work, even home. Occupational lung disease can result from inhalational exposure to minerals and dusts, microbes, animal and insect proteins, and chemicals and can have long-lasting effects even after the exposure ceases.
Chemical worker's lung refer to the development of lung disease in the work environment from inhalational exposure to chemicals. The U.S. Occupational Safety and Health Administration (OSHA) has established 8-hour time-weighted averages (TWA) on the airborne concentrations of hazardous chemicals. These permissible exposure limits (PELs) have been established for approximately 500 chemicals; however, many of the limits are outdated and there are many chemicals for which OSHA had not yet set a workplace exposure limit. [1]
Additionally, nanoparticles are engineered particles less than 100 nm. [2, 3] Commercially, nanoparticles are used in various industries. Nanoparticles like zinc oxide are widely used in sunscreens, paints, textiles, and other products and can lead to accidental occupational inhalational exposure. Few occupational exposure limits exist specifically for nanomaterials and certain nanoparticles may be more hazardous than larger particles of the same substance. Therefore, existing occupational exposure limits for a substance may not provide adequate protection from nanoparticles of that substance. For example, OSHA has issued a PEL nanoscale particles of titanium dioxide (TiO2) that exposure should not exceed 0.3 milligrams per cubic meter (mg/m3). By contrast, the recommended exposure limit for fine-sized TiO2 (particle size greater than 100 nm) is 2.4 mg/m3. Because exposure limits for most nanomaterials do not exist yet, OSHA recommends that worker exposure should be minimized by using the hazard control measures and best practices that include engineering controls, administrative controls, personal protective equipment and regular medical screening and surveillance. [2, 3]
Pathophysiology
Workplace exposure to inhaled chemicals can lead to changes in the airway, lung parenchyma, blood vessels, and pleura or a combination of these structures in the lung. Systemic manifestations may also be present, depending on the chemical exposure.
Airway manifestations
The nasal mucosa and airway are the first areas of contact with inhalational exposures to chemicals. Larger particles are trapped and deposited within the nares, whereas the smaller particles are deposited in the trachea, bronchi, and bronchioles; only particles smaller than 5 micrometers may reach the alveoli. More soluble gases may be directly absorbed from the nasal mucosa while lesser soluble gases may be absorbed further down the respiratory mucosa. This can lead to vascular dilatation, mucosal edema, and rhinorrhea resulting in sneezing, nasal stuffiness, drainage, epistaxis, and even septal perforation (eg, with arsenic, chromic acid).
Occupational rhinitis usually results in worsening of symptoms at the workplace and tends not to have seasonal variation in symptoms.
Tracheitis, acute and chronic bronchitis, and bronchiolitis can result from the airway inflammation. Bronchiolitis obliterans has also been reported with certain chemicals (eg, chlorine, phosgene, nitrogen dioxide). Manifestations include cough with and without sputum production, shortness of breath, and even hemoptysis.
Chemical irritation of the airway can result in the development of new onset asthma or worsening of prior symptoms of asthma. Higher molecular weight antigens stimulate the release of IgE. Patients with a history of atopy and smokers are at a higher risk for developing asthma. Lower molecular weight antigens can induce airway sensititzation without the mediation of IgE. Examples of substances that can result in asthma include acid anhydrides used in epoxy adhesives and paints. Isocyanates used in polyurethane paints and foam are commonly associated with asthma. [4]
A commonly asked employer question is why other coworkers do not have similar complaints of occupational asthma (OA). Development of OA is also genetically mediated with several different associated HLAs being implicated.
Chronic obstructive pulmonary disease (COPD) can develop following exposure to chemicals. [5]
Parenchymal manifestations
Chemicals like anhydrides, diisocyanates including trimellitic anhydrides, and other chemicals can result in hypersensitvity pneumonitis (HP). The onset may be acute, subacute, or chronic, depending on the intensity, duration, and susceptibility of the patient.
The list of chemicals that can result in HP continues to increase. Symptoms include fever, chills, fatigue, cough, shortness of breath, and cough. Recurrent exposure can lead to interstitial lung disease and pulmonary vascular pathologies.
Pulmonary vasculature involvement
As the pulmonary parenchymal involvement progresses, it may lead to the development of pulmonary arterial hypertension.
Lung cancer
Occupational lung cancer can result from exposure to a variety of chemicals used in the manufacturing of pesticides and water and flame repellents. These chemicals and be found in the National Toxicology Program Report on Carcinogens.
Etiology
The list of chemicals asociated with lung disease continues to increase. Traditionally the implicated industries included the manufacture polyurethane foam, molding, insulation, synthetic rubber, and packaging materials and include toluene diisocyanate (TDI) [6, 7, 8, 9] and trimellitic anhydride. However, with the development of newer chemical agents and with the novel use of existing agents the industries being associated with lung disease continue to expand.
As discussed earlier, nanoparticles, particularly engineered nanoparticles, are a relatively new, emerging occupational and environment exposure that can lead to the development of lung disease. [10, 11, 12] A unique feature of nanoparticles is their very large surface area-to-mass ratio, indicating their toxic effects may be more related to surface area than mass. [12] An increasing area of concern is that engineered nanoparticles may exhibit new or increased reactivity and increased toxic effects following inhalation exposure. [12] The Occupational Safety and Health Administration (OSHA) has a site dedicated to working safely with nanotechnology at https://www.osha.gov/dsg/nanotechnology/index.html. [3]
Epidemiology
Determining the actual prevalence rate of chemical worker's lung is difficult because of low reporting, poor appreciation of symptoms and signs associated with substance exposure, and lack of proper understanding of and diagnostic guidelines for the disease. Prevalence varies in accord with the distribution of the sexes in industry. No specific predisposition is noted for either sex. The kind of substance, the duration of exposure, and the total cumulative dose are more important than the age of an exposed individual.
Prognosis
The ultimate prognosis is related to the specific exposure. Mortality and morbidity vary with the substance and the frequency, intensity, and duration of inhalational exposure. Host factors include underlying cardiopulmonary disease and immunopathogenesis.
A study by Hart et al assessed ambient air pollution exposures and mortality. [13] The study concluded that cause-specific mortality (ie, lung cancer, cardiovascular and respiratory disease) were observed with particulate matter less than 2.5 micrometers in diameter, sulfur dioxide, and nitrogen dioxide, but not with particulate matter less than 10 micrometers in diameter.
Complications may include the following:
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Pulmonary fibrosis
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Lung nodules (benign or malignant)
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Bronchial hyperreactivity
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Right heart disease (eg, pulmonary hypertension, cor pulmonale)
