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.
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 list of chemicals that has been associated with lung disease continues to increase.
Nanoparticles are engineered particles less than 100 nm. 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 inhalational exposure in the occupational and personal settings. Only sparse data are available as to the respiratory morbidity that may be associated with these small particles.
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.
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 while the smaller particles are deposited in the trachea, bronchi, bronchioles while 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 dilation, 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.
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 like diisocyanate.
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.
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.
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.
The prevalence rate is unknown, but it is presumably higher than in the United States given the lack of reporting and regulatory bodies.
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.  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.
Data comparing the prevalence rates of chemical worker's lung among various races are not available; however, African Americans and Asians may have smaller lungs and, possibly, a higher risk of lung disease with the same exposure.
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.
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