In the 60-minute webinar, Mridu Gulati, MD, MPH of Yale University’s Interstitial Lung Disease Program, a renowned expert on ILDs in occupational illness, discussed known job-related exposures associated with ILD and (in the last 20 minutes) answered listener questions.
What is ILD?
First, Dr. Gulati introduces ILDs, noting they include all lung diseases that involve inflammation and/or scarring of lung tissue. Those that involve scarring are called pulmonary fibrosis—”a family of more than 200 different lung diseases that all look very much alike.” ILDs can be divided into those of known cause and those of unknown cause. ILDs of known cause include connective tissue diseases (autoimmune), medication-related, and exposures; idiopathic interstitial pneumonias, meanwhile, are the largest category of ILDs of unknown cause, of which IPF is included. Proving known causes can be challenging, she explains; for example, it typically takes years for symptoms and disease to occur, and people may not recall the exposure.
Two major types of PF with known exposure-related causes are reviewed in depth.
Pneumoconioses are “chronic lung diseases caused by inhaling dusts,” such as asbestosis; silicosis; and coal workers’ pneumoconioses/CWP, also known as “black lung.” To determine disease cause, doctors will generally ask questions regarding job history: titles held (including military); products made; materials/chemicals handled like asbestos, the mineral once prevalent in construction; exposure to gases, vapors, or dusts (like asbestos); ventilation quality; use of protective wear; etc.
Asbestosis signs happen 20+ years after exposure, with shortness of breath and cough coming on slowly. There is no proven treatment, but supportive care and (especially for severe disease) lung transplantation are effective. Diagnosis is through establishing exposure and testing: breathing/lung function (example, 6-minute walk test); oxygen levels; and a CT/ CAT scan to observe scarring patterns. (Lung biopsy is “usually not needed.”) Dr. Gulati emphasizes that prevention and regulation of asbestos works for reducing exposure.
Coal workers’ pneumoconiosis, which has made recent headlines, is caused by inhaling coal dust over many years, the dust containing particles of carbon and (of greater disease concern) silica. Though there is no treatment, the 1969 Federal Coal Mine Health and Safety Act “established regulations, medical monitoring and a lung benefits program.” CWP’s scarring pattern is “very different” from asbestosis; disease nodules progress over time to form large masses (called “progressive massive fibrosis”) that cause more symptoms.
Of growing medical interest, chronic hypersensitivity pneumonitis is also slowly progressive, with shortness of breath and a dry cough. Also called “bird fancier’s lung” when the result of long-term proximity to bird droppings, symptoms typically arise months to years after exposure. Lung scar is usually permanent, but stopping exposure helps, as can treatment with immune-suppressing drugs such as steroids. (Dr. Gulati notes that the newer IPF drugs have not been proven effective in patients with chronic hypersensitivity pneumonitis or pneumoconiosis.) CHP can occur where there is bacterial or fungal contamination: farm environments (moldy hay, for instance); contaminated hot tub and humidifier mist; isocyanates chemicals; and contaminated metalworking fluid and woodworking dust, for example. Diagnosis involves patient history and tests similar to pneumoconiosis, along with possible blood testing (though this can be misleading), biopsy, or (less invasive) bronchoscopy for lung sampling.
Exposure link to IPF?
In the last section, Dr. Gulati discusses whether these exposures may have a link to IPF.
IPF is believed to initiate from lung injury, which may result from exposure to pollutants on the job or in the environment (air pollution), from smoking, bacteria or fungus, or gastroesophageal reflux. Observational studies of hospital patients and self-reported questionnaires suggest that smoking, wood and metal dusts are associated with the disease. Further, a study of lung tissue from 23 IPF patients found increased aluminum and silica, while another found tungsten embedded in lung tissue of metal workers. Also, a study of air pollution suggested an association between increased pollutants and decreased lung function. But a firm connection between these exposures and IPF has yet to be established.
The webinar can also be accessed on YouTube where slides can be viewed in full-screen. (Slides can be obtained from the PFF by contacting their Patient Communication Center at firstname.lastname@example.org.)
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