Resurgence of Pneumoconiosis

How inhalation exposure contributes to pulmonary disorders

Innovations in Pulmonology & Sleep Medicine | Winter 2020

David Rosenberg, MD

Inhalation of organic and inorganic substances causes significant nonmalignant lung disease. These exposures, however, are often overlooked in the clinical setting.

If you don’t think about occupational or other exposures, you might not make an accurate diagnosis,” explains David Rosenberg, MD, Division of Pulmonary, Critical Care and Sleep Medicine at University Hospitals Cleveland Medical Center; and Assistant Clinical Professor of Medicine, Case Western Reserve University School of Medicine.

Dr. Rosenberg highlights several conditions where inhalation exposure may contribute to pulmonary disorders.

SILICOSIS

Inhaling the crystalline form of silica can cause silicosis. Despite newer workplace standards, more than 2.3 million workers still are exposed to crystalline silica, either alone or in combination with other minerals, Dr. Rosenberg says.

“Silica is cytotoxic. It can kill or damage lung cells and interacts with inflammatory cells in the lungs,” he says. “Also, silica causes cytokine production, which can damage the lung in various ways.”

Silicosis can produce symptoms within weeks following high-intensity exposure, although this is rare. More typically, silicosis takes 10 or more years to show symptoms.

“Chronic simple silicosis is characterized by small, sharply marginated micronodules, generally in the dorsal upper lobes,” Dr. Rosenberg says. “Often lung function is preserved, and patients have few respiratory problems. Simple silicosis can develop into progressive (or complicated) massive fibrosis, with large conglomerate masses that can be confused with lung cancer. Radiographically, patients with silica exposure not uncommonly have eggshell calcifications.”

Physicians should be aware that patients with silica exposure are at increased risk for tuberculosis, and those with silicosis are clearly at risk for lung cancer. These patients should be screened regularly. Workplace silica exposure also can increase patients’ risk for chronic obstructive pulmonary disease, chronic bronchitis or inflammatory reactions outside of the lungs, leading to rheumatic diseases, chronic kidney disease or scleroderma.

“If you have a patient who’s been coughing for at least three months a year for two consecutive years, ask about dust — and especially silica — exposure,” says Dr. Rosenberg.

COAL WORKERS’ PNEUMOCONIOSIS

Particles from coal mining can accumulate in the lungs, putting miners at risk for coal workers’ pneumoconiosis (CWP), better known as black lung disease.

Despite decreases in coal production, there’s been an uptick in the prevalence of CWP, possibly due to changes in mining practices that expose workers to ever smaller particles, which potentially can penetrate deep into the lungs.

Surveillance data for 2018 show that about 10 percent of coal workers who worked in mining 25 or more years have CWP. The migration of former coal miners to Northeast Ohio may explain the increased incidence in our region, says Dr. Rosenberg. If you have patients with micronodular changes, especially in the upper lobes, it may indicate CWP.

Radiographically, manifestations of coal workers’ pneumoconiosis and silicosis are essentially identical, Dr. Rosenberg says, although the pathologic findings are distinct. As with silicosis, small nodules associated with simple CWP generally don’t cause lung impairment. However, the disease can progress, and patients diagnosed with CWP should be followed carefully.

ASBESTOSIS

Asbestosis is a form of pneumoconiosis that results from inhaling friable asbestos fibers. Patients typically don’t exhibit symptoms for at least 20 years after exposure.

Unlike silica, which has a crystalline structure, asbestos has fibers that are either long, thin and straight (amphibole), or curved (chrysotile). Both are fibrogenic in the lungs, and the more asbestos a person inhales (or if the person also smokes), the greater the risk for asbestosis.

“The straight fibers have the greatest propensity to get into the lungs and get deposited in the alveoli structures where they cause inflammation,” Dr. Rosenberg says. “From the lungs, they can be transported through the lymph system to other parts of the lungs and body.”

A characteristic finding signifying asbestos exposure is pleural calcifications on a chest X-ray or CT scan.

Early on, asbestosis is asymptomatic. As it progresses, however, patients can experience shortness of breath along with crackles on examination and even clubbing. It is also associated with the development of lung cancer. As asbestosis progresses, pulmonary hypertension and right-sided heart failure can occur. Asbestos exposure also predisposes patients for the development of mesothelioma.

Clinicians should ask patients presenting with interstitial lung disease about employment in potentially high-risk occupations, such as textiles, shipbuilding or demolition. Family members can also be at increased risk of asbestos-related disorders through laundering contaminated clothing.

HYPERSENSITIVITY PNEUMONITIS

Hypersensitivity pneumonitis (HP), also called extrinsic allergic alveolitis, is a complex and potentially progressive lung disease that occurs after exposure to inciting agents, often organic chemicals, explains Dr. Rosenberg. It is a common cause of interstitial lung disease, although an inciting factor may not be found.

HP is commonly called farmer’s lung disease when related to exposure to moldy hay and related antigens, or bird fancier’s disease, as it’s common among individuals exposed to bird proteins. It’s often misdiagnosed as asthma or a viral illness.

“Hypersensitivity pneumonitis is generally an upper lobe disease, as opposed to having a lower lobe predominance as we observe with other forms of interstitial lung disease, such as asbestosis,” Dr. Rosenberg says. “Acute HP is characterized by small airway obstruction, ground glass opacification on high-resolution CT scans and small upper lobe micronodules.”

Clinicians should ask patients with suspected HP if they have a hot tub or sauna at home; if they are frequently around animals, grains or flowers; and if they are exposed at work to plastics or electronics. It’s important to catch HP early. Once it becomes chronic, it’s more difficult to diagnose and may present like idiopathic pulmonary fibrosis.

BOTTOM LINE

“Inhalation-related lung diseases are prevalent, and the possibilities for exposure are endless,” Dr. Rosenberg says. “Clinicians should think about different types of exposures when evaluating patients with pulmonary manifestations.”

For more information about pneumoconiosis, or for assistance diagnosing patients, contact Dr. Rosenberg at 216-553-1649.