Pneumoconiosis: what is it, causes, symptoms, treatment, prognosis

What is pneumoconiosis?

Pneumoconiosis Is any lung diseasecaused by inhalation of organic or inorganic dust and airborne fibers. Patients usually encounter these inhalants in the workplace, which is why pneumoconiosis is also called an occupational disease. The most common types of pneumoconiosis are asbestosis, silicosis, anthracosis, beryllium disease. These respirable dust particles cause inflammation and pulmonary fibrosisleading to irreversible lung disease. Prevention is based on workplace exposure and health regulations.

Signs and symptoms

The symptoms of pulmonary pneumoconiosis often depend on the severity of the disease. Simple anthracosis may have few or no symptoms and only appear on an x-ray. Progressive massive fibrosis can cause severe breathing difficulties. Common signs and symptoms of pneumoconiosis may include:

• cough;
• profuse sputum production;
• shortness of breath.

Causes and risk factors

Pneumoconiosis results from the accumulation of small, inhaled particles that cause an inflammatory response in the lungs. Fibrous pneumoconiosis is predominant and is caused by inhalation of particles such as silica, asbestos fibers, beryllium, talc and coal dust. The patient's history usually reflects long-term exposure to harmful inhalants, since interstitial lung disease caused by dust is hidden. Exposure to these inhalants usually occurs in the workplace. The duration of work is correlated with the risk of pneumoconiosis.

Pathogenesis

The lung response to mineral dust depends on many variables, including particle size, shape, solubility and reactivity. For example, particles larger than 5-10 microns are unlikely to reach the distal airways, then as particles smaller than 0.5 μm move into and out of the alveoli, often without significant deposits and injuries. Particles with a diameter of 1 to 5 microns are most dangerous, as they settle on the branching of the distal airways. Coal dust is relatively inert, and large quantities of it must settle in the lungs before the disease becomes clinically detected.

Silica, asbestos and beryllium are more reactive than coal dust, resulting in fibrotic reactions at lower concentrations. Most of the inhaled dust is trapped by the mucous membrane and quickly removed from the lungs due to the movement of the cilia. However, some particles collide with alveolar bifurcations, where macrophages accumulate and absorb the entrained particles.

Pulmonary alveolar macrophage is a key cellular element in the initiation and maintenance of pulmonary injury and fibrosis. Many particles activate inflammasomes and induce IL-1 production. The more reactive particles cause macrophages to secrete a number of products that mediate the inflammatory response and initiate fibroblast proliferation and collagen deposition.

Some of the inhaled particles can reach the lymphatic vessels either by direct drainage or inside migratory vessels. macrophages and thereby initiate an immune response to the components of particles and / or own proteins that are modified particles. This then leads to an increase and expansion of the local reaction. Smoking worsens your exposure to any respirable mineral dust, more with asbestos than with any other particulate matter.

Epidemiology

Pneumoconiosis is one of the most common occupational diseases in the world, especially in developing countries. From 1990 to 2017, the number of cases of the disease among both sexes increased by 81.1%. Age-standardized prevalence was significantly higher in males. The incidence also increased with age, and significantly more in men. According to the 2010 Global Burden of Disease study, pneumoconiosis was responsible for 125,000 deaths. In 2016, the Global Burden of Disease estimated 3,495 people died from asbestosis. The prevalence of pneumoconiosis among workers exposed to occupational dust is on the rise. In the Chinese province of Jiangsu, 9,243 cases were reported between 2006 and 2017, of which the majority are silicosis and pneumoconiosis of miners. In developed countries such as the UK, asbestosis accounts for the majority of cases. These illnesses can lead to other serious illnesses. For example, exposure to silica increases the risk of tuberculosis, cancer and emphysema of the lungs.

Diagnostics

The diagnosis is made with long-term exposure to one of the high-dose inhalants in addition to radiologic evidence of pulmonary fibrosis. A biopsy is rarely required. The three main criteria are exposure to inhalants, a characteristic chest X-ray, and the absence of a disease that could be mistaken for pneumoconiosis. In the case of asbestosis, pleural plaques on radiographs are pathognomonic. Signs of silicosis appear after 10-20 years of work in such an environment. The x-ray will look the same as for miner's pneumoconiosis, with small interstitial nodules in the upper and middle zones of the lungs. CT scans of both areas will show small nodules diffusely across the lungs, but more heavily concentrated in the upper area of ​​the lungs. To distinguish progressive massive fibrosis from lung cancer, you can use MRI. On T2-weighted images, lung cancer will appear as high signal intensity lesions, whereas progressive massive fibrosis has a low signal intensity abnormality.

Symptoms of pneumoconiosis are generally nonspecific and may overlap with other comorbid lung diseases such as chronic bronchitis, COPD and emphysema. Careful professional history should be taken into account, considering both exposure and duration of inhalation exposure. Patients may complain about dyspnea, decreased exercise tolerance, gradual onset of unproductive cough. In the case of miner's pneumoconiosis, black pigmented sputum may form. On physical examination, it can be noted tachypnea and wheezing at the end of inhalation. Friction or wheezing can be heard on auscultation of the lungs. Cardiac auscultation may reveal PJ2 accentuation at the left upper border of the sternum.

Pulmonary function tests can show the typical limiting picture with chronic obstruction air flow, a decrease in the forced vital capacity of the lungs (FVC), but maintaining the ratio OFV1-FZHEL. Diffusion capacity is often reduced and may precede a decrease in lung volume. The forced vital capacity of the lungs of patients, the forced expiratory volume in one second is proportionally reduced, and their forced expiratory flow is from 25% to 75% of the FVC. Severe pulmonary fibrosis can lead to hypoxemia, pulmonary hypertension, and right ventricular failure.

There is evidence of an increase in certain markers in serum and urine in pneumoconiosis. The researchers found that SMRP and fibulin-3 were elevated in subjects with pneumoconiosis, indicating exposure to asbestos. They hope that a combination of serum SMRP and Fibulin-3, CEA and 8-OHdG in urine can be used to test workers. The development of a breath test for pneumoconiosis is also being studied. Researchers describe the detection of pentane, C5-C7 alkanes and methylated alkanes in the breath of people with pneumoconiosis as a possible way to detect this disease.

Treatment

There is no specific treatment for pneumoconiosis, so instead the focus is on improving the patient's quality of life by stopping the progression and minimizing the impact complications. Patients are advised to quit smoking immediately and be vaccinated against fluas getting the flu will seriously worsen the condition.

Oxygen therapy, inhalers, and steroids can help manage the condition day in and day out. Short-term therapy corticosteroids can be used to treat exacerbations of this condition. In intensive care, patients with pneumoconiosis who were admitted to the intensive care unit in connection with the first an episode of acute respiratory failure, non-invasive mechanical ventilation may be required lungs.

Forecast

The prognosis of the disease depends on the specific type of pneumoconiosis, the duration of exposure to mineral dust, the level of exposure, and whether the patient is a smoker.

In the long term, patients with asbestosis and talc pneumoconiosis are at increased risk the development of lung cancer and malignant mesothelioma (cancer of the membranes lining the lungs and abdominal cavity). The risk of lung cancer is especially high in smokers with asbestosis.

Because men take most of the jobs associated with a high risk of pneumoconiosis, the majority of deaths from pneumoconiosis occur in men.

Complications

The main complication is the progression of simple pneumoconiosis to progressive massive fibrosis. The disease includes other possible complications:

• progressive respiratory failure;
• lungs' cancer;
• pulmonary tuberculosis (but now rarely);
• heart failurecaused by pressure in the lungs.

Prophylaxis

Prevention is important because the disease cannot be cured or reversed. The Occupational Safety and Health Administration sets out standard prevention guidelines for workers at risk of pneumoconiosis. These are general preventive measures:

• wearing a mask;
• washing areas of skin in contact with dust;
• safe removal of dust from clothing;
• washing your face and hands thoroughly before eating, drinking, or taking medication;
• quit smoking;
• inform your doctor and employer about any symptoms of pneumoconiosis;
• regular chest x-rays and medical examinations.