PNEUMOCONIOSIS

By-Anubhav Agrawal,514

CONTENTS

• Introduction• Pathogenesis• Classification• Silicosis• Diagnosis

INTRODUCTION• Pneumoconiosis is an occupational lung disease and a restrictive lung

disease caused by the inhalation of dust, often in mines and from

agriculture.

• In 2013, it resulted in 260,000 deaths, up from 251,000 deaths in 1990. Of

these deaths, 46,000 were due to silicosis, 24,000 due to asbestosis and 25,000

due to coal workers pneumoconiosis.

• The first recorded mention of breathlessness among handlers of grain was

done by Ramazzini, the father of occupational medicine, in 1713.

• The term "black lung" was coined when medical professionals

discovered the blackening of miners' lungs in post-mortem.

• The first documented case of an asbestos-related death was reported in

1906 when the autopsy of an asbestos worker revealed lung fibrosis.

PATHOGENESISFor clinical pneumoconiosis to develop, 3 essential factors are

required:

• Exposure to specific substance: coal, appear relatively inert and may

accumulate in considerable amounts with minimal tissue response;

while silica and asbestos, have potent biologic effects.

• Particles of appropriate size to be retained in lung (1-5μm)

• Exposure for a sufficient length of time (usually around 10 years)

CLASSIFICATIONDepending upon the type of dust, the disease is given different names:

• Coal worker's pneumoconiosis (also known as miner's lung, black lung or anthracosis) — coal,

carbon

• Asbestosis — asbestos

• Silicosis— crystalline silica dust

• Bauxite fibrosis — bauxite

• Berylliosis — beryllium

• Siderosis — iron

• Byssinosis — cotton

• Silicosiderosis — mixed dust containing silica and iron

• Labrador lung (found in miners in Labrador, Canada) — mixed dust containing iron, silica and

anthophyllite, a type of asbestos

SILICOSIS• Silicosis (previously miner's phthisis, grinder's asthma, potter's rot and

other occupation-related names) is a form of occupational lung disease

caused by inhalation of crystalline silica dust, and is marked by

inflammation and scarring in the form of nodular lesions in the upper

lobes of the lungs. It is a type of pneumoconiosis.

• Silicosis resulted in 46,000 deaths globally in 2013 down from 55,000 deaths

in 1990.

CLASSIFICATIONThree forms of silicosis:

• Acute silicosis: occurs with exposure to fine dust with high quartz content;

very heavy exposure for months, shows symptoms within weeks to months

of exposure,

• Accelerated silicosis: shows rapidly progressive symptoms after 5 to 10 years

of high exposure to fine dust of high silica content.

• Chronic silicosis: the most common form, results from long-term exposure

(10 to 20 years or longer) to dust containing less than 30% silica content.

CLINICAL FEATURES• Chronic cough

• Dyspnea (shortness of breath) that worsens with exertion.

• Fatigue

• Loss of appetite

• Chest pains

• Acute silicosis patients may also have fever and experience rapid, unintended

weight loss.

Silicotuberculosis: Pulmonary tuberculosis occurs in about 25% of patients

with acute or classic silicosis

DIAGNOSISPositive indications on patient assessment:

• Shortness of breath

• Chest X-ray may show a characteristic patchy, subpleural, bibasilar

interstitial infiltrates or small cystic radiolucencies called honeycombing.

Pneumoconiosis in combination with multiple pulmonary rheumatoid

nodules in rheumatoid arthritis patients is known as Caplan's syndrome.

• For uncomplicated silicosis, chest x-ray will confirm the presence of

small (< 10 mm) nodules in the lungs, especially in the upper lung

zones. Using the ILO classification system, these are of profusion 1/0 or

greater and shape/size "p", "q", or "r". Lung zone involvement and

profusion increases with disease progression. In advanced cases of

silicosis, large opacity (> 1 cm) occurs from coalescence of small

opacities, particularly in the upper lung zones. With retraction of the

lung tissue, there is compensatory emphysema. Enlargement of the

hilum is common with chronic and accelerated silicosis. In about 5-10%

of cases, the nodes will calcify circumferentially, producing so-called

"eggshell" calcification. This finding is not pathognomonic (diagnostic)

of silicosis. In some cases, the pulmonary nodules may also become

calcified.

• PA chest radiograph of an 80-

year-old man who was a miner

decades ago shows multiple large

opacities (arrows, large opacity =

parenchymal opacity greater

than 1 cm) and several tiny

rounded opacities in the right

lower and left mid/lower lung

zones. With the history of

exposure, adequate lag time and

chest radiographic findings, the

patient has findings consistent

with coal worker

pneumoconiosis.

• Image shows small nodules

predominantly in the

middle-to-upper lung zones,

several of which are

calcified. Eggshell

calcification is present in the

bilateral hilar lymph nodes.

The large mass in the

infrahilar region of the right

lung is consistent with

progressive massive fibrosis.

• Silicosis with progressive

massive fibrosis. Image

shows large, conglomerate

nodules in both the middle

and upper lung zones.

Peripheral hyperlucency

represents emphysematous

lung tissue secondary to

central migration of the

large nodules. Bilateral

upper lobe volume loss is

also noted.