PARTICLE SIZE AND CHEMISTRY:

Pneumoconioses

This information is additional to Davidson’s Principles and Practice of Medicine. /Hierdie inligting is aanvullend tot Davidson’s Principles and Practice of Medicine.

Pneumoconioses refers to the accumulation of dust in the lung and the tissue reactions to it. It excludes asthma, bronchitis, emphysema, malignancy and purely pleural lesions.

Diagnosis rests on a careful occupational history, a typical radiological appearance and the exclusion of other causes of the clinical picture.

In taking history it is important to identify the specific dust to which the patient has been exposed, for example in jobs such as fitters, grinders, and carpenters.

Of the pneumoconioses asbestosis and silicosis are the commonest. PARTICLE SIZE AND CHEMISTRY:

Particles above 10-15 µm do not penetrate beyond the upper airways. These include pollens and windblown dusts, and have little or no effect on chronic respiratory disease.

Particles below 10 µm in size are created by burning of fossil fuels in industrial processes resulting in products from gases and fumes of vapors. Particles 2,5-10 µm (silica, aluminum and iron) mostly deposit high in the tracheobronchial tree. Particles less than 2,5 µm contains sulphates, nitrates and organic compounds and deposit more often in the terminal bronchioles and alveoli. The smallest particles, les than 0,1 µm in size, remain in the air stream and deposit only on a random basis.

Besides the size, characteristics of the particles and the solubility of gases, the actual chemical composition, mechanical properties, immunogenicity and infectivity of inhaled material determine in a large part the nature of the disease found in exposed persons.

SILICOSIS:

Silicosis results from the inhalation of dust containing silica. This is toxic to macrophages, which it kills by initiating a fibrotic reaction. The most common source of free silica is quartz that is a component of most classes of rock - a prominent component of the earth’s crust.

Occupational history:

The risk in gold-miners is well known, but there is also a risk of silicosis in underground work in asbestos, copper, tin, and diamond mineworkers. Surface work in the ore crushing plant also presents a risk. Occupational exposure to silica is associated with mining, quarrying, drilling, tunneling, and sand blasting.

Forms of Silicosis: 1. Chronic silicosis a. Simple silicosis b. Complicated silicosis (PMF) 2. Accelerated silicosis 3. Acute silicosis

4. Silica dust and pulmonary tuberculosis

5. Silica dust and chronic obstructive lung disease 6. Silica dust and other health effects

a. Scleroderma

b. Systemic lupus erythematosus c. Rheumatoid arthritis

Chronic or classic silicosis usually follows one or more decades of exposure to respirable dust containing quartz.

Chronic silicosis may be asymptomatic or result in insidiously progressive exertional dyspnea or cough. A latency of 15 years or more since onset of exposure is common. Radiographically it presents with small (less than 10 mm) rounded opacities, predominantly in the upper zones.

Accelerated silicosis results from heavier exposures, often with duration of 5-10 years.

Acute silicosis is the consequence of intense exposures to high levels of dust that contain a significant proportion of silica. The reported exposure period is usually from several months up to about 5 years.

Progressive massive Fibrosis (PMF):

PMF occurs when one or more groups of small nodules in the lungs coalesce to form larger (over 10 mm) shadows on the chest radiograph. This progressive illness may occur even after exposure to silica-containing dust has ceased. This results in a clinically significant compromise of lung functions and symptoms of dyspnea.

Clinical Manifestations of Silicosis:

Patients with silicosis can be asymptomatic. The primary symptom is usually dyspnea, first noted with activity and later also reported in rest.

Severe respiratory disability usually indicates the development of PMF, tuberculosis or obstructive lung disease.

Respiratory failure is the most common outcome of end-stage massive fibrosis.

Association with Tuberculosis:

Tuberculosis can complicate all forms of silicosis.

Radiological features:

The classical picture of silicosis shows multiple rounded opacities 2-5 mm in diameter, usually in the upper two thirds of the lung fields.

Eggshell calcification of the hilar lymph nodes is an uncommon but important diagnostic feature.

Progressive massive fibrosis (PMF) refers to the presence of opacities larger than 1 cm in diameter. They are usually seen in the upper lung fields, and can be confused with tuberculosis or malignancy.

Diagnosis:

The diagnosis is made on a significant history of exposure to silica and radiological abnormalities consistent with silicosis.

Lung biopsy is rarely required to establish the diagnosis, but tissue samples and culture may be helpful where the differential diagnosis includes tuberculosis, neoplasm, or PMF.

Prognosis and complications:

• Simple silicosis as compared to PMF is rarely disabling.

• PMF may be disabling and progress to cor pulmonale and death. • Silicosis predisposes to tuberculosis.

• Scleroderma has been found to be related to silica exposure. Treatment:

There is no specific treatment for silicosis. The lack of a specific therapy for silicosis emphasizes the crucial role of primary prevention. Prevention remains the principle goal in dealing with this occupational disease. Exposures can be reduced through improved ventilation, personal protection (e.g. respirators) and education of workers and employers.

Symptomatic treatment, removal from further exposure and the possibility of alternative employment must be considered. Therapy is directed largely at the complications of the disease. ASBESTOS RELATED LUNG DISEASE:

South Africans may be exposed to three types of asbestos: • Chrysotile (white)

• Amosite (brown) • Crocidolite (blue)

These asbestos fiber types have strikingly different physical characteristics: chrysotile tends to be wavy and long, and occurs in bundles; crocidolite is needle shaped with many long fibers; and amosite is similar to crocidolite but generally thicker.

All three minerals have been mined extensively in South Africa in the Northern Cape and North West Province (crocidolite), Northern Province (crocidolite and amosite) and Mpumalanga (crysotile).

The mining of asbestos in South Africa has ceased except for chrysotile mining in Mpumalanga. Amosite mining stopped in 1992, and crocidolite mining in 1997.

Uses of asbestos: • Fireproof textiles

• Insulation for boilers and pipes • Cloth • Paints • Paper • Wire insulation • Cement pipes • Gaskets • Brake linings

• Roofing and floor products • Ship construction

ASBESTOS RELATED LUNG DISEASE:

1) Nonmalignant pleural manifestations: a) Pleural plaques

b) Diffuse pleural thickening c) Acute benign pleural effusions 2) Asbestosis (Pneumoconiosis) 3) Malignant mesothelioma 4) Lung cancer

a) Pleural plaques

Pleural plaques are the most common manifestation of asbestos exposure and exposure to asbestos is the most frequent cause of pleural plaques. They may be small or extensive, commonly occur in the lateral and posterior midlung zones, and can invade the mediastinum or pericardium. Pleural calcifications frequently develop in these lesions.

Treatment:

They are markers of asbestos exposure no specific treatment is required. b) Diffuse pleural thickening:

The fibrotic response can be localized or diffuse, and either unilateral or bilateral.

Clinical and physiological manifestations:

When mild, diffuse pleural thickening can be asymptomatic. The diffuse nature of the lesion often lead to pulmonary symptoms, including dyspnea, dry cough, and chest pain and can cause a restrictive lung function pattern.

Radiographic features:

Diffuse pleural fibrosis presents as a continuous pleural opacity extending over more than 25% of the pleural surface of a lung.

Treatment:

There is no specific therapy for asbestos related pleural fibrosis. Very rarely pleurectomy may be required.

c) Acute benign pleural effusions:

Acute benign pleural effusions are common pleural manifestations in asbestos exposed persons. The designation “benign” refers to the lack of evidence of malignancy. Benign effusions do not presage the development of malignant mesotheliomas, but is a risk factor for the development of pleural thickening.

2) ASBESTOSIS (Pneumoconiosis):

The term asbestosis is reserved for the diffuse interstitial fibrosis of the lung parenchyma caused by the inhalation of asbestos fibers. Rarely, residence or work near a mine of asbestos can result in exposure sufficient to cause lung fibrosis. Family members repeatedly exposed to asbestos on work clothes have been known to develop asbestosis.

Epidemiology:

The prevalence of parenchymal asbestosis among asbestos workers increases as the length of employment increases. The mortality in asbestos workers who have smoked is higher than in non-smoking co-workers.

Natural history:

The level and duration of exposure appear to be prognostic factors. Because work sites around the world increasingly meet recommended control levels, high-level exposure is now uncommon and clinical asbestosis is becoming a less severe disease.

Clinical picture:

Symptoms:

In the early phases the disease may be asymptomatic. Dyspnea on exertion is the earliest symptom of asbestosis. Cough may be absent in the early stages, but in the later stages it may become quite distressing.

Signs:

Late inspiratory bilateral basal crepitations are typical of the interstitial lung disease Clubbing of the fingers may occur. The clinical findings in asbestosis resemble those of other interstitial lung diseases.

Radiology:

The interstitial changes asbestosis is predominantly in the lower zones of the lungs. The presence of pleural plaques provides useful evidence that the parenchymal process is asbestos related.

Lung function tests:

A restrictive pattern with decreased lung volumes and diffusion is the usual abnormality, but smoking may contribute to a mixed pattern of restriction and airflow limitation.

Diagnosis:

The diagnosis of asbestosis must always be based on an appropriate exposure history. Exposures of over 10-20 years are usually necessary. The presence of asbestos bodies or asbestos fibers in sputum and on biopsy indicates past or present exposure.

Management:

There is no specific treatment, but management of complications is important. Complications include respiratory failure, cor pulmonale, and lung cancer (particularly in smokers). Because of the risk of lung cancer and mesothelioma, medical surveillance is recommended.

3) MALIGNANT MESOTHELIOMA:

Most instances of mesothelioma occur in persons who have been exposed to asbestos fibers.

Epidemiology:

In 1960 the association between asbestos and mesothelioma was demonstrated. In patients with asbestos exposure cigarette smoking contributes to the risk of lung cancer, but not to mesothelioma.

Natural history:

Malignant mesotheliomas are locally invasive, spreading along the pleural wall and invading the lung, mediastinal lymph nodes and other thoracic and abdominal structures.

Clinical and radiographic features:

Pleural mesotheliomas are found mainly in males in the age group of 50-70years of age. Chest pain is the most common symptom, and patients can also complain of cough, weight loss, and fever. A pleural effusion may be present and can be hemorrhagic.

Radiographic abnormalities found in malignant mesothelioma include a thick pleural peel along the lateral chest wall with an irregular nodular surface, and pleural effusions.

Diagnosis:

The diagnosis requires cytological or histological confirmation and biopsy is usually required.

Treatment and prognosis:

Median survival time is approximately 8-12 months; fewer than 20% of patients are alive at 2 years. Pleurectomy, pneumonectomy, radiation therapy and chemotherapy do not prolong survival.

4) LUNG CANCER:

Epidemiology:

In 1968 the association between asbestos exposure and lung cancer was demonstrated.

Treatment and prognosis:

The therapeutic approaches are similar to non-asbestos induced carcinoma. The survival at 5 years is 8-10 percent.

COAL WORKER’S PNEUMOCONIOSIS (CWP):

CWP occurs in surface and underground workers on the colliers in South Africa. The colliers are concentrated in northern KwaZulu-Natal, Mpumalanga and northern Free State.

Coal workers’ pneumonoconiosis (CWP) is the parenchymal lung disease that results from the inhalation and deposition of coalmine dust and the tissue’s reaction to its presence.

In addition to CWP, coal mine dust exposure increases a miner’s risk of developing chronic bronchitis and emphysema.

The prevalence of radiographic changes of simple CWP is related to the duration and intensity of dust exposure. The complicated form of CWP: progressive massive fibrosis (PMF).

Clinical features:

Simple CWP may be asymptomatic. Chronic cough and sputum production are the most common symptoms. With more severe airflow obstruction, dyspnea can be noted, and cough and sputum production are more frequent. Eventually cor pulmonale and edema of the lower limbs may occur.

Caplan’s syndrome:

An association between nodular opacities (PMF) in the lungs of coal miners and seropositive rheumatoid arthritis was described in 1953. Today the syndrome includes other pneumoconiosis, e.g. asbestosis and silicosis.

The radiograph in simple coal worker’s pneumoconiosis shows small opacities that first appear in the upper zones. Progressive massive fibrosis (PMF) is characterized by one or more large opacities greater than 1 cm in diameter, with upper lobe predominance.

The radiological appearance may be indistinguishable from silicosis.

Diagnosis:

The diagnosis of CWP can be made in the presence of an adequate history (at least 5–10 years of coal mine exposure) and a characteristic chest radiograph.

Management of coal workers lung’ diseases:

There is no specific therapy for CWP. Management is directed at prevention, early recognition, and treatment of complications.

Workers with PMF should not be exposed to further dusty work. SIDEROSIS:

Siderosis, due to the inhalation of iron dust and fumes, is seen in arc welders, metal polishers, iron miners, and oxyacetylene-torch cutters. Iron particles in the lung do not lead to fibrosis. The radiological appearance is similar to that of simple silicosis, but siderosis causes neither symptoms nor functional impairment.

BERYLLIOSIS:

Beryllium may produce an acute pneumonitis or, more commonly, chronic interstitial pneumonitis. One should inquire specifically about occupational exposure to beryllium in the manufacture of alloys, ceramics, and high technology electronics and before 1950 the production of fluorescent lights.

ORGANIC DUSTS

Specific diseases associated with organic dusts include asthma and hypersensitivity pneumonitis. Three occupational groups are singled out for discussion:

1) Cotton dust (byssinosis):

Cotton dust related disease is recognized world wide in the textile industry. Respiratory protection equipment to control dust levels has been highly successful.

Higher grades of impairment are seen in workers exposed to high levels of dust and for higher durations. There is an additive effect of cotton dust and cigarette smoking.

2) Grain dust:

The presentation of disease in grain elevator employers or workers in flour or feed mills is virtually identical to the finding in cigarette smokers, i.e. persistent cough, mucus hyper secretion, wheeze and dyspnea on exertion and reduced FEV1. The effect of grain dust

exposure is additive to that of cigarette smoking. 3) Farmer’s lung:

This condition results from exposure to moldy hay end straw, containing spores of thermophilic actinomycetes that produce hypersensitivity pneumonitis (mycrospora faenae, aspergillus fumigatus).

The prevalence of the disease varies in association with rainfall that determines the amount of fungal growth.