Mesothelioma Demographic Statistics ANDSTRING Frequency

Author: http://www.PainsAway.Info

The number of individuals affected by asbestos-related disease is slowly increasing. However, whether this is secondary to a true increase in incidence or due to increased recognition is debated.

The prevalence of benign pleural plaques in the non�asbestos-exposed general population is extremely low. The prevalence in environmentally exposed general populations in industrial societies is approximately 0.5-8%. Frequencies in exposed individuals are 3-58%, depending on occupation. The development of plaques depends on the length of exposure or the amount of time that has passed since the first exposure, as opposed to being dependent on a threshold dose, which is the case for asbestosis. The prevalence of pleural plaques is 10% in exposed individuals 20 years after exposure, rising to 50% after 40 years.

The prevalence of diffuse pleural thickening is not known, although it is reported to occur with frequency equal to that of pleural plaques. Thickening is a common concomitant finding to asbestosis, with a reported associated incidence of 10%.

The frequency of benign, asbestos-related pleural effusions in exposed individuals is reported to be 3-7%. However, this number may be an underestimate, because most patients are asymptomatic; therefore, effusions are subclinical and undetected. The incidence rises with increasing levels of asbestos exposure.

Asbestosis is reported to develop in 49-52% of adults with industrial asbestos exposure, after a latency period of 40-45 years.

Approximately 2000-3000 cases of malignant mesothelioma, or 7-13 cases per million general population, are diagnosed annually in the United States.

Epidemiologic studies predicted a decline in incidence in the United States after the year 2000, with a peak incidence in the United Kingdom in 2020. The prediction is probably applicable to benign pleural plaques also, because the latency period is similar. Lung cancer develops in as many as 25% of asbestos workers. In asbestos-exposed nonsmokers, the incidence of lung cancer is 5 times that of the general population. In exposed individuals, smoking further increases the risk of bronchogenic carcinoma by 80-90 fold.

The incidence of asbestos-related lung and pleural disease in the remainder of the industrialized world remains similar to that of the United States. In the United Kingdom, asbestos use was highest in the 1970s, later than in the United States; therefore, the peak incidence of disease lags as well. Legislation regarding asbestos varies from country to country, and although crocidolite is rarely used internationally, other forms of asbestos remain in use.

After the onset of symptoms, severe asbestosis may lead to respiratory failure and death over 12-24 years. Respiratory failure may be accelerated by the development of Caplan syndrome; pulmonary hypertension; or malignancy, including lung cancer or mesothelioma.

No treatment for asbestosis is effective. The primary strategy is prevention, through the worldwide elimination of asbestos use and the replacement of asbestos with safe synthetic products.

Mesothelioma tends to appear late and is usually associated with an extremely poor prognosis. The median survival is 10 months or less, and most patients die within 2 years.20

See also the following related Medscape topics:
CME Advances in the Systemic Therapy of Malignant Pleural Mesothelioma
CME/CE Interstitial Lung Disease and Pulmonary Hypertension

No race predilection exists for asbestos-related disease.

Mesothelioma has a male-to-female ratio of approximately 4:1. Asbestos-related disease in women is uncommon and is usually confined to spouses of industrial workers, as well as to secretarial and domestic staff working in asbestos industries.

A minimum latency period of 8-10 years is required for an asbestos-related pleural effusion to develop; this is usually the earliest manifestation of asbestos-related disease. Similarly, a latency period of more than 20 years is required for the development of asbestosis. As a result, most patients with asbestos-related disease are older than 40 years.

Mesothelioma usually is seen after a longer latency period, with most patients in the sixth-to-eighth decades of life.

* Pleural plaques are not reported to cause symptoms.
* Diffuse pleural thickening may be associated with symptoms and signs comparable to those arising from other causes of fibrothorax, such as dyspnea. The restriction of lung function rarely may be severe enough to warrant decortication of the lung.
* The clinical picture in benign, asbestos-related pleural effusion varies from asymptomatic patients to patients with an acute episode of pleuritic chest pain and pyrexia.
* Asbestosis may cause an insidious onset of progressive dyspnea in addition to a dry cough. Clinical findings of basal inspiratory crackles associated with reduction in vital capacity and diffusion capacity are also seen.
* Asbestosis is usually diagnosed on the basis of certain clinical, functional, and radiographic findings outlined by the American Thoracic Society (ATS).21 However, these guidelines have not been updated since the routine clinical use of high-resolution computed tomography (HRCT) scanning began in the early 1990s.22, 23 Findings based on the ATS criteria include the following:
o Reliable history of nontrivial asbestos exposure
o Appropriate interval between exposure and detection (usually >10 y)
o Abnormal chest radiographic findings
o Restrictive lung disease as indicated by pulmonary function test results
o Abnormal diffusing capacity
o Bilateral crackles at the lung bases that are not cleared by coughing
* Clinical symptoms in malignant mesothelioma are frequently present 6-8 months prior to diagnosis. Symptoms include localized chest wall pain and weight loss. Cough and dyspnea may also be present.

The international staging system for malignant mesothelioma is as follows:

* Tumor
o T1a – Tumor limited to ipsilateral parietal pleura
o T1b – Additional scattered foci of visceral pleural involvement
o T2 – T1 plus involvement of diaphragmatic muscle and/or confluent visceral tumor (including fissures) or direct extension to the pulmonary parenchyma
o T3 – Locally advanced (but potentially resectable) tumor encasing the lung with at least 1 of the following features:
Involvement of endothoracic fascia
Extension into mediastinal fat
Solitary focus of chest wall invasion
Nontransmural involvement of pericardium
o T4 – Locally advanced, unresectable tumor encasing the lung, with at least 1 of the following features:
Multifocal or diffuse chest wall involvement
Transdiaphragmatic peritoneal spread
Direct extension to contralateral pleura
Involvement of vital mediastinal structures
Direct extension to the spine
Transpericardial disease, with or without pericardial effusion or myocardial involvement
* Node
o N0 – No regional nodal metastases
o N1 – Ipsilateral bronchopulmonary or hilar nodal enlargement
o N2 – Ipsilateral mediastinal (including internal mammary) or subcarinal nodal enlargement
o N3 – Contralateral mediastinal, contralateral internal mammary, or supraclavicular nodal enlargement
* Metastasis
o M0 – No distant metastases
o M1 – Distant metastases present
* Staging
o Stage Ia – T1a, N0, M0
o Stage Ib – T1b, N0, M0
o Stage II – T2, N0, M0
o Stage III – Any T3, M0; any N1, M0; any N2, M0
o Stage IV – Any T4, any N3, any M1

Preferred Examination

HRCT scanning is playing an increasingly important role in the diagnosis of diffuse interstitial lung disease. However, chest radiography remains the initial modality for the detection and characterization of pleural and parenchymal disease. Ultrasonography has a role in characterizing pleural effusions and guiding pleural aspiration and biopsy. Nuclear medicine study has a limited role in the investigation of asbestos-related intrathoracic disease. Gallium-67 (67 Ga) citrate testing has been used to differentiate benign from malignant, asbestos-related pleural disease and to give a quantitative index of inflammatory activity.24
Limitations of Techniques

The limitations of chest radiography in the diagnosis and evaluation of asbestos-related disease are well recognized. The quality of the radiograph and the size, shape, position, and degree of calcification determine whether the radiologist can detect pleural plaques on the image. While the identification of bilateral, scattered, calcified, costal, and diaphragmatic pleural plaques is virtually diagnostic of asbestos exposure, studies have shown an 11% false-positive rate with chest radiographs. In particular, extrapleural fat mimics pleural thickening and is a significant cause of false-positive readings. Conversely, a high false-negative rate has also been reported.

Computed tomography (CT) scans have long been known to be more sensitive and specific than chest radiographs for the diagnosis of asbestos-related pleural disease.25, 26

Radiographic-pathologic studies have shown that chest radiographic findings are normal in as many as 20% of patients with asbestosis. HRCT scanning is more sensitive and specific than other studies, particularly when images are obtained with the patient in the prone position, which allows differentiation of mild parenchymal changes from dependent density (increased attenuation of the posterior, usually basal, lung, which is gravity induced and secondary to nonaeration of dependent alveoli).27

Nuclear medicine studies have been used in small series, but their exact role remains unclear. …