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1. Pleural Plaques

Pleural plaques are the most common condition resulting from asbestos exposure.  There is a long latency period (10-30 years) between asbestos exposure and the development of pleural plaques.  The development of pleural plaques depends on the length of exposure or time from the first exposure to asbestos rather than to a threshold dose.  This is in contrast to asbestosis (Brown 1994).

Pleural plaques are characterised pathologically by discrete elevated areas of hyaline fibrosis and usually arise from the parietal pleura.  They tend to lie adjacent to relatively rigid structures such as the ribs, vertebral column and the tendinous portions of the diaphragm (Hillerdal & Lindgren., 1980).  Typically, they do not involve the costophrenic angles or lung apices.  Plaques usually develop on the parietal pleura.  They may very rarely occur in the lower aspects of the interlobar fissures, and are usually associated with extensive parietal pleural plaque disease (Rockoff et al., 1987).  The number and size of pleural plaques is extremely variable, and may display calcification.  Unilateral plaques occur in approximately one third of cases (Genevois et al., 1998).

On chest X-rays, they are usually seen on the posterolateral chest wall between the 7th and 10th ribs, on the lateral wall between the 6th and 9th ribs on the dome of the diaphragm, and over the pericardium (Fletcher & Edge., 1970).  CT scans may reveal plaques in these areas and also beneath the anterior aspects of the upper ribs.

The pathogenesis of pleural plaques remains uncertain despite much speculation.  Pleural plaques commonly contain abundant numbers of asbestos fibres, usually chrysotile, but asbestos bodies are absent.  Previously, it was suggested that fibres caused direct mechanical irritation of the parietal pleura (the "scratching theory").  The more accepted theory is that short asbestos fibres reach the parietal pleura by passage through lymphatic channels and induce an inflammatory reaction (Hillerdal., 1980).  Other possibilities include direct migration of fibres through the visceral pleura or via the blood supply.

Pleural plaques may slowly progress in size and amount of calcification, independent of any further asbestos exposure.  There is no evidence that they undergo any malignant transformation (e.g. into mesothelioma or carcinoma).  Generally, it is accepted that pleural plaques (in the absence of any other asbestos-related disorder) do not result in any increased rate of malignancy or loss of lung function.  

References

1. Browne K. 1994. Asbestos-related disorders. In: Occupational Lung Disorders 3rd Ed, ed WR    Parkes, Butterworth Heinenmann. 449-459

2. Hillerdal G & A Lindgren. 1980. Pleural plaques: A correlation of autopsy findings to radiographic findings and occupational history. Eur J Respir Dis. 61(6):315-319

3. Rockoff SD, E Kagan, A Schwartz et al. 1987. Visceral pleural thickening in asbestos exposure: the occurrence and implications of thickened interlobar fissures. J Thorac Imag. Vol 2:58-66

4. Genevois PA, V de Maertelaer, A Madani et al. 1998. Asbestosis, pleural plaques and diffuse pleural thickening: three distinct benign responses to asbestos exposure. Eur Respir J. 11(5):1021-7

5. Fletcher DE & DR Edge. 1970. The early radiologic changes in pulmonary and pleural asbestosis. Clin Radio 21:355-365

6. Hillerdal G. 1980. The pathogeneisis of pleural plaques and pulmonary asbestosis: possibilities and impossibilities. Eur J Respir Dis 61:129-138

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