PLEURAL PLAQUES AND LUNG FUNCTION

Albert Miller

Saint Vincent Catholic Medical Centers, Jamaica, New York

To the Editor :

Van Cleemput and coworkers (1) are to be congratulated for utilizing HRCT scan to quantitate the extent of asbestos-related pleural plaques (PP) and to estimate relationships with lung function and asbestos exposure. Unfortunately, their subjects, asbestos cement workers, had only slight plaquing. Using an alternative CT method for estimating plaque surface (2), all their subjects who had PP were in the lowest grade, 1 of 3. Additionally, standard spirometric measurements and diffusing capacity (DL_CO) were normal compared with reference values and with control subjects.

It is difficult to relate one variable, in this case PP, to another, such as pulmonary function, when the spectrum of each variable is limited. Jarad and colleagues (2) reported a greater effect of PP on FVC, FEV₁, and TLC using a quantitative score based on HRCT rather than one based on the chest radiograph; both scores showed highly significant effects.

The authors did not report degree of PP on their subjects' chest radiographs, for which semi-quantitative (3) and quantitative (4) indices have been published based on the International Labour Office Classification of Radiographs (5). In a study of 1,536 insulators, 950 of whom had PP, there was a significant decrease in FVC with increasing PP. Regression analysis demonstrated a highly significant (p < 0.0001) inverse relationship between "integrative index" of PP and FVC after adjustment for the independent effects of duration of exposure, presence and profusion of irregular opacities indicative of interstitial fibrosis, and cigarette smoking. There was no such relationship for insulators with diffuse pleural thickening (PT), who constituted 17.2% of all those with PT, despite the considerably greater impact of diffuse PT on FVC.

Many investigators, including Schwartz and colleagues (6), have reported similar effects of PP on FVC in studies of workers from various asbestos trades that were confined to PP, or in which PP were clearly distinguished from diffuse PT.

It must be concluded that when sufficient numbers of workers with a sufficient extent of PP are analyzed, there is a significant effect on pulmonary function attributed to the PP.

	References

1. Van Cleemput J, De Raeve H, Verschakelen JA, Rombouts J, Lacquet LM, Nemery B. Surface of localized pleural plaques quantitated by computed tomography scanning. No relation with cumulative asbestos exposure and no effect on lung function. Am J Respir Crit Care Med 2001; 163: 705-710 [Abstract/Free Full Text].

2. Jarad N, Wilkinson P, Pearson MC, Rudd RM. A new high resolution computed tomography scoring system for pulmonary fibrosis, pleural disease, and emphysema in patients with asbestos-related disease. Br J Ind Med 1992; 49: 73-84 [Medline].

3. Oliver LC, Eisen EA, Greene R, Sprince NL. Asbestos-related pleural plaques and lung function. Am J Ind Med 1988; 14: 649-656 [Medline].

4. Lilis R, Miller A, Godbold J, Chan E, Selikoff IJ. Pulmonary function and pleural fibrosis: quantitative relationships with an integrative index of pleural abnormalities. Am J Ind Med 1991; 29: 145-161 .

5. International Labour Office. International classification of Radiographs of Pneumoconioses. Occupational safety and health series No. 22. Geneva: 1980.

6. Schwartz DA, Fuortes LJ, Galvin JR, Burmeister LF, Schmidt LE, Leistikow BN, LaMarte FP, Merchant JA. Asbestos-induced pleural fibrosis and impaired lung function. Am Rev Respir Dis 1990; 141: 321-326 [Medline].

From the Authors:

We thank Dr. Miller for his interest in our article (1) and his relevant comments.

We did not consider it useful to evaluate the extent of the pleural plaques on chest x-rays, since in the majority of our subjects plaques were visible only on CT. Because the alternative method of Al Jarad and colleagues (2) was intended for scoring all types of asbestos-related pleural changes, including diffuse pleural fibrosis, it is unavoidable that circumscribed pleural plaques attain values only at the lower end of the scale.

We were aware that some studies found effects of asbestos-related pleural lesions on pulmonary function (3, 4). However, in line with several other studies (cited in our paper), we found no effect of pleural plaques on pulmonary function, not even a trend. We agree with Dr. Miller's comment that the size of our group and the somewhat limited spectrum of the pleural plaques may have restricted our ability to detect any effect on lung function. On the other hand, we believe that much more extensive plaques are exceptional (at least as an isolated feature) and, therefore, not very representative for the average case today. As we discussed in our article, a consistent problem with the studies describing a relation between pleural plaques and pulmonary function, is that they included substantial proportions of subjects with diffuse pleural thickening, as well as an unknown number of subjects with subradiological asbestosis (since these studies relied on chest x-ray and not CT). Not only the presence and extent of plaques, but also the probability of asbestosis increases with time since initial exposure. Thus, in one study (3), the subjects with plaques were 10 years older, had been exposed 8 years longer to asbestos, and had 11 more years since initial exposure than those without plaques. In the other study (4), 17% of the cases had diffuse pleural fibrosis, and 862 of the 1,584 studied subjects had parenchymal fibrosis that was already detectable on chest x-ray. In their 1990 study, Schwartz and colleagues (5) found substantial lung function decreases resulting from diffuse pleural thickening, but they stated that "the lung volumes and DL_CO were virtually indistinguishible between sheet metal workers with circumscribed plaques and those with normal pleura."

In conclusion, although we appreciate Dr. Miller's comments, we do not think that they invalidate our observations and conclusions. The truth is probably that very large pleural plaques are likely to impact on pulmonary function, but the more common ones are unlikely to do so in a statistically detectable, let alone clinically relevant way. Of course, this does not imply that pleural plaques are an irrelevant consequence of exposure to asbestos.

KU Leuven, Leuven, Belgium

	References

1. Van Cleemput J, De Raeve H, Verschakelen JA, Rombouts J, Lacquet LM, Nemery B. Surface of localized pleural plaques quantitated by computed tomography scanning. No relation with cumulative asbestos exposure and no effect on lung function. Am J Respir Crit Care Med 2001; 163: 705-710 .

2. Jarad NA, Wilkinson P, Pearson MC, Rudd RM. A new high resolution computed tomography scoring system for pulmonary fibrosis, pleural disease, and emphysema in patients with asbestos-related disease. Br J Ind Med 1992; 49: 73-84 .

3. Oliver LC, Eisen EA, Greene R, Sprince NL. Asbestos-related pleural plaques and lung function. Am J Ind Med 1988; 14: 649-656 .

4. Lilis R, Miller A, Godbold J, Chan E, Selikoff IJ. Pulmonary function and pleural fibrosis: quantitative relationships with an integrative index of pleural abnormalities. Am J Ind Med 1991; 29: 145-161 .

5. Schwartz DA, Fuortes LJ, Galvin JR, Burmeister LF, Schmidt LE, Leistikow BN, LaMarte FP, Merchant JA. Asbestos-induced pleural fibrosis and impaired lung function. Am Rev Respir Dis 1990; 141: 321-326 .