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Asbestos pleural disease
Br. J. Dis. Chest (1982) 76, 1
ASBESTOS
PLEURAL
DISEASE
G. BRITTON
MARK The London Hospital
(Whitechapel),
London
Summary
The lung function tests on 88 asbestos workers known to have an asbestos-related abnormality on the chest radiograph have been analysed with respect to pleural disease. The degree cf intrapulmonary and pleural disease were assessedby reading posteroanterior and both oblique films according to a modified IL0 U/C Classification (1971). The results show a highly significant decrease in lung function with increasing pleural abnormality. Analyses suggest that these changes cannot be wholly accounted for by confounding variables such as airways obstruction and/or pulmonary fibrosis. We conclude that pleural thickening alone, particularly when severe, contributes to the decreased vital capacity and to any resultant disability.
An assessment of the effect of asbestos pleural disease is made difficult by the possible additional presence of pulmonary fibrosis and/or airway obstruction. Harries (1970) noted that men with pleural abnormality had more symptoms and lower lung function values than men without pleural abnormality. Lumley (1977) showed significant impairment in submaximal exercise testing in men with diffuse pleural thickening. However, controversy remains as to whether pleural thickening can occur alone without any associated intrapulmonary fibrosis and whether it can give rise to disability. We have reviewed the results obtained from a group of asbestos workers in an attempt to answer these questions. , Patients and Methods One hundred asbestos workers were included in the study. Approximately half had been referred for lung function testing as part of an assessment relating to claims for compensation; the remainder were under the care of The London Hospital or the East Ham Asbestos Clinic. All the men were seen at the London Hospital between August 1976 and August 1977, and all had a detectable abnormality on their chest radiograph which was thought to be related to their previous asbestos exposure. The various manifestations which can result from exposure to asbestos, including the pleural changes are listed in Table I. A medical history, including full details of present and past occupation, was followed by clinical examination. Lung function tests included simple spirometry, measurement of lung volumes, rebreathing PCOZ and transfer factor by the methods described by Hughes and Empey (1972) and the predicted values were those of Cotes (1975). Posteroanterior, lateral and right and left oblique chest radiographs were read ‘blindly’ by the author and were classified according to a modified form of the IL0 U/C International Classification (1971) by comparison with standard films. The modifications included an assessment of
Murk G. Britton Table
I.
Manifestations
of asbestos exposure
1. Asbestos bodies 2. Asbestos pleural changes (a) Plaque formation (i) Hyaline (C) Calcified (b) Pleuritic reaction (pleuritis) (2) Pleural effusion (acute) (iz) Pleural thickening (chronic) 3. Asbestosis (pulmonary fibrosis) 4. Asbestos granuloma (asbestoma) 5. Carcinoma (a) Bronchus (b) ? Larynx and others 6. Mesothelioma (a) Pleural (b) Peritoneal
pleural disease for each side separately, and the use of the oblique films in conjunction with the posteroanterior film, allowed a more accurate measurement of the width (thickness) and extent of the disease anteriorly and posteriorly. The author’s ability to use the IL0 U/C Classification has been verified by comparing his readings of 100 standard films with those of 15 expert readers. The IL0 U/C Classification 1971 does not allow a clear distinction to be made between plaques and diffuse pleural thickening. In our study both types of pleural disease were assessed together under the heading of pleural thickening, but, a note was made of which type was predominant, according to the criteria of Sheers and Templeton (1968) for differentiation between the two types. The pleural disease was assessed by grading the width, extent, and involvement of the costophrenic angles for each side separately as follows: IL0 Width Extent Costophrenic
angle
U/C Grading abc 012 No/Yes
Numerical
Code
o-3 o-2 o-1
A numerical grading for expressing the extent of pleural disease was calculated for each subject by multiplying the ‘extent’ and ‘width’ of the pleural disease for each side separately, and adding each side’s score together with the values for the costophrenic angles if these were involved, thus giving a possible score from 0 to 14. The subjects were then divided into five groups (Groups I-V) according to their scores. Pleural calcification was graded on an O-3 scale for each of the possible five sites of calcification, namely right and left chest walls, right and left diaphragms and ‘other’ sites. A score was calculated by addition giving a possible range from 0 to 15 and the subjects were then divided into three groups (Group A, B and C) according to their scores. The means, standard deviations and standard error of the means were calculated for each group and the differences between the group means were identified using a one-way analysis of variance. Trends across the five pleural groups (I-V) and the three calcification groups (A, B and C) were assessed using a linear term in the analysis of variance and confirmed by the Spearman rank corre-
Asbestos Pleural Disease
3
lation coefficient using the actual scores rather than the groupings. In studying the joint effect of pleural and pulmonary disease a two-way analysis of variance was computed. Significance levels are quoted for the effect of the two conditions and where there is an interaction between them. If the interaction is significant the effect of the pleural disease is then dependent on the amount of pulmonary disease.
Fig. 1. Serial radiographs of the patient described, pleural reactions and resultant pleural thickening
showing
the
development
of bilateral
acute
Mark G. Britton
4
RESULTS
There were 93 males and seven females ranging in age from 32 to 83 with a mean of 56.6 + 8.9 years. Twelve subjects have been excluded from this study because of other chest conditions which would have affected their lung function. The reasons for exclusion included carcinoma of the lung, mesothelioma, emphysema, tuberculosis, bronchiectasis, severe ankylosing spondylitis and previous thoracic surgery. The case history of one subject, a 34-year-old lagger, with details of serial lung function and serial radiographs illustrates the possible sequential changes in the development of diffuse pleural thickening. C.C. - -5.00
Pleuritic reactions Predicted L. R. vital capacity t t .. . .. .. .. . .. .. *. . .. .. . .. . .. .. .. . .. .. .. .. . .. . .. .. .. . .. . .. .. .. . ..
. .. .. 0-e . .. .. ..a........ c’\.
\
4.00 A----A,,
Litres
Vital capacity
\
“A
I
0
l.
.\
3.00
.-.-o-O
2.00
1.00 t,
Transfer factor 9.0 mmol min-1 kPa-1 (86% predicted) ,
0 70
, 71
, 72
, 73
, 74
, 75
, 76
, 77
, 78
, 79
Years Fig. 2. Serial
lung
function
tests
on the
patient
described
in relation
to the
bilateral
acute
pleuritic
reactions
Case history The patient had been a lagger since leaving school at the age of 15 in 1960 and had been a lifelong non-smoker. He had been under yearly follow-up at a chest clinic since 1970. In April 1974 he was asymptomatic, but three months previously had experienced mild left pleuritic pain which had lasted for approximately two weeks. His radiograph at this time showed a left pleural reaction with a small basal effusion. Six months later and without intervention the radiograph showed partial resolution of the changes on the left but a similar pleural reaction and effusion on the right. A later radiograph showed considerable residual pleural thickening which is shown more clearly on the computerized tomograms of the chest (Fig. 3). Serial lung function tests at various stages of his illness are shown in Fig. 2.
Asbestos Pleural Disease
Fig. 3. A CAT scan (1978) of the patient marked on the left anterior chest wall
described,
showing
bilateral
pleural
thickening,
most
Table II divides the group of 88 workers according to the extent of pleural disease and shows age, exposure to asbestos, and relevant lung function tests. By virtue of the definitions used most of the subjects with plaques alone were either Group II or III and most of Groups IV and V had varying degrees of diffuse pleural thickening. The results show that the workers in Group V (i.e. with moderate to severe pleural thickening) are slightly younger, but details of exposure for the groups do not differ significantly. There is a statistically significant trend for the vital capacity, expressed as litres (P < 0.005) and as a percentage of predicted value (P < O.OOl), to decrease with increasing pleural score. Neither the transfer factor nor the FEVJFVC ratio show any significant trend between the groups. The absolute peak flow values do show a similar decreasing trend but this does not reach statistical significance. Details of vital capacity and transfer factor (TF), both expressed as a percentage of the predicted value, the FEVl/FVC ratio and the degree of dyspnoea according to the MRC Questionaire (1966) g ra d’m g are considered in relation to both extent of pleural disease and degree of pulmonary fibrosis in Table III. These analyses show a significant trend of decrease of vital capacity with increase of pleural score in all three groups with different degrees of pulmonary fibrosis. The values for the FEVi/FVC ratio do not show a statistically significant trend either within or between the profusion score groups. However in three of the groups FEVi/FVC ratio is less than 70% and it would appear that this added airway obstruction may influence the vital capacity as seen especially in one group (Group 3, profusion score l/1-2/3) w h ere the vital capacity would appear
(NS=P>0.05)
Spearman
rank
correlation
above
7 and
of variance
6,
linear
term
49.0 (k3.5)
7
V: 9 and
Group
Analysis
58.6 (k1.7)
15
IV:
Group
4 and
8
55.7 (k1.4)
31
111:3,
Group
5
55.2 (zb2.2)
2
26
1 and
II:
Group
58.4 (k3.1)
9
Age
and
1:O
n
to asbestos,
Group
exposure
score
of age,
Pleural
Table 11. Details lung
five
NS
NS
NS
NS
23.3
18.8 (f4.1)
NS
NS
2.49 (kO.18)
2.98 (50.23)
3.19 (kO.14)
3.39 (kO.18)
litres
19.2 (k2.6) 25.9 (k2.1)
with
Vital
3.85 (kO.38)
groups
20.2 (f4.7)
exposure
of
Length
the
(k3.6)
for
1943 (k3.5)
1946 (22.6)
1943 (zb1.7)
(k2.3)
1946
(k4.6)
1940
Date of 1st exposure
function
P
P
P
71.3 (f3.7)
73.7 (k3.4) 60.0 (k3.3)
77.4 (25.2)
68.7
(k2.4)
(+2.01
72.5
73.6 (f4.7)
FEVl/ FVC (%)
of asbestos
80.2
degrees
(k2.6)
86.6 (k3.3)
92.8 (k6.8)
a/o pred.
capacity
varying
pred.)
TF
NS
NS
73.5 (k6.1)
65.7 (-t-3.3)
65.4 (k3.1)
71.2 (k4.1)
72.0 (k5.8)
(%
pleural
NS
NS
364 (+42)
(+W
412
(k64)
450
(litreslmin)
PEFR
disease
$
Group V 9 and above
8
Group IV 6, 7 and
66
80
88
86
93
85
66
73
75
75
70.5
72.4
71.4
73.3
72.8
--___
score
__~
O/O-l
function,
Two-way analysis of variance P values for: Effect of pleural score Effect of profusion score Interaction
3
4
10
5
Group III 3, 4 and
6
of lung
Profusion
Details
~_~--___
1.5
I
III.
Group II 1 and 2
Group 0
____~
Pleural score
Table
dyspnoea
2.0
1.5
1.8
1.8
1.0
VC
-~ ~- -
-.__
JO
and
57
87
76
86
92
70
75
65
69
69
pred.)
pred.)
(?A pred.) 0.003 0.14 0.55
3
7
10
9
2
TF
Profusion
with
VC
grading
TF
l/1-2/1
degrees
(“A pred.) 0.97 0.007 0.87
76.2
70.6
66.0
71.0
77.6
FEVl/ FVC (9;)
score
varying
FEVJFVC 0.68 0.81 0.93
2.7
2.0
2.2
2.1
1.0
Dyspnoea
__~-
of asbestos
2
1
1
4
11
n
-~~
(76)
48
60
77
90
92
VC (96 pred.)
pleural
Dyspnoea 0.07 0.04 0.99
51
51
60
55
60
TF (9: pred.)
scoye > 212
disease
60.6
80.3
68.9
72.5
75.3
FEVI/ WC (%)
pulmonary
Profusion
and
3.0
2.5
2.6
3.0
1.0
Dyspnoea
B (mild
Group
(NS=P>0.05)
rank
Spearman
linear
correlation
of variance
Analysis
l-4
calcification)
0
exposure
form
of age,
calcification):
calcification):
score
Details
Group C : (moderate/severe 5 and above
A (no
IV.
Group
Calcification
Table
:
to asbestos,
12
28
48
n
and
Age
the
three
P
P
1932 (k2.6)
1943 (st1.9)
1948 (k1.3)
Date of 1st exposure
for
P
function
P
63.6 (k1.5)
58.3 (k1.4)
52.5 (k1.3)
lung
with
P
P
31.3 (k5.1)
23.1 (k2.5)
18.8 (21.6)
Length of exposure
groups
NS
NS
NS
65.9
(+6.3)
74.2
(1k4.8) NS
68.5 (k3.3)
69.2
TF pred.)
83.7 (k3.1)
(%
of pleural
(22.5)
vc wed.)
degrees
81.8 (k2.8)
(%
different
P
P
(k36)
370
(zk22)
390
435 (519)
PEFR (litresimin)
calcification
Asbestos Pleural Disease
9
to be lower than appropriate considering the general trend. There is no significant trend of transfer factor within each profusion score group but changes between the groups show decreasing values with increasing pulmonary fibrosis. Table IV gives details of age, exposure and lung function for the three groups with different degrees of pleural calcification. There is a downward trend of VC and TF with increasing calcification but this does not reach statistical significance. The workers in Group C, those with moderate/severe calcification, tend to be older and to have been exposed to asbestos earlier in life and for longer.
DISCUSSION Becklake et al. (1970) reported small but consistent reductions in lung function in asbestos workers with pleural abnormalities, and Harries (1970) showed that men with pleural abnormalities had more symptoms and signs and lower lung function values than those without pleural abnormality, suggesting that some men with extensive pleural fibrosis were dyspnoeic as a result. However, Jones and Sheers (1973) supported the earlier findings of Leatheart (1968) and stated that localized pleural plaques are not associated with symptoms or abnormal physical signs. In a study of lung function at rest and during progressive submaximal exercise in a group of men with varying degrees of asbestos-related pleural abnormality (Lumley 1977), diffuse pleural thickening and to a lesser extent non-calcified pleural plaques were associated with substantial functional abnormality, but, pleural calcification was not associated with any significant functional impairment. Our study has shown increasing impairment of lung function with increasing severity of pleural disease irrespective of the degree of pulmonary fibrosis. However, the presence of coexistent airways obstruction, to be expected in a group of industrial workers in this age range, can undoubtedly influence the vital capacity, as shown by one group in particular. The FEVr/FVC ratios do not show any particular trend with increasing pleural abnormality and although the peak flow values do show a trend, this does not reach significance, so it is unlikely that airways obstruction can account for all the changes seen. The IL0 U/C Classification (1971) was designed for the reading of posteroanterior radiographs alone. The use of oblique views in addition allows a clearer view of pleural changes on the anterior and posterior chest walls, which are only seen ‘face-on’ in posteroanterior views, thus permitting a more realistic assessment of the total pleural disease present. In this study, oblique films were used and measurements of pleural disease were made for each side independently. Where possible distinction was made between plaques, which are described as being circumscribed, and diffuse pleural thickening. The accuracy of an assessment of underlying intrapulmonary fibrosis from a radiograph showing extensive pleural disease is questionable and some new method of assessment such as CAT scanning is needed. However, our data suggest that the decrease in vital capacity seen in the few patients with severe pleural disease was not due to fibrosis alone. In the three patients in Group V, in whom a zero profusion score was recorded, the transfer factor was within normal limits. One of the three (the case described) showed no evidence of intrapulmonary disease throughout nine years observation includ-
Mark G. Britton
10
ing a CAT scan. The substantial fall in his lung volume occurred at the time of his pleuritic reactions, suggesting cause and effect. This type of patient who has no evidence of intrapulmonary fibrosis does not qualify for compensation by Industrial Injuries Disablement Benefit. The sequence illustrated by the case history lends support to the theory that an acute pleuritic reaction plus effusion may be the precursor to pleural thickening (Gaensler & Kaplan 1971) and as the reaction may be virtually asymptomatic if the effusion is small, the majority of such episodes probably go undetected. Despite the difficult problems of apportioning reduction in lung function to airways obstruction, intrapulmonary fibrosis and pleural thickening when all three may occur together, the analyses we present suggest that the trends of reduction in vital capacity with increasing grades of pleural involvement, are unlikely to be wholly the result of airways obstruction and/or intrapulmonary fibrosis. Thus it is concluded that pleural involvement alone, particularly when severe, contributes to a decrease of vital capacity, and to any resultant disability. ilCKNOWLEDGEMENTS
I thank Dr A. Hanson, Dr P. Lesley Bidstrup and Dr D. T. D. Hughes for allowing me to study their patients and for their encouragement and advice. I would also thank Stephen Evans and David Brown for their statistical advice and Dr L. Kreel for the EM1 scan on the case history. I am grateful to Cape Industries for their financial support. REFERENCES BECKLAKE, M. R., E. (1970) Lung
Bull. Physiopath.
FOURNIER-MASSEY,
G.,
MCDONALD,
J.
C.,
SIEMIATYCKI,
J. & ROSSITER,
C.
function in relation to chest radiographic changes in Quebec asbestosworkers. r.+%p. 6, 637.
COTES, J. E. (1975) Lung Function. Assessment and Application in Medicine, 3rd ed., pp. 281-287. Oxford : Blackwell Scientific Publications. GAENSLER, E. A. & KAPLAN, A. I. (1971) Asbestos pleural effusion Ann. intern. Med. 74, 178. HARRIES, P. G. (1970) The effects and control of diseases associated with exposure to asbestos in a naval dockyard. M.D. Thesis, London. HUGHES, D. T. D. & EMPEY, D. W. (1972) Ten years experience in running a pulmonary function laboratory. Br. med. J. 4, 470. I.L.O. U/C (1971) International Classification of Radiographs of Pneumoconioses, Occupational Safety and Health Series No. 22. Geneva: International Labour Office. JONES, J. S. P. & SHEERS, G. (1973) In: Biological Effects of Asbestos, ed. P. Bogovski, J. C. Gibson, V. Timbre11 and J. C. Wagner, pp. 243-8. Scientific Publications No. 8. Lyon: International Agency for Research on Cancer. LEATHEART, G. L. (1968) Pulmonary function tests in asbestos workers. Trans. Sot. occup. Med.
18, 49. LUMLEY, K. P. S. (1977) Physiological changes in asbestos pleural disease. In: ed. W. H. WaIton, p. 781. Oxford and New York: Pergamon Press. MEDICAL RESEARCH COUNCIL COMMITTEE ON RESEARCH INTO CHRONIC Questionnaire on Respiratory Symptoms. London. SHEERS G. & TEMPLETON, A. R. (1968) Effects of asbestos in dockyard workers.
Inhaled Particles IV BRONCHITIS BY.
(1966)
med. J. 3, 574.
ASBESTOS
PLEURAL
DISEASE
G. BRITTON
MARK The London Hospital
(Whitechapel),
London
Summary
The lung function tests on 88 asbestos workers known to have an asbestos-related abnormality on the chest radiograph have been analysed with respect to pleural disease. The degree cf intrapulmonary and pleural disease were assessedby reading posteroanterior and both oblique films according to a modified IL0 U/C Classification (1971). The results show a highly significant decrease in lung function with increasing pleural abnormality. Analyses suggest that these changes cannot be wholly accounted for by confounding variables such as airways obstruction and/or pulmonary fibrosis. We conclude that pleural thickening alone, particularly when severe, contributes to the decreased vital capacity and to any resultant disability.
An assessment of the effect of asbestos pleural disease is made difficult by the possible additional presence of pulmonary fibrosis and/or airway obstruction. Harries (1970) noted that men with pleural abnormality had more symptoms and lower lung function values than men without pleural abnormality. Lumley (1977) showed significant impairment in submaximal exercise testing in men with diffuse pleural thickening. However, controversy remains as to whether pleural thickening can occur alone without any associated intrapulmonary fibrosis and whether it can give rise to disability. We have reviewed the results obtained from a group of asbestos workers in an attempt to answer these questions. , Patients and Methods One hundred asbestos workers were included in the study. Approximately half had been referred for lung function testing as part of an assessment relating to claims for compensation; the remainder were under the care of The London Hospital or the East Ham Asbestos Clinic. All the men were seen at the London Hospital between August 1976 and August 1977, and all had a detectable abnormality on their chest radiograph which was thought to be related to their previous asbestos exposure. The various manifestations which can result from exposure to asbestos, including the pleural changes are listed in Table I. A medical history, including full details of present and past occupation, was followed by clinical examination. Lung function tests included simple spirometry, measurement of lung volumes, rebreathing PCOZ and transfer factor by the methods described by Hughes and Empey (1972) and the predicted values were those of Cotes (1975). Posteroanterior, lateral and right and left oblique chest radiographs were read ‘blindly’ by the author and were classified according to a modified form of the IL0 U/C International Classification (1971) by comparison with standard films. The modifications included an assessment of
Murk G. Britton Table
I.
Manifestations
of asbestos exposure
1. Asbestos bodies 2. Asbestos pleural changes (a) Plaque formation (i) Hyaline (C) Calcified (b) Pleuritic reaction (pleuritis) (2) Pleural effusion (acute) (iz) Pleural thickening (chronic) 3. Asbestosis (pulmonary fibrosis) 4. Asbestos granuloma (asbestoma) 5. Carcinoma (a) Bronchus (b) ? Larynx and others 6. Mesothelioma (a) Pleural (b) Peritoneal
pleural disease for each side separately, and the use of the oblique films in conjunction with the posteroanterior film, allowed a more accurate measurement of the width (thickness) and extent of the disease anteriorly and posteriorly. The author’s ability to use the IL0 U/C Classification has been verified by comparing his readings of 100 standard films with those of 15 expert readers. The IL0 U/C Classification 1971 does not allow a clear distinction to be made between plaques and diffuse pleural thickening. In our study both types of pleural disease were assessed together under the heading of pleural thickening, but, a note was made of which type was predominant, according to the criteria of Sheers and Templeton (1968) for differentiation between the two types. The pleural disease was assessed by grading the width, extent, and involvement of the costophrenic angles for each side separately as follows: IL0 Width Extent Costophrenic
angle
U/C Grading abc 012 No/Yes
Numerical
Code
o-3 o-2 o-1
A numerical grading for expressing the extent of pleural disease was calculated for each subject by multiplying the ‘extent’ and ‘width’ of the pleural disease for each side separately, and adding each side’s score together with the values for the costophrenic angles if these were involved, thus giving a possible score from 0 to 14. The subjects were then divided into five groups (Groups I-V) according to their scores. Pleural calcification was graded on an O-3 scale for each of the possible five sites of calcification, namely right and left chest walls, right and left diaphragms and ‘other’ sites. A score was calculated by addition giving a possible range from 0 to 15 and the subjects were then divided into three groups (Group A, B and C) according to their scores. The means, standard deviations and standard error of the means were calculated for each group and the differences between the group means were identified using a one-way analysis of variance. Trends across the five pleural groups (I-V) and the three calcification groups (A, B and C) were assessed using a linear term in the analysis of variance and confirmed by the Spearman rank corre-
Asbestos Pleural Disease
3
lation coefficient using the actual scores rather than the groupings. In studying the joint effect of pleural and pulmonary disease a two-way analysis of variance was computed. Significance levels are quoted for the effect of the two conditions and where there is an interaction between them. If the interaction is significant the effect of the pleural disease is then dependent on the amount of pulmonary disease.
Fig. 1. Serial radiographs of the patient described, pleural reactions and resultant pleural thickening
showing
the
development
of bilateral
acute
Mark G. Britton
4
RESULTS
There were 93 males and seven females ranging in age from 32 to 83 with a mean of 56.6 + 8.9 years. Twelve subjects have been excluded from this study because of other chest conditions which would have affected their lung function. The reasons for exclusion included carcinoma of the lung, mesothelioma, emphysema, tuberculosis, bronchiectasis, severe ankylosing spondylitis and previous thoracic surgery. The case history of one subject, a 34-year-old lagger, with details of serial lung function and serial radiographs illustrates the possible sequential changes in the development of diffuse pleural thickening. C.C. - -5.00
Pleuritic reactions Predicted L. R. vital capacity t t .. . .. .. .. . .. .. *. . .. .. . .. . .. .. .. . .. .. .. .. . .. . .. .. .. . .. . .. .. .. . ..
. .. .. 0-e . .. .. ..a........ c’\.
\
4.00 A----A,,
Litres
Vital capacity
\
“A
I
0
l.
.\
3.00
.-.-o-O
2.00
1.00 t,
Transfer factor 9.0 mmol min-1 kPa-1 (86% predicted) ,
0 70
, 71
, 72
, 73
, 74
, 75
, 76
, 77
, 78
, 79
Years Fig. 2. Serial
lung
function
tests
on the
patient
described
in relation
to the
bilateral
acute
pleuritic
reactions
Case history The patient had been a lagger since leaving school at the age of 15 in 1960 and had been a lifelong non-smoker. He had been under yearly follow-up at a chest clinic since 1970. In April 1974 he was asymptomatic, but three months previously had experienced mild left pleuritic pain which had lasted for approximately two weeks. His radiograph at this time showed a left pleural reaction with a small basal effusion. Six months later and without intervention the radiograph showed partial resolution of the changes on the left but a similar pleural reaction and effusion on the right. A later radiograph showed considerable residual pleural thickening which is shown more clearly on the computerized tomograms of the chest (Fig. 3). Serial lung function tests at various stages of his illness are shown in Fig. 2.
Asbestos Pleural Disease
Fig. 3. A CAT scan (1978) of the patient marked on the left anterior chest wall
described,
showing
bilateral
pleural
thickening,
most
Table II divides the group of 88 workers according to the extent of pleural disease and shows age, exposure to asbestos, and relevant lung function tests. By virtue of the definitions used most of the subjects with plaques alone were either Group II or III and most of Groups IV and V had varying degrees of diffuse pleural thickening. The results show that the workers in Group V (i.e. with moderate to severe pleural thickening) are slightly younger, but details of exposure for the groups do not differ significantly. There is a statistically significant trend for the vital capacity, expressed as litres (P < 0.005) and as a percentage of predicted value (P < O.OOl), to decrease with increasing pleural score. Neither the transfer factor nor the FEVJFVC ratio show any significant trend between the groups. The absolute peak flow values do show a similar decreasing trend but this does not reach statistical significance. Details of vital capacity and transfer factor (TF), both expressed as a percentage of the predicted value, the FEVl/FVC ratio and the degree of dyspnoea according to the MRC Questionaire (1966) g ra d’m g are considered in relation to both extent of pleural disease and degree of pulmonary fibrosis in Table III. These analyses show a significant trend of decrease of vital capacity with increase of pleural score in all three groups with different degrees of pulmonary fibrosis. The values for the FEVi/FVC ratio do not show a statistically significant trend either within or between the profusion score groups. However in three of the groups FEVi/FVC ratio is less than 70% and it would appear that this added airway obstruction may influence the vital capacity as seen especially in one group (Group 3, profusion score l/1-2/3) w h ere the vital capacity would appear
(NS=P>0.05)
Spearman
rank
correlation
above
7 and
of variance
6,
linear
term
49.0 (k3.5)
7
V: 9 and
Group
Analysis
58.6 (k1.7)
15
IV:
Group
4 and
8
55.7 (k1.4)
31
111:3,
Group
5
55.2 (zb2.2)
2
26
1 and
II:
Group
58.4 (k3.1)
9
Age
and
1:O
n
to asbestos,
Group
exposure
score
of age,
Pleural
Table 11. Details lung
five
NS
NS
NS
NS
23.3
18.8 (f4.1)
NS
NS
2.49 (kO.18)
2.98 (50.23)
3.19 (kO.14)
3.39 (kO.18)
litres
19.2 (k2.6) 25.9 (k2.1)
with
Vital
3.85 (kO.38)
groups
20.2 (f4.7)
exposure
of
Length
the
(k3.6)
for
1943 (k3.5)
1946 (22.6)
1943 (zb1.7)
(k2.3)
1946
(k4.6)
1940
Date of 1st exposure
function
P
P
P
71.3 (f3.7)
73.7 (k3.4) 60.0 (k3.3)
77.4 (25.2)
68.7
(k2.4)
(+2.01
72.5
73.6 (f4.7)
FEVl/ FVC (%)
of asbestos
80.2
degrees
(k2.6)
86.6 (k3.3)
92.8 (k6.8)
a/o pred.
capacity
varying
pred.)
TF
NS
NS
73.5 (k6.1)
65.7 (-t-3.3)
65.4 (k3.1)
71.2 (k4.1)
72.0 (k5.8)
(%
pleural
NS
NS
364 (+42)
(+W
412
(k64)
450
(litreslmin)
PEFR
disease
$
Group V 9 and above
8
Group IV 6, 7 and
66
80
88
86
93
85
66
73
75
75
70.5
72.4
71.4
73.3
72.8
--___
score
__~
O/O-l
function,
Two-way analysis of variance P values for: Effect of pleural score Effect of profusion score Interaction
3
4
10
5
Group III 3, 4 and
6
of lung
Profusion
Details
~_~--___
1.5
I
III.
Group II 1 and 2
Group 0
____~
Pleural score
Table
dyspnoea
2.0
1.5
1.8
1.8
1.0
VC
-~ ~- -
-.__
JO
and
57
87
76
86
92
70
75
65
69
69
pred.)
pred.)
(?A pred.) 0.003 0.14 0.55
3
7
10
9
2
TF
Profusion
with
VC
grading
TF
l/1-2/1
degrees
(“A pred.) 0.97 0.007 0.87
76.2
70.6
66.0
71.0
77.6
FEVl/ FVC (9;)
score
varying
FEVJFVC 0.68 0.81 0.93
2.7
2.0
2.2
2.1
1.0
Dyspnoea
__~-
of asbestos
2
1
1
4
11
n
-~~
(76)
48
60
77
90
92
VC (96 pred.)
pleural
Dyspnoea 0.07 0.04 0.99
51
51
60
55
60
TF (9: pred.)
scoye > 212
disease
60.6
80.3
68.9
72.5
75.3
FEVI/ WC (%)
pulmonary
Profusion
and
3.0
2.5
2.6
3.0
1.0
Dyspnoea
B (mild
Group
(NS=P>0.05)
rank
Spearman
linear
correlation
of variance
Analysis
l-4
calcification)
0
exposure
form
of age,
calcification):
calcification):
score
Details
Group C : (moderate/severe 5 and above
A (no
IV.
Group
Calcification
Table
:
to asbestos,
12
28
48
n
and
Age
the
three
P
P
1932 (k2.6)
1943 (st1.9)
1948 (k1.3)
Date of 1st exposure
for
P
function
P
63.6 (k1.5)
58.3 (k1.4)
52.5 (k1.3)
lung
with
P
P
31.3 (k5.1)
23.1 (k2.5)
18.8 (21.6)
Length of exposure
groups
NS
NS
NS
65.9
(+6.3)
74.2
(1k4.8) NS
68.5 (k3.3)
69.2
TF pred.)
83.7 (k3.1)
(%
of pleural
(22.5)
vc wed.)
degrees
81.8 (k2.8)
(%
different
P
P
(k36)
370
(zk22)
390
435 (519)
PEFR (litresimin)
calcification
Asbestos Pleural Disease
9
to be lower than appropriate considering the general trend. There is no significant trend of transfer factor within each profusion score group but changes between the groups show decreasing values with increasing pulmonary fibrosis. Table IV gives details of age, exposure and lung function for the three groups with different degrees of pleural calcification. There is a downward trend of VC and TF with increasing calcification but this does not reach statistical significance. The workers in Group C, those with moderate/severe calcification, tend to be older and to have been exposed to asbestos earlier in life and for longer.
DISCUSSION Becklake et al. (1970) reported small but consistent reductions in lung function in asbestos workers with pleural abnormalities, and Harries (1970) showed that men with pleural abnormalities had more symptoms and signs and lower lung function values than those without pleural abnormality, suggesting that some men with extensive pleural fibrosis were dyspnoeic as a result. However, Jones and Sheers (1973) supported the earlier findings of Leatheart (1968) and stated that localized pleural plaques are not associated with symptoms or abnormal physical signs. In a study of lung function at rest and during progressive submaximal exercise in a group of men with varying degrees of asbestos-related pleural abnormality (Lumley 1977), diffuse pleural thickening and to a lesser extent non-calcified pleural plaques were associated with substantial functional abnormality, but, pleural calcification was not associated with any significant functional impairment. Our study has shown increasing impairment of lung function with increasing severity of pleural disease irrespective of the degree of pulmonary fibrosis. However, the presence of coexistent airways obstruction, to be expected in a group of industrial workers in this age range, can undoubtedly influence the vital capacity, as shown by one group in particular. The FEVr/FVC ratios do not show any particular trend with increasing pleural abnormality and although the peak flow values do show a trend, this does not reach significance, so it is unlikely that airways obstruction can account for all the changes seen. The IL0 U/C Classification (1971) was designed for the reading of posteroanterior radiographs alone. The use of oblique views in addition allows a clearer view of pleural changes on the anterior and posterior chest walls, which are only seen ‘face-on’ in posteroanterior views, thus permitting a more realistic assessment of the total pleural disease present. In this study, oblique films were used and measurements of pleural disease were made for each side independently. Where possible distinction was made between plaques, which are described as being circumscribed, and diffuse pleural thickening. The accuracy of an assessment of underlying intrapulmonary fibrosis from a radiograph showing extensive pleural disease is questionable and some new method of assessment such as CAT scanning is needed. However, our data suggest that the decrease in vital capacity seen in the few patients with severe pleural disease was not due to fibrosis alone. In the three patients in Group V, in whom a zero profusion score was recorded, the transfer factor was within normal limits. One of the three (the case described) showed no evidence of intrapulmonary disease throughout nine years observation includ-
Mark G. Britton
10
ing a CAT scan. The substantial fall in his lung volume occurred at the time of his pleuritic reactions, suggesting cause and effect. This type of patient who has no evidence of intrapulmonary fibrosis does not qualify for compensation by Industrial Injuries Disablement Benefit. The sequence illustrated by the case history lends support to the theory that an acute pleuritic reaction plus effusion may be the precursor to pleural thickening (Gaensler & Kaplan 1971) and as the reaction may be virtually asymptomatic if the effusion is small, the majority of such episodes probably go undetected. Despite the difficult problems of apportioning reduction in lung function to airways obstruction, intrapulmonary fibrosis and pleural thickening when all three may occur together, the analyses we present suggest that the trends of reduction in vital capacity with increasing grades of pleural involvement, are unlikely to be wholly the result of airways obstruction and/or intrapulmonary fibrosis. Thus it is concluded that pleural involvement alone, particularly when severe, contributes to a decrease of vital capacity, and to any resultant disability. ilCKNOWLEDGEMENTS
I thank Dr A. Hanson, Dr P. Lesley Bidstrup and Dr D. T. D. Hughes for allowing me to study their patients and for their encouragement and advice. I would also thank Stephen Evans and David Brown for their statistical advice and Dr L. Kreel for the EM1 scan on the case history. I am grateful to Cape Industries for their financial support. REFERENCES BECKLAKE, M. R., E. (1970) Lung
Bull. Physiopath.
FOURNIER-MASSEY,
G.,
MCDONALD,
J.
C.,
SIEMIATYCKI,
J. & ROSSITER,
C.
function in relation to chest radiographic changes in Quebec asbestosworkers. r.+%p. 6, 637.
COTES, J. E. (1975) Lung Function. Assessment and Application in Medicine, 3rd ed., pp. 281-287. Oxford : Blackwell Scientific Publications. GAENSLER, E. A. & KAPLAN, A. I. (1971) Asbestos pleural effusion Ann. intern. Med. 74, 178. HARRIES, P. G. (1970) The effects and control of diseases associated with exposure to asbestos in a naval dockyard. M.D. Thesis, London. HUGHES, D. T. D. & EMPEY, D. W. (1972) Ten years experience in running a pulmonary function laboratory. Br. med. J. 4, 470. I.L.O. U/C (1971) International Classification of Radiographs of Pneumoconioses, Occupational Safety and Health Series No. 22. Geneva: International Labour Office. JONES, J. S. P. & SHEERS, G. (1973) In: Biological Effects of Asbestos, ed. P. Bogovski, J. C. Gibson, V. Timbre11 and J. C. Wagner, pp. 243-8. Scientific Publications No. 8. Lyon: International Agency for Research on Cancer. LEATHEART, G. L. (1968) Pulmonary function tests in asbestos workers. Trans. Sot. occup. Med.
18, 49. LUMLEY, K. P. S. (1977) Physiological changes in asbestos pleural disease. In: ed. W. H. WaIton, p. 781. Oxford and New York: Pergamon Press. MEDICAL RESEARCH COUNCIL COMMITTEE ON RESEARCH INTO CHRONIC Questionnaire on Respiratory Symptoms. London. SHEERS G. & TEMPLETON, A. R. (1968) Effects of asbestos in dockyard workers.
Inhaled Particles IV BRONCHITIS BY.
(1966)
med. J. 3, 574.