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Polyvinyl Chloride Pneumoconiosis: Epidemiological Study of Exposed Workers
Giuseppe Mastrangelo, M.D4 Maurizio Manno, M.D.; Guido Marcer, M.D.; Giovanni Battista Bartolucci, M.D.; Carla Gemignani, M.D.; Giulia Saladino, M.D.;
Lorenzo Simonato, M.D; and Bruno Saia, M.D.
Among 1216 workers who were employed in a polyvinyl -ide production factory and who had had no previous exposure elsewhere, 20 cases of pneumoconiosis
were found. Chest x-ray abnormalities were characterized by limited profusion, irregular type and low gravity. All 20 workers had been exposed to high PVC dust levels. The chest x-ray changes were observed after a minimum ex posure of five years and, in a small percentage of cases, were associated with slight restrictive respiratory function
impairments. Moreover, in the whole group of workers 388 cases (31.9%) were found with non-specific x-ray abnor
malities mainly related to age and smoking.
Polyvinyl chloride (PVC) dust is particularly relevant
to a consideration of the anatomical, clinical and radiological signs of pneumoconiosis found in workers ex posed to "inert" dusts because of the high annual produc tion of PVC and the number of exposed workers.
Within the framework of a national survey on vinyl chloride hazards to humans, co-ordinated by the Chemical Workers Unions, the authors examined the working population of plants producing PVC in Porto Marghera, Italy. One group of workers was exposed to PVC dust, another group worked in departments polluted only by vinyl chloride monomer (VCM).
The characteristics and prevalence of pulmonary radiological abnormalities found are reported and their pathogenic mechanism is discussed in this article
ods and Population
environmental dust samples were collected and both concentration in air and particle size were measured In
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the drying, sacking and blending departments, PVC dust concentrations were higher than the TLV (10 mg/m* of total dust) in about 60% of the samples. In the polymerization departments, no concentration higher than the TLV was found. In the samples taken, particles with diameters of 1 pm to 5 jen constituted 4.5% to 30.9% of total dust weight.
All the workers answered the European Coal and Steel Community (ECSC) questionnaire for chronic bronchitis and emphysema,' and were submitted to chest x-ray (ac cording to ILO standards) and spirographic examination (Godart-Expirograph, Bilthoven, Holland). Chest x-ray films were read by two independent physicians utilizing the ILO/UC Pneumoconiosis Classification, 1971.* For statistical analysis, a consensus'reading was used. For each worker examined, present and past working histories were carefully recorded and particular consideration was given to previous dust exposure. Of the total, 1,216 sub jects had had no past exposure to organic or inorganic dusts; 731 had been exposed to PVC dust (employed in drying, sacking and blending of polymer); and 465 had been exposed to monomer alone.
Results Table 1 shows the mean and standard deviation of age
and of length of exposure, the number of subjects and the percentage of smokers in the two groups; those exposed to PVC dust and those not exposed There are no signjfi cant differences in age and smoking habits, but the dura tion of exposure is higher in the workers not exposed to dust.
In 20 subjects (16%). we diagnosed a typical pneumoconiosis, i.e.. chest x-ray changes (irregular opacities or frankly micronodular images) Of at least class 1 profusion, according to the ILO/UC classification The
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Table 1. -- Age, Exposure, Number ol Subjects and Percentage ot Smokers In PVC Dust Exposed and Non-Exposed Groups.
PVC Oust exposed group
PVC dust non-exposed group
Age (Years)
Mean
5.0.
37.7 8.8 35.7 8.5
t Exposure (Years)
Mean
S.D.
6.1 4.0 6.6 4.5
No. ot Subjects
731 485
% Ot Smokers
73.9
68.7
mean age of this group was 44.9 ( 5.2) years and the mean length of exposure was 11.6 ( 5.4) years; 16 sub jects (80%) were either smokers or ex-smokers.
Table 2 summarizes the distribution of cases in relation to age and length of exposure. In all age groups there is an increase of disease prevalence associated with increasing length of exposure. In the case of x-ray changes, 16 sub
jects had class 1/0 profusion; two cases, class 1/1; one case, class 2/1; and one case, class 2/2. In spite of age and the considerable exposure, the majority of cases observed were in a low profusion category, thus indicating a slow evolution of the disease. The changes were characterized by irregular opacities: ten cases were type "s"; three cases, type "t"; six cases, type "p"; and one case, type "r." The opacities were diffused, mainly over median lobe areas. Two subjects showed slight restrictive spirographic impairment. All had had jobs which involved high air borne dust levels (mostly drying and sacking) for at least five years. None of the 20 subjects was in a group unexnosed to dust. None of them had experienced previous Occupational exposure to organic or inorganic dusts. We considered the above alterations to be PVC pneumo coniosis.
In 388 subjects (31.9%) we found slight chest x-ray alterations consisting of linear or irregular vanishing
opacities, or both, classified as class 0/1 profusion; the re maining 808 subjects were class 0/0.
Table 3 reports the total population distribution, ex cluding 20 subjects with PVC pneumoconiosis. Results are presented in a twoway table -- each entry reports the number of observations. Samples are classified according
to age (three classes) and polyvinyl chloride dust ex posure: "PVC +" represents presence and "PVC -- absence. In the table, "x-ray +" indicates the classes with class 0/1 profusion. To assess the influence of both risk in dicators we performed a two-way analysis of variance for proportions (Snedecor and Cochran).* The column mean is adjusted for row effects and vice versa. We also tested whether row and column effects were additive or whether interaction was present. The results (Table 4) show that both age and exposure were significant factors influenc*
ing x-ray abnormalities -- since the interaction is not significant, the effects are simply additive.
The square of a multiple-partial association coefficient for qualitative data was calculated to measure the degree of association between the dependent variable (x-ray changes) and'each of the two predictor variables (age and exposure).4 Age and exposure are alternately held cons tant. Age is a most important factor. When exposure is held constant. 33.2% of the x-ray changes are shown to depend upon age; when age is held constant, 6.5% are shown to depend upon exposure.
Table 5 summarizes the distribution of cases (same subjects as Table 3) according to smoking habits in workers exposed and not exposed to PVC dust. In Table6, the two-way analysis of variance for proportions shows that both risk indicators have a significant influence on chest abnormalities.
There is no interaction of factors. Habitual smoking plays a major role and, when exposure is held constant, is shown to be responsible for 17.1 % of the changes. When smoking habits are held constant, exposure to PVC dust is shown to be responsible for 8.9% ot the x-ray abnor malities.
Discussion X-ray changes of at least class 1 profusion, found in 20
subjects, are considered PVC-induced pneumoconiosis. This claim is based on the following: (1) Reading of the chest films was performed by two independent physi cians, who were not informed of the age, job, length of ex posure or clinical history of workers. A consensus reading was required for the pneumoconiosis diagnosis. (2) Special attention was given to the absence of any previous occupational exposure to organic or inorganic dusts. (3) The changes were found in workers who had ex perienced prolonged exposure in departments with demonstrated PVC dust pollution. The length of exposure was about 12 years on the average and never less than five. No radiographic signs of pneumoconiosis were found in subjects working in departments free of PVC dust, although the average period of exposure was longer
Table 2 -- Distribution ot PVC Pneumoconiosis in Age and Exposure Classes
(The percentage on the group of same age and exposure is shown in parentheses).
PVC Oust Exposure (Years)
<5 5-10
> to
< 30
--
Age (Years)
31-40
41-50
--_
2(2 4) 2 (3.8)
5(8.3) 8(9 0)
> 50
--
1(591 2(9.5)
Journal of Occupational Medicine/Vol. 21, No. 8/August 1979
Table 3. -- Distribution ot Cases with Class 0/1 and 0/0 Profusion According to Age and PVC Dust Exposure.
PVC + X-ray + X-ray
PVC X-ray + X-ray -
< 30
20 133
17 119
Age (Yaars) 31-40 41-50
78 197
45 158 .
123 108
55 67
> 50
35 17
15 9
541
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Table 4. -- Two-Way Analysis a\ Variance lor Proportions (Same cases as in Table 3).
Source ol Variation
Age
PVC Oust exposure interaction Error
Degrees of Freedom
3 1 3 1188
Sum ol
Squares
30.9713 0.7843 0.9882
227.9403
Mean Squares
10.3238 07843 0.3294 0.1919
F
53 81* 4.09t 172
p <0.01 tP <0.05
Table 5. -- Distribution ol Cases with Clast 0/1 and 0/0 Profusion According to Smoking end PVC Dust Exposure.
PVC + X-ray + X-ray -
PVCX-ray + X-ray -
Nonsmokers
40 147
25 127
Smokers
216 308
107 226
in these workers (Table 1).
Previous experimental data on animals and reports of
human lung biopsy indicated the possibility that the im
pairments described above can be attributed to PVC dust
inhalation. In 1970, S^ende et aP reported a case of
pneumoconiosis in a worker exposed to PVC dust. Chest
x-ray films showed small patches which became denser
ward the hilum. Biopsy revealed multiple granuloma-
us centers consisting of foreign amorphous material sur-
junded by granulation tissue composed of histiocytes,
lymphocytes, plasma cells, eosinophils and foreign body
giant cells Such centers were associated with moderate
diffuse fibrosis.
A histiocytic-macrophage reaction in alveolar septa,
observed by Frongia et al6 in guinea pigs exposed to PVC
dust in a sacking department, developed into lesions with
multiple granulomatous centers with giant cells during
the course of exposure. Rats exposed to a similar working
environment developed marked thickening of in
teralveolar septa with an evolution similar to that in the
guinea pigs.
v
Such experimental and pathologic data confirm the
results of this epidemiological study. Lung changes are
directly related to PVC dust while VCM exposure alone
fails to cause these changes. Therefore, unlike Lilis et al.7
we believe that pulmonary changes are not pathogenical-
ly similar to other vinyl chloride induced abnormalities
(fibrosis of the liver, scleroderma-like skin changes,
peripheral vascular damage).
In the present study there was only a 1.6% prevalence
of pneumoconiosis in a total population of 1,216 subjects
Nevertheless, in workers exposed to effective risk of
pneumoconiosis (731 subjects) the prevalence rose to 2.7% Waxweiler et al* reported pulmonary fibrotic changes associated with respiratory function impairments in 96 subjects exposed to PVC dust. Lilis et al7 studied the chest x-ray films and changes in respiratory function of groups of PVC production workers who had experienced exposure of different degree and length. They found a 4.3% to 22.7% prevalence of chest.x<ay changes (small, linear, reticular and/or rounded opacities) and spirographic impairments related to the duration of exposure and to the presence of chest x-ray changes. As these authors did not employ either the ILO/UC International Classification or any other, no comparison concerning the reported prevalence can be made with the present data.
Apart from 20 cases of pneumoconiosis, mild non specific alterations (profusion of 0/1 class) were found both in the group exposed to PVC dust and in the group exposed to VCM alone. Such changes are related mainly to age and smoking habits, and the role of exposure is minor.
References
1 Commission of therEuropean Communities Notes on the 1967 ECSC Questionnaire for Studying Chronic Bronchitis and Pulmonary Emphysema. 1972. A Minetie. 0 Brille. R van der lende. F SannaRandaccio. and U Smidl (Eds) Industrial Hypene and Medicine Texts No 14. Office for Official Publications of the European Com munities. Luxembourg, 197J.
2. lacobson C and Lainhart W$ ILOUC 1971 International classification of radiographs of the pneumoconioses. Med Radtogr Phorogr *6 67.1972.
S Snedecor GW and Cochran VVG Statistical Methods. Sixth Edi tion Ames, the Iowa State University Press. Eighth Printing 197b. pp
472-901. 4 Blalock HM Social Statistics, Second Edition New York.
McGraw-Hill Book Company. 1972. pp 456459 5 S/ende B. Lapis K. Nemes A, and Pinter A. Pneumoconiosis
caused by the inhalation of polyvinyl chloride dust Med Lav bl 43343b. 1970
b. Frongia N. Spina/zold A. and Bucarelti A Lesioni polmonari sperimentali da malazione protungata di polveri di PVC in ambiente di favoro Med Lav 65.J2I-342. 1974
7 Lilis R. Anderson H. Miller A, and Seliioff l| Pulmonary changes among vinyl chloride polvmerization workers Chest 69 299-30.1. 197b
8 Waxweiler R|. Stringer W. Falk H. et al NIOSH, Neoplastic risk amony vinyl chloride polymerization workers. 1-16 Ann \> Acad Sci 271 4048. iy7b
Table 6. - Two-Way Analysis of Variance lor Proportions (Same cases as in Table 5).
Source of Variation
Smoking PVC oust exposure interaction Error
*P < 0 CM
542
Degrees ol Freedom
i l j 1192
Sum ol Squares
7 8850 1 7647 0 1023 251 9125
Mean Squares
7 8650 * 784 7 0 1023 0 2113
F
3? 31* 8 44* <1
Polyvinyl Chloride Pneumoconiosis/Mastrangelo et al
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