Occupational Medicine Advance Access originally published online on August 1, 2006
Occupational Medicine 2006 56(7):504-506; doi:10.1093/occmed/kql055
© The Author 2006. Published by Oxford University Press on behalf of the Society of Occupational Medicine. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Occupational paraffin-induced pulmonary fibrosis: a 25-year follow-up
Alexis Descatha1,
Dominique Mompoint2 and
Jacques Ameille1
1 Occupational Health Department, Poincaré University Hospital, AP-HP, 104 bd Raymond Poincaré, 92380 Garches, France
2 Medical Imaging Department, Poincaré University Hospital, AP-HP, 104 bd Raymond Poincaré, 92380 Garches, France
Correspondence to: Alexis Descatha, Occupational Health Department, Poincaré University Hospital, AP-HP, 104 bd Raymond Poincaré, 92380 Garches, France. E-mail: alexis.descatha{at}rpc.aphp.fr
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Abstract
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Abstract Exogenous lipid pneumonia can exceptionally be caused
by occupational exposure to paraffin. The authors report a case
of severe interstitial pulmonary disease induced by occupational
exposure to paraffin, leading to delayed fibrosis over a 25-year
follow-up, despite cessation of exposure.
Keywords Occupational disease; occupational lung disease; oil
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Introduction
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Exogenous lipid pneumonia (ELP) is an uncommon condition. The
great majority of cases of ELP are related to aspiration of
liquid paraffin ingested for the treatment of constipation.
Occupational ELP is rare with only four out of 44 cases reported
in a French nationwide retrospective study of ELP [
1]. Very
few well-documented cases have been published.
We report a case of severe interstitial pulmonary disease induced by occupational exposure to paraffin, with a 25-year follow-up.
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Case report
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A 35-year-old non-smoking woman was admitted to a Paris hospital
in 1979 for exertional dyspnoea, purulent sputum and weight
loss. She had no significant medical history and did not take
any medicine.
She was a former seamstress in Portugal, until her arrival in France, in 1971. A few months later, she obtained a job as an unskilled worker in a cardboard crockery factory. Her task consisted of tending and refilling a machine that covered cardboard plates and cups with paraffin for waterproofing. Solid blocks of paraffin were introduced into the machine and heated with subsequent release of fumes and projection of paraffin droplets. The workshop comprised several of these machines, with no aspiration system. Pipes were covered by a thick coating of paraffin (Figure 1). At the end of the workshift, the workers had white hair due to deposition of aerosolized paraffin. Paraffin was the only form of occupational exposure in this workshop [2].
Initial physical examination revealed bilateral crepitations
in both lung bases. Pulmonary function tests showed a restrictive
pattern [vital capacity (VC): 45% of predicted, total lung capacity
(TLC): 66% of predicted]. The diffusion capacity for CO was
30% of predicted, PaO
2 was normal (93 mmHg), but PaCO
2 was decreased
(32 mmHg). The posteroanterior chest radiograph was normal.
Bronchoalveolar lavage (BAL) showed an increased total cell count (783 x 103/ml), with a high percentage of lymphocytes (58%). Alveolar macrophages contained numerous large empty vacuoles which were stained with oil red 0 (Figure 2).
The diagnosis of paraffin-induced ELP was proposed, exposure
to paraffin was discontinued and steroid therapy was initiated.
In 1980, an improvement of respiratory function was observed (VC: 70%, TLC: 75%). However, exertional dyspnoea, cough and sputum persisted with frequent exacerbations. Radiological investigations remained normal or near normal for 10 years. In 1989, a slight interstitial infiltrate appeared on the chest radiograph characterized by discrete bilateral ill-defined reticulonodular opacities, mainly in the lower lungs. A small subpleural condensation in the right lower lobe was also detected on high-resolution computed tomography (CT). Progressive fibrosis appeared with loss of volume, haziness and a diffuse reticulonodular pattern (Figure 3), with no discernable low-density lipoid alveolitis on the mediastinal window.
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Figure 3. High-resolution axial CT scan performed in 2004 (a) shows lower lung volume loss, predominantly on the left. Extensive lung fibrosis is present with diffuse ground-glass, interlobular septal thickening, intralobular opacities, traction bronchiectasis and a predominantly subpleural honeycomb pattern. A minimum intensity projection in the coronal plane (b) elegantly illustrates these features.
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Parallel to the increase of interstitial opacities, progressive
deterioration of pulmonary function tests and blood gases was
observed, despite continuous steroid therapy and in 1996 lung
function was VC, 50%; TLC, 52%; PaO
2, 91 mmHg; and PaCO
2, 43
mmHg; and in 2004 the following: VC, 47%; TLC, 42%; PaO
2, 79
mmHg; and PaCO
2, 46 mmHg.
Further investigations were performed, including a standard laboratory work-up (with assay of serum phosphate, calcium and iron), specific autoantibodies research (anti-nuclear and anti-DNA antibodies, anti-mitochondrial and endoplasmic reticulum antibodies, anti-smooth muscle antibodies), angiotensin-converting enzyme test and a test for rheumatoid factors (standard latex agglutination and Waaler–Rose test reaction) and hepatitis and HIV serologies.
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Discussion
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In the absence of lung biopsy, the diagnosis of paraffin-induced
ELP cannot be confirmed with certainty. However, there is good
supportive evidence based on a history of heavy long-term occupational
exposure to paraffin, the absence of potential iatrogenic and
other environmental causes, negative immunological investigations
and the existence of similar cases in the same factory. Actually,
two similar cases were observed in the same factory [
2]. These
two subjects presented chronic productive cough and exertional
dyspnoea and a restrictive ventilatory impairment, with no abnormalities
on the chest radiograph. Furthermore, among 23 workers highly
exposed to paraffin in the same plant (from 2 to 14 years),
13 (56%) had chronic cough and phlegm and 15 (65%) had exertional
dyspnoea. A statistically significant reduction in FEV
1 and
FVC was observed in these subjects compared to less exposed
subjects [
3]. Although BAL is non-specific [
4], the presence
of oil-laden vacuoles in alveolar macrophages is highly suggestive
[
5]. The lymphocytic alveolitis observed in our case has also
been described in another case of occupational paraffin-induced
interstitial pulmonary disease [
6].
The contrast between the severity of pulmonary impairment and the normality of initial chest radiographs and CT scan is striking.
Long-term repetition of episodes of aspiration of oils usually produces non-specific lower lobe opacities presenting mixed alveolar and interstitial features or poorly demarcated lower zone mass-like lesions. CT usually suggests the diagnosis of ELP by showing a low-density consolidation, but this was not observed in the present case. Instead, subtle, bilateral, ill-defined basilar densities progressively increased leading to a less frequently described non-specific pattern of lower zone diffuse ground-glass attenuation, septal thickening and honeycombing, indicative of fibrosis [7].
Oil-mist-related occupational diseases, such as asthma or extrinsic allergic alveolitis, have been reported [8]. Repeated inhalation of paraffin in an occupational setting may also lead to severe pulmonary fibrosis. In the absence of curative treatment, primary prevention in the workplace remains essential. The various forms of exposure should be carefully monitored by occupational physicians, especially when paraffin may be aerosolized, particularly in cardboard crockery factories and the automobile industry.
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Conflicts of interest
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None declared.
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References
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Abstract
Introduction
