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A 38-Year-Old Welder With Dyspnea

and Iron Overload


Ariel Modrykamien, MD; Howard Christie, PA-C; Carol Farver, MD;
and Rendell W. Ashton, MD, FCCP
(CHEST 2009; 136:310313)
A
38-year-old man presented to the pulmonary
clinic with a 9-month history of progressive
bandlike burning pain around his chest and sharp
stabbing pain anteriorly, along with shortness of
breath. He had been a welder for 15 years, making iron
dumpsters in a plant. He noticed shortness of breath
when climbing stairs and moderate symptoms when
walking. He also reported a dry cough. He denied any
other systemic symptom and had no other medical or
surgical history. He was a nonsmoker.
Physical Examination
His vital signs were as follows: BP, 150/100 mm Hg;
heart rate, 78 beats/min; respiratory rate, 14 breaths/
min; temperature, 98.3F; and arterial oxygen satura-
tion, 98% while breathing room air. His physical exam-
ination was normal except for Velcro-type crackles in
both lung bases.
Laboratory Findings
Laboratory values at presentation showed a hemat-
ocrit of 50.4% with a hemoglobin concentration of 16.8
g/dL. Ferritin level was 1,634 ng/mL (normal range, 18
to 300 ng/mL), and iron level was 169 g/dL (normal
range, 30 to 140 g/dL). Transferrin saturation was
62% (normal range, 11 to 46%). The patient had a
normal WBC and platelet count. His coagulation stud-
ies, liver function test, and kidney function test findings
were within normal limits. Blood glucose levels and
urinalysis findings were normal as well.
Pulmonary function tests revealed an FEV
1
/FVC
ratio of 76%, an FEV
1
of 78% predicted, and an FVC
of 85% predicted. Diffusing capacity of the lung for
carbon monoxide was 73% predicted, and diffusing
capacity of the lung for carbon monoxide corrected for
his alveolar ventilation was 105% predicted.
A bronchoscopy was performed showing a normal
airway. A bronchial washing and transbronchial bi-
opsies of the right middle lobe revealed abundant
hemosiderin-laden macrophages. Cultures for bacte-
rial and fungal infections, viruses, and AFB were all
negative. Serum markers for autoimmune diseases,
such as antinuclear antibody, rheumatoid factor, SM,
RNP, SSA, SSB, centromere, scleroderma IgG, and
Jo-1 antibodies, were negative. Markers for vasculitides,
such as cytoplasmic antineutrophil cytoplasmic antibody,
perinuclear antineutrophil cytoplasmic antibody, and glo-
merular basement membrane antibody, were negative as
well. The patient underwent a video-assisted thoraco-
scopic surgery with right upper, middle, and lower lobe
wedge biopsies (Fig 1, 2) due to the lack of diagnosis.
From the Respiratory Institute (Drs. Modrykamien and Ashton,
and Mr. Christie) and Department of Anatomic Pathology (Dr.
Farver), Cleveland Clinic, Cleveland, OH.
The authors have no conflicts of interest to disclose.
Manuscript received December 15, 2008; revision accepted
December 31, 2008.
Reproduction of this article is prohibited without written permission
from the American College of Chest Physicians (www.chestjournal.
org/site/misc/reprints.xhtml).
Correspondence to: Ariel Modrykamien, MD, Respiratory Insti-
tute, A90, Cleveland Clinic, 9500 Euclid Ave, Cleveland, OH
44195; e-mail: modryka@ccf.org
DOI: 10.1378/chest.08-2954
Figure 1. Pulmonary parenchyma with diffuse brown pigment
involving 70 to 80% of thoracoscopic biopsy, centered around the
small airways (hematoxylin-eosin, original 12.5).
CHEST Postgraduate Education Corner
PULMONARY AND CRITICAL CARE PEARLS
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Radiology Findings
Chest radiography was normal, and a high-resolution
CT scan of the chest showed bilateral diffuse centri-
lobular ground-glass nodular opacities (Fig 3).
What is the diagnosis?
Figure 2. Brown hemosiderin pigment is present predominantly
within alveolar macrophages surrounding the bronchovascular
area of the biopsy (hematoxylin-eosin, original 200).
Figure 3. CT scan of the chest showing diffuse centrilobular
ground-glass nodular opacities.
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Diagnosis: Welders siderosis (pneumoconiosis
siderotica)
Discussion
Welders siderosis or pneumoconiosis siderotica
was originally characterized by Doig and McLaugh-
lin as a lung disease caused by the inhalation of iron
dust. In their report, the authors described 16
electric arc welders who remained in a good state of
health despite the diagnosis of siderosis. They con-
cluded that this entity was not associated with respi-
ratory symptoms or functional impairment.
Pneumoconiosis can be classified as fibrotic or
nonfibrotic, depending on the presence of fibrosis in
the lung biopsy specimen. Fibrotic pneumoconioses
usually present with symptoms such as cough and
dyspnea, differentiating it from nonfibrotic forms.
Silicosis, coal worker pneumoconiosis, asbestosis,
talcosis, and berylliosis are examples of fibrotic pneu-
moconiosis, whereas baritosis, stannosis, and sidero-
sis are nonfibrotic forms.
Welding involves mixtures of metals such as iron,
manganese, silica, chromium, nickel, and others. In
situations where the ventilation is poor or the weld-
ing activity is performed in confined spaces, the
probability for the development of lung disease
increases. The acquired disease depends on the
specific fume exposure, the coating of the rods, the
welding operation performed, and the metal welded.
Therefore, it is essential to distinguish welders
pneumoconiosis, which refers to the effect of inhal-
ing heterogeneous dusts generated by welding, from
welders siderosis, which is the effect of inhaled
iron oxide particles alone.
Environmental levels of fumes and particles are
thought to be directly related to the development of
lung disease. Hence the Occupational Safety and
Health Administration of the US Department of
Labor updated the permissible exposure limit estab-
lished for welding fumes to 5 mg/m
3
. However,
despite this updated regulation, there are still reports
of acute lung diseases in welders exposed to levels as
low as 4.3 mg/m
3
.
Because welders siderosis is a nonfibrotic pneu-
moconiosis, it was originally thought not to be
associated with respiratory symptoms. Neverthe-
less, some authors described symptomatic disease
with interstitial fibrosis in arc welders. It is
thought that these cases might have occurred
secondary to concomitant inhalation of silicates
and iron (silicosiderosis).
Some reports have described the occurrence of
welders siderosis associated with systemic iron over-
load. Three cases of welders siderosis with elevated
ferritin, serum iron level, and serum transferring
saturation have been reported. None of these pa-
tients had hemochromatosis, thalassemia, or sider-
oblastic anemia, and there was no history of multiple
blood transfusions, iron ingestion, or alcohol con-
sumption. The authors concluded that iron overload
seemed likely to be due to occupational exposure.
Chest CT imaging in patients with pneumoconio-
sis siderotica demonstrates small nodules that are
more prominent in the middle third of the lung.
These nodules indicate radiopaque accumulation of
iron particles in macrophages aggregated along the
peribronchovascular bundle. These changes are usu-
ally reversible and may completely resolve after
cessation of exposure.
It is important to differentiate welders siderosis
from two other entities: idiopathic pulmonary hemo-
siderosis and metal fume fever.
Idiopathic pulmonary hemosiderosis is a rare in-
terstitial lung disease of unknown etiology that oc-
curs preferentially in children. Its clinical presenta-
tion varies from an acute and fulminant form with
diffuse alveolar hemorrhage to a more subacute
presentation with cough, dyspnea, repetitive hemop-
tysis, and anemia. Sputum and BAL fluid examina-
tion show multiple hemosiderin-laden macrophages,
and the lung biopsy confirms a bland alveolar hem-
orrhage with variables degrees of fibrosis. Metal
fume fever, or Monday morning fever, is a self-
limiting inhalation fever attributed to a number of
metal oxide fumes. It presents with fever, headache,
fatigue, and dyspnea within 3 to 10 h after the
exposure to heated metals, including galvanized
steel, zinc oxide, magnesium oxide, and chromium.
Its diagnosis is based on clinical suspicion, and
preventive strategies are aimed at reducing fume
exposure.
Clinical Course
Our patient with welders siderosis presented with
symptoms of chest pain, severe shortness of breath,
and cough. Although patients with nonfibrotic pneu-
moconiosis usually present without respiratory symp-
toms, on occasion, they may be symptomatic. The
presence of iron overload was thought to be related
to the inhalation of iron dust because he did not have
a history for other sources of endogenous or exoge-
nous iron overload. We recommended the patient to
wear respiratory protection (respirator) and encour-
aged him to work in areas with an effective ventila-
tion system. We also recommended that all welders
in his plant be screened for serum ferritin, total iron
level, and iron binding capacity.
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Clinical Pearls
1. Welders siderosis is a nonfibrotic pneumoconi-
osis caused by the inhalation of iron dust.
2. Pneumoconiosis siderotica is typically, but not
always, asymptomatic.
3. Iron overload can complicate the presentation of
this entity. It is important to exclude hemochroma-
tosis, thalassemia, sideroblastic anemia, multiple
blood transfusions, iron ingestion, and alcohol con-
sumption in this clinical scenario.
4. Chest CT imaging shows diffuse, centrilobular,
ground-glass, nodular densities.
5. Pathologic changes are reversible, and complete
resolution is possible following cessation of exposure.
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