Autor : Rey, Darío R.1
1Consultant physician in Pulmonology, Hospital Gral. de Agudos Dr. E. Tornú
https://doi.org./10.56538/ramr.PHVI8364
Correspondencia : Darío R. Rey E-mail: darioraul.rey@gmail.com
Received: 12/9/2021
Accepted: 8/2/2022
The possibility exists that the global
workforce, which is approximately 140 million people, may suffer from an
occupational disease in practically every task it performs.1
However, despite that risk in the working population, few
published studies have estimated the incidence of these lesions or diseases,
their final cost in terms of medical expenses, the health of the affected individual
and economic losses related to hours of work. Methodological failure,
inconsistency between the members of the research population or poor records
are factors that cause differences in the notification of occupational diseases
and probably contribute to this situation.2
As a consequence of changes in
manufacturing practices and the use of new materials, occupational medicine
specialists continue describing associations between new types of exposure and
chronic forms of diffuse parenchymal lung disease (DPLD). In order to
understand the association between exposure and disease, specialized
physicians must see a high index of suspicion regarding the potential toxicity
of occupational and environmental exposure.
The diffuse interstitial lung
disease (DILD) related to the inadequate exposure or poor protection of
workers in different tasks, such as the usufruct of coal and asbestos deposits,
construction, manufacturing, work in shipyards and quarries, and agricultural
work, has been recognized as an occupational risk a long time ago.
Interstitial lung diseases caused
by exposure to substances present in the workplace (OCCUP DILDs) are a group of
significant, preventable diseases. Many different agents cause
the OCCUP DILD, some of which are correctly defined, and some have been poorly
characterized. The list of causative agents keeps growing. Once considered as
“pneumoconiosis”, the list of known causes of OCCUP DILD extends far beyond
coal, silica and asbestos. Clinical, radiological and pathological
presentations of OCCUP DILD are similar to the non-work-related forms of the
disease due to the complex list of pulmonary depuration and repair of the lesion.
The attending physician must have a high index of suspicion and keep a detailed
occupational record in order to look for potential exposure whenever he/she
sees a patient with a DILD. Recognizing an OCCUP DILD is especially important
due to the implications related to primary and secondary prevention of diseases
among the exposed co-workers of the index case.
A study of the American Thoracic
Society published in 2019 collected a literature review and data summary
regarding the occupational contribution to the burden of the main
non-malignant respiratory diseases. The purpose of the study was mainly to
inform about diffuse interstitial fibrosis, hypersensitivity pneumonitis, sarcoidosis and other non-infectious, granulomatous
diseases.
The result indicated that
exposure in the workplace contributes essentially to the presence of multiple
chronic respiratory diseases, for example: asthma (16%), COPD (14%), chronic
bronchitis (13%), idiopathic pulmonary fibrosis (26%), hypersensitivity
pneumonitis (19%), granulomatous diseases, including sarcoidosis (30%), pulmonary
alveolar proteinosis (29%) and
tuberculosis (2.3% in cases of silica exposure).
The conclusion of the study
establishes the urgent need to improve clinical suspicion and knowledge of the
public health regarding the contribution of occupational factors.3
Litow et al classify the OCCUP DILDs into four conditions (frequently
overlapped from the clinical point of view):
A. Pneumoconiosis,
defined as non-cancer pulmonary reaction to inhaled mineral or organic
dusts and resulting modification of the parenchyma structure.
B. Hypersensitivity
pneumonitis (HN), also known as “extrinsic allergic alveolitis”.
Substantial number of disorders of the organism’s immune response to the
inhalation of organic or chemical antigens, associated with histopathological, granulomatous-like changes.
C. Granulomatous diseases with
reaction of foreign body or chronic, immune diseases.
D. Interstitial diffuse
fibrosis, as a reaction to a severe pulmonary lesion, including the
inhalation of irritants.4
The following table shows some of
the numerous examples of OCCUP DILDs. Given the fact that a lot of cases in
the literature are referred to as exceptional, we should consider individual propensity,
thus it may occur that one causative agent causes different pulmonary
interstitial responses.
The most widely known paradigms
of OCCUP DILDs are SILICOSIS and ASBESTOSIS. The acute form of silicosis may
adopt a pattern similar to pulmonary alveolar proteinosis
(PAP), whereas the non-tumor clinical form of asbestosis can be manifested as
an idiopathic pulmonary fibrosis (IPF).
OCCUP DILD SIMILAR TO PAP
PAP is an exceptional disease. Both
the surfactant secreted by the huge number of type II pneumocytes
and the imperfect removal of the surfactant by alveolar macrophages play a role
in the physiopathology of this condition.
PAP is classified into two
essential forms: congenital or acquired. The most common
variant is the acquired, and is divided into two sub-classes, autoimmune and
secondary, related to a causal factor. Acquired autoimmune PAP is the
most common. Secondary PAP is related to chronic inflammatory processes,
tumors, hematologic diseases, immunosuppressor
syndromes, and inhalation of inorganic or organic particles.
Abraham and McEuen
studied twenty-four cases of PAP through optical and electron microscopy to
check if the PAP was associated with silica exposure. A large number of birefringent particles was found in 78% of the cases, as
opposed to control groups.
The environmental history that
was researched correlated well with the results of analyzed particles, for
example, silica “sandblasting”, metal fumes in welders and cement particles.5
Silicosis is generally a chronic
pneumoconiosis. It is not common for the silicosis to adopt an accelerated or
acute form; there aren’t many publications due to its low frequency of
presentation.
The accelerated variant occurs
between 5 to 10 years after exposure to dust with high concentrations of
silica and if the person didn’t wear respiratory protection.
The acute variant is developed a
few years after very intense, brief exposure. It is similar to PAP, due to the
accumulation of lipoprotein PAS (periodic acid-Schiff) positive material in
the alveolar spaces; and the chest CT shows the radiographic crazy paving
pattern. It is difficult to differentiate silicoproteinosis
from PAP; the right thing to do is to have good occupational anamnesis. A
whole-lung lavage may delay the unfortunate evolution of this form of
silicosis.6-8
Attached is a case report of a
worker who performed sandblasting of metal pieces for five years without
personal protection (he was unaware of the risk). Dyspnea FC IV and severe
hypoxemia were observed, and the chest CT showed the crazy paving pattern. The evolution
was fatal (Figures 1 and 2).
There are some publications in
the literature where the form of OCCUP DILD similar to PAP is induced by the
inhalation of indium (used in the electronic industry), aluminum (for the
industry of metallization, ship construction, used as dust or for welding),
cotton dust (it can be used in cotton bale carding machines), titanium (used by
painters, mechanics, artificial jewelry manufacturers and titanium dioxide
producers); and there is a case report published in 2018 regarding years of
chronic inhalation of chlorine (used for tanning leather in a tannery).9-15
Recent epidemiological
research suggests that occupational and environmental exposure, as well as the
inhalation of irritants, contribute to cases of IPF, which then ceases to be
idiopathic.
Exposure to asbestos may create
radiographic and histopathological changes similar to
IPF.17
We should also include smoking, sawdust or wood dust, silica,
aluminum, and agricultural activities. The genetic variation among the
population may explain the differences in the susceptibility of the
presentation of varied patterns of interstitial diseases, even with the same
causative agent.
Between 1997 and 2000, Ekström et al investigated the effects of smoking in
occupational exposure and found that the fact of being a smoker represented a
great danger of developing severe forms of IPF, as well as a direct
relationship between the smoking load and higher risks.18
It is possible that in many IPF
patients, the fibrosis isn’t idiopathic because it was caused by occupational
exposure. Misdiagnosis can be due to inadequate anamnesis or lack of evident
suspicion in the causative agent. Some examples of the types of exposure that
contribute to the IPF pathogenia are: organic dust in
agriculture, livestock farming, metal, wood and asbestos dust.
One study conducted in Italy in
2008 found two groups of activities with a particularly high risk of developing
UIP that increased as long as the occupational exposure continued: gardeners,
veterinarians, farmers and metal workers. People who had their own experience
with exposure to the inhaled agent had a higher risk of developing UIP.19
Siderosis is the accumulation of excess iron oxide in the alveolar macrophages,
and was described in 1946 by Buckell et al.20
Gothi et al published a case report of
a welder with IPF associated with siderosis who had
been exposed for 40 years to metal fumes; and confirmed that it was originated
by siderosis through transbronchial
biopsy, with moderate functional loss one year after diagnosis, but without
major changes in the chest CT.21 Another similar report is that
of McCormick et al, in which a patient showed IPF secondary to siderosis even though he had worn a welder’s protective
mask for 20 years.22
For a long time, it was thought
to be pneumoconiosis with “benign” evolution, given the lack of signs, symptoms
or fibrosis. It is also known as “arc-welders disease” because of the
aspiration of welding fumes with poor respiratory protection or without any
protection at all.23
Aluminum dust has also been an
IPF producer; there are publications about it in the literature. In 1990, Jederlinic et al published 9 cases of workers from a
factory of abrasives, with a mean exposure of 25 years. Radiographic and
functional findings were followed up with biopsy, confirming pulmonary
aluminosis.24
In 2014, Raghu et al published a
similar case of IPF caused by aluminum with bad evolution in a worker who had
mechanized, sanded, drilled and rectified Corian for
16 years. This is a synthetic material consisting of one third of acrylic resin
and two thirds of aluminum trihydrate. Due to the
fact that it is thermoformable and acid-resistant, it
is used for the manufacture of kitchen and bathroom countertops and counters.25
Sawdust, in the form of inhalable
particles, can deposit on the pulmonary parenchyma and damage the workers’
health.
It is known that sawdust is
carcinogenic to humans. Hancock et al carried out a meta-analysis of 85
studies in order to identify researches. The authors showed an elevated risk
in workers exposed to sawdust, and a lower risk in those who worked with soft
wood. The study provided important certainty of this occupational cancer,
suggesting a different effect between hard and soft woods.26 The study of Gustafson et al
established that wood dust could contribute to the incidence of IPF. To that end,
they provided a 30-question questionnaire to 757 individuals with this
disease, which was answered by 181 of them. Through statistical studies they
found a higher risk among workers who had been exposed to the dust of hard
woods and birch wood.27
Attached is a case report of IPF
caused by asbestosis in an individual who worked as an electrician and
manipulated insulation materials for 25 years without personal protection. The
chest CT shows pleural calcifications and peripheral signs of “honeycombing”
(Figure 3).
OCCUP DILD SIMILAR TO COMBINED PULMONARY FIBROSIS AND EMPHYSEMA (CPFE)
In 1990, Wiggins et al published
nine cases of CPFE, but the most important publication about this interstitial disease
was presented by Cottin et al with a cohort of 61
cases in which they emphasized the predominance of the condition in men, its
relationship with smoking, acceptably preserved lung volumes and severely
decreased DLCO (diffusing capacity for carbon monoxide). Chest CT: fibrosis or
“honeycombing” in lower lung fields and emphysema in upper fields, with
extremely bad prognosis associated with pulmonary hypertension. Survival is
lower in CPFE, compared to IPF or COPD.28,
29
Workers who manufacture tires may
suffer from pleural or pulmonary diseases because they are exposed to the
powder used to prevent adherence of the vulcanized surfaces of rubber. Vinaya et al published the case of a worker with CPFE who
had been exposed to powder aspiration for 26 years. The development of this
condition has also been associated with the use of agrochemicals30,
31 .
OCCUP DILD SIMILAR TO BRONCHIOLITIS OBLITERANS
Bronchiolitis obliterans
(BO) is an exceptional obstructive pulmonary disease of the small airways,
eventually fatal. It is characterized by the fibrosis of terminal and distal
bronchioles and an obstructive airflow pattern with progressive reduction of
the respiratory function. It is mostly seen as a non-infectious complication
and chronic rejection after lung transplantation. From the occupational point
of view, cases have been published of BO caused by artificial flavors of
popcorn, where diacetyl stands out. Other causes of
BO include exposure to toxins and inhaled gases, nitrogen oxides, sulfur
mustard, fiberglass.
American service members who
served in Iraq and Afghanistan suffered from BO after being exposed to a fire
in a sulfur mine, with elevated levels of SO2,
and possibly to emissions from open burn pits in military bases, where
batteries, plastic and waste had been disposed of by burning with jet fuel. Doujaiji and Al-Tawfiq, published
the case of a patient with BO caused by SO2
exposure in an oil refinery in the Persian Gulf.32,
33
In 1992 there was a series of 22
cases of BO among 257 textile workers in Spain who had been spraying the
fabrics with what seemed to be non-toxic dyes. Similar products caused a minor
situation in Algeria, with one death and 2 severe cases.34,
35
Experimental studies showed that
the textile paint that was used (Acramin FWR and Acramin FWN) was highly detrimental to the respiratory
system.36
Nanoparticles (NPs) are widely
used at present, and, due to their size, they are included in the range of
breathable elements, because they remain in aerial suspension as aerosols. They
are used in the paper, pharmaceutical, paint, and cosmetic industries. Cheng
et al published the case of an individual who developed BO after exposure to
titanium NPs in paint. Recent experimental research revealed inflammatory
phenomena and formation of granulomas after unprotected exposure to NPs.37
Cullinan et al published in 2012 six cases of BO in fiberglass workers, five of
which built vessels with that material, and the remaining worker was building a
cooling tower. The procedure was as follows: they had to build glass reinforced
plastic using resin mixed with styrene and phthalate plus methyl acetone
peroxide. The evolution was bad, with one death caused by respiratory failure,
two lung transplants and three survivors with poor lung function.38
On May 2000, the Bureau of
Occupational Health of Missouri, U.S.A, was informed about eight individuals
with BO who worked in a popcorn manufacturing plant. The national entity
(NIOSH, National Institute of Occupational Safety and Health) was notified of
this, and 135 workers were evaluated through questionnaires and spirometry. 117 workers finished the studies, and had a
respiratory obstruction rate 3.3 times higher than expected, and 2.6 times
higher than expected chronic cough rate.39 Diacetyl
is a volatile, water-soluble compound that vaporizes with heat, and is a
natural component of several foods, including beer and wine. Concentrated
formulae of diacetyl are used in the food industry,
as flavoring agents, and it is estimated that by 1995, 95 tons had been used
per year.40
If inhaled without respiratory protection or an adequate
ventilation, it can cause BO. Studies have been published in this regard.41
Diacetyl-induced BO among workers of the food industry is the most widely known
and published. After reviewing the literature, a publication has been found of
four cases in Brazil: young men, previously healthy, non-smokers. After 1 to 3
years of work without protection, there was obstructive spirometric
impairment between 25% and 44% of what was expected, and tomographic studies
showed air trapping, representative of BO, confirmed through biopsy.42
Just like Gulati and Kreiss, the BO diagnosis must include inspiratory and
expiratory chest CT, spirometry, and confirmatory
biopsy can be avoided in case of compatible exposure. The identification of the
causative agent and its cessation is still fundamental for the index case, as
well as prevention among co-workers who participate in similar types of
exposure. Hygiene and safety include the monitoring of environmental
ventilation, the use of respiratory masks and covering food containers in order
to avoid leaks.43, 44
The notification, study and
follow-up of similar cases produced by diacetyl or
analogous substances in coffee processing plants have been reported by
Reid-Harvey and Bailey.45, 46
OCCUP DILD SIMILAR TO PLEUROPARENCHYMAL FIBROELASTOSIS (PPFE)
PPFE is an exceptional pulmonary
disease, with rare radiological and histopathological
clinical characteristics. Since the 2013 classification, it has been recognized
as an idiopathic interstitial pneumonia resulting from the combination of
visceral pleura fibrosis and fibroelastosis changes
at the subpleural pulmonary parenchyma. The chest CT
provides characteristic images that raise the suspicion of this disease.
Present as a cause of various diseases, there isn’t a unique triggering factor
for PPFE; reports have been published of chemotherapy sequelae,
bone marrow transplant, collagenopathy or as a
consequence of lung transplant rejection.47-52
Despite its uncommon incidence
and prevalence, there are some publications that relate the PPFE with exposure
to toxic substances in the workplace. In 2011, Piciucchi
et al published the case of an individual with PPFE who had high exposure to
asbestos; and in 2018, Xu et al published a similar
case report in which both asbestos and silica were associated with this
condition.53, 54
The publication of Okamoto et al
reports the case of a patient with PPFE who works as a dental technician. These
artisans are exposed to an unlimited number of materials such as silver,
cobalt, chrome, nickel, silica, indium and titanium. The prevalence of
pneumoconiosis among them is estimated at 4.5%-23.6%, with a mean exposure of
12.8 to 28.4 years.55-57
However, regarding this
particular disease, cases have been published caused by chronic inhalation of
aluminum in individuals without respiratory protection, such as the reports of
Huang, Chino and Yabuchi. This metal generally produces
OCCUP DILD similar to IPF, but the repair mechanisms of the pulmonary
parenchyma show individual sensitivity that causes this response.58-60
OCCUP DILD SIMILAR TO DESQUAMATIVE INTERSTITIAL PNEUMONIA (DIP)
First described by Averil Liebow et al, the main
characteristic of DIP is the accumulation of macrophages both in the lumen and
walls of the alveoli. Patients with this disease are usually heavy smokers;
and the masculine gender is predominant. Clinical symptoms are non-specific,
and due to the fact that patients generally respond to treatment with steroids,
this disease has a better prognosis than IPF.61
The literature has published case
reports about work-related DIP. In many cases, the patient is a heavy smoker.
Abraham and Hertzberg studied 62
samples of DIP confirmed by biopsy using electronic microscopy and X-ray
scattering analysis, in search of inorganic particles. Seven out of seventeen
analyzed cases had an occupational history of exposure to that type of
elements, and high concentrations of those were found in their biopsies. The
authors certified specific classes of particles in 92% of the patients, that is
why they suggested a relationship between DIP and the worker’s profession.62
Interstitial lung diseases are
not commonly associated with primary aluminum production. OCCUP DILD induced by
aluminum is very rare, but the experience suggests that exposure to metal fumes
and dust may cause diffuse changes in the parenchyma, such as granulomas, PAP
or DIP.63
Lijima et al published the case report of a worker with a smoking load of 60
packs per year who developed DIP caused by aluminum exposure and showed
excellent evolution after corticosteroid treatment and smoking cessation. The
oriented anamnesis revealed certain tasks of aluminum processing that include
melting the metal in molds for engine covers and polishing the pieces.64
Blin et al published the case report of a patient with DIP who had been
exposed to asbestos working as a plumber and then worked as a caster, with
potential exposure to copper, bronze, iron, aluminum and zirconium alloys. He
had a smoking history of 30 packs per year, and had quitted 10 years before
the consultation.65
Zirconium is a
corrosion-resistant material used in the aerospace, airline, and nuclear power
industries. Thanks to scientific research tests, it is known that after
repeated use, it may cause a hypersensitivity skin reaction, forming granulomas
of epitheliolid cells. Experimental studies showed
lung alterations such as granulomas and interstitial fibrosis after exposure to
zirconium. There are few publications in humans regarding pulmonary diseases
related to zirconium.66
Kawabata et al studied 31 patients
with DIP of varied etiologies, where 93% of the patients were male smokers.
These patients had been followed-up for more than 99 months. 14 patients who
had been monitored for a longer period showed 5 cases of IPF and 4 of lung
cancer. The conclusion of this study was that, with time, DIP can progress to
IPF, despite the treatment.67
Coal power plants are still an
important source of power supply worldwide, so miners will continue suffering
from pneumoconiosis and dying because of it. After the approval of the Federal
Coal Mine Health and Safety Act of 1969 in the U.S.A., measures were adopted to
restrict exposure, thus causing a persisting reduction in the prevalence of
pneumoconiosis among coal workers in the U.S.A. from 1970 to 2000.68
Jelic et al studied, in 25 autopsies with microscopy and polarized light,
the number of intramacrophageal silica particles and
the degree of fibrosis in antracosilicosis, and in 21
cases, respiratory bronchiolitis associated with smoking. The proportion of
particles found was significantly higher in the cases of occupational disease
(331:4 p < 0.001).
The presence of intra-alveolar
macrophages full of particles of different fibrosis levels indicated a new
disease: chronic DIP, as a predecessor of diffuse fibrosis and emphysema
related to stone coal. Among smoking miners, smoking-related fibrosis wasn’t
significant in relation to occupational DIP.
Counting the number of
particle-laden macrophages in the BAL (bronchoalveolar
lavage) of miners can predict the disease and suggest prevention measures.69
OCCUP DILD SIMILAR TO LIPOID PNEUMONIA (LP)
LP, caused by the presence of
lipids in the alveoli, is a rare condition. It is classified into two main groups,
depending on the source of the oily substance: exogenous or endogenous. It has
an insidious onset and non-specific respiratory symptoms, such as dyspnea,
fever or cough. Tomographic findings include nodules, ground glass, crazy paving
or consolidation. Since this condition is not suspected, the diagnosis is
delayed or unnoticed. It may simulate many other lung diseases, including
carcinoma. LP is a chronic foreign body reaction, identified with lipid-laden
macrophages. The diagnosis requires a high index of suspicion and may be
confirmed through respiratory samples showing the macrophages. Treatment
guidelines are not properly defined. The aim of the diagnosis in the exogenous
form of the disease is to avoid exposure. Steroids as a therapeutic option seem
promising.70
Normally, exogenous LP is
associated with the accidental inhalation of oil laxatives to treat constipation,
as can be seen in the series of 44 cases of Gondouin
et al, where only 4 patients had an occupational origin.71 Fire-eaters are a workgroup
inside the entertainment industry. Possible complications of their work must
be taken into consideration. The normal procedure consists in blowing the pyrofluid against a burning stick, so there’s the risk that
the fire may propagate to the mouth.72
The first description in the
literature about this occupational hazard was related to accidental aspiration
and was reported in 1971. Since then, there were other publications of LP in
fire-eaters. It is easier to make the diagnosis of the clinical condition after
a good patient inquiry.73-76
According to Gentina
et al, fire-eaters use different pyrofluids, the
most common being the Kerdan, an oil product of
reduced viscosity that unfortunately spreads rapidly through the bronchial
tree after accidental inhalation.
Between October 1996 and January
2001, these authors reviewed seventeen subjects, ten of which had been working
as fire-eaters for years. Their mean age was 24.5 years, and they showed
pleural pain (100%), dyspnea (93.3%), fever of more than 38.5°C (93.3%), cough
(66.6%) and hemoptysis (26.6%). One patient suffered an hemodynamic shock and
had to be treated at the ICU, where he/ she developed a pleuropulmonary
infection. Upon discharge, he/she had a good evolution but with sequelae (opacity in the middle lobe and pleural scar).
Complete pulmonary resolution occurred after 14 days in fifteen patients.77
Apparently, according to
consulted publications, it is very common for the employees of gas stations to
practice fuel siphonage, which may be a potential
risk of aspirating liquids or vapor. Directed inquiry allows us to suspect the
cause of this particular LP and obtain diagnosis and treatment success.78-82
Sometimes, suspicion requires a
thorough inquiry. The patient from the study of Dhouib
et al lubricated cars for eight years with an oil spray without any
respiratory protection; this delayed his/her etiologic diagnosis for 2 years.83
Han et al reported three cases of
LP caused by the use of a paraffin aerosol. Their diagnosis was confirmed
through biopsy and through the study of the samples by x-ray diffraction. The
workers had long-term occupational exposure to paraffin, and the environmental
concentration of the product in the workplace was specifically higher than the
levels measured outdoors.84 Very exceptional cases of LP
were caused by herbicides or solvents used for dry cleaning in the laundry.85, 86
In short, a good patient
occupational inquiry is extremely useful because it generally provides us the
key to guide and elucidate the diagnosis.
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