Autor : Rubado Pilar1, Mirabal Yanina1, Taboada Martín1, Montoya Romina1, Martínez Fraga Alejandro1, Gullo Regina1, Renom Horacio1, Jordán Pablo1, Romera Andrés1, Barragán Horacio1
1Complejo Medico Policial Churruca-Visca - Autonomous City of Buenos Aires- Argentina
https://doi.org/10.56538/ramr.QTZP8357
Correspondencia : E-mail: pilar.rubado@gmail.com
ABSTRACT
Silicosis is caused by sustained
inhalation of silicon dioxide (SiO2).
Work in quarries and industries of ornamental rock, granite and slate, and
marble work, are the typically described types of exposure, together with
sandblasting. Denim sandblasting and the production of kitchen and bathroom
countertops have emerged more recently. Clinical presentations can be
classified into chronic silicosis (simple, complicated, and pulmonary
fibrosis), accelerated silicosis, and acute silicosis, depending on years of
exposure and individual factors. We present a clinical case of a 78-year-old
male patient with complicated chronic silicosis, asymptomatic, diagnosed in
the context of a pre-surgical examination.
Key words: Silicosis; Occupational diseases; Lung Diseases, Interstitial
RESUMEN
La silicosis es producida por la inhalación
mantenida de dióxido de silicio (SiO2). Los trabajos en canteras e industrias de
roca ornamental, granito y pizarra, y marmolerías son las exposiciones
clásicamente descriptas, junto al pulido con chorro de arena. El arenado
de jeans, producción de mesadas de cocinas y baños han surgido
más recientemente. Las presentaciones clínicas pueden
clasificarse en silicosis crónica (simple, complicada y fibrosis pulmonar),
silicosis acelerada y silicosis aguda, según los años de
exposición y factores individuales. Se presenta un caso clínico
de un paciente masculino de 78 años con silicosis crónica
complicada, asintomático, diagnosticado en contexto de un examen prequirúrgico.
Palabras clave: Silicosis; Enfermedades profesionales; Enfermedades pulmonares
intersticiales
Received: 12/06/2021
Accepted: 05/30/2022
INTRODUCTION
Silicosis is one of the oldest
known occupational lung diseases. It is caused by sustained inhalation of
silicon dioxide (SiO2),
mostly in the workplace, although it has also been described in the home
environment. With early suspicion, the patient can be isolated from the source
of exposure and change the prognosis and evolution of the disease. This work
proposes the publication of this clinical case for the purpose of emphasizing
the importance of patient inquiry in identifying diseases related to
environmental and work exposure and obtaining an early diagnosis of diseases
that are rare but can be prevented.
CLINICAL CASE
78-year-old male patient referred
by the Traumatology Service to do a pre-surgical study. The patient is a former
smoker (<5 p/y) with history of arterial hypertension, and has a pacemaker
due to a sinus node disease. As for his work, he is a retired police officer.
At the moment of the consultation, he is medicated with aspirin and enalapril; asymptomatic in the area of the respiratory
system. Oxygen saturation (Sp02) is 98% with inspired fraction of 0.21;
normal breath sounds, no adventitious sounds. The general physical examination
is unremarkable.
A spirometry
was performed, with the following results: FEV1/FVC, 54%; FEV1, 1.93 (75%);
FVC, 3.54 (107%), with evidence of mild obstruction. The chest X-ray shows heterogeneous
radiopacities with tendency to confluence, with
predominance of left upper lung field (Figure 1).
Due to the findings of the chest
X-ray, the patient was inquired again, and he said he worked in a
family-operated medal polishing shop (10 hours a week, for more than 10 years).
Chest tomography requested. The results showed bilateral masses in posterior
segments of upper lobes with spiculated borders,
fibro-cicatricial tracts, heterogeneous, with 58 mm ×
35 mm, and 35 mm × 28 mm calcifications. These images are associated with
bullae plus emphysema and bilateral mediastinal adenomegalies with calcifications (Figures 2A and 2B).
DISCUSSION
Silicosis is one of the oldest
known occupational lung diseases, and is included in the group of interstitial
diseases. It is produced by sustained inhalation of SiO2. Crystalline silica is a natural metal oxide.
Among the different varieties, the most abundant is the quartz, found in rocks
and sand. In a lower volume, there are other polymorphisms such as cristobalite and tridymite, both
from volcanic rocks, and stishovite, which doesn’t
have fibrotic potential1.
The silica is phagocytized by
alveolar macrophages, thus activating and perpetuating the inflammatory
process through inflammatory cytokines (tumor necrosis factor-alpha [TNF-a]
and interleukin-1 [IL-1]) that recruit inflammatory cells in the alveolar wall.
These cells release toxic derivatives of oxygen and proteolytic
enzymes that cause cellular damage and destroy the extracellular matrix, thus
producing a fibrotic response in the pulmonary parenchyma2.
There are multiple sources of
exposure, mainly in the workplace, but they may also occur in the home
environment (home exposure). Work in quarries and industries of ornamental
rock, granite and slate, and marble work, are the typically described types of
exposure, together with sandblasting.1
In the early ‘90s, new industries
emerged involving denim sandblasting, mostly in Turkey, also including the production
of kitchen and bathroom countertops with quartz. If countertops are grinded
without dust suppression, they generate a dust level 300 times above the
recommended value3.
In Israel, approximately 3,500 workers cut and process countertops that contain
93% of silica as raw material4.
In 2000, the existence of 3.2 million people exposed to silica was reported in
the European Union5.
In 2007, a 4-year follow-up study was published in which 145 former denim
sandblasting workers were evaluated, 83 of which were reevaluated in 2011; 6.2%
(9 individuals) had died, with an average age of 24 years, and the prevalence
of silicosis among the remaining 74 survivors increased from 55.4% to 95.9%,
with evidence of radiographic progression in 82%6. The SWORD (Surveillance of
Work-Related and Occupational Respiratory Disease) report described 216 cases
of silicosis from 600,000 exposed workers between 1996 and 2017 in the United
Kingdom7.
A study conducted in 132 companies of 31 different sectors in Chile estimated that
5.4% have a high probability of exposure to silica8. Real figures regarding its prevalence
in Argentina are unknown.
The risk of developing silicosis
depends on several factors. First, the magnitude and duration of the exposure,
given by the calculation of the cumulative dose (see Table 1) and individual
sensitivity, which is determined by genetic and environmental factors. The
silica dust, after being inhaled, is deposited in the lungs and presents a
complicated process of depuration that leads to its retention, because the
mechanisms of defense and ciliary clearance lose
effectiveness. Those mechanisms are boosted by smoking or the presence of some
respiratory underlying condition, such as COPD (chronic obstructive pulmonary
disease)1.
This justifies the fact that there isn’t any safe, zero-risk exposure
threshold. However, in Argentina, there is a maximum permissible concentration
of crystalline silica (cristobalite) regulated
through Resolution N° 295/2003 of the Ministry of Labor, Employment and Social
Security, which is 0.05 mg/m³; and 0.1 mg/m³ for quartz1.
Clinical presentations can be
classified into chronic silicosis (simple, complicated, and pulmonary
fibrosis), accelerated silicosis, and acute silicosis. The first are the most
common and can be observed after 10 to 15 years of exposure. Patients with
simple silicosis tend to be asymptomatic, with 2-5 mm centrilobular
nodule images predominating in the upper lobes and posterior segments. Thus,
silicosis can progress to the complicated type in patients with dyspnea and
cough, nodules bigger than 1 cm that tend to merge forming conglomerate masses
of irregular shapes, marked retraction, and cicatricial
emphysema. Patients usually show mediastinal adenopathies with calcifications. In pulmonary fibrosis,
the predominant symptom is also dyspnea with images similar to idiopathic
pulmonary fibrosis. Accelerated silicosis requires from 5 to 10 years of
exposure, with features intermediate between chronic and acute silicosis, but higher frequency of progression to severe forms of the
disease. Finally, acute silicosis is manifested after less than 5 years of
exposure, generally very high levels of exposure, with dyspnea, weight loss and
rapid progression to respiratory failure. Radiologically,
we observe a bilateral perihilar alveolar pattern
with “ground glass” opacities, similar to alveolar proteinosis;
that is why it is also called “silicoproteinosis”
(Table 2).
The diagnosis is based on the
presence of exposure to silica, radiological findings and exclusion of other
diseases. As regards the exposure, as we were saying, most cases occur in the workplace
environment, so it is important to evaluate current and past activities and to
describe the type of work that was carried out, and the mechanisms of
protection used, both environmental and individual. Radiological studies
(Rx-CAT) are essential for the diagnosis and evaluation of disease
progression. Other diagnostic studies are indicated only in atypical cases or
if the patient has a poorly-documented history of exposure. Anatomopathological
studies are required in exceptional cases.
Lung function tests are necessary
for follow-up and to assess possible progression. The spirometry
shows the presence or absence of ventilatory defects
(obstructive and non-obstructive) and facilitates the diagnosis of other
diseases. A decrease in the forced expiratory volume on the first second (FEV1)
can be observed in patients exposed to silica, which has a synergistic effect
with smoke in smoker patients. If the spirometry is
altered, we recommend to do a complete functional
assessment1.
Regarding the diffusing capacity for carbon monoxide (DLCO), it is reduced in
the complicated forms of the disease. SpO2 measured with pulse oximeter,
arterial blood gases, and exercise tests, such as
the 6-minute walk test (6MWT), together with the clinical severity assessment,
allow us to outline the behaviors.
There isn’t any
effective treatment for this disease, that is why
prevention is essential. Among the preventive measures, engineering controls
come first: eliminate exposure by substituting raw materials, making changes
and adjustment of processes, insulation and ventilation. To control the respirable dust levels within the legal limits is an
important measure, together with the use of personal protective elements, since
we must remember that the damage threshold is variable among patients.
Early diagnosis and
prevention of complications are part of the secondary prevention. People
exposed to silica should participate in a health surveillance program that
includes medical record, spirometry and chest X-ray
on a periodic basis, and according to clinical symptoms.
Tertiary prevention
makes reference to avoiding disease progression, treating the obstructive
defect, if present, providing home oxygen supply,
giving the influenza and pneumococcal vaccines and possible transplantation. We
recommend the screening and treatment of the latent tuberculous
infection. It is worth mentioning that association with autoimmune diseases has
been described: sclerodermia, rheumatoid arthritis
and systemic lupus erythematosus (SLE), among others,
even lung cancer.
CONCLUSION
We present this case
because it is a rare, underdiagnosed disease. In the exposed case, the patient
gets to an advanced age with no symptoms.
The physician has to identify
the patient’s work and environmental history that could imply exposure, since
it is a preventable disease that doesn’t have a treatment. Decree N° 658/96 of
occupational diseases enumerates the most frequent activities that involve
exposure1. From the
occupational point of view, when a patient is diagnosed with silicosis, he must
avoid exposure, also the disease has to be declared as an occupational disease,
and the patient must relocate his/her job or be declared as disabled. In the
work environment, it would behave as a surveillance event that imposes better
epidemiologic surveillance measures to prevent new cases.
Conflict of interests
The authors declare
that there is no conflict of interests.
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