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Genetic susceptibility in pneumoconiosis.Toxicol
Lett. 2007 Feb 5;168(3):249-54. Epub 2006
Nov 16
A large number of
cellular mediators such as cytokines, antioxidants and growth factors
have been implicated in the pathogenesis of chronic inflammatory and
fibrotic diseases. Common functional polymorphisms in these genes have
been shown to influence individual susceptibility to these diseases.
Silicosis, coal worker pneumoconiosis, progressive massive fibrosis
and berylliosis are examples of fibrotic pneumoconiosis and are
characterized by irreversible fibrotic lesions in the lung resulting
from chronic dust inhalation. Although the materials are the major
contributory factors of the disease pathogenesis, not all individuals
exposed to similar levels develop disease. This suggests that there is
a genetic predisposition to their development. Therefore, an
understanding of genetic variability and the interaction between
genetic and environmental factors is crucial to the identification of
high-risk individuals and prevention and treatment of these diseases.
Expression
level and significance of TGF-beta1, PDGF, CTGF in serum of patients
with pneumoconiosis.Sichuan
Da Xue Xue Bao Yi Xue Ban. 2006
Sep;37(5):754-6, 793.
OBJECTIVE: To
explore the TGF-beta1, PDGF, CTGF serum expression significance in the
occurrence and development of pneumoconiosis. METHODS: The serum
levels of TGF-beta1, PDGF, CTGF in 70 patients with pneumoconiosis
(including 29 patients with silicosis and 41 patients with coal
pneumoconiosis) and 77 healthy individuals were detected by means of
enzyme linked immunosorbent assay (ELISA). RESULTS: The serum levels
of TGF-beta1, PDGF, CTGF in patients with pneumoconiosis were (44.95
+/- 23.72) ng/mL, (56.95 +/- 55.68) ng/mL, (346.70 +/- 259.49) pg/mL,
the serum levels of control group were (6.81 +/- 4.99) ng/mL, (30.96
+/- 21.63) ng/mL, (307.49 +/- 235.40) pg/mL. There were significantly
statistical differences between the case group and the control group
in the serum levels of TGF-beta1 and PDGF (P < 0.05). There was no
significantly statistical difference between the two groups in the
serum levels of CTGF (P > 0.05). The serum levels of TGF-beta1 and
PDGF in the patients with silicosis were higher than those in the
patients with coal pneumoconiosis, and there was significantly
statistical difference between the two groups (P < 0.05). The serum
levels of TGF-beta1 and PDGF in the patients with pneumoconiosis
decreased with the pneumoconiosis stage going up (P < 0.05). There was
the bivariate correlation not only between the serum levels of
TGF-beta1 and PDGF in the whole objects but also the serum levels of
CTGF and PDGF (P < 0.05). CONCLUSIONS: The serum levels of TGF-beta1,
PDGF, CTGF in the patients with pneumoconiosis may correlate with the
pathological stages, styles and degree of pneumoconiosis.
Respiratory symptoms and functional status in workers exposed to
silica, asbestos, and coal mine dusts.
J Occup Environ Med. 2000;42(11):1076-84
This study aims
to provide further understanding of physiologic and symptomatic
changes and radiographic abnormalities due to exposure to silica,
asbestos, and coal dusts. Questionnaires and pulmonary function tests
were given to 220 silica, 277 asbestos, and 511 coal workers from
three different industries in China. Posteroanterior chest radiographs
were classified as stages 0, I, II, and III according to degree of
parenchymal fibrosis. Significantly poorer pulmonary function and a
higher prevalence of dyspnea and chronic cough were observed in
workers with pneumoconiosis than those without, irrespective of dust
type. Workers with stages II and III silicosis had worse pulmonary
function and more common symptoms relative to workers with equivalent
coal workers' pneumoconiosis or asbestosis. After adjusting for
relevant confounders, reductions in the spirometric parameters and
single breath diffusing capacity for carbon monoxide (DLCO) and the
occurrence of respiratory symptoms were associated with increasing
stage of silicosis, whereas lower DLCO and the occurrence of symptoms
were associated with increasing stage of asbestosis and coal workers'
pneumoconiosis. The study suggests that despite the differences in
degree and pattern due to exposure to different fibrogenic dusts,
respiratory impairments of all of the workers are associated with the
presence and progression of parenchymal fibrosis and smoking.
Recent advances in the pathogenesis and clinical assessment of mineral
dust pneumoconioses: asbestosis, silicosis and coal pneumoconiosis.
Eur Respir J. 1989
Nov;2(10):988-1001
Recent
investigations of the fundamental mechanisms of the mineral dust
diseases have substantially increased our understanding of the
pathogenesis of the pneumoconioses. In all the mineral dust
pneumoconioses, the initial early lung lesion is a fibrosing
macrophagic alveolitis. The additional contribution of other lung cell
populations is currently under investigation and may identify specific
processes for each of the pneumoconioses. Clinical investigations have
also progressed with new tools such as Gallium-67 lung scanning,
bronchoalveolar lavage analyses, and CT scanning of the thorax; their
established values are reviewed in this paper, and areas where
progress is needed are considered. The clinical progress in the
mineral dust diseases is clearly linked to the basic understanding of
the mechanisms of these diseases.
Mixed pneumoconiosis: silicosis, asbestosis, talcosis, and
berylliosis. Chest.
1979 Jun;75(6):726-8
Mixed
pneumoconiosis is pulmonary disease due to two or more inhaled mineral
irritants. Chronic disease due to beryllium has not been a component
of any described mixed pneumoconiosis. A man with occupational
exposure to a combination of dusts developed severe pulmonary disease.
Silicosis, talcosis, asbestosis, and berylliosis were all documented
by an open biopsy of the lung. The varieties of mixed pneumoconiosis
are summarized.
Relationship between
autoimmune diseases and pneumoconiosis.Sangyo
Igaku. 1992 Sep;34(5):421-31
In recent years,
with the aging of patients with pneumoconiosis, autoimmune diseases as
a complication have been observed. One of the reasons for this may be
that autoimmune diseases are prone to develop among the elderly. On
the other hand, it has been reported that dust itself, such as silica
for example, has adjuvant effect. A review of the recent literature
published in Japan and abroad was made to clarify the relationship
between pneumoconiosis and autoimmune diseases and the following
results were obtained. 1) Disorders which accompany pneumoconiosis:
Scleroderma, rheumatoid arthritis, systemic lupus erythematosus (SLE),
and disorders of the kidney and liver have been reported. In Japan,
about 30 cases of pneumoconiosis accompanied with autoimmune diseases
have been reported. In many of the reports, patients with
pneumoconiosis and scleroderma have a past history of exposure to
silica. In both case studies and case control studies, patients with
rheumatoid arthritis and history of silica exposure are prone to
develop pneumoconiosis. 2) Immunological studies of patients with
pneumoconiosis: As for humoral immunity, elevation of polyclonal
gamma-globulin, especially IgG, has been often reported together with
high positive rate of autoantibodies such as antinuclear antibodies.
In cellular immunity, decreased delayed type skin reaction and
decreased CD4/8 ratio have been reported. In human leukocyte antigen (HLA)
typing the elevated frequency of DR4 has been reported. In the study
of BAL increased production of superoxide anion O2- by alveolar
macrophages has been observed. 3) Experimental studies: Silica is well
known for its toxicity to cells and also for its adjuvant effect. In
the German Democratic Republic, patients with scleroderma and history
of long term silica exposure are recognized as patients with
occupational disease even though pneumoconiosis is not clearly
demonstrated on X-ray film. It is difficult from this review to nrake
a definite conclusion regarding the relation between silicosis and
autoimmune diseases. There is a need to repeat this review of the
literature on autoimmune diseases and pneumoconiosis in the near
future.
Long-term
outcome after resection of non-small cell lung carcinoma complicated
by pneumoconiosis.Surg
Today. 2006;36(10):869-73.
PURPOSE: Lung
cancer resection in patients with respiratory complications is
associated with a high surgical risk and the operative indications are
usually serious. Consequently, the long-term results are unclear. We
aimed to clarify the validity of surgery for non-small cell lung
cancer (NSCLC) in patients with pneumoconiosis. METHODS: We reviewed
the clinical and pathological data of 122 patients undergoing
resection of NSCLC with pneumoconiosis (n = 34: group A) or without
pneumoconiosis (n = 88: group B) to assess treatment outcomes and
prognostic factors. RESULTS: Among the treatment factors,
intraoperative blood loss was significantly greater in group A (723.2
+/- 647.3 ml) than in group B (466.4 +/- 450.7 ml) (P = 0.0067),
although the operative times (207 +/- 103.4 min vs 196.1 +/- 53.5 min,
respectively) and postoperative drainage period (8.3 +/- 4.2 days vs
8.5 +/- 5.7 days, respectively) did not differ significantly between
the two groups (P = 0.9466 and P = 0.6355, respectively). Among the
postoperative complications, the incidence of hemorrhage was
significantly higher in group A (29.4%) than in group B (7.9%) (P =
0.0022). The 5-year survival rates did not differ significantly
between the two groups, (45.9% and 55.7% for groups A and B
respectively) (P = 0.9424). CONCLUSIONS: The coexistence of
pneumoconiosis does not adversely affect postoperative survival or the
treatment of NSCLC, although it is associated with increased
intraoperative blood loss and postoperative hemorrhage. Thus, if
precautions are taken to minimize hemorrhage, surgery cannot be
excluded as a treatment option for NSCLC in patients with
pneumoconiosis.
The inorganic dust pneumoconioses.Clin
Rev Allergy. 1985 May;3(2):235-47
Collectively,
the pneumoconioses represent a spectrum of pulmonary diseases
initiated by inorganic dust exposure. Although multiple humoral
and cellular immune alterations have been demonstrated in these
interstitial and commonly fibrotic lung diseases, the exact role
of immune changes in disease pathogenesis presently is undefined.
Insight into disease mechanisms may have to await the careful
characterization of suitable animal models, along with analysis of
local, human bronchopulmonary immune responses through the vehicle
of bronchoalveolar lavage.
Immunopathogenesis of
asbestosis, silicosis, and coal workers' pneumoconiosis.
Clin Chest Med. 1983 Jan;4(1):3-14
From these
discussions, it is apparent that immunologic aberrations occur in
several inorganic dust diseases. Although the role of these
immunologic mechanisms in disease pathogenesis remains
speculative, recent studies demonstrating the regulation of
fibroblast proliferation by macrophage and asbestos or silica
interaction support a role for this cell type in the
immunopathogenesis of disease. Future cellular and humoral
investigations of the bronchoalveolar lavage in workers with
pneumoconiosis may clarify the immunologic contributions in the
development of fibrosis observed in these diseases.
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