| Wood
charcoal and activated carbon dust pneumoconiosis in three workers.
Am J Ind Med. 2007 Mar;50(3):191-6.
BACKGROUND: Data
on prevalence of lung diseases due to inhalation of carbonaceous
materials other than mineral coal is very limited. METHODS: We present
three cases of wood charcoal pneumoconiosis, two due to activated
carbon, and one from wood charcoal artisan handling. To our knowledge,
no clinical cases of wood charcoal pneumoconiosis, from artisan
handling has been published so far. CLINICAL CASES: The three cases
had their X rays classified by two B-readers as p/q round opacities
with profusion ranging from 2/2 to 3/3. HRCT of two of them showed a
diffuse centrilobular ground glass nodular pattern with subpleural
small areas of consolidations. Transbronchial biopsies showed
deposition of black pigment in the bronchiolar interstice similar to
the histological appearance of simple coal workers pneumoconiosis,
with no signs of fibrosis. Spirometry showed no abnormalities in the
three cases. CONCLUSIONS: The authors point out to a probably
underestimated respiratory occupational risk related to wood charcoal
manipulation, which must be addressed mostly in developing countries,
where deficient workplace conditions can lead to exposure above limit
levels.
Role of pyrite in
formation of hydroxyl radicals in coal: possible implications for
human health. Part Fibre
Toxicol. 2006 Dec 19;3:16
ABSTRACT:
BACKGROUND: The harmful effects from inhalation of coal dust are
well-documented. The prevalence of lung disease varies by mining
region and may, in part, be related to regional differences in the
bioavailable iron content of the coal. Pyrite (FeS2), a common
inorganic component in coal, has been shown to spontaneously form
reactive oxygen species (ROS) (i.e., hydrogen peroxide and hydroxyl
radicals) and degrade nucleic acids. This raises the question
regarding the potential for similar reactivity from coal that contains
pyrite. Experiments were performed to specifically evaluate the role
of pyrite in coal dust reactivity. Coal samples containing various
amounts of FeS2 were compared for differences in their generation of
ROS and degradation of RNA. RESULTS: Coals that contain iron also show
the presence of FeS2, generate ROS and degrade RNA. Coal samples that
do not contain pyrite do not produce ROS nor degrade RNA. The
concentration of generated ROS and degradation rate of RNA both
increase with greater FeS2 content in the coals. CONCLUSION: The
prevalence of coal workers' pneumoconiosis can be correlated to the
amount of FeS2 in the coals. Considering the harmful effects of
generation of ROS by inhaled particles, the results presented here
show a possible mechanism whereby coal samples may contribute to CWP.
This suggests that the toxicity of coal may be explained, in part, by
the presence of FeS2.
Mechanistically
identified suitable biomarkers of exposure, effect, and susceptibility
for silicosis and coal-worker's pneumoconiosis: a comprehensive
review.J
Toxicol Environ Health B Crit Rev. 2006 Sep-Oct;9(5):357-95.
Clinical
detection of silicosis is currently dependent on radiological and lung
function abnormalities, both late manifestations of disease. Markers
of prediction and early detection of pneumoconiosis are imperative for
the implementation of timely intervention strategies. Understanding
the underlying mechanisms of the etiology of coal workers
pneumoconiosis (CWP) and silicosis was essential in proposing numerous
biomarkers that have been evaluated to assess effects following
exposure to crystalline silica and/or coal mine dust. Human validation
studies have substantiated some of these proposed biomarkers and
argued in favor of their use as biomarkers for crystalline silica- and
CWP-induced pneumoconiosis. A number of "ideal" biological markers of
effect were identified, namely, Clara cell protein-16 (CC16) (serum),
tumor necrosis factor-alpha (TNF-alpha) (monocyte release),
interleukin-8 (IL-8) (monocyte release), reactive oxygen species (ROS)
measurement by chemiluminescence (neutrophil release), 8-isoprostanes
(serum), total antioxidant levels measured by total equivalent
antioxidant capacity (TEAC), glutathione, glutathione peroxidase
activity, glutathione S-transferase activity, and platelet-derived
growth factor (PDGF) (serum). TNF-alpha polymorphism (blood cellular
DNA) was identified as a biomarker of susceptibility. Further studies
are planned to test the validity and feasibility of these biomarkers
to detect either high exposure to crystalline silica and early
silicosis or susceptibility to silicosis in gold miners in South
Africa.
IL18 and
IL18R1 polymorphisms, lung CT and fibrosis: A longitudinal study in
coal miners.Eur
Respir J. 2006 Dec;28(6):1100-5.
It has been suggested that interleukin (IL)-18 plays a role in the
development of inflammatory and fibrosing lung diseases. Associations
of polymorphisms in the genes coding for IL-18 (IL18 /G-656T, C-607A,
G-137C, T113G, C127T) and its receptor (IL18R1 /C-69T) with coal
workers' pneumoconiosis (CWP) were studied in 200 miners who were
examined in 1990, 1994 and 1999. Coal-dust exposure was assessed
according to job history and ambient measures. The main health outcome
was lung computed tomography (CT) score in 1990. Internal coherence
was assessed by studying CT score in 1994, 4-yr change in CT score and
CWP incidence and prevalence. CT score in 1990 was a good predictor of
radiographic grade in 1999 and, therefore, an appropriate subclinical
quantitative trait. The IL18 -137C allele was associated with lower CT
score in 1990 and 1994 (1.24 versus 1.69 and 1.57 versus 2.46,
respectively), slower progression of CT score between 1990 and 1994
and lower pneumoconiosis prevalence in 1999 relative to the G allele
(0.33 versus 0.77 and 8.2 versus 19.6%, respectively). Smoking- or
dust-adjustment, and stratification on IL18R1 genotype and adjustment
for haplotype effects did not change the conclusions. In conclusion,
the results of the present study suggest a role for IL18 in reducing
the development of this fibrosing lung disease.
Apoptosis and
Bax expression are increased by coal dust in the polycyclic aromatic
hydrocarbon-exposed lung.Environ
Health Perspect. 2006 Sep;114(9):1367-73
BACKGROUND:
Miners inhaling respirable coal dust (CD) frequently develop coal
workers' pneumoconiosis, a dust-associated pneumoconiosis
characterized by lung inflammation and variable fibrosis. Many coal
miners are also exposed to polycyclic aromatic hydrocarbon (PAH)
components of diesel engine exhaust and cigarette smoke, which may
contribute to lung disease in these workers. Recently, apoptosis was
reported to play a critical role in the development of another
pneumoconiosis of miners, silicosis. In addition, CD was reported to
suppress cytochrome P450 1A1 (CYP1A1) induction by PAHs. METHODS: We
investigated the hypothesis that apoptosis plays a critical role in
lung injury and down-regulation of CYP1A1 induction in mixed exposures
to CD and PAHs. We exposed rats intratracheally to 0.0, 2.5, 10.0,
20.0, or 40.0 mg/rat CD and, 11 days later, to intraperitoneal beta-naphthoflavone
(BNF) , a PAH. In another group of rats exposed to CD and BNF, caspase
activity was inhibited by injection of the pan-caspase inhibitor Q-VD-OPH
[quinoline-Val-Asp (OMe) -CH2-OPH]. RESULTS: In rats exposed to BNF,
CD exposure increased alveolar expression of the proapoptotic mediator
Bax but decreased CYP1A1 induction relative to BNF exposure alone.
Pan-caspase inhibition decreased CD-associated Bax expression and
apoptosis but did not restore CYP1A1 activity. Further, CD-induced
lung inflammation and alveolar epithelial cell hypertrophy and
hyperplasia were not suppressed by caspase inhibition. CONCLUSIONS:
Combined BNF and CD exposure increased Bax expression and apoptosis in
the lung, but Bax and apoptosis were not the major determinants of
early lung injury in this model.
Changes of
tumor necrosis factor, surfactant protein A, and phospholipids in
bronchoalveolar lavage fluid in the development and progression of
coal workers' pneumoconiosis.Biomed
Environ Sci. 2006 Apr;19(2):124-9.
OBJECTIVE: To
evaluate the alterations of biomarkers in the development and
progression of coal workers' pneumoconiosis (CWP). METHODS: The type
and number of cells, and the levels of tumor necrosis factor-alpha (TNF-alpha),
pulmonary surfactant protein, phospholipids and fibronectin in
bronchoalveolar lavage fluid were assayed in 14 health active coal
miners, 21 coal miners without CWP and 13 miners with CWP of 0/1 to
1/1. RESULTS: Compared to active coal miners without CWP (8.23 microg/mL),
TNF-alpha concentration was gradually decreased when dust exposure was
stopped (5.90 microg/mL). Elevated surfactant protein A (SP-A) level
and phosphatidylglycerol (PG) to phosphatidylinositol (PI) ratio were
found in miners actively exposed to coal dust (6528 ng/mL for SP-A and
10. for PG/PI), and both parameters decreased when CWP progressed from
CWP (0/1) (3419 microg/mL for SP-A and 5.9 for PG/PI) to CWP (1/1)
(1654 microg/mL for SP-A and 5.5 for PG/PI). CONCLUSION: Biomarkers in
bronchoalveolar lavage fluid can be used to screen coal miners at high
risk of developing coal workers' pneumoconiosis.
Micronodules
and emphysema in coal mine dust or silica exposure: relation with lung
function.Eur
Respir J. 1998 Nov;12(5):1020-4.
The aim of
this study was to investigate the respective effects of micronodules
and pulmonary emphysema, detected by computed tomography (CT), on lung
function in workers exposed to silica and coal mine dust. Eighty-three
subjects exposed to silica (n=35) or to coal mine dust (n=48), without
progressive massive fibrosis, were investigated by high-resolution and
conventional CT scans to detect micronodules and to quantify pulmonary
emphysema by measuring the relative area of the lung with attenuation
values lower than -950 Hounsfield units. Sixty-six (54.5%) subjects
had evidence of micronodules on CT scans. Smokers had micronodules
more rarely than nonsmokers. Significant correlations were found
between the forced expiratory volume in one second (FEV(1); %
predicted) (r=-0.41, p<0.001), FEV1/vital capacity (VC) (r=-0.61,
p<0.001), diffusing capacity of the lung for carbon monoxide (DL,CO)
(r=-0.36, p<0.001) and the extent of emphysema. No difference was
demonstrated in the linear relationships between the extent of
emphysema and the pulmonary function according to the type of exposure
or the presence of micronodules on CT scans. This study suggests that
micronodules detected by computed tomography have no influence, by
themselves, on pulmonary function and that they should only be
considered as a marker of exposure.
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