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At least 19 recordsLinked to original sources

DNA methylation and expression of p16(INK4A) gene in pulmonary adenocarcinoma and anthracosis in background lung.

The p16 (CDKN2/MTS-1/INK4A) tumor-suppressor gene is frequently inactivated by DNA methylation in lung carcinomas. To clarify whether background anthracosis may play a role in DNA methylation and inactivation of the p16 gene, we examined DNA methylation of the p16-promoter region by methylation-specific polymerase chain reaction, and p16 expression immunohistochemically, and compared the results with the level of background anthracosis which was measured by an original quantitative method. At autopsy, DNA methylation of the p16 gene was observed in 6/19 tumors (32%) from patients who had died of pulmonary adenocarcinoma. The degree of background anthracosis (the effect of extrinsic carcinogenic factors) (mean absorbance value, A = 0.715) of the cases with p16-gene methylation was significantly higher than that without methylation (mean A value = 0.298). p16 expression was inactivated in all tumors with p16-gene methylation. The mean A value of black dust matter deposition in cases with normal expression of p16 (A = 0.151) was significantly lower than cases with abnormal expression of p16 (A = 0.531). These results indicate that the level of background anthracosis is closely associated with inactivation of p16 expression and also DNA methylation of the p16-gene promoter region in pulmonary adenocarcinogenesis. Int. J. Cancer (Pred. Oncol.) 84:609-613, 1999.

Adenocarcinoma↗

The implication of anthracosis in the development of pulmonary adenocarcinoma.

The relationship between anthracosis, which is the deposition of black dust matter in the lung parenchyma, and the development of pulmonary adenocarcinoma has not been fully characterized. In order to clarify whether background black dust matter deposition could be implicated in the development of pulmonary adenocarcinoma, we measured the level of anthracosis at autopsy in 47 patients who had died of pulmonary adenocarcinoma. Both lungs of all 47 cadavers were examined. Twenty-micrometer sections were cut from formalin-fixed, paraffin-embedded blocks of the largest cut surface of each lung. Black dust matter was extracted from the sections and blotted onto a nitrocellulose membrane. The density of the blotted black dust matter was then analyzed using an imaging densitometer. There were no significant differences in the density of black dust matter deposition between lungs affected by pulmonary adenocarcinoma and control lungs. However, well differentiated adenocarcinomas tended to develop more frequently than poorly differentiated ones in lungs showing less deposition. We found a very strong correlation between the degree of black dust matter deposition and smoking history. Patients with severe anthracosis tended to have a poorer prognosis than those with mild anthracosis.

Adenocarcinoma↗

Esophageal anthracosis: lesion mimicking malignant melanoma.

A case of anthracosis of the esophagus is reported. The patient was a previously healthy 69-year-old Japanese woman. A black and slightly elevated lesion was detected in her esophagus by upper gastroesophageal fiberoscopic examination. Endoscopically, the lesion looked like malignant melanoma. Thoracic esophagotomy was then performed. Histological examination revealed a pigmented lesion beneath the mucosal epithelial layer. The lesion consisted of an aggregation of histiocytes containing an abundance of tiny black pigments. A few mature lymphocytes and plasma cells were also evident in the periphery of the lesion. Histologically, these findings looked like lymph nodes in the pulmonary hilus; however, no lymph nodal structure was evident in the esophageal wall. Traction diverticula were also noted in the pigmented lesion. The patient has remained well without disease for 9 months since the surgery. Although anthracosis is a rare condition in the esophagus, the present case gave warning to pathologists and clinicians that it does indeed occur. Endoscopists and pathologists should differentiate anthracosis from malignant melanoma because the treatment and outcome are quite different for each.

Aged↗

[Liver and blood enzyme spectra of rats with model anthracosis based on feeding a diet with additional amounts of methionine and pyridoxine].

The data obtained during studies of the enzymic spectrum of the liver and blood of rats with experimental anthracosis fed the diet containing additional quota of methionine and pyridoxine are presented. It was established that introduction of additional quota of methionine and pyridoxine in the animals' diet with an optimal fat content reduced the negative manifestations on the part of the enzymic systems of the liver and blood characteristic of experimental anthracosis and thus promoted retardation of fibrous process in the lungs. Additional introduction into the diet of rats with experimental anthracosis of methionine alone appeared ineffective.

Animals↗

Pulmonary anthracosis in children.

We report two cases of children with malignancies and subpleural nodules found on computed tomography (CT) scan. In both cases the diagnosis was anthracosis. This pathologic condition has never been reported in children. Causes of anthracosis include a smoking environment, living in urban areas and air pollution.

Air Pollutants↗

Studies on pulmonary anthracosis. With special reference to the mineral constitution of intrapulmonary particulate pollutants in the human lung.

In order to investigate anthracosis of the human lung, especially its causal relationship with atmospheric pollution and the occurrence of lung cancer, intrapulmonary particulate pollutants (IPP) from autopsy cases and patients lobectomized because of lung cancer were separated by alkali digestion of the lung tissue, and their elemental constitution was analyzed by a wavelength-dispersive X-ray fluorescence spectrometer. Silicon was the most abundant mineral constituent of non-carbonaceous fraction of IPP, followed by calcium, magnesium, iron, aluminum and other trace elements. The levels of silicon and aluminum in IPP were significantly higher in individuals treated at Saitama Medical School Hospital than in those from Tokyo. Farmers showed higher levels of silicon and aluminum than other occupational categories, whereas male blue-collar workers showed higher levels of calcium and lead than farmers. The level of iron in IPP of male smokers tended to be higher than in non-smokers. In cases of lung cancer, especially of the hilar type, the levels of iron, calcium, copper, lead, chromium and nickel in IPP tended to be higher than in non-lung cancer cases, whereas the levels of silicon and aluminum were lower than in non-lung cancer cases. On the basis of these results, pulmonary anthracosis was considered to be etiologically related to the occurrence of lung cancer.

Adolescent↗

[Effect of methionine, retinol, tocopherol and pyridoxine on fibrogenesis in the lungs and vitamin metabolism in rats in an anthracosis model].

It has been discovered in rat experiments that the diet containing an additional amount of methionine and pyridoxine and optimal quantity of fat favoured to a certain degree the retardation of the development of pulmonary fibrosis and reduced the disorders in metabolism of vitamins, characteristic for animals with experimental anthracosis. On the contrary, introduction of an additional amount of retinol into the above complex aggravated the development of pulmonary fibrosis and alterations in vitamin metabolism. At the same time the negative manifestations seen in the animals with experimental anthracosis were removed to a certain measure by administering additional doses of vitamin E.

Animals↗

[Charcoal smoke causes bronchial anthracosis and COPD].

BACKGROUND: Bronchopulmonary disease due to inhalation of smoke from open woodfires represents a major health problem in developing countries. Due to increasing migration such patients also present to medical services in Europe. CASE REPORT AND DISCUSSION: An 84-year-old Afghan housewife who never smoked nor has a history of exposure to inorganic dusts, presents with chronic obstructive pulmonary disease (COPD) in association with bronchial anthracosis and stenosis of a bronchus. The complaints are found to be caused by chronic inhalation of smoke from an open woodfire which was used for cooking. The main complaints of "woodsmoke-associated lung disease" are cough und dyspnea with bronchial obstruction. Radiology and bronchoscopy usually reveal changes which are similar to pneumoconiosis of miners but without patients' relevant exposure. There is a frequent association of anthracotic bronchial stenosis and infection with tuberculosis. CONCLUSION: Since patients rarely recognize the risks of woodsmoke inhalation, they hardly report their exposure. Thus, the anamnesis is crucial to establish the right diagnosis and guide the patient to the appropriate diagnostic and therapeutic procedures.

Afghanistan↗

The implication of background anthracosis in the development and progression of pulmonary adenocarcinoma.

In order to characterize the relationship between background anthracosis and pulmonary adenocarcinogenesis, surgically resected tissues of 66 cases of stage I pulmonary adenocarcinoma, 4 cm or less at their greatest dimension, were examined. These cases were diagnosed based on the classification of small-sized adenocarcinoma of the lung (Noguchi et al., Cancer 75, 1995). Thirteen cases were diagnosed as types A (localized bronchioloalveolar adenocarcinoma, LBAC) and B (LBAC with alveolar collapse), 40 cases as type C (LBAC with a focus of fibroblastic proliferation), 8 as type D (poorly differentiated adenocarcinoma) and 5 as types E (bronchial gland type adenocarcinoma) and F (true papillary adenocarcinoma). The 5-year survival rate of types A and B cases was 100%, while those of type C, type D and types E and F were 52%, 48% and 39%, respectively. Nuclear accumulation of abnormal p53 protein in non-replacement type adenocarcinomas (types D, E and F) was detected more frequently than that in replacement type adenocarcinomas (types A, B and C) (P < 0.05). In each case, black dusty material was extracted from tumorous lesions and non-tumorous regions and blotted onto a nitrocellulose membrane. The anthracotic index (AI) was calculated with a densitometer. AIs of non-tumorous regions in early and replacement type adenocarcinomas (types A and B) were significantly less than in relatively advanced (type C) and poorly differentiated (type D) adenocarcinomas (P < 0.05). These results indicated that adenocarcinoma developing in heavily anthracotic lungs readily progresses to an advanced stage, or that adenocarcinoma with a less favorable prognosis tends to develop in severely anthracotic lungs.

Adenocarcinoma↗

[The effect of qualitatively different fatty components of the diet on mitochondrial membranes in animals with experimental anthracosis].

The diets with qualitatively different content of fat were found to produce structural and functional alternations in liver mitochondria of rats with experimental anthracosis. It was established in particular that the increase of the vegetable oil quota in the diet of rats affected the structure and function of mitochondria whereas the diet whose fat component included butter, lard, sunflower oil, and margarine at a ratio of 1:1, 5:1:0.5 reduced the untoward effect of coal dust and exercise on the mitochondrial membranes.

Animals↗

The role of soluble acids from oxidative-hydrolytic breakdown of coal in the development of the fibrous process in anthracosis.

The oxidative-hydrolytic mechanism of interaction of coal with tissue medium and the formation of humic acids (HA) and polycarboxylic acids (PCA) from coal in the organism were demonstrated. The composition of PCA obtained from the coal withdrawn from the organism of animals was investigated by gas-liquid chromatography by means of which 28 acids of the aromatic series were identified. The method of elemental spectral analysis revealed the transition of a number of macro- and microelements into the medium of the organism. It has been shown experimentally that the decrease in the mass of coal correlates with the fibrogenic process. The conclusion has been drawn that the soluble products of the oxidative-hydrolytic breakdown of coal in the organism are among the fibrogenic factors of pneumosclerosis in anthracosis. The initial mechanism in the development of fibrosis is the damage caused by polycarboxylic acids to the microcirculatory bed of the lungs and the structures of the aerohematic barrier.

Animals↗

[New morphological aspects of pathogenesis of pneumofibrosis in anthracosis].

The death of the alveolar macrophage stimulating the activation of fibroblast in pneumoconiosis is not a single trigger mechanism of pneumofibrosis in anthracosis. Alteration of the microcirculatory bed and lung aerohematic barrier plays an essential pathogenetic role in coal pneumoconiosis. Polycarbonic acids which are formed in the organism from coal as a result of its oxidative-hydrolytic degradation are the cause of the damage and loss of the structural components of the aerohematic barrier.

Anthracosilicosis↗