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V Vallyathan

Publications and source records attributed to V Vallyathan.

At least 109 records · Page 6Linked to original sources
PubMed1985

In vitro biologic toxicity of native and surface-modified silica and kaolin.

An in vitro study of the biologic responses of surface-modified and native silica and kaolin was made to provide comparative information on the suppression of cytotoxicity by pulmonary surfactant. The release of alveolar macrophage cytoplasmic enzyme, lactate dehydrogenase (LDH), and lysosomal enzymes beta-N-acetylglucosaminidase (beta-NAG) and beta-glucuronidase (beta-GLUC) and sheep blood-cell hemolysis were monitored as indicators of cell membrane damage and cytotoxicity. Surface modification of silica and kaolin with dipalmitoyl lecithin (DPL) resulted in complete abrogation of cytotoxicity of both minerals. These findings indicate that surface modification of minerals with different adsorption properties by pulmonary surfactant generally lessens their prompt adverse effects.

Acetylglucosaminidase↗
PubMed1985

Lung carcinoma by histologic type in coal miners.

Histologic types of lung carcinoma were studied in 171 coal miners in the National Coal Workers' Autopsy Study. These miners had an average underground mining tenure of 29 +/- 14 years and an average smoking history of 31 +/- 23 pack-years. The proportion of carcinomas by cell type were: squamous cell carcinoma, 30%; adenocarcinoma, 27%; small-cell undifferentiated carcinoma, 26%; large-cell undifferentiated carcinoma, 9%; and other carcinomas, 8%. More tumors were observed in the right lung and in the upper lobes of both lungs than in the left lung and in the lower lobes of both lungs, respectively. The majority of the tumors were centered on cartilaginous airways (81%) as compared with the peripheral regions of the lung (19%). Squamous cell carcinomas predominated in the older miners and in larger airways. Adenocarcinomas were more common in the peripheral lung. No significant interaction was demonstrated between cell type and years of underground mining. The data indicate that lung carcinoma in coal miners differs little in its pathologic features from men in the general population who smoke cigarettes. No effect of coal mine dust exposure on lung carcinoma histogenesis was demonstrated.

Adenocarcinoma↗
PubMed1984

Comparative in vitro cytotoxicity of volcanic ashes from Mount St. Helens, El Chichon, and Galunggung.

Dry sedimented volcanic ash samples from each of three widely separated volcanoes of the "Circum Pacific" region have been subjected to mineralogic analysis and in vitro tests for cytotoxicity. The ash samples from the three different volcanoes varied in particle size, surface area, and concentration of silica. Total crystalline silica in the respirable fraction of ashes was 1.5% (Mount St. Helens, Moses Lake); 1.36% (Galunggung, Bandung-1); 1.95% (Gallunggung, Bandung-2); and 1.72% (El Chichon, Tuxtla). Hemolysis as an index of cytotoxicity was measured by in vitro tests on sheep blood erythrocytes and indicated wide differences in hemolytic activity among ash samples. Alveolar macrophage cytosolic (lactate dehydrogenase) and lysosomal (beta-glucuronidase and beta-N-acetyl glucosaminidase) enzymes were measured as an index of cellular integrity following dust exposure. Hemolysis and release of enzymes from alveolar macrophages were greater with volcanic ash from Galunggung (Bandung-1) and El Chichon (Tuxtla) than the other ashes. Although crystalline silica induced an effect similar to volcanic ash from Galunggung (Bandung-1) on the release of enzymes from alveolar macrophages, the hemolytic potency of silica was much greater. Light and electron microscopic observations of dust-exposed alveolar macrophages indicated that the ash particles were readily phagocytized. These results indicate that volcanic ash is moderately cytotoxic and that exposure may lead to overt reactions and the exacerbation of preexisting chronic inflammatory processes.

Air Pollutants↗
PubMed1983

Mount St. Helens' volcanic ash: hemolytic activity.

Volcanic ash samples from four Mount St. Helens' volcanic eruptions were subjected to mineralogical, analytical, and hemolytic studies in order to evaluate their potential for cytotoxicity and fibrogenicity. Plagioclase minerals constituted the major component of the ash with free crystalline silica concentrations ranging from 1.5 to 7.2%. The in vitro hemolytic activity of the volcanic ash was compared to similar concentrations of cytotoxic and inert minerals. The ash was markedly hemolytic, exhibiting an activity similar to chrysotile asbestos, a known fibrogenic agent. The hemolysis of the different ash samples varied with particle size but not with crystalline silica concentration. The results of these studies taken in conjunction with the results of our animal studies indicate a fibrogenic potential of volcanic ash in heavily exposed humans.

Air Pollutants↗
PubMed1983

Pulmonary response to Mount St. Helens' volcanic ash.

The pulmonary response to a sedimented sample of Mount St. Helens' volcanic ash from the first eruption was studied at 1, 7, 28, 90, and 180 days postintratracheal administration of 1 or 10 mg of ash in specific-pathogen-free rats. One day administration of volcanic ash all animals exhibited a marked inflammatory cell response centered on respiratory bronchioles in which polymorphonuclear leukocytes predominated. At 7 days the reaction was characterized by mononuclear cellular infiltrates. The macrophages within the respiratory bronchioles and alveoli contained intracytoplasmic ash particles. At 28 days the intraalveolar aggregates of mononuclear cells had condensed to form granulomas. Most of the granulomas contained foreign body-type giant cells and some showed central necrosis. The granulomas enlarged in size from 28 days until the termination of the experiment at 180 days with progressive increase in the amount of collagenous tissue. The results of these studies suggest that the volcanic ash may pose a risk for pneumoconiosis in heavily exposed human populations.

Air Pollutants↗
PubMed1983

Pneumoconiosis and lung function in a group of kaolin workers.

In June 1981, 65 current and former workers at a kaolin mine and mill were examined by chest radiography, spirometry, and a questionnaire. Five (13%) of 39 current workers and 3 (19%) of 16 former workers with 5 yr or more of exposure had radiographic evidence of pneumoconiosis. Among the 8 workers with pneumoconiosis, conglomerate upper lobe lesions were present in one half. No pneumoconiosis was observed among 8 current workers with less than 5 yr of exposure. Lung function testing showed significant reductions (p less than 0.05) in FVC, FEV1, and peak flow rate in kaolin workers compared with that in a control group. Environmental sampling during the testing period showed airborne dust to be composed of kaolinite (96%) and titanium dioxide (4%). Additional controlled epidemiologic studies among kaolin workers are needed to generate reliable prevalence data for pneumoconiosis and to assess the impact of dust exposure on pulmonary function.

Adult↗
PubMed1983

Kaolin and the lung.

Explore the source record for details and available documents.

Environmental Exposure↗
PubMed1983

Inhalation studies of diesel exhaust and coal dust in rats.

The preliminary 12-month data of an ongoing two-year chronic inhalation study into the effects of diesel exhaust and coat dust on rats are reported. The study design consists of four exposure regimens: coal dust, diesel exhaust, coal dust plus diesel exhaust, and filtered air (control). Total respirable particulate is being maintained at 2 mg/m3 in all exposure groups. Animals are being serially sacrificed and subjected to immunologic, biochemical, physiological, microbiological, and pathological evaluations. Extracts of diesel emissions showed marked mutagenic activities in the Ames Salmonella his reversion assay. Mutagenic compounds were not however found in the urine of the exposed animals, nor were sister chromatid exchanges detected in peripheral lymphocytes. No changes were observed in cytochrome P450 enzyme activity in lung microsomes of exposed rats. Physiological tests showed no evidence of pulmonary function impairment in any group. Light microscopic examination of the lungs showed dust deposition with the formation of macules in all exposed groups. The preliminary results revealed few pathological effects of significance and no evidence of synergism between diesel exhaust and coal dust.

Animals↗
PubMed1982

Secalonic acid D toxicity in rat lung.

Toxicity of the mycotoxin secalonic D (SAD) was examined histopathologically in rats. Dose response was studied by intragastric and intratracheal instillation, and SAD was given in suspension in Krebs-Ringer phosphate solution at doses well below the reported LD50 values for both rats and mice. A full autopsy was performed on rats sacrificed 1--69 d after instillation. Responses differed markedly depending on the route of administration. Histopathological lesions were observed only in the lungs of rats receiving SAD intratracheally. At 24 h after treatment, the lungs of affected animals showed an acute polymorphonuclear reaction in the distal airways and adjacent alveoli and there was necrosis of airway epithelium. The latter resulted in the development of typical lesions of bronchiolitis obliterans. The initial acute inflammatory response in the peripheral lung became granulomatous at 3 d and the granulomas contained numerous foreign body type giant cells. Between 3 and 7 d the granulomas and bronchiolitis obliterans increased in severity; thereafter they tended to resolve. On termination of the experiment at 69 d there were a few small residual granulomas; however, no significant irreversible pulmonary injury was observed.

Animals↗
PubMedDate not supplied

Does coal mine dust present a risk for lung cancer? A case-control study of U.S. coal miners.

This paper evaluates the relationship between the risk of lung cancer mortality and coal mine dust exposure under control by cigarette smoking status. Two case-control studies based on 317 white male lung cancer mortality cases are presented. A one-to-one matched-case design allows examination of the risk of coal mine dust exposure and cigarette smoking. A two-to-one matched-case design was employed to examine the lung cancer risk of coal mine dust exposure independent of cigarette smoking. Based upon these data, no evidence of a coal mine dust exposure-lung cancer risk was found, although the expected increased risk for lung cancer in cigarette smokers was observed. There was no evidence of an interactive effect between cigarette smoking and coal mine dust exposure.

Coal Mining↗
PubMedDate not supplied

Cigarette smoking and inorganic dust in human lungs.

Whole left lungs from 18 smokers and 16 nonsmokers were obtained at autopsy and studied to determine the severity of subclinical emphysema and elemental dust loads of aluminum and silicon. Lungs selected were from individuals with work histories in non-dusty occupations and were sex- and age-matched by decade. Whole lung Gough sections were studied and emphysema was graded on a 0 to 100 score. Concentrations of aluminum and silicon were determined in homogenized-lyophilized lung of all 34 cases by plasma emission spectrometry. In addition, histological sections from 9 pairs of age-matched smokers and nonsmokers were studied by light microscopy and scanning electron microscopy in concert with semiquantitative x-ray spectrometric analysis of aluminum and silicon content in specific anatomical regions. The results of these studies indicate that aluminum and silicon concentrations increase in smokers with increased cigarette smoking. As expected, severity of pulmonary emphysema was associated with heavy cigarette smoking.

Adult↗
PubMedDate not supplied

Presence of stable coal radicals in autopsied coal miners' lungs and its possible correlation to coal workers' pneumoconiosis.

Stable coal radicals (SCRs) were detected by electron spin resonance (ESR) spectroscopy in the lung tissue of autopsied coal miners. The SCR concentrations were measured in the lung tissues from 98 coal miners with and without (a) coal workers' pneumoconiosis (CWP), (b) cancer, and (c) a history of cigarette smoking. Concentrations of SCRs were also determined in the lungs of nonminer controls. The SCR concentration was related to longer mining tenure, CWP disease severity, lung cancer, and cigarette smoking. The mean concentration of SCRs in the lung tissues of miners with 30 +/- 1.4 y of coal mining exposure was 5.3 +/- 1.3 x 10(17) spins/g versus controls who had a nondetectable level (less than 10(15) spins/g). An increase in disease severity was accompanied by a progressive increase in SCR concentration. A SCR concentration of 4.8 +/- 0.7 x 10(17) spins/g was found for simple CWP (with moderate coal macules) versus 7.8 +/- 4.6 spins/g lung tissue for complicated CWP (with progressive massive fibrosis). Significantly higher (i.e., 10 x 10(17] concentrations of SCR in the coal miners' lung tissues were associated with an exposure history in the anthracite regions of northeastern Pennsylvania. These results indicate a possible role for SCRs in the disease process. Furthermore, ESR appears to be an adequate methodology for the quantitation of coal dust retained in the lung and for distinguishing exposures to anthracite and/or bituminous coal.

Aged↗
PubMedDate not supplied

Roles of epidemiology, pathology, molecular biology, and biomarkers in the investigation of occupational lung cancer.

The pathology and molecular biology of lung cancer demonstrate that these tumors evolve through a series of mutations, molecular changes, and corresponding morphologic changes. To elucidate how occupational and environmental factors influence lung cancer histogenesis it is important not only to understand epidemiology and the interactions between etiologic agents but also to integrate information from pathology, biochemistry and molecular biology. This review focuses on the range of techniques currently available for characterizing lung cancer and how their prudent use can be beneficial in the identification of occupational carcinogens. Because many occupational and environmental lung cancers are caused by multiple etiologic agents, the integration of histology with cellular, biochemical and molecular biomarker techniques may provide new approaches for understanding the disease process.

Biomarkers↗
PubMedDate not supplied

Reactive oxygen species and silica-induced carcinogenesis.

Although silica has recently been designated as a carcinogen, its mechanism of carcinogenesis is not fully understood. Recent studies suggest that free-radical reactions may play an important role in the initiation and progression of cancer. This article summarizes literature on the generation of reactive oxygen species (ROS) directly from silica and from silica-stimulated cells. It also summarizes information concerning the role of ROS in silica-induced DNA damage as well as in silica-induced cell proliferation, including the effects of silica on the activation of nuclear transcription factors, induction of growth factors and oncogene expression, redox regulation of the p53 tumor suppressor gene, induction of apoptosis, and division of damaged cells. Understanding the role of ROS in silica-mediated reactions may help develop therapeutic agents to block silica-induced free radical reactions and thus prevent or attenuate silica-induced carcinogenesis.

Animals↗