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Biomedical subjects

A Churg

Publications and source records attributed to A Churg.

At least 109 records · Page 6Linked to original sources
PubMed1988

Direct enhancement by cigarette smoke of asbestos fiber penetration and asbestos-induced epithelial proliferation in rat tracheal explants.

Tracheal explants from Sprague-Dawley rats were briefly exposed to cigarette smoke or air (control) and then to amosite asbestos. Asbestos fibers in or under the tracheal epithelium were counted and extent of hyperplastic lesions was ascertained at 24 hours, 72 hours, and 1 week after exposure. Smoke-exposed cultures showed significantly greater numbers of fibers in the epithelium and greater proliferative activity compared to findings in cultures not exposed to smoke. These observations indicate that very short exposure to cigarette smoke can directly affect the response of the epithelium to asbestos fibers and that smoke exposure need not be concurrent with asbestos exposure for such event to occur. These reactions may play a role in the greater incidences of lung cancer and asbestosis seen in asbestos-exposed workers who smoke.

Animals↗
PubMed1988

Malignant peritoneal mesothelioma after remote abdominal radiation.

Peritoneal mesothelioma in a 61-year-old man, occurred 26 years after abdominal radiotherapy for a testicular seminoma. The patient had no history of asbestos exposure. After asbestos, radiation is the second most frequent defined cause of mesothelioma in North America, but the number of well-documented cases is small; this case represents only the fifth example of peritoneal mesothelioma after therapeutic irradiation of the abdomen.

Combined Modality Therapy↗
PubMed1988

Association of lung cancer and airway particle concentration.

Using 15 autopsy lungs containing nonresected lung cancers, we evaluated the exogenous mineral particle content of the upper and lower lobe parenchyma and of the upper and lower lobe bronchial mucosa. The bronchial mucosa from the lobe with the cancer was found to contain about three times the median mineral particle load of the bronchial mucosa from the lobe without the cancer, a statistically significant difference. No such difference was seen for mineral content of the parenchyma. This observation suggests that mineral particle deposition or accumulation in the bronchial mucosa may be related to respiratory carcinogenesis.

Adult↗
PubMed1988

Effects of cigarette smoke on tissue uptake and retention of iron oxide in the guinea pig.

We have previously shown that cigarette smoke increases retention and tissue penetration of asbestos, a pathogenic dust. To determine whether these same phenomena occur with an inert dust, we administered iron oxide particles to guinea pigs by intratracheal instillation. Half of the animals were exposed to cigarette smoke. Animals were killed at 1 day, 1 wk, and 1 month. Numbers of particles in airway epithelia and walls were counted in histologic sections of one lung, and the other lung was analyzed chemically for iron content. In both smoke-exposed and nonexposed groups, the chemically determined concentration of iron in the lung tissue decreased between 1 day and 1 month; however, the concentration of iron was significantly greater in the smoke-exposed group at 1 day and 1 wk. By 1 month, there was no significant difference between the 2 groups. The number of particles in the epithelia of respiratory bronchioles also decreased in both smoke-exposed and nonexposed groups between 1 day and 1 month, but the smoke-exposed group had significantly more intraepithelial particles at 1 day and 1 wk than did the nonexposed group. The number of particles in the walls of respiratory bronchioles increased between 1 day and 1 month in both smoke-exposed and nonexposed groups; the difference between these groups was significant only at 1 wk, when airway walls of the smoke-exposed animals contained more particles.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Quartz but not iron oxide causes air-flow obstruction, emphysema, and small airways lesions in the rat.

Recent epidemiologic studies have suggested that some workers exposed to inorganic dusts develop air-flow obstruction independent of or greater than that produced by cigarette smoke; the morphologic basis of this effect is unknown. To investigate this problem, we administered saline alone, 10 mg iron oxide (an inert dust), or 10 or 30 mg of quartz to rats by intratracheal instillation. Animals were killed after 30 days, and pulmonary function and morphologic changes were examined. The iron oxide group was similar to the saline control group in all functional and morphometric parameters. However, both quartz-exposed groups showed evidence of air-flow obstruction, with more severe abnormalities in the high dose group. These findings correlated with morphometric observations of emphysema and thickened airway walls, with changes again more severe in the high dose group. Early silicotic nodules were also present in the latter animals. We conclude that in addition to the classic lesions of nodular silicosis, quartz can produce morphologic and functional changes of air-flow obstruction; no such changes are seen with iron oxide. These observations may explain the air-flow obstruction seen in workers exposed to mineral dusts.

Airway Obstruction↗
PubMed1988

Chrysotile, tremolite, and malignant mesothelioma in man.

The question of whether chrysotile asbestos ever causes mesothelioma in man has become a major public and occupational health issue. Review of the literature suggests that only 53 acceptable cases of chrysotile-induced mesothelioma have ever been reported; of these, 41 cases have occurred in individuals exposed to chrysotile mine dust, all of it naturally contaminated with tremolite. Ten cases have occurred in secondary industry workers, but here the suspicion of amosite or crocidolite contamination is high. Analysis of lung asbestos content indicates that induction of mesothelioma by chrysotile requires, on average, as great a lung fiber burden as induction of asbestosis by chrysotile, whereas amphibole (amosite or crocidolite)-induced mesotheliomas appear at a several hundred-fold smaller lung burden. Tremolite alone has definitely produced mesothelioma in man, particularly when exposure has been to long, high aspect ratio, fibers. Analysis of tremolite:chrysotile fiber ratios in human lung suggests that some, but not all tremolite is removed in milling chrysotile ores. The low incidence of mesothelioma in secondary chrysotile users may reflect the small amount of tremolite left in the product. These observations indicate that although chrysotile asbestos can produce mesothelioma in man, the total number of such cases is small and the required doses extremely large. The data are consistent with the idea that mesotheliomas seen in chrysotile miners and some secondary industry workers are produced by the tremolite contained in the chrysotile ore, but that the short length and low aspect ratio of the tremolite make its carcinogenicity quite low. However, these data are very indirect, and a role for the chrysotile fiber itself is still possible.

Asbestos↗
PubMed1988

Environmental pleural plaques in residents of a Quebec chrysotile mining town.

We report four cases of pleural plaques found at autopsy in individuals who resided in or near the chrysotile mining town of Thetford Mines, Quebec, and who had never been employed in the chrysotile mining and milling industry. Three of these patients were farmers, and one was a road construction worker. Lung asbestos content of these cases was compared with that of a group of nine persons living in the same vicinity who did not have pleural plaques. The plaque group was found to have an equal chrysotile content but about a fourfold elevation in median tremolite content, a statistically significant increase. Fiber sizes were the same in both groups. Also, one plaque case had an elevated level of relatively long titanium oxide fibers. These observations suggest that environmental pleural plaques in this region of Quebec are probably caused by exposure to tremolite derived from local soil and rock and that other types of mineral fibers such as titanium oxide may occasionally also be the cause of such lesions.

Aged↗
PubMed1988

Cigarette smoke potentiates asbestos-induced airflow abnormalities.

It has been suggested that exposure to both asbestos and cigarette smoke can produce worse parenchymal lung disease than exposure to asbestos alone. Using a guinea pig model of asbestos administration that produces primarily airway disease and associated airflow abnormalities, we showed previously that the combination of asbestos and smoke acts synergistically to produce more marked increases in tissue collagen, fibrosis of airway walls, and early interstitial fibrosis than are seen with asbestos alone. To investigate the functional effects of these morphological and biochemical abnormalities, pulmonary function tests for volumes and flows, including lung volumes, pressure-volume curves, and flow-volume curves, were performed. By themselves, both smoke and asbestos produced increases in total lung capacity (TLC), residual volume (RV), and functional residual capacity (FRC); the two agents together made all these changes worse than either one alone. Both smoking and asbestos moved the pressure-volume curve upward, and the effects of the two agents together were again greater than either alone. Similarly, both smoke and asbestos decreased flows, and the two agents produced more severe impairment than either one by itself. The changes in volumes, pressure-volume curve, and flows correlated with both increased thickness of small airway walls and increases in airspace size. These observations indicate that, at least in this guinea pig model, cigarette smoke can potentiate the functional consequences of asbestos exposure.

Asbestos↗
PubMed1988

Clearance of chrysotile asbestos from human lung.

In contrast to amphibole asbestos, chrysotile asbestos fails to accumulate in human lungs. The reason for this phenomenon is not known. To examine this problem, we extracted chrysotile and tremolite fibers from the lungs of 11 chrysotile miners and millers whose last exposure was within 2 years of death and 12 chrysotile miners and millers whose last exposure was greater than 12 years (7 with last exposure 12-15 years and 5 with last exposure 22-25 years) before death. Fibers were extracted by bleach digestion, and concentrations, compositions, and sizes were determined by analytical electron microscopy. Native UICC Canadian chrysotile was used as a composition standard. Compared to the standard, there was minor loss of magnesium at 2 years and additional very slight loss after 12 years. The ratio of chrysotile to tremolite concentration did not change with time. There was also no evidence of increasing fiber length with time from last exposure. These data indicate that accumulation of amphibole compared to chrysotile in human lungs does not reflect either long-term dissolution of chrysotile or long-term preferential clearance of chrysotile compared to amphibole. Contrary to results of animal studies, fiber length in humans does not increase with time since last exposure. These findings imply that the failure of chrysotile to accumulate in human lungs reflects events that occur early after exposure rather than long-term clearance mechanisms.

Aged↗
PubMed1988

Significance of crystalline inclusions in lung granulomas.

We describe six examples of nonnecrotizing lung granulomatosis in which there were numerous polarizable crystalline inclusions. The crystals were easily visible in routine H&E-stained slides and were so prominent that the question of a pneumoconiosis or other exogenous source was raised. There was no clinical history to suggest an inhalational source, however, and no patient used intravenous drugs. In one case, an atypical mycobacterial infection was proven to be etiologic, while sarcoidosis was documented in three. A review of 63 additional consecutive lung biopsies and 24 extrapulmonary biopsies showing nonnecrotizing granulomatous inflammation demonstrated crystals in almost two-thirds of cases. X-ray spectroscopy and histochemistry demonstrated that the crystals contained mainly calcium oxalate and calcium carbonate and thus represented products of cellular metabolism. These findings emphasize that crystalline inclusions are common in lung granulomas of varying etiology. They may be numerous, and their presence does not necessarily indicate a pneumoconiosis or other exogenous source.

Adult↗
PubMed1988

Pleuropulmonary disease during bromocriptine treatment of Parkinson's disease.

Pleuropulmonary disease has been observed in eight patients with Parkinson's disease treated with bromocriptine or its related compound, mesulergine. The pleuropulmonary changes included pleural effusions, pleural thickening, and parenchymal lung disease. The patients developed symptoms from nine months to four years after starting treatment with bromocriptine that varied in dosage from 22 to 50 mg daily, while the patient receiving mesulergine was taking 6 mg daily. No other cause was found for the pleuropulmonary changes. In six patients the medication was discontinued with subsequent clinical, physiologic, and radiologic improvement. In two patients bromocriptine treatment was continued for one to two years, and in one patient there was further physiologic and radiologic progression of the pleuropulmonary changes. These findings suggest a causal relationship between bromocriptine treatment and pleuropulmonary disease. We recommend a chest roentgenogram and pulmonary function evaluation prior to bromocriptine treatment with follow-up studies if the patient develops respiratory symptoms. Physicians prescribing bromocriptine should be aware of this side effect to ensure early recognition and prompt withdrawal of bromocriptine therapy.

Aged↗
PubMed1987

Accumulation of long asbestos fibers in the peripheral upper lobe in cases of malignant mesothelioma.

Animal studies suggest that mesothelioma is most effectively induced by fibers longer than 8 mu. However, studies of asbestos fibers recovered from human lungs in cases of mesothelioma indicate that, at least in large-scale samples, relatively few fibers meet this size criterion, perhaps implying that the animal data do not apply to man. Since asbestos concentration in lung is known to be extremely inhomogeneous, it is also possible that long fibers may selectively accumulate in specific sites, such as under the pleura. To examine this possibility, we selected ten cases of mesothelioma that contained relatively large amounts of amosite asbestos and extracted fibers from an 0.5-cm-thick strip of subpleural tissue and an area 3-cm deep to the subpleural sample for upper and lower lobes. Amosite fibers were identified and sized by electron microscopic techniques. Fibers in the peripheral upper lobe were significantly longer, broader, and of higher aspect ratio than those in the central upper lobe. The lower lobe showed a reverse pattern, with longer fibers and broader fibers in the central sample. These data indicate that the two lobes behave differently in regard to fiber size, with selective accumulation of long fibers in the peripheral upper lobe, but not in the peripheral lower lobe. Whether these differences reflect differences in initial deposition of fibers within the lung, or, more likely, specific redistribution of fibers, is unclear, but in either case, accumulation of long fibers immediately under the upper lobe pleura may be important in the genesis of mesothelioma.

Asbestos↗
PubMed1987

Types, numbers, sizes, and distribution of mineral particles in the lungs of urban male cigarette smokers.

We analyzed the exogenous mineral particle concentration, size, type, and distribution for particles larger than 0.1 micron in the left lungs of 10 long-term male cigarette smokers. The mean number of particles found was 465 +/- 295 X 10(6)/g dry lung, of which 80% were kaolinite, micas, feldspars, free silica, and talc. Lead particles were extremely rare, despite their ubiquity in urban air. Overall there were no differences in particle concentration in upper vs lower lobes or central vs peripheral sampling sites. However, a significant correlation was found for upper lobe (r = 0.68), but not lower lobe (r = 0.08), particle concentration and amount of cigarette smoking. Overall, the geometric mean particle size was 0.6 +/- 2.1 microns; 56% of the particles in the upper lobes were larger than 0.75 micron in diameter, compared to 17% in the lower lobes, and the mean upper lobe particle size was greater than the mean lower lobe particle size for all individual mineral types. There was a remarkable homogeneity of mean particle size from patient to patient (mean intercase arithmetic particle size +/- SD of 0.8 +/- 0.1 micron). Particle size was not affected by the amount of smoking. We conclude that contrary to some published acute deposition data, there are no long-term differences in upper vs lower lobe particle concentration; total upper lobe particle retention is influenced by the amount of smoking as measured by pack-years, whereas total lower lobe particle retention appears to be independent by the amount of smoking; particles retained in the upper lobe are somewhat larger than those retained in the lower lobe, but the amount of smoking does not appear to influence retained particle size; the size of long-term retained particles most likely reflects largely atmospheric particle burden; and in the absence of overwhelming dust loads, the lung is able to regulate retained particle concentration and size in a fairly narrow range.

Health↗
PubMed1987

Immunohistochemistry of meningiomas including the angioblastic type.

Immunohistochemical techniques were used to determine the intermediate filament content of normal arachnoidal cells, meningiomas (including the so-called hemangiopericytoma of the meninges), soft tissue hemangiopericytoma, and the normal pericyte. Arachnoid granulations and all types of meningioma stained similarly: positive for vimentin and variably positive for keratin. Soft tissue hemangiopericytomas and normal pericytes were negative for both vimentin and keratin. This suggests that the "hemangiopericytoma" of the meninges is a variant of meningioma and not of pericytic origin.

Arachnoid↗
PubMed1987

Aluminum-induced pulmonary fibrosis: do fibers play a role?

A 50-yr-old man with a history of 19 yr of work in the aluminum smelting industry, including 14 years in the potrooms, was found to have diffuse interstitial fibrosis, slightly more severe in the upper zones. He died of respiratory insufficiency 5 yr after initial presentation. Analysis of lung by electron optical techniques revealed 15,000,000,000 nonfibrous particles and 1,300,000,000 fibrous particles of aluminum oxide/g dry lung, values representing approximately a 1,000-fold increase over background exposure. The nonfibrous particles had a geometric mean diameter of 0.4 mu, and the fibers had a geometric mean length of 1.0 mu, a width of 0.06 mu, and an aspect ratio of 16. X-ray diffraction demonstrated alpha but not gamma aluminum oxide. These studies indicate that previous suggestions relating aluminum-induced fibrosis to the presence of gamma aluminum oxide are not correct. Although pulmonary fibrosis in this case may be a response to a very high total aluminum particle burden, the presence of large numbers of fibers raises the possibility that fibers play a role in aluminum fibrosis.

Aluminum↗
PubMed1987

Cigarette smoke makes airway and early parenchymal asbestos-induced lung disease worse in the guinea pig.

In order to assess the effects of cigarette smoke and asbestos exposure, we divided guinea pigs into 4 groups: smoking or nonsmoking, and asbestos-exposed or not asbestos-exposed groups. Asbestos-exposed animals were given a single intratracheal instillation of 5 mg UICC amosite, a dose and method of administration that we have previously shown produces morphologic changes in the small airways as well as minimal interstitial fibrosis. Animals were smoked 5 days per week for 6 months. By itself, smoking did not affect lung collagen content, small airways wall thickness, or the volume fraction of tissue surrounding airways, but it did cause a significant increase in alveolar mean linear intercept (Lm). Asbestos alone increased collagen content, airway wall thickness, and tissue volume fraction surrounding airways, the latter measure used to assess interstitial fibrosis. An unexpected finding was that asbestos also increased Lm. The two agents administered together caused more severe changes of all types than were produced by either agent alone, and the interaction between the 2 was generally synergistic. Smoke-exposed animals retained 3 times the asbestos fiber burden of those not smoke-exposed; the increase in retention was greater for short than for long fibers. We conclude that cigarette smoke can potentiate the fibrosis induced by asbestos, possibly because of increased fiber retention. As well, in this model, asbestos or asbestos plus cigarette smoke produces increases in alveolar size.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗