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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The contributions of several recent reports to the definition of pulmonary effects of PVC dust inhalation are reviewed. Granulomatous reaction, with inclusion of PVC particles in macrophages and histocytes, and associated interstitial pulmonary fibrosis have been found to lead to exertional dyspnoea, diffuse micronodular chest radiographic opacities and restrictive pulmonary dysfunction. The effects of vinyl chloride (VC) monomer (gas) on proteins and the immunologic mechanisms triggered by the altered protein are possible mechanisms for the development in some cases of interstitial pulmonary fibrosis secondary to VC exposure. Vinyl chloride, a confirmed carcinogen, has been associated with, among other malignant tumors, a significant increase in the incidence of lung cancer. The magnitude of this effect has not yet been completely evaluated.
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PMID:Review of pulmonary effects of poly(vinyl chloride) and vinyl chloride exposure. 733 34

The Tyler Asbestos Workers Program is a continuing study of 1,105 former amosite asbestos workers. This report includes a study of six former workers, five of whom died and had autopsies, and one who underwent a lobectomy. Five of these men were exposed to asbestos for three months or less. Four had lung cancer, and one a rectal carcinoma. All were cigarette smokers. Ferruginous (asbestos) body content of the upper and lower lobes of the lungs was quantitated by a digestion technic. Tissue sections from upper and lower lobes were independently quantitated for fibrosis and ferruginous bodies, and chest roentgenograms were examined for interstitial fibrosis. (Control lung tissue was obtained from consecutive autopsies of 52 adults who did not have a known occupational exposure to asbestos.) Relatively low ferruginous body counts (less than 700/g lung tissue) were associated with mild degrees of fibrosis, and higher counts (greater than 10,000/g) with moderate to severe fibrosis. Mild to moderate pulmonary fibrosis could be identified on tissue sections before interstitial changes were detectable by chest roentgenograms.
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PMID:Pulmonary fibrosis, carcinoma, and ferruginous body counts in amosite asbestos workers. A study of six cases. 736 73

Lung cancer was found in 20 (9.8%) of 205 patients with cryptogenic fibrosing alveolitis (CFA) or 12.9% of the 155 patients in this series followed to death. An excess relative risk of lung cancer of 14.1 was found in patients with CFA compared to the general population of comparable age and sex, allowing for the lengths of follow-up of the CFA patients. The relative risk for male smokers was (observed/expected) 15+1.06 = 14.2, and for female smokers (O/E) 2/0.3 = 6.7. Only one male and one female non-smoker had lung cancer. These data suggest that there is an excess risk of lung cancer not wholly accounted for by age, sex, or smoking habit. The distribution of histological types was not obviously different from that found in lung cancer without pulmonary fibrosis. Large opacities suggestive of lung cancer were present at the time of first hospital attendance for symptoms relating to CFA in four of the 20 patients. Finger clubbing was present in 19 (95%) compared with 116/185 (63%) of those so far not developing cancer. There were no other clinical differences at presentation. In particular, cancer was not found especially in those with longer survival from the onset of symptoms of CFA or with a greater initial radiographic change.
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PMID:Cryptogenic fibrosing alveolitis and lung cancer. 743 10

Despite extensive research, the role of the commonly employed tumour markers in the diagnosis of lung carcinoma is yet to be clarified. The utility of a new marker, CYFRA 21-1, in the preoperative evaluation of patients with bronchogenic carcinoma was investigated. CYFRA 21-1 was determined with a radiometric assay in serum of 280 patients with lung cancer and 208 patients with various nonmalignant lung diseases. The levels of the marker were significantly higher in lung cancer patients. Among benign lung diseases, elevated CYFRA 21-1 levels were found in pulmonary fibrosis. Using a cut-off of 3.2 ng.ml-1 (95th percentile of levels obtained in benign lung disease), the total sensitivity of the marker was 48%. The best sensitivity was obtained in squamous cell lung cancer (60%). The highest values of CYFRA 21-1 were found in metastatic lung cancer, and the marker sensitivity was more elevated in stage IIIb and IV. On the other hand, 40% of patients with surgically resectable lung cancer had CYFRA 21-1 levels above the cut-off. We conclude that CYFRA 21-1 may be satisfactorily employed in the differential diagnosis between malignant and benign lung diseases in association with other clinical and radiological data.
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PMID:CYFRA 21-1 as a tumour marker for bronchogenic carcinoma. 754 May 61

The present studies were done to clarify the significance of foamy alveolar macrophages (FAM) in lung diseases, and the mechanism of the production of macrophages in rabbit lungs. Human subjects consisted of 18 normal volunteers (NV) and 47 patients with lung disorders: chronic bronchitis (CB), 7 cases; pulmonary fibrosis (PF), 8 cases; old pulmonary tuberculosis (OPT), 7 cases; lung cancer (LC), 20 cases; and bronchiectasis (BE), 5 cases. In each case, over 30 macrophages in the BALF were observed by transmission electron microscopy. There were no significant differences in the percentage of FAm in the BALF among NV, CB, and PF. Furthermore, OPT and LC were not significantly different. Many more FAM were seen in OPT and LC than in NV, CB, and PF (p < 0.005). The percentage of FAM obtained from BE was much higher than that from OPT and LC (p < 0.005). These results suggest that the grade of foamy change in macrophages differs among lung diseases. Three groups of rabbits were studied. Group I rabbits (n = 6) were control, Group II rabbits (n = 6) underwent bronchial clamping, and Group III rabbits (n = 6) underwent complete replacement of blood with saline. The number of macrophages and type II cells was much greater in Group II rabbits than in Group I rabbits. In Group III rabbits, the number of macrophages was lower than in Group I rabbits. In Group III rabbits, vacuole-like structures were seen in the cytoplasma of type II cells, but not from in macrophages. These findings suggest that anoxia and blood flow are important for the appearance of macrophages in alveolar space. Group III rabbits had few alveolar macrophages. Therefore, alveolar macrophages may be derived from monocytes in blood.
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PMID:[Foamy alveolar macrophages in various lung diseases, and their origin in rabbit lungs]. 756 96

This study was designed to test the hypothesis that the risk of lung cancer from asbestos exposure is confined to persons with radiographic evidence of pulmonary fibrosis. Occupational and smoking histories were obtained from 271 patients with a confirmed diagnosis of primary lung cancer and 678 referents (279 with other respiratory disease and 399 with cardiac disease). Histories were reviewed blind to assess the timing, duration, and probability of exposure to asbestos. To allow for a lag between asbestos exposure and the development of lung cancer, subjects were classified by the time they had spent in an occupation entailing definite or probable exposure more than 15 years before diagnosis. The presence and extent of fibrosis was assessed blindly from chest radiographs by three readers and scored for small opacities with the ILO 1989 International Classification of Radiographs of the Pneumoconioses. 93 (34.3%) cases had worked in an occupation with definite or probable asbestos exposure compared with 176 (25.8%) referents (crude odds ratio for lung cancer 1.49, 95% CI 1.09-2.04). After adjustment for age, sex, smoking history, and area of referral, the odds ratio (95% CI) was 2.03 (1.00-4.13) in the subgroup of 211 with a median ILO score for small parenchymal opacities of 1/0 or more, and 1.56 (1.02-2.39) in the 738 with a score of 0/1 or less (ie, those without radiological evidence of pulmonary fibrosis). These results suggest that asbestos is associated with lung cancer even in the absence of radiologically apparent pulmonary fibrosis.
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PMID:Is lung cancer associated with asbestos exposure when there are no small opacities on the chest radiograph? 767 17

Obstetrician-gynecologists reviewed patient records of women delivering during January 1986-December 1992 to determine the maternal mortality rate and trends and the causes of maternal deaths in the maternity ward at the National University of Singapore. There were 26,173 deliveries and 9 maternal deaths (a maternal mortality rate of 22.9/100,000). The causes of maternal deaths were pulmonary embolism (underlying condition, systemic lupus erythematosus [SLE]), hemorrhage from multiple sites (thrombotic thrombocytopenia), acute exacerbation of SLE with interstitial pneumonitis, pulmonary fibrosis (systemic sclerosis), fulminant hepatitis (prior hepatitis and liver disease), and cerebral embolism (rheumatic heart disease with mitral valve replacement). There were also three incidental maternal deaths bringing the maternal mortality rate up to 34.4/1000. The incidental causes of death included septicemia from perforated peptic ulcer (uncontrolled thyrotoxicosis), multiple metastases from lung cancer, and suicide (family dispute over adoption of newborn). A cesarean section preceded 4 (44%) of the 9 maternal deaths. Two of these deaths were incidental maternal deaths. Cesarean section was related to two of the remaining six (33%) deaths. These findings show that traditional direct causes of maternal death (hemorrhage, sepsis, embolism, or hypertension) were not responsible for the maternal deaths at this tertiary facility. Instead, the women tended to have medical conditions that placed them at high risk of death regardless of pregnancy status.
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PMID:Maternal mortality: evolving trends. 781 Nov 98

The question whether silica is carcinogenic is not new, but there has been a resurgence of research over the last two decades with the use of more powerful epidemiological methodologies. There is sufficient evidence for the carcinogenicity of crystalline silica in animals. A large number of cohort and case-control studies consistently suggest a modest excess of lung cancer in workers with occupational silica exposure (relative risk less than 2). However, in many studies, the association is confounded by exposures to cigarette smoke, and environmental cocarcinogens like radon daughters, polyaromatic hydrocarbons and asbestos. The excess risk of lung cancer is more pronounced in workers with silicosis (relative risk of 2 to 4). Silica may act as a direct carcinogen or indirectly by the adsorption of cocarcinogens such as polyaromatic hydrocarbons from cigarette smoke or industrial pyrolysis products, and/or by impairing pulmonary clearance, thereby increasing the effective dose and duration of exposure to these carcinogens. Pulmonary fibrosis itself may be a precursor to the development of lung cancer.
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PMID:Silica and lung cancer: a continuing controversy. 784 60

Deposition, clearance, retention, and durability of inhaled particles in lung are important factors for induction of pulmonary fibrosis or lung cancer. To study the deposition and clearance of aluminium silicate ceramic fibers from the lung, male Wistar rats were exposed to ceramic fibers, with a mass median aerodynamic diameter (MMAD) of 3.7 microns, for 6 hr/day, 5 days/week for 2 weeks. The average exposure concentration was 27.2 mg/m3 (SD 9.0). The rats were killed at 1 day, 1 month, 3 months, and 6 months after the end of exposure, and the fiber numbers and dimensions were measured with a scanning electron microscope. No significant difference in length of residual ceramic fibers in the lungs was found among the groups. The geometric mean diameter and number of ceramic fibers, however, decreased according to the clearance period. These findings suggest that the fibers were dissolved at their surface.
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PMID:Clearance of inhaled ceramic fibers from rat lungs. 788 24

A range finding study for experimental induction of pulmonary fibrosis in which female Syrian golden hamsters received five subcutaneous injections of 0.8, 0.6, 0.4, 0.2 or 0 mg of N-methyl-N-nitrosourethane (MNUR) once a week or once per two weeks revealed most of the animals of the 0.8 mg group to die of acute pulmonary injury due to MNUR while typical interstitial pneumonia was induced in the 0.6 mg group. Based on these results hamsters were given five subcutaneous injections of 0.6 mg/animal of MNUR once per two weeks and then reared without any treatment for 12 weeks. Marked interstitial edema and intraalveolar infiltration of macrophages due to alveolar capillary damage were seen in treated animals at week 1, and secondary diffuse fibrotic thickening of the alveolar septa, as evidenced by increased type III collagen demonstrated immunohistochemically, was marked thereafter. The content of hydroxyproline in the lung was significantly increased from week 4. The present study indicates that lung injuries attributable to primary damage of alveolar capillaries progress to diffuse alveolar fibrosis in hamsters treated with MNUR, suggesting that this animal model might be of advantage for pathogenetic analysis of the relationship between pulmonary fibrosis and lung cancer development.
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PMID:Experimental induction of pulmonary fibrosis in Syrian golden hamsters by N-methyl-N-nitrosourethane. 789 38


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