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Query: UMLS:C0032273 (pneumoconiosis)
 1,578 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunological abnormalities in 30 patients with asbestosis were investigated by examining the cytoxicity of natural killer (NK) cells and antibody dependent cellular cytotoxicity by killer (K) cells from peripheral blood lymphocytes; the effects of interferon on NK activity was also examined. Fifteen men and 15 women (mean age 58; range 40-72) with asbestosis but who were free of complications such as tuberculosis, carcinoma, or steroid treatment were the subjects for study. There were nine cases of type 1, 19 cases of type 2, and two cases of type 3 disease as described in the ILO classification of pneumoconiosis. They were all textile workers with a mean duration of 18 years (3-40 years) since first exposure to chrysotile. Controls matched for age and sex were selected from a population without occupational exposure to asbestos. The activity of the NK and K cells in patients with asbestosis was significantly lower than in the control group, but the populations of NK and K cells in the peripheral blood lymphocytes were not significantly different in the two groups. An in vitro experiment showed that the increase in the cytotoxicity of the NK cell after treatment with interferon-alpha was significantly lower in the subjects than in the controls. These results indicate that one of the defence mechanisms in relation to cancer is deficient in patients with asbestosis.
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PMID:Reduced killer cell activity of lymphocytes from patients with asbestosis. 397 49

The mortality experience of 5,406 men (cohort I) employed at one aluminum smelter on Jan. 1, 1950, and 485 men employed at a second plant (cohort II) on Jan. 1, 1951, is reported. For each man, the total number of years of exposure to tars, the number of years since first exposure to tars, and an index of exposure to tars expressed in tar-years were calculated. More than 99% of the men in the first cohort and 98% of the men in the second cohort were traced. Of the 1,539 men in cohort I who were deceased as of December 31, 1977, death certificates were obtained for 1,432 (93%). Of the 92 men in cohort II who were deceased as of December 31, 1977, death certificates were obtained for 80 (87%). The results showed that men in cohort I died of the following causes at approximately the same rate as or less frequently than men of similar age in the Province of Quebec: tuberculosis; circulatory disease; hypertensive heart disease; trauma; leukemia and aleukemia; and malignant neoplasms of the pancreas, genital organs, brain, intestine, and rectum and other abdominal areas. There were no deaths from pneumoconiosis or Alzheimer's disease. Although the observed and expected numbers of deaths in some of the cause-of-death categories were small, men in cohort I died of the following causes more frequently than did men of similar age in the Province of Quebec: respiratory disease; pneumonia and bronchitis; malignant neoplasms (all sites); malignant neoplasms of the stomach and esophagus, bladder, and lung; other malignant neoplasms; Hodgkin's disease; and other hypertensive disease. Mortality from malignant neoplasms of the bladder and lung was meaningfully related to numbers of tar-years and of years of exposure. Exposure-response relationships were less clear for malignant neoplasms of the esophagus and stomach and for other malignancies. Mortality from respiratory disease for men with 21 or more tar-years of exposure was approximately twice that of persons never exposed to tars. The apparent excess of other hypertensive disease was restricted to men never exposed to tars. Malignant neoplasm of the lung was the only cause of death in cohort II that was in excess of that expected at Quebec provincial rates.
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PMID:Mortality of aluminum reduction plant workers, 1950 through 1977. 406 80

Silica is not generally considered to be a carcinogen, however, occupations characterized by high exposure to crystalline silica have excessive rates of lung cancer mortality. Respiratory cancer excesses have been reported from North America and from Europe for the following dusty trades in which exposure to silica is a common factor: iron and steel foundry workers, steel casting workers, sand blasters, metal molders, non-uranium miners, and ceramic workers. These findings have been reinforced by two reports from the Swedish Pneumoconiosis Register and the Ontario Ministry of Labor indicating that silicotics have statistically significant risks of lung cancer mortality. Animal studies suggest that silica can be an initiating carcinogen or can act as a cocarcinogen or promoter when combined with benzo(a)pyrene. We propose three candidate hypotheses and two pathways for silicocarcinogenesis.
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PMID:Does occupational exposure to silica cause lung cancer? 630 Dec 70

Cohort studies in three American asbestos factories were undertaken to investigate the effect of fibre type and manufacturing process on lung cancer, mesothelioma, and asbestosis. Reports have been published on a chrysotile textile plant in South Carolina and a mainly textile plant in Pennsylvania, which also used amphiboles. In the third plant in Connecticut friction products and packings were made from chrysotile only. In a cohort of 3641 men employed for one month or more, 1938-58, 3513 (96.5%) were traced, 1267 (36%) had died, and death certificates were obtained for 1228 (96.9%). Individual exposures were estimated (in mcpf . years) from impinger measurements. Life table analyses using Connecticut mortality rates gave an SMR for all causes of 108.5 (USA 107.9). The SMR (all causes) for men who had worked for less than a year was 129.9 and for those who had worked for a year or more, 101.2. The equivalent SMRs for respiratory cancer were 167.4 and 136.7 respectively. Excluding men who had worked for less than a year, there was possible evidence of some increase in risk of lung cancer with increasing exposure, supported also by a "log-rank" (case-control) analysis, of the same order as that observed in chrysotile mining and milling. These findings may be compared with chrysotile textile manufacture where the risk of lung cancer was some 50-fold greater. It is suggested that the differences in risk are perhaps related to the higher proportion of submicroscopic fibres in textile manufacture that may result from the traumatic carding , spinning, and weaving processes. No case of mesothelioma was found, consistent with a much lower risk of this tumour with chrysotile than with amphiboles. Twelve deaths (nine in men with very short and low asbestos exposure) were given ICD code 523 (pneumoconiosis); all but two were ascribed to anthracosilicosis or silicosis and none to asbestosis.
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PMID:Dust exposure and mortality in an American chrysotile asbestos friction products plant. 632 94

The history of pneumoconiosis research in Switzerland from the 16th century to the present day is briefly summarized. The concerns and aims of a silicosis research group founded at the end of World War II by faculty members of Zurich University, Federal Institute of Technology (ETHZ) and by the SUVA (Swiss national accident insurance) are presented. The salient results of interdisciplinary research on the pathogenicity of particle size and fibrogenicity of various mineral and non-mineral dusts are discussed, and related questions of cancer epidemiology are considered.
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PMID:[Pneumoconiosis research in Switzerland in the past and today]. 636 39

This paper reports on the evaluation of 21 epidemiological studies concerning investigations in the Man-Made Mineral Fibers (MMF) industries. First conditions of exposure were described. Concentrations of respirable fibers at the production and further treatment of MMF in older plants were in average about a few fibers per cm3, today in most cases remarkable below 1 fiber/cm3. In the old factories also there has been an exposure with very fine fibers with a diameter below 1 micron and this is comparable from its amount with the conditions nowadays. About 55000 workers exposed to MMF were investigated, most of them handling glass fibers. Several thousands of this workforce had a duration of exposure of 20 years or more and a latency time of 30 years or more. No case of mesothelioma was found. A most of the identified cases of pneumoconiosis could be attached to a prior or a concomitant exposure to silica if the occupational exposure was carefully examined. At the recent time there is no wellfounded suspicion that pneumoconiosis is caused by the exposure in the MMF-industries. A few authors supposed, that unspecific structural changes of the lung as occuring also in a greater amount in dependency of smoking habits and age are found more frequently among the employees of this industry than among the common population. Neither the workers with such unspecific structural changes of the lung nor the other members of the workforces had prejudices of lung function. At present time a risk due to MMF to get sick with cancer of the bronchopulmonic system, especially with lung cancer can neither be proved nor be excluded. The epidemiological studies carried out until now were not capable to point out a possibly existing risk in such a ordner of magnitude. It is uncertain if it will be feasable to prove such a risk by using more subtilized methods. This depends at one side on the possibility of clearing up and registering the confounding risk factors. On the other side it must be considered, that the exposure with fibrous dusts even in the old MMF-factories was very much lower than the exposure in the asbestos-industry. It is indispensable to take into account the most important confounding risk factors (smoking habits, preexposure and concomitant exposure with dangerous working materials) in further epidemiological investigations.
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PMID:[Findings in the bronchopulmonary system of workers employed in the industrial production and processing of synthetic mineral fibers]. 636 2

A historical prospective mortality study was conducted at a nickel company with mines, mills, and a smelter in Ontario, Canada. All men were included in the study who worked for a total of at least 6 months and were employed at some time between 1950 and 1976. Mortality was ascertained and observed number of deaths (O) were compared with expected number of deaths (E), on the basis of the person-years method with the use of rates for Ontario males. There were 804 O compared to 743 E (P less than .001). However, the excess was more than accounted for by the increase in accidental and violent deaths (O = 242; E = 150). Deaths from circulatory diseases and all cancers were roughly equal to E. Laryngeal cancer mortality was significantly increased due to an excess in miners (O = 4; E = 1.00). Lung cancer mortality was somewhat increased (O = 46; E = 37.5); no nasal cancers were observed. Three deaths were due to pneumoconiosis. Sinter plant workers showed a significant increase of cancer deaths (O = 13; E = 6.7; P = .015).
J Natl Cancer Inst 1984 Dec
PMID:A mortality study of 11,500 nickel workers. 659 36

Previous employees of a mining company, engaged in mining of crocidolite at Wittenoom Gorge in Western Australia between 1943 and 1966, have been traced to determine their incidence of asbestos-related diseases. Of 6200 male employees, 220 (3.5%) have developed pneumoconiosis and 26 have developed pleural mesothelioma. No cases of peritoneal mesothelioma have been identified. Prior to 1978, 60 men had died from respiratory cancer other than mesothelioma, compared with 38.25 expected from the mortality experience of all Western Australian males. The incidence of pneumoconiosis and mesothelioma and the mortality from other respiratory cancer all increased with duration of employment, interval from first employment, and level of occupational exposure, indicating a strong relationship between intensity of asbestos exposure and these diseases. The mortality ratio for respiratory cancer, excluding mesothelioma (1.57), was nearly twice that for all nonrespiratory causes of death, suggesting a two-fold increase in mortality from respiratory cancer compared with all Western Australian males. Variation of mortality from respiratory cancer by duration of employment and occupational exposure suggests that at least 30% of respiratory cancer deaths other than mesothelioma may be due to asbestos exposure. The major part of this excess is accounted for by respiratory cancer occurring in men with previously diagnosed pneumoconiosis.
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PMID:The incidence of pneumoconiosis, mesothelioma and other respiratory cancer in men engaged in mining and milling crocidolite in Western Australia. 722 17

The cancer incidence among asbestos workers in the Sennan District and its surrounding of Osaka Prefecture, Japan, and the results of a mass survey in the above area since 1957 were evaluated from view points of epidemiology. During the period from 1953 to 1979, 107 patients with asbestosis were admitted to this Hospital. Twenty-six (24%) of them died of various carcinoma; 21 had lung cancer, 2 pleural mesothelioma and 3 had stomach cancer. Respiratory insufficiency due to pulmonary asbestosis was responsible for 41 deaths (38%). by a cohort survey of the 297 asbestos workers in the same district, 4 cases of lung cancer, and 3 cases of gastric cancer were detected and cases of cohort survey were followed up for 19 years. Fifty-seven (10%) of 556 cases of silicosis and 14 (11%) of 125 cases of pneumoconiosis other than silicosis or asbestosis were found to have lung cancer, but no mesothelioma. These results indicate that lung cancer and mesothelioma are associated more frequently with asbestosis than with non-asbestos pneumoconiosis (p less than 0.001 as tested by chi2-test). The standardized mortality ratio of lung and stomach cancer among the inhabitants of the Sennan District was calculated based on the statistics during the period of 10 years (1968-1977). the ratio of observed death to expected death of both cancers was smaller than 1.1, and there was no significant increase of death of lung and stomach cancer, although the risk of lung cancer tended to increase among male inhabitants. Discussions were made on the problems related to asbestos industry.
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PMID:Asbestos and cancer in the Sennan District of Osaka. 731 84

Over-expression of the c-erbB-2 oncogene-encoded p185 protein product has been implicated in the pathogenesis of a wide variety of human malignancies, including lung cancer. Over-expression of p185 can be detected immunologically by quantification of the extracellular domain of p185 (c-erbB-2 oncopeptide) in extracellular fluid in vitro and in serum in vivo. An enzyme-linked immunosorbent assay (ELISA) for the c-erbB-2 oncopeptide was used to examine banked serum samples of 11 pneumoconiosis patients who subsequently developed lung cancer and serum samples from 11 hospital controls matched for age, sex, ethnic group and smoking as well as 55 unmatched general population controls. The mean serum level for the c-erbB-2 oncopeptide in human neu units/ml in the lung cancer cases (1,756 +/- 549 HNU/ml) was statistically significantly elevated (p < 0.001) in comparison to the mean level in the matched controls (976 +/- 488 HNU/ml) or the general population controls (888 +/- 655 HNU/ml). Defining a positive elevation of the serum c-erbB-2 oncopeptide as any value more than 2 standard deviations above the mean of the matched controls, 64% (7 of 11) of the lung cancer cases were positive compared to 0% (0 of 11) matched controls and 5% (3 of 55) of the unmatched controls. In addition, 4 of the 7 c-erbB-2 oncopeptide-positive cancer cases had positive serum samples prior to the time of disease diagnosis (average = 35 months). These results suggest that serum c-erbB-2 oncopeptide may be elevated at an early stage of pulmonary carcinogenesis and that further prospective study of the utility of this biomarker is warranted.
Int J Cancer 1994 Feb 01
PMID:Detection of increased amounts of the extracellular domain of the c-erbB-2 oncoprotein in serum during pulmonary carcinogenesis in humans. 790 54


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