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PubMed1984

Cigarette smoke, asbestos, and small irregular opacities.

The long-term inhalation of cigarette smoke is associated with the appearance of diffuse small irregular opacities of mild profusion on chest roentogenograms of some subjects in a limited number of reports. Human histologic and experimental animal studies have shown the presence of pulmonary interstitial fibrosis. The radiographic abnormalities may be explained by interstitial fibrosis, although bronchiolar wall thickening may also be involved. Because asbestos causes diffuse pulmonary fibrosis, the literature was reviewed for evidence concerning an interaction between cigarette smoke and asbestos in the frequency of pulmonary asbestosis. A majority of 14 prevalence studies and 7 cohort studies of asbestos workers with information on smoking habits have shown a positive interaction between the 2 agents. The interaction appears to be additive rather than synergistic. Smoking may exert an effect on the frequency of pulmonary asbestosis by increasing the effective fiber dose retained in the lungs through interference with clearance.

Animals↗
PubMedDate not supplied

A cross-country comparative overview of the asbestos situation in ten Asian countries.

Information about asbestos issues at the national level was compiled for ten Asian countries (China, Indonesia, Japan, Korea, Malaysia, Philippines, Singapore, Taiwan, Thailand, and Vietnam) regarding 1) bans and consumption levels; 2) occupational exposure limits (OELs) and medical follow-up schemes; and 3) statistics and compensation status of asbestosis and mesothelioma victims. Only Singapore and recently Japan have adopted a total ban an asbestos. China, a major producer of chrysotile, showed an increasing consumption trend, which was typical of the less industrialized countries. Considerable differences between countries existed in OELs (0.1 to 5.0 fibers/mL) and medical follow-up of exposed workers. National statistics for asbestosis and mesothelioma were available for only the industrialized countries, where reported cases as well as compensated cases were relatively few. There is need to improve the quality and quantity of information, but the available information attests to unfavorable conditions in the less industrialized countries. Hence the experience of industrialized countries regarding asbestos and its use should be utilized to the fullest to improve the situation worldwide.

Asbestos↗
PubMedDate not supplied

Mining and mendacity, or how to keep a toxic product in the marketplace.

The corruption of medical evidence about the hazards of asbestos began with the Canadian mines. Quebec at one time boasted ten of the 13 mines in Canada. Work conditions in the mines were harsh, and the mills were full of airborne fiber. Given the size of the industry, the Quebec mines were where occupational asbestosis should first have been identified, but research at the mines was done in company towns, where clinics were staffed by company doctors. Since the late 1920s U.S. parent companies and their Canadian subsidiaries have maintained that there is little if any disease among mine workers. Asbestosis in textile workers, they have claimed, has been due to the conditions in that industry and not the inherent dangers of asbestos. That fiction continues to shape the discourse about the usefulness of asbestos.

Asbestos, Serpentine↗
PubMed1980

Clinical observations following asbestos exposure.

There is a spectrum of clinical entities following occupational exposure to asbestos. Methods of evaluation for these problems are reviewed. Nonmalignant clinical conditions include asbestos warts, asbestos bodies, parenchymal fibrosis (asbestosis), pleural fibrosis and calcification, and benign asbestotic pleural effusion. Asbestosis, though a benign process, is a significant cause of death. Malignant conditions associated with asbestos exposure include lung cancer, accounting for about 20% of all deaths among insulation workers and significantly related to cigarette smoking. The lung cancers tend to occur more frequently in the lower lobes and are more peripheral. Pleural and peritoneal mesothelioma and some excesses in gastrointestinal cancers are found with asbestos exposure, although these are not related to cigarette smoking. Increased rates of malignancy first become significant after 20 years from onset of exposure and are also related to duration of exposure. Difficulties with the use of death certificate data are reviewed.

Asbestos↗
PubMed1990

The relationship between fibrosis and cancer in experimental animals exposed to asbestos and other fibers.

The association between occupational asbestos exposure and the development of both pulmonary fibrosis or asbestosis and pulmonary carcinomas is well documented. It has been suggested that the two pathological conditions are associated with asbestos-related carcinomas developing from areas of asbestosis and not occurring when exposure has been too low to produce this type of pulmonary scarring. Experimental inhalation studies so far published have not been designed to examine this association specifically, but many publications have reported that asbestos samples producing high levels of fibrosis is experimental animals are also very carcinogenic. Samples of asbestos or man-made fibers that produce little fibrosis also produce few tumors. These works are reviewed. In order to examine the association between fibrosis and tumor production in more detail, groups of animals with and without pulmonary tumors and with individual fibrosis measurements were assembled from a number of inhalation studies undertaken over a period of years at this Institute. It was found that animals with pulmonary tumors had almost double the amount of pulmonary fibrosis as animals of similar age that did not. In a few of the animals where tumors were found at an early stage of development, their origin from fibrotic areas could be confirmed, although in most cases where tumor deposits were widespread this was not possible. Experimental confirmation of the site of origin of most pulmonary tumors in asbestos-treated rats would require new studies with rats examined specifically at an age when early tumors would be expected.

Animals↗
PubMed2002

The attribution of lung cancers to asbestos exposure: a pathologic study of 924 unselected cases.

We studied a series of 924 nonselected surgical cases of lung carcinoma (without occupational history in clinical records) by histologic examination and light microscopic determination of asbestos body (AB) concentration to determine cancers attributable to asbestos exposure. Lower lobes showed higher concentrations, but no significant associations were recorded between concentrations and histologic type of the lung carcinomas. Histologic asbestosis was demonstrated in 56 cases considered definitely asbestos-related. In 12 of them, the demonstration of asbestosis was attained only after repeated examination of additional sections, suggested by thefinding of more than 1,000 ABs per gram of dry weight (gdw), an indicator of occupational asbestos exposure. In the 56 cases, the media

Air Pollutants↗
PubMed1992

Lymphocyte-macrophage alveolitis in nonsmoking individuals occupationally exposed to asbestos.

A disordered immunologic activity has been observed in humans and animal models of asbestosis and silicosis. To characterize the lung immunologic response following long-term occupational exposure to asbestos, bronchoalveolar lavage (BAL) was performed on 28 nonsmoking individuals. Increased BAL lymphocytes were observed in one third. Lung lymphocytes were predominantly of the CD4+ helper-inducer subtype with increased CD4+/CD8+ ratio and increased surface expression of DR antigen consistent with the activation phenotype. Histologic evaluation of lung tissue from two individuals with lymphocytic-macrophage alveolitis and asbestos exposure revealed an infiltration of alveolar walls with chronic inflammatory mononuclear cells (lymphocytes). Interferon gamma was spontaneously released by BAL cells from 19 (76 percent) of 25 of the individuals with asbestos exposure and only one of ten normal controls. The release of interferon gamma by BAL cells could be further stimulated with concanavalin A and suppressed by cyclosporine. Although asbestosis is characterized by a predominant alveolar macrophage alveolitis, there is a subgroup with lymphocytic alveolitis and activated lymphocytes participating in the inflammatory response, especially in those without respiratory impairment early in the course of the disease process.

Adult↗
PubMed1993

Asbestos-related pleural plaques and lung cancer.

The English-language literature was reviewed to evaluate a possible relationship between asbestos-related pleural plaques and lung cancer in the absence of parenchymal asbestosis. There were six cohort studies in which the comparison group was limited to unexposed persons or the general population, four lung cancer case-control studies, and three autopsy studies. Of the 13 investigations, only 3 supported the hypothesis that lung cancer risk is elevated among persons with pleural plaques over the risk in unexposed people: 2 cohort studies from the same city in England with much the same data and 1 case-control study. These three studies had the most defects in design. The other ten studies failed to confirm the hypothesis. Thus, the weight of the evidence favors the conclusion that persons with asbestos-related pleural plaques do not have an increased risk of lung cancer in the absence of parenchymal asbestosis.

Asbestosis↗
PubMed1994

Pleural plaques and risk for bronchial carcinoma and mesothelioma. A prospective study.

From the general population in the county of Uppsala, Sweden, 1,596 men with pleural plaques fulfilling strict radiologic criteria were identified from 1963 until June 1985. The men have been followed prospectively for 16,369 person-years. The number of mesotheliomas and bronchial carcinomas was compared with the age- and year-specific expected incidence from the official cancer registry of Sweden. Fifty bronchial carcinomas occurred, while 32.1 were expected after correction for smoking habits, a difference which was statistically significant. Patients with radiologic asbestosis were overrepresented among those with bronchial carcinoma. The risk for patients with pleural plaques without asbestosis was increased 1.4 times, which was statistically significant. There were 9 mesotheliomas, while only 0.8 were expected. The mean latency time from first exposure to diagnosis of bronchial cancer was 44.1 years and for mesothelioma was 48.1 years. Thus, pleural plaques on the chest roentgenogram indicate significant exposure to asbestos, with an increased risk for mesothelioma and possibly also for bronchial carcinoma. Any person found to have plaques on chest roentgenogram should be informed of them and should be persuaded to stop smoking.

Adolescent↗
PubMed1995

Do radiographic criteria for emphysema predict physiologic impairment?

OBJECTIVE: The functional consequences of pulmonary emphysema have been estimated from autopsy studies. This antemortem study correlates structure as assessed by criteria applied to chest radiographs and function in earlier disease. SUBJECTS AND METHODS: Four thousand one hundred seven male shipyard and construction workers had chest radiographs scored for asbestosis using International Labour Office criteria and for emphysema using five criteria: hyperlucent lung fields, low flat diaphragms on posteroanterior views, low flat diaphragms on lateral radiographs, a wide retrosternal space, and bullae. Total lung capacity (TLC) was measured by planimetry of radiographs and forced vital capacity (FVC) and flows by spirometry: TLC minus FVC equaled residual volume (RV). All were expressed as percentage of predicted (% pred) adjusted for height, age, and duration of cigarette smoking. Linear regression modeling examined the influence of each emphysema criterion on function measurements. RESULTS: Four hundred three (10.1%) of 4,107 men had two or more emphysema criteria and 24.5% had asbestosis. Prevalence of 2 criteria varied by smoking status and was present in 20% of current smokers, 7.5% of ex-smokers, and 2% of never smokers. The TLC % pred and RV/TLC increased and % pred of FEV1/FVC and FEF25-75, FEV1, and FVC decreased with increasing radiographic emphysema criteria. Forty-four (10%) had normal results of spirometry with two or more radiographic emphysema criteria. CONCLUSION: Impairment of airway function worsened with each additional radiographic criteria of emphysema. These criteria were more strongly associated with an increase in RV/TLC than an increase in TLC.

Asbestosis↗
PubMed1978

Crackles (rales) in the interstitial pulmonary diseases.

There is renewed interest in the classification and methods of recording adventitious pulmonary sounds. This is a study of the importance of fine crackles (rales) in the diagnosis and estimation of the severity of diffuse infiltrative pulmonary disease. Among 272 cases documented by lung biopsy, bilateral fine crackles were heard in 60 percent of those with interstitial pneumonias and asbestosis but in only 20 percent of those with sarcoidosis and other granulomatoses. These incidences were identical in 335 patients diagnosed clinically. In 322 selected ambulatory patients with chronic obstructive pulmonary disease, fine crackles were recorded in only 10 to 12 percent, while coarse crackles were not uncommon in patients with chronic bronchitis. In workers exposed to asbestos, crackles correlated with exposure. In serial studies of such workers, the occurrence of crackles alone appeared to be a random event, while among those with crackles together with one other of five criteria, almost one-half developed asbestosis within four to six years. Fine crackles correlated with pathologic severity, with radiographic honeycombing, and with physiologic abnormalities.

Asbestosis↗
PubMed1980

Presence of asbestos bodies in organs other than the lung.

This study was designed to test the hypothesis that subjects with many asbestos bodies in their lungs at autopsy would also have asbestos bodies in various other organs. The subjects included 19 cases with diagnosis of asbestosis at death (two of these had mesothelioma, five had lung cancer) and 18 with pleural plaques but not asbestosis. Occupational histories were obtained from relatives. In subjects occupationally exposed to asbestos, large numbers of asbestos bodies were found in the lungs, and in most of these, asbestos bodies were found in many of the other organs examined. In the 18 cases with only pleural plaques found at autopsy, considerably fewer asbestos bodies were found in the lungs. The number of other organs with one or more asbestos bodies ranged from 32 percent to 62 percent of the sites examined. The findings seem to confirm the hypothesis of the study.

Aged↗
PubMed1984

Exercise alveolar-arterial oxygen pressure difference in interstitial lung disease.

Abnormality of gas exchange is best evaluated by the exercise alveolar-arterial oxygen pressure difference, P(A-a)O2. We studied the P(A-a)O2 in 168 patients with sarcoidosis, desquamative interstitial pneumonia (DIP), usual interstitial pneumonia (UIP), berylliosis, and asbestosis who were seen for clinical and disability consultations. The increase of P(A-a)O2 with exercise was greatest in UIP (mean 16 mm Hg), least in sarcoidosis (mean 1 mm Hg), and intermediate in DIP, berylliosis, and asbestosis (means 9, 9, and 7 mm Hg, respectively). The increase was best predicted by the single breath diffusing capacity (Dsb), and it occurred in patients with sarcoidosis and DIP if the Dsb was less than 50 percent predicted and in patients with the other diseases if the Dsb was less than 70 percent predicted. However, the magnitude of the increase could not be predicted from resting tests, even when multilinear regression equations were used. We conclude that for clinical evaluation of patients with interstitial lung disease, the exercise test with arterial blood gas measurement adds important information if the Dsb is less than 70 percent predicted. For disability evaluation, the invasive exercise study may be helpful when there is a wide discrepancy between clinical findings and resting physiologic studies.

Adult↗
PubMed1989

Gallium lung scanning and bronchoalveolar lavage in crocidolite-exposed workers.

Gallium lung scanning is widely used to evaluate pulmonary inflammation in patients with interstitial lung disease but has not previously been reported in crocidolite-exposed workers. In order to characterize the pulmonary inflammation caused by crocidolite inhalation, GLS and BAL findings were related to chest x-ray film changes graded according to the ILO classification of roentgenograms of pneumoconioses. In individuals with roentgenographic evidence of asbestosis (CXR greater than or equal to 1/0, n = 15), 13 had a positive GLS and 13 had an abnormal BAL. In asbestos-exposed individuals with equivocal chest x-ray film changes (CXR 0/1, n = 12), six had a positive GLS and six had BAL changes (both GLS and BAL abnormal in three). In individuals with a normal chest x-ray film (CXR 0/0 n = 8), two had a positive GLS and two BAL changes (both abnormal in 1). These data demonstrate that most subjects with crocidolite-induced asbestosis have an abnormal GLS and BAL. In addition, many individuals with asbestos exposure and equivocal or no chest x-ray film changes have an abnormal GLS and/or BAL, suggesting the presence of active subclinical pulmonary inflammation in these individuals.

Asbestos↗
PubMed1999

A historical cohort mortality study of workers exposed to asbestos in a refitting shipyard.

To investigate the risks of developing asbestos-related diseases we conducted a historical cohort mortality study on 249 ship repair workers (90 laggers and 159 boiler repairers) in a single U.S. Navy shipyard in Japan. We successfully identified the vital status of 87 (96.7%) laggers and 150 (94.3%) boiler repairers, and, of these, 49 (56.3%) and 65 (43.3%) died, respectively, during the follow-up period from 1947 till the end of 1996. Our in-person interviews with some of the subjects clarified that asbestos exposure was considered to be substantially high in the 1950-60s, decreased thereafter gradually but remained till 1979 in the shipyard. The laggers, who had handled asbestos materials directly, showed a significantly elevated SMR of 2.75 (95% C.I.: 1.08-6.48) for lung cancer. The risk developing the disease was greater in the laggers after a 20-year latency (SMR = 3.42). Pancreatic cancer yielded a greater SMR than unity (7.78, 90% C.I.: 2.07-25.19) in a longer working years group. Four laggers died from asbestosis. The boiler repairers, who had many chances for secondary exposure to asbestos and a few for direct exposure, showed no elevation of the SMR of lung cancer overall, but there was a borderline statistically significant SMR of 2.41 (90% C.I.: 1.05-5.45) in a longer working years group. One boiler repairer died from mesothelioma and four from asbestosis.

Adult↗
PubMed2001

Epidemiology of occupational asbestos-related diseases in China.

In 1950s and 60s, asbestosis had been a major health hazard for asbestos exposed workers. In the late 1970s, lung cancers with or without asbestosis were found among asbestos workers. All cohort studies on asbestos workers and on chrysotile miners in China showed excess deaths from lung cancer. In a large scale of cohort study on asbestos workers, a synergistic effect was found between cigarette smoking and asbestos exposure in the production of lung cancer. There have been not so many cases of malignant mesotheliomas reported, so far. In the cohort of chrysotile miners, 4 cases of pleural mesothelioma were observed. In the large scale of cohort study on asbestos workers in 9 factories using only chrysotile only one case of pleural mesothelioma was detected for 10 years' observation. In another 2 cohort studies, 2 cases of peritoneal mesotheliomas were found, one in Shanghai asbestos factory where a small amount of crocidolite had been used in 1960s, and one in Anqing asbestos factory that was located near tremolite mine. Further study is needed especially for the relationship between exposure to Chinese chrysotile and malignant mesotheliomas.

Asbestos↗
PubMed2003

Clinical study of asbestos-related lung cancer.

We analyzed the characteristics of 120 patients of primary lung cancer supposed to be induced by exposure to asbestos. Most of 120 patients were male and the age ranged from 47 to 87 years with a median of 70 years. No particular tendency was observed in the histological types of the lung cancer in 120 patients. Forty of the 120 patients were heavy smokers. When the occupational history was analyzed, most of the patients had been exposed to asbestos in former Japanese naval shipyard, commercial shipyards, construction industry and ironworks. The term of asbestos exposure was 2 to 60 years with a median 27 years. Lung cancers appeared after 15 to 69 years with a median 43 years from the initial exposure to asbestos. Lung cancer was accompanied by asbestosis in 35 patients and by pleural plaques in 77. Twenty-two patients had both asbestosis and pleural plaques. The number of asbestos bodies per 5 g wet lung tissue for 72 patients whose lung tissues obtained from autopsy or surgery was more than 150 bodies which meant the number of occupational asbestos exposure. As for the kinds of asbestos fibers of 32 patients, 14 patients exposed to crocidolite, 10 patients to amosite and 8 patients to chrysotile.

Age of Onset↗
PubMed1986

Asbestos related interstitial pneumonitis associated with glomerulonephritis and lymphomatoid granulomatosis.

We report a case of pulmonary asbestosis in a patient who also developed glomerulonephritis and lymphomatoid granulomatosis. The pulmonary reaction was unusual, characterized clinically by an acute onset of symptoms after a prolonged latent period and morphologically by an interstitial pneumonitis with prominent desquamative features and a paucity of fibrosis. The association of pulmonary asbestosis with glomerulonephritis and lymphomatoid granulomatosis has been hitherto unreported.

Asbestosis↗