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PubMed1998

Progression of asbestosis predicts lung cancer.

STUDY OBJECTIVES: To explore whether the progression of asbestosis correlates with the risk of lung cancer among patients with asbestosis. DESIGN: A group of 85 asbestosis patients (78 men and 7 women) were radiographically followed up between 1979 and 1987. Two or three posteroanterior radiographs taken from each patient in 1978 to 1979, 1983 to 1984, and 1986 to 1987 were classified according to the International Labour Office 1980 classification and were used to divide the patients into progressors and nonprogressors. Follow-up for cancer was done automatically through the files of the Finnish Cancer Registry from the time of determination of the progression status to December 31, 1994. Predictors of lung cancer risk were studied with a logistic regression model, and the standardized incidence ratio (SIR) was calculated for lung cancer. RESULTS: Of the 24 male patients with progressive small opacity profusion, 11 (46%) developed lung cancer, as opposed to 5 (9%) of the 54 male patients without progression. The SIR for lung cancer was 37 (95% confidence interval, 18 to 66) for the progressors and 4.3 (1.4 to 9.9) for the nonprogressors. In both groups, all the lung cancer cases occurred among smokers or ex-smokers. None of the seven female patients showed progressive small opacity profusion. One of them developed lung cancer. In the logistic regression model including all 85 asbestosis patients, radiographic progression of small opacity profusion (p=0.0009) and current smoking (0.0021) were significant predictors of lung cancer morbidity. CONCLUSIONS: Asbestosis patients with radiographic progression of small opacity profusion over a few years are at a higher risk of lung cancer than those with a less aggressive course of the disease. The progression of pulmonary fibrosis may be an independent risk factor that, in addition to smoking history and the intensity of asbestos exposure, could be used to estimate lung cancer risk.

Adult↗

PubMed1985

Asbestosis. Bronchoalveolar lavage fluid proteins and their relationship to pulmonary epithelial permeability.

We measured levels of albumin and immunoglobulins in serum and bronchoalveolar lavage (BAL) fluid in 28 men with asbestosis and 11 control subjects. The half-time clearance of inhaled diethylene triamine pentacetate labelled with technetium-99m (99mTc-DTPA) from the lungs (t1/2LB) was measured in 26 patients with asbestosis and in 31 normal nonsmoking controls. In those individuals in whom immunoglobulins were detected in BAL fluid, the mean IgG:albumin ratio in BAL fluid was 0.30 (range, 0.11 to 0.97), significantly less than the ratio of 0.43 (0.28 to 0.66) in control subjects (p less than 0.05). There was no significant difference in IgA:albumin ratios between patients and control subjects. The mean BAL:serum albumin ratio in patients with asbestosis was 2.3 X 10(-3) (range, 0.2 to 9.5 X 10(-3), significantly greater than the ratio of 1.2 X 10(-3) (0.5 to 2.0 X 10(-3] in control subjects (p less than 0.02). The t1/2LB was significantly shorter in both smokers and nonsmokers with asbestosis, compared with 31 normal nonsmoking controls, but there were no relationships between t1/2LB and BAL:serum albumin ratio or any other BAL protein levels in either smokers or nonsmokers with asbestosis.

Adult↗

PubMed1989

The discriminatory value of the P(A-a)O2 during exercise in the detection of asbestosis in asbestos exposed workers.

Asbestosis is commonly associated with abnormalities of gas transport but since most asbestos workers are smokers and smokers also commonly have abnormalities in P(A-a)O2, the actual specificity and sensitivity of the P(A-a)O2 has been unknown. The P(A-a)O2 was measured at rest and exercise in 92 asbestos-exposed patients. These patients were divided into five groups based on their x-ray and pulmonary function status; normal, CAO, CAO and pleural disease, pleural disease alone and asbestosis with or without CAO. The P(A-a)O2/VO2(mm Hg)/L of O2 was the most discriminatory measurement of gas transport between groups, with mean values of 14.45 +/- 9.24 for normal, 19.04 +/- 10.52 for CAO, 16.85 +/- 8.94 for CAO and pleural disease and 34.07 +/- 21.54 for asbestosis with or without CAO. The P(A-a)O2/VO2 was of high specificity if greater than 35 mm Hg/L of O2 with only two out of 65 patients without asbestosis being considered abnormal. It was of low sensitivity in that only nine out of 27 patients with asbestosis would be detected if this were the sole criterion for diagnosis.

Asbestosis↗

PubMed1995

CT for asbestosis: value and limitations.

CT is more sensitive than clinical evaluation for the detection of asbestosis but is inevitably less sensitive and less specific than pathologic evaluation. For the asbestos-exposed individual, CT is useful for the evaluation of suspected lung masses, particularly rounded atelectasis [15], for identifying pleural plaques, and for confirming unequivocal asbestosis (grade 2 or grade 3 [8]). CT also will identify and quantify emphysema as a cause of physiologic impairment. Because clinicians commonly use CT to resolve clinical uncertainties, radiologists often feel pressured to categorize disease as unequivocally present or absent. Gamsu et al. [8] show that the borderline between normal and abnormal is not always sharply defined. In the absence of pathologic proof, the diagnosis of asbestosis must be based on a thoughtful evaluation of the likelihood of asbestosis by use of all available clinical, physiologic, and radiologic information. The scoring systems used by Gamsu et al. [8] offer a practical approach to defining the likelihood of asbestosis based on CT appearances.

Asbestosis↗

PubMed1997

Asbestosis: clinical spectrum and pathogenic mechanisms.

Asbestosis is a diffuse pulmonary fibrotic process caused by the inhalation of asbestos fibers. Despite extensive investigations, the precise mechanisms regulating asbestos-induced lung damage are not fully understood. This review summarizes the important clinical manifestations and pathogenic mechanisms of asbestosis. We focus on the relatively new information that has emerged over the last several years. The diagnosis of asbestosis is often easily established by well-characterized criteria. Pulmonary physiologic testing and high-resolution computed tomography can detect clinically occult disease. The finding of asbestos bodies in the bronchoalveolar lavage fluid confirms that an individual has been exposed to asbestos but is of unclear significance in diagnosing asbestosis. Evidence reviewed herein suggests that asbestos pulmonary toxicity is due in part to the physical properties of the fibers, iron-catalyzed reactive oxygen species (ROS), and macrophage-derived cytokines and growth factors. Special emphasis is given to the hypothesis that iron-catalyzed hydroxyl radicals (HO.-) have a pivotal role in causing asbestosis. Definitive proof of this hypothesis is difficult to obtain since HO.- are highly reactive and their deleterious effects to cells may have occurred years prior to disease presentation. Despite these limitations, considerable data firmly support the notion that ROS have an important role in causing asbestos toxicity. Further, the iron content of asbestos or the redoxactive iron associated with or mobilized from the surface of the fibers is important in generating HO.- as well as in activating inflammatory cells. There also appears to be a close association between asbestos-induced ROS production and cellular toxicity and DNA damage. The full expression of asbestos-induced diseases likely involves the contribution of cytokines, growth factors, proteases, and other inflammatory cell products. Many of the mechanisms by which asbestos- and inflammation-induced ROS activate specific genes in pulmonary cells remain to be elucidated.

Asbestosis↗

PubMed1990

A study on the dose-response relationship between asbestos exposure level and asbestosis among workers in a Chinese chrysotile product factory.

The dose-response relationship for asbestos exposure in a chrysotile product factory was studied. The past gravimetric dust concentration values, obtained from different worksites, were converted into fiber concentration values according to conversion factors that were worked out by simultaneous sampling in this study. The conversions were made so that exposure could be expressed in fiber-years (f-yr). Asbestosis was diagnosed on the basis of chest radiographs and occupational histories. Cumulative dust exposure (f-yr) was calculated up to the date of diagnosis for asbestosis patients, and up to September 1982 for the remaining workers. A dose-response relationship expressed as fiber-years exposed vs cumulative prevalence of asbestosis was established by the life table method on the basis of these data. Predicted 3 and 1% prevalence of asbestosis corresponded to 43 and 22 f-yr exposure, respectively. Considering that a worker can work for 35 years, these doses are commensurate with dust concentrations of 1.22 and 0.63 f/ml, respectively. It is recommended that 1 f/ml be taken as the maximum allowable concentration of airborne asbestos dust for the workplace with an anticipated prevalence of about 2% asbestosis after 35 years of exposure.

Air Pollutants, Occupational↗

PubMedDate not supplied

Risk factors for asbestosis in workers of asbestos mills.

The analysis was based on a set of fifteen factors, characterising: the value of exposure to dust hazard, social status of the subjects involved, presence of diseases in the anamnesis, habits, etc., with the aim of establishing their effect on the possibility of developing asbestosis among the female workers of asbestos mills. Mathematical methods of pattern recognition were used for this multifactorial analysis. The decisive rule, obtained on the "training" principle, helped to differentiate the observations made in a reference group with the following accuracy: "without asbestosis": 87.5% correct answers, and "with asbestosis": 88.9% correct answers, which confirms the possibility of predicting the individual risk of developing asbestosis by analysing the set of risk factors. The use of the improved dermatoglyphic technique contributed to demonstrating the significance of the genotype in producing a predisposition towards asbestosis. The experience acquired demonstrates the possibility of medico-occupational selection for work involving asbestos exposure with simultaneous improvement of dust abatement measures at the factory.

Asbestosis↗

PubMed1988

Different patterns of gas exchange response to exercise in asbestosis and idiopathic pulmonary fibrosis.

To analyse the pattern of pulmonary gas exchange during maximal exercise (Emax) in asbestosis, we compared nine subjects with this disease (1 female/8 male), aged 54 +/- 11 yrs (mean +/- SD), to nine patients (1 female/8 male) with idiopathic pulmonary fibrosis (IPF) of a similar age, height, weight and smoking history, both at rest and during Emax. No differences were observed in dynamic and static lung volumes between the groups. However, patients with IPF had a lower DLCOsb and KCO (p less than 0.005 and 0.05, respectively). At rest, both groups showed mild arterial hypoxaemia (76 +/- 11, asbestosis, vs 77 +/- 11 mmHg, IPF), widened AaPO2 (32 +/- 14 vs 31 +/- 13 mmHg) and slight increases in VD/VT (47 +/- 12 vs 46 +/- 11%), respectively. During Emax, PaO2 fell to 51 +/- 7 mmHg in patients with IPF whereas those with asbestosis had PaO2 of 73 +/- 21 mmHg (p less than 0.05). Conversely, those with asbestosis were able to reduce VD/VT (from 47 +/- 12 to 39 +/- 10%, p = 0.01) as opposed to those with IPF (from 46 +/- 11 to 47 +/- 13%). Furthermore, DLCOsb and AaPO2 during Emax were highly correlated only in IPF (r: -0.84, p less than 0.01). Despite the finding that both diseases represent a diffuse pulmonary fibrosis with a similar degree of resting ventilatory impairment, the pattern of gas exchange during exercise is different in each. These differences may be related to the underlying morphology of each process, which probably includes more airway disease and less pulmonary vascular involvement and/or a different degree of interstitial fibrotic change in asbestosis.

Asbestosis↗

PubMed1979

The problems of asbestosis in Spain.

About 50 cases of asbestosis have been descirbed in Spain from 1948 through 1974. Since 1975 the Instituto Territorial de Barcelona, Servicio Social de Higiene y Seguridad del Trabajo, has initiated a survey of all the industries with an asbestosis risk in the Barcelona area. Nearly 300 cases of asbestosis have been detected to date. Given the poor hygienic conditions of most of the industries, with an asbestosis risk, and the considerably large number of exposed people, it can easily be predicted that a rapid increase of the incidence of the disease in the years to come will occur. Most of the observed cases in Barcelona were from two fibrocement industries. Of a total of 1003 workers examined, 247 (about 25%) had asbestosis.

Adult↗

PubMed1979

The role of histocompatibility (HLA) antigens in asbestosis.

Histocompatibility antigens on the A, B and C loci have been studied in 172 asbestos workers, 92 of whom had radiographic evidence of asbestosis and 80 of whom had normal radiographs. Within each population, 77 were selected who matched for age, sex, duration from first exposure, duration of exposure and approximate heaviness of exposure. Results were also compared with 174 normal unexposed volunteers. No differences of statistical significance were found in the frequency of histocompatibility antigens tested when the matched or the total population of asbestos workers with and without asbestosis were compared. There was, however, a consistent trend of increase in B27 amongst those with asbestosis (11%) and this reached conventional significance (P < 0.05) when the 92 asbestotics were compared with the whole group having normal radiographs (asbestos workers 5.0% and volunteers 5.2%). Amongst the group having asbestosis, those with HLA-B27 had a significantly shorter exposure to the dust (13.5 years) compared with those without asbestosis (22.3 years), although the mean radiographic profusion score for the two categories was similar. No statistical differences could be found when B5, B8 and B12 were analysed in a similar way, but there was a trend suggesting that B5 was less frequent amongst a small group of cases showing radiographic progression over a three-year follow-up, compatible with the suggestion that this antigen might be linked with with some protective effect.

Asbestos↗

PubMed1977

HLA antigens in asbestosis.

One hundred thirty-four workers in an asbestos factory who had been in contact with asbestos for about 20 years, were typed for 22 HLA antigens of the A and B loci. In this group, 22 workers were diagnosed as asbestosis patients on the basis of chest radiography and clinical findings; the remaining 112 were without signs of asbestosis. In the group of asbestosis patients an increase of B27 antigen was observed in comparison with the group without asbestosis (27-27% and 9-82% respectively). The relative risk = 3-44 is significant at the level of p less than 0-05. These results may indicate that a genetic factor, connected with HLA locus has influence on the development of asbestosis under conditions of contact with asbestos.

Asbestosis↗

PubMed1997

Histopathological features of pulmonary asbestosis with particular emphasis on the comparison with those of usual interstitial pneumonia.

We examined 40 autopsy cases of pulmonary asbestosis which were defined by occupational history, lung fibrosis and asbestos bodies (ABs) to clarify histopathological features. Thirty four patients were males and six were females. The mean age was 64.1 +/- 1.6. Gross findings of 39 cases (one case was examined only microscopically) showed that pleural adhesion in 31/39, visceral pleural thickening in 37/39, and pleural plaques in 26/33 except of 6 cases with severe adhesion. Four cases had no or only mild pleural adhesion or pleural thickening, and no pleural plaques. Grossly, lung fibrosis of asbestosis can be divided into two types of honeycombing (HNCB) predominant fibrosis (16 cases), and atelectatic induration predominant fibrosis (23 cases). Histologically, the honeycombing type fibrosis showed peripheral acinar fibrosis like in usual interstitial pneumonia (UIP), whereas the atelectatic induration type exhibited non-peripheral acinar fibrosis with intraluminal organization unlike in UIP. In our study, the lung fibrosis was more intensive in the lower lobes, posterior and subpleural zones, although in eight cases the upper lobes were more intensively involved than the lower lobes. The degree of asbestos body formation on each case was varied. Four cases with typical honeycombing and fibrosis grade 3 were counted only small numbers of asbestos bodies, and lacked one or two above-described pleural changes, and these cases were similar to idiopathic or usual interstitial pneumonia (UIP). As for complications of asbestosis, 13 cases (32.5%) had lung cancer and 14 cases (35%) presented diffuse alveolar damage (DAD) pathologically. It is concluded that asbestosis cases of honeycombing type without pleural changes can not be distinguished even from UIP, if asbestos bodies (ABs) were not found histologically. Therefore, great care needs to be taken in identifying them. We also have examined the quantitatave counts of asbestos bodies and asbestos fibers in ten cases. Acute exacerbation of UIP is a well recognized entity in Japan, similar condition may occur in pulmonary asbestosis.

Asbestosis↗

PubMed1999

[Clinical course of asbestosis under the existing conditions in extraction and processing of serpentine asbestos].

The authors followed changes in clinical course of asbestosis, comparing groups of individuals working in exposure to chrysotile-asbestos dust, patients having so-called late asbestosis and reference group (individuals with absent or minimal roentgenologic changes in lungs). Analysis of 530 case histories proved increase of average length of service in dusty conditions before asbestosis development, longer progression of pulmonary fibrosis. Asbestosis progression does not depend on medical resolutions. "Late" asbestosis occurs in retired workers who were engaged into auxiliary occupations. Low baseline values of respiratory function and associated respiratory infection worsen the overall prognosis.

Asbestos, Serpentine↗

PubMed1998

Fibroblast mitogens in bronchoalveolar lavage (BAL) fluid from asbestos-exposed subjects with and without clinical evidence of asbestosis: no evidence for the role of PDGF, TNF-alpha, IGF-1, or IL-1 beta.

Asbestosis is a fibrotic lung disease resulting from inhalation of asbestos fibres. Its pathogenesis is poorly understood but probably involves stimulation of fibroblast proliferation and collagen production by mediators released from inflammatory and resident lung cells. In vitro studies have implicate PDGF, TNF-alpha, IGF-1, TGF-beta, and IL-1 in asbestosis, but the role of these mediators in vivo is not known. This study aimed to characterize mediators in bronchoalveolar lavage (BAL) fluid from patients exposed to asbestos with (n = 24) or without (n = 34) asbestosis, compared with ten normal subjects. Human lung fibroblasts were exposed to serial dilutions of BAL fluids and the effects on fibroblast proliferation were assessed. The median mitogenic activity of BAL fluid from asbestos-exposed (17 per cent above medium control, range 3-44 per cent) and asbestosis (14 per cent, range 2-60 per cent) groups was higher than that of BAL fluid from controls (10 per cent, range 2-20 per cent; P < 0.01 and P < 0.05, respectively), but there was no significant difference between the patient groups. The mitogenic activity of BAL fluids was not reduced by incubation with neutralizing antibodies to PDGF-AA, PDGF-AB, PDGF-BB, TNF-alpha, IGF-1, and IL-1 beta. We conclude that BAL fluids from patients exposed to asbestos contain mitogens for human lung fibroblasts, but that PDGF, TNF-alpha, IGF-1, or IL-1 beta do not contribute to this activity.

Adult↗

PubMed1996

Lung cancer and asbestos exposure: asbestosis is not necessary.

Recent commentaries on the issue of asbestos-related lung cancer have raised important points. One major question is whether lung cancer can be attributed to asbestos exposure in the absence of asbestosis. This review attempts to place the debate in the proper context for establishing causation. Relevant epidemiologic and pathologic studies are analyzed, as well as the scientific basis for each position in the debate. The assertion that asbestosis must be present in order to attribute a lung cancer to asbestos exposure does not meet accepted standards for establishing causation. In addition, some evidence has been incorrectly cited in support of this position. This discussion can benefit from clearer definitions of asbestosis, a more thorough evaluation of the available scientific information, and a proper context for determining causation. This review of the available evidence indicates that lung cancers can occur as a result of asbestos exposure, in the absence of clinical or histologic asbestosis. Causation in an individual should be assessed by considering duration of exposure, intensity of exposure, and appropriate latency.

Asbestos↗

PubMed1983

Asbestosis and tuberculosis.

The frequent association between silicosis and tuberculosis has been known for a long time. However, the possible interrelationship between asbestosis and tuberculosis is not entirely clear, and some reports on the subject are contradictory. The incidence of tuberculosis was determined in three groups of people: 1) those with asbestosis, 2) those exposed to asbestos dust but without asbestosis, and 3) healthy people without pneumoconiotic exposure. Chest X-rays of 2,846 workers surveyed in this department between 1976 and 1980 were reviewed. Since only one case of active tuberculosis was detected, residual tuberculosis was the type encountered and this was diagnosed solely on its radiological signs. The incidence of tuberculosis was: 3.87% (N = 257) for group 1; 3.45% (N = 1,215) in group 2; and 3.93% (N = 1,374) for group 3. Statistical analysis confirms the lack of significant differences in the incidence of tuberculosis in the three groups. From these findings, it is concluded that asbestosis is not an influential factor in the appearance and development of tuberculosis.

Adolescent↗

PubMed1992

Patterns of asbestosis in New Jersey.

Hospital discharge data from New Jersey were used to identify cases of asbestosis for the 8 years 1979-1986. Multiple admissions were deleted so that each individual was counted once at the time of his/her first hospitalization with an asbestosis diagnosis. White males had the highest age-adjusted average annual discharge rate of 19.3 cases/100,000 population, followed by black males (12.3 cases/100,000) and white females (1.2 cases/100,000). The discharge rate was positively associated with age in each race/sex category. The relationship between rates for black males and white males depended on age: under 65 years, the rates were almost equal, and at 65 years and older, the white rates were nearly twice the black rates. There were two areas of the state where the rates were highest: the north-central and southwest regions. These two areas represent manufacturing and shipbuilding applications of asbestos, respectively. During the years 1979-1986, the annual percentage increase in asbestosis rates was 20% for white males, 17% for black males, and 8% for white females. Continued surveillance will reveal when the rates for asbestosis stop increasing.

Adult↗

PubMed1986

Enzyme activities of lung lavage in asbestosis.

We analyzed lung lavage supernatant for amylase, lactate dehydrogenase (LD), alkaline phosphatase (ALP), beta-glucuronidase (beta G), and albumin, and a differential count was made of the cellular component of lung lavage in 18 normal controls and 36 long-term asbestos workers of the mines and mills of Québec. The men were concomitantly evaluated by the usual clinical, radiological, functional parameters and 67Ga lung scan. In 7 workers without asbestosis and normal 67Ga scan, lavage enzyme activities, albumin and cell counts were comparable to those of controls. Of 9 without sufficient criteria for asbestosis but increased 67Ga lung uptake, cell counts documented significant increases in the mean number of macrophages (X 2), lymphocytes (X 2) and neutrophils (X 3). Supernatant analyses showed significant increases in amylase (X 4-5), LD (X 2.5), ALP (X 1.5) and beta G (X 2-4). These changes were comparable to those in the lavage of workers with well established asbestosis except that in the latter, the lymphocyte count was slightly lower but the neutrophil count higher (p less than 0.05). These data document that enzyme activities of lung lavage can differentiate asbestos workers with early or late asbestosis from controls and asbestos workers without disease.

Adult↗