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PubMed2006

Matrix metalloproteinases promote inflammation and fibrosis in asbestos-induced lung injury in mice.

Inhalation of asbestos fibers causes pulmonary inflammation and eventual pulmonary fibrosis (asbestosis). Although the underlying molecular events are poorly understood, protease/antiprotease and oxidant/antioxidant imbalances are believed to contribute to the disease. Implicated in other forms of pulmonary fibrosis, the matrix metalloproteinases (MMPs) have not been examined in asbestosis. We therefore hypothesized that MMPs play a pathogenic role in asbestosis development. Wild-type C57BL/6 mice were intratracheally instilled with 0.1 mg crocidolite asbestos, causing an inflammatory response at 1 d and a developing fibrotic response at 7, 14, and 28 d. Gelatin zymography demonstrated an increase in MMP-9 (gelatinase B) during the inflammatory phase, while MMP-2 (gelatinase A) was profoundly increased in the fibrotic phase. Immunohistochemistry revealed MMP-9 in and around bronchiolar and airspace neutrophils that were often associated with visible asbestos fibers. MMP-2 was found in fibrotic regions at 7, 14, and 28 d. No increases in RNA levels of MMP-2, MMP-9, or MMP-8 were found, but levels of MMP-7, MMP-12, and MMP-13 RNA did increase at 14 d. The MMP inhibitors, TIMP-1 and TIMP-2, were also increased at 7-28 d after asbestos exposure. To confirm the importance of MMP activity in disease progression, mice exposed to asbestos were given daily injections of the MMP inhibitor, GM6001. MMP inhibition reduced inflammation and fibrosis in asbestos-treated mice. Collectively, these data suggest that MMPs contribute to the pathogenesis of asbestosis through effects on inflammation and fibrosis development.

Animals↗
PubMed1997

Respiratory impairments due to dust exposure: a comparative study among workers exposed to silica, asbestos, and coalmine dust.

We conducted a comparative study of pulmonary dysfunction among workers who were exposed to silica, asbestos, or coalmine dust. The results showed that all three groups of dust-exposed workers, even those without radiographic signs of pneumoconiosis, had decreased spirometric parameters and diffusing capacity (DLco) in both nonsmokers and smokers. Pulmonary function was further decreased when pneumoconioses were present in the three groups. In accord with increasing radiographic categories, pulmonary function in the workers with either silicosis or asbestosis was even lower, whereas in those with coal workers' pneumoconiosis (CWP), it changed relatively little. Workers with mild to moderate (radiographic category I-II) silicosis or asbestosis showed similarly decreased DLco, but those with silicosis showed lower FEV1/FVC than those with abestosis. The workers with CWP also showed a lower FEV1/FVC than those with asbestosis. The major impairment patterns for silica workers, asbestos workers, and coal miners were mixed, restrictive and mixed, and obstructive, respectively. Smoking obviously increased the prevalence of obstruction for all the groups. We conclude from the present study that all the three dusts cause functional abnormalities that precede radiographic changes of pneumoconiosis. We should pay more attention to respiratory impairment in the initial stage of silicosis and CWP.

Adult↗
PubMed1985

A respiratory epidemiological study of stevedores intermittently exposed to asbestos in a South African port.

The prevalence of asbestosis in stevedores intermittently transporting crocidolite asbestos in a South African port was found to be 30% in a cross-sectional survey. Diagnostic criteria are discussed in terms of the low index of suspicion for industrial diseases, the high probability of missing slight radiological changes, and the attribution of radiological lesions to other diseases, particularly tuberculosis, in a high prevalence area. Results are compared with other studies. Asbestosis was not associated with tuberculosis. Smoking was not significantly associated with asbestosis, other respiratory signs and symptoms, or radiological abnormality.

Adult↗
PubMed1992

Electron microscopy analysis of mineral fibers in human lung tissue.

In the present study, lung samples from 126 autopsied cases were examined to determine the content of mineral fibers using analytical transmission electron microscopy (ATEM). The cases were divided into four groups (22 lungs of persons exposed to ambient environmental pollution, 32 cases of mesothelioma, 38 cases of primary lung cancer, and 34 asbestosis cases, 13 of these with additional pleural plaques). Fibers were counted, measured, and mineralogically identified using a combination of X-ray microanalysis and electron diffraction of the non-oriented fiber. Concentration of fibrous particles (defined as particles above 1 micron in length with roughly parallel long sides and an aspect ratio of 5:1 and greater) was calculated as fibers 10(6)/g dry lung weight. The concentration of chrysotile was found to be similar throughout the groups except for two cases in the asbestosis group with comparably high numbers of chrysotile. However, a remarkable difference for amphiboles could be observed between the groups. Asbestos bodies were mostly found in the asbestosis group. There was a rather good correlation between numbers of amphibole fibers and asbestos bodies, with an average ratio of 10:1. For comparison purposes between occupationally exposed/non-exposed individuals, a transition was found in the concentration range of 3-10(7) asbestos fibers/g dried lung weight.

Analysis of Variance↗
PubMed1995

Asbestos-induced visceral pleural fibrosis reduces pulmonary compliance.

To determine the nature of respiratory functional impairment caused by asbestos-induced visceral pleural fibrosis (VPF) and to discover which pulmonary physiological variable best reveals it, we examined 59 asbestos-exposed construction workers having asbestos-related changes on chest radiographs. Computed tomography scans of the thorax were also performed. Visceral pleural fibrosis was diagnosed in 29 subjects: seven had only VPF, 17 had VPF and pleural plaques, and five had VPF, plaques, and asbestosis. In subjects without VPF, 23 had plaques, six had plaques and asbestosis, and one had only minor fibrotic parenchymal changes insufficient for a diagnosis of asbestosis. Flow-volume spirometry, body plethysmography, static and dynamic compliance, and pulmonary diffusing capacity for carbon monoxide were measured. The subjects with VPF had significantly lower static (p = 0.005) and dynamic (p = 0.007) compliance values than those without. Other respiratory function variables failed to show any significant differences. We conclude that the measurement of static and dynamic compliance is a useful method in assessing pulmonary function impairment caused by visceral pleural fibrosis.

Adult↗
PubMed1978

Asbestos exposure and related neoplasia. The 28 year experience of a major urban hospital.

In a retrospective study of 49 cases of asbestosis, a steady increase in the frequency of diagnosis of asbestosis and asbestos-related neoplasia is documented from a major urban hospital since 1960. Although in the majority of cases the subjects were exposed to asbestos in a neighboring shipyard, in 20 per cent of the cases, asbestos exposure was in industries not related to shipbuilding, reflecting its widespread use. This selective population of patients with asbestosis more often than not had an associated neoplasm. The most likely accompanying tumor was pleural mesothelioma, and among cell types of lung cancer, adenocarcinoma was notably frequent.

Adenocarcinoma↗
PubMed1980

Further observations on cytoplasmic hyaline in the lung.

Cytoplasmic hyaline material resembling Mallory's alcoholic hyaline has previously been described in pulmonary alveolar cells of patients with asbestosis. We present 14 new cases of cytoplasmic hyaline found in patients with a variety of processes causing damage to the alveolar lining; these include cases of radiation pneumonia, diffuse interstitial fibrosis, organizing bacterial pneumonia, as well as asbestosis. Hyaline was found only in the setting of an unusual type II cell change, which ultrastructurally appeared to represent squamous metaplasia. We conclude that pulmonary cytoplasmic hyaline is not specific for asbestosis but rather is a nonspecific reaction to injury;

Adult↗
PubMed1983

Asbestos exposure. An update on pleuropulmonary hazards.

Asbestos exposure is causally related to the development of asbestosis, bronchogenic carcinoma, malignant mesothelioma, and nonmalignant pleural disorders. Clinical and roentgenographic manifestations of asbestosis mimic other diffuse fibrotic lung diseases. However, a concomitant finding of pleural plaques strongly suggests the diagnosis. The manifestations of bronchogenic carcinoma related to asbestos exposure are varied and do not differ from those unrelated to asbestos exposure. Malignant mesothelioma signals previous asbestos exposure. Nonmalignant pleural disorders may not cause any symptoms but should alert the physician to other concurrent or potential asbestos-related diseases. To diagnose asbestos-related diseases, physicians should bear in mind the long latent period and should take a careful, comprehensive occupational and environmental history. Cigarette smoking markedly increases the risk for development of bronchogenic carcinoma in asbestos workers and increases the mortality due to asbestosis.

Aged↗
PubMed2005

Predictors of lung cancer among asbestos-exposed men in the {beta}-carotene and retinol efficacy trial.

Despite numerous published studies, debate continues regarding the risk of developing lung cancer among men exposed occupationally to asbestos, particularly those without radiographic or functional evidence of asbestosis. The beta-Carotene and Retinol Efficacy Trial (CARET), a study of vitamin supplementation for chemoprevention of lung cancer, has followed 4,060 heavily exposed US men for 9-17 years. Lung cancer incidence for 1989-2002 was analyzed using a stratified proportional hazards model. The study confirmed excessive rates of lung cancer among men with radiographic asbestosis. Comparison of study arms revealed a strong, unanticipated synergy between radiographic profusion category and the active intervention. In the large subgroup of men with normal lung parenchyma on chest radiograph at baseline, there was evidence of exposure-related lung cancer risk: Men with more than 40 years' exposure in high-risk trades had a risk approximately fivefold higher than men with 5-10 years, after adjustment for covariates. The effect in these men was independent of study intervention arm, but pleural plaques on the baseline radiograph and abnormal baseline flow rate were strong independent predictors of subsequent lung cancer. Residual confounding by subclinical asbestosis, exposure to unmeasured lung carcinogens, or differences in smoking are unlikely to explain these observations better than a carcinogenic effect of asbestos per se.

Adult↗
PubMed1994

The human evidence: parenchymal and pleural changes.

Asbestos inhalation can cause fibrotic reactions both in the lung parenchyma and in the pleura. The incidence and relative proportions of these lesions in any cohort will be dependent on: (1) the time factor: both asbestosis and pleural plaques are progressive diseases and the longer the time from exposure, the more the changes; (2) the dose-response: the more intense the exposure, the earlier and the more advanced is the asbestosis. However, pleural plaques are only moderately dependent on the exposure level and will occur after approximately 30 years in most persons who develop them, even after fairly low exposure; (3) the early lesions are difficult to diagnose radiologically and are prone to overdiagnosis. Considerable caution is necessary when evaluating results if only such lesions are reported. It is generally accepted that the occurrence of radiological asbestosis is a risk factor, particularly for bronchial carcinoma. However, pleural plaques have been considered to be relatively harmless. Recent data have indicated, however, that they can be indicators of sufficient exposure to increase the risk of other asbestos-related diseases, including lung cancer and mesothelioma.

Asbestos, Serpentine↗
PubMed1982

Asbestos-related diseases. Algorithm for forensic pathological diagnosis.

The pathological diagnosis and proof of asbestos causation in environmental-occupational diseases is based on a spectrum of increasingly sophisticated determinations with greater confidence in detection of asbestos bodies and fibers. These include the following: pathology (histology) and/or thick smears of lung, microincineration, bulk chemical digestion, and electron beam instruments. The requisites of medical and forensic asbestos causation differ, and do not always require the full range of these analytical techniques. The need and significance of some of these determinations, as expressed in number of asbestos bodies and fibers, may be related in many cases to the evidence of asbestosis; to the gross and microscopic pathological findings (asbestosis, lung carcinoma, mesothelioma); the exposure history (type, duration, intensity, and period of latency); and nature of the asbestos mineral. An algorithm for the forensic pathological diagnosis of asbestosis and of asbestos-related diseases is proposed.

Asbestos↗
PubMed1996

The pneumoconioses.

The stringent industrial hygiene regulations that have been introduced in North America, Europe, and Australasia have led to a decline in the incidence and prevalence of silicosis, coal workers' pneumoconiosis, and asbestosis. Although new cases of asbestosis are not occurring, an appreciable number of mesotheliomata are still being diagnosed, and there has yet been little, if any, decline in the latter tumor. These new cases are nearly entirely due to exposure to amphiboles in the 1940s and 1950s. It is expected that by about the year 2000 the incidence of mesothelioma will begin to decrease in the United States and Canada. Meanwhile there is an undue preoccupation with more and more sensitive methods of detecting asbestosis, silicosis, and coal workers' pneumoconiosis, eg, magnetic resonance imaging, bronchoalveolar lavage, and so forth. Much effort is being made in trying to detect disease in groups of workers with extremely low exposures and no symptoms. Smaller and smaller effects are being detected, with the ultimate aim appearing to be detecting nothing at all. Efforts should be made at surveying other populations exposed to agents that have recently been introduced and that could conceivably have long-term effects.

Asbestos, Amphibole↗
PubMed2000

Pathology and pathophysiology of pneumoconiosis.

Cellular and molecular mechanisms, as well as associated gene expressions, in silicosis and asbestosis are widely investigated, and compound mechanisms involved in initiating inflammation and progression to fibrosis are comprehensively studied, though not yet totally understood. Recent advances in this field, especially concerning pathophysiology of these pneumoconioses, are reviewed in this article. Silicosis and asbestosis are two major types of pneumoconiosis. Although the clinico-pathologic features presented are apparently different, silicosis and asbestosis are both interstitial lung diseases caused by chronic exposure to airborne inorganic dusts, and the pathology of these two diseases is essentially a fibrosis.

Asbestosis↗
PubMed1973

Epidemiological and quantitative relationships between mesothelioma and asbestos on Tyneside.

Thirty-five necropsied cases of diffuse malignant mesothelioma of pleura and six cases of mesothelioma of peritoneum are reported. Occupational histories from 40 cases showed that 32 cases (80%) were definitely exposed to asbestos; six cases (15%) were probably exposed and two (5%) had no known exposure. The mean latent interval was 34 years. Occupational histories of 56 control patients matched in pairs for age and sex with 28 of the mesothelioma cases revealed definite exposure to asbestos in 12 controls (21%), probable exposure in 11 (20%), and no evidence of exposure in 33 (59%). The difference in incidence of exposure between mesotheliomas and controls is statistically highly significant. Six-micron histological sections of lung, available in 39 mesothelioma cases, contained coated asbestos fibres in 36 cases (92%). Sixteen cases of mesothelioma showing fibres were free of asbestosis; asbestosis was slight in 14 cases, moderately severe in five cases, and severe in one case. The incidence of asbestos bodies in sections from mesothelioma cases was significantly higher than in a previously reported series of routine necropsies examined by lung smear. Counts of coated and uncoated asbestos fibres were performed on samples of lung tissue from 33 mesothelioma cases. No fibres were identified in one case and only occasional coated fibres in a second case. The remainder gave counts ranging from 154 thousand to 684 million fibres per gram dry weight. Uncoated fibres were invariably present and usually comprised 50 to 80% of the count. No relationship was found between total fibre count and the latent period of the mesothelioma. Fibre counts were also performed on lung samples from 18 smear-positive and 30 smear-negative routine necropsies. Cases with numerous coated fibres in the smear gave total fibre counts similar to those of mesothelioma cases without asbestosis. Routine cases with only one fibre in the smear usually yielded only occasional fibres on analysis. Coated and uncoated fibres were found in 13 out of 30 smear-negative cases, indicating a true incidence of 56% of exposure to asbestos in the whole necropsy series. When compared with the mesothelioma series the difference in incidence of fibres remains statistically significant. The data suggest that, on Tyneside, exposure to asbestos sufficient to cause an appreciable risk of developing mesothelioma has usually occurred through occupational exposure rather than by general environmental pollution by asbestos.

Adult↗
PubMed1973

The optical and electron microscopic determination of pulmonary asbestos fibre concentration and its relation to the human pathological reaction.

The quantitative extraction of asbestos fibres from asbestotic lung by alkali digestion has been refined by maceration of the tissue without prior drying, the minimum use of centrifugation, and the adoption of phase contrast microscopy. Preliminary experiments suggested that, using this technique, asbestos fibre counts were accurate to within at least +/- 20% and in most instances to within +/- 10%. The method was used to assess asbestos concentrations in lung tissue showing various degrees and forms of fibrosis. The results, as determined by light microscopy, indicated that uncoated fibres generally outnumbered coated fibres. In mild and moderate asbestosis there was a progressive increase in concentration of asbestos fibres, both coated and uncoated, with increasing severity of fibrosis, whereas in severe asbestosis no correlation existed between the fibre concentration and the form or the extent of the pathological reaction. It is suggested that the severe fibrosis results from the supervention of non-specific inflammatory processes. Asbestos fibre diameter distributions, gauged by electron microscopy, were fairly constant irrespective of the degree of fibrosis. Optically visible fibres constituted between 12 and 30% of the total, so that an optical count may be said to give an approximate indication of the total asbestos concentration and, so far as asbestosis is concerned, may well serve for comparative purposes. The relation between asbestos and neoplasia will, however, require identification and quantitation of particular types of the mineral by microanalytical techniques.

Asbestos↗
PubMed1992

The Small Area Health Statistics Unit: a national facility for investigating health around point sources of environmental pollution in the United Kingdom.

STUDY OBJECTIVE: The Small Area Health Statistics Unit (SAHSU) was established at the London School of Hygiene and Tropical Medicine in response to a recommendation of the enquiry into the increased incidence of childhood leukaemia near Sellafield, the nuclear reprocessing plant in West Cumbria. The aim of this paper was to describe the Unit's methods for the investigation of health around point sources of environmental pollution in the United Kingdom. DESIGN: Routine data currently including deaths and cancer registrations are held in a large national database which uses a post code based retrieval system to locate cases geographically and link them to the underlying census enumeration districts, and hence to their populations at risk. Main outcome measures were comparison of observed/expected ratios (based on national rates) within bands delineated by concentric circles around point sources of environmental pollution located anywhere in Britain. MAIN RESULTS: The system is illustrated by a study of mortality from mesothelioma and asbestosis near the Plymouth naval dockyards during 1981-87. Within a 3 km radius of the docks the mortality rate for mesothelioma was higher than the national rate by a factor of 8.4, and that for asbestosis was higher by a factor of 13.6. CONCLUSIONS: SAHSU is a new national facility which is rapidly able to provide rates of mortality and cancer incidence for arbitrary circles drawn around any point in Britain. The example around Plymouth of mesothelioma and asbestosis demonstrates the ability of the system to detect an unusual excess of disease in a small locality, although in this case the findings are likely to be related to occupational rather than environmental exposure.

Asbestosis↗
PubMed1975

Prevalence of asbestos bodies in a necropsy series in East London: association with disease, occupation, and domiciliary address.

The prevalence of asbestos bodies was measured in lung sections in a necropsy series carried out at the London Hospital (1965-66) after exclusion of all known asbestos factory workers and cases of asbestosis and of mesothelioma. Associations were sought between the presence and number of asbestos bodies with the patients' sex, domiciliary address, occupation, industry, and diseases recorded at necropsy. Asbestos bodies were present in 42% of the 216 men in the series and in 30% of the 178 women. The number of bodies in the positive cases was small in comparison with the numbers seen typically in asbestosis; thus there were less than 6 asbestos bodies per 6-75 mm-3 lung tissue in 107 of the total 145 positive cases in contrast to 1 000 or more in asbestosis. In comparison with the overall series, an increased number of asbestos body positives was present in males with carcinoma of stomach and females with carcinoma of breast. In view of this finding lung sections were counted in further post-mortem examples of these carcinomas making a total of 50 males with carcinoma stomach and 82 females with carcinoma breast. Thirty-five positive cases were found in the carcinoma stomach group as against 22-7 expected and 38 in the carcinoma breast group against 26-35 expected. There was no excess of observed over expected asbestos body positives in 51 males with carcinoma of bronchus. There was an excess of asbestos body positives (60-9%) in heavy manual workers and in both heavy and light manual male workers in the shipping (61%), electrical and engineering (56%), and transport (54%) industries. The incidence in male clerical workers was 12-8%. The incidence of asbestos body positives according to home address was highest (53% in males, 45% in females) in patients living in the industrial and cockland area due east of the hospital. The incidence fell in the less industrial areas north-east of the hospital. Consideration of possible environmental sources of the inhaled asbestos suggests that in this survey occupation, industry, and comiciliary area all play a part. The comparatively minor intensity of asbestos pollution in our positive cases showed a positive association with carcinoma of stomach and breast, possibly playing a direct pathogenic role in carcinoma of stomach. No positive association was identified with any other neoplastic disease including carcinoma of bronchus.

Adolescent↗
PubMed1986

Hazards of lung biopsy in asbestos workers.

An investigation into the problem of the frequency and hazards of lung biopsy in asbestos workers was performed in two ways. The first study was into the frequency of lung biopsy among 2907 long term asbestos insulation workers in 1981-3 and the second was into the frequency of fatal complications of lung biopsy in 168 deaths from asbestosis among 2271 consecutive deaths of asbestos insulation workers 1967-76. Only 25 (0.9%) of the 2907 asbestos insulation workers reported having had either an open lung biopsy, a needle biopsy, or a transbronchial biopsy. Seven (24%) of these men suffered difficulties as a result of the biopsy. Lung biopsies had been performed on 14 of the 168 workers who died of asbestosis. Three (21%) of these 14 patients had died within 30 days of biopsy as a direct result of the procedure. In most cases there is no need for lung biopsy to establish a diagnosis of asbestosis; generally, it may be defined by history of exposure, clinical and radiological findings, and other well established non-invasive diagnostic procedures. Certainly, legal and compensation recommendation for biopsy should be considered with the possibility of death in mind. If biopsy is performed precautions should be taken, including adequate observation in hospital.

Asbestosis↗