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PubMed1980

Clearance of asbestos bodies from the lung: a personal view.

In histological sections asbestos bodies in human lungs may be either transparent, yellow, strongly Perls-positive structures as described in published reports, or opaque, black structures, the ferroprotein coating having been converted into haemosiderin. The transparent asbestos bodies fragment into segments; the black asbestos bodies disintegrate into a mass of haemosiderin granules that accumulate as dense deposits, particularly near to blood vessels. The presence of haemosiderin granules indicates that asbestos bodies have broken down. When a patient has died with a mesothelioma there is little evidence of phagocytic activity in many areas of the lung. When exposure to asbestos ceased many years before a mesothelioma developed there may be few recognisable asbestos bodies remaining in the lung.

Adult↗

PubMed1983

Tobacco consumption and asbestos exposure in patients with lung cancer: a three year prospective study.

During the three years 1979-81, all patients with bronchial carcinoma of World Health Organisation types I to IV were given a questionnaire to determine occupation, smoking habits, and exposure to asbestos. Chest x rays were screened for the presence of pleural plaques. Of the men, 96.2% were current or ex-smokers, as were 71% of the women. In those who had never smoked 70% had an adenocarcinoma. In smokers the risk of getting other types was greater, but the risk of getting an adenocarcinoma was also considerably increased compared with the normal population. Of the men, 35.8% were occupationally exposed to asbestos and 15.6% were carriers of radiological plaques, a frequency five to six times greater than expected. Practically all asbestos exposed patients with lung tumours were smokers or ex-smokers and their total tobacco consumption was as high as that of non-exposed patients. The average latency from first exposure to asbestos to diagnosis of the lung tumour was 37 years. Even if strict regulations are warranted for the use of asbestos, this cannot prevent future asbestos cancers resulting from exposure that has already occurred. Elimination of smoking seems the only way to reduce such tumours.

Adenocarcinoma↗

PubMed1987

Ferruginous bodies and pulmonary fibrosis in dead low to moderately exposed asbestos cement workers: histological examination.

Histological slides from the lungs of 89 dead asbestos cement workers have been examined with respect to ferruginous bodies and fibrosis. The results have been compared with individually matched controls with no known exposure to asbestos, and related to asbestos exposure, expressed as duration of exposure and cumulative asbestos dose, and smoking habits. The asbestos cement workers studied had been employed for on average 15 years, with a mean cumulative dose of 26 fibre-years per ml (f-y/ml). Clear dose-response relations between exposure (duration of exposure and cumulative asbestos dose) and level of ferruginous bodies were found. An association was evident already at a low cumulative dose (1-10 f-y/ml). Fibrosis was more common and more pronounced among the exposed workers than among controls. An association between ferruginous bodies and fibrosis was also found. Among the controls, but not among exposed workers, there was an association between smoking history and fibrosis.

Asbestos↗

PubMed1988

Immune response in shipyard workers with x ray abnormalities consistent with asbestos exposure.

The association of cellular and humoral immune responses with asbestos exposure was studied in two groups of 150 workers each from a shipyard population and compared with a population of Red Cross blood donors. One of the shipyard groups had both chest x ray evidence of asbestos exposure and work assignments that necessitated direct handling of asbestos. The other shipyard group had normal chest x ray films and no job assignments involving the direct handling of asbestos. Cellular immune responses studied were mitogen activation and measures of T helper and T suppressor cells. Humoral immune measures were IgG, IgA, and IgM. In shipyard workers with asbestos related x ray abnormalities there was a significant increase in pokeweed mitogen stimulation. In both shipyard groups compared with Red Cross blood donors were found (1) significantly higher IgG and IgA levels and (2) greater numbers of T helper and T suppressor cells; because of the disproportionately large number of T suppressor cells, Th/Ts ratios were lower than in the Red Cross controls. Observations of differences in humoral and cellular immune response may point the way to the early diagnosis of the clinical manifestation of asbestos related disease.

Asbestos↗

PubMed1988

Lobe of origin in the attribution of lung cancer to asbestos.

Lung cancer originates most commonly in the upper lobes in the general population but among workers with asbestosis it is most common in the lower lobes. Published data on lobar distribution were used to estimate the probabilities that lung cancer among asbestos workers is attributable to exposure to asbestos. This attribution varies directly with the relative risk. Critical values of the relative risk at which attribution of lung cancer to asbestos equalled its attribution to other causes, mainly smoking, were calculated. At a relative risk above 2.81 upper lobe cancers were more likely to be due to asbestos than not. For middle and lower lobe cancers, the critical relative risk was 1.55. These critical values were compared with published standardised mortality ratios reported for cohorts of workers with asbestosis. Since the ratios ranged from 6.3 to 9.1, the probability that lung cancer in such cases is due to asbestos is high regardless of lobe of origin. In many cohorts unstratified by the presence or absence of asbestosis the risk ratios are below one or both of these critical values. Since risk ratios are so high among workers with asbestosis, the ratios must be lower for workers without asbestosis than the overall ratios for unstratified cohorts. Therefore, the critical values may be useful in workers without asbestosis among such cohorts to estimate the upper limit of the probability that lung cancer in a given lobe is due to exposure to asbestos.

Asbestos↗

PubMed1989

Alterations in the laryngeal mucosa after exposure to asbestos.

The laryngeal mucosa of 195 workers in an asbestos cement factory (Salonit Anhovo, Yugoslavia) and in a control group was examined. The factory manufactures asbestos cement products containing about 13% of asbestos (8% amosite, 12% crocidolite, and 80% chrysotile) of different provenance. Alterations in the laryngeal mucosa were more frequent in the factory workers than in the control group. The changes, mostly consistent with chronic laryngitis, were closely related to the degree of workplace pollution and less so to the duration of employment Ten workers exhibiting the most severe clinical changes underwent biopsy, the results of which showed histomorphological changes characteristic of hyperplastic chronic laryngitis. Four tissue specimens were examined also by scanning electron microscopy and in three of them asbestos fibres were found on the epithelial surface. No case of laryngeal carcinoma was identified. On the basis of our results it is thought that asbestos related changes of the larynx should receive more attention and that the use of the term "laryngeal asbestosis" is justified. The clinical picture is non-specific but in view of their frequency such changes should be considered a consequence of exposure to asbestos.

Adult↗

PubMed1996

Survival in cohorts of asbestos cement workers and controls.

OBJECTIVES: To measure the impact on survival of being exposed to asbestos cement dust. METHODS: Survival of 866 asbestos cement workers and 755 controls was studied with Cox's proportional hazards regression models with age as the basic time variable. The effect of cumulative exposure up to the age of 40 was investigated in an internal analysis of 635 asbestos cement workers who had dose estimates. RESULTS: The death risk was higher for the asbestos cement workers than for the controls with a hazard ratio (HR) of 1.15 (95% confidence interval was 1.00 to 1.31). The increased risk found seemed to be confined to the period 20-40 years from start of employment. The estimates of the cohort effect were almost unaffected by adjustment for smoking habits. The estimates of the exposure effect rose with increasing dose (< 4 fibre-years/ml (f-y/ml): HR = 1.00, 4-9.9 f-y/ml: HR = 1.06, > or = 10 f-y/ml: HR = 1.35, for workers with at least five years of employment), and were higher when restricted only to deaths from malignant or non-malignant respiratory disease. However, none of the point estimates were significantly increased. Median age at death was two years lower in the high than in the low, exposure group. CONCLUSIONS: The results indicate that even a moderate asbestos exposure may shorten the median duration of life in an exposed population. Compared with the estimated effect on duration of life from ever being a smoker, that of ever being an asbestos cement worker was less, although that of having a high exposure was similar.

Adult↗

PubMed2002

Asbestos fibreyears and lung cancer: a two phase case-control study with expert exposure assessment.

AIMS: To assess the cumulative effect of asbestos on lung cancer risk where the exposure is assessed by an expert rating. METHODS: 1678 male cases and controls were enrolled in a population based matched case-control study, focused on occupational risk factors, carried out in West Germany. The exposure to asbestos was computed as lifelong working hours. For a validation subsample of 164 matched pairs from this study the intensity of asbestos exposure was further assessed by a panel of experts in order to obtain an estimate of the cumulative exposure on a time by intensity scale (fibreyears). The information on duration of asbestos exposure in the original study was combined with the fibreyears following the two phase case control study paradigm. RESULTS: The number of exposed subjects in the validation subsample was 75 cases and 71 controls. The percentage of subjects with a cumulative exposure < or =1, 1 to < or =10, and >10 fibreyears was 16%, 15%, and 15% for the cases and 18%, 16%, and 9% respectively for the controls. The smoking adjusted odds ratios for the fibreyears based on an unconditional logistic regression were 0.81, 1.02, and 1.60 respectively with increasing exposure categories (not significant). The coefficient (beta) for a log transformed trend was 1.156. Applying the two phase paradigm, these odds ratios became 0.86, 1.33, and 1.94; the latter reached significance and the beta coefficient was 1.178. CONCLUSIONS: The two phase paradigm allowed us to obtain a more precise estimate of the effect of asbestos on lung cancer. Results are consistent with a doubling of the lung cancer risk with 25 fibreyears asbestos exposure.

Adult↗

PubMed1982

Pulmonary asbestos and dust content in East Anglia.

Measurements were made of the asbestos fibre and dust content of samples from 96 surgically excised lungs; 42 necropsies on patients with lung cancer, 11 necropsies on patients with non-pulmonary malignancies, and 59 necropsies on patients without any malignant disease. The patients' ages ranged from 45 to 74 years at the time of study. None of the patients had asbestosis. The distribution of fibres and dust content of the lungs showed a log-normal distribution. There was no significant difference in fibre counts or dust content between men and women, and between lung cancer and non-cancer patients. The only group with an association with a high asbestos fibre count was four necropsy cases of pleural mesothelioma. There was no significant relationship between asbestos fibre count and dust content of the lung. The present data suggest that asbestos fibre counts below 100,000 per gram of dried lung are not related to specific asbestos disease, although in the surgical cases who were closely questioned on their residential and occupational histories most of those with fibre counts above 30,000 per gram dried lung had had occasions of definite or very likely asbestos exposure.

Adenocarcinoma↗

PubMed1987

Asbestos pleural effusion: a clinical entity.

In a case-control study asbestos exposure in 64 consecutive men with idiopathic pleural effusion and 129 randomly sampled age matched male controls was compared. Furthermore, seven women and 64 men with idiopathic pleural effusion were studied, including a three year re-examination, in an attempt to identify characteristics that might distinguish asbestos exposed from non-exposed patients. Asbestos exposure was significantly (p less than 0.01) more frequent in men with idiopathic effusions than in controls. The idiopathic effusions seen in asbestos exposed patients were compatible with the diagnosis "asbestos pleural effusion." Two features were characteristic of patients with asbestos pleural effusion: a chest radiograph at the initial examination showing converging pleural linear structures or rounded atelectasis or a history of recurrent pleural effusion, or both.

Adolescent↗

PubMed2003

Activation of p38 MAP kinase by asbestos in rat mesothelial cells is mediated by oxidative stress.

Asbestos fibers are biopersistent particles that are capable of stimulating chronic inflammatory responses in the pleura of exposed individuals. Exposure of pleural mesothelial cells, the progenitor cell of malignant mesothelioma, to asbestos induces an array of cellular responses. The present studies investigated whether the p38 mitogen-activated protein kinase cascade was induced under asbestos-exposed conditions. p38 plays a vital role in the response to stressful stimuli and enables the cell to enter an inflammatory state characterized by cytokine production. Western blot and in vitro kinase assays showed increases in dual phosphorylation and actual activity of p38 after exposure to fibrous and nonfibrous (milled) crocidolite; in contrast, polystyrene beads and iron (III) oxide had no such effects. In common with other asbestos-induced events, this was shown to be an oxidative stress-sensitive effect, inasmuch as preincubation with N-acetyl-L-cysteine or -tocopherol (vitamin E) ameliorated the effect. The present studies show that p38 activity is important for crocidolite-induced activator protein-1 DNA binding, inasmuch as an inhibitor of p38, SB-203580, reduced this activity. Crocidolite-induced cytotoxicity was also reduced with SB-203580, indicating a role for p38 in asbestos-mediated cell death. Our studies suggest that p38 activity could be a crucial factor in the chronic immune response elicited by asbestos and may represent a target for future pharmacological intervention.

Animals↗

PubMed1983

Early fibrogenicity of asbestos fibers in visceral peritoneum.

Different asbestos types and milled asbestos cement were inoculated intraperitoneally into mice. Mesenteric tissue (appendices epiploicae) was examined by transmission electron microscopy at different intervals between 2 h and 3 weeks after exposure to asbestos. As early as 2 h after asbestos administration, the investigated tissues exhibited focal mesothelial cell loss barring the basement membrane, which at some points was even disrupted. Severe cell damage, obviously caused by the mineral fibers, was discernible in the remaining mesothelial cells. At a later stage, the whole peritoneal sheet underwent inflammatory and diffuse fibrotic processes. The early surface irritation is due to the mechanical influence of the penetrating asbestos fibers. The results confirm our previously published findings with the scanning electron microscope that asbestos has distinct fibrogenic properties.

Animals↗

PubMed1994

p53 protein accumulation in lung carcinomas of patients exposed to asbestos and tobacco smoke.

Primary lung carcinomas often carry mutations in the p53 tumor suppressor gene. Most of these mutations alter the conformation of the p53 protein into a more stable phenotype that makes it immunohistochemically detectable. Asbestos is a carcinogen that can cause deletions in chromosomes and possibly also gene mutations. In this study we examined 70 primary lung carcinomas for p53 protein accumulation using a polyclonal antihuman p53 antibody, CM-1. Patients were interviewed about their occupational and smoking history and classified according to their anamnestical asbestos exposure. Presence of asbestos bodies (AB) was evaluated from histologic samples of peripheral nontumorous lung tissue using both 5-microns-thick sections stained with Perls' iron and 30-microns-thick unstained sections. Abnormal accumulation of p53 protein was found in 36 tumors (51%), more often in patients exposed to asbestos than in patients without exposure (67% versus 40%, p = 0.027). Significant association was also noticed between the accumulation of p53 and the asbestos content of lung tissue: 35% of the p53-positive patients had more than one AB/cm2 compared with 14% of p53-negative cases (p = 0.046). Patients with strongly p53-positive tumors were heavier smokers (57.2 +/- 38.2 pack-years) than patients with p53-negative or lightly positive tumors (38.9 +/- 19.9 pack-years) (p = 0.017). Our findings indicate that both asbestos exposure and heavy smoking can cause abnormal p53 protein accumulation suggestive of mutated p53.

Aged↗

PubMed1987

Mechanisms of macrophage accumulation in the lungs of asbestos-exposed subjects.

Chronic asbestos exposure is associated with the accumulation of mononuclear phagocytes in the lower respiratory tract. This process can be both protective and injurious, since macrophages can aid in asbestos clearance yet also modulate structural derangements of the alveolar walls. To understand why macrophages accumulate in the lungs of asbestos-exposed persons, 2 possible mechanisms were evaluated using alveolar macrophages from subjects with histories of chronic high exposure to airborne asbestos: enhanced recruitment of blood monocytes to the lung, and an increased rate of replication of macrophages in situ. Monoclonal antibody analysis with antibodies that detect surface antigens on the majority of circulating blood monocytes but only on a minority of mature alveolar macrophages demonstrated that an increased proportion of alveolar macrophages of asbestos workers expressed monocyte lineage antigens, suggesting the presence of "young" newly recruited macrophages and thus enhanced recruitment. Culture of the alveolar macrophages from these subjects with [3H]thymidine followed by autoradiography demonstrated an increased proportion of alveolar macrophages synthesizing DNA, suggesting the macrophages are replicating at an increased rate in situ. These observations are consistent with the concept that both enhanced recruitment of blood monocytes and increased local proliferation of alveolar macrophages contribute to the accumulation mononuclear phagocytes in the lung of persons with chronic asbestos exposure.

Asbestos↗

PubMed1989

Alveolar macrophages from patients with asbestos exposure release increased levels of leukotriene B4.

The alveolar influx and subsequent activation of inflammatory cells such as neutrophils and eosinophils are believed to be important in the pathogenesis of many interstitial lung disorders, including asbestosis. Indices of lower respiratory tract abnormalities detected by bronchoalveolar lavage (BAL) were investigated in 93 asbestos-exposed workers as well as in smoking (n = 12) and nonsmoking (n = 10) control subjects. Patients with clinical asbestosis (n = 12) exhibited increases in both BAL neutrophils and BAL eosinophils, expressed as both percentage of total cells and total numbers, when compared to asbestos-exposed workers without asbestosis (n = 81) and control subjects. Significantly greater numbers of BAL neutrophils were also found in asbestos-exposed workers without asbestosis than in either smoking or nonsmoking control subjects. These abnormalities correlated significantly with in vitro BAL alveolar macrophage production of the potent leukocyte chemotaxin, leukotriene B4 (LTB4). For example, basal, unstimulated LTB4 production was 3.1 +/- 0.8 ng/10(6) alveolar macrophages for patients with asbestosis, 1.05 +/- 0.2 ng/10(6) cells in asbestos workers without asbestosis, 0.9 +/- 0.2 ng/10(6) cells in control nonsmokers, and 0.2 +/- 0.05 ng/10(6) cells in control smokers. Stimulated LTB4 release from BAL alveolar macrophages (A23187 or arachidonate) was even more pronounced in asbestos workers with or without asbestosis, suggesting an in vivo priming effect on alveolar macrophage synthesis of LTB4. Cell-free BAL supernatants from asbestos-exposed patients with or without asbestosis also contained significantly greater amounts of LTB4 than did those from control subjects, indicating enhanced in vivo production of this inflammatory mediator.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1990

The degree of roentgenographic parenchymal opacities attributable to smoking among asbestos-exposed subjects.

Considerable controversy surrounds the question of whether cigarette smoking has the potential to increase the prevalence of small opacities on chest roentgenographs among asbestos-exposed workers. To compare the relative contribution of smoking with other predictors of the presence of roentgenographic small opacities, we examined 661 men enrolled in a double-blind, randomized trial designed to assess the efficacy of vitamin A and beta-carotene in the prevention of lung cancer among workers with heavy occupational asbestos exposure. Subjects in the study population had a mean latency of 35 yr from first asbestos exposure and a mean of 28 yr in their trade. The prevalence of roentgenographic abnormalities consistent with asbestos exposure was 26% for pleural abnormalities alone, 10% for parenchymal abnormalities alone, and 20% for pleural and parenchymal abnormalities together. We investigated occupation, age, latency from first asbestos exposure, and smoking status as predictors of roentgenographic small opacities. Smoking history, independent of latency, contributed to the prevalence and extent of small opacities, but its effect was less than that of latency. We conclude, that in the setting of heavy occupational exposure to asbestos, cigarette smoking confers added risk for the development of roentgenographic small opacities.

Aged↗

PubMed1991

Cellular and molecular basis of the asbestos-related diseases.

Asbestosis is an inflammatory and fibrotic process of the alveolar structures mediated, at least in part, by cytokines released by "activated" alveolar macrophages. The process of phagocytosis and "activation" of alveolar macrophages is poorly understood. Are all macrophages activated or only subpopulations? Which cytokines are up-regulated? How does the local milieu modulate profibrotic and antifibrotic mediators? Is protein release accompanied by up-regulation of gene transcription? Is there an ordered sequence of cytokine activity? What roles do neutrophils and lymphocytes play? How can disease progression best be quantified absent further exposure? Answers to these questions are important to direct rational strategies at interdicting the fibrotic process. The question of cancer and asbestos is more vexing. The processes of inflammation, fibrosis, and carcinogenesis appear to be closely intertwined. For example, proto-oncogenes such as c-sis (PDGF B-chain) are up-regulated in activated alveolar macrophages from fibrotic lungs; these and possibly others may play an important role in asbestos carcinogenesis. Second, asbestos can transfect DNA into cells. Furthermore, DNA can adhere to asbestos fibers, and these fibers are capable of direct transmigration into cells. The questions of the mechanisms of cigarette smoke cocarcinogenicity and latency remain. Lastly, if the bronchial epithelium is highly metaplastic throughout from cigarette smoking, what triggers a single (or several) nidus of cells to transform into carcinoma? Malignant mesothelioma poses the most challenging questions because of association with brief asbestos exposure by history. Mesothelial cells are susceptible to minute environmental manipulations, and changes occur after exposure to all fiber types. Yet epidemiologic studies point toward long amphiboles as having greater mesothelioma risk. To test this hypothesis, experimental data must be generated differentiating tumorigenesis risk from short, chrysotile fibers that can migrate to the parietal pleura from the associations of long amphiboles persisting in lung tissue. Despite the future decreasing numbers of clinical cases of asbestos-related disease, solving the important mechanistic questions remaining will contribute significantly to our understanding of fibrosis and cancer.

Animals↗

PubMed2005

Residential proximity to naturally occurring asbestos and mesothelioma risk in California.

RATIONALE: Little is known about environmental exposure to low levels of naturally occurring asbestos (NOA) and malignant mesothelioma (MM) risk. OBJECTIVES: To conduct a cancer registry-based case control study of residential proximity to NOA with MM in California. METHODS: Incident MM cases (n = 2,908) aged 35 yr or more, diagnosed between 1988 and 1997, were selected from the California Cancer Registry and frequency matched to control subjects with pancreatic cancer (n = 2,908) by 5-yr age group and sex. Control subjects were selected by stratified random sampling from 28,123 incident pancreatic cancers in the same time period. We located 93.7% of subjects at the house or street level at initial diagnosis. Individual occupational exposure to asbestos was derived from the longest held occupation, available for 74% of MM cases and 63% of pancreatic cancers. Occupational exposure to asbestos was determined by a priori classification and confirmed by association with mesothelioma. MAIN RESULTS: The adjusted odds ratios and 95% confidence interval for low, medium, and high probabilities of occupational exposures to asbestos were 1.71 (1.32-2.21), 2.51 (1.91-3.30), and 14.94 (8.37-26.67), respectively. Logistic regression analysis from a subset of 1,133 mesothelioma cases and 890 control subjects with pancreatic cancer showed that the odds of mesothelioma decreased approximately 6.3% for every 10 km farther from the nearest asbestos source, an odds ratio of 0.937 (95% confidence interval = 0.895-0.982), adjusted for age, sex, and occupational exposure to asbestos. CONCLUSIONS: These data support the hypothesis that residential proximity to NOA is significantly associated with increased risk of MM in California.

Adult↗