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PubMedDate not supplied

The role of analytical SEM in the determination of causation in malignant mesothelioma.

The causative relationship between asbestos exposure and mesothelioma is firmly established. Some information in this regard comes from analysis of the fiber content of lung tissue by means of analytical electron microscopy. The author has had the opportunity to study the lung asbestos content of 396 cases of mesothelioma, including 28 peritoneal cases, by means of analytical scanning electron microscopy. The highest fiber levels occurred in patients who also had asbestosis, which was found in 12% of pleural and 43% of peritoneal cases. Elevated tissue asbestos content was identified in 87% of pleural and 75% of peritoneal cases. Peritoneal cases that are asbestos related have on average a higher lung fiber burden than pleural cases. Mesotheliomas in women have elevated tissue asbestos content in about 60% of cases, and many of these had a history of exposure as a household contact of an asbestos worker. The main fiber type identified in our series was amphibole, predominantly amosite. These fibers have been demonstrated to reach the target tissue, the pleura.

Asbestos, Amosite↗

PubMed2000

The use of a task-based exposure assessment model (T-BEAM) for assessment of metal fume exposures during welding and thermal cutting.

Elevated disease rates have been documented among construction workers for cancer, pneumonoconiosis, asbestosis, and silicosis. However, methodologies for exposure assessment in construction are not well described in the U.S. literature. Working through a cooperative agreement with the National Institute for Occupational Safety and Health (NIOSH), the Center to Protect Workers' Rights--a research arm of the Building and Construction Trades Department, AFL-CIO--has developed and used a "Task-Based Exposure Assessment Model (T-BEAM)" for construction. The characteristic elements of T-BEAM are: (1) an emphasis on the identification, implementation, and evaluation of engineering and work practice controls; and (2) use of experienced, specially trained construction workers (construction safety and health specialists) in the exposure assessment process. A task-based approach was used because tasks, or specialized skills, form the single greatest thread of continuity in the dynamic environment of construction. Workers in the construction industry come from several crafts and are typically employed by a large number of contractors throughout their career. Project types (e.g., residential or industrial rehabilitation) are also highly variable and present unique health risks. Finally, because construction involves building, renovating, or dismantling physical surroundings, the work site is constantly changing. Between 1995 and 1996, T-BEAM was applied to the collection of approximately 200 personal exposure measurements associated with "hot work tasks"--welding and thermal cutting. Data were collected with the assistance of specially trained, journeyman ironworkers, pipe fitters, and boilermakers on nine construction sites located throughout the United States. Portable local exhaust ventilation was provided to participating contractors with the intent of measuring its impact on exposure. Results indicate that data collected in a standardized, systematic fashion from multiple work sites can be used to characterize exposures among sampled trades. Comparison of results to American Conference of Governmental Industrial Hygienists (ACGIH) threshold limit values (TLVs) demonstrate a significant health hazard among sampled trades posed by welding and thermal cutting fume, manganese, nickel, and chromium VI. Direct estimates of the probability of exceeding the ACGIH TLV for respirable particulate suggests that boilermakers (100%) and ironworkers (71%) are at greatest risk. Other task variables evaluated with respect to exposure include task, whether work was performed indoors or outdoors, intermittency of work, and use of ventilation. Use of local or mechanical ventilation reduced mean exposures to fumes significantly.

Adult↗

PubMed1987

Asbestos-induced changes in rat lung parenchyma.

Fischer 344 rats have been exposed to UICC crocidolite by whole-body inhalation procedures for periods of 1 d to 12 mo. Material was obtained from the same location in the left lung, and the numbers of cells in the parenchyma were identified and determined by transmission electron microscopy. An immediate increase (1 d of exposure) was evident in the number of type II cells, suggesting a direct action of the dust on these cells. The number of interstitial and alveolar macrophages showed a significant increase after 3 mo of exposure. The number of alveolar macrophages containing dust particles after a 1-d exposure was 49%, and the corresponding value after 12 mo of exposure was 92%. The longer periods of exposure were associated with an increase in the number of particles per macrophage. Polymorphs appeared in the interstitium at airway bifurcations, prior to their appearance in the alveolar space. These bifurcations were also the initial sites where evidence of cell damage and collagen deposition was seen. In this experiment crocidolite appears to be weakly fibrogenic, and other factors may be needed to produce the marked lesions seen in human asbestosis.

Animals↗

PubMedDate not supplied

National Occupational Health Service policies and programs for workers in small-scale industries in China.

Over the 14 years since economic reform began, and the restructuring of the economy to encourage international trade, a large number of township enterprises have been developed and put into operation in the Peoples Republic of China. From 1978 to 1991, the number of enterprises has increased 11.5 times; the number of employees has increased 2.4 times; the fixed assets have increased 13.7 times; and the value of the total output has increased 22.5 times. In this article, a report is given on a sample survey in 30 counties in 1990, which showed that 82.69% of rural industrial enterprises had at least one type of occupational hazard in their work environments. Workers engaged in at least one type of hazardous working environment accounted for 33.91% of the blue-collar workers. Physical examinations were performed for seven types of occupational diseases: silicosis, coal worker's pneumoconiosis, asbestosis, chronic lead poisoning, benzene analogs poisoning, chronic chromium poisoning, and noise-induced hearing loss. The total detectable rate of the seven types of occupational diseases was 4.4% among those workers. In addition, 11% had illnesses suspected of being (though not proven to be) caused by occupational exposures. Most township enterprises do not provide basic occupational health services. The coverage of five routine occupational health service activities provided for township enterprises were very limited, from 1.4 to 36%.

China↗

PubMed1979

Evaluation of dust exposure in asbestos cement manufacturing operations.

Previous investigations of the health of workers of the asbestos cement industry have demonstrated dose-response relationships for the diffuse radiographic changes of asbestosis and pulmonary function impairment. Studies of the mortality experience of past employees have also identified levels of cumulative exposure above which an excess of respiratory cancer could be detected. These epidemiologic studies were based on particulate concentrations determined by the midget impinger. We attempted to develop information that might lead to conversion of particulate to fiber concentrations in the industry in order that the risk assessment could be related to the current membrane filter methods. Pairs of impinger and membrane filter samples were taken in the various areas of the plant. Personal samples were also taken to determine the current exposure of workers. The ratio of fiber concentration to particle count varied from 0.63 to 2.5. Por correlation (0.18) was obtained at low fiber and particle counts and good correlation (0.91) was demonstrated in dustry areas where asbestos and silica were handled in a dry form. The concentration of fibers in 80% of the personal samples was less than 2 fibers/cc, and 60% were less than 0.5 fibers/cc. The results also show that no one conversion factor can be used for all areas of this type of operation.

Asbestos↗

PubMed2005

Evidence for excess colorectal cancer incidence among asbestos-exposed men in the Beta-Carotene and Retinol Efficacy Trial.

The relation between asbestos exposure and colorectal cancer remains controversial. The authors of this 1984-2004 US study examined the association among 3,897 occupationally exposed participants in the Beta-Carotene and Retinol Efficacy Trial (CARET) for chemoprevention of lung cancer, followed prospectively for 10-18 years. When a Cox stratified proportional hazards model was used, risks of colorectal cancer were elevated among male heavy smokers exposed to asbestos. Their relative risk was 1.36 (95% confidence interval: 0.96, 1.93) when compared with that for CARET heavy smokers not exposed to asbestos, after adjusting for age, smoking history, and intervention arm. The presence of asbestos-induced pleural plaques at baseline was associated with a relative risk of 1.54 (95% confidence interval: 0.99, 2.40); colorectal cancer risk also increased with worsening pulmonary asbestosis (p = 0.03 for trend). A dose-response trend based on years of asbestos exposure was less evident. Nonetheless, these data suggest that colorectal cancer risk is elevated among men occupationally exposed to asbestos, especially those with evidence of nonmalignant asbestos-associated radiographic changes.

Adult↗

PubMed1984

Cancer in a factory using amosite asbestos.

The paper describes the mortality experience of 5969 men employed in a factory where insulation board was manufactured using amosite asbestos from 1947 to 1979. 422 (7%) of the men were known to have died by the end of 1980. Among the 4820 men engaged in the manufacture of insulation board a doubling of the risk of lung cancer has occurred (57 deaths observed; 29 deaths expected). An excess is present both in men who entered the factory before and after 1960. Among the 2461 for whom smoking information is available a detectable excess risk is limited to current smokers exposed to higher levels of asbestos. Apart from five deaths from mesothelioma no statistically large or significant excesses of mortality from cancers of other sites have occurred, but further follow-up of the cohort is in progress. Nine deaths from asbestosis have been recorded. The results are discussed in the light of other studies of the effects of exposure to amosite asbestos.

Adult↗

PubMed1988

Direct enhancement by cigarette smoke of asbestos fiber penetration and asbestos-induced epithelial proliferation in rat tracheal explants.

Tracheal explants from Sprague-Dawley rats were briefly exposed to cigarette smoke or air (control) and then to amosite asbestos. Asbestos fibers in or under the tracheal epithelium were counted and extent of hyperplastic lesions was ascertained at 24 hours, 72 hours, and 1 week after exposure. Smoke-exposed cultures showed significantly greater numbers of fibers in the epithelium and greater proliferative activity compared to findings in cultures not exposed to smoke. These observations indicate that very short exposure to cigarette smoke can directly affect the response of the epithelium to asbestos fibers and that smoke exposure need not be concurrent with asbestos exposure for such event to occur. These reactions may play a role in the greater incidences of lung cancer and asbestosis seen in asbestos-exposed workers who smoke.

Animals↗

PubMed1996

Glutathione S-transferase and N-acetyltransferase genotypes and asbestos-associated pulmonary disorders.

BACKGROUND: Humans vary in their ability to metabolize endogenous and exogenous compounds. Glutathione S-transferases (GSTs) and N-acetyltransferases (NATs) are enzymes involved in the detoxification of hazardous agents. The GSTM1 and GSTT1 genes exhibit null (i.e., deletion) polymorphisms; in specific individuals, homozygous deletion (i.e., both copies lost) of these genes can be detected. Polymorphism of the NAT2 gene results in slow and fast acetylators of potentially toxic substances. The GSTM1-null and the NAT2 slow-acetylator genotypes have been associated with increased risks for the development of environmentally induced cancers. PURPOSE: We assessed whether homozygous GSTM1-null or GSTT1-null genotypes or the NAT2 slow-acetylator genotype were associated with increased risks for the development of malignant and nonmalignant asbestos-related pulmonary disorders in a cohort of Finnish construction workers. METHODS: The study population consisted of 145 asbestos insulators who were classified as having been exposed to high levels of asbestos; 69 of these individuals had no pulmonary disorders (control subjects), and 76 had either malignant mesothelioma (n = 24) or nonmalignant pulmonary disorders, such as asbestosis and/or pleural plaques (n = 52). Lymphocyte DNA and the polymerase chain reaction were used to determine the GSTM1, GSTT1, and NAT2 genotypes of the study subjects. Odds ratios (ORs) and 95% confidence intervals (CIs) estimating the relative risks of disease associated with specific genotypes were calculated from 2 x 2 tables by use of Fisher's exact method. RESULTS: Risks for the development of asbestos-related pulmonary disorders were not affected significantly by homozygous deletion of the GSTM1 or GSTT1 genes. However, the risk of developing both malignant and nonmalignant pulmonary disorders for individuals with a NAT2 slow-acetylator genotype was more than twice that observed for those with a NAT2 fast-acetylator genotype (OR = 2.3; 95% CI = 1.1-4.7); the risk of developing malignant mesothelioma for NAT2 slow acetylators was increased almost fourfold (OR = 3.8; 95% CI = 1.2-14.3). Individuals who lacked the GSTM1 gene and possessed a NAT2 slow-acetylator genotype had a risk of developing malignant and nonmalignant pulmonary disorders that was approximately fivefold greater than that observed for those who had the GSTM1 gene and a NAT2 fast-acetylator genotype (OR = 5.1; 95% CI = 1.6-17.6); these individuals had a fourfold increased risk of developing nonmalignant pulmonary disorders (OR = 4.1; 95% CI = 1.1-17.2) and an eightfold increased risk of developing malignant mesothelioma (OR = 7.8; 95% CI = 1.4-78.7) when compared with the same reference group. CONCLUSIONS: Individuals with homozygous deletion of the GSTM1 gene and a NAT2 slow-acetylator genotype who are exposed to high levels of asbestos appear to have enhanced susceptibility to asbestos-related pulmonary disorders.

Acetylation↗

PubMed1996

Silicosis among foundry workers. Implication for the need to revise the OSHA standard.

To evaluate the risk of pneumoconiosis among workers in a Midwestern automotive foundry, medical records and silica sand exposure data were analyzed for 1,072 current and retired employees with at least 5 years of employment as of June 1991. Approximately half of these employees had worked at the foundry for 20 or more years. Sixty workers were found to have radiographic evidence of pneumoconiosis. Twenty-eight workers had radiographs consistent with silicosis, of which 25 were consistent with simple silicosis and three with progressive massive fibrosis. The prevalence of radiographic changes consistent with silicosis increased with: number of years worked at the foundry (6% for 20-29 years and 12% for 30 or more years); cigarette smoking (12.2% among smokers with high silica exposure vs. 4.4% among never smokers with high silica exposure); work area within the foundry (cleaning room, core room, mold area, core knockout); and quantitative silica exposure (0.3-2.7% of workers at the current Occupational Safety and Health Administration (OSHA) standard and 4.9-9.9% of workers above the OSHA standard). In addition, the odds of developing radiographic changes consistent with silicosis were increased for African Americans (odds ratio = 2.14, 95% confidence interval 0.85-5.60) in comparison with whites. (The risk was similar when silica exposure was equal, but African-American workers on average had greater exposure to silica, despite having a similar duration of work as white workers.) Another eight workers had radiographic evidence of asbestosis, and 24 had pleural plaques. These asbestos-related changes were not associated with increasing exposure to silica but rather were associated with being in the maintenance department and performing repair work. After controlling for cigarette smoking, race, and exposure to silica at another job besides the foundry, the authors found a 1.45 increased risk of developing a radiograph consistent with silicosis after 20 years of work at the current OSHA standard, and a 2.10 increased risk after 40 years of work at the current OSHA standard. On the basis of these findings, the authors recommend maintaining silica air levels no higher than the exposure level of 0.05 mg/m3 recommended by the National Institute for Occupational Safety and Health.

Black People↗

PubMed1992

Asbestos-related lung disease.

Asbestos is a versatile fibrous mineral that can cause lung disease and death. Asbestosis, benign pleural disease, lung cancer, and mesothelioma can all result from inhaling asbestos. The history of disease and exposure risks are discussed. The difficult assessment of risk and the long latency period for development of disease demand evaluation and regular surveillance of asbestos-exposed workers.

Asbestos↗

PubMed1997

Pulmonary involvement in unusual multisystem disorders.

The clinical syndrome of interstitial lung disease encompasses a number of clinical disorders that affect the alveolar walls, interstitium, and vicinal structures including small airway and pulmonary vasculature. The syndrome has more than 200 causes including bacterial, viral, fungal, protozoal, and parasitic infections; collagen vascular disorders including systemic lupus erythematosus, rheumatoid arthritis, progressive systemic sclerosis, ankylosing spondylitis, mixed connective tissue disease, Sjögren's syndrome, and various vasculitides; hypersensitivity lung disease or extrinsic allergic alveolitis; inorganic neumoconioses including silicosis, asbestosis, and berylliosis; drug-induced and iatrogenic entities; and disorders of unknown origin including sarcoidosis, idiopathic pulmonary fibrosis, eosinophilic granulomatosis, lymphangioleiomyomatosis, and bronchiolitis obliterans-organizing pneumonitis. Apart from these, there are many uncommon metabolic and immune disorders that can involve pulmonary interstitium. Recently developed epidemiologic, immunologic, and molecular biology techniques undoubtedly will add to the list other entities that may produce interstitial lung disease.

Female↗

PubMed2000

The past and present of pneumoconioses.

Pneumoconioses are still a common cause of chronic lung disease. In industrialized countries, improvements in working conditions and dust control measures have led to a decrease in the incidence of severe forms of silicosis, coal worker pneumoconiosis, and parenchymal asbestosis. However, the diversity of settings in which silica and asbestos are used fuels a continued input of cases, and the burden of cases related to remote exposures is still considerable. Overall, the clinical picture of the classic pneumoconioses and their complications has not changed substantially. However, their limits and links have expanded toward systemic and connective tissue disease, idiopathic pulmonary fibrosis, and antineutrophil cytoplasmic autoantibody-positive vasculitides. Immunologically mediated occupational lung diseases have emerged, such as berylliosis and hard-metal disease. Advances in imaging, mineralogic analysis of bronchoalveolar lavage fluid, and immunologic techniques have been instrumental in describing new patterns of disease and are helpful in litigious or difficult cases.

Antibodies, Antineutrophil Cytoplasmic↗

PubMed1987

Comparison of bronchoalveolar lavage helper/suppressor T-cell ratios in sarcoidosis versus other interstitial lung diseases.

In order to compare the frequency of elevated lymphocyte proportions and elevated Leu3/Leu2 (helper/inducer to suppressor/cytotoxic) ratios in sarcoidosis with those in clinically similar interstitial lung diseases (ILDs), bronchoalveolar lavage (BAL) lymphocyte proportions and Leu3/Leu2 ratios were determined for 20 patients with sarcoidosis and 30 patients with other (non-sarcoidosis) ILDs [cryptogenic fibrosing alveolitis (seven), lung connective tissue disease (seven), extrinsic allergic alveolitis (four), lymphoproliferative disease (two), and asbestosis (ten)], as well as in eight control subjects. BAL lymphocyte proportions were elevated above control values in 19 (95%) patients with pulmonary sarcoidosis (mean value 36 +/- 3%) but also in 12 (39%) patients with non-sarcoidosis ILDs (mean value 17 +/- 4%). Leu3/Leu2 ratios were over 2.5 in 15 (75%) of the sarcoidosis patients (mean ratio 4.4 +/- 1). In all control subjects, however, and in all but one of the non-sarcoidosis groups, Leu3/Leu2 ratios were below 2.5 (p less than 0.001 for each compared to sarcoidosis patients). Helper/suppressor ratios over 2.5 are found in the majority of our sarcoidosis patients and, unlike raised lymphocyte proportions alone, are not commonly seen in other ILDs, suggesting that evaluation of BAL helper/suppressor cell ratios may be of value in the investigation of patients with ILD.

Adult↗

PubMed1989

The role of bronchoalveolar lavage in the assessment of diffuse lung diseases.

Bronchoalveolar lavage is a safe and simple technique for sampling the inflammatory cells of the lung. However, while its use in the evaluation of pulmonary pathogenic mechanisms is both well accepted and described, its clinical utility is more controversial. Marked variation in results may occur through variation in the lavage procedure. Standardisation of the lavage technique and laboratory processing of the specimen are essential for reliable results. This review examines the current clinical role of bronchoalveolar lavage in the assessment of patients with diffuse lung diseases, and immunocompromised patients with pulmonary infiltrates. In this latter category, for patients with Acquired Immunodeficiency Syndrome, lavage is of equal efficacy to lung biopsy and can establish the cause of pulmonary infiltrates in over 90% of cases. Bronchoalveolar lavage can detect abnormalities in patients with diffuse lung diseases prior to the development of irreversible fibrosis. Lavage features have been described for sarcoidosis, cryptogenic fibrosing alveolitis, extrinsic allergic alveolitis, connective tissue diseases, and asbestosis. In cryptogenic fibrosing alveolitis lavage data may be used to indicate a subsequent deterioration in the patient's condition, or predict a favourable response to therapy.

Alveolitis, Extrinsic Allergic↗

PubMed1991

The clinical relevance of asbestos-induced pleural fibrosis.

Asbestos-induced pleural fibrosis is the most common radiographic abnormality among asbestos-exposed persons. Circumscribed pleural plaques and diffuse pleural thickening account for more than 90% of the asbestos-induced chest wall abnormalities, and their prevalence is expected to increase for the next 15 to 20 years. Several investigators have recently found that pleural plaques and diffuse pleural thickening independently contribute to the development of restrictive lung function. The work presented in this paper indicates that asbestos-induced pleural fibrosis is also associated with evidence of interstitial lung abnormalities, even among those with normal parenchyma on chest X-ray film. These parenchymal abnormalities include an increased percentage of lymphocytes on bronchoalveolar lavage and an increase in the interstitial changes observed on high-resolution chest computerized tomography (HRCT) scan. However, neither a lymphocytic alveolitis nor an interstitial parenchymal fibrosis influenced the relationship between pleural fibrosis and restrictive lung function. We conclude that asbestos-induced pleural disease contributes to the development of restrictive lung function and identify a group of exposed individuals who are at excess risk of asbestosis.

Asbestos↗

PubMed1991

The Veterans Administration's Asbestos Abatement Program.

1. The Veterans Administration has developed a program of asbestos abatement for its more than 1000 buildings, where health care personnel from 173 hospitals and 238 ambulatory care clinics are likely to encounter respirable asbestos. 2. This is a costly program, which has averaged about $25 million annually for the past ten years. 3. The VA has banned the use of new asbestos products containing more than 1% of asbestos in building construction or renovation projects. 4. Industrial hygiene engineering programs have been ordered instituted at all VA medical centers to monitor dust levels in compliance with OSHA and EPA requirements. 5. Health surveillance programs, managed by an environmental health physician at each medical center, have been instituted for all personnel who have been identified to have breathed asbestos fibers in excess of OSHA-EPA threshold limit values. 6. The health care program focuses on the identification of asbestosis and asbestos-related cancer through periodic X-ray films, lung function tests, and electrocardiographic and physical examination screening. 7. The program also stresses cessation of smoking.

Air Pollution, Indoor↗

PubMed1992

[Three cases of lower respiratory tract infection worsened after rhinovirus infection].

We experienced three cases of lower respiratory tract infections worsened after Rhinovirus infection. Case 1: A 42-year-old male with diffuse panbronchiolitis was admitted to our hospital with the complaint of dyspnea on November 21, 1988. Rhinovirus was isolated from nasal washing and P. aeruginosa was cultured from transtracheal aspiration (TTA). Case 2: A 67-year-old male, whose underlying disease was pulmonary asbestosis, was admitted to our hospital complaining of pyrexia on June 12, 1990. Rhinovirus was isolated from TTA and H. influenzae and others were cultured from TTA. Case 3: A 64-year-old male with pulmonary emphysema was admitted to our hospital with a complaint of dyspnea on August 11, 1989. On December 17, 1989 the patient developed rhinorrhea and complained of purulent sputum, pyrexia and dyspnea after five days. Rhinovirus was isolated from nasal washing and TTA and S. nonhaemolyticus and others were cultured from TTA. As indicated in this report, it is interesting to study the relationship between viral infection of the upper respiratory tract and bacterial infection of the lower respiratory tract.

Adult↗