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PubMed1986

Lung asbestos content in long-term residents of a chrysotile mining town.

The effects of long-term exposure to very small amounts of chrysotile asbestos are controversial. To examine this problem, the lung asbestos content from 7 long-term (25 yr and greater) residents of Thetford Mines, Quebec, who were never employed in the chrysotile mining and milling industry, was analyzed. Thetford Mines is a chrysotile mining town with a demonstrated ambient atmospheric concentration of chrysotile asbestos approximately 200 to 500 times that in urban areas of North America. Data on the residents' lungs were compared with those obtained from 20 long-term (25 yr and greater) chrysotile industry workers from Thetford Mines and 20 members of the general population of Vancouver. The median concentrations of chrysotile and tremolite in the Thetford residents were only about one fiftieth of those of the chrysotile workers, but about 10 times that of the population of Vancouver. Because long fibers of asbestos are generally thought to be more dangerous than short ones are, the sizes of fibers from these 3 groups were also examined. The fiber size distribution of the asbestos from the Thetford residents was significantly longer than that of the Vancouver population, and resembled that of the chrysotile workers. Because epidemiologic studies have consistently failed to find an increased respiratory disease incidence in lifelong residents of Quebec chrysotile mining towns who were never employed in the chrysotile industry, these findings imply that even asbestos burdens much higher, and fiber size distributions much longer, than those of the general population of most North American cities, are not associated with demonstrable pathologic effects.

Aged↗

PubMed1983

Interaction of asbestos with metaplastic squamous epithelium developing in organ cultures of hamster trachea.

The normal mucociliary epithelium of the respiratory tract in chronic cigarette smokers often is replaced focally by a metaplastic squamous epithelium. Because asbestos workers who smoke have a substantially greater risk of bronchogenic carcinoma than nonsmokers, we hypothesized that interaction of asbestos with squamous epithelium might be a contributing factor. To address this question, an in vitro model was developed to study the interaction of asbestos with both mucociliary and squamous epithelium. Explants of tracheas from hamsters were cultured in either a chemically defined minimal essential medium, which maintains a differentiated epithelium, or a nutritionally complex medium, which encourages the development of squamous metaplasia. Scanning electron microscopy (SEM) was used to measure quantitatively the development of a squamous epithelial surface on the explants. The interaction of chrysotile and crocidolite asbestos with cells of the mucociliary and squamous epithelium was studied using both SEM and transmission electron microscopy (TEM). Long fibers of asbestos were cleared, whereas shorter fibers were phagocytized by cells of the mucociliary epithelium. In contrast, asbestos was phagocytized by superficial squamous cells regardless of fiber length, and fibers penetrated between intercellular junctions in the metaplastic epithelium. The relevance of these interactions to the induction of bronchogenic carcinoma is discussed.

Animals↗

PubMed2002

The asbestos dilemma: I. Assessment of risk.

This paper gives a critical review of current problems related to quantitative health risk assessment of exposure to asbestos, and particularly to chrysotile, the only type of asbestos still available on the market. The paper reviews types, sources, uses and the main recognised health effects of asbestos, paying particular attention to the health-related properties of fibres and the role of their biopersistence. The main focus is on yet unresolved issues which introduce a large margin of uncertainty into the published quantitative risk assessments: 1) Are all asbestos types equally dangerous or is chrysotile asbestos less dangerous than amphiboles? 2) Are health effects of asbestos fibres threshold or non-threshold effects? 3) Are errors in mathematical modelling of risks so great as to make the risk evaluations worthless? Attention is also given to errors in estimates of past exposures, uncertainties and unspecificities of models and to the unfeasibility of practical application of some well recognized risk assessment models.

Asbestos↗

PubMed1983

Interactions of chrysotile and crocidolite asbestos with red blood cell membranes. Chrysotile binds to sialic acid.

Chrysotile and crocidolite are commonly used forms of asbestos. Hemolysis has been widely used as a test of membrane injury, and it has been shown previously that chrysotile causes rapid breakdown of red blood cells (RBCs), whereas crocidolite is only weakly hemolytic. A reasonable hypothesis set forth to explain the cytotoxic effects of chrysotile maintains that positively charged chrysotile fibers bind to negatively charged sialic acid residues on RBC membranes causing clustering of membrane proteins and increased cell permeability to Na and K ions. Our studies presented here provide two lines of evidence in direct support of this hypothesis. (a) Morphologic--Ultrastructural techniques showed that both chrysotile and crocidolite asbestos bind to and distort more than 85% of RBCs treated for 15 minutes. The distorting effects of chrysotile, but not crocidolite, were almost totally ablated by pretreating the cells with neuraminidase. In addition, gold-conjugated wheat germ agglutinin was used to label the distribution of sialic acid groups on RBC membranes. Pretreatment of the RBCs with chrysotile, but not crocidolite, reduced the number of gold-conjugated wheat germ agglutinin-labeled sites to less than 30% of the control level. (b) Biochemical--The thiobarbituric acid assay was used to determine the percentage of sialic acid that remained with the cell pellet after neuraminidase and/or asbestos treatment. Asbestos treatment alone caused no release of sialic acid from the cells. Neuraminidase treatment for 3.5 hours removed more than 80% of the sialic acid from cell surfaces. Chrysotile, but not crocidolite, asbestos prevented neuraminidase-mediated removal of sialic acid from RBCs. In addition, x-ray energy spectrometry of freeze-dried cells showed that RBCs distorted by chrysotile, but not by crocidolite, exhibited significant alterations in intracellular Na:K ratios. The morphologic and biochemical data strongly support the hypothesis that chrysotile asbestos binds to sialic acid groups on RBC membranes. Consequently, the sialic acid residues are redistributed on the surfaces of distorted cells which then are unable to maintain a normal Na:K balance with the surrounding medium.

Animals↗

PubMed1984

Dependence of asbestos- and mineral dust-induced transformation of mammalian cells in culture on fiber dimension.

The abilities of chrysotile and crocidolite asbestos, glass fibers of differing dimensions, and nonfibrous mineral particulates to induce morphological transformation of Syrian hamster embryo cells in culture were compared. Chrysotile and crocidolite asbestos induced morphologically transformed colonies which were indistinguishable from transformed colonies observed following treatment with known chemical carcinogens. A linear, dose-dependent increase in the frequency of transformed colonies was observed. The slope of the dose-response curve on a log-log scale was approximately 1, which is consistent with a one-hit mechanism for their induction. The transforming potency of chrysotile asbestos was decreased by milling of the fibers but not by extraction with an organic solvent. Chrysotile asbestos was nearly twice as potent in inducing morphological transformation as crocidolite asbestos. Glass fibers were also very active in this assay. Thin glass fibers with an average diameter of 0.1 to 0.2 micrometer were as active as asbestos. In contrast, two nonfibrous particulates, alpha-quartz and Min-U-Sil, were inactive over the same concentration range used for the fibrous dusts; however, both were active at higher doses. The effect of varying fiber dimension on induction of morphological transformation was examined with glass fibers. When compared on a per-weight basis, thick glass fibers [average diameter, 0.8 plus/minus 0.06 micrometer (S.E.)] were 20-fold less potent than thin fibers [average diameter, 0.13 plus/minus 0.005 micrometer] in inducing cell transformation. When the average fiber length of thin glass fibers was reduced from 9.5 to 1.7 micrometer by milling the fibers in a mortar and pestle, a 10-fold decrease in transforming activity resulted. When the average fiber length was reduced to 0.95 micrometer, transforming ability was totally absent. The cytotoxic potencies of the various mineral dusts correlated with their transforming potencies. The varying abilities of the mineral dusts to induce cell transformation in vitro are similar to their abilities to induce mesotheliomas in vivo. Thus, this system provides a unique model for studying the mechanism of mineral fiber tumorigenesis and for comparing the relative risks of mineral dusts.

Animals↗

PubMed1986

Gallium scanning in differentiating malignant from benign asbestos-related pleural disease.

In order to assess the utility of 67gallium citrate in delineating malignant pleural mesothelioma from benign asbestos-related pleural disease, 49 patients with malignant mesothelioma and 16 with benign asbestos-related pleural disease were studied. Seven patients with malignant mesothelioma had no history of asbestos exposure, while the remaining 58 patients were exposed. Forty-three of the 49 patients (88%) with malignant mesothelioma had a positive 67gallium scan including 36 of the 42 (86%) patients with asbestos exposure and all 7 patients without a history of asbestos exposure. Three of 16 patients (19%) with benign asbestos-related pleural disease had a positive scan. 67Gallium radionuclide imaging is nonspecific but may be valuable in noninvasive monitoring of asbestos-exposed populations, which have a high risk for the late development of benign and/or malignant pleural disease.

Asbestosis↗

PubMed2006

Asbestos mineral analysis by UV Raman and energy-dispersive X-ray spectroscopy.

The applicability of a UV micro-Raman setup was assessed for the rapid identification of fibrous asbestos minerals using 257 and 244 nm laser light for excitation. Raman spectra were obtained from six asbestos reference standards belonging to two basic structural groups: the serpentines (chrysotile) and the amphiboles (crocidolite, tremolite, amosite, anthophyllite, and actinolite). The UV Raman spectra reported here for the first time are free from fluorescence, which is especially helpful in assessing the hydroxyl-stretching vibrations. The spectra exhibit sharp bands characteristic of each asbestos species, which can be used for the unambiguous identification of known and unknown asbestos fibres. Evident changes of the relative band intensities sensitively reflect the chemical substitutions that typically occur in asbestos minerals. The elemental composition of the asbestos reference samples was analysed by using a scanning electron microscope equipped with an energy-dispersive X-ray (EDX) spectrometer. The discussion of the experimental results in terms of EDX analysis sheds new light on the structural and vibrational consequences of cation distribution in asbestos minerals.

Journal Article↗

PubMed2001

Physicochemical Studies on the Adsorption Properties of Asbestos.

Toxic asbestos fibers are known to be carriers of carcinogenic polyaromatic hydrocarbons (PAH) when ingested by human lungs. To clarify the asbestos-PAH interactions, the adsorption properties of four different asbestos, namely amosite, anthofillite, crocidolite, and chrysotile (termed AMOS, ANTHO, CROX, and CHRYS, respectively), toward pyrene (py) were investigated by electron paramagnetic resonance (EPR) and fluorescence spectroscopy, both steady state and time resolved. Pyrene was labeled with a nitroxide TEMPO radical (py-T) for the EPR study. EPR provided information on the adsorption ability of the surface toward py-T and on the interactions between py-T and surface sites, mainly cooperative in nature. Pyrene molecules organize on AMOS samples in a packed layer; the radical works as a separator and prevents the attaching of the py-T molecules at the surface, but the N-O groups of the few adsorbed molecules directly interact with the surface. The interacting sites at the ANTHO surface are quite far from each other; therefore py-T instead of py may form a monolayer at the asbestos surface. The surface of CROX strongly adsorbs both excimers of py and monomers of py-T, orienting the nitroxide groups toward the polar sites at the surface. The surface of CHRYS is the most adsorbing toward py and py-T, but the nitroxide group does not directly interact with the surface. By increasing concentration, py-T saturates the CROX and the CHRYS surface interacting sites, and then forms a disordered liquid-like multilayer. The close average distance calculated for py-T adsorbed at the CROX surface (12 Å) suggests that the py-T molecules intercalate in an "up-and-down" conformation. The chemical composition of the different asbestos and their different structural properties affect the distribution of the polar sites at the external surface, modifying the adsorption properties. This study confirms the synergetic effect between the toxicity of the asbestos fibers and the adsorption of polyaromatic hydro carbons at their surface, which mainly depends on the surface properties of the asbestos. Copyright 2001 Academic Press.

Journal Article↗

PubMed1983

Airway function in lifetime-nonsmoking older asbestos workers.

Previous studies of lung function in asbestos workers have documented airflow limitation in many of the workers, but the specific influence of asbestos exposure could not be clearly differentiated from the effects of the cigarette smoking habit. In this study, airway function was evaluated in lifetime-nonsmoking, long-term workers of the mines and mills of Québec. The 17 asbestos workers in this study had worked for an average of 28 years in the mines and mills of the local asbestos industry and did not have any other respiratory industrial dust exposure. They did not have a history of previous pulmonary disease and did not meet the usual diagnostic criteria for chronic bronchitis, emphysema, or asthma. Seven of the workers met the diagnostic criteria for asbestosis and 10 workers did not. The latter group of workers did not differ from a matched control group except in terms of a higher isoflow volume (p less than 0.05). The workers with asbestosis, however, had a restrictive pattern of lung function, increased isoflow volume, and increased upstream resistance at low lung volumes (p less than 0.01). Lung biopsy in three of the patients with the disease demonstrated peribronchiolar alveolitis and fibrosis with obliteration and narrowing of the small airways. These data on lifetime-nonsmoking, long-term asbestos workers provide further evidence of small airway obstruction associated with asbestos exposure and independent of the smoking habit. This airflow limitation was observed predominantly in workers with a restrictive pattern of lung function associated with peribronchiolar alveolitis. The lifetime-nonsmoking asbestos workers without restrictive patterns of lung function had minimal dysfunction of the peripheral airways.

Aged↗

PubMedDate not supplied

Pulmonary function of nonsmoking female asbestos workers without radiographic signs of asbestosis.

Researchers disagree about whether exposure to asbestos causes significant respiratory impairments and airway obstruction in the absence of radiographic asbestosis and smoking. To obtain confirmatory information, the authors examined pulmonary function of 208 nonsmoking female asbestos workers who did not have asbestosis and 136 controls. The authors observed an overall lower single-breath carbon monoxide diffusing capacity in the asbestos workers than in controls. In addition, significant decreases in percentage vital capacity, percentage forced vital capacity, and percentage mean forced expiratory flow during the middle half of the forced vital capacity were evident in the older workers. Logistic regression analysis revealed that asbestos exposure was associated with abnormal single-breath carbon monoxide diffusing capacity, vital capacity, and mean forced expiratory flow during the middle half of the forced vital capacity among the older workers. The age-related decline in vital capacity, forced vital capacity, and mean forced expiratory flow during the middle half of the forced vital capacity was significantly greater in the asbestos workers than the controls. The findings imply that asbestos-exposure per se contributes predominantly to restricted lung volume and reduced single-breath carbon monoxide diffusing capacity. Asbestos may also cause slight airway obstruction, especially in workers who are heavily exposed.

Adult↗

PubMed1992

Chronological assessment of asbestos exposure on cell composition in murine lung.

To elucidate immune pathogenic mechanisms in asbestosis, lung and spleen lymphoid cell populations were analyzed at defined time intervals (1, 2, 3, 6, and 12 weeks during exposure and 4, 24, and 48 weeks post-exposure) in asbestos-exposed and unexposed (control) mice. Polymorphonuclear leukocytes and macrophages were increased in the lung tissue histologic sections of asbestos-exposed mice compared to controls. No consistent changes were observed in percentages of lung or spleen helper, suppressor, or total lymphocyte populations after asbestos exposure. The numbers of B cells (identified by anti-IgG) in minced lung preparations of asbestos-exposed animals were increased after 12 weeks of exposure. There also was an increase in IgG production in asbestos-exposed mice after 12 weeks exposure and at 4 weeks post-exposure with a return to near baseline levels 24 and 48 weeks after initial exposure. Collectively, these studies demonstrate stimulatory effects of inhaled asbestos fibers on B cells and IgG production after 12 weeks of continuous inhalation of asbestos fibers in a dust generation chamber.

Animals↗

PubMed1998

Upregulation of the PDGF-alpha receptor precedes asbestos-induced lung fibrosis in rats.

Platelet-derived growth factor-AA (PDGF-AA) and its matching alpha receptor (PDGF-R alpha) are upregulated in rat lung fibroblasts (RLFs) after exposure to chrysotile asbestos fibers in vitro, which results in asbestos-induced RLF proliferation. We now report our in vivo observations, which show an increase in the expression of PDGF-R alpha mRNA, but not PDGF-beta receptor mRNA, in asbestos-exposed rat lungs when compared with RNA from air-exposed (sham) and iron-exposed lungs. Western analysis of membrane preparations confirmed the observations on mRNA expression by demonstrating an increase in PDGF-R alpha peptide expression in the asbestos-exposed rat lungs, compared with that in the air-exposed lungs. Immunohistochemistry for the PDGF-R alpha was performed on air- and asbestos-exposed rat lungs and revealed a clear increase in staining within interstitial and subepithelial compartments in the exposed animals. These observations, along with our previous report demonstrating an increase in the PDGF-AA isoform expression immediately after asbestos-exposure, suggest a scenario in which a potent lung mesenchymal cell mitogen, PDGF-AA, and its alpha-receptor are upregulated prior to the development of a fibroproliferative lung lesion, and thus may play a central role in the pathogenesis of asbestos-induced lung fibrosis.

Animals↗

PubMed1989

Chrysotile asbestos inhalation induces tritiated thymidine incorporation by epithelial cells of distal bronchioles.

Previous studies in a rat model of asbestosis have demonstrated increased incorporation of tritiated thymidine by bronchiolar and alveolar epithelial cells 19 to 72 h after a single, 5-h exposure to chrysotile asbestos. This increase in thymidine labeling occurred at the first alveolar duct bifurcations, where terminal bronchioles end and where asbestos deposition is most concentrated. To determine whether airways more proximal than the terminal bronchioles exhibit a similar type of proliferative response to asbestos, incorporation of tritiated thymidine by airway epithelial cells was determined by light microscopic autoradiography. Incorporation by the epithelium in regions of the trachea, mainstem bronchi, and bronchioles was measured in lung tissue from sham-exposed and chrysotile asbestos-exposed rats, zero and 33 h after exposure. Sham-exposed animals and those studied immediately after exposure exhibited no increases in tritiated thymidine incorporation at any airway level. Tritiated thymidine incorporation by epithelial cells of bronchioles in peripheral regions of the lungs was significantly increased, as much as 20-fold, 33 h after chrysotile exposure. In the same asbestos-exposed animals, epithelial cells of the trachea, the bronchi, and the larger bronchioles did not exhibit increased cell labeling. The fact that asbestos was deposited throughout all airway levels, yet increased thymidine incorporation is observed primarily in the peripheral bronchiolar regions, raises interesting questions regarding the mechanisms of asbestos-induced cell proliferation.

Animals↗

PubMed1993

Localized inflammatory pulmonary disease in subjects occupationally exposed to asbestos.

In reviewing pathology materials from patients occupationally exposed to asbestos, we identified eight patients with either localized nodules in their lung or unusual pathologic changes. The chest radiographs of six patients showed isolated parenchymal nodules thought to represent primary neoplasms. In three cases, pathologic examination of these nodules showed intraluminal fibrosis and inflammation of the distal airways, a pattern of change frequently referred to as "bronchiolitis obliterans organizing pneumonitis." In each instance, asbestos bodies were present in association with the fibroinflammatory tissue. In one case, the nodule showed a desquamative interstitial pneumonitis type pattern, and asbestos bodies were present admixed with the alveolar macrophages and occasionally within their cytoplasm. In one case, the nodule was composed of nonspecific inflammation and fibrosis with focal bronchiolitis obliterans and frequent asbestos bodies scattered throughout the area of inflammation and fibrosis, and in another case, necrotizing inflammation association with Aspergillus fungal organisms was identified. Granulomatous inflammation was the dominant pulmonary pathologic change in one patient, and the other patient's lung biopsy specimen showed a diffuse lymphocyte-plasma cell interstitial pneumonitis. The cases reported suggest that asbestos may cause localized lesions in the lung that clinically and radiographically are misinterpreted as cancer and that pathologically show inflammation and fibrosis of the distal airways. In addition, our observations suggest that asbestos may cause granulomatous inflammation, a desquamative interstitial type pneumonitis, and a lymphocytic interstitial pneumonitis type pattern. Our conclusions that asbestos may cause these pathologic changes are supported by case reports in the clinical and pathologic literature, clinicopathologic studies, and by experimental studies.

Aged↗

PubMed1994

Airways obstruction from asbestos exposure. Effects of asbestosis and smoking.

OBJECTIVE: To define the apparent steps in developing airways obstruction vs restrictive lung disease in men exposed to asbestos for more than 20 years who had never smoked vs cigarette smokers. DESIGN: Physiologic signs of asbestosis were studied in cross-sectional age-matched groups of never, current, and ex-cigarette smoking workers. SETTING AND PARTICIPANTS: The study included 8,720 asbestos-exposed construction and shipyard workers in the United States. MEASUREMENTS: FVC, FEV1, FEF25-75, and FEF75-85 were measured by spirometry and total lung capacity (TLC) by planimetry of standard chest radiographs and adjusted for height, age, and duration of cigarette smoking and expressed as percentage of predicted. TLC minus FVC yielded RV. We compared means and mean residuals (measurement minus group mean) expiratory flows and lung volumes in 1,146 men with pulmonary asbestosis age matched to 1,146 without asbestosis who had similar durations of asbestos exposure and to 370 men without asbestos exposure. Next, flows and volumes were regressed against the International Labour Office (ILO) profusion scale of irregular opacities on chest radiographs (PIO) and the duration of asbestos exposure for 1,777 never smokers (NS), 4,550 current smokers, and 2,393 ex-smokers. RESULTS: Asbestos exposure in NS men decreased expiratory flows and increased TLCs compared with unexposed NS men. Further reductions in flows and FVC and increases RV/TLC with radiographic asbestosis were not statistically significant. As the PIO increased from 1/1 to 3/3, obstruction and air trapping increased significantly but TLC did not. CONCLUSIONS: Asbestos exposure reduced flows and produced air trapping after 20 years in workers who never smoked. Smoking increased these abnormalities.

Adult↗

PubMed1986

Fibronectin and procollagen 3 levels in bronchoalveolar lavage of asbestos-exposed human subjects and sheep.

To evaluate the potential interest of levels of fibronectin and procollagen 3 in bronchoalveolar lavage fluid as markers of fibrogenic activity, we characterized the time course of changes in fibronectin and procollagen 3 levels in the tracheal lobe of sheep exposed to nonfibrogenic and fibrogenic materials. We correlated these observations with those of bronchoalveolar lavage in long-term asbestos workers in various stages of disease activity. Following studies before exposure, the tracheal lobe of three groups of 24 sheep were exposed once to 100 ml of phosphate-buffered saline solution (PBS), to 100 mg of latex beads in 100 ml of PBS, or to 100 mg of chrysotile fibers in 100 ml of PBS. Bronchoalveolar lavages were obtained at 0, 1, 2, 4, 8, and 12 months after exposure, and four or five sheep per group were killed after each lavage for histopathologic analysis. Fibronectin in bronchoalveolar lavage fluid increased significantly only in the asbestos-exposed sheep to values two to three times above controls or latex-exposed sheep and remained elevated during the 12 months of the study. Levels of procollagen 3 in bronchoalveolar lavage fluid were increased significantly only during the first two months following exposure in the asbestos-exposed sheep only. In the asbestos workers without disease, levels of fibronectin and procollagen 3 in bronchoalveolar lavage fluid were comparable to controls, but these levels were significantly elevated in those with asbestos-associated alveolitis or asbestosis. This study documents that the measurement of levels of fibronectin and procollagen 3 in bronchoalveolar lavage fluid assesses fibrogenic activity of alveolitis and should be useful to predict its progression in a fibrotic process. In asbestos workers the potential use of these markers is primarily related to early detection of asbestos-induced pulmonary injury.

Adult↗

PubMedDate not supplied

Non-asbestos related diffuse malignant mesothelioma.

AIMS: The association between asbestos exposure and the development of malignant mesothelioma is well known. Nonetheless, a proportion of patients suffering from this disease do not appear to have documented exposure to asbestos fibers from any known source. Available information suggests that a true "background" incidence of this disease exits raising the possibility that other factors contribute to its etiology. This paper will review existing data related to non-asbestos related mesothelioma and suggest avenues for further research. METHODS AND STUDY DESIGN: A comprehensive electronic MEDLARS search of the literature pertinent to non-asbestos related malignant mesothelioma was performed including the years 1996-2001. Hand searches were also carried out to supplement electronically derived information and literature pre-dating 1996. The resulting references were stratified into the following categories and reviewed; (1) radiation associated mesothelioma, (2) familial mesothelioma, (3) dietary factors, (4) childhood mesothelioma and (5) the role or SV40. RESULT: Available information suggests that genetic factors may play a larger role in the etiology of this disease than currently appreciated. The interplay of genes and environment require further elucidation in the pathogenesis of mesothelioma. The role of diet is poorly understood with few studies directly addressing this issue. Whether other environmental or infectious agents are involved in mesothelioma development remains speculative. CONCLUSION: The biology of mesothelioma is an enigma. Although this disease appears to occur in the absence of asbestos exposure, the genetic and biological differences between asbestos related and non-asbestos related tumors is unclear. Additional epidemiological and laboratory studies are needed to provide a better understanding of the relationship between environmental and non-environmental causes of mesothelioma.

Adolescent↗

PubMed1992

Ventilatory function in Nigerian asbestos factory workers.

Ventilatory function indices; forced vital capacity (FVC), forced expiratory volume in one second (FEV1), the percentage of vital capacity in one second (FEV1%) and peak expiratory flow rate (PEFR) were measured to find the effect of asbestos fiber on lung function in 95 male Nigerian asbestos factory workers (aged 25-55 years). The results were compared with a control group of age and sex-matched Nigerians from the same area that were not exposed to asbestos fiber or any known air pollutant. The results were also compared with expected values calculated from linear regression equations worked out for healthy Nigerians. The mean values of FVC, FEV1 and PEFR were significantly lower in the asbestos factory workers than in the control group (P less than 0.01, 0.05 and 0.001 respectively). FEV1 in asbestos factory workers showed a statistically significant negative correlation with the duration of service (P less than 0.05). The reduced FVC and FEV1 and normal FEV1% in asbestos factory workers is indicative of restrictive lung defect and may be attributed to asbestos fiber exposure. Frequent monitoring of the health of these factory workers and control measures should be stepped up in the factory.

Adult↗