Journal of Toxicology and Environmental Health

Our medical research library holds 29 studies published in Journal of Toxicology and Environmental Health (1976–1997). Each entry links to the study's record on PubMed and, where there is one, to the publisher's page and a free full text. 29 have an abstract, the authors' own summary as PubMed records it: open "Abstract" to read it.

About the journal

• Publisher: Taylor & Francis
• Published: 1975–1997, United States
• Language: English
• ISSN: 0098-4108 (print)
• Its record in the NLM Catalog

1990s

• Ferritin adsorption on amosite fibers: possible implications in the formation and toxicity of asbestos bodies. B. Fubini, F. Barceló, C. Otero Areán. 1997;52(4):343-52. PubMed · Publisher

  Abstract

  In order to investigate how endogenous iron can be deposited in vivo on inhaled mineral fibers during early stages of formation of asbestos bodies, in vitro experiments were performed on the adsorption of ferritin onto amosite asbestos. The mineral dust was found to adsorb the protein from an aqueous solution containing 0.3 mg/ml horse spleen ferritin. In order to simulate physiological conditions the aqueous solution was adjusted with 150 mM saline. Polyacrylamide-SDS gel electrophoresis of the desorbed protein showed subunits of approximately 13 and 15 kD, aside from the 20-kD subunit present in the native protein. This suggests that as a result of interactions between ferritin molecules and the solid surface of the mineral fibers, the protein iron core may be released or partially exposed. Data indicate these interactions may have implications in the observed mineral fiber toxicities.

• In vivo accumulation of iron on crocidolite is associated with decrements in oxidant generation by the fiber. A.J. Ghio, A. LeFurgey, V.L. Roggli. 1997;50(2):125-42. PubMed · Publisher

  Abstract

  In vivo exposures to fibrous silicates are characterized by the formation of asbestos bodies. These structures consist of the original fiber with a coating of inexact composition, but it will include iron and protein. We tested the hypothesis that this iron, accumulated on asbestos bodies, participates in electron transport and oxidant generation. Thirty-day-old, male guinea pigs were intratracheally instilled with 1.0 mg crocidolite. Six months later, the animals were anesthetized, euthanized, and the fibers were isolated from the lungs. Energy-dispersive x-ray analysis and x-ray photoelectron spectroscopy confirmed an accumulation of metal onto the fiber after in vivo exposure. Stains for iron demonstrated a heterogeneous distribution of the metal on the silicate, while the uptake of a commercially available polyclonal antibody to ferritin localized to beaded enlargements along the coated fibers. Chelatable [Fe3+] associated with the fiber increased after in vivo exposure. However, oxidant generation by asbestos bodies was decreased relative to uncoated fibers despite the elevation in the concentration of metal associated with the crocidolite. We conclude that iron is accumulated onto fibers in the lungs of guinea pigs. Some portion of this accumulation of iron is in the form of ferritin, and this metal is not chemically reactive in oxidant production. Asbestos bodies may represent a successful attempt by the host to sequester the metal adsorbed to the surface of a fiber and diminish the oxidative challenge introduced by a fibrous silicate. Subsequently, the generation of free radicals by the fibrous silicate is diminished.

• Distinctive profile of alveolar macrophage-derived cytokine release induced by fibrogenic and nonfibrogenic mineral dusts. I. Lemaire, S. Ouellet. 1996;47(5):465-78. PubMed · Publisher

  Abstract

  Groups of 7 Wistar rats each received a single intratracheal instillation of either saline (control), UICC chrysotile B asbestos (5 mg), or very short 4T30 chrysotile asbestos fibers (5 mg). Five animals in each group were killed at 1, 3, and 6 wk posttreatment and analyzed by bronchoalveolar lavage (BAL) for BAL cell populations and cytokine production in conjunction with histopathological assessment of lung tissue. Chrysotile B and short 4T30 chrysotile fibers induced chronic inflammatory reactions characterized by alveolar macrophage (AM) accumulation that resulted, respectively, in lung fibrosis and resolving granuloma. Alveolar macrophages (AM) obtained from rats treated with UICC chrysotile B and short 4T30 chrysotile produced enhanced levels of interleukin-1 (IL-1) and interleukin-6 (IL-6), both spontaneously and in response to lipopolysaccharide (LPS). A different pattern of response was observed for tumor necrosis factor-alpha (TNF-alpha). Fibrogenic chrysotile B caused biphasic changes characterized by significant inhibition of LPS-induced TNF-alpha release by AM 1 and 3 wk after treatment, followed by stimulation of spontaneous and LPS-induced TNF-alpha at 6 wk. In contrast, no significant change in spontaneous and LPS-induced TNF-alpha release was seen with AM from animals with resolving granuloma (4T30 group). Thus, modulation of AM-derived TNF-alpha was correlated under these conditions with the fibrogenic potential of asbestos dusts. These data support a role for TNF-alpha in fibrosis and suggest that TNF-alpha may represent a useful marker of lung damage induced by fibrogenic dusts.

• Alveolar macrophage cytokine and growth factor production in a rat model of crocidolite-induced pulmonary inflammation and fibrosis. K.E. Driscoll, J.K. Maurer, J. Higgins, et al. 1995;46(2):155-69. PubMed · Publisher

  Abstract

  The present study was undertaken to further define the role of alveolar macrophages (AM) in the pulmonary response to crocidolite fibers. Briefly, groups of 4 male F344 rats were intratracheally instilled with saline or saline suspensions of crocidolite at 2 or 20 mg/kg body weight. Animals were sacrificed 3, 7, 14, and 28 d after exposure and the lung response was characterized by analysis of bronchoalveolar lavage fluid (BALF) for markers of lung injury and inflammation. AM obtained in BALF were cultured and their production of the pro-inflammatory cytokines, tumor necrosis factor alpha (TNF alpha), and interleukin-1 (IL-1) were characterized along with fibronectin, a protein known to stimulate fibroblast migration and proliferation. Lung hydroxyproline content was determined 28 d after exposure and lung histopathology was characterized on d 28 and 90 after exposure. Crocidolite instillation resulted in transient dose-related pulmonary inflammation as evidenced by increased numbers of BALF neutrophils at the low dose and neutrophils, macrophages, and lymphocytes at the high dose. Cytotoxicity and increased permeability were demonstrated by increased levels of BALF lactate dehydrogenase (LDH) and total protein, respectively. AM TNF alpha and IL-1 production were increased only at the high crocidolite dose. This cytokine response was greatest at d 3 and decreased thereafter. AM TNF alpha and IL-1 release were positively correlated with the increased BALF neutrophils. In contrast to TNF alpha and IL-1, AM fibronectin release was increased at both the low and high doses, with the magnitude of response increasing over time. Consistent with previous acute asbestos inhalation studies, histopathology revealed inflammation localized at the level of the terminal bronchioles and alveolar ducts. Fibrosis was demonstrated at both doses by increased trichrome staining of lung tissue sections. Only the high dose resulted in a detectable increase in lung hydroxyproline. Given the bioactivities of TNF alpha, IL-1, and fibronectin, their increased production after crocidolite exposure indicates they contribute to the pulmonary inflammation and fibrosis occurring with this mineral fiber. In addition, the correlation of increased AM TNF alpha and IL-1 production with increased BALF neutrophils supports a role for these cytokines in crocidolite-induced inflammatory cell recruitment. Lastly, association of a persistent increase in AM fibronectin production with an eventual increase in lung collagen deposition extends the growing database indicating this response is a predictive marker of pulmonary fibrosis.

• Pulmonary response of mice to fiberglass: cytokinetic and biochemical studies. I.Y. Adamson, H. Prieditis, C. Hedgecock. 1995;46(4):411-24. PubMed · Publisher

  Abstract

  It has been suggested that glass fibers in the respirable size range may pose a health hazard similar to asbestos because of the similarities in physical characteristics. To compare the pulmonary cell response with that described earlier with crocidolite asbestos, we administered a milled fiberglass sample to mice by intratracheal instillation. Little effect was seen at a dose of 0.1 mg, but at 1 mg there was epithelial injury and an inflammatory cell response concentrated at bronchiolar-alveolar duct regions. Cellular incorporation of tritiated thymidine showed that repair of both bronchiolar and alveolar epithelium occurred rapidly. This was followed by an extended increase in cell labeling, particularly in peribronchiolar fibroblasts, from 2 to 8 wk after fiber instillation. Granulomas formed at this site and later there was morphologic evidence of fibrosis, which was confirmed biochemically by a significant increase in lung collagen at 4-16 wk. Although 10 times higher dose is required, the results show that the lung response to fiberglass in this experimental system is similar to that described previously for crocidolite asbestos; the sites of cell injury and repair are the same, and the subsequent fibrotic response produces small airway disease.

• Cytotoxic effects of quartz and chrysotile asbestos: in vitro interspecies comparison with alveolar macrophages. J. Schimmelpfeng, A. Seidel. 1991;33(2):131-40. PubMed · Publisher

  Abstract

  Cytotoxic effects of DQ12 quartz and chrysotile asbestos on alveolar macrophages of different animal species were compared in vitro. The type of cell reaction toward the cytotoxic dusts was always the same: a loss of cell viability (trypan blue dye exclusion test) was accompanied by the release of cytoplasmic and lysosomal enzymes. The extent of cellular destruction depended upon the amount of dust applied. In the range of 50-100 micrograms/ml quartz or chrysotile asbestos, species-specific variations were observed in the sensitivity of the cells. At this concentration alveolar macrophages of dogs, monkeys, and human patients were damaged to a greater extent than the cells from rats and cattle. Simultaneous incubation of the cells with quartz and L-alpha-dipalmitoyl lecithin resulted in a reduction of the cytotoxic quartz effect. The extent of the protective effect varied according to the species. In the case of chrysotile asbestos no reduction of the fibers cytotoxicity was observed in the presence of L-alpha-dipalmitoyl lecithin.

1980s

• Functional and biochemical effects on rat lung following instillation of crocidolite and chrysotile asbestos. S. Hirano, M. Ono, A. Aimoto. 1988;24(1):27-39. PubMed · Publisher

  Abstract

  Groups of rats received a single intratracheal instillation of saline (control), 1.6 mg crocidolite, and 1.6 mg chrysotile. At 1, 3, 6, 9, and 12 mo after instillation, respiratory functional tests were performed and the lungs were biochemically analyzed. Throughout 12 mo, obstructive small-airway abnormalities with air trapping were observed in the asbestos-treated rats. The degree of airway obstruction and air trapping was higher in the chrysotile-treated group than in the crocidolite-treated group. Lung weight increased significantly in both asbestos-treated groups. Collagen and elastin content of unit lung weight significantly increased in the chrysotile-treated group compared with the control and crocidolite-treated group throughout the experimental period up to 12 mo. However, the collagen and elastin content of unit lung weight in the crocidolite-treated group was not as different from the control group. These results indicate that chrysotile is more fibrogenic than crocidolite, as has been suggested in histopathological studies.

• Asbestos-induced changes in rat lung parenchyma. N.F. Johnson. 1987;21(1-2):193-203. PubMed · Publisher

  Abstract

  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.

• Physical and microchemical alterations of chrysotile and amosite asbestos in the hamster lung. G. Kimizuka, N.S. Wang, Y. Hayashi. 1987;21(3):251-64. PubMed · Publisher

  Abstract

  The physical and microchemical alterations of chrysotile and amosite asbestos (Union International Contre le Cancer standard samples) in the hamster lung and in vitro following acid treatments were studied by scanning electron microscopy (SEM) and x-ray energy-dispersive spectrometry (XEDS). Following intratracheal instillation, the ratio of short chrysotile fibers (less than 5 microns in length) decreased initially from 38% to 13% in the hamster lung, but increased again to 56% 2 years after the instillation. The majority of these new short chrysotile fibers had diameters less than 0.05 micron. Contrary to this, short amosite fibers (less than 5 microns in length) decreased from 41% initially to 4% 2 yr after instillating into the hamster lung. The diameters of amosite fibers appeared much less altered than that of chrysotile during the same time period. After 2 yr in the hamster lung, 33% of chrysotile and 68% of amosite found were asbestos bodies. The Si/Mg ratios of chrysotile fibers with diameters less than 0.2 micron were significantly higher than those with diameters between 0.2 and 0.6 micron in all groups: this relationship was reversed in all amosite groups. The Si/Mg ratios of the instillated and acid-treated chrysotile fibers were both higher than that of the same-sized control fibers. Acid treatments of chrysotile fibers in asbestos bodies from the hamster lung further altered their Si/Mg ratio. The Si/Mg ratios of the instillated amosite fibers were lower than that of the same-sized control fibers, but the difference between them disappeared following acid treatments. The hamster lung disposed of both chrysotile and amosite fibers smaller than 5 microns efficiently. Chrysotile and its asbestos bodies appeared to lose Mg ions and to fragment continuously in the hamster lung, and also in vitro with acid treatments. Amosite appeared also to fragment but lose more silicon than magnesium ions, at a much slower rate than that of chrysotile, presumably from the difference in their basic structures.

• Sequence of bronchoalveolar lavage and histopathologic findings in rat lungs early in inhalation asbestos exposure. C.M. Smith, S. Batcher, A. Catanzaro, et al. 1987;20(1-2):147-61. PubMed · Publisher

  Abstract

  To assess the early cellular inflammatory response of the lungs, 7 rats per group were exposed nose-only to 13 mg/m3 of chrysotile asbestos, 7 h/day for 2, 4, or 6 wk. Lung histopathology and bronchoalveolar lavage (BAL) were analyzed. In exposed animals, dose-related bronchiolitis and fibrosis were found that were not seen in control rats (p less than 0.001). In exposed rats, total BAL cells were increased six-to sevenfold over matched controls, and more cells were retrieved with longer exposure (p less than 0.001). In the BAL, counts of macrophages, lymphocytes, and polymorphonuclear cells (PMNs) were each elevated in the exposed rats (each p less than 0.001). PMNs seen histologically and in the BAL may be related to the time period examined. PMNs and lymphocytes observed throughout this 6-wk study support the idea that these cells may have an important role in the early events of asbestos lung injury.

• Early response of the visceral pleura following asbestos exposure: an ultrastructural study. R.F. Dodson, J.O. Ford. 1985;15(5):673-86. PubMed · Publisher

  Abstract

  The acute in vivo response of the visceral pleura following intracheal instillation of amosite asbestos was examined by light microscopy and by transmission and scanning electron microscopy in the guinea pig model. Asbestos fibers were observed close to the pleura in all time periods but were never found within the pleura or subpleural regions proper. Thus, pleural changes occurred in the absence of direct fiber contact. Morphological changes in the pleural and subpleural areas were seen as early as 2 h after exposure and were associated with pathological alterations of the underlying parenchyma. The normally squamous mesothelial cells became pleomorphic in experimental animals, ranging from slightly cuboidal, to protruding "columnar-like" cells, to more bizarre forms. While many organelles remained unaltered, an increase in vacuolization in portions of the pleura indicated localized and advanced intracellular responses. Beginning at 4 h postexposure, varied numbers of particulate-free macrophages were seen on the pleural surface, and were considered an extension of the inflammatory response occurring in the underlying parenchyma. Early proliferation of the mesothelial cells, in limited areas of the pleura, and cytoplasmic extensions into the pleural space were also observed. Distortions of the basal lamina and smooth-muscle bundles accompanied the morphological changes in the pleural cells. A trend toward normality was observed in the longer time frames, but some areas of pleural change persisted through 3 mo postexposure.

• Lung and pleural "free-cell responses" to the intrapulmonary deposition of particles in the rat. B.E. Lehnert, Y.E. Valdez, S.H. Bomalaski. 1985;16(6):823-39. PubMed · Publisher

  Abstract

  Deposition of a high lung burden of particulate carbon or latex in the mouse elicits a biphasic macrophagic response, with the early increase in the size of the population of the alveolar macrophages (AM) being mainly due to an influx of mononuclear phagocytes from the blood compartment and the later phase being due to the egression of interstitial macrophages (IM). In the present study, we investigated the lung's free-cell response in the rat to the intrapulmonary instillation of microspheres and determined the contributions of newly arrived blood monocytes to the macrophagic response over a 30-d period. As of 24 h after deposition, the lavageable population size increased approximately fivefold. Most of the increase in the free cell population was due to a recruitment of polymorphonucleated leukocytes (PMN), although the size of the AM population nearly doubled. Only about 13% of the AM on d 1 were positive for myeloperoxidase activity, suggesting that recruitment of mononuclear phagocytes from the blood compartment plays a limited role in the early expansion of the AM pool in the rat. As of 14 and 30 d after particle deposition, lavaged AM numbers continued to be elevated; the enlarged sizes of the AM populations at these times could be explained, in part, by a continuing influx of blood monocytes. In a parallel component of the study, we also investigated how the pleural cell population might be affected during the lung's free-cell response to the particulate burden. No acute influx of PMN into the pleural space (PS) accompanied the early free-cell response; the chemotactic factors initially involved in recruitment of the PMN into the lung apparently did not reach the PS in significant or biologically active concentrations, or they were inoperable in the pleural compartment. On the other hand, the numbers of macrophages in the PS were significantly elevated on d 1 and 14 after particle deposition in the lung. The macrophagic response in the PS subsided by d 30, but at this latter sacrifice time, pleural mast-cell and lymphocyte numbers were significantly increased and decreased, respectively. These results indicate that the deposition of particles into the lung can lead to numerical alterations in the cell types composing pleural cell populations.

• Relative effects of asbestos and wollastonite on alveolar macrophages. W.H. Pailes, D.J. Judy, H. Resnick, et al. 1984;14(4):497-510. PubMed · Publisher

  Abstract

  Rabbit alveolar macrophages were exposed in culture to chrysotile asbestos, wollastonite, or latex, and the effects on various biochemical and physiological parameters related to cellular viability and fibrogenicity were determined. Exposure of alveolar macrophages to asbestos, wollastonite, or latex for 3 d has no effect on oxygen consumption or cellular volume. However, treatment of alveolar macrophages with as little as 25 micrograms asbestos/ml for 1 d increases lysosomal enzyme release and decreases membrane integrity, i.e., decreases trypan blue exclusion and increases leakage of cytosolic enzymes. In contrast, exposure of alveolar macrophages to wollastonite or latex at 250 micrograms/ml does not induce lysosomal enzyme release or alter membrane integrity even after 3 d of exposure in culture. These data suggest that chrysotile asbestos damages rabbit alveolar macrophages, while wollastonite, a potential substitute for asbestos, is far less cytotoxic.

• Hemolysis by chrysotile asbestos fibers. I. Influence of the sialic acid content in human, rat, and sheep red blood cell membranes. J.P. Pelé, R. Calvert. 1983;12(4-6):827-40. PubMed · Publisher

  Abstract

  Complete removal of accessible sialic acids from human, rat, and sheep red cell membranes does not inhibit the hemolytic properties of chrysotile asbestos fibers. After 60 min of contact, the percentages of hemolysis are comparable between the treated and the nontreated groups. Nevertheless, with low concentrations of fibers the initial velocity of hemolysis of rat and sheep red blood cells is lower in the neuraminidase-treated group. Although sialic acids are not essential for the expression of the hemolytic activity of asbestos, we suggest that these acids could play a role during the first seconds or minutes of the hemolytic process by increasing the electrostatic attraction between the red blood cell membranes and the fibers. However, it is clear that asbestos fibers provoke hemolysis by acting on some other cell membrane component(s).

• Method for removing the ferruginous coating from asbestos bodies. R.F. Dodson, M.G. Williams, G.A. Hurst. 1983;11(4-6):959-66. PubMed · Publisher

  Abstract

  A new technique for removing the ferruginous coating from ferruginous bodies is described. The tissue from occupationally exposed individuals was digested in bleach and the material collected on a Nucleopore filter. The ferruginous bodies were localized by light microscopy and either cleaned on the marked filter or transferred to a marked area on a clean filter. The chemical treatment consisted of an 8% oxalic acid bath used at various temperatures. It was determined that at 75 degrees C the reaction resulted in removal of the ferruginous coat, leaving an exposed core for further analysis. This procedure overcomes the previous analytical problems of core analysis caused by the ferruginous coating.

• Modification of the in vitro activities of amosite asbestos by surface derivatization. P.H. Evans, R.C. Brown, A. Poole. 1983;11(4-6):535-43. PubMed · Publisher

  Abstract

  The in vitro cytotoxicity of amosite asbestos and its silanized and bovine serum albumin conjugated derivatives were studied in two cell lines. The overall cytotoxicity of amosite towards Chinese hamster lung cells (V79-4) was not affected by derivatization, although the rate of cell-particle interaction was reduced. Protein derivatization virtually abolished the cytolytic action of amosite to the macrophage-like cell line (P388D1), although this derivatized material still induced the release of arachidonate. These results confirm that the in vitro cytotoxic effect of fibrous particulates toward V79-4 cells is mainly dependent on fiber size, while the response of macrophage-like cells is more sensitive to alterations in surface chemistry. The relationship between these results and the pathogenicity of asbestos is discussed.

• A procedure for the isolation of amosite asbestos and ferruginous bodies from lung tissue and sputum. M.G. Williams, R.F. Dodson, C. Corn, et al. 1982;10(4-5):627-38. PubMed · Publisher

  Abstract

  A comprehensive scheme is described for isolating amosite asbestos and ferruginous bodies from fixed and unfixed human lung tissue and sputum. This qualitative procedure avoids many of the problems associated with previous isolation techniques and illustrates the advantages of brief bleach digestions. The samples are digested in prefiltered Wright laundry bleach (9.2% sodium hypochlorite), collected on 0.2-microns Nucleopore filters by vacuum filtration, rinsed with distilled water and absolute ethanol, and examined visually for excessive residue. If organic residues are suspected or are known to occur, the sample is treated sequentially with 2% potassium permanganate, 8% oxalic acid, and 9.2% sodium hypochlorite, and rinsed with distilled water and absolute ethanol. The ethanol, potassium permanganate, and oxalic acid steps can be repeated as often as needed until the desired sample volume has been filtered. The entire procedure allows large volumes to be filtered and yields filters that have extremely clean backgrounds. Filtration can be completed in as little as 15 min, as opposed to the hours or days recommended for other procedures. The technique is applicable to specimens fixed in Saccomanno's fixative or glutaraldehyde, and to those in an unfixed state. The procedure does not appear to damage the gross morphology of the amosite fibers, and it does not produce a detectable change in their elemental composition when determined by energy-dispersive X-ray analysis.

• Effects of particulate matter on rates of membrane uptake of polynuclear aromatic hydrocarbons. D.R. Bevan, S.C. Riemer, J.R. Lakowicz. 1981;8(1-2):241-50. PubMed · Publisher

  Abstract

  Investigations of the mechanism of particle-enhanced uptake of benzo [a] pyrene into model membranes and microsomes have been extended by studying the effects of particulates on the rates of uptake of four additional polynuclear aromatic hydrocarbons (PAH) into model membranes. Adsorption of dibenzo [a, h] anthracene, benzo [g,h,i] perylene, and 3-methylcholanthrene to the surface of particles resulted in enhanced rates of membrane uptake of these PAH. Adsorption to the fibrous asbestos minerals (chrysotile and anthophyllite) produced the greatest enhancement in membrane uptake rates compared to uptake from microcrystalline dispersions of the PAH. Adsorption of these PAH to nonfibrous minerals resulted in uptake rates intermediate between those of the asbestos-adsorbed and microcrystalline states. In contrast, adsorption of dibenzo-[c,g] carbazole to particles did not result in enhanced uptake. In this case, the rates of uptake in the absence and presence of particles were all extremely high, presumably as a result of the high water solubility of this PAH. The methods described in this paper permit characterization of particles-PAH mixtures in terms of the rate of PAH uptake into membranes.

• Increased risk of lung cancer in pesticide-exposed male agricultural workers. E. Barthel. 1981;8(5-6):1027-40. PubMed · Publisher

  Abstract

  The cancer morbidity in a large group of male German agricultural workers exposed to pesticides was investigated through a retrospective cohort study. A total of 169 malignant tumors were diagnosed in 1658 men who began to work with pesticides between 1948 and 1972, and who continued this type of activity for at least 5 yr. The SMR (standardized mortality ratio) of 2.0 for lung cancer morbidity (mortality) in these pesticide-exposed subjects was significantly higher than that for the general male population of the German Democratic Republic. A positive correlation between the duration of employment and the mortality due to lung cancer (mainly undifferentiated and small-cell carcinomas) suggested a dose-effect relation. The smoking habits of the exposed men did not differ from those of the general male population of the German Democratic Republic. Because the subjects had been exposed to many different substances, the study does not permit any conclusions to be drawn in respect to the carcinogenicity of individual pesticides. The increased mortality due to lung cancer is presumably the result of an additive effect of different pesticide ingredients or of by-products whose carcinogenic effect has been definitely or tentatively established through experimental or epidemiologic studies (e.g. arsenic, asbestos, chlorinated dibenzodioxins, DDT). The results of the present investigation emphasize the need for effective measures to protect workers during occupational contact with pesticides.

• Measurement of blood flow and vascular permeability changes in response to 12-O-tetradecanoyl-phorbol-13-acetate and to asbestos fibers. J.A. Hamilton, P. Vadas, J.B. Hay. 1981;8(1-2):205-14. PubMed · Publisher

  Abstract

  The hyperemia (increased blood flow) and vascular permeability changes induced in rabbit skin by the tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate and by asbestos fibers have been quantitated. The resultant hyperemia, measured with radiolabeled microspheres, was inhibited in both cases by steroidal and nonsteroidal anti-inflammatory drugs. Since the inflammatory responses resulting from exposure to these agents might be important for the subsequent development of neoplasms, it is proposed that such a specific and quantitative technique be used to analyze the components of these inflammatory responses in more detail.

• Serum protein concentrations and respiratory tract abnormalities following short-term exposure to amosite: a comparison between former asbestos workers and unexposed controls. D.R. Nash, N.G. Fortson, J.W. McLarty, et al. 1981;7(5):733-44. PubMed · Publisher

  Abstract

  A group of 176 former asbestos workers and 76 unexposed controls of similar age were evaluated and compared for concentrations of serum immunoglobulins, alpha 1-antitrypsin, carcinoembryonic antigen (CEA), pulmonary function, radiographic appearance of the lungs, rales, cellular atypia and ferruginous bodies in sputum, and smoking habits. Test subjects were evaluated as a single group and also according to years of exposure to asbestos. Both test and control populations were independently subjects to parametric and nonparametric correlation analyses. Partial correlations were also determined for both groups after controlling for age, race, sex and smoking habits. Analysis of variance was used to compare test and control groups. Smoking, particularly heavy smoking, was an important variable influencing abnormalities of the respiratory tract and CEA in former asbestos workers but not in controls. Except for immunoglobulin A (IgA), serum proteins, CEA, and alpha 1-antitrypsin were not significantly different between test and control subjects. Analysis of variance revealed significant increases between test and control groups for cellular atypia, X-ray abnormalities, rales, and pulmonary restriction. Partial correlation analysis of the asbestos-exposed group revealed important correlations between ferruginous bodies in sputum, rales, and radiographic appearance of the lungs.

• Asbestos and cancer in Finland. M.S. Huuskonen. 1980;6(5-6):1261-5. PubMed · Publisher

  Abstract

  Cancer mortality of men with diagnosed asbestosis was studied in Finland. Of the 174 men registered as having asbestosis, 56 had died before 1977, whereas the number of expected deaths based on the Finnish male population was only 23.4. The respective figures for lung cancer were 19 observed and 2.1 expected. The mean age of these 19 lung cancer patients was 57.8 yr, and lung cancer was the cause of death (underlying cause) in 35% of all diseased men with asbestosis. The proportion of lung cancer mortality from all deaths among Finnish men 55-64 yr old is 10.8%, which is clearly lower than that among the men with asbestosis. No excess of other malignancies was found in Finland among workers with asbestosis.

• Asbestos and metals as carcinogens. T. Norseth. 1980;6(5-6):1021-8. PubMed · Publisher

  Abstract

  Increased incidences of lung carcinoma and pleural mesothelioma in humans exposed to asbestos have been irrefutably established. Different forms of asbestos may have different tumorigenic activities, depending on surface properties, durability, and size of the fibers. A number of metals, such as nickel, chromium, and arsenic, are known to be carcinogenic to humans; for beryllium and cadmium the epidemiologic evidence is less extensive. All these metals also induce genetic toxicity in vitro. For chromium the molecular mechanism of metal tumorigenesis has been extensively investigated; the hexavalent form is generally a much more potent mutagen than is chromium (III). Solubility seems to be necessary for the genotoxicity of nickel. At present it cannot be concluded that all metals act by the same carcinogenic mechanism, even though direct modification of DNA seems to be the common experimental finding.

• Historical perspectives of occupational cancer. P. Bogovski. 1980;6(5-6):921-39. Historical article PubMed · Publisher

  Abstract

  Three topics are discussed in this review, which is not intended to give even a short description of the history of occupational cancer. First, the present state and possible future trends of occupational cancer are examined. Such factors as rapid industrialization, increasing amounts of chemical compounds in the environment, and discoveries of new occupational carcinogens such as asbestos and vinyl chloride indicate that occupational cancer is likely to become more frequent in the future. The controversial issue of the proportion of cancers related to occupation is briefly considered. The upward trend of estimates of various authors during a quarter of a century indicates a growing proportion of occupational cancers in the overall incidence of cancer. Second, some lessons from the past are considered. Careful observations and alertness of physicians and proper documentation of occupational cancer cases are pointed out. Interdisciplinary teamwork and international cooperation have been useful in the past and continue to be desirable. Some details of the studies of skin cancer caused by mineral oil are informative. Individual susceptibility, whether genetically determined or due to pathological conditions, needs further study. As an example of the predictive value of animal experiments, skin cancer related to the oil shale industry in Estonia is discussed. The third topic--input from experimental cancer research--deals mainly with the problem of modifying factors. Experimental data on such factors could facilitate investigations of life-style effects, using the proposed classification of modifying factors. The problem of nasal cancer in woodworkers may be easier to solve by taking into account some experimental data on tannin-containing material. Some possibilities for future action and suggestions for further research are outlined.

1970s

• Asbestos fibers in wines: relation to filtration process. A. Gaudichet, M. Bientz, P. Sebastien, et al. 1978;4(5-6):853-60. PubMed · Publisher

  Abstract

  Asbestos fibers were counted by using the transmission electron microscope in 42 wines from France and abroad. Fifteen samples were found to be significantly positive for chrysotile asbestos. Concentrations were in the range of 2--64 X 10(6) fibers per liter. Technical investigations showed that the abestos content of the wines was related to the process by which they were filtered. On the other hand, we found that abandoning the use of asbestos for filtering wines would not alter the wine from the enological point of view.

• Induction of pulmonary carcinoma in rats by chronic inhalation of dust from pulverized asbestos pipe covering. B.K. Leong, R.J. Kociba, H.C. Pernell, et al. 1978;4(4):645-59. PubMed · Publisher

  Abstract

  Rats and hamsters were exposed to the dust of pulverized asbestos pipe covering at an average concentration of 85 mg/m(3) for 6 h/d, 5 d/wk, for 7 mo, followed by a lifetime observation period. In rats, the pulmonary responses were alveolar adenomatous proliferation, nonprogressive fibrosis, squamous metaplasia, and a substantial incidence of pulmonary carcinoma formation. A smaller group of hamsters exposed under these conditions experienced an earlier onset of mortality than control hamsters, which were not subjected to the exposure regimen. Although this prevented conclusive evaluation of the pulmonary response in this species, no pulmonary neoplasms were noted in the surviving hamsters.

• Variation of properties of chrysotile asbestos subjected to milling. A.M. Langer, M.S. Wolff, A.N. Rohl, et al. 1978;4(1):173-88. PubMed · Publisher

  Abstract

  Mechanical milling is commonly used to produce short chrysotile asbestos for experimental purposes. Such manipulation also decreases fiber crystallinity, alters Si-O and Mg-O interlayer bonding, induces coordination changes in the brucite layer, diminishes the ability of fiber to reduce specific free radicals and physisorb organic molecules, and decreases hemolytic potency and antagonist sorption capabilities. The degree of alteration is related to the time of milling. Results of biological experimentation with these materials must be interpreted with caution. Interaction mechanisms in the biological setting are suggested for chrysotile fiber.

• Consumer talcums and powders: mineral and chemical characterization. A.N. Rohl, A.M. Langer, I.J. Selikoff, et al. 1976;2(2):255-84. PubMed · Publisher

  Abstract

  Representative consumer talcums and powders, including 20 body powders, baby powders, facial talcums, and also one pharmaceutical talc, were analyzed to determine their mineralogical and chemical composition. Where known, all were formulated prior to 1973. Of the 20 products 10 contained detectable amounts of tremolite and anthophyllite, principally asbestiform, while some also contained fragmented forms of these minerals. The amounts ranged from tenths of a percent to over 14% by weight; two contained detectable amounts of chrysotile asbestos fiber. Eight contained quartz, seven ranging from 2 to 5%, with one as high as 35%. The analyses showed that the consumer products examined were rarely the pure mineral talc, but rather were mixtures of various minerals; some samples consisted of three to five minerals, only one of which was talc. Other common mineral phases included chlorite, platy serpentine, pyrophyllitem mica, and carbonate minerals. Kaolin additive was identified in two products. The single pharmaceutical talc examined contained only a trace amount of quartz. The chemical composition of these products, including both major oxide and trace element content, correlated with their mineral components. Four samples contained substantial concentrations of nickel, cobalt, and chromium, suggesting latice substitution or the presence of trace mineral phases. Geological provenance of the talcs may be ascertained on the basis of chemistry. Possible adverse health effects from intermittent use of these products, especially those that contain asbestiform and fragmented anthophyllite and tremolite, chrysotile, quartz, and trace metals, are presently unknown and warrnat evaluation.

• Quantitative relationship of fecal asbestos to asbestos exposure. H.M. Cunningham, R.D. Pontefract, R.C. O'Brien. 1976;1(3):377-9. PubMed · Publisher

  Abstract

  A method is descirbed for isolating chrysotile fibers from feces and counting them with an electron microscope. The detection limit was 150,000 fibers per gram feces; average recovery was 85.5%. When the method was used to check the asbestos in feces of people subjected to industrial exposure vs. controls, the means were significantly different (p less than 0.02). Duplicate fecal samples were found to check within an average of +/- 31.1% of their means.

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