Science

Our medical research library holds 49 studies published in Science (1937–2012). 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. 20 have an abstract, the authors' own summary as PubMed records it: open "Abstract" to read it. For 10 studies PubMed has no abstract for, we give the abstract printed in the article or, where there is none, a summary we wrote from it, each labeled as such.

About the journal

• Publisher: American Association for the Advancement of Science
• Published: 1880 to the present, United States
• Language: English
• ISSN: 0036-8075 (print), 1095-9203 (electronic)
• Absorbed: Scientific Monthly
• Its record in the NLM Catalog

2010s

• Loss of the tumor suppressor BAP1 causes myeloid transformation. A. Dey, D. Seshasayee, R. Noubade, et al. 2012;337(6101):1541-6. PubMed · Publisher · Free full text

  Abstract

  De-ubiquitinating enzyme BAP1 is mutated in a hereditary cancer syndrome with increased risk of mesothelioma and uveal melanoma. Somatic BAP1 mutations occur in various malignancies. We show that mouse Bap1 gene deletion is lethal during embryogenesis, but systemic or hematopoietic-restricted deletion in adults recapitulates features of human myelodysplastic syndrome (MDS). Knockin mice expressing BAP1 with a 3xFlag tag revealed that BAP1 interacts with host cell factor-1 (HCF-1), O-linked N-acetylglucosamine transferase (OGT), and the polycomb group proteins ASXL1 and ASXL2 in vivo. OGT and HCF-1 levels were decreased by Bap1 deletion, indicating a critical role for BAP1 in stabilizing these epigenetic regulators. Human ASXL1 is mutated frequently in chronic myelomonocytic leukemia (CMML) so an ASXL/BAP1 complex may suppress CMML. A BAP1 catalytic mutation found in a MDS patient implies that BAP1 loss of function has similar consequences in mice and humans.

2000s

• Immunology. How frustration leads to inflammation. L.A. O'Neill. 2008;320(5876):619-20. Comment PubMed · Publisher

  Summary

  This Perspective commented on a study by Dostert et al., published in the same issue, on how inhaled particles such as asbestos and silica lead to inflammation and lung disease. The author first outlined background on inflammation. Cellular receptors such as Toll-like and NOD-like receptors recognize harmful agents. Inflammasomes are multiprotein complexes containing caspase-1, which processes prointerleukin-1β into its mature form. Nalp3 is one inflammasome component, and it was already known to sense monosodium urate, the cause of gout. The author then summarized the findings of Dostert et al. Reducing Nalp3 expression in macrophages attenuated asbestos-induced caspase-1 activation and interleukin-1β secretion. Asbestos triggered potassium efflux. Asbestos fibres underwent 'frustrated' phagocytosis, and disrupting actin filaments with cytochalasin D inhibited interleukin-1β secretion. Inhibitors of reactive oxygen species and of NADPH oxidase reduced interleukin-1β production, while reducing thioredoxin increased it. Mice exposed to airborne chrysotile asbestos showed increased cell numbers in bronchoalveolar lavage fluid. Nalp3-deficient mice recruited fewer cells, had impaired cytokine production and were resistant to asbestos-induced lung injury. The author noted that how reactive oxygen species affect Nalp3 activation was unknown. He concluded that the study highlighted the importance of testing the interleukin-1 receptor antagonist anakinra as a treatment to slow the progression of asbestosis and silicosis. He added that Nalp3 itself might be a drug target.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Innate immune activation through Nalp3 inflammasome sensing of asbestos and silica. C. Dostert, V. Pétrilli, R. Van Bruggen, et al. 2008;320(5876):674-7. PubMed · Publisher · Free full text

  Abstract

  The inhalation of airborne pollutants, such as asbestos or silica, is linked to inflammation of the lung, fibrosis, and lung cancer. How the presence of pathogenic dust is recognized and how chronic inflammatory diseases are triggered are poorly understood. Here, we show that asbestos and silica are sensed by the Nalp3 inflammasome, whose subsequent activation leads to interleukin-1beta secretion. Inflammasome activation is triggered by reactive oxygen species, which are generated by a NADPH oxidase upon particle phagocytosis. (NADPH is the reduced form of nicotinamide adenine dinucleotide phosphate.) In a model of asbestos inhalation, Nalp3-/- mice showed diminished recruitment of inflammatory cells to the lungs, paralleled by lower cytokine production. Our findings implicate the Nalp3 inflammasome in particulate matter-related pulmonary diseases and support its role as a major proinflammatory "danger" receptor.

• Division for Planetary Sciences meeting: Martian methane: rocky birth, then gone with the wind?. G. Schilling. 2005;309(5743):1984-5. News PubMed · Publisher

1990s

• Disordered biopyriboles, amphibole, and talc in the Allende meteorite: products of nebular or parent body aqueous alteration?. A.J. Brearley. 1997;276(5315):1103-5. PubMed · Publisher

  Abstract

  Transmission electron microscope observations of the Allende carbonaceous chondrite provided evidence of widespread hydrous phases replacing enstatite in chondrules. Calcic amphibole and talc occur in thin (less than 0.3 micrometer) crosscutting veins and as alteration products of primary chondrule glass in contraction cracks within the enstatite. In addition, talc and disordered biopyriboles were found replacing enstatite grains along cracks and fractures. Although rare hydrous phases have been reported in calcium- and aluminum-rich inclusions in the Allende meteorite, these observations suggest that aqueous fluids played a much more significant role in the mineralogical and geochemical evolution of Allende than has previously been thought.

• 'Natural' cancer prevention trial halted. K. Peterson. 1996;271(5248):441. News PubMed · Publisher

  Summary

  This news report in Science described the National Cancer Institute's (NCI) announcement that two clinical trials it sponsored, in which volunteers took beta carotene to prevent cancer and heart disease, had yielded negative results. The report noted that two years earlier a Finnish study had suggested that beta carotene might raise the risk of lung cancer in smokers, a result many researchers had dismissed as a fluke. The Beta Carotene and Retinol Efficacy Trial (CARET), led by Gilbert S. Omenn of the University of Washington, Seattle, gave its 18,314 participants, who were smokers and people exposed to high levels of asbestos, daily doses of beta carotene, vitamin A, or a placebo for about 8 years. Those taking beta carotene had 28% more lung cancers and 17% more deaths than the group taking a placebo. Omenn stopped the $42 million trial on 10 January, 21 months early, and said the investigators did not know why these effects were observed. The second trial, the $22.5 million Physicians' Health Study, involved 22,071 doctors, 11% of them smokers, who took beta carotene or a placebo every other day for 12 years. The regimen did no harm, but it did not appear to help prevent cancer or cardiovascular disease. NCI Director Richard Klausner concluded that beta carotene is no magic bullet and that there is no substitute for stopping smoking.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Chrysotile, tremolite, and mesothelioma. J.C. McDonald, A.D. McDonald. 1995;267(5199):776-7. Comment · Letter PubMed · Publisher

  Summary

  In this letter, the authors returned to a question they had raised in 1990: whether mesothelioma deaths among Quebec chrysotile miners and millers might have been caused by contamination with fibrous tremolite, an amphibole. Their cohort comprised almost 11,000 men born between 1891 and 1920 and followed continuously since 1966. By the end of 1992, 37 mesothelioma deaths had been identified among 8000 deaths from all causes. Twenty-four were from Thetford Mines and 13 from Asbestos, including five from a small asbestos products factory that had used crocidolite. For the 24 Thetford cases, up to 10 surviving controls with the same year of birth were sought, and two cases with too few controls were excluded. Years worked in each of 15 Thetford-region mines were calculated, excluding employment within 20 years of death. Case employment was concentrated in five central mines (Area A). There, the control-to-case ratio of man-years was 5.3, compared with 21.6 in 10 peripheral mines (Area B). Electron microscopy data on lungs from 83 cohort members who died of other causes (58 Area A, 25 Area B) showed geometric mean concentrations of fibers 5 micrometers or longer per microgram of dried lung of 7 versus 13 for chrysotile (not significant) and 32 versus 7 for tremolite (P = 0.0002). The authors concluded that the relatively rare mesothelioma cases mainly or perhaps wholly resulted from amphibole contamination. They stressed that these findings reflected long, heavy exposures 20 to 70 years earlier.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Asbestos Regs to Be Re-examined. C. Holden. 1992;255(5052):1639. PubMed · Publisher

• No meeting of the minds on asbestos. R. Stone. 1991;254(5034):928-31. News PubMed · Publisher

• Asbestos and carcinogenicity. J.C. McDonald, A.D. McDonald. 1990;249(4971):844. Comment · Letter PubMed · Publisher

  Summary

  In this letter, the authors responded to a letter by William J. Nicholson et al. (Science, 18 May). That letter had alleged that there had been 67 or more cases of mesothelioma among Quebec chrysotile miners and millers, and attributed the estimate to J. C. McDonald. The authors stated that their cohort was 11,379 persons born between 1891 and 1920 and employed for 1 month or more. By the end of 1975 the cohort had 11 mesothelioma cases among 4,547 deaths, and 18 cases were known by 1978. A follow-up to 1990 was nearly complete. More than 70% of the cohort had died, and a subsample study suggested the eventual number of cases may be about 30. At least seven of these cases had been exposed to crocidolite in a small local factory, and one had substantial amosite exposure. Citing Montana tremolite data, the authors suggested that the remaining cases might possibly be attributed to fibrous tremolite contamination, roughly estimated at about 1.5%. They contrasted this with crocidolite-exposed gas mask and cigarette filter workers, in whom 16 to 19% of all deaths were attributed to mesothelioma. They defended well-controlled lung fibre studies and argued that the amphibole hypothesis concerns mesothelioma, not lung cancer. They cited textile plants where a chrysotile-only plant had one mesothelioma case, against 12 and 14 or more in mixed-exposure plants. They concluded that spending billions of dollars to control a minuscule or nonexistent risk seemed strange and sad.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Asbestos removal. W.K. Reilly. 1990;248(4959):1064-5. PubMed · Publisher

  Summary

  In this letter, William K. Reilly, Administrator of the US Environmental Protection Agency (EPA), responded to Philip H. Abelson's editorial "The asbestos removal fiasco" (2 March, p. 1017). That editorial had blamed EPA policies for large sums spent removing asbestos from buildings. Reilly stated that EPA requires removal only when demolition or renovation threatens to release significant amounts of asbestos fibers into the air. He said that many building owners were removing asbestos because of concerns about property devaluation, insurance and liability that may be unrelated to actual health risks. EPA recommended that asbestos-containing material in good condition and unlikely to be disturbed generally be contained in place, and it warned that poorly conducted removal can increase risk. On fiber type, he acknowledged evidence that chrysotile may be less likely to cause some asbestos-related diseases. However, he noted that the National Academy of Sciences and other organizations maintain that chrysotile is a human carcinogen that can cause all asbestos-related diseases. He described the data Abelson cited as important but inconclusive. He said EPA was assessing actual exposure levels in buildings through research by the Health Effects Institute. He also argued that air monitoring can supplement, but not replace, physical inspection, because it cannot predict future fiber releases. He listed ongoing EPA policy reviews, an evaluation of the asbestos-in-schools program and guidance on managing asbestos in place.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Asbestos: scientific developments and implications for public policy. B.T. Mossman, J. Bignon, M. Corn, et al. 1990;247(4940):294-301. PubMed · Publisher

  Abstract

  Asbestos is a commercial term for a group of fibrous minerals often associated with the development of pulmonary interstitial fibrosis (asbestosis), lung cancer, and malignant mesothelioma in occupationally exposed individuals. The pathogenicity of different forms of asbestos varies--long, thin amphibole fibers are most pathogenic, particularly in the induction of mesothelioma. Available data do not support the concept that low-level exposure to asbestos is a health hazard in buildings and schools. The concentration of asbestos fibers in air, type of asbestos, and size of fibers must be considered in evaluation of potential health risks.

• EPA and asbestos removal. J. Berry. 1990;248(4963):1595. Letter PubMed · Publisher

• In reply: asbestos, carcinogenicity, and public policy. K.S. Crump. 1990;248(4957):799. PubMed · Publisher

• In reply: asbestos, carcinogenicity, and public policy. S.W. Samuels. 1990;248(4957):795-6. PubMed · Publisher

• In reply: asbestos, carcinogenicity, and public policy. W.J. Nicholson, E.M. Johnson, J.S. Harington, et al. 1990;248(4957):796-9. PubMed · Publisher

  Summary

  In this letter, the authors responded to an article by Mossman et al. in Science that supported the "amphibole hypothesis" and suggested little cancer risk from chrysotile asbestos. They argued that lung burdens of fiber types were nearly worthless for predicting mesothelioma, because chrysotile can disappear from lung tissue and tremolite burden is proportional to chrysotile inhaled. They cited four studies of mainly chrysotile textile workers, in which lung cancer risk rose by 1.0 to 2.8% per fiber-year per cubic centimeter. In five studies of amosite or mixed exposures the rise was 0.5 to 4.3%, and for crocidolite miners it was 2.1 to 5.8%. They also cited rat inhalation studies in which chrysotile produced the most cancers for equal exposures, findings that short chrysotile fibers outnumbered amphiboles in pleural tissue, and evidence that chrysotile transfers DNA into cells. They criticized the building air data used by Mossman et al., noting that no fibers were found in 83% of samples and that short-term sampling misses episodic releases. Agency estimates gave 4 to 12 cancer deaths per 100,000 for a 13-year school exposure at 0.002 fiber per cubic centimeter, or 800 to 2400 cases among 20 million pupils. They concluded that the EPA's school asbestos regulation was in the mainstream of U.S. regulatory action.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• In reply: asbestos, carcinogenicity, and public policy. B.T. Mossman, J. Bignon. 1990;248(4957):799-802. PubMed · Publisher

• The asbestos removal fiasco. P.H. Abelson. 1990;247(4946):1017. Editorial PubMed · Publisher

  Summary

  In this signed editorial, the author argued against large-scale removal of asbestos from buildings in the United States, which he said could cost $50 to $150 billion. He stated that airborne asbestos levels in buildings containing asbestos are harmlessly small and essentially the same as outdoor levels, that undamaged asbestos does not shed fibers, and that removal releases fibers that could cause more cancer in workers than leaving the asbestos in place would cause in occupants. He criticized federal regulations for grouping chrysotile, which makes up about 95 percent of asbestos in place in the United States, with the amphibole crocidolite, and he described differences between the two minerals in composition, shape, solubility and persistence in tissue. He cited four epidemiological studies of Quebec chrysotile mining localities that, he wrote, showed no statistically significant excess disease in women with lifelong exposure to mine dust. He also criticized the Environmental Protection Agency (EPA) for promoting the unproven view that a single fiber can cause cancer, for being slow to measure indoor and outdoor fiber levels, and for recommending bulk sampling and visual inspection in schools rather than air measurement. He noted the EPA's own estimate that half of removal projects are done improperly. He concluded that regulations should account for the differing hazards of the asbestiform minerals and that indoor air standards should be based on actual fiber measurements.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

1980s

• EPA proposes ban on asbestos. M. Sun. 1986;231(4738):542-3. PubMed · Publisher

• Risk from exposure to asbestos. J. Aroesty, K. Wolf. 1986;234(4779):923. Letter PubMed · Publisher

• Indoor air pollution: a public health perspective. J.D. Spengler, K. Sexton. 1983;221(4605):9-17. PubMed · Publisher

  Abstract

  Although official efforts to control air pollution have traditionally focused on outdoor air, it is now apparent that elevated contaminant concentrations are common inside some private and public buildings. Concerns about potential public health problems due to indoor air pollution are based on evidence that urban residents typically spend more than 90 percent of their time indoors, concentrations of some contaminants are higher indoors than outdoors, and for some pollutants personal exposures are not characterized adequately by outdoor measurements. Among the more important indoor contaminants associated with health or irritation effects are passive tobacco smoke, radon decay products, carbon monoxide, nitrogen dioxide, formaldehyde, asbestos fibers, microorganisms, and aeroallergens. Efforts to assess health risks associated with indoor air pollution are limited by insufficient information about the number of people exposed, the pattern and severity of exposures, and the health consequences of exposures. An overall strategy should be developed to investigate indoor exposures, health effects, control options, and public policy alternatives.

• Endemic pleural disease associated with exposure to mixed fibrous dust in Turkey. A.N. Rohl, A.M. Langer, G. Moncure, et al. 1982;216(4545):518-20. PubMed · Publisher

  Abstract

  Pleural mesothelioma, lung cancer, pleural calcification and fibrosis, and interstitial parenchymal fibrosis have been observed among inhabitants of several villages in south-central Turkey. Earlier reports have stated that environmental and lung tissue samples from this area contained the fibrous zeolite mineral erionite, and this mineral has generally been assumed to be the agent responsible for these endemic pathological conditions in the absence of asbestos outcroppings and usage. Several different kinds of asbestos minerals in addition to erionite have now been found in environmental samples taken from the villages where these diseases occur. The lung tissues of mesothelioma patients from these villages contain both fibrous zeolites and asbestos minerals.

• Indoor airborne asbestos pollution: from the ceiling and the floor. P. Sebastien, J. Bignon, M. Martin. 1982;216(4553):1410-12. PubMed · Publisher

  Abstract

  Electron microscopic measurements of the concentrations of airborne asbestos were carried out inside and outside an office building having ceilings sprayed with a crocidolite-containing material and floors covered with vinyl-chrysotile tiles. Under normal conditions in this building, constructed 10 years ago, the two asbestos-containing materials released fibers into the air. This is the first measurement of elevated (up to 170 nanograms per cubic meter) concentrations of indoor airborne asbestos associated with the weathering of asbestos floor tiles during their service life. Asbestos flooring is used in a large number of buildings and represents the third largest use of asbestos fibers in the United States and in Europe, ranking after roofing and asbestos-cement pipe.

• Asbestos surface charge heterogeneity and biological effects. W.G. Light. 1981;213(4515):1534. Letter PubMed · Publisher

• Asbestos as a cofactor in carcinogenesis among nickel-processing workers. A.M. Langer, A.N. Rohl, I.J. Selikoff, et al. 1980;209(4454):420-2. PubMed · Publisher

  Abstract

  It has been widely assumed, especially in the absence of other explanations, that lung cancer and nasal sinus cancers observed among nickel smelter workers are the result of the carcinogenicity of nickel. Although there may be such influence, supplementary hypotheses are also possible. The nickeliferous ores from at least one major smelter in New Caledonia (excess numbers of cancers have been found in these smelter workers) are derived from serpentinized host rocks which contain large amounts of chrysotile asbestos. Analysis indicates that nickel ores from this area are heavily contaminated by these fibers. The deposits are mined for their nickel content, but workers may be exposed to the asbestos fibers contained in the deposits. Hygiene measures limited to the avoidance of nickel may be inadequate under such circumstances and should be reevaluated so as to prevent the inhalation of asbestos-containing dusts.

• Asbestos-induced epithelial changes in organ cultures of hamster trachea: inhibition by retinyl methyl ether. B.T. Mossman, J.E. Craighead, B.V. MacPherson. 1980;207(4428):311-3. PubMed · Publisher

  Abstract

  The epithelium of the hamster trachea in organ culture undergoes hyperplasia and squamous metaplasia after exposure to the amphibole types of asbestos, crocidolite and amosite. These changes are inhibited when the synthetic vitamin A analog, retinyl methyl ether, is incorporated into the culture medium. These findings suggest a possible use for retinoids in the prevention and treatment of respiratory tract disease associated with environmental exposure to asbestos.

• Surface charge heterogeneity in amphibole cleavage fragments and asbestos fibers. J.E. Schiller, S.L. Payne, S.E. Khalafalla. 1980;209(4464):1530-2. PubMed · Publisher

  Abstract

  Aspect ratio and electrophoretic mobility data for amphibole particles reveal that short fibers and blocky cleavage fragments have a smaller net charge than highly elongated particles. Asbestos fibers and cleavage fragments of the same dimensions exhibit the same net negative surface charge but positively charged ends and negatively charged lateral surfaces.

1970s

• Chrysotile asbestos in a California recreational area. W.C. Cooper, J. Murchio, W. Popendorf, et al. 1979;206(4419):685-8. PubMed · Publisher

  Abstract

  Dustfall along roads and trails being used recreationally in the Clear Creek area of San Benito County, California, located in the New Idria serpentinite, was found to be 90 percent or more chrysotile asbestos. Personal samplers worn by motorcyclists using one of the trails showed concentrations of airborne fibers ranging from 0.3 to 5.3 fibers per milliliter, according to methods prescribed for monitoring occupational exposures. The present workplace standard for brief exposures to asbestos is 10 fibers per milliliter; 5 fibers per milliliter is the proposed standard. The average total dust concentration estimated from personal samplers was approximately 20 milligrams per cubic meter of roughly 90 percent chrysotile. To our knowledge, this is the first demonstration of asbestos exposures of this magnitude, in size ranges known to be pathogenic, resulting from natural deposits not associated with mining, milling, or industrial use.

• Congress considers asbestos indemnity bill. R.J. Smith. 1979;204(4394):712. PubMed · Publisher

• Health hazards of asbestos. D.H. Wegman. 1979;206(4419):677-8. PubMed · Publisher

• Ingested mineral fibers: elimination in human urine. P.M. Cook, G.F. Olson. 1979;204(4389):195-8. PubMed · Publisher

  Abstract

  Sediment in human urine examined by transmission electron microscopy contains amphibole fibers which originate from the ingestion of drinking water contaminated with these mineral fibers. The ingestion of filtered water results in the eventual disappearance of amphibole fibers from urine. These observations provide the first direct evidence for the passage of mineral fibers through the human gastro-intestinal mucosa under normal conditions of the alimentary canal.

• State officials alerted to school asbestos hazard. R.J. Smith. 1979;204(4390):285. PubMed · Publisher

• Comparison of rhapidosomes and asbestos microfibrils. W.G. Hutchison, R.I. Harker, M.M. Allen. 1978;200(4348):1401-3. PubMed · Publisher

  Abstract

  Rhapidosomers (cylindrical nucleoprotein rods of bacterial origin) show great structural similarity to the microfibrils of chrysotile asbestos when negatively stained and observed with the electron microscope. If the negative stain is omitted, the asbestos retains its structural detail whereas the rhapidosomes appear to be unstructured bodies. When the microscope is adjusted into a selected area diffraction mode, the asbestos shows characteristic electron diffraction patterns whereas the rhapidosomes appear to be amorphous to electron diffraction.

• Asbestos pollution. J.T. Hack. 1977;197(4305):716. PubMed · Publisher

• Asbestos pollution. A.N. Rohl, A.M. Langer, I.J. Selikoff. 1977;197(4305):716-8. PubMed · Publisher

• Asbestos: trouble in the air from Maryland rock quarry. L.J. Carter. 1977;197(4300):237-40. PubMed · Publisher

• Chrysotile asbestos: effects of human exposure. A.N. Rohl, A.M. Langer, I.J. Selikoff. 1977;198(4323):1202. PubMed · Publisher

  Summary

  This letter replied to a letter by John T. Hack about environmental asbestos pollution in Rockville, Maryland. The authors agreed that the pollution was primarily chrysotile from the Rockville quarry. They disputed Hack's suggestion that studies of chrysotile miners and millers in Quebec, Canada, exonerated the quarry's crushed rock as a carcinogen, and his claim that these workers' general health was comparable to that of Quebec Province as a whole. They noted that latent periods for asbestos-related malignancy appear to extend from 20 to 40 years or more from the onset of exposure, and that exposure intensity influences both disease risk and latency. They cited McDonald and Becklake's own list of asbestos-associated diseases in Canada. They argued that the Quebec studies grouped about 4000 workers by total exposure in 'MPCF-years' rather than by years since onset of exposure, which mixed workers with short and long latency periods. Even so, workers with 400 to 800 MPCF-years had a 2.1 elevated risk of respiratory cancer, and those above 800 MPCF-years had a 3.6 times elevated risk. The authors considered these figures conservative. They also cited the Beaudry Commission's findings of poor worker education, dangerous methods, negligent inspection and a lack of medical surveillance in the Quebec industry, as well as an IARC conclusion that reassurance was unwarranted. They concluded that chrysotile mining and milling had been established as hazardous.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Chrysotile asbestos: health effects. J.T. Hack. 1977;197(4310):1232-4. PubMed · Publisher

• Environmental asbestos pollution related to use of quarried serpentine rock. A.N. Rohl, A.M. Langer, I.J. Selikoff. 1977;196(4296):1319-22. PubMed · Publisher

  Abstract

  Crushed serpentinite quarried in Montgomery County, Maryland, has been extensively used for paving roads and other surfaces. The mineral assemblage includes antigorite or lizardite as well as chrysotile and tremolite. Air samples taken in the vicinity of serpentine-paved roads show that chrysotile concentrations are about 10(3) times greater than those typically found in urban ambient air in the United States.

• NAS Committee on Asbestos: Discovery of a Special Relationship. N. Wade. 1976;193(4254):661-4. PubMed · Publisher

• Exposure to asbestos in the use of consumer spackling, patching, and taping compounds. A.N. Rohl, A.M. Langer, I.J. Selikoff, et al. 1975;189(4202):551-3. PubMed · Publisher

  Abstract

  Analysis of representative samples of spackling, patching, and jointing compounds, purchased at retail stores in the New York City area, has shown that some contain asbestos minerals as well as other biologically active substances. Measurements suggest that home repair work involving the use of such materials may result in exposure to dust at concentrations sufficient to produce disease.

• Asbestiform amphibole minerals: detection and measurement of high concentrations in municipal water supplies. P.M. Cook, G.E. Glass, J.H. Tucker. 1974;185(4154):853-5. PubMed · Publisher

  Abstract

  Ashestiform amphibole minerals, which have been demonstrated to be associated with human health problems, have been detected in substantial quantities in municipal water supplies taken from western Lake Superior Water. The total concentrationl of amphibole minerals in the Duluth, Minnesota, water supply, as measured by x-ray diffraction for daily samples of suspended solids averages 0.19 milligram per liter with large fluctuations due to seasonal and climatological effects on lake circulation. Electron microscopic examination of these water samples confirms the presence of asbestiform amphibole fibers. A conservatiue estimate of the fiber count for 1973 Duluth water supply samples is (1 to 30) x 10(6) amphibole fibers identifiable by electron diffraction per liter of water with a mass concentration of 1 to 30 micrograms per liter.

• Ferromagnetic contamination in the lungs and other organs of the human body. D. Cohen. 1973;180(4087):745-8. PubMed · Publisher

  Abstract

  Contaminating particles which are ferromagnetic have been found in the human body. Their distribution was measured by applying an external magnetic field to the torso for a short time, and then, in a shielded room, mapping the steady magnetic field around the torso due to the magnetized particles. Maps of subjects show various distributions, including particles in the stomach from food cans and in the lungs from are welding. The fields from these two sources are strong enough to be detected with a flux-gate magnetometer, without the need for a shielded room. This simplicity of detection of larger amounts of ferromagnetic contamination suggests that this method may be used in two applications: in detecting the presence of large amounts of asbestos (ferromagnetic and harmful) in the lungs of asbestos workers, and in tests of the condition of the lung where FE(3)O(4) dust (ferromagnetic and harmless) would be used as an inhaled tracer material.

• Asbestos contamination of parenteral drugs. W.J. Nicholson, C.J. Maggiore, I.J. Selikoff. 1972;177(4044):171-3. PubMed · Publisher

  Abstract

  Chrysotile asbestos has been found in approximately one third of the samples from two sets of 17 widely used parenteral drugs.

• Talc-treated rice and Japanese stomach cancer. R.R. Merliss. 1971;173(4002):1141-2. PubMed · Publisher

  Abstract

  The Japanese prefer talc-dusted rice in their diet. The incidence of stomach cancer in Japan is unusually high. Most talc has some asbestos contaminants. Epidemiologic evidence is presented that the asbestos-contaminated talc on rice in the diet is the carcinogen or cocarcinogen responsible for the high incidence of Japanese stomach cancer.

1960s

• Natural Occurrence of Amino Acids in Virgin Crocidolite Asbestos and Banded Ironstone. J.S. Harington. 1962;138(3539):521-2. PubMed · Publisher

  Summary

  This short report gave further details of amino acids found naturally with virgin crocidolite asbestos from the North-Western Cape, Republic of South Africa. The author had earlier reported fluorescent oils containing polycyclic aromatic hydrocarbons and amino acids in crocidolite and amosite asbestos but not in chrysotile. Fiber samples were taken from cobs of asbestos in a way intended to make contamination extremely unlikely. They were extracted under reflux for 1 hour with boiling 80 percent ethanol-water and then dried, giving a brownish-yellow oily extract equal to 0.025 percent of the asbestos sample. Two extractions of the surrounding country rock gave 123 mg/100 g and 42 mg/100 g of oil. Paper chromatography showed three amino acids in both country rock extracts and eight in the crocidolite extract. Quantitative column chromatography of the crocidolite extract found ten amino acids. Serine was the most abundant at 0.095 mg/100 g of fiber, and the total was 0.268 mg/100 g (0.00027 percent). The author noted that, except for serine, all of these amino acids had been found by earlier workers in fossils, marine mud and sedimentary rocks. Virtually the same amino acids had been found in Gunflint chert, which is also a banded ironstone formation. The concentration in crocidolite was low compared with other settings, such as 0.0026 to 0.03 percent in fossils and 0.02 percent in Middle Huronian ironstones.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

1950s

• Tubular crystals of chrysotile asbestos. T.F. Bates, L.B. Sand, J.F. Mink. 1950;111(2889):512-3. PubMed · Publisher

  Summary

  The authors used electron microscopy to examine the crystal form of chrysotile asbestos and to compare it with the clay mineral endellite, which the senior author and colleagues had described in 1949 as forming tubular crystals. Electron micrographs were taken at The Pennsylvania State College and at the National Bureau of Standards. The illustrated samples were halloysite (dehydrated endellite) from Real County, Texas, and chrysotile synthesized by Bowen and Tuttle. The micrographs of synthetic chrysotile showed multiple tubes made of concentric cylinders, with a uniform diameter within each cylinder and a similar increase in diameter from one cylinder to the next. They also showed conical development of the tubes and longitudinal splitting. Well-defined discontinuities in the concentric layers, not seen in halloysite, were of unknown significance. The authors explained tubular growth by a slight misfit in dimensions between the two sheets of a 1:1 layered structure. This misfit produces curvature when the bonds between layers are too weak to stretch the lattice. In chrysotile, such a discrepancy exists between the magnesium-hydroxyl (brucite) sheet and the silicon-oxygen sheet. The authors concluded that both natural and synthetic chrysotile crystallize as hollow cylindrical tubes, and that there is a general structural analogy and a striking resemblance between the tubular crystals of endellite and chrysotile.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

1940s

• Filtration of citrated plasma. L. Rane, D.M. Baldwin. 1945;101(2628):494-6. PubMed · Publisher

  Abstract

  Large amounts of fresh citrated plasma can be filtered easily through specially prepared asbestos-composition pads without clotting. A description of the technique is given.

1930s

• An asbestos KCl bridge and a simple calomel electrode. C.E. Zobell, S.C. Rittenberg. 1937;86(2239):502. PubMed · Publisher

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