Document ZBzzQNQ39B395Dmo02aeme2MJ
Asbestos Timetables
(By History of usage. Knowledge & Disease association)
(Up to the passage of the occupational Safety & Health Act of 1970, including the IHF documents)
by
Dr. R. A. Lemen
History of Asbestos Usage
2500 B.C
The use of asbestos dates back thousands of years when asbestos fibers were being incorporated into pottery (Agricola, 1556; Noro, 1968).
1880 A.D. Early 1888s
1895 1903 @ 1904
1/13/06
The modern industry dates from about 1880, when asbestos was used to make heat and acid resistant fabrics (Hendry, 1965; and Heuper, 1965).
Crocidolite, meaning "woolly stone", asbestos was first found northwest of the Cape Province of South Africa, but was not actively mined until the demands for asbestos during World War II (Cilliers and Genis, 1961; Hall, 1930; Sleggs et al., 1961;
and Sluis-Cremer, 1970).
In England a patent was awarded for railroad brake linings containing asbestos (Raybestos-Manhattan, 1968).
Friction brake products sold in the United States (Raybestos-Manhattan, 1968).
Second deposit of asbestos was found in South Africa in northeast Transvall and
was named amosite, in 1918, from the village Amosa, which was the acronym
for the term Asbestos Mines of South Africa. Production began in the mid-
1920s, by Cape Asbestos Company the same company already mining and
Droducina crocidolite (
. 1948: and Sluis-Cremer. 1970).
Johns-Manville ran full page advertisements in The Saturday Evening Post saying [asbestos] "Serves More People in More Ways than any Institution of its kind in the World." Included in this ad were products for the home builder, the industrial and commercial builder and the automobilists. Asbestos was also being used by American steel companies for insulation of large furnaces (cirkei,
1910).
Highlights in the production history of asbestos
1866 1870 1871
Asbestos used as heat insulation (Bowies, 1937) Asbestos cement used as a boiler coverina in 1870 ( Openina of the first asbestos factory in Great Britain (
. 1903) . 1953)
1874 1890 @ 1890
Commercial production of asbestos insulation materials in 1874 ( . 1903) The first processing of Canadian asbestos into textile in the U.S. (Berger, 1963) The asbestos cement pipe industry had its origins in Italy ( . 1973)
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1903 1904 1906 1928 1944
1963
Asbestos cement production in the U.S. began in 1903 (Berger, 1963)
Flat asbestos cement board was produced in the U.S. in 1904 ( 1958)
Asbestos was first used as a brake lining in 1906 (, 1953)
The first pipe making machines were imported into the U.S. (Berger, 1963) Asbestos spraying of deckheads and bulkheads begun in British Navy Ships
(Harries, 1968; and Harries, 1971).
The spraying of British Navy ships with asbestos was discontinued (Harries, 1968;
and Harries, 1971).
Early Knowledge Of The Health Effects From Exposure To Asbestos
Lung Disease
61-114 A.D. 1899
1902 1906 1906 1908
1911
1912 1912
Pliny the Younger wrote of the illness of slaves who worked with asbestos
Lucy Dean, Women Inspector of Factories, writes in the 1899 Annusl Report on the Health of Workers for 1898, that "[T]he evil effects of asbestos dust have instigated a microscopic examination of the mineral dust [asbestos] by HM Medical Inspector.. ., the effects have been found to be injurious as might have been expected." She continues "the worker can continue for a very long time apparently unaffected, before the symptoms of the evil become marked." (Dean, 1899).
Adilaide Anderson, Lady inspector of Factories included asbestos among the dusts known to cause injury to man in a publication on dangerous industries in England (Anderson, 1902).
*****The fjrst recor(je(j case 0f asbestosis was reported, in London, in a 33 year old man who worked in an asbestos textile plant for 14 years, by a Charing Cross Hospital physician Dr. Montague Murray in 1906 (Murray, 1907).
Numerous deaths (@50) reported in a French asbestos textile factory (Auribauit,
1906).
Italian physician reviewed the cases of 30 asbestos workers seen in a Turin clinic between 1894-1906, having a serious pulmonary disease, thought to be tuberculosis, however, which was extremely progressive, unlike the typical tuberculosis case (Scarpa, i908).
Reported in the Annual Report of HM Chief Inspector of Factories for 1910 that a Professor J.M. Beattie, of Sheffield University in the UK, had shown mild degree of fibrosis in experimental animals after inhalation of asbestos containing dust (Collis, 1911).
The American Association for Labor Legislation mentioned asbestos related disease in their Industrial Diseases (, 1912)
The government of Canada Department of Labour included asbestos related diseases as an industrial disease (1912).
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1914
1918 1918 1924
1925
1927 1927
1927 1928
Case report of a woman having worked in a German asbestos factory and dying of an acute lung illness resembling pleural pneumonia, however, on autopsy there were . . large number of crystals of a peculiar nature" (Fahr, i9i4). This was the 1st case reported in Germany and was presented to the medical society of Hamburg.
The first description in the medical literature on x-ray changes in 15 individuals exposed to asbestos (Pancoast et at., 1918).
It was reported in the Bulletin of US Labor Statistics that American and Canadian, insurance companies would not insure asbestos workers due to the un-healthy conditions in the industry (Hoffman, 191S)
Case report of asbestosis, with extensive fibrosis and more so in the right lung, in a 33 year old woman who had worked in asbestos factories for 20 years. This case had pleural thickening over the entire surface of the lung with dense adhesions on the chest wall and the pericardium. There were also tuberculosis lesions present (Cooke, 1924).
Pancoast & Pendergrass published their review of the present knowledge on the pneumoconiosis, including asbestosis, in The American Journal of Roentgenology and Radium Therapy, a journal read by mainstream general medicine radiologists (Pancoast & Pendergrass, 1925).
First complete description of asbestosis,1 including the naming of the disease and a description of "curious bodies", observed in lung tissue (Cooke, 1927).
Description of asbestosis observed in lung tissue, appearing first in 1924 (Cooke, 1924) and three years later in 1927 (McDonald, 1927; Cooke, 1927; Cooke and Hill, 1927; and Oliver, 1927). Also, McDonald (1927) and Cook & Hill (i 927) described 11 peculiar Bodies in the lungs.
First official claim for asbestosis reported in the United States (Lanza, 1936).
In May, 4 cases of asbestosis reported with one case having no histological evidence of tuberculosis. The study report stated that it had been known for sometime that workers exposed to asbestos materials suffer from pulmonary disabilities (Simson, 1928). One case, a South African asbestos mill worker, was only exposed 12 months died of rapid TB and on autopsy was found to have moderate fibrosis.
Asbestosis is a chronic lung disease due to the inhalation of asbestos fibers, either of the amphibole or serpentine type, and is characterized by diffuse interstitial fibrosis and frequently is associated with pleural fibrosis or pleural calcification. X-ray changes are usually small irregular opacities occurring mainly in the lower and middle lung fields. The pulmonary fibrotic changes develop slowly over the years--often progressively, even without further exposures--and their radiographic detection is a direct correlate of their extent and profusion. In some cases, minor fibrosis with considerable respiratory impairment and disability can be present. Pulmonary hypertension is frequently associated with advanced asbestosis and the resultant cor-pulmonale (right-sided heart failure) may be the cause of death. In some cohorts this has accounted for 12 to 20% of the deaths (Kieinfeid et ai., 1967 and Knge, 1966). Asbestosis is a progressive disease even in the absence of further exposure (osha, i986). Individuals diagnosed with pulmonary asbestosis are at a higher probability of developing and dying of cancer of one or other forms (hmso, i949;
Buchanan, 1965; O'Donnell, et al,, 1966; Lewinsohn, 1974; and Berry, 1981).
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1928 1929 1929 1929 1930 1930 1930
1930 1930
1930 1930 1931 1931 1931 1932
On December 1, a case report of asbestosis was published in which all other causes were excluded including tuberculosis (Seiler 1928).
Cooke and Gloyne independently describe curious bodies found in pulmonary asbestosis (Cooke, 1929 & Gloyne, 1929).
Stewart & Haddow (1929) demonstrate asbestos bodies in the sputum of asbestos workers.
"***An article in the British Medical Journal reviewed occupational induced dust diseases, including asbestos related disease (Bridge, 1929).
The first reported case of asbestosis in the United States (Mills, 1930).
Lynch and Smith (1930) reported on "asbestos bodies" found in the sputum of asbestos exposed workers.
*****Five additional early studies led many investigators to conclude that people exposed to asbestos dust, including manufacturing, developed the disease "asbestosis" (Merewether and Price, 1930; Merewether, 1930; Wood and Gloyne, 1930; Wood and Page, 1930; Soper, 1930). Merewether and Price (1930) in their report found 28.1 percent of the 374 asbestos textile workers examined with pulmonary fibrosis and for those with greater than 20 years exposure, 80% had x-ray abnormal! Jes. Even after excluding any of those with other known or suspected dust exposure history, there remained 26.2 percent with pulmonary fibrosis that could only be explained as a result of their asbestos exposure.
Suppression of dust was recommended to control lung fibrosis, caused by asbestos, in a report issued by HM Chief Inspector of Factories (Merewether &
Price, 1930).
*****The Journal of the American Medical association published statistical highlights of the report by Merewether, 1930 (jama, 1930). The JAMA was mailed, by 1920, to 48% of U.S. doctors but estimated to be read by 80% of U.S. physicians (Fishbein, 1947). JAMA also in a latter edition reported the Mills, 1930, case of asbestosis (jama, 1930).
*****The Asbestos Worker, a trade union journal for the asbestos worker made reference to asbestosis (____ , 1930).
It was demonstrated that disease occurred even after short periods of exposure and that radiographic changes occurred in workers exposed less than 5 years
(Donnelly, 1930).
Asbestos induced discrete pleural thickening (pleural plaques) were first reported by Sparks (1931). He also described small irregular calcareous deposits in the lower parts of the lung.
Asbestos exposure studies continued to be reported showing the development of asbestosis (Lynch and Smith, 1931; Sparks, 1931; Stewart et al., 1931).
Another study discussed the case of asbestosis in a wired-haired terrier used as a ratter in an asbestos factory (Schuster 1931).
Asbestosis after asbestos exposure indicating how the x-ray is different than that
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1932 1932 1932
1933
1933 1933
of silica exposed workers. (Russell, 1932).
Asbestosis, it's identification and control discussed in a UK Government publication (UK, 1932).
*****Concerns were raised in The Lancet, the American/British medical journal, about asbestos building materials and health risks (___ 1932).
The disease asbestosis was causally liked with end-product usage of asbestos containing materials, as early as 1932, when a maintenance employee, working with asbestos containing insulation products, developed the disease. A workers' compensation claim was even awarded, in this case, without any medical challenge (Russell, 1932).
Asbestos exposure study and the development of "asbestosis" in 7 cement mixers cases and a dog. This study reported asbestosis cases among production workers and described the slow development of the disease with the patient often free of symptoms for several years. This report re-reported the case of asbestosis in a 10 year old rough-hairr.d terrier dog used as a ratter in an asbestos factory that had been reported in 1931 by Schuster (Eiiman, 1933)2.
Ellman discussed a case of asbestosis from asbestos insulation used on lead pipes (Ellman, 1933).
Merewether (1933-34) commenting on Professor Beattie's study of experimental animal reported in HM Annual Report of 1910, said "Although definite proof was not forth-coming at the time, there were reasonable grounds for suspicion that the inhalation of much asbestos dust was to some extent harmful, and form then onwards the British Factory Department pressed for the installation of exhaust ventilation in the more dusty processes." (Coins, 1911).3
1934
Studies linking asbestos exposure with to asbestosis (Wood and Gioyne, 1934;
Donnelly, 1934).
1935 1935
1935 1936
Reports linking asbestos exposures with asbestosis (Egbert, 1935 & Fulton et ai.,
1935).
In the study by Lanza et al. (1935), of asbestos textile workers, they found overall 43 percent had fibrosis (lung scaring); 58 percent of workers with 10-15 years exposure; and 87 percent of workers with over 15 years exposure had x-ray changes.
Asbestosis found in a welder (Jacobson, 1935).
The IHF, first called the Air Hygiene foundation (1936-1941), was
2 This study and others followed describing the latent period for disease development where they found the
longer the duration of exposure the greater the risk of developing disease. 3 3 Asbestosis is not specific to humans and has occurred in animals other than under experimental situations. Besides the terrier described above by Ellman (1933) and Schuster (1931), Webster (1963) described asbestosis in donkeys hauling asbestos ore. Environmentally induced asbestosis has also been found in field rats living in and around an asbestos mill and also in baboons living near an asbestos mill (Webster, 1963).
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1936 1936
founded in 1936, under the auspices of the Mellon Institute. It's membership was comprised of a cross-section of large industrial companies. IHF conducted medical and industrial hygiene surveys, including in the asbestos industry & produced a digest - the Industrial Hygiene Digest which provided health & safety information to members. The IHF meetings were also covered by various news and wire services, such as the Wall Street Journal & The New York Times as well as the Associated Press and United Press International. (McMahon, j.f., 1939 & castieman, b.i., 1990). The Foundation was labeled by at least by one person, Vandiver Brown, who described to C.J. Stover, the publisher of Asbestos, Dec. 4, 1936 it as "the creature of industry and the one institution upon which employers can rely completely for a sympathetic appreciation of their viewpoint."(Castieman, 1990)
Studies linking asbestosis with exposure to asbestos (Donnelly, 1936 & Egbert et
al,, 1936).
McPheeters (1936) described continued exposure to asbestos could increase the fibrosis in existing asbestotics and reported some evidence that asbestosis develops more rapidly in younger persons.
1938
1939 1940 1940 1940 1942
*****United States Public Service Health study of 541 men and women in three asbestos textile factories finding asbestosis dose-response related and later used for setting guidance limits for occupational exposure to asbestos of 5 mppcf (Dreessen et al., 1938).
Asbestosis in a person handling asbestos at a chemical plant (Arnold et ai., 1939).
Asbestosis in a chemical worker (Wold, 1940). Asbestosis in a shipyard Insulator (Kuhn, 1940).
Asbestosis in a chemical worker (Schrumpf, 1941).
The first description of typical pleural plaques was by Porro et al., (1942).4
4 and then by Siegal et al., (1943) in talc workers and then in the 1950's in asbestos workers (Smith,1952; Jacob & Bohlig, 1955; Fehre, 1956; and Frost et al., 1956) The plaques are progressive and do cause adverse respiratory symptoms, such as dyspnea (breathlessness) and decrements in pulmonary function while it is more likely that diffuse pleural thickening will cause functional impairment (McMillan and Rossiter, 1982; Sheers, 1979; Rosenstock and Hudson, 1986; Rosenstock et al., 1988). Pleural thickening is considered a marker of past exposures (Hiiierdai, 1980). There is evidence that persons with pleural plaques are more likely to develop asbestos-induced parenchymal fibrosis than those without such plaques (Rosenstock, 1994). Asbestos-induced pleural plaques are a progressive disease (McMillan and Rossiter, 1982).
There is evidence that individuals with asbestos-induced pleural plaques are at a marked increased risk of developing and dying of lung cancer or malignant mesothelioma. Fletcher (1972) reported asbestos-exposed workers diagnosed with pleural plaques were at a 137 percent greater risk from dying of cancer of the lung (16 obs. vs. 6.74 exp.) and at 2900 percent increased risk of dying from mesothelioma (3 obs. vs. 0.10 exp.) when compared to the general population of the same age but not occupational exposed to asbestos. The workers included sheetmetal workers, plumbers, electricians, welders, laborers, engineers, and other crafts workers. In another study of shipyard workers, Edge (1976) reported that workers with mixed
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1942 1942 1944
1944
1945 1946 1949 1947 1951 1953 1953
1955 1956
1956
1956 1957 1958 1959 1960 1960
Asbestosis in a worker who worked wearing an asbestos apron (Williams, 1942).
Asbestosis was reported among insulators (Hoiieb & Angrist, 1942).
The industrial journal, Heating and Ventilation, published an article discussing dusts, including asbestos, as hazards within the industry (Hutchinson, 1944).
Industrial Hygiene Digest (IHD) published two abstracts, one on asbestosis among 132 workers showing 29% with radiological evidence of the disease, some in workers with less than 3 years exposure; second, an abstract by the pioneer cancer researcher, Dr. W.C. Hueper, stating that asbestos was among the chemical and physical agents known to cause occupationally induced cancer
(IHD, 1944).
Asbestosis among pipe coverers (Fieisher et ai., 1946).
Asbestosis in an insulator (Kennaway & Kennaway, 1947, & Mallory et al., 1947).
Asbestosis in an insulator (Franchlnl & Canepa, 1949).
Asbestosis in and insulator (Frost, 1950).
Asbestosis in a plumber/insulator (stoiietai., 1951).
Asbestosis in insulators (van Luyt, 1953; Isselbacheretal., 1953; &Weiss, 1953). McLaughlin raised the issue of preventing end product users and dust diseases when he mentioned sprayed-on asbestos containing materials (McLaughlin, 1953).
Asbestosis in a plumber's helper (Sander, 1955).
Asbestosis in insulation workers (Ahlborg & Hansson, 1956; Hampe, 1956; Molfino & Sannini,
1956; & Frost etal., 1956).
The annual report of the UK Chief Inspector of Factories mentioned "lagging" (insulation work) as being recognized as hazardous (___ 1956).
Asbestosis in a pipefitter (Markset et at., 1957).
Asbestosis in insulators (Pendergrass, 1958 & Van der Schoot, 1958)
Asbestosis in insulators (Hertz & Reinwein, 1959).
Asbestosis in a bricklayer (Whitmore et ai., i960).
Over 20 cases of asbestosis among miners in the Transvaal asbestos
asbestos exposures and pleural plaques (without evidence of pulmonary fibrosis) had a 2.5 times greater risk of developing carcinoma of the bronchus, when compared to the matched controls without plaques. Also, Edge (1979) found that workers with asbestos- induced pleural plaques, but with no other radiographic evidence of pulmonary fibrosis, were at a 375 percent increased risk of dying of lung cancer and at a 950 percent increased risk of dying of lung cancer and mesothelioma compared to controls not exposed to asbestos and who did not have either pleural plaques or fibrosis (42 obs. vs. 4 exp.) and that smoking could not explain the increase in lung cancer in these workers.
Dr. R.A. Lemen Asbestos Timetable
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1960
1961 1961 1961 1961 1961
mining region of South Africa (Wagneretai., i960). Asbestosis in insulators and sprayers (Anderson SCampagna, I960; Ahlmark et al., 1960;
Keal, 1960; Wagner et al., 1960; & Eisenstadt & Wilson, 1960).
Asbestosis in insulators (Ambrosi & cavaiio, 1961). Asbestosis in a shipyard worker (Castieman & Kibbee, 1961). Asbestosis in carpenter and insulator (Heard & Williams, 1961). Asbestosis in a plasterer (Teiischi & Rubenstone, 1961). Asbestosis in a person doing automotive undercoating (Brugsch & Baviey, 1961).
1962 1962 1963 1963 1963 1963
1965 1964
Asbestosis in insulators and refinery workers (Eisenstadt, 1962).
Asbestosis in hod carrier, iron worker, shipyard worker, bricklayer, carpenter, and insulators (Cordova et al., 1962).
Asbestosis in insulators (Bogetti, 1963).
Asbestosis in a plumber (Castieman & Kibbee, 1963).
Asbestosis in insulators (Farina & Mazzanti, 1963, & Leathart 8, Sanderson, 1963).
*****As a result of some of these report, the American Medical Association (AMA), Council on Occupational Health, published in the Archives of Environmental Health, in August, a whole thesis titled "The Pneumoconioses", in which asbestosis was discussed. This document was to alert physicians throughout the United States of the hazards of dust exposure and disease and how to recognize and treat them. The report was reprinted by the AMA and circulated widely (Mayer et al., 1963).
Asbestosis in insulators (Seiikoff, 1965).
Asbestosis in insulators and brake repair workers (McVittie, 1965).
Cancer of the Lung5 6 5
5 Asbestosis frequently precluded or was found in conjunction with lung cancer among workers exposed to asbestos (Merewether, 1949; Doll, 1955; Buchanan, 1965). This lead some to speculate that asbestosis was necessary and somehow associated in the etiology of lung cancer among those exposed to asbestos, some attributing this association to the "scar" theory of carcinogenesis. This is not strongly supported for all asbestos-associated lung cancers according to Hillerdal (1994), since he observed that a majority of tumors were squamous cell cancers and not adenocarcinomas. Adenocarcinomas were found most commonly among patients with asbestosis and in the lower lobes of the lung, where asbestosis is most prevalent (Karjaiainen, 1994). It is true, however, in some cases of advanced asbestosis, that scar carcinomas may develop as an outgrowth of uncontrolled fibrogenesis, just like they do with usual interstitial pneumonitis (UIP), the typical pathologic lesion in asbestosis (Cullen, 1987). Asbestos exposure appears to
Dr. R.A. Lemen Asbestos Timetable
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1942 1942 1944
1944
1945 1946 1949 1947 1951 1953 1953
1955 1956
1956
1956 1957 1958 1959 1960 1960
Asbestosis in a worker who worked wearing an asbestos apron (Williams, 1942).
Asbestosis was reported among insulators (Hoiieb & Angrist, 1942).
The industrial journal, Heating and Ventilation, published an article discussing dusts, including asbestos, as hazards within the industry (Hutchinson, 1944).
Industrial Hygiene Digest (IHD) published two abstracts, one on asbestosis among 132 workers showing 29% with radiological evidence of the disease, some in workers with less than 3 years exposure; second, an abstract by the pioneer cancer researcher, Dr. W.C. Hueper, stating that asbestos was among the chemical and physical agents known to cause occupationally induced cancer
(IHD, 1944).
Asbestosis among pipe coverers (Fieisher et ai,, 1946).
Asbestosis in an insulator (Kennaway & Kennaway, 1947, & Mallory et al,, 1947).
Asbestosis in an insulator (Franchini & Canepa, 1949).
Asbestosis in and insulator (Frost, 1950).
Asbestosis in a plumber/insulator (stoiietai., 1951).
Asbestosis in insulators (van Luyt, 1953; Isselbacher et al., 1953; & Weiss, 1953). McLaughlin raised the issue of preventing end product users and dust diseases when he mentioned sprayed-on asbestos containing materials (McLaughlin, 1953).
Asbestosis in a plumber's helper (Sander, 1955).
Asbestosis in insulation workers (Ahlborg & Hansson, 1956; Hampe, 1956; Molfino & Sannini,
1956; & Frost et al., 1956).
The annual report of the UK Chief Inspector of Factories mentioned "lagging" (insulation work) as being recognized as hazardous (___ , 1956).
Asbestosis in a pipefitter (Markset et al., 1957).
Asbestosis in insulators (Pendergrass, 1958 & Van der Schoot, 1958)
Asbestosis in insulators (Hertz & Reinwein, 1959).
Asbestosis in a bricklayer (Whitmoreetai., i960).
Over 20 cases of asbestosis among miners in the Transvaal asbestos
asbestos exposures and pleural plaques (without evidence of pulmonary fibrosis) had a 2.5 times greater risk of developing carcinoma of the bronchus, when compared to the matched controls without plaques. Also, Edge (1979) found that workers with asbestos- induced pleural plaques, but with no other radiographic evidence of pulmonary fibrosis, were at a 375 percent increased risk of dying of lung cancer and at a 950 percent increased risk of dying of lung cancer and mesothelioma compared to controls not exposed to asbestos and who did not have either pleural plaques or fibrosis (42 obs. vs. 4 exp.) and that smoking could not explain the increase in lung cancer in these workers.
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1960
1961 1961 1961 1961 1961
mining region of South Africa (Wagner et at, i960). Asbestosis in insulators and sprayers (Anderson &Campagna, I960; Ahlmark et at, 1960;
Keal, 1960; Wagner et at, 1960; & Eisenstadt & Wilson, 1960).
Asbestosis in insulators (Ambrosi & Cavaiio, 1961). Asbestosis in a shipyard worker (Castieman & Kibbee, 1961). Asbestosis in carpenter and insulator (Heards. Williams, 1961). Asbestosis in a plasterer (Teiischi & Rubenstone, 1961). Asbestosis in a person doing automotive undercoating (Brugsch & Baviey, 1961).
1962 1962 1963 1963 1963 1963
1965 1964
Asbestosis in insulators and refinery workers (Eisenstadt, 1962).
Asbestosis in hod carrier, iron worker, shipyard worker, bricklayer, carpenter, and insulators (Cordova et at, 1962).
Asbestosis in insulators (Bogetti, 1963).
Asbestosis in a plumber (Castieman & Kibbee, 1963).
Asbestosis in insulators (Farina & Mazzanti, 1963, & Leathart & Sanderson, 1963).
*****As a resu|t of some of these report, the American Medical Association (AMA), Council on Occupational Health, published in the Archives of Environmental Health, in August, a whole thesis titled "The Pneumoconioses", in which asbestosis was discussed. This document was to alert physicians throughout the United States of the hazards of dust exposure and disease and how to recognize and treat them. The report was reprinted by the AMA and Circulated Widely (Mayer etal., 1963).
Asbestosis in insulators (Seiikoff, 1965).
Asbestosis in insulators and brake repair workers (McVittie, 1965).
Cancer of the Lung5 6 5
5 Asbestosis frequently precluded or was found in conjunction with lung cancer among workers exposed to asbestos (Merewether, 1949; Doll, 1955; Buchanan, 1965). This lead some to speculate that asbestosis was necessary and somehow associated in the etiology of lung cancer among those exposed to asbestos, some attributing this association to the "scar" theory of carcinogenesis. This is not strongly supported for all asbestos-associated lung cancers according to Hillerdal (1994), since he observed that a majority of tumors were squamous cell cancers and not adenocarcinomas. Adenocarcinomas were found most commonly among patients with asbestosis and in the lower lobes of the lung, where asbestosis is most prevalent (Karjaiainen, 1994). It is true, however, in some cases of advanced asbestosis, that scar carcinomas may develop as an outgrowth of uncontrolled fibrogenesis, just like they do with usual interstitial pneumonitis (UIP), the typical pathologic lesion in asbestosis (Cullen, 1987). Asbestos exposure appears to
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1935
1936 1938 1938 1942 1944 1947
1949
*****Lynch and Smith (1935) in the United States and Gloyne (1935) in the United Kingdom both associated occupational asbestos exposure with lung cancer. Lynch and Smith reported epidermoid carcinoma of the right lung in a 57 year old man who also had pulmonary asbestosis and who had began as a weaver in an asbestos textile plant in 1913 and died in 1934. Gloyne reported two cases of squamous carcinoma of the lung in women workers, the first age 35 who had spent 8 years as a spinner in a textile plant and survived 9 years after that exposure before death. The second woman was 71 who lived 15 years after two brief periods of 6 months and 13 months working in a mattress factory. Both women also had asbestosis.
Reports appeared in the medical literature of lung cancers occurring in asbestos exposed workers (Egbert and Geiger, 1936; Gloyne, 1936; Middleton, 1936).
Reports appeared in the medical literature of lung cancers occurring in asbestos workers (Hornig, 1938 & Koelsch, 1938).
German physicians began calling lung cancer an occupational disease of asbestos workers (Nordman, 1938).
Hueper (1942) in his classic book on cancer discusses asbestos related lung cancers.
The American Medical Association talks of asbestos and it's relationship to lung cancer (jama, 1944).
The Chief Inspector of Factories in Great Britain reported on all of the known cases of asbestosis (235), in Great Britain, where 13% were due to lung cancer when only 1% of all deaths were due to this cause. Among women, known to have asbestosis, 8% had lung cancer when, at that time very few women smoked and the amount of female lung cancer was quite rare (Merewether,
1949).
The American Medical Association ran an editorial urging increased attention, by the medical profession, to asbestos exposed workers, because of their risk developing lung cancer (jama, 1949)6
increase the risk for all histological types of lung cancer (Karjaiainen, 1994). It is more likely that asbestosis is not a precursor to lung cancer, but that both are independent diseases related with a dose-response from exposure to asbestos, and that cancer of the lung can and does occur in the absence Of asbestosis (Roggli et al., 1994; Abraham, 1994; Karjaiainen, 1994; Hillerdal, 1994; and Jones et al., 1996). McDonald et al. (1994) have presented epidemiological data showing increased risk of lung cancer in occupations with exposure to asbestos in the absence of radiological evidence of pulmonary fibrosis. Hillerdal (1994), in a well designed study having sufficient statistical power, found lung cancer to occur in patients with bilateral pariental pleural plaques but without radiological evidence of asbestosis.
6 The relative risk for lung cancer has varied from 1.0 (Knox et al., 1968) to 17.6 (Eimes and Simpson, 1971) with an average 9.8 relative risk. The prognosis and treatment of asbestos induced lung cancer is no different than lung cancer having another etiology. It appears that all cell types of lung cancer occur in asbestos workers and that the presence or absence of one cell type cannot be used to prove or disprove and association of asbestos exposure with the lung cancer (Churg,
1985).
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1955 1960
1965 1964 1966 1966
1968 1968 1968
*****Epidemiological evidence from a United Kingdom cohort of 113 men who had worked for more than 20 years and were employed before 1930 in an asbestos textile plant was reported by Doll in 1955 which showed a ten-fold excess risk of lung cancer (Doit, 1955). This study has proven to be the pivotal study for the causal association of asbestos exposure and lung cancer.
The E.l. Du Pont De Nemours & Company sponsored a book published by Lea & Febiger on Modern Occupational Medicine which had a chapter by Schepers on Occupational Chest Diseases. In the chapter and section on asbestos Schepers concludes that "[P]ulmonary carcinoma has been observed with such high frequency in employees of the asbestos industry that a causal relationship has been accepted by most authorities." He further discusses the causal association of mesothelioma with asbestos exposure and that even a single month of exposure with no additional exposure can result in asbestosis 30 years later. Finally, Schepers talks about "[Cjases are currently cropping up in men and women who had worked as pipe insulators on liberty ships during the second world war without since having had any further asbestos exposure" (Schepers,
I960).
*****The New York Academy of Sciences held a conference on "The Biological Effect Asbestos" (Selikoff and Churg, 1965).
*****By 1964 there were more than 700 articles in the worldwide medical literature dealing with health effects associated with asbestos exposure (Ozonoff,
1988).
The widely read American/British medical journal The Lancet ran an editorial on March 5, 1966 discussing the wide news coverage of the "dangers of asbestos", resulting from the New York Academy of Science Conference and the need for the risks of asbestos to be know and to control exposures (Lancet, 1966).
Citing this conference the United States government, program on occupational health of the National Center for Urban and Industrial Health, sponsored a two day seminar, in December of 1966, that outlined the need for expanding the governments role in protecting asbestos exposed individuals. The seminar proceedings stated that "It has been known since the early 1900's that excessive exposure to asbestos gives rise to the disabling pulmonary disease "asbestosis." More recently, evidence has been developed that the incidence of respiratory tract, and other malignancies in asbestos workers is excessive." (Brown, 1967).
So much concern was express that some governmental, some industry, some labor, and some academia were jointly embarked on ways to eliminate exposures to asbestos (Brown, 1968; Selikoff, 1968; Jobe, 1968; and Hutchinson, 1968).
J.B. Jobe, Vice President of Johns-Manville Corporation described their need to participate in jointly sponsored studies as ". . . another stride to cope with environmental problems involved with its [industry's] operations and products"
(Jobe, 1968).
On October 12, a report appeared in the popular periodical The New Yorker magazine on asbestos and its' associated health hazards in a 22 page article tiled The Magic Mineral. Now not only the scientific community knew of the hazards of asbestos but now one of the most widely read lay publications was telling its' readership of the dangers faced by persons exposed to asbestos
(Brodeur, 1968).
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Mesothelioma (cancer of the linings of the chest and abdomen)7 8
1943- 1946
Reports of pleural (chest) and peritoneal (abdominal) tumors associated With asbestos exposures appeared (Wedler, 1943 a, b and Wyers, 1946).
1947
Mesothelioma of the pleura, with no fibrosis of the lung, found on pathologic examination in a 37 year old insulation worker with a history of cutting asbestos containing insulation board (Mallory etai., 1947).
1949 1952
Further reports of mesothelioma and association with asbestos exposure
(Doig, 1949; Merewether, 1949; & Wyers, 1949).
Cases of mesothelioma reported (Smith, 1952) and Cartier (1952) reported on a pleural mesothelioma with no asbestosis.
1953
Discussion of two previously unpublished cases of pleural mesothelioma (Weiss,
1953).
1958
1960
1963
Pleural mesothelioma in insulation worker (Van der school, 1958).
*****Wagner et al's. study of miners, millers, and transporters of asbestos and of non-mining residents looked at 47 cases, occurring between 1956 and 1960 and found primarily mesothelioma of the pleural occurring in one part of South Africa, the northwestern portion of the Cape Province, known to have many asbestos mines. Their study is attributed to confirming epidemiologically an association between exposure to asbestos and mesothelioma. The fact that residential exposures were also occurring have attributed to the fact that lowlevel, non-occupational exposures to asbestos could be hazardous (Wagner et
at., 1960).
The first study, in the United States, to report mesothelioma with asbestos exposure was reported (Mancuso and Coulter, 1963)
1964
A second study in the United States, of insulation workers, found an association of asbestos exposure and mesothelioma (Seiikoff et ai,, 1964).
PRODUCT USAGE AND DISEASE78 9
7 The ratio of occurrence for mesothelioma in the pleural area to the peritoneal area appears to be associated with the degree of exposure (Newhouse et ai., 1972). Among the number of occupational exposed groups studied approximately 5-7% of the deaths have been due to mesothelioma (Gilson, 1973; Hammond and Seiikoff, 1973; and Seiikoff, 1976). Another estimate has projected that as many as 11% of all asbestos workers' deaths in England will be from mesotheliomas (Newhouse and Berry, 1976).
8 Other malignant disease patterns have also been reported from epidemiological studies of asbestos workers, the most common of which is gastrointestinal tract cancer with a relative risk Of 0.5 (Meurman et al,, 1974) to 3.1 (Mancuso and El-Atar, 1967 and Seiikoff, 1974). Reports Of gastrointestinal tract cancers associated with asbestos exposure have been reviewed by the World Health Organization (WHO) (1989) in which they have concluded that "overall, there seems that there is a correlation between lung cancer and gastrointestinal cancer rates in occupational cohorts [exposed to asbestos] which is not due to chance" (who, 1989).
9 Worker exposure has been found in the shipyard industry; the construction industry; the brake repair and transportation industry; the electronic and electrical industries; the paint industry; the optical goods industry; the plumbing industry; and other general industry manufacturing sectors
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1932
1932 1933 1934 1935 1935 1935 1935
1939 1939 1940 1940
Lung Disease (Asbestosis)
The disease asbestosis was causally linked with end product usage of asbestos containing materials, as early as 1932, when a maintenance employee, working with asbestos containing insulation products, developed the disease. A workers' compensation claim was even awarded, in this case, without any medical challenge.(Russell, 1932).
Concerns were raised in The Lancet, the American/British medical journal about asbestos building materials and health risks (___ 1932).
Ellman discussed a case of asbestosis, from asbestos insulation used to lead pipes (Ellman, 1933).
Asbestosis in a boiler riveter (Wood and Gioyne, 1934).
Asbestosis in a welder(Jacobson, 1935).
Asbestos use in brake linings is mentioned by Fulton et al. (Fulton et ai., 1935).
Asbestosis in 5 plants among workers having more than 3 years employment including one making brake and clutch friction products (Lanza etai., 1935).
Asbestosis mentioned as a consequence from exposure in industries and processes such as the sawing, grinding and turning of brakes, in the dry state
(HMSO, 1935).
Asbestosis in an asbestos handler at a chemical plant (Arnold et ai., 1939).
Asbestosis reported in brake manufacturing workers beginning in 1928 and discusses wet methods for control Of dust (George & Leonard, 1939).
Asbestosis in a chemical worker (Wolf, 1940).
Asbestosis in a shipyard insulator (Kuhn, 1940).
(niosh, 1990; Lloyd, 1975; and Nicholson et ai.. 1962). Exposures in the construction industry varied as shown in the study by Reitze et al. (1972) when they measured fiber counts from spraying asbestos onto buildings. They found 70 fibers/ml 10 feet from the nozzle of the spray gun and at 25 feet from the nozzle, 3 fibers/ml. This indicates that not only were the spray operators at risk, of exposure, but also the auxiliary workers such as carpenters, pipefitters, welders, electricians, plumbers, etc. (Reitze et al., 1972).
Diseases in non-occupational exposed persons living near industrial sources of asbestos and familial exposures to asbestos occurred when the worker brought home asbestos containing material from the worksite or when the worker did not shower or wore the same clothes home that had been worn during the work process (Wagner et al., I960; Newhouse and Thompson, 1965; Bohlig and Hain, 1973; Nicholson, 1975; Anderson etal., 1976; and NIOSH, 1995). Also domestic exposures have been associated with household repairs, and do-it-yourself construction, using products containing asbestos or when disturbing products containing asbestos (Rohi et ai., 1975). Pets, of owners with asbestos-related occupations or the hobbies of a household member involving asbestos containing materials, have lead to the animal's developing mesothelioma (Giickman et ai., 1983).
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Mesothelioma (cancer of the linings of the chest and abdomen)7 8
1943 - 1946 1947 ,1949 1952
1953
1958 1960
1963 1964
Reports of pleural (chest) and peritoneal (abdominal) tumors associated with asbestos exposures appeared (Wedler, 1943 a, bandWyers, 1946).
Mesothelioma of the pleura, with no fibrosis of the lung, found on pathologic examination in a 37 year old insulation worker with a history of cutting asbestos containing insulation board (Mallory et at., 1947).
Further reports of mesothelioma and association with asbestos exposure
(Doig, 1949; Merewether, 1949; & Wyers, 1949).
Cases of mesothelioma reported (Smith, 1952) and Cartier (1952) reported on a pleural mesothelioma with no asbestosis.
Discussion of two previously unpublished cases of pleural mesothelioma (Weiss,
1953).
Pleural mesothelioma in insulation worker (Van der Schoot, 1958).
*****Wagner et al's. study of miners, millers, and transporters of asbestos and of non-mining residents looked at 47 cases, occurring between 1956 and 1960 and found primarily mesothelioma of the pleural occurring in one part of South Africa, the northwestern portion of the Cape Province, known to have many asbestos mines. Their study is attributed to confirming epidemiologically an association between exposure to asbestos and mesothelioma. The fact that residential exposures were also occurring have attributed to the fact that lowlevel, non-occupational exposures to asbestos could be hazardous (Wagner et
al,, 1960).
The first study, in the United States, to report mesothelioma with asbestos exposure was reported (Mancusoand Coulter, 1963)
A second study in the United States, of insulation workers, found an association of asbestos exposure and mesothelioma (Seiikoff et ai,, 1964).
PRODUCT USAGE AND DISEASE
7 The ratio of occurrence for mesothelioma in the pleural area to the peritoneal area appears to be associated with the degree of exposure (Newhouse et ai., 1972). Among the number of occupational exposed groups studied approximately 5-7% of the deaths have been due to mesothelioma (Gilson, 1973; Hammond and Seiikoff, 1973; and Seiikoff, 1976). Another estimate has projected that as many as 11% of all asbestos workers' deaths in England will be from mesotheliomas (Newhouse and Berry, 1976).
8 Other malignant disease patterns have also been reported from epidemiological studies of asbestos workers, the most common of which is gastrointestinal tract cancer with a relative risk Of 0.5 (Meurman etal., 1974) to 3.1 (Mancusoand El-Atar, 1967 and Seiikoff, 1974). Reports Of gastrointestinal tract cancers associated with asbestos exposure have been reviewed by the World Health Organization (WHO) (1989) in which they have concluded that "overall, there seems that there is a correlation between lung cancer and gastrointestinal cancer rates in occupational cohorts [exposed to asbestos] which is not due to chance" (who, 1989).
9 Worker exposure has been found in the shipyard industry; the construction industry; the brake repair and transportation industry; the electronic and electrical industries; the paint industry; the optical goods industry; the plumbing industry; and other general industry manufacturing sectors
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1932
1932 1933 1934 1935 1935 1935 1935
1939 1939 1940 1940
Lung Disease (Asbestosis)
The disease asbestosis was causally linked with end product usage of asbestos containing materials, as early as 1932, when a maintenance employee, working with asbestos containing insulation products, developed the disease. A workers' compensation claim was even awarded, in this case, without any medical challenge.(Russeii, 1932).
Concerns were raised in The Lancet, the American/British medical journal about asbestos building materials and health risks (___ 1932).
Ellman discussed a case of asbestosis, from asbestos insulation used to lead pipes (Ellman, 1933).
Asbestosis in a boiler riveter (Wood and Gloyne, 1934).
Asbestosis in a welder{Jacobson, 1935).
Asbestos use in brake linings is mentioned by Fulton et al. (Fulton et ai., 1935).
Asbestosis in 5 plants among workers having more than 3 years employment including one making brake and clutch friction products (Lanza etai., 1935).
Asbestosis mentioned as a consequence from exposure in industries and processes such as the sawing, grinding and turning of brakes, in the dry state
(HMSO, 1935).
Asbestosis in an asbestos handler at a chemical plant (Arnold et ai., 1939).
Asbestosis reported in brake manufacturing workers beginning in 1928 and discusses wet methods for control Of dust (George & Leonard, 1939).
Asbestosis in a chemical worker (Wolf, 1940).
Asbestosis in a shipyard insulator (Kuhn, 1940). .
(NiosH, 1990; Lloyd, 1975; and Nicholson et ai., 1982). Exposures in the construction industry varied as shown in the study by Reitze et al. (1972) when they measured fiber counts from spraying asbestos onto buildings. They found 70 fibers/ml 10 feet from the nozzle of the spray gun and at 25 feet from the nozzle, 3 fibers/ml. This indicates that not only were the spray operators at risk, of exposure, but also the auxiliary workers such as carpenters, pipefitters, welders, electricians, plumbers, etc. (Reitze et al., 1972).
Diseases in non-occupational exposed persons living near industrial sources of asbestos and familial exposures to asbestos occurred when the worker brought home asbestos containing material from the worksite or when the worker did not shower or wore the same clothes home that had been worn during the work process (Wagner et al., I960; Newhouse and Thompson, 1965; Bohlig and Hain, 1973; Nicholson, 1975; Anderson et al., 1976; and NIOSH, 1995). Also domestic exposures have been associated with household repairs, and do-it-yourself construction, using products containing asbestos or when disturbing products containing asbestos (Row et ai., 1975). Pets, of owners with asbestos-related occupations or the hobbies of a household member involving asbestos containing materials, have lead to the animal's developing mesothelioma (Giickman et al., 1983).
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1940 1941 1941
1942 1942 1946 1947 1949 1950 1951 1953 1953,
1955 1955 1956
1956
1957 1957
1958 1959 1960 1960
1961 1961 1961
Asbestosis among 148 brake lining manufacturing workers (stone, 1940).
Asbestosis in a chemical worker (Schrumpf, 1941).
Risk of asbestosis disease among brake grinders and drillers discussed
(Brachmann, 1941).
Asbestosis in a worker who worked wearing an asbestos apron (Williams, 1942).
Asbestosis among insulators (Holleb and Angrist, 1942).
Asbestosis among pipe coverers (Fieisheretai., 1946).
Asbestosis in an insulator (Kennaway and Kennaway, 1947 & Mallory et al.,1947). Asbestosis in an insulator (Franchini and Canepa, 1949).
Asbestosis in an insulator (Frost, 1950).
Asbestosis in a plumber/insulator (Stoll et at, 1951).
Asbestosis in insulators (van Luyt, 1953 & Weiss, 1953). McLaughlin raised the issue of preventing dust diseases when he mentioned sprayed on asbestos containing materials (McLaughlin, 1953).
Asbestosis in a plumber's helper (Sander, 1955).
Asbestosis in insulators of pipes and boilers (McLaughlin, 1955).
Asbestosis in insulation workers (Ahlborg and Hansson, 1956; Hampe, 1956; Molfino and
Sannini, 1956; & Frost et al., 1956).
The annual report of the U.K. Chief Inspector of Factories mentioned ''lagging" (insulation work) as being recognized as hazardous (___ , 1956).
Asbestosis in a pipefitter (Marksetetal., 1957).
Asbestosis in insulators; workers sawing and cutting finished asbestos materials; workers tearing out old insulation; and spraying asbestos on walls and ceilings (Thomas, 1957).
Asbestosis in an insulators (Pendergrass, 1958 & Van derSchoot, 1958).
Asbestosis in insulators (Hertz and Reinwein, 1959).
Asbestosis in a bricklayer (Whitmore etai., i960).
Asbestosis in an insulators and sprayers (Anderson and Campagna, I960; Ahlmark et al.,
1960; KeaI, 1960; Wagner et al., I960; & Eisenstadt and Wilson, 1960).
Asbestosis in insulators (Ambrosi and Cavallo, 1961).
Asbestosis in a shipyard worker (Castleman and Kibbee, 1961).
Asbestosis in carpenter and insulator (Heard and williams, 1961).
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1961 1961 1962 1962 1963 1963 1963 1963
1964
1965 1965 1966 1968 1969 1971 1971 1971 1971 1971
1971
Asbestosis in a plasterer (Telischi and Rubenstone, 1961).
Asbestosis in an person doing automotive undercoating (Brugschand Baviey, 1961).
Asbestosis in insulators and refinery workers (Eisenstadt, 1962).
Asbestosis in hod carrier, iron worker, shipyard worker, bricklayer, carpenter, and insulators (Cordova et al., 1962).
Asbestosis in insulators (Bogetti, 1963).
Asbestosis in a plumber (Castleman and Kibbee, 1963).
Asbestosis in insulators (Farina and Mazzanti, 1963 & Leathart and Sanderson, 1963).
*****As a result of some of these reports, the American Medical Association (AMA) Council on Occupational Health published in the Archives of Environmental Health in August 1963 a whole thesis titled "The Pneumoconioses", in which asbestosis was discussed. This document was to alert physicians throughout the country of the hazards of dust exposure and disease and how to recognize and treat them. The report was reprinted by the AMA and circulated widely (Mayer, etai., 1963).
***`*By 1964 close to 50 medical articles were published, the majority in English, describing some 150 plus cases of non-cancerous lung disease (asbestosis) among end product users of asbestos containing products. Many of these products were used in construction of buildings and, as with any building, through periodic maintenance asbestos was disturbed and released.
Asbestosis in insulators (Seiikoff, 1965).
Asbestosis in insulators and brake repair workers (McVittie, 1965).
Asbestosis in insulators (Gilson, 1966).
Asbestosis in insulators (Harries, 1968).
Asbestosis from childhood exposure to asbestos from father's work clothes
(Teyssier and Lesobre, 1968).
Asbestosis in pipe insulators (Murphy et ai., 1971).
Asbestosis in insulators (Harries, 1971).
Asbestosis in joiners (Fletcher, 1971).
Asbestosis in shipyard repair workers (Ferris et ai., i97i).
Lumley et al., (1971) discussed the potential health hazards from buildings insulated with sprayed asbestos.
Occupational Safety and Health Act of 1970 (OSHAct) became effective (April 29) and asbestos officially regulated under this new act (May)10
10 Official U.S. Government regulations for asbestos prior to the OSHAct were covered under the Walsh Healy Act as early as the early 1950s and the Longshoremen's Act in 1960.
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1942 1951 1953 1953 1954 1958 1958 1960 1961 1962 1962 1962 1963 1963
1964 1964
1965
CANCER FROM ASBESTOS PRODUCT USAGE
Lung cancer in insulators (Hoiieb and Angrist, 1942).
Lung cancer in a pipe coverer (Stoll et at, 1951).
Mesothelioma in a shipyard insulator (Weiss, 1953).
Lung cancer in a contractor's helper sawing asbestos board (isseibacher, 1953).
Lung cancer in plumbers, gas fitters and steam fitters (Breslow et al., 1954).
Mesotheliomas in insulators (Van DerSchoot, 1958).
Lung cancer in insulator (Schomagei, 1958).
Pleural mesothelioma in refinery worker (Eisenstadt and Wilson, i960).
Lung cancer in insulators (Frankel and DeJager, 1961).
Mesothelioma in refinery foremen (Eisenstadt, 1962).
Mesothelioma in shipyard workers (McCaugheyetat, 1962).
Lung cancer in a hod carrier, iron worker, shipyard worker, bricklayer, carpenter, and insulators (Cordova et al., 1962).
Mesothelioma in a plumber (Castleman and Kibbee, 1963).
Mesotheliomas have also been observed in pets. In one study of 18 dogs diagnosed with mesothelioma, the owners for 16 were identified and 12 were able to identify possible sources of asbestos exposure. Nine of the dogs owners had asbestos-related occupations or hobbies, five had remodeled their homes, five had residential proximity to an industrial source of asbestos, and five used flea powders known to contain asbestos-like fibers (Glickman et al., 1983).
Lung cancer, stomach cancer, colon cancer, rectal cancers, and pleural and peritoneal mesotheliomas in insulators (Selikoff et al., 1964).
*`***ln October 1964 a watershed event occurred that brought broader international attention to the hazards of work with asbestos and to products containing asbestos, when the New York Academy of Sciences held a conference on the "Biological Effects of Asbestos" with presentations by over 80 of the World's leading researchers on asbestos. This conference was widely covered by the news media and the proceedings were published in 1965 in a 766 page Annals (Selikoff and Churg, 1965). [While this conference reported on the known health
effects exposure to asbestos (asbestosis and cancers) a major theme was the emphasis placed on the areas of prevention, including dust control techniques, community and other indirect exposures, and the significance of air pollution control.]
C.G. Addingley of the British Belting and Asbestos Ltd. industry stated that "We do not believe there is any safe limit.. . . Therefore, I would like it to be clearly
Dr. R.A. Lemen Asbestos Timetable
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understood that we do not accept four fibers per cc. as a safe maximum limit in the asbestos industry." (Addingiey, 1965).
1965
1965 1965 1965 1965
1967
John Wells of the American Asbestos industry, U.S. Rubber Co., said "Our own conclusion, as we began seeing what was happening in our own process, was that the only safe amount of asbestos dust exposure was zero and that the efforts in terms of achieving that lay basically in engineering, and, secondly, in education." (Weils, 1965).
Mesothelioma in insulators (Selikoff et al., 1965).
Mesothelioma in laggers and pipe fitters (Owen, 1965).
Mesothelioma in plumbers and boiler repair workers (Elmes and Wade, 1965).
Mesothelioma from domestic exposures to asbestos insulation, in wives of asbestos workers and from neighborhood exposures (Newhouse and Thompson,
1965).
Mesothelioma in a boiler maker, plasterer, builder of bakery ovens, and two women with sons that were insulators (Lieben and Pistawka, 1967).
Regulations for asbestos11 * 12
11 It has long been known that suppression of dust was the best method to control diseases associated with exposures to dusts and was described by Ramazzini, 1713 and Oliver, 1902. In the United Kingdom, the Chief Inspector of Factories, in London, recommended to one factory, after having experienced five deaths due to phthisis (asthma like disease), exhaust ventilation and annual medical examinations (The chief inspector of Factories, 1910). Merewether and Price, (1930) were among the very firsts to set forth very specific recommendations for dust suppression in the asbestos industry that included: 1) application of efficient localized exhaust ventilation at dust producing points; 2) substitution of enclosed mechanical methods for hand conveyance, and for dusty hand work generally; 3) effective enclosure of dust-producing machines; 4) substitution of wet methods instead of dry material handling; 5) elimination of certain dust-producing appliances; 6) abandonment of settling chambers in manufacturing processes, to the utmost extent; 7) effectual separation of processes to prevent unnecessary exposure to dust; 8) wide spacing of dust-producing machines in new factories and, as far as practicable, in existing works; 9) use of sacks of close texture material for internal work; 10) efficient cleaning systems with wide use of vacuum methods; 11) storage of asbestos and other goods outside workrooms; and 12) exclusion of young persons from specially dusty work. Safety Engineering magazine ran an article in 1931 on "The Very Least an Employer Should Know about Dust and Fume Diseases'1 warning that dust including asbestos could be seriously harmful and that controlling the dust was necessary (Willson, 1931). McPheeters (1931) suggested engineering dust controls methods for the prevention of asbestosis. Many others have also given methods for preventive actions from hazardous dusts, including the classic work of the United States Public Health Service (Bloomfield and Daiiavaiie, 1935 and Dreessen et at., 1938). For asbestos disease control Lanza (1935) also described the serious hazard faced by the industry with dust and recommended studies on its control as related to disease prevention. However, not much attention was given to hygiene, in the early history Of exposure to asbestos (Sellikoff and Greenberg, 1991).
The National Cancer Institute's pioneer cancer researcher Wilhem C. Hueper, as early as 1942, in his historic book Occupational Tumors and Allied Diseases recommended controlling asbestos by methods of wetting, closed production, ventilation or other engineering controls, as well as personnel protective devices (Hueper, 1942). Fleischer, et al, in 1946, expanded this advise
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1931 1938
1946 1951 1960
Regulation jointly prepared by the British government and the industry being regulated (, 1931).
The United States Public Health Service introduced a guidance limit of 5 mppcf, as a guide for the control of asbestos dust even though they found 3 cases of asbestosis below this recommended guidance (Dreessen et at., 1938). [Fulton et al. (1935) reported 2 of 20 workers exposed to an average asbestos dust concentration of 4.64 mppcf for greater than five years to have both clinical and radiographic evidence of asbestosis.]12
This recommended guidance concentration for exposure to asbestos of 5 mppcf, was later adopted by the newly organized American Conference of Governmental Industrial Hygienists (ACGIH) in the U.S. (Acgih, 1946).13
Asbestos standard for contractors performing Federal Supply Contracts under the Walsh-Healey Public Contracts Ac* of 5 mppcf (Dol, i 951).
Department of Labor (DOL) standard for employers under the Longshoremen's Act of 5 mppcf (dol, i960).
and gave even more extensive guidance for dust control to end product users of asbestos containing materials, when in their study of the construction of naval vessels, recommended wetting the material, exhausting the dust where possible, employing respirator usage by the workers, isolating dusty operations in order to protect other workers not directly working with asbestos, and providing room ventilation. Flesher et al. concluded that "There are no established figures for permissible or safe dustiness in pipe covering operations." They also describe that "During the handling, unwrapping and unrolling of the asbestos [material], considerable dust arises, but appears to settle readily. A very fine water spray should be used for wetting down the material as a high velocity spray stirs up dust." Pertaining to the use of saws, used to cut the end product, Flesher et al. recommend that"... the band saw should be enclosed in a room by itself and should be equipped with adequate local exhaust ventilation both above and below the saw table." Further, Flesher et al. point out that end product users such as ". . . asbestos pipe covering differs markedly from the asbestos textile industry where dust concentrations for an operation do not fluctuate widely and where a worker will usually remain at a specific job for some years." Finally, the Fleisher et al. recommendations were some of the most extensive ever made and were published in a prominent professional journal of that time.
12l2Since 1938 several studies have shown asbestosis occurring in workers at concentrations below 5 mppcf (Fleischer et al., 1946; Leathart & Sanderson, 1963; Marr, 1964; Selikoff et al., 1965).
13 Commenting on the effectiveness of such a guidance concentrations S.A. Roach of the University of London stated that . .5 million particles per cu. Ft., are simply standards, although I hope I did not use the word 'safe.' These are standards which are actually used, although they are not ever expressed as being safe standards." Roach further went on to state that even if this was dropped to 2 million particles per cu. ft. that this would not necessarily be a "perfectly safe level of dust" (Roach, 1965). It is interesting to note that a worker would not be able to see this concentration of dust in the ambient air and would not see any dust until a concentration of between 20 to 40 mppcf was reached (Hemeon, 1955). Warren Cook in 1942 said "This [5 mppcf] is a very small concentration, so small in fact that the condition may look good even to a critical eye and still present an exposure greater than this low limit (Cook, 1942). The 5 mppcf guidance concentration remained in effect until the 1960s (dol, i960).
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1968 1969 1971 1971 1971
1971 1971
ACGIH proposed a new guidance limit of 12 fibers/milliliter or 2mppcf (ACGIH, 1968).14
DOL adopted a new standard for asbestos of 12 fibers/ml or 2 mppcf under the standard for employers under the Walsh-Healey Act (dol, 1969).
The ACGIH recommended, in April, a new guidance limit of 5 fibers/ml
(ACGIH, 1971).
On April 28th the Occupational Safety and Health Act of 1970 became effective
(OSHAct, 1970).
On May 29 Occupational Safety and Health Administration (OSHA) adopted the ACGIH recommendation of 12 fibers/milliliter or 2 mppcf as a legal standard under the provisions of the new OSHAct using consensus recommendations as initial start-up standards, after which they would develop their own official standards using the OSHAct promulgation procedures (osha, 1971).
On November 17th, NIOSH Director sent a letter to OSHA recommended a reduction of the current OSHA asbestos standard of 12 fibers/cc to 5 fibers/cc
(NIOSH, 1971).
On December 7, OSHA set an emergency legal standard of 5 fibers/ml
(OSHA, 1971).
1972
1972 1972
1972
1975 1976
On January 12, OSHA issued an emergency standard covering the ship repairing, shipbuilding, shipbreaking and longshoring industries. This held the same requirements as the December 7, 1971 emergency legal standard (osha,
1972).
On January 12th, OSHA proposed to modify their existing 12 fiber/cc or 2 mppcf standard to 5 fibers/cc (osha, 1972).
On February 25th, NIOSH sent OSHA it's first criteria document on asbestos recommending that OSHA promulgate a standard for asbestos of 2 fibers/cc based on a count of fibers greater than 5 micron in length and an aspect ratio (length to width) of 3:1 (NiosH, 1972).
On June 7th, OSHA promulgated a new standard for asbestos of 5 fibers/cc, intended to prevent asbestosis and that would provide some degree of protection against asbestos induced cancers. This standard would be lowered to 2 fibers/cc in July 1976 (osha, 1972).
On October 9th, OSHA proposed to revise it's asbestos standard to 0.5 fibers/cc and to designate asbestos as a carcinogen (osha, 1975).
In December, NIOSH sent to OSHA a revised recommended asbestos standard recommended OSHA promulgate a new standard for asbestos of 0.1 fibers/cc based on it's carcinogenicity and the available technology of the phase contrast microscope to only measure fibers accurately down to this concentration. NIOSH stated that this recommendation was intended to 1) protect against the non-carcinogenic effects of asbestos, and to 2) materially reduce the risk of asbestos-induced cancer and that only a ban on asbestos could assure
14 The British, thereafter, adopted a new counting method for fibers and instead of a concentration based on total dust particles actual fibers were counted if they met the criteria of greater than 5 um in length and had an aspect ratio of 3:1 or greater (Lane, 1968).
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protection against the carcinogenic effects of asbestos (NiosH, 1976).
1980
1983 1984 1986 1992 1994
On April 17lht the NIOSH/OSHA Working Group on Asbestos recommended that there is no safe level of exposure to asbestos and discussed the inadequacy or the current OSHA standard of 2 fibers/cc recommending a reduction to 0.1 fiberS/CC (NIOSH/OSHA, 1980).
On November 4th, OSHA publishes Emergency Temporary Standard (ETS) for Asbestos of 0.05 fibers/cc (OSHA, 1983).
On March 7th, the OSHA ETS for asbestos was invalidated by the U.S. Circuit Court of Appeals for the Fifth Circuit.
On June 17th, OSHA issued two revised standards, one for general industry and a second for the construction industry, at 0.2 fibers/cc <osha, 1986).
On June 8th, OSHA deletes non-asbestiform, tremolite, anthophyllite, and actinolite (osha, 1992).
On October 11th, OSHA promulgates a new rule for asbestos setting the Permissible Exposure Level at 0.1 fibers/cc with an excursion limit of 1.0 fiber/cc over a sampling period of 30 minutes (osha, 1994).15 16 *
Human Evidence of Disease18 by Fiber Type
15 RISK FROM EXPOSURE The higher the exposures the higher the risks and the lower the exposures the lower the risks. The exposure-response relationship for lung cancer is linear (Peto, 1989). At the current OSHA standard the risk of death is 3.4 per 1,000 at 0.1 fibers/cc (osha, 1986). Even at this new limit it can be clearly seen that the risk for dying from cancer is not zero nor does it even approach it. The WHO (1989) stated that "[TJhe human evidence has not demonstrated that there is a threshold exposure level for lung cancer or mesothelioma, below which exposure to asbestos dust would not be free of hazard to health". This continues to support what the industry said in 1965 that the only safe level to prevent disease is zero and it also supports the finding that nonmalignant respiratory diseases need not be present before cancer of the lung or mesothelioma can develop.
There is marked enhancement of the risk of lung cancer in workers exposed to asbestos who also smoke cigarettes (Selikoff et al,, 1968; Berry et al., 1972; Hammond and Selikoff, 1973; Hammond et al., 1979; and Seiikoff et ai., 1968). Data from Hammond et al. (i979) and Weiss <i971) suggest cigarette smoking may also contribute to the risk of asbestosis. Smoking, however, has not been found to be associated with an increased risk of pleural or peritoneal mesothelioma, or cancers of the stomach, colon and rectum, which occur with equal frequency among smoking and non-smoking asbestos workers. OSHA attributes asbestos exposure with 79.4 percent of the lung cancer deaths among asbestos-exposed workers who smoke and 77.2 percent of lung cancer deaths among non-smokers (osha, 1986).
16Other diseases reported in asbestos exposed workers include laryngeal cancer (Bianchi et ai., 1978;
Hinds et al., 1979; Stell and McGill, 1973; Morgan and Shettigara, 1976; Newhouse and Berry, 1973; and Shettigara and
Morgan, 1975; and Doll and Peto, 1985); oropharyngeal cancer (Selikoff et ai., 1970); multiple primary cancer (Dohner etal., 1975); Suicides (Wagoner et al., 1973 and Robinson et al., 1979); Ovarian cancer (Parkes, 1973; Acheson and Gardner, 1983; and Doll and Peto, 1985); renal cancer (Selikoff et al., 1979 and MacLure, 1987); penile
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1960 1962 1971 1973 1976 1988
Wagner et al. McNulty Harrington et al. Webster Jones et al. Armstrong et al.
Crocidolite Chrysotile 17
cancer (Raffn and Korsgaard, 1987); bladder cancer (Bravo et al., 1988); breast cancer (Doniach et al., 1975) and leukemia, multiple myeloma and Waldenstrom's Macroglobulinemia (Parkes, 1973; Kagan etai.,
1977; Gerber, 1970; and Kishimoto et al., 1988).
''Conclusions concerning the carcinogenicity of Chrysotile Asbestos The results from animal bioassays present a strong case that there is no safe form of asbestus. Wagner et al. (1979), then with the U.K.s Medical Research Council (MRC), have shown that a commercial grade, predominantly short fiber Canadian chrysotile, which is used primarily for paint and plastic tile fillers, can induce mesotheliomas when injected intrapleurally into rats, and induce primary lung neoplasm when the animals are exposed by inhalation. Not only does it appear that chrysotile is as potent as crocidolite and the other amphiboles in inducing mesotheliomas after intrapleural injections (Wagneretai., 1973), but also equally potent in inducing pulmonary neoplasm after inhalation exposures (Wagneretai., 1974). In terms of degree of response related to the quality of dust deposited and retained in the lungs of rats, chrysotile appears to be much more fibrogenic and carcinogenic than the amphiboles (Wagner et al., 1974). Epidemiologic evidence combined with the animal data supports the role that all fiber types, including chrysotile, are responsible in the etiology of lung cancer and mesothelioma as well as other cancers.
The 1984 Report of the Royal Commission on Matters of Health and Safety Arising from the Use of Asbestos in Ontario concludes that "All fibre types can cause all asbestos-related diseases,. . ." (Dupre1 et al., 1984). This supports the finding of reported cases of mesothelioma among brake mechanics exposed to chrysotile (Langer et ai,, 1982; and Haucharek, 1987). Mancuso (1988; 1990) further contends, based upon his analysis of railroad machinists, that commercial chrysotile asbestos has caused mesotheliomas and that the risk is greater than previously asserted. There is further concern that chrysotile is rarely found in its pure form and that most chrysotile deposits are contaminated with the amphibole tremolite, which is agreed by experts to be a toxic form of asbestos (Sebastien et ai., 1989). In the most recent review of the evidence, Stayner, Dankovic, and Lemen, of the National Institute for Occupational Safety and Health conclude that "Given the evidence of a significant lung cancer risk, the lack of conclusive evidence for the amphibole hypothesis, and the fact that workers are generally exposed to a mixture of fibers, we conclude that it is prudent to treat chrysotile with virtually the same level of concern as the amphibole forms Of asbestos" (Stayner, Dankovic, and Lemen, 1996).
Chrysotile fibers are much more chemically and biologically reactive than amphibole fibers and because of this reactivity with the tissues, they lose their structural elements and divide into smaller fibrils, making their recognition difficult by the usual analytical methods. In fact, many of the fibers are removed from the lung and exhaled back through the bronchi or removed by the
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1957
Cartier, P.18
1960
Wagner etal. 19
1973a,b
McDonald
1974
McDonald et al.
1972
Kogan et al.
1973
Borow et al.
1973
Wagoner et al.
1973
Enterline and Henderson
1983
Dement et al.
1979
Robinson et al.
1977
Liddell et al.
1977
McDonald et al.
1977
Selikoff
1979 1979
Nicholson et al. Rubino et al.
1980
Boutin et al.
1983
McDonald et al.
lymphatic system to other organs Of the body (Marten et al., 1989; Davis, 1979; Davis et at., 1986a; and Davis et ai., 1986b). The concentration of dust in the lungs of rats exposed to Canadian chrysotile was only 1.8% - 2.2% of the dust concentration in the lungs of animals exposed to amphiboles (after 24 months of inhalation exposures). Yet the lung tumor incidence and degrees of pulmonary fibrosis were similar in all groups. These findings support the idea that chrysotile fibers cause more cellular injury, fibrosis and lung cancer, than the amphiboles, while at the same time are less readily detected in the tissue after the damage is done. Churg et al. (1989a) concludes that the failure of chrysotile to accumulate in the lung is a result of preferential chrysotile clearance during the first few days to weeks after exposure and that dissolution plays no role in the clearance and that the preferential clearance may be a result of fragmentation and rapid removal of the chrysotile fibers. Suzuki et al. (1998) in 92 consecutive cases of mesothelioma observed that the major asbestos type identified in the mesothelial tissues was chrysotile when compared to the chrysotile fiber burden in the lungs of the same cases (79.0% vs. 28.3% respectively). Malorni et al. (1990) suggests that fiber penetration can rearrange the cytoskeletal apparatus of the cell and that this could indicate an interaction between the chrysotile fibers and the normal mitotic process, since giant multinucleated cells are formed. Churg et al. (1989b) further believes that the short fibers may be more fibrogenic than previous animal data suggest and deserves further study.
18 2 cases Of diffuse mesothelioma (Arch Industr Hyg, vol. 5, p. 262). 19 discusses chrysotile as cause of mesothelioma (Brit j industr Med, i960, voi. 17, p. 268).
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1987 1990 1996
1960 1965 1976 1977 1983 1986 1989 1989
1986 1988
1974 1979 1989
Huncharek Piolatto et al. Stayneretal.
Wagner et al. Scheapers20 Selikoff Seidmanetal. Johnson et al. Seidmanetal. Finkelstein Ribak et al.
McDonald et al. Amandusetal.
Meurman Meurman Timo
etal. etal.
Amosite
Tremolite Anthophyllite
SUMMARY OF THE KNOWLEDGE CONCERNING THE HEALTH EFFECTS ASSOCIATED WITH EXPOSURE TO ASBESTOS
Early reports of lung disease and exposure to asbestos (asbestosis) first appeared at the turn of the 20th Century and continued to the present time. By the mid through late 1920s it became well established that the fibrotic disease of the lungs, by then named asbestosis, was causally associated with exposure to asbestos. Evidence that lung cancer was also causally associated with asbestos exposure began appearing in the mid-1930s and became well recognized as such, by the scientific community, by 1955, however, several well recognized medical organizations accepted this fact prior to then. Mesothelioma or cancer of the linings of the chest and abdomen, were first reported in asbestos exposed persons as early as1943 and it became well established, in the scientific community, as a marker tumor in persons exposed to asbestos by 1960. End-product users of asbestos containing products were shown to be at risk of developing
20 Ann N Y Acad Sci, 1965, vol. 132, p.246
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non-malignant lung diseases in the 1930s and cancer in the 1940s. It was shown in the 1960s that non-occupational exposures and those workers wearing contaminated work clothing home also carried a risk of asbestos associated diseases to family members.
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