8
British Journal of Industrial Medicine, 1976, 33, 115-122 Thirty-two cases of mesothelioma in Victoria, Australia: a retrospective survey related to occupational asbestos exposure JAMES E. H. MILNE Industrial Hygiene Division, State Health Department, 5 Parliament Place, Melbourne 3002 Victoria, Australia Milne, J. E. H. (1976). British Journal ofIndustrial Medicine, 33, 115-122. Thirty-two cases of mesothelioma in Victoria, Australia: a retrospective survey related to occupational asbestos exposure. Mesotheliomas have been reported in four states in Australia. Crocidolite has been mined and milled at Wittenoom in West Australia where five cases of mesothelioma were re- ported after exposure of high intensity. The 32 cases of mesothelioma reported in this paper occurred during a period of 11 years in Victoria; 29 were pleural and three peritoneal. There were 22 autopsies. End occupations were misleading in 66 % of cases. Two of the three sub- jects with peritoneal mesothelioma were siblings, and there was no evidence of occupational or other exposure to asbestos in either. There was a significant prevalence of pulmonary asbestos bodies in the tumour series as compared with an unselected consecutive series of 200 routine autopsies (0 01 > p > 0 001). The occupational history was as effective a method of assessing 'true' asbestos exposure as the pulmonary asbestos body count. Five cases had had a duration of exposure of one year or less, but they had had heavy exposure. The latent interval before tumour development was 25 years or longer in each case. There was no known exposure to asbestos in five cases (16 %). The rare association of mesothelioma with types of asbestos other than crocidolite may not exist and could be explicable on the basis of the proportion (16%) of these tumours arising randomly in the population. Australia is a political federation comprising seven and peritoneum and an earlier exposure to asbestos. states, Victoria being the most densely populated Crocidolite has been noted to be peculiarly potent in (3 3 million) and most highly industrialized. Around this respect compared with other types of asbestos the capital, Melbourne, which is a port with a popu- such as chrysotile, amosite, or anthophyllite (Gilson, lation of 2 million, there has been rapid industrial 1973). development. Asbestos use and processing has Of those occupationally exposed to asbestos only markedly increased. Asbestos is not mined in a small percentage develop mesothelioma; but not Victoria. The crocidolite mine in West Australia is all mesotheliomata are related to asbestos exposure now closed, and open cut mining of chrysotile has (Webster, 1972). only recently begun in New South Wales. Mesotheliomata were regarded until recently as Mesothelioma in other Australian states rare tumours. There appears to be a clear relationship between West Australia the development of serosal tumours of both pleura At Wittenoom in the far north-west, crocidolite was 115 on October 10, 2020 by guest. Protected by copyright. http://oem.bmj.com/ Br J Ind Med: first published as 10.1136/oem.33.2.115 on 1 May 1976. Downloaded from

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Page 1: Thirty-two cases in Victoria, Australia: to exposure · British JournalofIndustrial Medicine, 1976, 33, 115-122 Thirty-two casesof mesothelioma in Victoria, Australia: a retrospective

British Journal of Industrial Medicine, 1976, 33, 115-122

Thirty-two cases of mesothelioma inVictoria, Australia: a retrospective surveyrelated to occupational asbestos exposure

JAMES E. H. MILNEIndustrial Hygiene Division, State Health Department, 5 Parliament Place, Melbourne 3002Victoria, Australia

Milne, J. E. H. (1976). British Journal ofIndustrial Medicine, 33, 115-122. Thirty-two cases ofmesothelioma in Victoria, Australia: a retrospective survey related to occupational asbestosexposure. Mesotheliomas have been reported in four states in Australia. Crocidolite has beenmined and milled at Wittenoom in West Australia where five cases of mesothelioma were re-ported after exposure of high intensity. The 32 cases of mesothelioma reported in this paperoccurred during a period of 11 years in Victoria; 29 were pleural and three peritoneal. Therewere 22 autopsies. End occupations were misleading in 66% of cases. Two of the three sub-jects with peritoneal mesothelioma were siblings, and there was no evidence of occupationalor other exposure to asbestos in either. There was a significant prevalence of pulmonaryasbestos bodies in the tumour series as compared with an unselected consecutive series of200 routine autopsies (0 01 > p > 0 001). The occupational history was as effective a methodof assessing 'true' asbestos exposure as the pulmonary asbestos body count. Five cases hadhad a duration of exposure of one year or less, but they had had heavy exposure. The latentinterval before tumour development was 25 years or longer in each case. There was noknown exposure to asbestos in five cases (16%). The rare association of mesothelioma withtypes of asbestos other than crocidolite may not exist and could be explicable on the basis ofthe proportion (16%) of these tumours arising randomly in the population.

Australia is a political federation comprising seven and peritoneum and an earlier exposure to asbestos.states, Victoria being the most densely populated Crocidolite has been noted to be peculiarly potent in(3 3 million) and most highly industrialized. Around this respect compared with other types of asbestosthe capital, Melbourne, which is a port with a popu- such as chrysotile, amosite, or anthophyllite (Gilson,lation of 2 million, there has been rapid industrial 1973).development. Asbestos use and processing has Of those occupationally exposed to asbestos onlymarkedly increased. Asbestos is not mined in a small percentage develop mesothelioma; but notVictoria. The crocidolite mine in West Australia is all mesotheliomata are related to asbestos exposurenow closed, and open cut mining of chrysotile has (Webster, 1972).only recently begun in New South Wales.

Mesotheliomata were regarded until recently as Mesothelioma in other Australian statesrare tumours.

There appears to be a clear relationship between West Australiathe development of serosal tumours of both pleura At Wittenoom in the far north-west, crocidolite was

115

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116 James E. H. Milne

mined underground until recently. Evidence frompersonal observation, from workmen's accounts,and from published investigations (McNulty, 1962;Major, 1968) indicates that exposure to asbestoswas high both in the mine and the nearby millingplant, but not of long duration due to itinerantlabour. Five cases of pleural mesothelioma have beenreported, and McNulty (1972) noted that one caseoccurred after an elapsed time of only 13 yearsafter eight months' exposure in the mill.

New South WalesBarnes (1972) gave details of 13 cases of pulmonarymalignancy and asbestosis, accepted by the DustDiseases Medical Authority; pleural mesotheliomaoccurred in three.

QueenslandMortimer and Campbell (1968) described two casesof pleural mesothelioma related to industrialasbestos exposure.

Mesothelioma in Victoria

Riddell (1966) reported three cases of pleural meso-thelioma presenting at the Austin Hospital between1962 and 1965. In 1967 an ongoing survey in-corporating all cases diagnosed since 1962 was set up.In each case the diagnosis was confirmed independ-ently by other pathologists and the occupationalhistories were to be personally assessed by theauthor. By the end of 1973, 29 cases of pleuralmesothelioma had been investigated. Fifteen of thesehave been previously reported (Milne, 1969). Therewere three cases of peritoneal mesothelioma makinga total of 32.

Source of case and findingsA total of 23 cases presented at the Thoracic Unitof the Austin Hospital, Melbourne. The remainingnine cases were found at seven other institutions inVictoria. At the time of writing only one patient isalive. Autopsy has been carried out in 22. Thediagnosis in the remaining 10 was made by pleuralbiopsy. Of the 10 biopsies, seven were made atthoracotomy and tissue macroscopically consistentwith mesothelioma was seen.The original diagnosis was not made in all cases by

the same pathologist but all tissue sections have beenseen by at least two pathologists who agreed thatthe diagnosis was mesothelioma. Sections from fourcases have been sent to individual members of theUICC panel in England for opinion and in each casethe diagnosis was confirmed.

Assessment and grading of asbestos exposure

Asbestos bodiesHistological sections of macroscopically normal lung

parenchyma taken as a routine autopsy procedure weresearched for asbestos bodies. Solitary fragments andgranules were disregarded, and unless an unmistakablybeaded body was seen it was not considered as a positivefinding. 'Mature' bodies as described previously elsewhere(Milne, 1971), however, were included. Provided aclubbed head and a group of beads were seen the objectwas regarded as an asbestos body.Some attempt at quantification was made, by categoriz-

ing subjects as follows:Asbestos bodies in any one sectionNone1-34-1011-20More than 20

Not seen±

The writer assessed and counted the asbestos bodies.There were 21 cases where routine lung sections had beentaken at autopsy. Of these, 11 showed asbestos bodies bylight microscopy and four revealed asbestos bodies afterdigestion (Xipell and Bhathal, 1969). Thus asbestosbodies were seen in 15 out of 21 cases in which tissuewas available for examination.

Occupational historyEvidence was obtained from the patient if possible, other-wise from relatives, friends, acquaintances, and medicalrecords. According to the occupational history a categorywas ascribed as follows:

'Nil' No history of exposure. No likelihood of ex-posure.'Possible' Patient had worked in an industry whereasbestos could have been contacted.'Probable' Patient had worked in an industry whereasbestos was clearly known to have been used but wherethe patient's exact mode and duration of contact wasunknown.'Certain' Patient had worked in an industry whereasbestos usage was established and where there wasclear evidence that the patient had been in contact withthe asbestos in the course of his work.Thus (see Table 1) 14 subjects had 'certain' exposure to

asbestos. No history of any sort of exposure could beelicited in five subjects; of these the writer was able tointerview two and close relatives of the other three. Noleading questions were asked at the outset but eventuallythese were introduced. Exposure to asbestos was cate-gorically denied in all cases. The relatives claimed to havefull awareness of the patient's working conditions. Thetwo patients interviewed were rational and intelligent andgave sensible answers to questions. One had become anadministrator but had worked as a carpenter with no ex-posure whatsoever to asbestos. The other gave heroccupation as housewife; her only industrial experiencehad been in handling photographic chemicals and shefirmly denied having been exposed to asbestos.

Some illustrative case histories

One common factor among those with certainhistory of asbestos exposure was the long delay or'elapsed time' before development of mesotheliomaafter their exposure to asbestos had begun. Often the

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A retrospective survey related to occupational asbestos exposure 117

TABLE 1MESOTHELIOMA AND OCCUPATIONAL ASBESTOS EXPOSURE

Case Sex Asbestos Exposure Brief description of employment Endbodies occupation

Past Duration Estimatedintensity

1940-65

1942-45

1942-47

1942-451935-501939-68

1942-68

1930-45

1930-42

1943-44

1920-501942

Mild

Heavy

Heavy

HeavyHeavyHeavy

Heavy

Heavy

Heavy

Heavy

HeavyHeavy

Certain 1942-43 Heavy

1941-45

1910-?1941-66

1925-30Nil

1930Nil

Unknown

UnknownModerate

MildNil

Very mildNil

Uncertain Very mild

Nil Nil1938-39 Heavy1937-51 Heavy

1936 Heavy

Uncertain UncertainUncertain Heavy

Nil Nil

1920-? Uncertain

1920-45 Moderate

Nil Nil

1928-68 Heavy

Loaded packs of asbestos-bound weld- Trucking rods driverBound welding rods with crocidolite Invalid

pensionerBound welding rods with crocidolite Ledger

operatorBound welding rods with crocidolite HousewifeBound welding rods with crocidolite ForemanExposed to dust from lagging, strip- Dockyardping asbestos workerExposed to dust from lagging, strip- Dockyardping asbestos workerExposed to dust from lagging, strip- Dockyardping asbestos workerExposed to dust from lagging, strip- Labourerping asbestosExposed to dust from lagging, strip- Dockyardping asbestos workerLagged steam pipes with asbestos BarmanCarded asbestos in confined space X-ray

crystallo-grapher

Sprayed insulation containing asbestos Sewingmachinemechanic

Munitions factory Tram con-ductress

Munitions factory PensionerWelder in railway shop, near asbestos WeldermattressesWelder-loose asbestos lying about StoremanTextile worker. Dressmaker Dressmaker

Father worked in asbestos/cement HousewifeCarpenter, denied asbestos exposure Manager

Aircraft engineer Aircraftengineer

Domestic servant HousewifeInsulator, spraying asbestos CarpenterWelded railway trucks with asbestos- Pensionerbound electrodesSwept asbestos and lagged as dock- Pensioneryard workerFitter and turner PensionerWorked in dockyards in Holland Carpenter

Itinerant worker, then PMG for 30 Telephoneyears technicianMade asbestos gaskets as youth Chicken

farmerBoiler room attendant, stripping insu- PensionerlationPacked photographic chemicals HousewifeDenied asbestos exposureInsulated, using asbestos in dockyards Process

worker

M

F

F

FM

M

M

M

M

M

M

M

2

3

456

7

8

9

10

1112

Probable

Certain

Certain

CertainCertainProbable

Certain

Certain

Certain

Probable

CertainCertain

13 M

++++

No autopsy

No autopsy

No autopsy

+++

No autopsy

No autopsy

++

No autopsy++

Not seen+ Lung

digestionNo autopsy+ Lung

digestionNot seen

Not seenNo autopsyNo autopsy

No autopsy

Not seen+ Lung

digestionNot seen

Not seen

+ Lungdigestion

Alive

14

1516

1718

1920

21

222324

25

2627

28

29

30

31

32

F

MM

MF

FM

M

FMM

M

MM

M

M

M

F

M

Possible

PossibleProbable

PossibleNil

PossibleNil

Possible

NilCertainCertain

Certain

PossibleProbable

Nil

Possible

Certain

Nil

Certain

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118 James E. H. Milne

On the some scaleLondo*- iVienna

FIG. 1. Australia showing the seven state

intensity of exposure was high althougwas relatively short. Case 13 illustrate

Case history no. 13The patient was a sewing machine mecyears who also ran a small shopelectrical goods. He had left school atyears and had joined a firm engageinsulating. For a year he had workedand his job had been to spray asbestopreviously coated with a black aasbestos was supplied in large papergrey in colour. These bags were emptiman into a hopper feeding a garnewhich shredded the asbestos to an ev(

before feeding it to the spray gun. Thecartridge respirator with a felt filtecalled the profusion of the asbestos disuch that invariably each day someescaped filtration and got into his i

sprayed. The patient suffered no furthedust exposure, having been a sevmechanic ever since.Such an occupational history pros

dence of asbestos exposure. In otlevidence was not at first clear butenabled elucidation of a better picture,and 16.

Case history no. 10When this man died, autopsy revealpleural tumour. There was some medicthat his exposure was said to have occhad worked in the Railways Depart

years previously. The departmental records relatingto time of exposure were good, because asbestos hadbeen used in their workshops some 20 years beforethe man's death, and at that time the question offuture development of pneumoconiosis had beenraised. Further investigation of the patient's history,through interview of the widow, revealed that in

ueensland 1943 (about 18 years before his death) he hadstarted work in a naval dockyard where otherinformation indicated that asbestos exposure washigh. Thus the history of asbestos exposure was

New classed as 'probable' and related to his dockyardSouthWales exposure, not to his more recent work in the Rail-

ways Department.rora

Case history no. 16This man died in 1969, aged 66 years, having emi-

)Tasmania grated from England in 1966. The cause of death, atautopsy, was pleural mesothelioma. His occupa-tion had been 'welder', and an occupational history

DS. was obtained from his wife and daughter. Detailswere sent to England for investigation by theMedical Inspector of Factories for the area in whichhe had worked.

,h the duration It appeared he had been a rivetter and welder ins these points. railway workshops where lagging was carried out

and asbestos mattresses and pre-formed sectionswere in use. It was said that he had had no direct

chanic aged 44 contact with asbestos nor had he handled this in thestocked with course of his work. His history of asbestos exposurethe age of 14 was classified as 'probable' and further search of thed in acoustic histological sections of lung parenchyma (where nowith this firm asbestos bodies were seen by the pathologist) re-

os on to a wall vealed at least six individual asbestos bodies in onetdhesive. The section alone, tending to confirm the occupationalbags and was classification.ied by anothertting machine Peritoneal mesotheliomataen consistencypatient wore a There were three cases. One subject had worked onr and he re- the docks and shipyards in Glasgow as a shipwright,ast, which was and as an engine room insulator handling asbestose of the dust for about 40 years. The other two subjects, Cases 21nostrils as he and 22, presented special features:r occupational Case 21 A man aged 38 years when he died, whoseving machine occupation had been 'aircraft engineer'. Careful

search of the lung tissue sections taken routinelyvided firm evi- at autopsy failed to reveal evidence of asbestosher cases the bodies. The diagnosis of peritoneal mesotheliomainvestigation was made independently by three pathologists onas in Cases 10 the microscopic features. The macroscopic appear-

ance of the tumour was one of intense widespreaddiffuse thickening of the peritoneum, which was re-garded as characteristic. Interview of his wife (and

led a primary later of an elder brother) revealed that he had beenSal puzzlement apprenticed as a turner and fitter. After apprentice-urred when he ship he worked on aircraft engines. The highest:ment only 10 rating which could be ascribed to his exposure to

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A retrospective survey related to occupational asbestos exposure 119

asbestos was 'possible', and even this appeareddoubtful.Case 22 A woman aged 57 years when she died.The diagnosis of peritoneal mesothelioma had beenmade originally by the two pathologists who hadseen most of the cases of pleural mesothelioma at theAustin Hospital. The woman had married again afterthe death of her first husband, and the change ofname had concealed the fact that she was the eldersister of Case 21 who had died from a similartumour. Her close relatives would not budge fromthe position that she had no occupation other thanrural housework. There was no evidence of asbestosexposure. A brother gave the evidence on which thefamily tree (Fig. 2) is based. In this family of 10there had been five deaths from malignancy. Two ofthese were caused by peritoneal mesothelioma, twoby 'cancer of the stomach', and one by 'cancer in thelung'.

Died aged 78yearsO- Died aged 59yeors(Lung concer) (Cancer of stomach & brain)

Case 22 Died Case 21Died aged 57years (Cancer Died aged 38yeors

(Peritoneal of (Peritonealmesothelioma) stomach) mesothelioma)

FIG. 2 Family tree of Cases 21 and 22 (details wereprovided by living siblings).

The brother was adamant that there had been nofamily exposure to asbestos. The father had beenemployed as a labourer, and later as an inspectorwith the Board of Works, engaged in maintenanceof sewers. Any piping with which he had come intocontact was of pottery construction. He had been aheavy smoker for many years.The coincidence of two members of one family

developing peritoneal mesothelioma without evi-dence of asbestos exposure is remarkable.

End occupations'End occupation' is taken in this context to mean theoccupation followed by the patient at the time oftumour diagnosis. In this series the 'end occupation'could have been misleading in at least 21 cases (66 %),(see Table 1). A typical example was Case 9, a'labourer', formerly 'lemonade maker'. In fact thisman had worked for 12 years before the second worldwar at the naval dockyard in Malta, exposed tohigh concentrations of asbestos dust. Case 11 hadbeen a 'barman' for 15 years before his death but hehad been a lagger for 30 years.

It is of some interest that Case 1 called himself'truck-driver'; Case 2 'invalid pensioner'; Case 3'ledger operator'; Case 4 'housewife'; Case 5 'fore-

man'. These people were all shown to have workedat the same firm in the same room on the same pro-cess using South African crocidolite during a similarperiod of time. The firm's name had changed, thepatients had lost contact with each other, and theydid not know of the others' illness until they wereadmitted to hospital many years later.Case 23 was a 'carpenter' but had been an asbestos

sprayer in 1938 and 1939. Case 30 whose end occupa-tion was 'retired pensioner' and who was said to haveworked as an 'engine driver', had worked as a boilerroom engineer and lagger for several years about 30years previously.

Discussion

Relationship to asbestos exposureAsbestos bodies The only estimate of the populationprevalence of pulmonary asbestos bodies in Victoriais that of Xipell and Bhathal (1969). In an un-selected consecutive series of 200 autopsies, using adigestion technique, they found asbestos bodies in 87cases (Table 2). The same digestion technique was

TABLE 2ASBESTOS BODIES IN Two SERIES OF

AUTOPSIES

Autopsy Asbestos bodies Total

Seen Not seen

Routine .. .. 87 113 200Mesothelioma .. 15 6 21

Total .. .. 102 119 221

x2 = 7-14 One degree of freedom P < 0-01.

used to reveal asbestos bodies in four cases in ourseries in which asbestos bodies were not easily seenby light microscopy. Asbestos bodies were found in15 out of 21 autopsied cases in the present series. Thedifference is significant at the 1 % level (see Table 2).The two familial cases of peritoneal mesothelioma

did not produce any evidence of asbestos bodies.Of the 10 cases on whom autopsy was not per-

formed, seven were considered to have certainly beenexposed to asbestos, one probably exposed, and twopossibly exposed.

There was no evidence of occupational asbestosexposure in one case in which the subject's father hadworked for a short time in an asbestos/cementfactory many years previously. On the basis of the'neighbourhood cases' noted by Newhouse andThompson (1965), she was allotted a category of'possible'.

Occupational history Considering the total group

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120 James E. H. Milne

of 32 patients, there were 27 patients about whomsome possible history of exposure to asbestos couldbe elicited. Thus there were two parameters, namely:

exposure historythe finding of asbestos bodies

as pointers to the 'true incidence' of asbestos expo-sure.Comparing the two, the value of x2 was 0-62

which indicated no significant difference betweenthem as indicators of 'true' asbestos exposure 0*5 >p > 03.

Type of asbestos exposureIt has not been possible to analyse the series accord-ing to the type of asbestos exposure. Crocidolite issaid to have an enhanced carcinogenic effect ascompared with other forms of asbestos, but therewas no way of testing this hypothesis quantitativelyin our series since most patients suffered a mixedexposure. A small subgroup who shared a commonsource of exposure, however, were exposed solely toimported crocidolite ('Cape blue' asbestos). Thesewere Cases 1 to 5 and they were all employed in themanufacture of welding electrodes of the earliesttype, in which asbestos string was wound around thecoated iron electrodes giving rise to clouds of blueasbestos dust. The earliest date at which exposurebegan was 1935. Three of the five in the subgroupwere women engaged on a temporary basis duringthe war; their exposure ceased about 1945. Thustheir exposure to crocidolite was of short durationbut of high intensity. There was an elapsed time of atleast 20 years between start of exposure and develop-ment of mesothelioma in all five. McNulty's case,mentioned previously, was of similar exposurepattern (high intensity and short duration) and thedevelopment of a mesothelioma followed only 13years later. This may be related to the fact thatAustralian crocidolite consists of very fine fibres. Thesusceptibility of Australian workers to both localand imported crocidolite has been clearly demon-strated and in Victoria some neoplastic outcome ofthe West Australian conditions may be revealed inthe future as itinerant workmen move from state tostate.

Duration of exposure, elapsed time, and latent intervalThe exposures as listed show a range of durationfrom six months to nearly 30 years. One envisagesa product relationship between duration of exposureand intensity (US Public Health Service Report,1972) to give an index indicative of total number offibres inhaled and some measure of carcinogeniceffect. When a critical 'dose level' has been reached,a response may be stimulated (for example, meso-thelioma) which requires a latent interval of manyyears to manifest itself.With exposures of long duration, which cease only

on the eventual diagnosis of mesothelioma, one hasno idea when the critical level of exposure mighthave been sufficient to induce carcinogenesis. InCase 1, for example, this would be impossible toestablish because exposure was continual from 1940to 1965. Therefore 'elapsed time' as estimated insuch cases, gives no indication of the latent intervalbetween dose and response.A more accurate estimate of the latent interval can

be made with short well-delineated exposures. Inthe series there were five cases, all male, for whom theduration of exposure was a year at the most, andwhose exposure began about 25 years or earlierbefore tumour development. Probably the mostreliable witness was Case 12, an x-ray crystallo-grapher, who understood the importance of ac-curacy in giving his occupational history. He gavefirm evidence that the duration of his exposure wasonly six months in 1942. This indicates a latentinterval of 25 years, after heavy exposures toasbestos imported into Australia.The reported West Australian case suggests that

for the finer Australian crocidolite with heavy ex-posures of short duration, the latent interval beforemesothelial tumour development could be even less.That we in Victoria are now seeing the results of theindustrial conditions of about 30 years ago is shownby the fact that no case in our series began exposureafter 1943.

Occupational groupsThe occupations involved showed a similarity tothose seen in larger series investigated in othercountries. Of 27 subjects with a history of possibleexposure, occupationally, to asbestos, eight hadworked in dockyards, five had worked bindingcrocidolite string on to welding rods, and three werewelders. Other occupations involved were lagging,asbestos spraying, and asbestos carding.

Mesothelioma with no exposure to asbestosOne of the features of most series of carefully in-vestigated cases of mesothelioma is the presence ofthose whose past history, either occupational ordomestic, does not include exposure to asbestos.Webster (1972) noted that the South AfricanAsbestos Tumour Reference Panel had registered179 cases of pleural mesothelioma by the end of 1969.The environmental history was known in 148 casesand 24 (16%) of these showed no evidence ofasbestos exposure. McDonald et al. (1970) studiedall fatal malignant mesothelial tumours known topathologists in Canada 'between 1959 and mid-1968'. Using a technique of obtaining occupationalhistories 'blind', only 20% of male cases and onefemale case were demonstrated to have had occupa-tional exposure to asbestos. Greenberg and LloydDavies (1974) investigated 413 notifications of meso-

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A retrospective survey related to occupational asbestos exposure 121

thelioma in the United Kingdom and accepted 246cases as definite, of which, in 38 cases (15%) therewas no history of any exposure to asbestos aftercareful inquiry.Of the 32 cases in this Australian series five

(16%) were devoid of evidence which might indicatea link with asbestos. The numbers are much less thanin the South African and English series but the per-centages are very similar. In neither series was a'blind' technique used. In our series in spite of directquestioning, patients and close relatives remainedunmoved in their denial of exposure to asbestos.

It seems clear that some mesothelial tumours (atleast 15 Y) are unrelated to asbestos exposure.Furthermore in the present climate of opinion somesubjects could mistakenly be categorized as havinga possible exposure (or even probable exposure) toasbestos, because of its widespread use, and Case 19in our series may be one such. Given intensive inter-rogation, a large proportion of any industrial popula-tion might 'confess' to asbestos exposure. This mayexplain the discrepancy between McDonald's re-sults and those of other workers.Webster (1965) pointed out that mesotheliomata

occur in families, and although many workers havebeen exposed few have ultimately developed thetumour. These two factors indicate that there is somepredisposition to serosal tumour formation incertain individuals, sometimes exhibited as afamilial trait. The occurrence of two cases of peri-toneal mesothelioma in one family, neither of whomcould be regarded as having significant asbestos ex-posure, lends support to this view.The presence, in our series, of five cases (16 %)

lacking evidence of exposure to asbestos also lendscredence to the theory that mesotheliomata havebeen in existence in larger numbers in the communitythan we had been aware. The search for thesetumours has become intense of latter years, and con-sequently recognition has probably been facilitated.Moreover a further point comes out of this in rela-tion to the type of asbestos causing mesothelioma.There is evidence linking crocidolite exposure withthe later development of mesothelioma. Other typesof asbestos, for example, chrysotile, rarely inducemesothelioma. Perhaps this rarity does not exist infact. If at least 15% of all known mesotheliomataare unrelated to asbestos and occur 'spontaneously'for no obvious reasons, there exists the possibilitythat such tumours may also randomly but rarelyoccur in a population of workers exposed to chryso-tile, particularly a large population; so that the co-incidence of two factors in time and place may havegiven rise to an erroneous idea of cause and effect.

Conclusions

This small series provides confirmatory evidence

that in Victoria, as elsewhere in the world, there is arelationship between occupational exposure toasbestos and the subsequent development of amesothelial tumour, after an elapsed time of theorder of 20 years. Exposure times in five cases wereof less than one year's duration but these were ofhigh intensity.'End occupations' bear little relationship to past

occupational exposure. The occupational history isequally effective as an asbestos body count toindicate past exposure to asbestos. The mostcommon occupation in the series was 'dockyardemployee'.

In five of the cases (16%) there was no evidence ofexposure to asbestos, despite intensive investigation.This figure is similar to that found in other largerseries. It indicates that mesotheliomata do occurunrelated to asbestos exposure, possibly in largernumbers than previously suspected, and may serveto show that the so-called rare association of meso-thelial tumours with types of asbestos other thancrocidolite, is in fact non-existent.Two cases of peritoneal mesothelioma in siblings

who had no history of asbestos exposure probablyrepresent a remarkable coincidence of familial cancerincidence.

My gratitude is expressed to the following who haveassisted with this paper: Professor H. Attwood, Dr A. J.Christophers, Dr J. Riddell, Dr J. Ireton, Dr A. Parkin,Dr G. Price, Dr J. Clarebrough, Dr A. Campbell andmembers of the staff of the Austin Hospital ThoracicUnit, Dr R. Motteram, Dr R. Doig, Dr J. Hicks, Dr S.Pilbeam, and Dr A. Jackson. Mrs M. Griffiths has typedmany drafts; Dr B. McCloskey, Chief Health Officer, hasgiven permission to publish the paper.

References

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Gilson, J. (1973). Asbestos cancer: past and futurehazards. Proceedings of the Royal Society ofMedicine,66, 395-403.

Greenberg, M. and Lloyd Davies, T. A. (1974). Meso-thelioma register 1967-68. British Journal of IndustrialMedicine, 31, 91-104.

McDonald, A., Harper, A., El Attar, O., and McDonald,J. (1970). Epidemiology of primary malignant tumoursin Canada. Cancer, 26, 914-919.

McNulty, J. C. (1962). Malignant pleural mesotheliomain an asbestos worker. Medical Journal of Austratia,2, 953-954.

(1972). Personal communication.Major, G. (1968). Asbestos dust exposure. In Proceedings

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Milne, J. E. H. (1969). Fifteen cases of mesotheliomaassociated with occupational exposure to asbestos.Medical Journal of Australia, 2, 669-673.

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122 James E. H. Milne

(1971). Developmental changes in asbestos bodiesand their significance. Transactions of Society ofOccupational Medicine, 21, 118-121.

Mortimer, R. and Campbell, C. (1968). Asbestos expo-sure and pleural mesotheliomata. Medical Journal ofAustralia, 2, 720-722.

Newhouse, M. L. and Thompson, H. (1965). Mesothe-lioma of pleural and peritoneum following exposureto asbestos in the London area. British Journal ofIndustrial Medicine, 22, 261-269.

Riddell, J. (1966). Three cases of mesothelioma. MedicalJournal of Australia, 2, 554-558.

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standard, Sect. V, pp. 12-13, National Institute forOccupational Safety and Health. US Department ofHealth, Education, and Welfare, Washington, DC.

Webster, I. (1965). Biological effects of asbestos. Sect. IX.Mesotheliomatous tumours in South Africa. Annals ofthe New York Academy of Sciences, 32, 1-766.(1972). The pathology of asbestosis. In Medicine in

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Received for publication 16 June 1975Accepted for publication 19 January 1976

The February (1976) IssueMyocardial infarction in car assembly workers P. J. Baxter, W. G. White, C. F. B. Sanderson, G. M. Barnes,

C. S. Baxter, and R. M. Acheson

Absence attributed to sickness in oil tanker crews J. T. Carter

Significance of irregular small opacities in radiographs of coalminers in the USA H. E. Amandus, N. L. Lapp,G. Jacobson, and R. B. Reger

Follow-up of ventilatory lung function in a group of cement workers M. Saric, I. Kalacid, and A. Holetic

Induction of fibrogenesis by lung antibody-treated macrophages D. M. Lewis and R. Burrell

Biochemical changes during the initial stages of industrial lead exposure G. I. Benson, W. H. S. George,M. H. Litchfield, and D. J. Seaborn

Activity of erythrocyte &-aminolevulinic acid dehydrase and its change by heat treatment as indices of leadexposure M. Chiba

Plasma concentrations of the oxime Pralidoxime Mesylate (P2S) after repeated oral and intramuscular adminis-tration P. Holland and D. C. Parkes

Notes and miscellaneaAre glass fibres carcinogenic to man? A critical appraisal J. Milne

Book review

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