Beris Penrose

'So Now They Have Some Human Guinea Pigs': Aluminium Therapy and Occupational Silicosis

In the late-1930s corporate scientists at McIntyre Porcupine Gold Mine, Canada believed they had made a breakthrough in the prevention and treatment of the deadly and widespread occupational disease, silicosis. Their research indicated that powdered aluminium countered the effects of silica dust in the lungs. Based on this, they patented and marketed a powdered aluminium product which workers would inhale before their shifts. Aluminium therapy, as it became known, was taken up in Australia, the United States and, especially, Canada between 1944–79. However, given that the data supporting the therapy was not solid, that there were clear conflict of interest concerns, and that despite the seriousness of the disease mining companies chose to ignore advice that the only preventive against silicosis was removing silica dust from the workplace air, it is argued that the use of aluminium therapy was a reckless approach to protecting workers' health, safety and lives.

Silicosis: 'Public Enemy No. 1'

Silicosis is an incurable occupational disease caused by inhaling microscopic particles of silica dust. The dust damages the lungs, which become fibrous and lose their elasticity. Consequently, workers become increasingly short of breath even on the slightest exertion.¹ According to William Sands, a Queensland metal miner affected by silicosis: 'It caught me that way that I could hardly breathe or walk. I could hardly get home' from work.² Apostmortem examination of a Canadian worker employed in the crushing room of a quartz quarry for only six months a year for four years illustrates the destructive nature of this disease. His lungs

bulged out of the chest when the thorax was opened; the pleura was very much thickened and was strongly bound to the parietal pleura with adhesions. The lung sank in water. It cut with much resistance and grating. The majority of the lung was non-air holding ... microscopic sections show scarcely any areas of lung tissue approaching normal. The fibrous tissue was massive.³

Although lung diseases in miners had been recognised for centuries,⁴ the rise of industrialism with its factory system, intensification of work, extensive rail and road networks, development of global mineral resources, ever increasing technological changes, and rapid urban and industrial growth, vastly increased the number of workers exposed to silica dust and the quantity of dust to which they were exposed. In the 1860s England's first medical inspector of factories E.H. Greenhow linked dust to lung diseases in metal miners. In the same decade German pathologist Friedrich von Zenker coined the term 'pneumokoniosis' to describe lungs saturated with coal dust and in 1870 France's Dr. Visconti coined the term 'silicosis' to describe the lung disease specifically caused by inhaling silica particles.⁵

Workers at risk were mostly men employed in a range of industries and occupations including metal mining, quarrying and tunnel construction; ore milling; foundry work where silica was used for sandblasting; the manufacture of ganister—a fine-grained material consisting of crushed or ground siliceous stone mixed with fire clay that was used for lining blast furnaces and for road building; brick and tile making; building and construction; road building; stone masonry and stone cutting. Women, as well as men, employed in cutlery grinding, the pottery industry or the manufacture of scouring powders were also at risk.

Wherever doctors and medical researchers looked they found silicosis and, frequently before the 1950s, tuberculosis. In 1906 Walter Summons estimated that goldminers in Bendigo, Victoria were dying from tuberculosis at a rate six times that of other adult males.⁶ J.H.L. Cumpston, who became Australia's first director general of the Commonwealth Department of Health, examined 1,805 metal miners in Western Australia in 1910 and found fibrosis in 33% of rock drillers, 24% of dry treatment workers, 7% of nonmachine miners and 3% of truckers.⁷ At Broken Hill during 1910–12 the death rate from pneumonia in underground miners was four times greater than in all males in New South Wales.⁸ Ten years later H.G. Chapman, head of the Technical Commission of Inquiry into silicosis at Broken Hill, found that underground miners had tuberculosis at a rate 20 times that of the general population.⁹ In 1934 it was found that 111 of the 268 stonemasons examined were 'suffering from moderate or advanced fibrosis, silicosis or some manifestation of tuberculosis, either simple or complicating a fibrosis..'¹⁰

Overseas, studies of Cornish tin miners,¹¹ American metal miners¹² and South African goldminers¹³ also found a high mortality rate from silicosis or tuberculosis. In 1927, 268 of the 454 British sandstone workers examined had fibrosis.¹⁴ In 1928, of the 208 New York City tunnel excavators examined, 118 had evidence of silicosis.¹⁵ In 1933 over 11 percent of the 1,641 foundry workers examined in Massachusetts had silicosis with or without tuberculosis.¹⁶ The following year 78 of the 125 granite cutters in New York City stone cutting yards showed evidence of silicosis.¹⁷ In the late-1930s, of those workers in Britain who died from silicosis the average duration of employment was 40.1 years. However, the average duration of employment for workers manufacturing scouring-powders it was 7.8 years before their deaths; and for those employed in sandblasting, 10.3 years.¹⁸ By the 1940s silicosis, by now one of the most widespread occupational diseases, had been labelled by Americans 'public enemy No. 1.'¹⁹

'Our gift to humanity'—aluminium²⁰ therapy

In the United States the adoption of workers' compensation legislation by an ever increasing number of American states from the 1910s had stimulated corporate interest in medical research of occupational diseases. While the 'no-fault' laws ended labour–management disputes over who caused the occupational injury or disease it did not do away with conflict. As Anthony Bale suggests, the compensation laws simply shifted the battleground to medical questions over the diagnosis of occupational diseases, the definition of disability, and the length of time thought to be adequate for recuperation. In Pennsylvania in the early 1930s, for instance, 'medical testimony was involved in 80% of all contested cases for termination or modification of [compensation] benefits..'²¹

This process stimulated a transformation within the medical community. From around 1920 laboratory-oriented studies into occupational diseases and exposures to various toxins began to replace the previously favoured field studies that had been based on direct observation of factory conditions and work processes; examination of hospital and medical records; and interviews with employees and employers. Scientific work shifted 'from practical toward more theoretical questions' and the audience for this work shifted from laypersons to a 'specialized audience of physicians and hygienists.'²² Corporations began to set up their own medical research facilities or to fund academic research into occupational diseases.²³

The industrial base in Australia was too small to support corporate research on this scale; however, medical inquiry into occupational diseases also experienced a shift from, what Vicente Navarro has termed, macrocausality to microcausality.²⁴ A key turning point in this process was the creation of the Commonwealth Division of Industrial Hygiene in 1921 as a section of the Commonwealth Department of Health. This body, staffed by physicians under the direction of Duncan G. Robertson, viewed industrial hygiene through the prism of public health, focusing on the occupational disease rather than the underlying production processes that gave rise to it. As Richard Gillespie explains, this approach drew them 'into the laboratory to find scientific precision, rather than into the workplace; and it encouraged the quarantine of "susceptible" workers rather than removal of the source of the problem.'²⁵

In Canada corporate research developed on a smaller scale than in the United States. However, like its American counterpart, it was stimulated by the introduction of workers' compensation legislation. In Ontario in 1926 silicosis in miners was added to the list of compensable diseases. Previously compensation was available for 'miners' phthisis,' that is, tuberculosis or tuberculosis in conjunction with silicosis. The 1926 amendments included the stages of ante-primary, primary and secondary silicosis, derived from South African research into the disease that was devastating goldminers on the Witwatersrand. Workers with ante-primary stage silicosis exhibited the earliest detectable signs of the disease before it impaired their working capacity. Primary stage signified the presence of the disease and a slight impairment of working capacity. Secondary stage meant the workers' ability to work was seriously and permanently impaired or that they had tuberculosis, with or without silicosis. These stages were not rigid. South African investigators reported that miners with ante-primary silicosis could progress to primary silicosis within four and a half years of being removed from exposure to silica dust.²⁶

After the passage of the amendments the number of compensation claims in Ontario rose. This trend was not interrupted by laws passed in 1928 that required annual medical examinations of employed miners to locate and exclude from underground work those with early stages of silicosis; and pre-employment examinations of new recruits to ensure only strong, healthy men were hired in the mines.²⁷ The Ontario Mining Association admitted in 1940 that new cases of silicosis developed in previously healthy miners and many workers who had been removed from underground in 1926 and 1927 'became progressively worse instead of better.'²⁸

This should not have been a surprise. J.G. Cunningham, director of Ontario's Division of Industrial Hygiene, reported in 1930 that in two miners diagnosed with, and compensated for, ante-primary stage silicosis in 1927 and 1928 respectively the disease advanced, and in six miners with primary stage silicosis it had quickly progressed to secondary stage. Cunningham noted:

In the Porcupine area, of 27 primary cases compensated to 1 January 1930, 15 have died. Of 17 secondary cases compensated in 1926, 9 died in 1926. Since then 10 more secondary cases have been compensated and 6 have died. In the 15 death cases, the period which elapsed between the time they were compensated, which in most cases was shortly after disability arose, and the date of death, averaged sixteen months.²⁹

Ontario mining companies found there was a deficit of $1,100,000 in the silicosis fund and the Workmen's Compensation Board wanted them to establish an account 'to pay for incidence and progression on the basis of past experience.' As a direct result of the compensation crisis 'studies were undertaken by various parties to improve ... preventives and to develop others more effective.'³⁰ Leading this scientific research was McIntyre Porcupine Gold Mine in Schumacher, Ontario. McIntyre was a major gold producer in the Porcupine district where the largest number of silicosis cases had been reported.

A publication in 1924 by British medical researchers W.E. Gye and W.J. Purdy was the springboard for the research conducted by W.D. Robson, medical officer at the McIntyre Mines; James Denny, the company's chief metallurgist; and Dudley Irwin, pathologist at Toronto's Banting Institute. Prevailing opinion held that silicosis was caused by the physical damage of silica particles to lung tissue. James Newman, consulting mining engineer to Mount Morgan Gold Mining Company, said in 1911: 'It is admitted on all sides that the irritation and cutting of the lung tissues by particles of dust not only produce "fibrosis," a non-infective process, but also render the organs less able to resist tuberculosis.'³¹ In contrast, Gye and Purdy hypothesised that the destructive fibrosis of the lungs was not caused by mechanical damage from silica dust particles, but by a chemical reaction with the lung tissue. In 1932 Robson, Denny and Irwin began their research to find a substance or method to counteract this chemical effect.

After four years experimenting on animals they believed they had found a safe material that prevented the transformation of silica into silicic acid in the lungs—the process that they believed caused silicosis. They hypothesised that the disability from silicosis was not due to fibrosis of the lungs but from inflammation induced by the inhaled silica, which interfered with the exchange of gases that takes place in the lungs.³² In 1936, in what the Ontario Mining Association characterised as a 'brilliant piece of research,' Robson reported that powdered aluminium coated silica in the lungs, reducing inflammation and preventing silicosis in animals.³³ It was also stated that aluminium 'was an effective treatment in established silicosis.'³⁴ Further, there was 'no effect on the general health of the animals and no evidence of toxicity or damage to tissues' after breathing large quantities of it over long periods.³⁵ For their work Denny received the Leonard Medal, while Robson and Irwin received the McCharles Award from the University of Toronto.

To establish whether aluminium powder was toxic to humans, D.W. Crombie and J.L. Blaisdell from McIntyre Research Foundation,³⁶ a nonprofit company established by McIntyre Porcupine Gold Mine, examined x-rays of 125 workers engaged in manufacturing fine aluminium powder for paint and ink. The workers had been employed at the Aluminum Company of America's Pittsburgh plant for a period of years ranging from six to twenty-three and their exposure to high concentrations of aluminium dust had been considerable. Crombie and Blaisdell's findings were remarkable. Not only were there no abnormalities in the workers' lungs, but there was also evidence that tuberculosis in some employees 'had cleared and disappeared' over time.³⁷ Given the impressive results with laboratory animals and the reported harmlessness of inhaling large amounts of powdered aluminium, human trials began. By 1940, with the support of Ontario's Department of Health and the Workmen's Compensation Board, McIntyre mines facilitated the establishment of the Porcupine Clinic for Silicosis Research at Timmins, Ontario. Here Crombie, Blaisdell and G. MacPherson conducted clinical trials on volunteer miners with silicosis.

These trials showed 'conclusively' that aluminium powder was 'entirely harmless' and 'proved definitely beneficial' in some cases. Of thirty-four workers studied nineteen showed clinical improvement. These nineteen comprised seven miners who showed a definite improvement and twelve who showed a slight improvement.³⁸ Crombie warned that aluminium therapy 'cannot be regarded in any sense as a "cure" for silicosis insofar as restoring to normal lung tissue which has already undergone fibrotic change.' However, he recommended its use, believing it offered 'every prospect of preventing the development of human silicosis.' As a treatment for established silicosis, it improved symptoms of the disease as well as increasing miners' capacity to work.³⁹ W.D. Robson believed it was capable of halting the progression of silicosis.⁴⁰ Concurrent human studies carried out by J.W.G. Hannon from McIntyre Research on workers in the ceramic industry in Washington, Pennsylvania corroborated the Timmins' results that aluminium improved workers' 'morale, health and production capacity.'⁴¹ Hannon reported that 94 percent of the study subjects—143 workers disabled from silicosis—improved with the therapy.⁴² Dudley Irwin, one of the original McIntyre team members, reported that the results of the clinical trials 'surpassed even those anticipated from the animal experiments.'⁴³

By 1930 Ontario workers with ante-primary silicosis were awarded $500, those with primary silicosis $1,000, while secondary silicosis victims received 66.6 percent of their previous wage, as well as medical and hospital care. On death, families received a pension in accordance with the number of dependants.⁴⁴ Fifteen years later it was estimated that the cost of a case of silicosis was $11,000. Robson declared that if aluminium therapy could halt the progress of silicosis and prevent disability, the financial benefit to Ontario's mining industry would be enormous and the benefit to the workers, their families and communities would be incalculable.⁴⁵

It seemed that the universal antidote to silicosis had finally been found. In Canada it was enthusiastically taken up. In Quebec, Eugene Larochelle, secretary of Western Quebec Mining Association, commented: 'All mines where silica occurs are "Sold" on the treatment.'⁴⁶ In British Columbia the Workmen's Compensation Board encouraged the mining industry to adopt aluminium therapy by reducing the silicosis assessment rate for companies using it.⁴⁷ By 1948 it was reported that 'most of the mines in British Columbia have installed this therapy.'⁴⁸ In the United States D.R. Johns and S.J. Petronella from East Chicago, Indiana were so impressed with Hannon's investigations in Pennsylvania that they started aluminium therapy at Harbison Walker Refractories and Continental Foundry & Machine Company in East Chicago. Johns and Petronella reported that 23 of 75 workers who completed treatment at Continental Foundry & Machine showed definite improvement indicated by 'less cough, easier breathing, less fatigue, improved appetite.'⁴⁹

A booklet published in 1943 by the McIntyre Porcupine Mines assured miners there was 'no longer any need to be afraid that you will contract silicosis.' It concluded on this positive note:

Aluminum powder breathed into your lungs, combined with good ventilation and proper attention to water sprays, etc., below ground, will protect you from developing the disease 'Silicosis.'⁵⁰

Not surprisingly, Canadian workers then submitted to the procedure. In fact, by the late 1940s some miners, as well as their wives, were using it to 'cure' a variety of respiratory complaints.⁵¹

In Australia there were mixed responses to aluminium therapy. Both F. McCullum, Director General of Health for NSW's Department of Public Health, as well as A.J. Metcalfe, acting director-general of the Commonwealth Department of Health were cautious.⁵² Metcalfe advised that a long term project be established whereby Commonwealth Health Laboratory staff at Kalgoorlie investigates aluminium therapy 'under carefully controlled conditions.'⁵³ However, W.E. George, an expert on silicosis who visited the McIntyre Porcupine mine and laboratory in July 1946, was an enthusiastic supporter of the therapy.⁵⁴ In this he was encouraged by the Australasian Institute of Mining and Metallurgy who saw it as a means of 'preserving human life from the ravages of a disease which is still the bane of the mining industry.'⁵⁵ The Institute worked closely with the Queensland and Western Australian governments as well as Mount Isa Mines Ltd in 1945 to promote the therapy and to sponsor a visit to Australia by W.D. Robson.⁵⁶

Despite his reservations, McCullum acknowledged in July 1945 that Western Australian authorities had 'already approached the McIntyre Institute, Canada for permission to use their patented process..'⁵⁷ And when he was approached in December by the state government to use the medical officer at Kalgoorlie Health Laboratory 'for the technical aspects of aluminium therapy in that State,' he consented.⁵⁸ In November 1945 Queensland Premier Frank Cooper was reported to have said that 'Mount Isa Mines Limited anticipates the early installation of aluminium therapy treatment facilities..'⁵⁹

While the Commonwealth government was cautious about the therapy, by the end of World War II they were concerned about a labour shortage in the metal mining industry. From July 1939 to June 1945 employment in mining and quarrying had declined nationally from 54,400 to 43,800.⁶⁰ The Commonwealth government's greatest fear was that the industry's bad reputation for silicosis would exacerbate this trend. The Mining Industry Advisory Panel informed the Department of Post War Reconstruction that there was 'a hesitancy on the part of a generation that knows something of the experience of its predecessors in Mining—an experience in respect to industrial disease that none would willingly seek to emulate..'⁶¹ Perhaps it was also this concern that motivated Western Australian mines to take up aluminium therapy. Whatever the key driver was, by 1958 E.E. Brisbane, the state mining engineer, reported that 2,337 of the state's underground miners, representing 72 percent of Western Australia's total underground workforce, were using aluminium therapy.⁶²

Confidence in the therapy was so high an American observer declared, 'before long there shouldn't be any more new cases of silicosis ... no more at all. All that is needed is a good supply of aluminium dust and the proper equipment to disperse it.'⁶³ The 'proper equipment' was developed by the McIntyre team and it allowed aluminium to be administered to workers as a group or individually. The group method was used at Porcupine mines where fine particles of aluminium powder 5 microns in diameter were pumped into sealed mine change rooms at the beginning of shifts.

When the miners have assembled, the room is tightly closed. The [four] dispersal machines, situated in the corners of the room, are operated in series, one minute for each machine so as to obtain a uniform distribution of the aluminum dust throughout the chamber. The dusting period lasts about 10 minutes.⁶⁴

It was asserted that the process 'entails no inconvenience to the men or waste of company time.'⁶⁵ When given individually, a purpose-built inhaler was used. Sessions lasted for approximately ten minutes and workers stood erect, their noses clamped to force them to breathe through their mouths. Thirty to forty treatments were given each year, although some workers received up to sixty.⁶⁶

The sole supplier of the equipment and aluminium powder was McIntyre Research, which was also the patent holder. As its director, Robson informed Julius Kruttschnitt, Chair of Mount Isa Mines, that the 'right to use our aluminium powder process for the prevention and treatment of silicosis is our gift to humanity and we are anxious to do what we can to introduce it with the minimum amount of delay.'⁶⁷ The cost of the therapy in 1946 amounted to

1 dollar per man per year with a minimum charge of 200 dollars for treatment of those in the mine exposed to dusting. There are also the costs of the use of the plants and the price of injections and the powders which can be obtained from the McIntyre Research Company alone.⁶⁸

By mid-1945 around 12,000 Canadian miners and 6,700 American workers were being exposed to aluminium therapy. By 1946 the estimation was 15,000 Canadian and 8,000–10,000 American workers.⁶⁹ As Australian doctor W.E. George put it: 'So now they have some human guinea pigs working for them.'⁷⁰

Problems with the mass application of aluminium therapy

The widespread use of aluminium therapy, described as still experimental in 1944 by Leroy Gardner who was conducting simultaneous research on the subject at the Saranac Laboratory in New York State, raises four major issues.⁷¹ First, at the time the McIntyre team began their experiments it was well established that the cause of silicosis was the inhalation of silica dust and that eliminating it from the workplace air was the only guarantee that workers would not contract the disease. Yet, the focus of corporate scientific research at McIntyre Porcupine Mines was not the mine air, but workers' bodies. Attention, time, money and expertise were invested in altering the effects of silica once it had been inhaled. This methodology is fitting in a number of circumstances; for instance, where an infectious disease cannot be eliminated it is appropriate to build bodily defences with vaccines. However, occupational exposure to silica is not comparable, since it was possible to remove much of the dust. The greatest obstacle to this was employers' unwillingness to spend the money required to make workplaces safe. In this context, there was a danger that some employers would view the 'magic bullet' of aluminium therapy as a cheap alternative to eliminating their employees' exposure to silica dust.

An example of this was the plan by America's Air Hygiene Foundation to study the effects of adding aluminium to compounds used in foundries for dusting moulds—many of these compounds caused silicosis. The foundation acknowledged that the alternative was to control the dust hazard through exhaust ventilation, but this 'would require a very great expenditure.'⁷² While Robson maintained that aluminium therapy should be seen as an adjunct to lowering levels of atmospheric silica dust, some researchers, like Anthony Lanza, an American authority in silicosis, warned it could be viewed as a

wonderful cure-all which obviates the necessity of spending a considerable amount of money to install adequate ventilation and engineering control methods, and in fact, I have been informed that in certain localities where there is a silicosis hazard, men on being hired are required to agree to submit themselves to a course on aluminum therapy.⁷³

Given the concern that some employers could use aluminium therapy to evade their obligation to reduce or eliminate silica dust, comments such as those by W.E. George were reckless. He recommended the use of aluminium therapy where employers thought the hazard had been dealt with 'so far as is economically practicable' or where it was 'necessary' to expose workers to dangerously high concentrations of silica dust.⁷⁴

A second issue is the strength of the experimental data underpinning the therapy. In the animal studies aluminium inhibited the effects of comparatively pure quartz. However, conditions in industry were not comparable to those in a laboratory. Often workers were exposed to a mixture of mineral dusts, not just quartz, and environmental variables in the workplace differed from those in the laboratory.⁷⁵ As for the human trials conducted by or for the McIntyre team, concerns were raised that they involved only a small number of research participants. At the clinic in Timmins, Ontario, only thirty-four volunteers with silicosis took part in Crombie's study into the therapeutic benefits of aluminium therapy in workers with silicosis. Eighteen of these workers 'showed little or no disability' from their disease before the experiments began and only three of them had a 'definitely measurable disability due to silicosis ... but even in these the disability was not marked.'⁷⁶ The American Medical Association believed the numbers in the study were 'too limited to be of statistical significance.'⁷⁷

According to Lanza there was 'good evidence to show that aluminum will inhibit the action of silica in experimental animals. As far as I know, this is the only certainty with reference to this whole question.'⁷⁸ In Australia Director-General of Health F. McCullum believed 'the figures are so small that the evidence as to its curative properties is inconclusive.'⁷⁹ The American Medical Association cautioned in mid-1946:

Only prolonged unbiased observations, with adequate control cases, will demonstrate whether the prophylactic results obtained with animals are applicable to man ... it is recommended that the general application of aluminum therapy in industry be delayed until adequately and impartially controlled clinical observations demonstrates its effectiveness in preventing or alleviating silicosis in man.⁸⁰

In 1948 concerns were again raised that no satisfactorily controlled experiments had been conducted and the optimum dose of aluminium as a treatment for silicosis had not been determined.⁸¹ The American Medical Association believed that aluminium therapy should not have been introduced on a large scale in industry in the absence of scientifically-controlled experiments.⁸² Yet, it was introduced even though its value as a preventive had only been determined on the results from a small clinical trial in silicotic workers, from projections from animal studies and from Crombie and Blaisdell's assertion that aluminium was harmless after reviewing the x-rays of 125 Aluminum Company of America workers who manufactured aluminium powder. The claim that the general health of these 125 workers seemed better than 3,000 workers in other sections of the same plant, gave added weight to Crombie and Blaisdell's opinion.⁸³ It is possible of course that the workers' health appeared exceptional because sick workers left the company's employ, thereby skewing the results. This phenomenon known as the 'healthy worker effect' is not uncommon.

In Hannon's trials in Pennsylvania's ceramic industry, which were used to corroborate findings in the Timmins clinical trials, some reservations should also be raised. A number of workers in the industry were subjected to levels of occupational silica as high as 9,500 particles per cubic centimetre. The 'safe' exposure limit at the time varied from one authority to the next; for instance, the International Labour Organisation's conference in Johannesburg in 1930 recommended a limit of 6 million particles per cubic foot of air,⁸⁴ while the United States Bureau of Mines recommended 10 million particles per cubic foot of air, which was approximated to 300 particles per cubic centimetre.⁸⁵ Whichever standard was used, it is clear that the conditions in the ceramic industry were appalling. Workers were contracting disabling silicosis after less than four years exposure.⁸⁶ This compared with an average ten years exposure in Western Australia's notoriously unhealthy gold mines⁸⁷ and fifteen years exposure in Ontario and South African gold mines before workers contracted silicosis.⁸⁸ Clearly, less than four years represented a very rapid onset of the disease.

Hannon declared his trials successful because workers using aluminium therapy for four years did not show signs of silicosis.⁸⁹ However, his studies were not carried out under the scandalous conditions just mentioned. Fortunately for the ceramic workers, prior to his studies employers reduced dust levels to an average of 370 particles per cubic centimetre, the highest reading being 900 particles.⁹⁰ Given this, it cannot be proved that the absence of silicosis in ceramic workers during Hannon's study was a result of aluminium therapy. It is just as plausible that it was due to the improved working conditions.

In addition to the relatively small number of participants in the human trials, scientists elsewhere were unable to reproduce the results of the McIntyre team. Animal experiments by Carl Naeslund at Sweden's Karolinska Institute were so unsuccessful he cautioned against using aluminium on humans.⁹¹ In Britain investigators were not able to substantiate Robson's animal experiments in 1943, although by 1950 one of the principal investigators, in conjunction with other scientists, had achieved successful results.⁹² Similarly, human trials conducted by the British Medical Research Council could not demonstrate the beneficial effects of aluminium therapy.⁹³

In the United States John Berry at the University of Colorado conducted a study into the effect of aluminium in advanced silicosis. Twenty-six workers with this disease were treated with aluminium while another nine—a control group—believed they were being treated but were only given inhalations of room air. Berry stated that an 'impressive degree of subjective improvement was reported by the majority of the individuals in both groups. In the aluminium treated group, no objective changes were observed which could be convincingly attributed to the metallic therapy.'⁹⁴ Similarly, Leroy Gardner, at the Saranac Laboratory, replicated the results of Robson's animal experiments, but failed to replicate Crombie's clinical trial results that saw improvements in workers with silicosis.⁹⁵ Gardner tested American workers at an iron ore mine and a lead and zinc mine in New York State but 'failed to furnish convincing proof that aluminum treatment has any specific effect upon the symptoms of established silicosis.' Of a minority of workers who improved Gardner reported that there were compounding factors such as a change of occupation or the cure of an associated disease. Nonetheless, he concluded: 'whether symptomatic relief is physical or psychological its attainment is most desirable and no harm has been done.'⁹⁶

But surely harm was done. Silicosis is a very real and fatal disease producing observable, irreversible lung damage—a disease now shown to cause lung cancer. Robson, Hannon and Crombie promoted aluminium therapy on the basis that it would prevent silicosis in unaffected workers as well as improve the health of workers disabled from the disease. Given the danger that some employers could use the therapy as an alternative to reducing silica dust levels, it could be argued that aluminium therapy increased, rather than diminished, the risk to workers' health. Irving Tabershaw and Bernard Tebbens from Alabama's Department of Health reasoned that by using aluminium therapy on workers suspected of having silicosis 'the worker may continue on his job in a potentially hazardous silica environment without danger to himself.' This was despite their admission that there was:

still controversy regarding objective evidence of this improvement [in silicotics]. Pulmonary function tests are difficult to interpret and those clinicians using the rigid criteria of objective findings find improvement less remarkable.⁹⁷

Although aluminium therapy was never promoted as a placebo to improve workers' psychological outlook, it was often subjective, rather than objective, improvements that were commended by health professionals. Leroy Gardner reported in 1939 that he had found it 'impossible to obtain protective action with metallic aluminium dust,' although he had better results with aluminium hydroxide.⁹⁸ Still, he was sufficiently satisfied with the subjective improvements to recommend its use.⁹⁹

A third problem was that experts, including those who fully supported the therapy, admitted that its full effects would not be known for a decade because silicosis typically was a slow-developing disease.¹⁰⁰ E. Winn, chair of British Columbia's Workmen's Compensation Board, said it was 'a certainty' that 'it will be some time before the treatment will have been given for a sufficient period to warrant definite conclusions' about its effectiveness.¹⁰¹ N. Parkinson, the executive director of the Ontario Mining Association, admitted that although almost all mines were using aluminium therapy it was too soon to draw conclusions about its effectiveness.¹⁰² In Australia, W.E. George predicted it would be ten to fifteen years 'before it could be finally established whether aluminium treatment was proving effective,'¹⁰³ and D.A. MacGregor from West Virginia concurred.¹⁰⁴

Given the uncertainty over the cumulative effects of aluminium therapy on workers' health, Anthony Lanza warned of potential medico-legal concerns. In 1945 he cautioned: 'any pulmonary disease which the individual might suffer in subsequent years would be blamed upon this unusual form of treatment.'¹⁰⁵ Such concerns may have underpinned Robson's advice to Mount Isa Mines' management that it should obtain workers' consent before subjecting them to the therapy. He cautioned against forcing it on an unwilling miner, saying that, as

the process becomes better known and understood, [the miner] gradually realises that it involves no hazard. He finally reaches the conclusion that perhaps he is denying himself something that is free and worthwhile and he falls in line. From every viewpoint the introduction of the process should be a voluntary effort shared by management and labour alike.¹⁰⁶

By this time obtaining consent from research subjects in general had become a concern for scientists in a number of countries. In 1933 Britain's Medical Research Council adopted a policy of full consent on the advice of the Treasury solicitor as a means of avoiding liability for damages arising from clinical trials.¹⁰⁷ In 1946 the American Medical Association adopted a policy of voluntary consent from subjects of medical research as a requirement for experimentation.¹⁰⁸

Although the therapy was adopted widely despite the limited experimental data, it was not withdrawn as rapidly when preliminary data emerged indicating that it was not very effective as a preventive. After six years use by Ontario's mining industry, Andrew Riddell from the province's Silicosis Referee Board reported that in some miners the disease was progressing 'despite continual administration of aluminum, and in certain workers it has progressed on to definite silicosis since the beginning of the aluminum procedure.' As for being an effective treatment for silicosis, doubts were also emerging. Riddell said that in thirty-nine miners treated for silicosis by Crombie from 1940 to 1942, silicosis had progressed in 41 percent of them by 1945. Of another thirty-nine miners treated by Robson in 1943 and 1944 for very early stage silicosis, the disease had progressed in thirteen, or 33 percent, of them.¹⁰⁹ This was occurring concurrently with improvements in dust control, a requirement stipulated by McIntyre Research of all its licensees.

In Western Australia the state mining engineer, E.E. Brisbane, reported in 1956, after approximately a decade of using aluminium therapy, that 'there is yet no evidence of any decisive change.'¹¹⁰ Nonetheless, new mines, such as Fraser's Mine in 1957 and Croesus Mine in 1958, continued to be added to the list of those using the therapy.¹¹¹

The fourth issue raised by the extensive use of aluminium therapy was that McIntyre Research was not just the patent holder and sole supplier of the components needed for the therapy, but those associated with it were some of the principal scientific investigators into its effectiveness.

Any company that used the therapy became a license holder and was contractually obligated to refrain from publishing or permitting the publication of results of any prophylaxis, treatment or clinical observation carried out by them 'except with the written consent and approval of the licensor'—that is, McIntyre Research.¹¹² Such a stipulation restricted the process of free and open exchange of scientific ideas. As well, any discovery or invention made by the licensee became the property of McIntyre Research. Given the degree of control over research by the patent holder the possibility of scientific bias has to be considered. It is well recognised that any financial interest in the outcome of a researcher's work can produce a conflict of interest capable of influencing the quality of their research, the analysis and interpretation of their data, and the public disclosure of their discoveries. Such influences can lead scientists to downplay negative results or exaggerate favorable ones.

Conclusion

Over the period that aluminium therapy was used in northern Ontario—from 1943 until 1979—the incidence of silicosis in miners decreased. On average the years of exposure to silica dust before workers became disabled from silicosis increased from 12.5 years in 1926 to 23.7 by 1959. The average age of a miner when first diagnosed with silicosis rose from 39.7 years to 58.4 years and the average age at death from all causes in silicotic miners rose from 44.3 years in 1926 to 67.4 in 1959.¹¹³ However, this trend is also observable in other major metal mining countries such as Australia and South Africa where aluminium therapy was not used as extensively. Further, the period coincided with the development and installation of more effective methods of dust control and ventilation that reduced the formation and distribution of dust in the workplace. It also coincided with a reduction in the number of workers exposed to dangerously high levels of dust in the mines.¹¹⁴

When a company agreed to use McIntyre's aluminium therapy it signed a legal agreement stipulating that it would:

Keep dust at a minimum, obey all dust control legislation of the region where they mine is situated, furnish reports of dust counts to the licensor [McIntyre] on demand, allow the licensor free and uninterrupted access to any place on the property for inspection or dust counts, and permit inspection of personal records.¹¹⁵

That is, the company was obliged to tackle the problem at its recognised source—silica dust in the workplace air.

Had aluminium therapy achieved its stated goals of radically improving the health of already effected workers and preventing the disease in healthy workers, it is fair to expect that those workplaces using the treatment would have stood out conspicuously against those not using it. Yet, no published reports by authors unconnected with McIntyre Research have shown that to be the case. In fact, one paper published seventeen years after the adoption of aluminium therapy concluded:

It is not now possible to confirm or refute that aluminium prophylaxis does or does not prevent or retard the development of silicosis in miners. There is no proof of the value of aluminium treatment of established silicosis in man, and there is evidence that apparent improvement during such treatment is psychological.¹¹⁶

In Western Australia the last mention of aluminium therapy by the state mining engineer was in 1960, when he reported:

In some change rooms the dispersal of the powder has become rather haphazard due no doubt to the waning interest of both miner and management. Differences of opinion, between medical men, on the effectiveness of the treatment has not assisted the situation.¹¹⁷

The adverse effects of inhaling aluminium powder were never seriously studied while the therapy was in use. After it was discontinued in Canada, however, the Ontario Ministry of Labour, in 1987, commissioned studies into the health of miners who had been exposed to aluminium therapy to see if there were any long term health effects. In 1990 S.L. Rifat and others from the University of Toronto examined two groups of Canadian miners. One group had been exposed to the therapy; the other had not. They found that exposed miners did not perform as well as unexposed workers on cognitive state examinations; 'also, the proportion of men with scores in the impaired range was greater in the exposed than non-exposed group.' The greater exposure to aluminium therapy, the more likely it was that the miners scored in the impaired range. Rifat and her colleagues concluded that the 'findings are consistent with putative neurotoxicity of chronic aluminium exposure.'¹¹⁸

A follow up study was done some years later and the results presented in 1997. The second study contradicted the initial findings, showing that the proportion of miners with neurocognitive disorders who had been exposed to aluminium therapy was approximately the same as for men who had no exposure. Concerns were raised that the follow up sample was too small to 'allow for any definitive conclusion regarding the safety of historical exposure to McIntyre powder.'¹¹⁹

In 1944 W.D. Robson acknowledged that increased production associated with World War II intensified the demand for aluminium therapy. He felt that the treatment had been still in its preliminary phase, but nonetheless concluded that the 'need of those suffering from or subjected to the hazard of siliceous dust prevailed and a start [was] made' in using the therapy on a large scale in industry.¹²⁰ However, it does not matter whether the therapy was promoted out of altruism and a genuine desire to save workers' lives or from a desire to save industry money by offering employers a cheaper alternative to removing silica dust from the workplace air. Workers should not have been subjected to an unproven therapy that may have put their health at risk, when from the outset every authority on the disease recognised that the only real defence against silicosis was eliminating workers' exposure to silica dust.

Notes

¹ In 1997 the International Agency for Research on Cancer also confirmed that silica was a carcinogen. Beth Rosenberg, "Change in the World of Occupational Health: Silica Control, Then and Now," Journal of Public Health Policy 26 (2005): 192–202, 195.

^2. "Report of the Royal Commission on Health Conditions in Queensland Mines," Queensland Parliamentary Papers 3 (1911–1912): 539–843, 645.

^3. Andrew R. Riddell and H.E. Rothwell, "Some Clinical and Pathologic Observations on Silicosis in Ontario," Journal of Industrial Hygiene 5 (May 1928): 147–57, 151.

^4. D. Harrington and Sara J. Davenport, Review of Literature on Effects of Breathing Dusts with Special Reference to Silicosis (Washington DC: United States Bureau of Mines, 1937), Bulletin 400, 8–9.

^5. Elaine Katz, The White Death: Silicosis on the Witwatersrand Gold Mines: 1886–1910 (Johannesburg: Witwatersrand University Press, 1994), 24.

^6. Walter Summons, Miners' Phthisis: An Investigation at Bendigo into the Prevalence, Nature, Causes and Prevention of Miners' Phthisis and the Ventilation of the Bendigo Mines (Melbourne: Stillwell & Co., 1907), 23; B. Stewart Cowen, "Tuberculosis in a Mining Community," Intercolonial Medical Journal (20 September 1902), 432–38.

^7. Report of the Royal Commission on Pulmonary Diseases Amongst Miners," Western Australian Minutes and Votes and Proceedings of Parliament 2, Report No. 12 (1910–11): 1–107, 6. For accounts of earlier studies into silicosis Frank R. Kerr, see "A Brief Survey of the Various Inquiries into Pneumoconiosis and Tuberculosis among Australian Miners (1902–21)," Medical Journal of Australia (3 May 1924): 273–5; Marcus James, "The Struggle against Silicosis in the Australian Mining Industry: The Role of the Commonwealth Government, 1920–1950," Labour History 6 (November 1993): 75–95; Bradley Bowden and Beris Penrose, "Dust, Contractors, Politics and Silicosis: Conflicting Narratives and the Queensland Royal Commission into Miners' Phthisis, 1911," Australian Historical Studies 137 (October 2006): 89–107.

^8. A. J. Lanza, ed., Silicosis and Asbestosis (London: Oxford University Press, 1938), 15; Melville Birks, "Health Conditions at Broken Hill Mines," Journal of State Medicine 29 (April 1921), 1212.

^9. "Silicosis," Medical Journal of Australia 2, no. 15 (13 October 1923), 394.

^10. Keith Moore and C.A. Kuhlmann, Enquiry into the Effects of Occupation on the Pulmonary Condition of Stonemasons (Canberra: Commonwealth Department of Health, 1934), A1928 545/102 Section 1, Industrial Hygiene of Stone Masons, National Archives of Australia, Canberra (hereafter NAA), 13.

^11. John S. Haldane, Joseph Martin and R. Arthur Thomas, "Report to the Secretary of State for the Home Department on the Health of Cornish Miners," reprinted in "Report of the Royal Commission on the Ventilation and Sanitation of Mines: Appendix no. IX," Western Australian Minutes of Votes and Proceedings of Parliament 1 (1905): 151–67.

^12. Daniel Harrington and Anthony Lanza, Miners' Consumption in the Mines of Butte, Montana: Preliminary Report of an Investigation Made in the Years 1916–1919 (Washington DC: United States Bureau of Mines, 1921), Technical Paper 260; A.J. Lanza and Samuel B. Childs, Miners' Consumption: A Study of 433 Cases of the Disease Among Zinc Miners in Southwestern Missouri (Washington DC: United States Public Health Service, 1917) Bulletin no. 85; A.J. Lanza and Edwin Higgins, Pulmonary Disease among Miners in the Joplin District, Missouri and its Relation to Rock Dust in the Mines: A Preliminary Report (Washington DC: United States Bureau of Mines, 1915), Technical Paper 105.

^13.General Report of the Miners' Phthisis Prevention Committee (Pretoria: Government Printing and Stationery Office, 1916).

^14. C.L. Sutherland and B. Bryson (members of the Medical Board Appointed under the Refractories Industries [Silicosis] Scheme), Report on the Occurrence of Silicosis Among Sandstone Workers (London: HMSO, 1929), 29.

^15. Adelaide Ross Smith, "Silicosis in Rock Drillers in New York City. II Silicosis Among Rock Drillers, Blasters, and Excavators in New York City," Journal of Industrial Hygiene 11 (February 1929): 39–69, 44.

^16. Alton S. Pope and David Zacks, "Epidemiological Aspects of Silicosis and Tuberculosis," American Review of Tuberculosis 32 (1935): 229–42, 239.

^17. Adelaide Ross Smith, "A Study of Granite Cutting and Granite Cutters in the Vicinity of New York City," American Journal of Public Health 24 (1934): 831–4, 832.

^18. E.R.A. Merewether, "The Risk of Silicosis in Sand-Blasters," Tubercle 17 (June 1936): 385–9, 386–7.

^19. L.E. Hamlin, "Industrial Dust—The Pneumoconioses," Industrial Medicine 13, (March 1944): 223–39, 226.

^20. Australians use the word 'aluminium' while Americans use the word 'aluminum.' 'Aluminium' has been used throughout the paper except where direct quotes from American or Canadian sources have been used.

^21. Anthony Bale, "Medicine in the Industrial Battle: Early Workers' Compensation," Social Science and Medicine 28 (1989): 1113–20, 1115.

^22. Christopher Sellers, "'A Prejudice Which May Cloud the Mentality': An Overview of the Birth of Modern Science of Occupational Disease," in Environmental Hazards from the Workplace into the Community, edited by Helen E. Sheehan and Richard P. Wedeen (New Brunswick: Rutgers University Press, 1993), 231–63, 235.

^23. Christopher Sellers, Hazards of the Job: From Industrial Disease to Environmental Health Science (Chapel Hill and London: University of North Carolina Press, 1997), 183–4.

^24. Vicente Navarro, "Work, Ideology, and Science: The Case of Medicine,' International Journal of Health Services 10 (1980): 523–50, 541

^25. Richard Gillespie, "The Limits of Industrial Hygiene: Commonwealth Government Initiatives in Occupational Health, 1921–48", in Reflections on Medical History and Health in Australia, edited by Harold Attwood and Geoffrey Kenny (Melbourne: University of Melbourne Press, 1987), 101–20, 114.

^26. L.G. Irvine, "Silicosis in South Africa: A Symposium on the Histo-Pathology, Pathological Anatomy and Radiology of the Disease," Proceedings of the Transvaal Mine Medical Officers' Association, Special Supplement (23 October 1930), 43.

^27. For a more extensive study on the failure of medical monitoring to prevent silicosis see Beris Penrose, "Medical Monitoring and Silicosis in Metal Miners: 1910–1940," Labour History Review 69 (December 2004): 283–303.

^28. "Memorandum, Ontario Mining Association, 'Memorandum on the Use of Metallic Aluminum in the Prevention of Silicosis,' February 1940," A1928 545/109, Industrial Hygiene. Silicosis, Aluminium Therapy, NAA.

^29. J.G. Cunningham, "Silicosis in Canada," in Silicosis: Records of the International Conference held at Johannesburg, 13–27 August 1930 (Geneva: International Labour Office, 1930), 317–37, 324.

^30. "Memorandum, Ontario Mining Association," 1.

^31. "Report of the Royal Commission on Health Conditions in Queensland Mines," 747.

^32. D.W. Crombie, J.L. Blaisdell, and G. MacPherson, "The Treatment of Silicosis by Aluminum Powder," Canadian Medical Association Journal 50 (April 1944): 318–28, 319.

^33. "Memorandum, Ontario Mining Association," 6.; J.J. Denny, W.D. Robson and Dudley A. Irwin, "The Prevention of Silicosis by Metallic Aluminium I: A Preliminary Report," Canadian Medical Association Journal 37 (July 1937): 1–11, 10; F. Bremner, "Antidotal Rocks and Silicosis," Canadian Mining Journal 60 (October 1939): 589–95.

^34. D. Irwin, "The Contribution of Sir Frederick Banting to Silicosis Research," Canadian Medical Association Journal 47 (November 1942): 403–5, 405.

^35. J.J. Denny, W.D. Robson and Dudley A. Irwin, "The Prevention of Silicosis by Metallic Aluminium II," Canadian Medical Association Journal 40 (March 1939): 213–28, 227.

^36. The McIntyre Research Foundation was originally McIntyre Research Limited.

^37. Leroy U. Gardner and George W. Wright, The Current Status of Aluminum Therapy in Silicosis (Saranac Laboratory, 23 October 1944), A1928 545/109 Industrial Hygiene. Silicosis, Aluminium Therapy, NAA, 4; "Aluminum Therapy," Industrial Medicine 14 (November 1945): 40–6, 40, extract from Johns; and S.J. Petronella, "Aluminum Therapy for Silicosis," Monthly Bulletin Indiana State Board of Health (September 1945).

^38. W.D. Robson, "Progress in Aluminium Therapy," Proceedings of the Australasian Institute of Mining and Metallurgy 138 (1945): 23–30, 27.

^39. Crombie et al., 328.

^40. Robson, 29.

^41. "Aluminum Therapy," Industrial Medicine, 40.

^42. Paul J. Bamberger, "Aluminum Therapy in Silicosis," Industrial Medicine 14 (June 1945): 477–9, 477.

^43. Irwin, 405.

^44. Cunningham, 328.

^45. Robson, 29.

^46. "Letter, Eugene Larochelle, Secretary, Western Quebec Mining Association, Quebec, to E. J. Carlyle, Secretary, Canadian Institute of Mining and Metallurgy, Montreal, 5 July 1945," A1928 545/109, Industrial Hygiene. Silicosis, Aluminium Therapy, NAA.

^47. "Letter, Australian Scienti.c Liaison Office, Washington DC, to Director of Health, 'Miner's Phthisis,' (12 April 1945)," A1928 545/109, Industrial Hygiene. Silicosis, Aluminium Therapy, NAA.

^48. C.H. Vroom, "Silicosis as an Industrial and Compensation Problem in British Columbia," Chest 14 (January–February 1948): 63–77, 66.

^49. "Aluminum Therapy," Industrial Medicine, 40.

^50.Silicosis: What It Is and How It Can Be Prevented (Canada: Northern Miner Press, December 1943), no page numbers.

^51. Vroom, 67.

^52. F. McCullum, Director General of Health, to Dr Morris, Department of Public Health, NSW, 24 July 1945, A1928 545/109, Industrial Hygiene. Silicosis, Aluminium Therapy, NAA; Memorandum, A.J. Metcalfe, Acting/Director-General of Health, Commonwealth Department of Health, to Chairman, Secondary Industries Commission: "Report No 4: Health and Safety in the Mining Industry—By Mining Industry Advisory Panel Assisting the Secondary Industries Commission," 17 February 1947, A1928 545/109, Industrial Hygiene. Silicosis, Aluminium Therapy, NAA.

^53. Memorandum, A.J. Metcalfe to Chairman, Secondary Industries Commission

^54. "Notice, Australian Institute of Mining and Metallurgy, Melbourne 5 September 1946," A1928 545/109, Industrial Hygiene. Silicosis, Aluminium Therapy, NAA. In 1926 George took over as medical advisor to the Broken Hill's Bureau of Medical Inspection, which had been established after the Technical Commission of Inquiry to examine miners for lung diseases. Later he became the first Chief Medical Officer of NSW's Joint Coal Board after its creation in 1946.

^55. "Aluminium Therapy in Silicosis," Proceedings of the Australasian Institute of Mining and Metallurgy 138 (1945), 22.

^56. General Secretary, Australian Institute of Mining and Metallurgy, Melbourne, to Director General of Health, Canberra, 9 July 1945, A1928 545/109, Industrial Hygiene. Silicosis, Aluminium Therapy, NAA.

^57. F. McCullum, Director General of Health, Canberra, to Dr Morris, 24 July 1945.

^58. F. McCullum, Director General of Health, Canberra, Memorandum, 12 December 1945, A1928 545/109, Industrial Hygiene. Silicosis, Aluminium Therapy, NAA.

^59. Premier Frank A. Cooper, Queensland, to Right Honourable Prime Minister, Canberra, 29 November 1945, A1928 545/109, Industrial Hygiene. Silicosis, Aluminium Therapy, NAA.

^60. "Labour Report for 1943, No. 33," Australian Bureau of Census and Statistics: Labour Reports (Canberra: Commonwealth Government Printers, 1945), 96; "Labour Report for 1945 and 1946, No. 35," Australian Bureau of Census and Statistics: Labour Reports (Canberra: Commonwealth Government Printers, 1947), 101.

^61. "Fourth Report (Health and Safety) of the Mining Industry Advisory Panel, Secondary Industries Commission, Department of Post-war Reconstruction, 1946," A1658 553/1/1, NAA.

^62. "Report of the Department of Mines for the Year 1958," Western Australia Minutes and Votes and Proceedings of Parliament 3 (1960), 27.

^63. Quoted in David Rosner and Gerald Markowitz, Deadly Dust: Silicosis and the Politics of Occupational Disease in Twentieth-Century America (Princeton: Princeton University Press, 1991), 192.

^64. "Silicosis," Industrial Medicine 14 (October 1945), 816–17 [extract from D.A. MacGregor, "Silicosis – its Prevention and Treatment," West Virginia Medical Journal 4, (September 1945)].

^65. "Memorandum, M. du Toit, Mining Engineer, Government Scienti.c Mission (South Africa), Confidential Memo: 'The Present Status of Aluminium Therapy in Canada,' 11 August 1944," A1928 545/109, Industrial Hygiene. Silicosis, Aluminium Therapy, NAA.

^66. C.W. Rauschenbach, D.R. Johns, J.F. Larrabee, L.M. Hammar and B.F. Poracky, "Silicosis Study and Management in the Calumet Industrial Area," Industrial Medicine 17 (January 1948): 1–6, 6.

^67. "Letter, W.D. Robson, Medical Director, McIntyre Research Ltd, Schumacher, Ontario, to J. Kruttschnitt, Chairman, Mount Isa Mines, Mount Isa, 20 July 1945," A1928 545/109, Industrial Hygiene. Silicosis, Aluminium Therapy, NAA.

^68.Barrier Daily Truth, 23 August 1946.

^69. Dudley A. Irwin, "Morning Session, 3^rd Annual Industrial Medical and Surgical Conference, Michigan State Medical Society, Detroit (5 April 1945)," Industrial Medicine 14 (July 1945), 570; W.E. George, "A Report of a Visit to Canada and the United States of America (April–July, 1946) to Enquire Into the Use of Different Types of Aluminum Powder in the Prevention and Treatment of Silicosis, Together With a General Review of the Subject," Proceedings of the Australasian Institute of Mining and Metallurgy 143 (1946): 1–117, 46.

^70.Barrier Daily Truth, 23 August 1946.

^71. Gardner and Wright, 5.

^72. Quoted in Rosner and Markowitz, 193, n 40.

^73. "Letter, H.O. Hofmeyr, Australian Scienti.c Research Liaison Office, Washington D.C., to G. Malherbe, Department of Mines, Johannesburg, Union of South Africa, 20 March 1945," A1928 545/109, Industrial Hygiene. Silicosis, Aluminium Therapy, NAA.

^74. "Notice, Australian Institute of Mining and Metallurgy, Melbourne, 5 September 1946," A1928 545/109, Industrial Hygiene. Silicosis, Aluminium Therapy, NAA.

^75. Carl M. Peterson and Austin E. Smith, "Aluminum in the Prevention and Treatment of Silicosis," Journal of the American Medical Association 103 (27 April 1946), 1223; George, 17.

^76. Crombie, et al., 321.

^77. Ernest W. Brown and Walton van Winkle, "Present Status of Aluminum in the Therapy and Prophylaxis of Silicosis," Journal of the American Medical Association 140 (July 1949): 1024–9, 1027.

^78. Hofmeyr to Malherbe, 2.

^79. "Memorandum, F. McCullum, Director-General of Health, Canberra, 12 December 1945," A1928 545/109, Industrial Hygiene. Silicosis, Aluminium Therapy, NAA.

^80. Peterson and Smith, 1223. The Director of the Ohio Department of Health also advised caution, see Roger E. Heering, "Advances in Public Health," Ohio Journal of Science 66 (June 1946): 165–7, 165.

^81. John W. Berry, "Aluminum Therapy in Advanced Silicosis," American Review of Tuberculosis 6 (June 1948): 557–73, 558.

^82. Brown and van Winkle, 1025.

^83. Robson, 23.

^84. E.L. Collis, "Silicosis. A Critical Review of Literature," in Pneumoconiosis Abstracts (London: Sir Isaac Pitman & Sons, 1931), 60.

^85. R.R. Sayers, "Silicosis," Public Health Reports 49 (18 May 1934), 601.

^86. J.W.G. Hannon, "Aluminium Therapy in the United States," Proceedings of the Australasian Institute of Mining and Metallurgy 138 (1945): 31–5, 31.

^87. Keith Moore, "Silicosis Among Metal Miners in Western Australia," Medical Journal of Australia 1, no. 3 (15 January 1938): 147–53, 151.

^88. Crombie, et.al., 318; Prevention of Silicosis on the Mines of the Witwatersrand: Being a Report on the Investigations of the Miners' Phthisis Prevention Committee (Johannesburg, 1937), 25.

^89. J.W.G. Hannon, "The Utilization of Aluminum," Industrial Medicine 15 (September 1945): 527–8, 527.

^90. Hannon, 'Aluminium Therapy in the United States,' 31.

^91. Carl Naeslund, "The Prevention of Silicosis: Experimental Investigations on the Action of Certain Non-Siliceous Dusts and Silica in the Origin and Development of Silicosis," Journal of Industrial Hygiene and Toxicology 22 (January 1940): 1–30, 23.

^92. Thomas Belt and Earl J. King, "Failure of Aluminium to Prevent Experimental Silicosis," Journal of Pathology and Bacteriology 55 (January 1943): 69–73; E.J. King, B.M. Wright, S.C. Ray and C.V. Harrison, "Effect of Aluminium on the Silicosis-Producing Action of Inhaled Quartz," British Journal of Industrial Medicine 7 (January 1950): 27–36, 35.

^93. M.C.S. Kennedy, "Aluminium Powder Inhalations in The Treatment of Silicosis of Pottery Workers and Pneumoconiosis of Coal-Miners," British Journal of Industrial Medicine 13 (April 1956): 85–101.

^94. Berry, 571.

^95. Leroy U. Gardner, Morris Dworski and Anthony B. Delahant, "Aluminum Therapy in Silicosis: An Experimental Study," Journal of Industrial Hygiene and Toxicology 26 (September 1944): 211–3, 221.

^96. Gardner and Wright, 10.

^97. Irving R. Tabershaw and Bernard D. Tebbens, "The Use of Aluminum in Silicosis Control," Industrial Medicine 14 (September 1945): 709–11, 710.

^98. "Fourth Silicosis Symposium," Industrial Medicine 8, (August 1939), 355.

^99. Bamberger, 479; Carl U. Dernehl and Carl A. Nau, "Some New Aspects and Approaches to the Problem of Dust Diseases," Industrial Medicine 14 (September 1945): 744–54, 748.

^100. Gardner and Wright, 3; "Letter, S. R. Johnston, Secretary, Workmen's Compensation Board, Toronto, to E. J. Carlyle, Canadian Institute of Mining and Metallurgy, Montreal, 6 July 1945," A1928 545/109, Industrial Hygiene. Silicosis, Aluminium Therapy, NAA.

^101. "Letter, E.S.H. Winn, Chairman, Workmen's Compensation Board, Vancouver, to E.J. Carlyle, Canadian Institute of Mining and Metallurgy, Montreal, 10 July 1945," A1928 545/109, Industrial Hygiene. Silicosis. Aluminium Therapy, NAA.

^102. "Letter, N. F. Parkinson, Executive Director, Ontario Mining Association, to E.J. Carlyle, Canadian Institute of Mining and Metallurgy, Montreal, 2 July 1945," A1928 545/109, Industrial Hygiene. Silicosis. Aluminium Therapy, NAA.

^103.Barrier Daily Truth, 23 August 1946.

^104. "Silicosis," 817.

^105. Hofmeyr to Malherbe, 2.

^106. Robson to Kruttschnitt.

^107. Paul Weindling, "Human Guinea Pigs and the Ethics of Experimentation: The BMJ's Correspondent at the Nuremberg Medical Trial," British Medical Journal, (December 1996): 1467–70, 1469.

^108. Susan E. Lederer, Subjected to Science: Human Experimentation in America Before the Second World War (Baltimore: Johns Hopkins University Press, 1997), 140.

^109. Brown and van Winkle, 1028.

^110. "Report of the Department of Mines for the Year 1956," Western Australia Minutes and Votes and Proceedings of Parliament 3 (1958), 23.

^111. "Report of the Department of Mines for the Year 1957," Western Australia Minutes and Votes and Proceedings of Parliament 2 (1959), 25; "Report of the Department of Mines for the Year 1958," Western Australia Minutes and Votes and Proceedings of Parliament 3 (1960), 27.

^112. George, 43.

^113. Paterson, 595.

^114. A.H. Sellers and W.C. Wheeler, "Further Statistics on Silicosis Among Miners in Ontario," Industrial Medicine and Surgery (February 1964): 89–97, 90–4.

^115. George, 42–43.

^116. Paterson, 600–1.

^117. "Report of the Department of Mines for the Year 1960," Western Australia Minutes and Votes and Proceedings of Parliament 3 (1962), 27.

^118. S.L. Rifat, M.R. Eastwood, D.R. McLachlan and P.N. Corey, "Effect of Exposure of Miners to Aluminium Powder," Lancet (1990 Nov 10): 1162–5, 1162.

^119. "Northern Ontario Miners Health Survey," Occupational Disease Panel (Industrial Disease Standards Panel) Annual Report 1997/98, http://www.canoshweb.org/odp/html/an98.htm (accessed 15 May 2007).

^120. Robson, 30.

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