The Research Community, Risk and Evidence: 1912–1932

Abstract

The closely knit research community, centred on the South African Institute of Medical Research and the Miners’ Phthisis Medical Bureau, was created by the gold mining industry and the state between 1912 and 1916. This chapter describes the establishment and day-to-day working of that research community. It then documents the accumulation of evidence on the risks associated with exposure to silica dust, the synergy between silicosis and tuberculosis, the spread of infection in the mine compounds, the problems arising from the repatriation of sick miners and the declining living standards and malnutrition in the labour-sending communities. Despite the evidence, the chapter concludes, the Chamber of Mines and its Chief Medical Officer strenuously maintained that the mines were safe.

South Africa’s first silicosis crisis helped to make Johannesburg a world centre for research into occupational lung disease. From as early as 1902, science was a powerful tool in defining risk and shaping the legislative response. The complexion and dynamics of the research community came to exert a profound effect on the nature of scientific studies it produced, and the evidence it tendered to the various commissions of enquiry and parliamentary select committees.¹

The closely knit research community, centred on the South African Institute of Medical Research (SAIMR) and the Miners’ Phthisis Medical Bureau (Bureau), was created by the gold mining industry and the state between 1912 and 1916. Its members included L.G. Irvine, A. Sutherland Strachan, F.W. Simson, Wilfred Watkins-Pitchford, Anthony Mavrogordato, Spencer Lister, A.J. Orenstein and Andrew Watt. For the next half-century, the research agenda was set by the Chamber. The intimate relationship between the Chamber and the research community is epitomised by SAIMR. The Institute was founded in 1912 by the Witwatersrand Native Labour Association and the government in response to the high mortality rates from pneumonia and silicosis, which threatened recruitment from the north. In 1919, the SAIMR had a staff of seven; by 1926 that had grown to 75. William Gemmill was the WNLA’s long-term representative on the SAIMR’s Board.²

The SAIMR had two divisions. The Research Division’s primary focus was on silicosis and pneumonia, while the Routine Division carried out the diagnosis and treatment of miners and conducted medico-legal investigations. The Routine Division’s funding came from services to the mines and government departments. In 1919, the Division carried out over 60,000 diagnostic investigations.³ The Institute’s first Director was Wilfred Watkins-Pitchford, who in 1916 also became the first Director of the Bureau. Both positions were prestigious, and his combined salaries made him the highest paid health officer in South Africa.⁴ Despite his status, Watkins-Pitchford had limited authority: it was the Chamber which set the Institute’s research agenda. In addition, Watkins-Pitchford’s role at the Bureau was part-time, and his duties were purely administrative. He did not, for example, examine patients. The appointment of one person to head both the SAIMR and the Bureau raised concerns about the independence of the two organisations. The Bureau had no qualified pathologist and relied entirely for such reports on the SAIMR, thereby further blurring the boundaries between the two. As one Johannesburg specialist pointed out, it was important that in settling disputed compensation claims, an independent authority should tender evidence to the Bureau.⁵

The Miners’ Phthisis Medical Bureau, founded in 1916, was the first state organisation of its kind, and it conducted all entry, periodic and exit medicals of white miners. It also adjudicated compensation awards for both white and black mine workers. It was from this limited data set that it compiled the official disease rates. The Bureau’s primary role was to promote health and safety, but it had no capacity to conduct research. The Bureau interns were also poorly paid. In 1945, a full-time intern’s commencing salary was £1000 per annum, with £50 increments to a maximum of £1350.⁶ By comparison, a District Surgeon in the Transkei had a gross income of between £1500 and £2000.⁷

We have an account of the Bureau’s daily operations by Professor Arthur J. Hall, who was a delegate to the 1930 Silicosis Conference in Johannesburg. Hall found the Bureau was under-staffed and that the seven full-time clinicians devoted their mornings to examining the more than 30,000 white miners who attended annually. After each man’s work and medical history was taken, he was X-rayed and given a full clinical examination. The examinations were completed by midday, and after lunch the clinicians met to consider the cases. Because of the volume of work, the process was very rapid. Initially, Hall questioned why there was no similar supervision of black miners, but later accepted the explanation by the Bureau Director: since black miners worked on contracts for only a few months, they were not at risk from silicosis. Hall was also assured that blacks were subject to regular medical reviews during their service.⁸

As General Manager of Tropical Areas for the Chamber, William Gemmill routinely negotiated labour quotas with colonial governments. During one such assignment, Gemmill explained the Bureau’s role in the following way: ‘Every Mine Medical officer is by law an officer of the Miners Phthisis Medical Bureau, and is subject to the instructions of the Bureau in all Miners Phthisis matters affecting natives employed by the Mines.’⁹ In practice, the workloads of Bureau interns meant there was no such supervision. According to Dr Gerrit Schepers, who was a Bureau intern from 1946 until 1952, at no time did the Bureau supervise or evaluate mine medicals.¹⁰ Oluf Martiny, who served as a medical officer at the WNLA compound from 1954 until the early 1980s, made similar comments.¹¹

In political terms, the SAIMR and the Bureau were designed to achieve two outcomes. They were to placate the imperial authorities about the safety of the mines for migrant labour, and they were to placate the MWU about the safety of the mines for its white members. How the Institute’s first Director defined the Bureau’s role is significant. In a memo from 1917, Watkins-Pitchford wrote: ‘The Bureau assumes that its province in relation to the Mine Medical Officers is solely to secure the removal of cases of Pulmonary Tuberculosis from underground work systematically and without unnecessary delay.’¹²

Mine medicine was a bifurcated system in which the Bureau and the mine medical service operated separately.¹³ In September 1917, the Minister for Mines asked Watkins-Pitchford several questions about the duties and capacities of mine medical officers. Watkins-Pitchford admitted that he had no first-hand knowledge of mine medicine. To answer the Minister’s questions, he would have to investigate the work of medical officers, whether they were full or part-time, the number of miners each supervised, the nature and efficiency of the mine hospitals, and the sickness and death rates at each mine.¹⁴ In summary, after six years as Director of the SAIMR and a year as Director of the Bureau, which was in theory responsible for the supervision of mine medical officers, Watkins-Pitchford was not able to provide the most basic information about the workings of the Miners’ Phthisis Act in regard to medical supervision of 90 per cent of the workforce.

Despite its heavy workloads and apparent lack of coordination, the Bureau enjoyed a glowing international reputation. In March 1937, The Lancet commented on what it termed ‘the Bureau’s outstanding role’ in awarding compensation and in controlling and preventing disease. ‘The value of the records and experience of an established organisation such as this Bureau in assessing the effect of new technical measures is inestimable, and Dr Irvine [the Director] and his colleagues can be assured that their work is appreciated not only in the Transvaal but throughout the world wherever silicosis is a problem.’¹⁵

The Rand system of medical surveillance and research was stable over time, and from its foundation until the early 1970s the SAIMR had only four Directors. They were Dr Watkins-Pitchford (1912–1926), Dr Spencer Lister (1926–1939), Dr E.H. Cluver (1940–1959) and Dr J.H.S. Gear (1960–1973).¹⁶ That stability extended to the workloads of Bureau interns, which were much the same in 1950 as they had been during the First World War. Because of the lack of staff, the clinical examinations of white miners at the Bureau were always cursory. During November 1949, for example, each of the eight interns was required, on average, to carry out 30 clinical examinations in a morning.¹⁷

The other unchanging element was the limited circle of specialists who were employed by the state or the mining houses, and who dominated the science. Mine medicine in South Africa was more of a club than an open society, and a handful of men controlled the discipline. In December 1955, the Department of Mines approached the British specialist, Professor E.J. King, with the offer of appointment as Director of the newly created Pneumoconiosis Research Unit. Professor King declined, and a special sub-committee was appointed to make recommendations. Dr Orenstein was elected Chair of that Committee, which in turn nominated him as Director of the PRU. Orenstein was duly appointed to the position.¹⁸

A range of physicians saw at first hand the impact of silicosis and tuberculosis on black goldminers. These included company doctors who conducted pre-employment and periodic medicals at the WNLA compound or at individual mines, and the interns at the Bureau who carried out compensation reviews. District medical officers and missionary doctors in rural South Africa and in labour-sending states such as Basutoland (Lesotho) and Swaziland (eSwatini) saw the effects of mining on migrant workers. In addition, there were scientists at the SAIMR in Johannesburg who conducted research. Finally, there were medical specialists in the Department of Health who treated miners for tuberculosis and other diseases. Among that range of physicians, mine medical officers were best placed to identify occupational disease. However, their ability to intervene was compromised by two factors. First, their crushing workloads left them little time or energy for tasks not immediately related to their job. In addition to treating miners injured in accidents, they were responsible for daily sick parades, the examination of recruits, compound inspections and monitoring of work conditions underground.¹⁹ The other factor concerned divided loyalties to patients and to their employers, and the perceived consequences of criticising the companies.

The Mine Medical Officers’ Association

At a meeting in 1921, the Chamber created the Transvaal Mine Medical Officers’ Association (MMOA) to represent the medical practitioners who worked on the mines. At the inaugural general meeting, a draft constitution was adopted. The first elected officials included A.J. Orenstein as Vice-President and Dr A.I. Girdwood of the WNLA as Secretary. From its inception, the Association was supported by the Chamber, with the WNLA and the NRC funding the publication of the monthly proceedings.²⁰

Apart from dealing with mine accidents and serious infections, the principal duties of a mine medical officer were to conduct entry, periodic and exit examinations. The Miners’ Phthisis Act of 1925 made the employment of full-time medical officers compulsory, thereby to a degree professionalising the service. Medical officers were to examine every black recruit and certify him free from tuberculosis and fit for employment. They would also carry out periodic and exit examinations.²¹ In his commemorative history of the MMOA, A.P. Cartwright notes that the health of the black mineworker became almost an obsession with the mining companies. A balanced diet and ‘the healthy lives’ they led while employed on the mines usually resulted in a weight gain and an improvement in their general health. ‘It is of importance to many of the African communities south of the Equator that so many of their men return to their villages after a sojourn in South Africa in far better physical condition than most of them were when they left home.’²²

Despite the Chamber’s claims about the excellence of medical care, the mines’ health service had its critics. The medical corps consisted of a small number of senior officers supported by a group of young graduates who used the mines as a stepping stone to a better career. In the period between 1929 and 1935, for example, 13 out of 34 medical officers resigned from the service.²³ The workloads were no doubt a factor: a full-time medical officer on a medium sized mine would be responsible for 6000 men.²⁴ The workloads of the five full-time physicians at the WNLA hospital were also onerous. In addition to responsibility for more than 250 hospital patients, each doctor examined between 300 and 1200 black miners a day.²⁵ The corps’ status was such that they were referred to by their Johannesburg colleagues by the derogatory term ‘Kaffir Doctors’.²⁶

The Miners’ Phthisis Commissions held between 1919 and 1952 routinely commented on the inadequacy of the medical examinations and the obstacles black miners faced regarding compensation. The 1919 Commission, for example, was highly critical of WNLA’s medical officers for making it difficult if not impossible for the relatives of a deceased miner to receive an award. Services for living miners were no better. The Commission found that medical examinations were poor. Often there was no exit medical as required under the Act, not even for seriously ill men who had spent months in hospital. Without a certificate, a miner could not lodge a claim for compensation.²⁷ The findings of the 1919 Commission were endorsed by the Young (1930), Stratford (1943), Allan (1950) and Beyers (1952) Commissions. They are also consistent with recent research by Jaine Roberts on former miners from the Eastern Cape. Among her cohort of 205 men, 85 per cent had not received an exit examination as required by law.²⁸

Despite their limitations, the medical care and state regulation of South African mines were unique. From 1912 the industry was subject to a swathe of legislation covering most aspects of work, compounds, rations and medical care. By contrast, there was little regulation of factories, and virtually none of farms or the domestic sector where large numbers of black women were employed. The work conditions were far worse on the coal and asbestos mines, and they were certainly hazardous in smaller industries, especially in factories with less than 500 employees. There, pre-employment and regular health examinations were rare, and post-employment examinations non-existent. The availability of large numbers of migrant workers made it cheaper for employers to replace injured men and women rather than make workplaces safer. That pattern continued well into the apartheid era. As recently as 1976, the Erasmus Commission found that over 70 per cent of South Africa’s eight million workers were inadequately covered by occupational health and safety legislation.²⁹ In 1983, just 81 inspectors were responsible for worker safety in more than 35,000 factories.³⁰

Dealing with Risk

High mortality rates and the prospect of a ban on tropical recruiting led to the Miners’ Phthisis Commissions of 1902, 1912 and 1914. Those enquiries were bolstered by the work of international experts contracted by the Chamber. In evaluating the industry’s response to the ban, it is important to identify how the evolving contemporary science viewed the risks associated with gold mining.

In March 1913, under pressure from London, the government in Pretoria barred the Chamber from further recruiting in the north. In order to regain access to Tropicals, the Chamber needed to reduce miners’ death rates and to convince the British and South African governments that the mines were relatively safe. To that end, it commissioned Sir Almroth Wright and Spencer Lister in a futile attempt to find a vaccine for pneumonia.³¹ The Chamber also turned to Major W.C. Gorgas, Surgeon-General in the US Army, who had achieved fame for his work on the Panama Canal. Gorgas arrived in Johannesburg in December 1913. His brief was to investigate the causes of the high mortality rates from pneumonia and to find a remedy.

W.C. Gorgas was a scrupulous researcher and his report on the ecology of the mines was the first of its kind. In fact, there was no comparable research until the eve of majority rule. Gorgas found that the fatalities from pneumonia varied between individual mines. They also varied according to the origin of labour. Most cases occurred during the first months of service. Fatalities were highest among miners from Nyasaland, and lowest in recruits from the Cape, suggesting that immunity was a factor. Gorgas was highly critical of the mine rations which were inadequate for men performing hard labour. ‘I have never seen so large a proportion of the ration supplied by one article as is here supplied by mealie meal’, Gorgas wrote.³² The compounds were crowded and full of litter and miners wore wet and soiled clothes. The bucket system of disposing of waste added to the unsanitary conditions.

Gorgas modelled his recommendations on his Panama experience, where the scattering of workers from crowded barracks into single huts dramatically reduced the death rate from infectious disease. ‘And for the sanitation of pneumonia I would urge a similar measure on the Rand. Place your negro labourers in individual buildings, and bring in and place with them their families.’ Married men would form a permanent, skilled and efficient workforce. Gorgas noted that while the industry was spending a million pounds a year on recruitment, the construction of family locations would save the greater part of that expense. By housing labour in huts and providing an adequate diet, Gorgas was confident that in a year or two, immunity to infection would be greatly increased.³³

The Gorgas report is also a landmark in knowledge about tuberculosis and its synergy with silicosis. Gorgas argues forcefully that pneumonia and tuberculosis on the mines were linked by the conditions which gave rise to them, namely malnutrition, overcrowding and poor hygiene. Transmission was usually by means of the expectorated sputa of diseased men which, once dried and airborne, could enter the lungs of co-workers. In addition, miners’ phthisis lowered a workman’s resistance to tuberculosis. There was a high rate of infection: during 1912, over 1100 tuberculosis cases were repatriated by the WNLA. The annual mortality rate of 5.65 per 1000, while lower than for pneumonia, was significant. In comparison, the mortality rate from tuberculosis among men, women and children in London in 1911 was 1.03 per 1000; in New York City it was 1.67 per 1000. Given these facts, Gorgas predicted that ‘for the future, present conditions continuing, tuberculosis will cause you more trouble among natives than does pneumonia at present’. As with pneumonia, the most important preventative measure was the replacement of the compound system.³⁴

Dr Darling, who assisted major Gorgas, carried out a number of post-mortems in Johannesburg. In each of one set of 11 consecutive post-mortems of miners diagnosed as succumbing to pneumonia, the underlying cause of death was found to be tuberculosis.³⁵ Importantly, Gorgas noted, most men with miners’ phthisis died from incidental tuberculosis implanted upon a silicotic lung, rather than from silicosis itself. To Gorgas, the hygiene of silicosis was obvious: that of laying the dust, so that the particles of silica will not be floated in the air where they could be breathed. Gorgas also wanted regular medical examinations and the exclusion of infected men from the mines.³⁶

In his report, Gorgas recommended two structural reforms. The first was an end to the migrant labour system under which single men lived in compounds. The system was, he believed, inefficient in its use of labour and came at a high human cost. Gorgas suggested miners become a permanent workforce and live with their families in village settlements adjacent to the mines. The second proposal was to centralise the mine hospitals into one or more large facilities to achieve economies of scale and service the industry as a whole. Neither recommendation was adopted, and pneumonia remained a serious problem. According to the official data, between 1933 and 1938, it accounted for between 29.65 and 37.87 per cent of deaths from disease among miners.³⁷

There were several reasons for the Chamber’s rejection of the Gorgas’ recommendations. A stabilised work force was anathema to employers as it would have required wages capable of supporting a family.³⁸ It also went against the entrenched government policy, fiercely supported by the white electorate, of preventing black urban settlement. Centralising the hospital system had the obvious advantage of reducing duplication and costs. As noted earlier, the industry achieved similar aims in successfully centralising and streamlining the recruiting system with the setting up of the WNLA in 1896, and the NRC in 1912. However, centralisation of the hospital system would have enabled the state to exercise greater control over mine medicine and to collect more accurate data on mortality and morbidity rates. It might also have resulted in men with tuberculosis or silicosis dying in Johannesburg rather than in distant rural areas.

Soon after the release of the Gorgas Report, the newly appointed Miners’ Phthisis Prevention Committee (MPPC) wrote to the Minister of Mines about what it viewed as a looming crisis. It was particularly concerned at the rate at which tuberculosis converted an otherwise early case of silicosis into a life-threatening disease which was killing large numbers of miners. The Committee’s grim warning came after the passing of the first Miners’ Phthisis Acts and coincided with the release of the Tuberculosis Commission Report in 1914. According to the MPPC, every precaution should be taken to ensure that infected men were not recruited, and that conditions be improved to reduce the spread of disease. The Committee recommended that all recruits rejected on the Rand because of tuberculosis should have their passes endorsed to that effect. They should be repatriated wherever possible, or otherwise assessed by a government medical officer with a view to their treatment. Compound bunks should be designed to allow for thorough cleansing and a steam steriliser should be available for each compound. The room from which a patient had been removed should be immediately disinfected.³⁹ Once a month every room should be emptied and hosed out, the bunks boiled and all clothing and bedding sterilised. All room fixtures should be sprayed with a disinfectant and lime-washed. Underground tanks for drinking water should be covered and periodically emptied and cleansed. Ladder ways and incline shafts, travelling ways and stations should be systematically disinfected at least once a month. The question of supplying change houses should be given careful consideration. That final recommendation was the only one of the MPPC’s suggestions that was acted upon.

The 1912 Tuberculosis Commission

The Tuberculosis Commission promised by Prime Minister Botha in August 1911 was appointed in February 1912. Its brief was to investigate the causes and prevalence of tuberculosis among all racial groups, and to report on the steps which the government should take to prevent the spread of disease. The Commission was also to identify the extent and causes of mortality in black goldminers and their susceptibility to pneumonia.⁴⁰ It was the first commission into tuberculosis, and it took evidence from more than 600 witnesses. Dr A. John Gregory, the Medical Officer of Health of the Cape Colony, was appointed Chairman. Dr Gregory was one of the first public health officers in South Africa to campaign for a national response to tuberculosis. Unlike those who usually chaired or served on such commissions, he had no allegiance to the mining industry.⁴¹ Gregory was assisted by four commissioners, two of them closely linked to the mining industry. Dr G.A. Turner was the WNLA’s Chief Medical Officer. Dr Charles Porter, the Medical Officer of Health for the Johannesburg Municipality, oversaw two inspectors on the mines and claimed to have had more experience than anybody else in regard to mine sanitation. In eight years, he had never made a prosecution. The commissioners struggled to reach consensus, both during the Commission’s sittings and in compiling its final report. Gregory twice resigned from the Commission on the grounds that Turner and Porter had in effect been asked to sit in judgement on their own work, only to be persuaded by the Minister to remain.⁴² In the end, Gregory submitted a minority Report, and the two commissioners he clashed with responded with a supplementary statement.

The Commission’s deliberations coincided with those of Gorgas. The industry had a great deal at stake in Gregory’s report. The ban on Tropical recruiting was putting upward pressure on wages by reducing the labour supply. Because more miners were recruited within South Africa, it also threatened to make the actual disease burden more visible. In its final report from 1914, the Gregory Commission considered at some length historic evidence about the incidence of tuberculosis in southern Africa. It concluded that, given its ancient origins, the disease was almost certainly brought to the region by Arab traders. Over the last few centuries, it was on occasions described by European travellers, but never became widespread. This changed in the last 25 years. Many observers reported that tuberculosis was almost unknown among black South Africans in the past but recently had quickly become a ‘most serious menace’ in the large industrial centres.⁴³ The black industrial population consisted mainly of fit young men; the weak and ailing remained in the villages. The mines were one of the major sources of infection. All African labourers were adversely affected by the change from village life to unhygienic and crowded mine compounds.⁴⁴ The inhalation of ‘silicous dust’ was particularly harmful in predisposing miners to tuberculosis and pneumonia.⁴⁵ Of all the different groups working on the mines, Tropical recruits were particularly vulnerable. Subjected to an ‘enormously increased risk’ of infection, their mortality was almost five times that of miners from Natal and Zululand.⁴⁶

When a miner became ill, he wanted to return home. As a result, the actual rates of sickness and mortality were hidden. The official annual mining death rates were confined to those men who died at the mines. A more accurate figure required adding those deaths which took place on the journey to the Rand, the deaths of men who waited to be allocated to individual mines or repatriated at the WNLA compound, and those of repatriated men who died before they reached home or soon after. As Gregory explained it with regard to statistics for the years 1910 to 1912, ‘it is evident that while the death-rate has been going down, the repatriation rate has been steadily going up faster than the mortality has been diminishing, so that the total rate of wastage from death and disease increased in 1912 by 13 per cent over what it was in 1910. This well illustrates the fallacy involved if the health of mine natives on the Rand is considered merely on the recorded mortality and without reference also to repatriations.’⁴⁷ In contrast, tuberculosis rates in the white population were very low. Apart from mining, very few Europeans were employed in phthisis-producing occupations.⁴⁸

Tuberculosis in blacks was notable for its rapid course, and for the frequency with which it was fatal. Of 524 deaths from the disease occurring on 22 gold mines taken at random, almost 20 per cent died within a week of admission to hospital. There was also evidence of widespread under-reporting. Dr G.A. Turner from the WNLA carried out post-mortems of 88 miners at the WNLA hospital where the recorded cause of death was silicosis; he found that 59 (or two-thirds) of the deceased also had tuberculosis.⁴⁹ None of the Commissioners, including Dr Turner, disputed the link between silica dust exposure and tuberculosis.

The Commission cited four reasons why black miners were so vulnerable to tuberculosis. The first was the absence of immunity acquired in early childhood, the second was living in unhygienic and overcrowded compounds, and continuous and excessive labour. The most potent factor was the inhalation of silica dust, which depressed the powers of resistance to the bacillus. The final element was the pattern of recruitment, which possibly interacted with a ‘tribal or racial proclivity to the disease’.⁵⁰ Local recruits worked on six-month contracts while Tropicals and East Coasters were typically recruited for 12 months, with most East Coasters returning again and again. The Commission found that repeated contracts were a factor in the production of silicosis, and therefore a ‘powerful predisposing cause of pulmonary tuberculosis’. Tropical recruits, who often suffered from a series of other diseases, were unsuited for mine work, and the Commission strongly recommended that the ban should remain, and ‘no further recruiting of Tropicals … be permitted unless and until the Government is fully satisfied that there is no reasonable likelihood of the recurrence of such mortality’.⁵¹

Gregory’s findings confirmed those of William Gorgas, who made similar recommendations. Any scheme for combating tuberculosis must be based on the discovery and isolation of cases, the care of patients, and the safeguarding of co-workers and families from infection. That in turn required the breaking up of large compound dormitories into rooms housing not more than six miners, and sanatoria.⁵² In his minority report, Dr Gregory recommended that a government Mines Board of Health take over the current uncoordinated, fragmented, overlapping and ineffective management of mine medicine and sanitary inspection. Its responsibilities would include conducting all medical examinations, reviewing ventilation, dust levels, sanitation both in the compounds and underground in the mines, compound conditions and rations. The Board would be funded by an annual levy on the industry and would have the power to appoint and remove mine medical officers and to initiate research.⁵³ Gregory’s proposal to shift control of mine medicine from industry to the state was the most radical recommendation made by a Commission. It was strongly opposed by two of his fellow commissioners and never repeated. None of Dr Gregory’s recommendations were acted upon and the practice of returning sick miners to their homes continued. The Commission findings were ignored by subsequent enquiries: A.J. Orenstein was scathing in his references to Gregory, whose report he termed ‘of no value whatsoever’.⁵⁴ Today the Commission’s Report is the only one of its kind not readily available in South African libraries. There are, for example, no copies at the Wits Medical Library or at the NIOH.⁵⁵

The Tuberculosis Research Committee

Evidence that tuberculosis was being spread from the mines continued to mount. In February 1920, the Minister of Mines asked Dr L.G. Irvine, the Acting Chairman of the Bureau, to review the Bureau’s operations. Irvine reported that during the previous five months, just under 1400 black miners had radiographic examinations at the Bureau. The number of cases of tuberculosis complicated by silicosis (297) was far greater than those with pure silicosis (78). ‘The data given do not, of course, represent the total incidence of Tuberculosis amongst Natives working upon the Scheduled Mines. They obviously do not include any cases which have died from that disease in the Mine Hospitals, which during 1918 amounted to not less than 170 per 100,000 per annum.’ The data was disturbing and, according to Irvine, reducing the tuberculosis rate was one of the major challenges facing the industry.⁵⁶

Dr Irvine’s concerns were shared by the Secretary for Public Health, Dr J.A. Mitchell, who in August 1922 directed a tuberculosis specialist, Dr Peter Allan, to begin the first study of tuberculosis and repatriated miners. Allan was asked to examine the extent of the disease, the level of resistance, what happened to infected men returning from the mines and the effect of repatriations on the general population. Mitchell was certain that the mines were spreading infection and he wanted a report within three months.⁵⁷ Allan visited several villages and towns in the Eastern Cape, including Libode, Umtata and Kingwilliamstown. In estimating the infection rate, he interviewed magistrates, district surgeons and mission stations. He also conducted a number of medicals. The NRC helped him to trace former miners. The records of the Umtata Hospital showed a high prevalence of tuberculosis, with around 10 per cent of all admitted patients suffering from the disease. According to Dr Drewe from the Holy Cross Mission, Flagstaff, infection was very common. In his interim report Allan commented: ‘Much more time is required to investigate to what extent the repatriated native infects other natives.’⁵⁸

Having received Allan’s interim report, Dr Mitchell convened an informal conference to discuss tuberculosis. Held at the end of October 1922, it included the Director of Native Labour from the WNLA, Dr Girdwood; Dr A. J. Orenstein representing the MMOA; Dr Peter Allan; and the Director of the Bureau and the SAIMR, Dr Watkins-Pitchford. Dr Mitchell was in the chair. Mitchell told the delegates that when he first called the conference, it had been suggested that he had done so in response to Dr Orenstein’s recent remarks accusing the government of doing nothing about tuberculosis. According to Mitchell, the government realised the importance of tuberculosis among miners and would cooperate with the industry to improve the situation. Mr Whitehead, representing the Native Affairs Department, promised to fully cooperate while Mr Villiers, General Manager of the NRC, said that his organisation had already instructed its agents to keep an eye on men returning from the mines.

Dr Orenstein repeated his accusation that the government had done nothing to prevent the spread of disease. While Dr Allan’s study was valuable, it was still unknown how the disease was acquired.⁵⁹ The MMOA had given the matter considerable attention but nothing could be done unless the necessary research was funded. Even if it cost £50,000 it would be money well spent as the very existence of the mines depended upon the labour supply. The meeting agreed it was important to understand where infection occurred, how many men developed tuberculosis on the mines and how many brought the disease with them. A month later, Dr Peter Allan attended a meeting of the Mine Medical Officers’ Association in Johannesburg. With Dr Orenstein in the chair, Allan asked the meeting for estimates of how many men were repatriated with ‘open’ tuberculosis and how many had positive sputum? Dr Girdwood of the WNLA replied that there was no data but from the cases he examined the proportion of ‘open’ cases was high.⁶⁰

Allan soon found that there were no statistics on death and disease for the Transkei, so that information had to be obtained from medical practitioners. The records of the Umtata Hospital showed that tuberculosis was prevalent. Tuberculosis or sifubu had been present for at least 40 years and it was more common than formerly, with many children suffering from chest complaints. The NRC provided Allan with a list of men who had been compensated and then repatriated. Of the 112 miners Allan traced, half had died within a year and another 15 per cent within two years. Of the 47 cases who were still alive, only 28 had recovered sufficiently to work. It appeared that in the Transkei tuberculosis was common apart from infection brought from the mines. At the Holy Cross Mission, for example, only 10 per cent out of a consecutive sequence of 42 admissions may have been infected on the mines. Allan concluded that without extensive examinations and diagnostic tests, it was difficult to determine the extent to which infection in the general population came from returning miners.⁶¹ It was certain, however, that the danger of spreading infection was greatest with patients in whom the disease was advanced. The removal of such cases to a hospital was essential and wherever possible, Tuberculosis Dispensaries should be established.⁶²

Dr Allan submitted his final report to Mitchell in 1924. The main themes were the paucity of morbidity and mortality data, and patients’ lack of access to biomedical care. The report is notable, however, for its omissions. Allan does not mention exposure to silica dust, the synergy between silicosis and tuberculosis, the spread of infection in the mine compounds, the NRC’s repatriation policies or the declining living standards and malnutrition in the Reserves. Every one of those factors had featured in Gregory’s 1914 report.

Allan’s survey led to the creation of the Tuberculosis Research Committee (TRC) in 1925. The Chamber agreed to fund an international expert to guide the Committee’s research. Dr Lyle Cummins, famous for his theory of virgin soil infection, which explained high mortality rates in Africans by reference to their racial deficits, was appointed.⁶³ Dr Mitchell was concerned that Cummins would sandwich the work between visits to game parks and he preferred they ‘get somebody else’.⁶⁴ The TRC members included Dr L.G. Irvine as the Department of Mines representative; Mr H.M. Taberer, Native Labour Adviser to the Chamber; Dr Mavrogordato from the SAIMR; Dr Watkins-Pitchford, Director of the Bureau; Orenstein and Mitchell. The TRC was conflict ridden and there was a battle over jurisdiction between the Departments of Public Health and of Mines. J.A. Mitchell was highly critical of the gold mines. Writing in December 1922, he told his counterpart that the main cause of the spread of tuberculosis was the mines. He wanted the Department of Mines to pay the cost of investigating and treating the disease in miners and their families.⁶⁵

On his part, Orenstein insisted that he knew a great deal about the work and living conditions of migrant workers, and he was certain that the mines bore no responsibility for the spread of tuberculosis; a view which put him at odds with the Departments of Public Health and Native Affairs. Lyle Cummins was sure that silica dust played a major role in the tuberculosis rate and he wanted that question investigated. The only issue on which the Committee agreed was the urgent need for research. However, it took almost ten years before a report was completed.

Lyle Cummins, who attended the July meeting of the TRC in 1927, noted that among white miners, about 97 per cent of pulmonary tuberculosis cases were chronic or ‘secondary’, and only about 3 per cent acute or ‘primary’. In the case of black miners those figures were reversed. The Committee agreed that insufficient systematic work had been done to offer an explanation. Cummins then raised two adjacent questions: ‘Assuming that tuberculosis is an environmental disease, is mining on the Witwatersrand a phthisis-producing industry because conditions favour the lighting up of old foci, or because they render possible infections from without that would not occur apart from such conditions?’ To find an answer, Cummins suggested a study comparing the prevalence of tuberculosis in villages that were directly associated with the scheduled mines and villages which were not. There should also be a follow up of open-tuberculosis ‘repats’ and their families. Such an enquiry should explain whether miners were spreading tuberculosis and whether a high prevalence was peculiar to the scheduled mines.⁶⁶

Cummins believed it essential to compare the phthisis incidence and mortality and the ratio of tuberculous ‘repats’ to ‘deaths’ between Africans working in the gold mines and those working under the less strenuous and less dusty conditions in the coal and diamond mines. Such comparisons should take account of the length of time worked before phthisis developed. It was necessary to obtain a series of post-mortems of men killed in mine accidents to estimate the extent to which focal infections were present in healthy recruits. In rural areas, the disease seemed to take a more benign course. If the clinical types were found to be more severe on the Rand, that would suggest that, in addition to native susceptibility, some factor of aggravation existed on the mines. That factor might be exposure to silica dust or in repeated exogenous re-infection, either in the mines or in the compounds. Those factors (which are still highly relevant today), required careful investigation.

Mavrogordato agreed with Cummins that gold mining was a phthisis-producing industry. He wanted the tuberculosis incidence and mortality on the Rand compared with that of phthisis-producing industries in Great Britain, rather than with that of the general African population. In such industries in Great Britain, the average age of mortality was in late middle-age and old age, the tuberculous process being, as it were, superposed on a silicotic fibrosis. In black miners, in contrast, death or disease from tuberculosis was common in young adults and occurred before silicosis had become marked. Cummins wondered if the cause was silica dust inhaled over a relatively short period: ‘The question of the part played by silica dust in the tuberculosis of natives is of fundamental importance and every effort must be made to solve it.’⁶⁷

Cummins noted a contrast between the tuberculosis in the mine hospitals and that seen in the Transkei. In Johannesburg, the disease took an acute and generalised form characteristic of recent exogenous infection: in the Transkei tuberculosis was of the ‘modified’ type found in communities where infection had been present for some time.⁶⁸ During his visit to the Transkei, Cummins discussed that problem with district surgeons and medical missionaries, including Dr Macvicar. All were sure that the disease was widespread and that chronic cases were becoming more common. ‘It is undeniable, however, that many cases of “open” tuberculosis are repatriated [from the mines] every year and such cases are necessarily a risk to others.’ Cummins presented two research priorities. The first was to identify and remove carriers; the second was to conduct experiments in the prevention of tuberculosis on the mines. In the case of those repatriated, data on the period of survival might be collected by the NRC.⁶⁹

Lyle Cummins’ presentations to the Committee must have surprised Orenstein and Mitchell. The Chamber wanted Cummins as its international expert because of his virgin soil thesis, which attributed Africans’ high mortality rates to their lesser civilisation. Having viewed the evidence, Cummins abandoned that thesis in favour of dust as the causative factor. Cummins identified several sophisticated avenues for research, none of which were subsequently taken up by the Committee. Indeed, his views about dust exposure were completely erased from the Committee’s final report.

Orenstein was the only member of the Committee who denied outright that there was a major tuberculosis problem on the mines. He argued that over the previous 11 years, the average annual tuberculosis mortality rate was approximately 1.2 per 1000, resulting in 240 deaths per annum. He admitted that, in addition, a certain number ultimately died at home.⁷⁰ Orenstein was arguably the best-informed member of the Committee about tuberculosis in black miners. He was certainly the most experienced and, unlike the other members of the Committee, had access to two recently completed surveys of long-service miners. While the Committee was sitting, Dr Girdwood reported to the GPC, which Orenstein chaired, that the radioscopic examination of approximately 1800 long-service miners at the WNLA Compound had revealed around 8 per cent were suffering from tuberculosis. In an expanded study of 2023 long-service miners, half of whom were surface workers, Dr Girdwood found definite tuberculosis in 66 men and probable tuberculosis in another 59. In all, 18 per cent of the subjects had evidence of chest abnormalities.⁷¹ If those results were representative, there were thousands of carriers working underground. The situation was grave, and the Health Committee of the League of Nations offered to assist the Chamber with a further investigation.⁷²

The ILO co-sponsored the 1930 Silicosis Conference in Johannesburg in the hope of promoting workplace reform. In contrast, the Chamber viewed the Conference as a stage on which to convince the South African and British governments to lift the ban on Tropical labour. The Chamber invested heavily in persuading an international audience of experts that the mines were safe. Three years later, the ban was provisionally lifted.⁷³ In 1932, the final outcome of the TRC deliberations was published under the title Tuberculosis in South African Natives. Much of the report was written by Orenstein. It found that blacks were heavily tubercularised and that they would soon develop immunity like whites.⁷⁴ Dr B.A. Dormer, one of the leading specialists on tuberculosis, was unimpressed by the report and blamed Cummins. ‘This theory of racial susceptibility in primitive people was, to use modern parlance, sold to the Committee by Professor Lyle Cummins, who was its expert adviser.’⁷⁵ Like the Chamber, Dormer had expected Cummins to reprise his virgin soil thesis and therefore blamed him for what he saw as sloppy science.⁷⁶

Conclusion

The Commissions and allied investigations carried out from 1902 until the SAIMR’s report of 1932 all reached the same conclusions. Dust exposure was a major hazard, as was tuberculosis for migrant labour. The causes of lung disease were environmental rather than racial and therefore could only be reduced by major investment in work and living conditions, and not by the ‘seasoning of labour’. The ban should remain until the risks associated with silica dust had been removed. Gorgas and Cummins, who were recruited by the Chamber because of their status as world authorities, both identified silica dust exposure as a major hazard for migrant labour. Their recommendations were consistent with the then-ruling medical orthodoxy in Britain, the United States and Australia, as well as with findings of the South African Commissions of 1902, 1912 and 1914. And yet, until the advent of majority rule, these findings were obscured by the Chamber’s orthodoxy regarding mine safety.