Occupational Lead Poisoning in Battery Workers: the Failure to Apply the Precautionary Principle

Beris Penrose

Labour historians are now beginning to explore the history of occupational health and safety and its impact on workers and the community. An examination of past approaches to protecting workers' health can inform current debates over such things as the relevance of the Precautionary Principle advocated by those who seek to remove from the workplace substances suspected of being harmful. In the United States from the 1920s–60s the employer body, the Lead Industries Association, funded much of the research into occupational lead poisoning. The results, which rejected the Precautionary Principle, understated the adverse effects of lead and placed workers' lives in jeopardy. The politicisation of medical knowledge in the United States had a global impact that has not yet been fully examined. This article explores the influence of American research on the Australian medical community's approach to occupational lead poisoning in the early twentieth century, with particular reference to the battery industry.
Introduction
Jacqueline Corn, in her history of occupational health hazards in the United States, maintains that health and safety decisions have two components — value and science. Value refers to the amount of money society is willing to spend on protecting workers' health while science refers to the available scientific knowledge on which occupational health policies are based.1 Space does not permit a discussion of Corn's value component which implies all sections of society arrive at a consensus on what is an 'acceptable' level of occupational ill health to be borne by workers. It is Corn's second element — the available scientific knowledge — that is relevant here as she argues that the high incidence of occupational lead poisoning in early twentieth century America can be attributed to the absence of a scientific understanding of lead's adverse effects. She states that the scientific studies and surveys from which the medical description and definition of the lead hazard derived 'had not yet taken place'.2	1
Yet by the early years of the century the battery manufacturing industry (called the electric accumulator industry in Britain and the storage battery industry in the United States) was known to be dangerous. Between 1889 and 1904 factory inspectors in Germany, Britain and France identified it as hazardous after numerous workers contracted occupational lead poisoning — a situation corroborated in the American industry in 1914.3 This raises a fundamental issue on protecting workers' health — at what point does society have enough scientific or medical knowledge on the toxicity of a substance to remove it from the workplace.	2
One perspective insists on conclusive scientific proof of the causal relationship between particular toxins and ill health before action can be taken. This approach has been summed up by Jerome Nriagu as the 'Show Me the Data' paradigm. Fundamentally, after workers have been exposed to untested or incompletely tested toxins employers and governments have demanded conclusive proof of these substances' toxicity before removing them from the workplace. Any uncertainty arising from studies into the toxins has set in motion more studies, generating a constant stream of data but not necessarily conclusive proof. Nriagu calls this the cascading uncertainty principle. He explains that in a 'world of imperfect knowledge, especially if the industry controlled most of the information, it would always be easy to find uncertainty in any study'.4 Sanford Lewis terms it 'smokescreen uncertainty' to differentiate it from genuine scientific uncertainty. Lewis points to recent corporate response to hazards such as lead, asbestos and tobacco where smokescreen uncertainty was created through concealing knowledge, hiring scientists to create contrary opinions, developing 'independent' research organizations whose findings appeared impartial and by manipulating public relations, all to 'create an atmosphere of uncertainty and a "consensus" need for more study before action is taken'.5	3
In contrast, the Precautionary Principle, first proposed by German conservationists and now adopted as an environmental guideline by the United Nations and the European Union, maintains:6	4
When an activity raises threats of harm to human health or the environment, precautionary measures should be taken even if some cause and effect relationships are not fully established scientifically.7
Absence of conclusive scientific proof of a substance's toxicity is, therefore, no justification for failing to take decisive measures to protect health.	5
These opposing views draw attention to the vital question of scientific impartiality. Corn acknowledges the interplay between science and politics, nonetheless, she depicts science as a value-free body of knowledge developing along a linear process as new insights and discoveries based on objective and testable observations build upon accumulated wisdom. This view does not withstand rigorous scrutiny and has increasingly been challenged by social constructionists who see scientific knowledge as a product of its social context, reflecting the ideological, social and economic power relations within society.8 Scholarship into the history of occupational hazards such as synthetic dyes, asbestos, silica, radioactive paint and Weil's disease confirm that science has frequently been subordinated to corporate and economic interests, that adverse health effects of occupational hazards have at times been minimised or suppressed and that the partisanship of investigating scientists has sometimes been under question.9	6
Occupational lead poisoning also falls within this category. The most influential scientific studies on the effects of lead on the human body were conducted in the United States, the world's largest lead producer, and were funded principally by the Lead Industries Association from the 1920s–60s.10 This employer-sponsored research, which understated lead's adverse effects, had a profound impact on the medical profession globally, setting the parameters within which decisions on diagnosis, treatment and prevention of lead poisoning were based; decisions that ultimately failed to protect workers' health.	7
By looking at the battery manufacturing industry that, by the 1930s, was poisoning great numbers of workers in many countries11 this article shows, first, that had the Precautionary Principle been adopted when it first became apparent that the work process was dangerous numerous deaths and illnesses could have been prevented. Second, that the politicisation of medical knowledge in the United States impacted on the Australian medical community to the detriment of workers' health.	8
Lead Poisoning in the Early American Battery Industry
At the beginning of the twentieth century the United States had a poor record on workplace injuries, illnesses and deaths and lagged behind Europe in industrial hygiene and workers' compensation legislation.12 In response to this a broad-based movement grew from 1908–14, demanding safer, healthier workplaces and compensation for industrial injuries and death.13 During this period the first studies into occupational lead exposure were carried out and revealed that the American battery industry was renowned for low wages, long shifts, a high labour turnover, almost non-existent industrial hygiene measures and a rate of lead poisoning far above that found in European battery workers. Workers were exposed to lead dust or fumes at every step of the work process which involved casting and moulding lead grids or plates; trimming them; mixing lead oxides into a paste and applying this to the plates; and drying, forming, assembling and finishing the batteries.14	9
A review of 60 deaths from occupational lead poisoning in New York State in 1909–10 revealed that two were young migrant men from the same battery plant employed sawing and handling the lead plates. The plant was so dangerous a nearby doctor had treated both acute and chronic cases of lead poisoning more or less weekly over the preceding eight years; workers usually exhibited symptoms within 30 days of employment.15 The deliberate exploitation of inexperienced migrant workers, including children, for some of the most dangerous work, characterised the early years of the industry.16 Most at risk were eastern European, Italian and Greek workers. Many of whom left the industry after contracting lead poisoning and were replaced by new migrants, generating ever increasing numbers of workers with varying amounts of lead permanently stored in their bodies.17 Some employers deliberately hired workers for only short periods before symptoms of lead poisoning would become evident. Few safety measures were taken to protect these workers. As Alice Hamilton, a physician and pioneer in occupational health who conducted the first investigation into the battery industry in 1914, explained, 'one can hardly expect a foreman to show much solicitude for a gang of Poles or Italians whom he expects to lose in a few weeks' time'.18	10
No accurate statistics on the extent of lead poisoning were kept largely because of the high turnover but also because lead poisoning was not notifiable in every state.19 Where it was, some doctors were casual about submitting reports while others reported only severe cases. Collating statistics from death certificates was also problematic as workers dying from diseases caused by lead poisoning, such as renal, cardiac or neurological disorders, often had these, rather than lead poisoning, registered as the cause of death. Yet, from her study of the industry in 1914 Hamilton estimated that almost 18 per cent of American battery workers had lead poisoning. This compared with a rate of three per cent in the British battery industry and one per cent in Germany's largest battery plant.20	11
The most dangerous jobs were mixing and pasting the lead oxides, which were often applied to the lead plates by hand. Hamilton described the process where mixing was carried out at one end of the pasting room:	12
There is no exhaust over scales or mixer and the litharge or red lead is simply scooped up from the kegs and dropped into the scales, which are then emptied into the mixer. At the time this place was visited a workman was engaged in mixing oxides, and clouds of yellow dust were perceptible.21
Mixers and pasters were usually paid piece rates, ensuring a rapid work pace. That, along with shifts of nine or ten hours, guaranteed prolonged exposure to lead dust and fumes.22 Remuneration for this work was low. In 1914 pasters in Ohio received from $1.90 to $3.50 per day; a large plant in Philadelphia, where the pasters were 'all, or almost all, foreigners' paid $14–18 per week; while some New York City plants paid from $12–15 per week. Mixers in the Philadelphia plant were paid $9 per week for hand mixing lead oxide into paste.23 At the time the combined average weekly wage of office and factory workers in New York State was estimated at $12.85. So although some pasters received slightly more than the average wage this did not make up for the financial cost of lead poisoning, estimated to be $15–$25 in medical bills and about $45 in lost wages in the early stages of each bout.24 Nor did it compensate for the long-term cost of poor health and a shortened life.	13
Hamilton proposed reducing lead poisoning by abolishing low wages, long shifts and high labour turnover and by implementing safety measures to protect workers from lead dust and fumes.25 In an earlier study of the pottery trade she found that organised workers were less likely to develop lead poisoning than unorganised ones. In East Liverpool and Trenton, New Jersey, organised male potters had a lower incidence of lead poisoning than 'unorganized, underpaid, poorly housed, poorly fed' female potters who were 'subject to the worry and strain of supporting dependents on low wages'. Hamilton highlighted industrial relations rather than women's greater susceptibility to lead — a popular belief at the time — as the main cause of their higher rates of lead poisoning. She contrasted these New Jersey potters with fellow workers in Zanesville, Ohio, employed in tile and art pottery. Here both women and men were unorganised and their rates of lead poisoning were equally high.26	14
However, Hamilton's study came at a crucial moment in American medical and labour history. By 1914 more and more states had introduced workers' compensation acts and the demand for safety engineers and company doctors grew as employers tried to moderate the economic effects of the new legislation. Medical interest in occupational health expanded as the new legislation shifted the focus of employer/employee disputes away from who was at fault for an injury, to disputes over the medical definition and degree of occupational disability. Anthony Bale notes that doctors became the 'gatekeepers' for 'rationing benefits'.27 A new medical audience was created for occupational health. Whereas Hamilton addressed her studies to employers, employees, physicians and lay people, occupational health studies from the mid-1920s almost exclusively addressed a medical audience.28	15
As the broad-based movement for improvements in the workplace dissipated around the time of World War I the employer-sponsored National Safety Council came to dominate health and safety.29 Aided by an employer offensive in the 1920s that resulted in a massive decline of trade union membership, the rise of open shops and the supremacy of managerial prerogative over most workplace affairs, the Council promoted the hegemony of technicians, engineers and medical officers in occupational health.30 In this atmosphere it was not unusual to hear employers declare that lead poisoning could only be prevented by the producer, safety engineer and physician.31 Workers and unions had become marginalised and were given no role in protecting workers from lead exposure.	16
The National Safety Council identified workers' carelessness, laziness or poor personal hygiene as a major cause of occupational lead poisoning. Although migrants were given the most dangerous jobs in the lead trades, one commentator declared that this 'class of Eastern European peasant lacks the intelligence and initiative either to avoid the ordinary dangers of rough labor or to keep in efficient health'.32 Consequently, the Safety First movement sponsored by the National Safety Council promoted worker education programs, exonerating employers who exposed workers to a known poison and enforced long shifts, low wages and a frenzied work pace — all of which increased the chances of contracting lead poisoning. In an industry that annually poisoned countless numbers, it was the worker who was portrayed as a threat. Those with lead in their bodies from past occupational exposure were declared a 'potential risk' to employers who would bare the cost of future bouts of lead poisoning through compensation payments.33 The audience for Hamilton's appeals for improvements in industrial relations in combination with effective industrial hygiene measures had declined and continued to do so, particularly following changes in the philosophy and practice of medical inquiry into occupational diseases and a significant victory by the lead industry over public health in 1925.	17
First, an examination of the tetraethyl lead scandal is necessary. Between September 1923 and February 1925 at least 17 workers died and another 125 were hospitalised when manufacturing tetraethyl lead at the New Jersey plants of Standard Oil and DuPont Corporation, and the Ohio research plant of General Motors.34 In 1922 tetraethyl lead, a known poison, was first added to petrol to allow it to burn evenly and reduce the 'knock' in General Motors most recently developed high-compression, high-piwered motor that gave it a competitive advantage over its main rival, the Ford Motor Company. The public outcry over the workplace deaths and illnesses compelled General Motors to fund a study by the United States Bureau of Mines on the understanding that the Ethyl Gasoline Corporation — a joint venture of General Motors, Standard Oil of New Jersey and DuPont — would receive the results before publication for 'comment, criticism, and approval'. The Bureau of Mines' study was favourable to tetraethyl lead but disquiet within public and occupational health circles over the study's objectivity and reliability forced the United States Public Health Service to call a conference on 20 May 1925 to discuss the chemical's potential health effects.35	18
Proponents of tetraethyl lead blamed worker-carelessness for the deaths and illnesses and urged critics like Alice Hamilton and the American Federation of Labor to appreciate the chemical's centrality to America's industrial progress. Frank Howard of the Ethyl Gasoline Corporation, raising the issue of uncertainty in the scientific studies, asked if it was appropriate to abandon tetraethyl lead because 'some animals die and some do not die in some experiments'. From this conference came a further study, described as 'short-term, and in retrospect very limited', on the amount of lead in exhaust fumes that garage workers, petrol station attendants and chauffeurs in two cities were exposed to. The study, by Public Health Service under the direction of J.P. Leake, concluded that there were 'no good grounds for prohibiting the use of ethyl gasoline'. This was the last government study into the issue. Robert Kehoe, medical director of the Ethyl Gasoline Corporation, performed all subsequent investigations into tetraethyl lead.36 By the 1960s Kehoe boasted that 'in developing information on [tetraethyl lead], I have had a greater responsibility than any other person in this country'.37	19
According to Leake, industry funding of studies was appropriate as it 'was not felt justifiable that public funds should be again expended in such an elaborate study as that of 1925'.38 When Britain debated the introduction of leaded petrol in 1928 Leake testified to its safety before the Ministry of Health's investigating committee, as did A. Maxwell, vice-president and sales manager of the Ethyl Gasoline Corporation. Graham Edgar, the company's director of research offered the committee access to its technical personnel particularly Kehoe who had quickly become America's leading medical researcher into lead.39 Christian Warren believes the 1925 Public Health Service conference marked a turning point as Hamilton's leadership in the field of occupational lead poisoning from 1910 to 1920 gave way to Kehoe's.40	20
The growing prestige of the medical profession in the opening decades of twentieth century had produced a sea change where scientific inquiry based on laboratory work into the effects of lead supplanted studies like Hamilton's which observed workplace conditions, investigated work processes and interviewed employers and employees. Joseph Aub, a scientist at Harvard — the leading academic centre for research on industrial hygiene by the mid-1920s — stated that preventing lead's harmful effects was contingent upon understanding its action in the human body.41 This replicated a broader trend in the history of scientific medicine described by Vicente Navarro as a shift from macrocausality to microcausality; from focusing on the power relations of society to locate the cause of diseases to laboratory investigation into micro-organisms.42 The Harvard investigators, in seeking industry funding for their research, were highly critical of earlier American and European lead studies, believing they were politically motivated and their science untrustworthy. Aub, whose research was in part supported by the Lead Industries Association and its predecessor the Lead Institute,43 condemned the International Labour Organization's report on lead paint as biased because it called for its prohibition.44 Eventually Hamilton, Aub's co-worker at Harvard, found herself 'relegated to a second-class scientific status among her academic colleagues'.45 Yet, a scientific understanding of lead's effects on the body, while necessary, was not central to preventing lead poisoning. Eliminating occupational exposure to lead dust and fumes was. Moreover, much of the science from the late-1920s, funded by the Lead Industries Association, was flawed as will be shown.	21
Politicisation of Medical Knowledge
The Kettering Laboratory of Applied Physiology was founded by General Motors executive Charles Kettering who helped develop tetraethyl lead, and was funded by the Ethyl Gasoline Corporation and DuPont. Its first director was Robert Kehoe. The institution served as a vital link on lead research between industry and the academic community.46 William Graebner states that although industry 'engineered the development, dissemination, and perception of knowledge concerning the lead hazard' through the Kettering Laboratory, seemingly independent organisations like the American Public Health Association and the American Medical Association 'digested that science and attested to its worthiness'.47	22
One of the key arguments put forward by Kehoe was that lead in the body was normal after finding it in apparently unexposed villagers outside Mexico City.48 This was not a new concept. In fact, Leake's committee opposed prohibition of leaded petrol because 'as much lead was found in the excreta of persons who had no exposure to ethyl gasoline as was found in that of those who had'.49 Subsequently, wherever investigators looked they found lead; its ubiquity was used to confirm Kehoe's proposition. For instance, a Commonwealth Department of Health study of Broken Hill lead miners and Port Pirie lead smelter workers found that medical students, residents of Broken Hill not employed at the mines and workers at the Commonwealth Health Laboratory three-quarters of a mile from the Port Pirie smelters, had lead in their bodies.50 Other studies found lead in residents of Sydney, London, Manchester and Glasgow.51 Britain's final report approving tetraethyl lead in 1929 found lead in the urine of Londoners 'of the same order as that found by American and Australian investigators'.52	23
Only a minority of medical researchers believed this to be detrimental to health.53 In 1932 C. Myers of New York warned that cities were being blanketed in lead from car exhausts and that the 'harmlessness of the anti-knock gases will need modification as time goes on'.54 This would not happen until the 1960s and would require a determined fight against proponents of tetraethyl lead, like Kehoe. Myers was aware that lead contaminated much of the environment, not only from car exhausts and batteries, but from factory and smelter emissions; from the widespread use of the pesticide, lead arsenate; from lead paint in homes, factories, offices, public buildings, and on furnishings and toys; and from lead pipes in plumbing.55	24
In fact, the rural Mexicans in Kehoe's study were exposed to lead through pottery glazes.56 The five medical students in the Broken Hill study, apart from their general exposure to environmental lead, probably ingested it from the hospital food, which on one day contained 1.14 mg of lead per 926 g of food.57 Some of the unexposed Broken Hill residents could have ingested lead from their drinking water.58 As far back as 1916 it was reported that cattle grazing near the mines 'died from lead poisoning, fowls could not be reared, and in one instance a child died after sucking flowers contaminated with lead dust'.59 Workers at Port Pirie's Commonwealth Health Laboratory, it was stated, were 'not exposed to lead except in the forms of dust from the wharf, half a mile away and fumes from the smelter three-quarters of a mile away'.60 Yet, these findings were not considered significant enough to invalidate the hypothesis that lead was a normal element in the body.	25
Kehoe also argued that humans kept a natural equilibrium by excreting most of the absorbed lead. Therefore, lead in urine, faeces or body tissues was not indicative of poisoning. Diagnosis relied on proof of a significant occupational exposure in conjunction with acute, debilitating symptoms.61 The condition where lead had entered the body but had not yet caused acute symptoms, was defined as lead absorption.62 Although the distinction between poisoning and absorption had been used before Kehoe's research, it soon became universal and virtually unchallenged. By 1943 the American Public Health Association of which Kehoe was a member advised that 'certain levels of occupational lead exposure and absorption are compatible with normal healthy existence' and any ill effects 'are so tenuous and vague as to be purely speculative in character'.63	26
Absorption, in the absence of acute symptoms, became inconsequential. Ludwig Teleky, a former Austrian factory inspector forced to flee the Nazis in the late 1930s, had fought vigorously for the prohibition of lead paint in the 1920s as the only means of protecting painters from lead poisoning.64 Yet by 1940 he stated that lead absorption was 'of very little importance'.65 Secretary of the Lead Industries Association Felix Wormser proclaimed in 1947 there were two schools of thought on lead:	27
School A feels that inasmuch as lead is a cumulative poison — a word which needs careful defining — the effects on the body are ultimately disastrous no matter how small the amount ingested. On the other hand, school B refuses to accept this theory without scientific confirmation and is constantly accumulating data to disprove it.66
Robert Kehoe and Joseph Aub were proponents of School B. School A represented a minority position until the mid-1960s when the scientific community began to question the notion that lead workers could be either 'perfectly healthy' or 'classically intoxicated', and nothing else.67	28
It soon became a cliché that workers would have no health problems as long as a balance between absorption and elimination was maintained. The role of industrial hygienists was to preserve that balance through respirators, exhaust fans and adequate ventilation and the role of company medical departments was to purge the workforce of 'susceptible' workers who contracted lead poisoning despite these measures. Age, sex and race were the three main categories of susceptibility, with young workers, women and non-'whites' being deemed most at risk. But, there was also the category of individual susceptibility. In 1919 Hamilton had raised doubts about race susceptibility, stating that not only had this 'never been confirmed' but African American and white workers rarely performed the same tasks. Therefore, their exposure to lead dust and fumes was not comparable. In the white lead industry, for instance, only 15 per cent of employees were African American and they were usually employed in the more dangerous jobs, which explained their higher incidence of lead poisoning.68	29
Although several studies were done on battery workers in the 1920s and 1930s, none assessed the validity of the susceptibility theory. Only one, a Public Health Service study commissioned by the National Battery Manufacturers Association, even reported workers' ethnic or racial backgrounds. It revealed that in the mixing room of the plant surveyed 90 per cent of workers were African American, seven per cent were white and 2.4 per cent were migrants. The average monthly lead poisoning rate in these workers was 44 per cent. In the pasting room where the average monthly lead poisoning rate was 12 per cent, 48 per cent of workers were migrants, 26 per cent African American and 26 per cent white. In the lead burning areas where the average monthly rate was 4.4 per cent, 60 per cent of workers were migrants, 40 per cent white and none were African American. In the casting room where the average monthly rate was 0.18 per cent, 53 per cent of workers were migrants, 47 per cent were white and none were African American.69 Clearly, African Americans were employed in the most dangerous processes. Yet, no researcher questioned the notion of race susceptibility. In fact, it became so incontrovertible that in 1927 Hamilton recommended excluding African Americans from the battery industry because of their susceptibility and wondered if Filipinos 'who are entering this industry very rapidly will prove to resemble Negroes or white men in their susceptibility to lead'.70	30
The theory gave weight to calls for pre-employment medical examinations to eliminate 'predisposed' workers.71 This not only bolstered the role of medical experts in occupational health and safety, but also entrenched the notion that workers were to blame for lead poisoning. Elston Belknap, associate professor of medicine at Marquette University, Milwaukee, and consultant to Globe-Union Battery Company, advised employers to hire only workers of 'excellent physical quality'.72 The medical director of United States Refining Company at Carteret, New Jersey, excluded 'susceptible' people such as African American, Spanish, Turkish, Portuguese, Arab and southern Italian workers.73 DuPont's medical director hired only healthy men aged 21–45 years and excluded workers whose 'appearance indicates chronic slovenliness', or the 'wise guy' who 'will invariably fail to follow instructions and often take keen delight in disobeying them', as well as those 'afraid of lead work'. The latter were 'very liable to be constantly presenting subjective symptoms with no objective findings, and soon become a problem to the [medical] examiner'.74 Only healthy workers were hired because battery employers could not be expected to 'shoulder the responsibility of labor material already loaded with lead', according to Belknap.75	31
However, even the most scrupulous elimination of 'susceptible' workers failed to prevent lead poisoning. In 1931 the doctor at a new battery plant in New Jersey carefully scrutinised prospective employees, generally rejecting migrants, and conducted frequent physical examinations of employees to detect early cases of lead poisoning. Yet, shortly after production started a large number of workers became acutely ill with lead poisoning.76 The fact remained that lead emissions were not eliminated, battery workers were constantly exposed to a well-known toxin and the medical definition of lead poisoning allowed for the routine contamination of workers as long as they did not exhibit acute symptoms. Because of this battery manufacturing remained one of the most important sources of lead poisoning in the United States and workers viewed battery work as a 'last chance job' even during the 1930s depression.77 High labour turnover throughout the 1920s, 1930s and 1940s ensured unrecognised, undiagnosed, unreported and uncompensated cases of lead poisoning were turned out by the industry.78	32
The medical distinction between poisoning and absorption helped establish the legal division between the compensable disease of lead poisoning and the non-compensable condition of lead absorption. In the early years of the twentieth century social reformers anticipated that the financial cost placed on industry through workers' compensation would promote greater attention to occupational health and safety.79 They failed to predict legislative timidity that saw only 11 states cover lead poisoning, the most common industrial disease, by 1932;80 the exemption of small plants from compensation;81 the manipulation of the system by some employers who signed up battery workers as independent contractors not covered by compensation;82 or battery employers who preferred to pay workers' compensation and medical bills rather than install safety equipment.83 Workers who overcame numerous hurdles to receive compensation still assumed three-fourths to four-fifths of the financial cost of lead poisoning even under the most liberal laws.84	33
Nonetheless, doctors warned employers that lead workers were 'in search of easy money'. Aub cautioned that one case of lead poisoning in an industry was 'very apt to precipitate the appearance of other similar cases' and that weekly compensation cheques could bring on a neurosis in the worker that could only be cured by stopping payment.85 Doctors also questioned the long-term effects of lead. May Mayers, medical officer with the New York State Department of Labor, asserted that arteriosclerosis in lead workers was probably due to chronic alcoholism.86 Aub wrote that at one lead plant where there was 'undoubtedly a large amount of lead absorption, and there was a good deal of lead poisoning' lawyers were attempting to link permanent disabilities in from arteriosclerosis and nephritis to workers' lead exposure. Aub did not believe that a link between these diseases and long-term lead exposure had been proved.87 Interestingly, 30 life insurance companies in the United States and Canada disagreed. They reported that a worker who had suffered industrial lead poisoning 'would not be issued ordinary life insurance and would be "rated" up for a substandard form of insurance'. Hardly any company was prepared to issue health insurance or to attach a disability clause to these workers' policies because of the association between chronic, debilitating illnesses and lead poisoning.88	34
The politicisation of medical knowledge plus industry domination of occupational health and safety coincided with an unparalleled expansion of the battery industry. The 1920s, an era described as one of the most oppressive for labour,89 was one of the most profitable for the industry. In one year, from 1921–22 to 1922–23, battery exports from the United States rose by almost 35 per cent in volume and 43 per cent in value — including exports to Australia, which almost doubled from $123,000 to $221,000.90 Rising production, associated with an increase in car registration from 3.6 million to 17.5 million between 1916 and 1925,91 made the industry the largest single user of lead in America from the mid-1920s, annually consuming over 180,000 tons, worth more than $3 million.92 By 1931 it was conservatively estimated that the batteries in America's 25 million cars, contained 600 million pounds of lead.93	35
Although the United States had lagged behind Europe in industrial hygiene in the 1910s, by the 1930s it had become a global pacesetter.94 According to Kehoe the Kettering Laboratory was the 'only source of new information' on occupational and public health lead-standards; its findings shaped the theory and practice of those responsible for occupational and public health, including in Australia.95	36
Australian Consequences
During the 1920s American and British firms established battery plants in Australia to circumvent federal import tariffs on batteries. This resulted in an increase in the number of plants in Sydney from two or three small ones in the early 1920s to seven large ones by 1929.96 By that year local manufacturers supplied 70 per cent of the nation's replacement battery market.97 As head of the NSW division of industrial hygiene, established in 1923, Charles Badham conducted studies into occupational lead poisoning. His inspections of Sydney's battery plants revealed their hazardous and dirty states that he likened to that 'found in the white lead industry sixty years ago'. In 1927 and 1929 he recommended the cessation of battery production at Clyde Engineering and US Light and Heat respectively, until the workplaces were made safe. However, he had no authority to implement this as only the Chief Inspector of Factories could put these proposals into effect.98	37
US Light and Heat, a major American battery producer, was headquartered in Niagara Falls and helped found America's National Battery Manufacturers Association in 1924 as well as the Lead Industries Association in 1928.99 In 1930 D. Kelly, president of US Light and Heat, was also an ex-president of the National Battery Manufacturers Association.100 Another company criticised by Badham for its poor industrial hygiene was Vesta Battery Company, which had major plants in Chicago and Los Angeles producing 700,000 batteries annually. In 1930 Ward Perry, president of Vesta, was also president of the National Battery Manufacturers Association and Vesta employees staffed many Association committees. In 1931 Vesta merged with Consolidated Battery Company with plants in Philadelphia and Buffalo that manufactured 215,000 batteries annually. Herbert Warden Jr became president of the newly merged company — his father had founded the Electric Storage Battery Company (Exide), a company closely associated with Britain's Chloride Accumulator Works (later, Chloride Electrical Storage Company), the leading battery manufacturer in the British Empire and the third largest in the world. In the 1920s Chloride established a plant in Sydney to manufacture Exide batteries.101	38
Given the prominence of these companies in the American battery industry management should have been aware of the extreme lead-danger to workers. However, it appears that when companies were established in Australia they were inclined toward low standards of occupational health and safety until compelled by local authorities to improve them. Australian managers, likewise, should have at least been aware of the NSW regulations gazetted in 1928 to protect battery workers' health. Yet, conditions in Sydney's plants were so bad Badham wondered whether management understood that lead in the factory air inevitably caused poisoning in workers.102 Battery workers made up the majority of reported cases of lead poisoning in NSW in the 1930s.103 Of the 198 battery workers examined by Badham from 1927–33, 150 had lead poisoning with disability. One hundred per cent of mixers examined had disabling lead poisoning, as did 90 per cent of workers handling dry plates and 85 per cent of pasters.104 This followed an international trend that identified mixers and pasters as those most at risk.105	39
As global battery production intensified, the incidence of lead poisoning also rose. In France the number of battery workers with this disease, as a percentage of the total number of workers with it, rose from 12.5 per cent in 1921 to 32 per cent by 1924.106 In Britain, battery manufacturing had ranked sixth as the country's most dangerous lead industry from 1900–08; by 1919–20 it was first.107 Battery workers, who represented 4.6 per cent of all lead poisoned workers in 1909–11, made up 23 per cent by 1923–25.108 Increasing productivity and employers' non-compliance with Britain's 1904 regulations covering battery manufacturing were cited in the government's second study into the industry in 1924 as the reasons for this escalation.109 Even after new regulations were introduced in 1925, the incidence of lead poisoning continued to rise at Chloride's plant in Manchester 'as a result of expanding and changing trade'.110 In Sydney, too, Badham noted that increasing production in 1940 brought on 'several cases of lead poisoning ... in the larger and better equipped factories where no cases have occurred for several years'.111 In India increased battery production during World War II likewise resulted in an epidemic of lead poisoning.112	40
The hazardous state of Sydney's battery plants that unnecessarily exposed workers to lead dust and fumes has been outlined. What will be examined now is the influence of American, particularly Robert Kehoe's, theories on the Australian medical community. But first it needs to be said that long before America became the major centre for medical research into lead poisoning Australian physicians were engaged in their own research, discoveries and debates over the definition, diagnosis and long-term effects of lead poisoning.	41
As early as 1898 a Queensland government inquiry into lead poisoning in children found a number to be suffering from brain and nervous system damage from lead.113 By 1904 Brisbane doctor J. Lockhart Gibson identified paint as the source of this contamination. Throughout the following decades Gibson, A. Jefferis Turner and other doctors continued to report on the high incidence of paediatric lead poisoning in Queensland.114 While these findings were largely ignored by the international medical community,115 they sparked continued debate at home particularly among southern doctors where there were fewer painted wooden houses and fewer cases of paediatric lead poisoning. Although Queensland doctors and the state branch of the Operative Painters and Decorators Union had been lobbying the government to intervene since the early 1900s, the argument that there was no conclusive proof that lead paint caused paediatric lead poisoning was used to forestall legislation to regulate the use of paint until 1922.116	42
Subsequent studies by Queensland doctor L. J. Jarvis Nye from the late-1920s linked paediatric lead poisoning from paint with chronic nephritis. Despite this the federal government resisted calls to restrict lead paint use citing the harm it could do to Australia's oldest lead producer Broken Hill Propriety Ltd and concluded that: 'If it is conclusively proved that white lead as an ingredient in paint is injurious to health, we must find a substitute for it'.117 'Conclusive proof' was unlikely to be found while some sections of the Australian and American medical communities questioned Nye's work. In the mid-1940s Robert Kehoe, in his personal correspondence with Nye, rejected the link between lead poisoning and kidney disease.118 At home the head of Queensland's health department, the politically conservative Raphael Cilento,119 also cast doubt on Nye's theory and called for yet more studies to prove the connection.120	43
The Australian medical community was also familiar with occupational lead poisoning. In 1893 a NSW Board of Trade inquiry into lead poisoning at Broken Hill mines followed a strike by workers the previous year, as did the Technical Commission of Inquiry into lead poisoning at Broken Hill in 1919. Then in 1925 a Royal Commission into lead poisoning at Broken Hill Associated Smelters in Port Pirie was held. This became the subject of Richard Gillespie's influential study on the social construction of medical knowledge on lead poisoning. Medical experts Henry Chapman and Stewart Smith believed local doctors misdiagnosed cases of lead poisoning, agreeing with management that many were actually carbon monoxide poisoning or non-occupational illnesses. Chapman and Smith's narrow definition of lead poisoning categorised a number of previously diagnosed cases of lead poisoning as merely lead absorption, thereby mitigating management's concern over rising workers' compensation claims. Eventually local doctors were removed from the equation altogether after a medical board was established as the sole authority to diagnose lead poisoning. As Gillespie noted:	44
The definition of lead poisoning and its causes did not result from the unproblematic application of objective medical and technical knowledge. On the contrary, medical knowledge of lead poisoning was shaped within political and class structures that ensured that corporate interests would prevail.121
Up to the mid- to late-1920s the orientation of the Australian medical community was ostensibly toward Britain and Australian publications on lead poisoning frequently cited British authorities. But after American medical literature on lead research began to predominate globally, Australian physicians, unsurprisingly, were influenced. Badham said in 1925 that knowledge of lead poisoning over the past few years had flourished mainly through the work of Americans like Alice Hamilton, Joseph Aub and the United States Public Health Service's committee on tetraethyl lead.122 Queensland government pathologist J.V. Duhig, who investigated occupational lead poisoning at Mount Isa Mines in 1933, acknowledged that it was only within the previous eight to ten years that precise medical knowledge on the prevention of lead poisoning had developed.123 This was the era in which research sponsored by the American lead industry 'became the world's most important source of both theoretical and practical knowledge about the toxicity of lead'.124	45
Debates within the Australian medical community in the 1930s over lead poisoning remained largely within the parameters set by American researchers like Kehoe and Aub, whose works were frequently cited. G. C. Willcocks, whose 1933 paper on lead poisoning began with the statement that 'there is little to be said on the subject ... that is new', reiterated many of Aub's theories including the notion of compensation neurosis in lead poisoned workers.125 Even where disagreements arose within the medical profession they remained within the boundaries set by the American theorists. Badham was highly critical of Stewart Smith's contention that lead poisoning 'does not necessarily follow the chemical fact of absorption'.126 He believed there was only one condition — lead poisoning, with or without disability — and advised doctors not to demand a 'high degree' of this when diagnosing the disease.127 He also stated that company doctors used the term absorption rather than poisoning to conceal the real incidence of disease because the latter had to be reported.128 Yet, Badham used the artificial distinction himself when diagnosing workers for compensation.	46
The Australian medical community instinctively acknowledged the centrality of lead to modern industry but thought the hazard was controllable through fine-tuning the diagnostic criteria. Badham, for instance, advised doctors to take blood samples from workers because lead absorption induced changes in the blood cells. As a method of preventing lead poisoning, he stated, blood samples were 'preferable to a routine official inspection of these factories'.129	47
At Mount Isa Mines, whose production helped make Australia the world's second largest producer of lead, a medical board was established after the 1933 government inquiry led by Duhig. Douglas Shiels headed this board from 1934–36 — the exclusive agency responsible for diagnosing lead poisoning in Mount Isa workers. Shiels went on to head Victoria's industrial hygiene division in 1937. His research at Mount Isa, written almost exclusively for a medical audience, focused on the diagnostic significance of blood changes as well as lead in the urine and cited the works of Kehoe and Aub.130	48
By 1936 the Lead Industries Association acknowledged that, from their standpoint, the situation was 'growing better as appreciation of Dr Aub's and Dr Kehoe's work on lead permeates the medical fraternity'.131 This included the Australian medical profession.	49
Yet research from the Kettering Laboratory and from Australian physicians failed to protect battery workers from contracting occupational lead poisoning. In the laboratories researchers debated the diagnostic value of blood changes and lead in human excreta while in the battery plants workers continued to be exposed to lead. Throughout the 1930s small plants in NSW remained unsafe and new ones, which should have been clean, gave rise to severe cases of lead poisoning.132 In Brisbane in 1939/1940 three battery plants were reported to be poorly lit, poorly ventilated, had no adequate washing facilities and employed boys aged 15–17 years, 'some of whom were affected by lead'.133 Little seems to have changed in Queensland when eight years later, it was reported that compensation rates and labour turnover were high and 'far too many adolescents' were working in the battery trade.134	50
Conclusion
In 1849 during a cholera epidemic in London, Dr John Snow observed that a large number of cases occurred in the vicinity of a surface well in Broad Street, St James' parish. He advised removing the handle from the well's pump to prevent people consuming the water. When this was done the incidence of the disease declined rapidly in the immediate area.135 Proponents of the Precautionary Principle frequently cite this intervention because it occurred well before cholera's causative organism was discovered. Action was taken to protect public health even though the cause-effect relationship was not fully established scientifically. Had similar action been taken with occupational lead exposure the health and lives of hundreds of thousands of workers around the world would not have been jeopardised. However, the passion with which social reformers confronted occupational lead poisoning in the early twentieth century gave way to a tolerance of it in the absence of acute symptoms, following research funded by lead employers. Australian medical professionals, likewise, agreed with the fundamental tenets of this research, reinforcing recent scholarship that has shown, medical knowledge is constructed in a social context.	51
In 1992 battery workers in the United States remained amongst those most at risk of occupational lead poisoning,136 and a survey of recent literature in the medical publications' database PubMed has identified almost 30 studies of lead poisoning in workers manufacturing batteries as well as in workers, and their dependents, employed in battery salvaging in China, Columbia, the Dominican Republic, Germany, India, Iraq, Israel, Jamaica, Nicaragua, Russia, Taiwan and the United States.137 Yet, lead poisoning in today's battery workers should not be seen as an unfortunate but inevitable product of the work process. Rather it is the outcome of political and economic decisions made nearly three-quarters of a century ago, decisions that rejected the Precautionary Principle and ultimately failed to protect workers' health.	52
Endnotes 1. Jacqueline Karnell Corn, Response to Occupational Health Hazards: a Historical Perspective, Van Nostrand Reinhold, New York, 1992, p. 2. 2. Corn, Response to Occupational Health Hazards, p. 4. 3. Alice Hamilton, Lead Poisoning in the Manufacture of Storage Batteries (Bulletin of the United States Bureau of Labor Statistics, no. 165), Government Printing Office, Washington, D.C., 1915, p. 27; International Labour Office, 'Accumulators (Storage Batteries)', in Occupation and Health: an Encyclopaedia of Hygiene, Pathology and Social Welfare, vol. 1, International Labour Office, Geneva, 1934, p. 29. 4. Jerome Nriagu, 'Clair Patterson and Robert Kehoe's Paradigm of "Show Me the Data" on Environmental Lead Poisoning', Environmental Research, section A, vol. 78, August 1998, p. 74. 5. Sanford Lewis, 'The Precautionary Principle and Corporate Disclosure', in Carolyn Raffensperger and Joel A. Tickner (eds), Protecting Public Health and the Environment: Implementing the Precautionary Principle, Island Press, Washington, D.C., 1999, pp. 242–243. 6. Andrew Jordon and Timothy O'Riordan, 'The Precautionary Principle in Contemporary Environmental Policy and Politics', in Raffensperger and Tickner (eds), Protecting Public Health and the Environment, p. 16. 7. Lewis, 'The Precautionary Principle and Corporate Disclosure', p. 241. 8. Richard Gillespie, 'Accounting for Lead Poisoning: the Medical Politics of Occupational Health', Social History, vol. 15, no. 3, October 1990, pp. 303–331; Vicente Navarro, 'Work, Ideology, and Science: the Case of Medicine', International Journal of Health Services, vol. 10, no. 4, 1980, pp. 523–550; Karl Figlio, 'How Does Illness Mediate Social Relations? Workmen's Compensation and Medico-Legal Practices, 1890–1940', in P. Wright and A. Treacher (eds), The Problem of Medical Knowledge, Edinburgh University Press, Edinburgh, 1982, pp. 174–224. 9. D. Michaels, 'Waiting for the Body Count: Corporate Decision Making and Bladder Cancer in the U.S. Dye Industry', Medical Anthropology Quarterly, new series, vol. 2, no. 3, September 1988, pp. 213–232; D. Lilienfeld, 'The Silence: the Asbestos Industry and Early Occupational Cancer Research — a Case Study', American Journal of Public Health, vol. 81, no. 6, June 1991, pp. 791–800; David Rosner and Gerald Markowitz, Deadly Dust: Silicosis and the Politics of Occupational Disease in Twentieth-Century America, Princeton University Press, Princeton, 1991; David Egilman, 'The Asbestos TLV: Early Evidence of Inadequacy', American Journal of Industrial Medicine, no. 30, 1996, pp. 369–370; Claudia Clark, Radium Girls: Women and Industrial Health Reform, 1910–1935, University of North Carolina Press, Chapel Hill and London, 1997; Beris Penrose, 'Medical Experts and Occupational Illness: Weil's Disease in North Queensland, 1933–1936', Labour History, no. 75, November 1998, pp. 125–143. 10. William Graebner, 'Hegemony Through Science: Information Engineering and Lead Toxicology, 1925–1965', in D. Rosner and G. Markowitz (eds), Dying for Work: Workers' Safety and Health in Twentieth Century America, Indiana University Press, Bloomington, 1989, p. 141; Richard Wedeen, 'Shaping Environmental Research: the Lead Industries Association 1928–1946', Mount Sinai Journal of Medicine, vol. 62, no. 5, October 1995, pp. 386–389; Herbert Needleman, 'Clair Patterson and Robert Kehoe: Two Views of Lead Toxicity', Environmental Research, section A, vol. 78, August 1998, pp. 79–85; Nriagu, '"Show Me the Data"', pp. 71–8; Christian Warren, Brush with Death: a Social History of Lead Poisoning, Johns Hopkins University Press, Baltimore, 2000, p. 129. 11. International Labour Office, 'Accumulators (Storage Batteries)', p. 24. 12. David Rosner and Gerald Markowitz, 'The Early Movement for Occupational Safety and Health, 1900–1917', in J. Walzer Leavitt and R.L. Numbers (eds), Sickness and Health in America, University of Wisconsin Press, Madison, 1997, p. 468; Corn, Response to Occupational Health Hazards, pp. 4–5; Alice Hamilton, 'Industrial Lead-Poisoning in the Light of Recent Studies', Journal of the American Medical Association, vol. 59, no. 10, 7 September 1912, p. 777. 13. Rosner and Markowitz, 'The Early Movement for Occupational Safety and Health', p. 473. 14. Alice Hamilton, Lead Poisoning in the Manufacture of Storage Batteries; E.R. Hayhurst, Industrial Health-Hazards and Occupational Diseases in Ohio, University of Chicago, Chicago, 1915. 15. John B. Andrews, Deaths from Industrial Lead Poisoning (Actually Reported) in New York State in 1909 and 1910, reprinted from Bulletin of the United States Bureau of Labor, no. 95, Washington, D.C., 1912, pp. 263–265. 16. Hamilton, Lead Poisoning in Manufacture of Batteries, p. 9. 17. Alice Hamilton, 'Lead-Poisoning in Illinois', Journal of the American Medical Association, vol. 56, no. 17, 29 April 1911, pp. 1240–1244. 18. Alice Hamilton, 'Lead Poisoning in American industry', Journal of Industrial Hygiene, vol. 1, May 1919, p. 17. 19. Paul Holmes, 'Health Hazards in the Industries of Niagara Falls, N.Y.', Public Health Reports, vol. 35, no. 1, 2 January 1920, p. 13. 20. Hamilton, Lead Poisoning in Manufacture of Batteries, pp. 22, 27; Austin D. Reiley, 'The Problem of Ascertaining the Actual Rise in Mortality Caused by Unhealthy Trades', Journal of Industrial Hygiene, vol. 1, no. 3, July 1919, p. 110; Hamilton, 'Lead Poisoning in American Industry', p. 14. 21. Hamilton, Lead Poisoning in Manufacture of Batteries, p. 10. 22. Hamilton, Lead Poisoning in Manufacture of Batteries, pp. 12, 18; Hayhurst, Industrial Health-Hazards, pp. 201–202. 23. Hamilton, Lead Poisoning in Manufacture of Batteries, pp. 19, 23. 24. Industrial and Labor Information, vol. 2, no. 10, 9 June 1922, p. 25; Andrews, Deaths from Industrial Lead Poisoning, p. 263. 25. Alice Hamilton, 'Lead Poisoning in the United States', American Journal of Public Health, vol. 4, no. 6, June 1914, pp. 477–478. 26. Hamilton, 'Industrial Lead-Poisoning', p. 779. 27. Anthony Bale, 'Medicine in the Industrial Battle: Early Workers Compensation', Social Science of Medicine, vol. 28, no. 11, 1989, p. 1116. 28. Christopher Sellers, Hazards of the Job: from Industrial Disease to Environmental Health Science, University of North Carolina Press, Chapel Hill and London, 1997, p. 111. 29. Rosner and Markowitz, 'The Early Movement for Occupational Safety and Health', p. 473. 30. Sidney Lens, The Labor Wars: from the Molly Maguires to the Sitdowns, Anchor Books, New York, 1974, pp. 257–259; Daniel Berman, Death on the Job: Occupational Health and Safety Struggles in the United States, Monthly Review Press, New York, 1978, pp. 21, 77; David Rosner and Gerald Markowitz, 'Introduction: Workers Health and Safety: Some Historical Notes', in Rosner and Markowitz (eds), Dying for Work, pp. ix–xx; Richard Rabin, 'Warnings Unheeded: a History of Child Lead Poisoning', American Journal of Public Health, vol. 79, no. 12, December 1989, p. 1672; Rosner and Markowitz, 'The Early Movement for Occupational Safety and Health', p. 467. 31. J.S. Mark, 'Prevention and Control of Lead Poisoning in Industry', Journal of the Medical Society of New Jersey, vol. 28, October 1931, p. 773. 32. Quoted in Rosner and Markowitz, 'Introduction: Workers Health and Safety', p. xv. 33. E. Falconer, 'Lead Intoxication', California and Western Medicine, vol. 34, April 1931, p. 253. 34. Alice Hamilton, P. Reznikoff, G. Burnham, 'Tetra-Ethyl Lead', Journal of the American Medical Association, vol. 84, 16 May 1925, pp. 1481–1486. 35. David Rosner and Gerald Markowitz, '"A Gift of God"?: the Public Health Controversy over Leaded Gasoline During the 1920s', in Rosner and Markowitz (eds), Dying for Work, pp. 126–129. 36. Rosner and Markowitz, '"A Gift of God"?' 37. Herbert Needelman, 'The Removal of Lead from Gasoline: Historical and Personal Reflections', Environmental Research, vol. 84, no. 1, 2000, p. 24. 38. Great Britain Ministry of Health Committee on Ethyl Petrol, Minutes of Evidence taken before the Departmental Committee on Ethyl Petrol, His Majesty's Stationery Office, London, 1928, p. 56. 39. Great Britain Committee on Ethyl Petrol, Minutes of Evidence, p. 1; W.F. Machle, 'Tetra-Ethyl Lead Intoxication and Poisoning by Related Compounds of Lead', Journal of the American Medical Association, vol. 105, no. 8, 24 August 1935, p. 578; Rosner and Markowitz, '"A Gift of God"?', pp. 125–128; Needleman, 'Clair Patterson and Robert Kehoe'; Warren, Brush with Death, pp. 117–129. 40. Warren, Brush with Death, p. 129. 41. Quoted in Peter English, Old Paint: a Medical History of Childhood Lead-Paint Poisoning in the United States to 1980, Rutgers University Press, New Brunswick and London, 2001, p. 39. 42. Navarro, 'Work, Ideology, and Science', p. 541. 43. Graebner, 'Hegemony through Science' p. 148; Rabin, 'Warnings Unheeded', p. 1671; Wedeen, 'Shaping Environmental Research', p. 388; Sellers, Hazards of the Job, p. 174. 44. Sellers, Hazards of the Job, p. 159. 45. Sellers, Hazards of the Job, pp. 183–184. 46. Warren, Brush with Death, p. 130. 47. Graebner, 'Hegemony through Science', p. 155. 48. Robert Kehoe, G. Edgar, F. Thamann and L. Sanders, 'The Excretion of Lead by Normal Persons', Journal of the American Medical Association, vol. 87, no. 25, 18 December 1926, p. 2081; Robert Kehoe and F. Thamann, 'The Excretion of Lead', Journal of the American Medical Association, vol. 92, 27 April 1929, pp. 1418–1421; Robert Kehoe, F. Thamann and J. Cholak, 'On the Normal Absorption and Excretion of Lead. I. Lead Absorption and Excretion in Primitive Life', Journal of Industrial Hygiene, vol. 15, no. 5, September 1933, pp. 257–272. 49. Thomas Legge, Industrial Maladies, Oxford University Press, London, 1934, p. 50. 50. R.W. Tannahill, 'A Critical Survey of the Methods for the Determination of Lead in Biological Material', Medical Journal of Australia, vol. 2, 16 February 1929, pp. 194–201; R.W. Tannahill, 'The Excretion of Lead by Mine Workers at Broken Hill', Medical Journal of Australia, vol. 2, 16 February 1929, pp. 201–205; R.W. Tannahill, 'Lead Excretion of Workers at the Smelters, Port Pirie', Medical Journal of Australia, vol. 2, 16 February 1929, pp. 205–208. 51. Charles Badham, 'Basophilia and Lead Excretion in Lead Poisoning', Medical Journal of Australia, vol. 2, 16 December 1933, p. 818; Ronald Lane, 'Punctate Basophilia in the Diagnosis of Plumbism', Clinical Journal, vol. 61, 27 January 1932, p. 42; Legge, Industrial Maladies, p. 51; J. Chalmers, 'Lead Content of Human Blood', Lancet, vol. 238, 1940, pp. 447–450. 52. Legge, Industrial Maladies, p. 51. 53. C.N Myers, F. Gustafson and B. Throne, 'The Distribution and Diagnostic Significance of Lead in the Human Body', New York State Journal of Medicine, vol. 35, 1 June 1935, p. 582. 54. C.N. Myers, 'The Medico-Legal Aspects of Chronic Metallic Poisoning', International Journal of Medicine and Surgery, vol. 45, October 1932, p. 474. 55. Myers, Gustafson and Throne, 'The Distribution and Diagnostic Significance of Lead', pp. 580–582. 56. Needleman, 'Clair Patterson and Robert Kehoe', p. 80. 57. Tannahill, 'A Critical Survey', p. 198. 58. Tannahill, 'The Excretion of Lead', p. 203. 59. Thomas Oliver, Occupations from the Social, Hygienic and Medical Points of View, Cambridge University Press, Cambridge, 1916, p. 9. 60. R.Y. Mathew, 'The Blood of Workers Exposed to Lead', Medical Journal of Australia, vol. 2, 16 February 1929, p. 214. 61. Philip Donohue, 'The Prevention of Industrial Lead Poisoning', Minnesota Medicine, vol. 8, September 1925, p. 597; Lane, 'Punctate Basophilia', p. 43; Robert Kehoe, F. Thamann and J. Cholak, 'Normal Absorption and Excretion of Lead', Journal of the American Medical Association, vol. 104, no. 3, 12 January 1935, p. 90; Alice Hamilton, 'Medico-Legal Aspects of Industrial Poisonings', Bulletin of the New York Academy of Medicine, vol. 12, December 1936, p. 638. 62. Waldemar Dreessen, T. Edwards, W. Reinhart, R. Page, S. Webster, D. Armstrong and R.R. Sayers, The Control of the Lead Hazard in the Storage Battery Industry (United States Public Health Service Bulletin, no. 262), Government Printing Office, Washington, D. C., 1941. 63. American Public Health Association, Occupational Lead Exposure and Lead Poisoning: a Report Prepared by the Committee on Lead Poisoning of the Industrial Hygiene Section of the American Public Health Association, American Public Health Association, New York, 1943, p. 17. 64. Beris Penrose, 'Government Response to Lead Poisoning from Paint: Historical Lessons and Legacies', Labour and Industry, vol. 11, no. 1, August 2000, pp. 95–114; Robert Proctor, The Nazi War on Cancer, Princeton University Press, Princeton, 2000, p. 288, fn. 4. 65. Ludwig Teleky, 'Lessons From the History of Lead Poisoning: a Review of International Experience', Industrial Medicine, vol. 9, no. 1, January 1940, p. 19. 66. Felix Wormser, 'Facts and Fallacies Concerning Exposure to Lead', Occupational Medicine, vol. 3, no. 2, February 1947, p. 139. 67. Warren, Brush with Death, p. 216. 68. Hamilton, 'Lead Poisoning in American industry', p. 17. 69. A.E. Russell, R.R. Jones, J.J. Bloomfield, R.H. Britten and L.R. Thompson, Lead Poisoning in a Storage Battery Plant (United States Public Health Service Bulletin, no. 205), Government Printing Office, Washington, D.C., June 1933, pp. 9–10, 14, 23. 70. Alice Hamilton, 'The Storage Battery Industry', Journal of Industrial Hygiene, vol. 9, no. 3, August 1927, p. 368. 71. Donohue, 'The Prevention of Industrial Lead Poisoning'; G.H. Gehrmann, 'Prevention of Lead Poisoning in Industry', American Journal of Public Health, vol. 23, July 1933, pp. 687–692. 72. Elston Belknap, 'Control of Lead Poisoning in the Worker', Journal of the American Medical Association, vol. 104, no. 3, 19 January 1935, p. 207. 73. Mark, 'Prevention and Control of Lead Poisoning', p. 776. 74. Gehrmann, 'Prevention of Lead Poisoning', p. 688. 75. Belknap, 'Control of Lead Poisoning', p. 206. 76. Max Kummel, 'Medicolegal Aspects of Disability in Industrial Lead Poisoning', Journal of the Medical Society of New Jersey, vol. 28, April 1931, p. 238. 77. Donohue, 'The Prevention of Industrial Lead Poisoning', p. 597; C. McCord, H. Walworth, J. Johnston and P. Fisher, 'The Atmospheric Content of Lead and its Correlation with Basophilic Aggregation Tests in Exposed Storage Battery Workers', Industrial Medicine, vol. 6, no. 6, June 1937, p. 357. 78. Donohue, 'The Prevention of Industrial Lead Poisoning', p. 597; Russell, et al., Lead Poisoning in a Storage Battery Plant; Harriet Hardy, Challenging Man-Made Disease: Memoirs of Harriet L. Hardy, Praeger, New York, 1983; Hamilton, Lead Poisoning in Manufacture of Batteries, p. 22; J.D. Hackett, 'Storage Battery Plants, New York State, 1933', American Journal of Public Health, vol. 24, September 1934, p. 971; Kummel, 'Medicolegal Aspects', p. 329; Warren, Brush with Death, p. 86. 79. Quoted in Warren, Brush with Death, p. 78. 80. Alice Hamilton, 'Industrial Poisons', New England Journal of Medicine, vol. 209, 10 August 1933, p. 279. 81. McCord et al., 'The Atmospheric Content of Lead', p. 357. 82. Kummel, 'Medicolegal Aspects', p. 329. 83. Hardy, Challenging Man-Made Disease, p. 118. 84. Kummel, 'Medicolegal Aspects', pp. 328–329. 85. Joseph Aub, 'Relationship of Lead Poisoning to Industry', Industrial Medicine, vol. 1, no. 1, October 1932, p. 64. 86. May Mayers, 'A Study of the Lead Line, Arteriosclerosis, and Hypertension in 381 Lead Workers', Journal of Industrial Hygiene, vol. 9, no. 6, June 1927, p. 246. 87. Aub, 'Relationship of Lead Poisoning to Industry', p. 64; Charles Badham, 'An Investigation Concerning the Incidence of Lead Poisoning in Motor-Car Painters', Studies in Industrial Hygiene, no. 6, New South Wales Legislative Council and Legislative Assembly Papers, 1925–1926, Sydney, 1925, p. 100. 88. Kummel, 'Medicolegal Aspects', p. 328. 89. David Rosner and Gerald Markowitz, 'Safety and Health as a Class Issue: the Workers Health Bureau of America during the 1920s', in Rosner and Markowitz (eds), Dying for Work, p. 53. 90. Automotive Industries, vol. 50, no. 9, 28 February 1924, p. 527. 91. United States Bureau of Census, Historical Statistics of the United States, Colonial Times to 1970, part II, Government Printing Office, Washington, D.C., 1975, p. 716. 92. Battery News, vol. 1, no. 1, December 1926, p. 8. 93. Battery News, vol. 6, no. 1, October 1931, p. 17. 94. Pamela E. de Silver, Science at Work: a History of Occupational Health in Victoria, PenFolk Publishing, Blackburn, Victoria, 2000, p. 10; Sellers, Hazards of the Job, p. 112. 95. Quoted in Nriagu, 'Clair Patterson and Robert Kehoe's Paradigm', p. 73. 96. Electrical Review, 28 November 1930, p. 906; Electrical Review, 13 February 1931, p. 280; 'Report of the Director-General of Public Health, New South Wales, for the year 1930', Joint Volumes of Papers Presented to the Legislative Council and Legislative Assembly, New South Wales, 1930–32, vol. IV, 29th Parliament, Sydney, 1932, p. 390. 97. Electrical Review, 18 October 1929, p. 681. 98. 'Report of the Director-General of Public Health, New South Wales, for the Year 1929', Joint Volumes of Papers Presented to the Legislative Council and Legislative Assembly, New South Wales 1930–32, vol. IV, 29th Parliament, Sydney, 1932; 'Report of the Director-General of Public Health, New South Wales, for the Year 1930', p. 390. 99. Battery News, vol. 3, no. 1, December 1928, p. 34 100. Battery News, January 1930, p. 10; Battery News, vol. 5, no. 9, January, 1931, pp. 9, 14, 15; Battery News, May 1931, p. 22. 101. Battery News, January 1930, p. 10; Battery News, vol. 5, no. 9, January 1931, pp. 10, 13, 14; Electrical Review, 2 November 1928, p. 755. 102. 'Report of the Director-General of Public Health, New South Wales, for the Year 1930', p. 390; 'Report of the Director-General of Public Health, New South Wales, for the Years 1931 and 1932', Joint Volumes of Papers Presented to the Legislative Council and Legislative Assembly, New South Wales, 1933–1934, vol. I, 4th Session of the 30th Parliament, Sydney, 1934, p. 523. 103. G.C. Willcocks, 'Lead Poisoning', Medical Journal of Australia, vol. 2, 16 December 1933, pp. 813–816; also see New South Wales annual reports of director general of health throughout the 1930s. 104. Willcocks, 'Lead Poisoning', p. 814. 105. International Labour Office, 'Accumulators (Storage Batteries)', pp. 26, 31; 'Lead Poisoning Resulting from Manufacture of Storage Batteries', Journal of the American Medical Association, vol. 85, no. 18, 31 October 1925, pp. 1412–1413. 106. International Labour Office, 'Accumulators (Storage Batteries)', pp. 29, 24. 107. International Labour Office, 'Lead Poisoning', in International Labour Office, Occupation and Health: an Encyclopaedia of Hygiene, Pathology and Social Welfare, vol. I, Geneva, 1933, p. 124. 108. Thomas Legge, 'Twenty Years Experience of the Notification of Industrial Diseases', Journal of Industrial Hygiene, vol. 12, April 1920, p. 590; Legge, Industrial Maladies, p. 50. 109. C.W. Price and J.C. Bridge, 'The Manufacture and Repair of Electric Accumulators', Journal of Industrial Hygiene, vol. 7, no. 10, October 1925, p. 456. 110. Ronald E. Lane, 'The Prevention of Industrial Plumbism', Lancet, vol. 2, 25 July 1936, p. 206. 111. 'Report of the Director-General of Public Health, New South Wales, for the Year 1938', Joint Volumes of Papers Presented to the Legislative Council and Legislative Assembly, New South Wales, vol. V, 2nd Session of the 32nd Parliament, Sydney, 1940, p. 298. 112. Government of India Ministry of Labour, Environmental and Medical Studies in the Storage Battery Industry, Office of the Chief Adviser, Factories, New Delhi, 1953. 113. Report of Proceedings of the Board Appointed by the Government to Inquire into a Report upon the Subject of Chronic Lead Poisoning in Queensland from 30 May 1898 until 24 August 1898, Queensland State Archives (Brisbane): loc. no. A/5077, dept. no., 24/8150. 114. Penrose, 'Government Response to Lead Poisoning from Paint', pp. 100–101. 115. John C. Burnham, 'Biomedical Communication and the Reaction to the Queensland Childhood Lead Poisoning Cases Elsewhere in the World', Medical History, vol. 43, no. 2, April, 1999. 116. Penrose, 'Government Response to Lead Poisoning from Paint', p. 101. 117. Quoted in Penrose, 'Government Response to Lead Poisoning from Paint', p. 105. 118. Penrose, 'Government Response to Lead Poisoning from Paint'; Anthony Lanza, 'Epidemiology of Lead Poisoning', Journal of the American Medical Association, vol. 104, no. 2, 12 January 1935, p. 86; English, Old Paint, p. 26. 119. For Cilento's conservative role in the control of Weil's Disease see, Penrose, 'Medical Experts and Occupational Illness'. Also see Richard Gillespie, 'Epidemics and Power: Weil's Disease in North Queensland, 1929–1939', Occasional Papers on Medical History Australia, vol. 4, 1990, pp. 59–65. 120. Penrose, 'Government Response to Lead Poisoning from Paint', pp. 105–106 121. Gillespie, 'Accounting for Lead Poisoning', p. 327. 122. Charles Badham and H.B. Taylor, 'Lead Poisoning: Concerning the Standards Which Should be Used in Diagnosing this Industrial Disease, Together with a New Method for the Determination of Lead in Urine', Studies in Industrial Hygiene, no. 7, Joint Volumes of Papers Presented to the Legislative Council and Legislative Assembly, New South Wales, vol. 1, 1st Session of the 28th Parliament, 1927, p. 52. 123. 'Enquiry into Lead Poisoning and its Incidence', Queensland Parliamentary Papers, vol. 2, Brisbane, 1933, p. 176. 124. Warren, Brush with Death, p. 99. 125. Willcocks, 'Lead Poisoning', p. 125. 126. S.A. Smith, 'Some Aspects of Lead Absorption', Medical Journal of Australia, vol. 2, 26 September 1925, p. 391. 127. Badham and Taylor, 'Lead Poisoning: Concerning the Standards', p. 64; Badham, 'Basophilia and Lead Excretion', p. 819. 128. Badham, 'An Investigation Concerning the Incidence of Lead Poisoning', p. 91. 129. Badham, 'Basophilia and Lead Excretion', p. 820. 130. D.O. Shiels, 'The Concentration of Lead in the Urine of Workers at Mount Isa Mines Limited, Queensland, with Special Reference to its Value in the Diagnosis of Lead Poisoning', Medical Journal of Australia, vol. 1, no. 17, 25 April 1936, pp. 559–565; D.O. Shiels, 'The Ratio of Large to Small Lymphocytes in Persons Exposed to a Lead Hazard', Medical Journal of Australia, vol. 1, 20 June 1936, pp. 847–849; D.O. Shiels, 'Comparison of Punctate Basophilia and Ratio of Large to Small Lymphocytes in the Diagnosis and Prevention of Lead Poisoning', Medical Jounral of Australia, 10 April 1937, pp. 535–545. 131. Quoted in Wedeen, 'Shaping Environmental Research', p. 388. 132. 'Report of the Director-General of Public Health, New South Wales, for the Year 1930', p. 524; 'Report of the Director-General of Public Health, New South Wales, for the Years 1931 and 1932', p. 523; 'Report of the Director-General of Public Health, New South Wales, for the Year 1934', Joint Volumes of Papers Presented to the Legislative Council and Legislative Assembly, New South Wales, vol. III, Sydney, 1936, p. 122. 133. 'Annual Report of the Health and Medical Services of the State of Queensland for the Year 1939–40', Queensland Parliamentary Papers, vol. II, 3rd session of the 28th Parliament, Brisbane, 1940, p. 1060. 134. 'Annual Report on Health and Medical Services', Queensland Parliamentary Papers, vol. II, Brisbane, 1947–48, pp. 984–985. 135. Frederick Cartwright and Michael Biddiss, Disease and History, Barnes & Noble, New York, 1991, pp. 158–162. 136. 'Battery Reclamation Workers', Morbidity and Mortality Weekly Reports, 1 May 1992, p. 303. 137. The years surveyed were 1986–2002.

Content in the History Cooperative database is intended for personal, noncommercial use only. You may not reproduce, publish, distribute, transmit, participate in the transfer or sale of, modify, create derivative works from, display, or in any way exploit the History Cooperative database in whole or in part without the written permission of the copyright holder.