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Margaret Becklake was born in 1922 and grew up in Pretoria, South Africa. She trained in medicine at the University of the Witwaterstrand, Johannesburg, graduated with MB and BCh degrees in 1944, and then interned at the Johannesburg General Hospital. This was followed by postgraduate studies at what was then the British Postgraduate Medical School, Hammersmith, London, U.K., where she focused on respiratory function. On her return to Johannesburg in 1950, she was appointed a Junior Lecturer in Medicine at her alma mater and also Respiratory Physiologist to the Pneumoconiosis Bureau in Johannesburg. There she carried out her first epidemiologic studies, including the documentation of lung function in subjects living 1 mile above sea level, and of the effects of mine dust exposure and silicosis on lung function in Witwaterstrand gold miners. In 1957, she moved to Montreal, Canada, and worked in the Lung Function Laboratory of the Department of Medicine, Royal Victoria Hospital. In 1967, she set up a lung function laboratory in support of Professor Corbett McDonald's research program into the effects of exposure to asbestos in the chrysotile miners and millers of Québec. She was the recipient of a Medical Research Council of Canada Career Investigator award from 1968 to 1993. She is currently an Emeritus Professor at McGill University, with appointments in the Department of Epidemiology and Biostatistics and the Department of Medicine, as well as in the Respiratory Epidemiology and Clinical Research Unit of the Montreal Chest Institute and the Meakins Christie Laboratories.
PE: Few people start with the intent of becoming an epidemiologist. Can you describe how you came to epidemiology?
MB: I had studied medicine in Johannesburg during World War II and the word epidemiology did not appear in the curriculum. My postgraduate training took place in London after the war, during 1947 and 1948, at what was then the British Postgraduate Medical School. In those days, the answers to questions on disease mechanisms were expected to come from pathology. Clinical pathology rounds were held every day at lunchtime at the Postgraduate Medical School and involved specialists from all fields. This model of interdisciplinary activity fascinated both my husband and me, and we hoped to take it back to South Africa. At the Postgraduate Medical School, I was also involved in research in Professor McMichael's laboratory—research that focused on respiratory physiology and which became the subject for my own MD thesis.
We returned to Johannesburg in 1950 and I was offered a Junior Lectureship in the Department of Medicine at my alma mater. I set up one of the first clinical lung function laboratories in the country. In 1954, I was also appointed Physiologist to the Pneumoconiosis Bureau.
My contact with epidemiology really resulted from a chance conversation with Dr. John Gilson, who was Head of the Pneumoconiosis Research Unit in South Wales. Dr. Gilson focused on coal miner's disease. When I told him that the Miner's Bureau in Johannesburg was responsible for the compulsory preemployment and annual medical examinations (including chest x-ray) of every active miner, he pointed out what a remarkable opportunity this gave me to sample from their number and address epidemiologic questions. If he wanted to do the same thing, he would have to mount a field survey and go around to all the coal pits in England to get the information that was being systematically recorded on every active miner in South Africa.1,2 By that time, it had also become clear to me that case studies were insufficient to identify the various determinants of occupational respiratory disease.
PE: How did you come to study asbestos miners and millers?
MB: Our family moved to Québec in 1967. Early in the 1970s, I was invited by Professor Corbett McDonald, Head of what was then the Department of Epidemiology and Health, to set up a lung function laboratory. This laboratory would help support his research program into the ill health effects of exposure to chrysotile asbestos among miners and millers in Québec. The impetus for this study had come from the International Commission on Occupational Health, which had identified several important questions. One was whether there were differences in the health effects of exposure to the different types of asbestos fibers. In Québec, there was a group of miners and millers exposed primarily to chrysotile fibers, about which there was little published data.
PE: You had the experience of testing lung function on a large scale in the gold miners in South Africa.
MB: In our studies of South African gold miners, we had used resting and exercise lung function tests in very much the same way as we subsequently did in the chrysotile miners of Québec. The technologic challenges, however, were different. Johannesburg is situated at 6000 feet above sea level where the air is thin, and the minute ventilation and forced expiratory flow rates are increased. We had to establish what was “normal” at 6000 feet.3 I have maintained an interest in the determinants of normal lung function throughout my career.3–11
PE: What is the biggest difference between epidemiology as it was practiced when you started your career and epidemiology today?
MB: I think the biggest difference is in the technology. It is possible today to carry out much more complex and more rapid analysis of multivariable data. In our first studies of South African gold miners,1,2,12 we performed a number of lung function tests, none of which singly differentiated between miners with and without silicosis. Our statistical consultant proposed a discriminant analysis, following an approach to analysis used by Dr. Gilson in his studies of Welsh coal miners. We found it necessary to invert a matrix of approximately 240 data points. This analysis could not be carried out in South Africa, because we did not have access to a computer that had the memory or the processing speed to do the computation. We therefore mailed the data to England, where the computations were carried out over the course of several weeks with the aid of the computer belonging to a U.K. restaurant chain.
By contrast, we recently carried out a study of adult asthma among almost 16,000 subjects, with 8 major symptoms as outcomes and various risk factors.13 The analysis of approximately1.7 million data points of information could be completed on a desktop computer in a single day.
PE: Whom would you credit as having most strongly influenced your career?
MB: I would single out Professor Craib, who was Professor of Medicine when I was a medical student in Johannesburg. He was an interesting individual and an original thinker. He had grown up on a farm in the Eastern Cape Province, South Africa, and served in the South African forces in France in World War I where he earned 2 military crosses. He then trained in medicine in London because there were no medical schools in South Africa before 1922. In London he became interested in how the heart muscle generated the electric current that resulted in the electrocardiogram. In doing so, he challenged the concepts of Sir Thomas Lewis, Editor of the British Heart Journal and the doyen of cardiology in London. Professor Craib devised experiments to prove his point.
PE: This was the 1920s and he was challenging the professor?
MB: Absolutely. And he taught us in much the same way. He expected us to challenge everything that did not fit our clinical observations, whether or not it fitted current dogma. This is something that I have tried to follow all of my life.
PE: Who would you regard as the 2 or 3 most important epidemiologists during your lifetime and on what basis?
MB: I would say Sir Richard Doll, Dr. Archie Cochrane, Professor Corbett McDonald, and Dr. Kenneth Rothman. I have met the first 3. I know Dr. Rothman only through his book.14 In the case of Sir Richard Doll, his studies examining the link between cancer and cigarette smoking became the model for chronic disease epidemiology in the latter half of the 20th century. Dr. Cochrane was Head of the Medical Research Unit in Cardiff, Wales, close to the Pneumoconiosis Research Unit that Dr. Gilson headed. The close collaboration between Dr. Cochrane and Dr. Gilson no doubt accounts for Dr. Cochrane's approach to the study of occupational lung disease using a community-based approach. Most of the epidemiology I know comes from working with Professor McDonald on his asbestos studies. When you approached him with a project or a protocol, he would criticize it from many different aspects, and when you thought you really had no option but to abandon the project, he would turn it around and come to closure with a rather simple design. He always taught that “Le meilleur est l'enemi du bien” (The best is the enemy of the good). A good simple study plan is preferable to a more ideal but complex plan that takes longer to achieve and risks forfeiting the interest of all concerned. As I have already mentioned, Dr. Rothman I came to know through reading his book. I strongly endorse his view that “an epidemiological study should be regarded as an exercise in measurement, with accuracy as its goal.”14 It is an eloquent reminder of the importance of accurate measurement in epidemiology and has guided me in my research on lung function.
PE: Which do you think has been your most influential paper?
MB: I think my paper on “Asbestos-related diseases of the lungs and other organs, their epidemiology and implications for clinical practice.”15 When Professor McDonald was completing the first series of reports on his studies in asbestos miners, most were reported in epidemiology or public health journals, often not read by clinicians.16–21 I told him that I thought that they were extremely important to the practice of medicine, so he suggested I write a review from a clinical perspective. This coincided with an invitation from the Editor of the American Review of Respiratory Diseases, John Murray, to write a piece on the health effects of asbestos.
PE: Which is your most underappreciated paper?
MB: That was a paper by Umesh Lalloo and me—a nonsystematic review of the literature entitled, “The ‘healthy’ smoker: a phenomenon of health selection?”22 The healthy worker effect had been described in relation to mortality but not to morbidity. It was clearly related to morbidity in our own studies.23,24 In addition, the fact that the “healthy” worker and the “healthy” smoker effect both occurred in the same populations struck us as interesting because this implied that those whose lungs could stand cigarette smoke could also stand exposure to mine dust.
PE: How have you chosen the research questions that you want to address?
MB: As Professor Craib taught us to do: address questions garnered from listening to what patients, workers, their relatives or our colleagues tell us, and which do not fit current clinical dogma.
PE: Which of your contributions to the field would you most like to be remembered for?
MB: Probably for any contribution that I made to the evidence that work-related exposures to dusts could cause chronic obstructive pulmonary disease. In other words, this disease is not exclusively a cigarette-related disease. The information has been relatively slow to gather. It started out with my very first studies in South African gold miners.25 As the miners put it, “the x-ray does not tell the whole story.” At that time, disability compensation was given only to miners with x-ray evidence of silicosis. The miners’ experience was otherwise. There were men who were compensated for x-ray silicosis and yet were fit and able to work, whereas others without radiologic silicosis were disabled and unable to work as a result of what the miners were convinced was work-related disease.12 The germ of the idea was there. Most recently, a proceedings of a workshop on occupational contributions to the burden of airway disease estimated that it is of the order of 15%.26
PE: What have been your major interests outside of your epidemiologic activities?
MB: My husband grew up on a farm in South Africa, and our family has always been interested in the country around us, particularly its evolution through the seasons. We own a log cabin in a lovely part of Québec. As a family, probably because we have lived on 3 continents, we have also been interested in the economic, social, and political events of the world. These have regularly been subjects of our dinner table conversations. Living in Montreal helps. Not only do we enjoy living here, but it is a city that attracts visitors, including our extended family and friends.
PE: In your opinion, what has been epidemiology's most important contribution to society?
MB: I think it is the transfer of the concept of frequency and uncertainty into the public domain. This provides the public with some protection against the flamboyant claims of risk or benefit for drugs, drinks, or foods made in the lay press.
PE: Do you see risks for our profession?
MB: The biggest risk is the imbalance between the effort that we put into studying various issues versus their relative importance on the world scene. Of most concern to me, as someone who grew up in Africa, is the lack of involvement of the industrialized countries of the world in addressing the AIDS/tuberculosis (TB) epidemic, particularly in sub-Saharan Africa. Recently, I was involved with a course on protocol development for the study of lung diseases in the Durban area, South Africa. The participants from South Africa and neighboring countries all felt that every one of our protocols should deal with some issue pertinent to the HIV/AIDS/TB epidemic.
PE: You feel there is an opportunity for western epidemiologists to do more about HIV and TB in the Third World?
MB: Yes, particularly in exerting pressure in directing funding to care and treatment of AIDS victims, but also by encouraging research to be done locally. It is critically important that industrializing countries, whatever their level of industrialization, should have the means to carry out their own research to answer the questions they feel are important.
PE: Do you have any predictions about what the future might hold for our field?
MB: Epidemiology is a wonderfully useful and versatile discipline, and I expect it will increasingly be used in other fields. This corresponds very closely to Dr. Miettinen's description of epidemiology as a discipline, not a science.27
PE: Why have students always been such a priority for you?
MB: Students are our investment in the future. Also (something I learned from Professor Craib), students come to a set of facts with a fresh point of view. They have little baggage and are relatively uninfluenced by dogma. If you listen, their ideas can often be extremely refreshing and well worth considering.
PE: What would be the single most important piece of advice that you would give a new epidemiologist starting his or her career?
MB: Professsor McDonald used to quote a piece of graffiti from the London Underground. It said, “God is the Answer.” And underneath it somebody—presumably an epidemiology student—had written “But what is the question?” I would urge new epidemiologists to become involved in what you think are important questions. Concentrate on the “why” of what you are studying, not so much in the “how.” The methods can nearly always be worked out. Concentrate on the importance of the research question.
ABOUT THE INTERVIEWER
PIERRE ERNST trained as a respiratory physician and then studied epidemiology at McGill University. His first research experience was with Margaret Becklake, examining the effects of pleural disease on respiratory symptoms and lung function in asbestos workers and the determinants of respiratory health in young adults. Since then, his primary interests have been in the environmental determinants of asthma and in the pharmacoepidemiology of asthma and chronic obstructive pulmonary disease. He is currently a Professor of Medicine at McGill University.
Judy Eshelman carried out the transcription of this interview.
1.Becklake MR, du Preez L, Lutz W. Lung function in silicosis of the Witwaterstrand gold miner. Am Rev Tuberc. 1958;77:400–412.
2.Zwi S, Becklake MR. Respiratory function of Witwaterstrand gold-miners; a comparison between radiologically normal miners and control non-mining subjects. Br J Ind Med. 1958;15:258–261.
3.Goldman HI, Becklake MR. Respiratory function tests; normal values at median altitudes and the prediction of normal results. Am Rev Tuberc. 1959;79:457–467.
4.Ouellet Y, Poh SC, Becklake MR. Circulatory factors limiting maximal aerobic exercise capacity. J Appl Physiol. 1969;27:874–880.
5.Andrew GM, Becklake MR, Guleria JS, Bates DV. Heart and lung functions in swimmers and non athletes during growth. J Appl Physiol. 1972;32:245–251.
6.Seely JE, Guzman CA, Becklake MR. Heart and lung function at rest and during exercise in adolescence. J Appl Physiol. 1974;36:34–40.
7.Becklake MR, Leclerc M, Strobach H, Swift J. The N2 closing volume test in population studies: sources of variation and reproducibility. Am Rev Respir Dis. 1975;111:141–147.
8.Leech JA, Ghezzo H, Stevens D, Becklake MR. Respiratory pressures and function in young adults. Am Rev Respir Dis. 1983;128:17–23.
9.Becklake MR. Concepts of normality applied to the measurement of lung function. Am J Med. 1986;80:1158–1164.
10.White NW, Hanley JH, Lalloo UG, Becklake MR. Review and analysis of variation between spirometric values reported in 29 studies of healthy African adults. Am J Respir Crit Care Med. 1994;150:348–355.
11.Becklake MR, Kauffmann F. Gender differences in airway behaviour over the human life span. Thorax. 1999;54:1119–1138.
12.Becklake MR, Zwi S, Lutz W. Studies on the nature and aetiology of respiratory disability in Witwaterstrand gold-miners free of radiological silicosis. Br J Ind Med. 1959;16:290–296.
13.Manfreda J, Becklake MR, Sears MR, et al. Prevalence of asthma symptoms among adults aged 20–44 years in Canada. Can Med Assoc J. 2001;164:995–1004.
14.Rothman KJ. Modern Epidemiology, 1st ed. Boston: Little, Brown and Co; 1986.
15.Becklake MR. Asbestos-related diseases of the lung and other organs: their epidemiology and implications for clinical practice. Am Rev Respir Dis. 1976;114:187–227.
16.Becklake MR, Fournier-Massey G, McDonald JC, Siemiatycki J, Rossiter CE. Lung function in relation to chest radiographic changes in Quebec asbestos workers. I. Methods, results and conclusions. Bull Physiopathol Respir (Nancy). 1970;6:637–659.
17.Jodoin G, Gibbs GW, Macklem PT, McDonald JC, Becklake MR. Early effects of asbestos exposure on lung function. Am Rev Respir Dis. 1971;104:525–535.
18.McDonald JC, Becklake MR, Fournier-Massey G, Rossiter CE. Respiratory symptoms in chrysotile asbestos mine and mill workers of Quebec. Arch Environ Health. 1972;24:358–363.
19.McDonald JC, Becklake MR, Gibbs GW, McDonald AD, Rossiter CE. The health of chrysotile asbestos mine and mill workers of Quebec. Arch Environ Health. 1974;28:61–68.
20.Fournier-Massey G, Becklake MR. Pulmonary function profiles in Quebec asbestos workers. Bull Physiopathol Respir. 1975;11:429–445.
21.Becklake MR, Fournier-Massey G, Rossiter CE, McDonald JC. Lung function in chrysotile asbestos mine and mill workers of Quebec. Arch Environ Health. 1972;24:401–409.
22.Becklake MR, Laloo U. The ‘healthy smoker': a phenomenon of health selection? Respiration. 1990;57:137–144.
23.Ernst P, Dales RE, Nunes F, Becklake MR. Relation of airway responsiveness to duration of work in a dusty environment. Thorax. 1989;44:116–120.
24.Becklake MR. Epidemiology of spirometric test failure. Br J Ind Med. 1990;47:73–74.
25.Becklake MR. When the chest x-ray does not tell the whole story: a tale of miners, selection bias, and the healthy worker effect. Am J Respir Crit Care Med. 2001;164:1761–1762.
26.Balmes J, Becklake M, Blanc P. American Thoracic Society statement: occupational contribution to the burden of airway disease. Am J Respir Crit Care Med. 2003;167:787–797.
27.Miettinen OS. Theoretical Epidemiology: Principles of Occurrence Research in Medicine. New York: Wiley & Sons; 1985.
© 2004 Lippincott Williams & Wilkins, Inc.