Episode 44: The Great Smog

What was behind the mysterious increase in lung cancer deaths at the turn of the 20th century? The first of a three-parter investigating the cigarette-smoking link and causality, this episode looks at that early debate, which largely focused on environmental pollution. Along the way, we’re going to talk about toxic vapors — and not Miasma theory, but the actual literal Great Smog of London in 1952 that killed over 10,000 people — as well as the birth of the case-control study, Nazi attempts at tobacco control programs, and the rather prosaic beginnings of a debate that rages to this day. Plus a new #AdamAnswers about the medical cause of Game of Thrones greyscale featuring Dr. Jules Lipoff!


  • Bell, M. L., Davis, D. L. & Fletcher, T. A retrospective assessment of mortality from the London smog episode of 1952: the role of influenza and pollution. Environ Health Persp 112, 6–8 (2003).
  • Brunekreef B, Air Pollution and Life Expectancy: Is There a Relation? Occupational and Environmental Medicine, Vol. 54, No. 11 (Nov., 1997), pp. 781-784.
  • Des Voeux HC, Smoke and Fog, The Lancet, 1679-1680 (1904).
  • Logan WPD, Mortality in the London Fog Incident, 1952. The Lancet, 336-338 (1953).
  • Heirdorn KC, The Weather Doctor’s Weather Almanac: The Infamous London Smog of 1952, 2012.
  • HOFFMAN, F. L. CANCER AND SMOKING HABITS. Ann Surg 93, 50–67 (1931).
  • Morabia, A. Quality, originality, and significance of the 1939 “Tobacco consumption and lung carcinoma” article by Mueller, including translation of a section of the paper. Prev Med 55, 171–177 (2012).
  • Ochsner, A. My first recognition of the relationship of smoking and lung cancer. Prev Med 2, 611–614 (1973).
  • Ochsner, A. & bakey. Primary pulmonary malignancy: treatment by total pneumonectomy; analysis of 79 collected cases and presentation of 7 personal cases. Ochsner J 1, 109–25 (1999).
  • Parascandola, M. Two approaches to etiology: the debate over smoking and lung cancer in the 1950s. Endeavour 28, 81–86 (2004).
  • Press, D. J. & Pharoah, P. Risk Factors for Breast Cancer. Epidemiology 21, 566–572 (2010).
  • Proctor, R. Angel H Roffo: the forgotten father of experimental tobacco carcinogenesis. B World Health Organ 84, 494–495 (2006).
  • Proctor, R. N. The anti-tobacco campaign of the Nazis: a little known aspect of public health in Germany, 1933–45. Bmj 313, 1450 (1996).
  • Proctor, R. On playing the Nazi card. Tob Control 17, 289–290 (2008).
  • Winkelstein, W. Vignettes of the History of Epidemiology: Three Firsts by Janet Elizabeth Lane-Claypon. Am J Epidemiol 160, 97–101 (2004).
  • Proctor R, The history of the discovery of the cigarette–lung cancer link: evidentiary traditions, corporate denial, global toll. Tobacco Control. 21:2 (2013).


This is Adam Rodman, and you’re listening to Bedside Rounds, a monthly podcast on the weird, wonderful, and intensely human stories that have shaped modern medicine, brought to you in partnership with the American College of Physicians. This episode is called “The Great Smog,” and it’s the first of a three-parter on how the debate about what caused the dramatic increase in lung cancer — and the attempts to finger cigarette smoking in particular — revolutionized our ability to determine causality — that is, what exactly causes disease. And not just revolutionized — it cracked open fault lines that still smolder today. You can still see this debate regularly  exploited in the media, with constant stories about whether or not coffee drinking causes cancer, or whether eatings eggs is going to kill you. In this episode, we’re going to start in those early days of the debate, when it was generally assumed that environmental pollution was behind the great increase in lung cancer. Along the way, we’re going to talk about toxic vapors — and not Miasma theory, but the actual literal Great Smog of London in 1952 — the birth of the case-control study, Nazi attempts at tobacco control programs, and the rather prosaic beginnings of a debate that rages to this day.


We’re going to start in the early years of the 20th century, before the Great War. You’d have to forgive doctors in this period if they had a little bit of whiplash. Within a generation, the causative basis of medicine had fundamentally shifted under their feet. It’s hard to exaggerate how much an impact germ theory had on the minds, even decades before effective antibiotics. Take tuberculosis, largely accepted in the Germanic and English-speaking world to be caused by a “consumptive diathesis” — that is, hereditary in some way. Now it had been definitely shown to be caused by a small, round organism now called mycobacterium tuberculosis. There was now a reasonably cheap and easy test to identify this previously mysterious disease in sputum using techniques developed during the chemical revolution, and new therapies — like collapsing lungs to obliterate tubercular cavities — were developed. And with better understanding of the disease both incidence and mortality plunged. Tuberculosis was only one example; over a few decades dozens of diseases were identified as being infectious in nature. And by 1910, the first effective drug therapy for an infectious disease — Salvarsan, for syphilis — was introduced. 


I think you have to keep these dramatic changes in mind to understand the debate in the early years of the 20th century about another medical mystery — what was behind the dramatic increase of lung cancer at the beginning of the 20th century? Cancer, of course, is an ancient diagnosis, with descriptions dating back to the Egyptians and Greeks. By the nineteenth century, cancerous growth of all sorts of organs — the gut, the liver, the skin, the brain — had been well-described. But not of the lung. Lung cancer was virtually unknown. Isaac Adler, who wrote the first monograph on the subject in 1914, starts by writing, “One one point, however, there is nearly complete consensus of opinion, and that is that primary malignant neoplasms are among the rarest forms of disease.” 


Take, for example, the experience of Alton Ochsner, a preeminent chest surgeon, who would become one of America’s foremost anti-tobacco activists and who founded the Ochsner clinic in New Orleans, where I was lucky enough to rotate when I was a young medical student at Tulane. In 1920, Ochsner himself was a medical student at Washington University in St. Louis, when a patient with lung cancer was admitted to Barnes Hospital, and soon thereafter died. As Ochsner recalled it, the chief pathologist of the hospital gathered all the medical students into the autopsy because, “as he succinctly said, the condition was so rare he thought we might never seen another case as long as we lived.” 


Like I’ve discussed in previous episodes about the development of pathological anatomy, the standard of care throughout the 19th century was to perform an autopsy as soon as possible after death, often by the doctor who had been taking care of the patient. The idea was to “catch” the transition between life and death, and thereby identify the cause of death as accurately as possible. The practice began in the Paris Clinical School with Laennec, Bichat, Bayle, and colleagues, but it really took off in the German-speaking world starting in the middle of the 19th century.  This led to increasingly detailed statistics on post-mortem causes of death — as well as advanced methods of autopsy and determining cause of death. Carl von Rokistansky, for example, performed an estimated 30,000 autopsies, and supervised an additional 70,000, over the course of his career. Along the way he described a number of diseases, which is why there are so many “Rokitanksy’s” in medicine to torture medical students. Chief among them for pathologists in the “Rokitanksy technique” for performing an autopsy, which is still used today.  All of this is to say, by the early 20th century, there was a lot of detailed pathological data on cause of death when Adler sat down to write his first monograph on lung cancer. And this data was unequivocal — lung cancer was increasing, and dramatically. Just one example — in 1840 in England the estimated lung cancer rate was 177 per million, compared to almost 1,000 per million just 60 years later, with similar rates of increase noted in basically every country that kept detailed statistics.


Let’s go back to Ochsner. That single case of lung cancer back in St. Louis had made a profound impression on him. After medical school, he moved down to New Orleans and became a professor of surgery at Tulane University working in the busy Charity Hospital. In 1937 — 17 years later — he saw another case of lung cancer, which was surprising, but not truly shocking. But in the next six months, 8 more cases walked into his clinic. “Having been impressed with the extreme rarity of the condition 17 years previously, the sudden increase in incidence represented an epidemic, and there had to be some reason for it.”


Ochsner was convinced by the reality of the increase, but that was not the medical consensus. In reviewing the data, Adler actually dismissed it, writing, “It is the conviction of the writer, and he shares this belief with many others, that there is no absolute increase in the incidence of carcinoma.” Basically, he felt that the apparent increase in lung cancer was rather due to better ability to diagnose it. And this is most certainly true to a certain extent. In the early 19th century, many cases of lung cancer were likely misdiagnosed as either tuberculosis or pneumonia. Even today, with antibiotics, infection is still the cause of death of a plurality of patients with lung cancer (https://www.ncbi.nlm.nih.gov/pubmed/23194048), and in the 19th century would likely have the majority cause.  By the late 19th century, with Virchow definitively showing that cells, rather than tissues, were the seat of disease, microscopic analysis of tumors had become standardized, and more and more chemical stains were used, further increasing the ability to diagnose lung cancer. These techniques were showing that doctors were quite poor at diagnosing cancer during life. Adler quotes statistics from Friedrichschain Hospital, where over half of lung cancers were not diagnosed until after death with pathological methods.


The problem with this line of argument was that the most convincing evidence for an increase came from places that had well established autopsies — especially Germany. And hospital records there showed as well a dramatic increase. Adler discusses an alternative theory, that perhaps a dramatic increase in air pollution, especially from coal burning and road tarring , is behind the increase. But buried deep in his work, he makes one curious observation. The rate of lung cancer increase was far higher in men than in women. But this wouldn’t make sense if the reason were underdiagnosis, or if it were environmental air pollution, which would affect everyone equally.


Presciently, he writes, “the domestic life led by women, with their consequent retirement and immunity from the irritations and traumatisms which must be frequent in the more unprotected life of men (the abuse of tobacco and alcohol, the many trades and vocations which are accompanied by irritations of the respiratory organs, etc) has been adduced in explanation of this fact. The entire subject is not yet ready for final judgement.”


It may have not been ready for final judgement, but just a decade later the larger medical community had taken notice — wide recognition of the increase in lung cancer, but disagreement about whether it represented an absolute increase on the one hand, or that it was real and largely due to environmental pollution on the other. The idea that smoking tobacco might be behind the increase was a minority view. Chief among them was Alton Ochsner, whose experiences with patients with lung cancer convinced him that cigarette smoking was the culprit. All of his patients had been heavy smokers, and in 1939 he wrote with Michael Debakey, another great of medicine from Tulane, I might add, “In our opinion the increase in smoke with the universal custom of inhaling is probably a responsible factor [in the increase in pulmonary carcinoma], as the inhaled smoke, constantly repeated over a long period of time, undoubtedly is a source of chronic irritation to the bronchial mucosa.”


But Debakey and Ochsner were widely ridiculed. Tobacco by the 1930s was widespread and largely viewed as safe — and even healthy. Tobacco smoking, of course, is many centuries old, having spread from the New World to the old thanks to European colonizers. And concerns about its negative effects on the human body are equally old. For example, Kings James VI in 1604 wrote a treatise called “A Counterblaste to Tobacco,” where he calls tobacco smoking, “A custome lothsome to the eye, hatefull to the Nose, harmefull to the braine, dangerous to the Lungs, and in the blacke stinking fume thereof, neerest resembling the horrible Stigian smoke of the pit that is bottomelesse.”


Various anti-smoking societies had sprouted up across the West, but they usually operated on moralistic lines of thought — smoking was another intoxicant, like alcohol, leading the youth astray. That being said — despite the concerns of King James and legions of anti-smoking activists throughout the centuries, no one likely smoked many cigarettes until the late 19th century. Cigarettes would have to be hand-rolled, a time consuming process, and pipe smoking, with a need for fresh tobacco, was the norm. That is, until 1880, when James Bonsack invented his cigarette-rolling machine. It could roll 200 cigarettes a minute — over 20,000 cigarettes a day. Combine this vast industrial manufacturing capability, an increasingly sophisticated advertising industry, and the widespread use of cigarettes on both sides in WWI to calm soldier’s nerves, and you have the makings for widespread adoption of cigarette smoking. Take statistics from the US Department of Agriculture; around 1900 the per capita annual cigarette consumption in the US hovered around 0. By the great depression, it was about 1500, and by the end of WWII it was almost 3500. This chart is on the Twitter thread, by the way. And as tobacco companies grew, they developed more and more influence over governments. By Ochsner and Debakey’s time, the phrase “More Doctors Smoke Camels” was firmly ingrained in the public consciousness, and it was standard to doctors to offer a cigarette to patients prior to an exam.


They were arguing against powerful companies, and an overwhelming public perception that cigarettes were beneficial, or at least not harmful. But I think it’s important to recognize how they were making their argument. Anyone who listens to this show knows that I’m a little bit obsessed with the nature of medical epistemology — how doctors “know” things. Ochsner and Debakey were making one of the oldest medical arguments known to man, an argument from their own observation, or empiricism. This is still a valid — and popular — type of medical knowledge, hence the widespread use of case reports. But as the oft-referenced and even-more-often misunderstood quote goes, “the plural of anecdote is not data.”


The second type of medical knowledge is experimentation — essentially the scientific method. The most active researcher in this field was Angel Roffo, who had founded Argentina’s Institute of Experimental Medicine for the Study and Treatment of Cancer. In 1931, he showed that that tars distilled from tobacco smoke could cause cancer when applied to rabbit skin, and throughout the 1930s and 1940s he published dozens of studies — including one which identified polycyclic aromatic hydrocarbons in tobacco smoke, a known carcinogen. These experiments certainly concerned some within the tobacco industry, who quickly performed their own experiments and confirmed his findings — so much so that by 1961, the research director of Philip Morris would write that carcinogens were found in “practically every class of compounds in cigarette smoke.”


These experiments certainly had some impact — within tobacco companies, and in the public health apparatus of a single country, which I’ll talk about in a second, but otherwise they didn’t really convince anyone else. Naked rabbits with skin cancer, after all, are a far cry from cigarettes causing lung cancer.


Which, of course, brings us to the third type of medical knowledge — looking at large groups of human beings, or population medicine. So a quick refresher, which should be familiar to anyone who listens to Bedside Rounds. The first population study was done in the 1820s in Paris by Pierre Louis, who analyzed data on patients with pneumonia to determine that bloodletting was largely ineffective. Throughout the 19th and early 20th century, these sorts of studies became more and more common — retrospectively looking at data from large groups of patients to try and determine if an exposure or an intervention cause or cured disease. These initial studies were what we would today call retrospective cohort trials — looking at patients who were exposed to an intervention, and then seeing if a certain outcome was met. So Pierre Louis, for example, looked at patients who received early- and late-bloodletting, and looked to see if there was any difference in death rates. Many of the weaknesses of these sorts of studies were clear from the very beginning — there was no easy way to ensure that the populations being studied were equivalent, let alone whether there might be hidden confounders.


The field would be revolutionized by Janet Layne-Claypon, a physician-epidemiologist at the Medical Research Council in the UK. Fun fact — she was one of the first MD/PhDs. In 1912, she published a retrospective cohort study of babies either breast fed or those given cows milk. She found that the breast-fed babies gained more weight, but she also became frustrated at the possibility of confounders in her data — that there might be something fundamentally different about the two groups that she hadn’t realized. So when she set out to study breast cancer, she chose a different tact. She recruited 500 women with breast cancer, her “cases,” and then went about finding another 500 women as similar as she could find to the first group, except that they didn’t have breast cancer — her controls. By asking detailed questions of the two groups, she could potentially identify hidden risk factors for breast cancer. What she found still stands true today — women with no children, those who delayed childbirth, and women who didn’t breast feed are all at a higher risk of breast cancer. But more importantly — she had invented a potent new way to study risk factors for developing a disease. As an aside — in 1929, Layne-Clapton married, and as was tradition retired from civil service, thus prematurely ending the work of a ground-breaking physician scientist. How much scientific knowledge have we lost by essentially cutting out half the human population for most of our history?


But back to cigarettes. Like I mentioned earlier, experiments on animals didn’t really convince anyone, with one glaring exception — Nazi Germany. The Nazis, and Hitler in particular, were vehemently anti-smoking. The historian Robert Proctor has written several fascinating articles and a book on the subject. In the beginning of the 20th century, the Germans were arguably the most scientifically-advanced society on the planet, but with the rise of Nazism, a concern with the effects of smoking on health took a particularly eugenical bent. Hitler called cigarette smoking “the wrath of the Red Man against the White Man for having been given hard liquor,” and despite a powerful tobacco industry and lobby, Germany banned smoking in public places, street cars, in the SS and Luftwaffe, on active duty in the army, sale of cigarettes to anyone under the age of 18, and the sale of cigarettes to pregnant and young women, out of concern of the effects of smoke on the developing fetus. So it should be not be particularly surprising that some of the first research on the effects of cigarette smoking was completed in Nazi Germany first by Mueller in 1939, and then Shairer and Schoeniger in 1943. Mueller studied 86 males patients with lung cancer and found that only 3 were nonsmokers, and 56 were heavy smokers. He matched these with 86 “healthy men of the same age groups” and found 14 nonsmokers among them, and only 31 heavy smokers; Shairer and Schoeniger largely confirmed these results four years later. But these were relatively small groups, and it was not entirely clear how they had selected their controls. In 2013, Morabia reviewed the paper and re-analyzed the data, and was not impressed. He concludes, ”the study was of modest quality and evidence and did not add qualitatively new knowledge about the causal link of tobacco smoke and lung cancer compared to a report published 8 years earlier.” He is referring to a similar study in the US by Hoffman, 8 years earlier, with largely similar findings. 


And while these German researchers didn’t make a splash anywhere else in the world, in Germany and other fascist countries, it was increasingly accepted that smoking caused lung cancer. After all, Hitler, Mussolini, and Franco were all non-smokers, while Churchill, Roosevelt, and Stalin all smoked like chimneys. This fascist association took the wind out of the sails of the antitobacco movement, and as World War II ended, the world seemingly abandoned the tobacco hypothesis in favor of environmental pollution. 


This seems absurd to us now, but sometimes it’s easy to forget just quite how polluted — and deadly — high income countries were prior to modern environmental protections. The most dramatic example was probably the Great Smog of London. During World War 2, for almost a year between 1940 and 1941, over 2,000 German planes had relentlessly bombed civilians in London trying to break British morale — the Blitz, from the German word for lightning. Almost 20,000 people were killed in the city, and probably twice that number wounded. Not a decade later, a self-inflicted Great Smog struck the city, and in just five days left perhaps 12,000 dead, 140,000 hospitalized, and health impacts on survivors that would last a lifetime. 


Bad air was nothing new to the city of London. As early as 1661, John Evelyn had published the wonderfully-titled, Fumifugium, or, The inconveniencie of the aer and smoak of London dissipated together. It’s based on a miasmatic understanding of epidemic disease, but it showed a keen understanding of the effects of coal-burning, especially “sea coal,” high in sulfur dioxide, which was primarily used for heating and industry. He recommended switching to wood, which he felt was less polluting, and moving industry outside the city, where weather conditions were more favorable. The Fumifugium was famously summed up in iambic pentameter after Evelyn was elected to the Raol Society:


He shows that ’tis the sea-coal smoke

That always London does environ, 

Which does our lungs and spirits choke, 

Our hanging spoil, and rust our iron. 

Let none at Fumifuge be scoffing 

Who heard at Church our Sunday’s coughing


England was the first nation to industrialize, which added even more coal to the mix — not just burned to heat houses, but to power the great factories and railroads of Dickensien London. These are the famous “pea-soup” fogs, which Dickens described in the Bleak House:


“Fog everywhere. Fog up the river, where it flows among green aits and meadows; fog down the river, where it rolls defiled among the tiers of shipping, and the waterside pollutions of a great (and dirty) city…Chance people on the bridges peeping over the parapets into a nether sky of fog, with fog all round them, as if they were up in a balloon, and hanging in the misty clouds.”


By the early 20th century, it had become increasingly clear that these fogs were a cause of disease, and British doctors had started to agitate for change. One of these was HA Des Voeux, a physician who began to track increases in “smoke-fog” deaths during the “pea soupers” in the industrial cities of England, and worked with the Coal Smoke Abatement Society, one of the first environmental groups in history. In a report in 1905, he contracted “smoke-fog” to “smog,” and a dramatic new cause of disease was born. 


It was the destruction from the Blitz, ironically, that likely fueled the Great Smog. Great Britain had rebuilt rapidly after the war, opening scores of new electrical plants. Think the iconic Battersea Power Station, famously pictured on the cover of Pink Floyd’s Animals — the one with the giant floating pig that famously broke free from its moorings and drifted into the flight path of Heathrow. I’ve posted the video to the shownotes, not only because I think Animals is the best Pink Floyd album, but because you can clearly see the billowing smoke pouring out of the plant — fueled the same high-sulfur “sea coal” that Evelyn had complained about 400 years before.


December 4th, 1952 was unusually cold; Londoners fired up their coal stoves, or those with more modern houses turned on their electric heating. Unfortunately, a combination of environmental factors  joined together to make a subsidence inversion, trapping all those emissions into a thin strip less than 200 meters in height, choking the city of London. I’m posting some videos and photos to Twitter — but the effects were dramatic. Visibility in the city was less than a meter and city busses had to be evacuated from the street, led in a convoy by conductors on foot carrying flares and leading a “huge, red, metallic caterpillar” slowly winding through the streets to safety. A permanent dusk settled on the city; purse snatching increased, the police recommended that children stay home from school, not because of health effects, but because they might get lost in the darkness. There was no escape — the thick soupy smog permeated everything and every building. Movies were canceled since viewers couldn’t see the screen. Famously — and I’ll add, anecdotally, on the Isle of Dogs in the Thames, the blind helped the seeing through the streets, as visibility was so bad they couldn’t even see their feet. 


By the 9th — just five days later — wind and rain came, pushing the Great Smog out to sea. The city took a deep breath of fresh — or at least fresher — air. But the human toll was clear. In the days after the smog, doctors noted the increased emergency bed requests, undertakers noted that they were running out of coffins, and florists ran of flowers for funerals.  These anecdotes would be quickly born out by data. In February 1953, Dr. Logan, the chief medical statistician of the General Register Office, released a report on mortality statistics during the Great Smog. He first goes over mortality data from previous smog attacks; the worst previously recorded was in 1948 in the Meuse Valley in Belgium, which killed 64 people. What he found was death rates two orders of magnitude higher — almost 4,000 had died in just five days, with London death rates equivalent to those during the great cholera epidemic of 1854, and the flu epidemic of 1918-19. Respiratory diseases were especially increased, with 8 times the average deaths from bronchitis and pneumonia, and older people were especially affected. 


In retrospect, this number was an underestimate. Bell and her colleagues re-analyzed the government data and found that almost 12,000 deaths could be attributed to the Great Smog. More recently, researchers have analyzed the long-term health effects of the “natural experiment” of the Great Smog. For example, Bharadwaj and his colleagues found that exposure to the Great Smog in the first year of life increased the likelihood of childhood asthma was 20%, and adult asthma was 10%. Even in the unborn — in utero exposure led to an 8% increase of childhood asthma later in life.


So that a lifetime of toxic air — of power stations, road tarring, automobile exhaust, factories — might be behind the increase in lung cancer should have been a pretty natural assumption. And the political reaction to the Great Smog of London in Britain, as well as to similar pollution-fueled disasters around the world, like the famous Cuyahoga River Fire in 1969 in Cleveland, Ohio, challenges some of the assumptions we’ve made about the reaction to cigarettes and cancer. Because energy companies, like tobacco companies, were wealthy, politically connected, and had unarguably led to material benefits for citizens across the developed world. Yet the Clean Air Act was passed in 1956 in the UK and the Air Pollution Control Act in the United States in 1955 — both in direct response to public outcry from the health impacts of the Great Smog. I should point out that most of this legislation and benefits have been in wealthy countries — outdoor urban air pollution still causes almost 800,000 deaths a year worldwide, with indoor air pollution causing another 1.6 million, mostly in low– and middle-income countries. 


But the health effects have been dramatic — the Environmental Protection Agency in the United States estimates that in the year 2020, the Clean Air Act — which was the 1970 update to the Air Pollution Control Act — will save 230,000 adult lives, prevent 200,000 heart attacks, prevent 2.4 million asthma exacerbations, and lead to a reduction in 17 million lost work days. And while there have been economic costs to the stricter regulations, the EPA suggests that for every dollar spent, 30 are saved, with most of the savings in health expenditures; the most optimistic estimation puts those benefits at 90 dollars saved for every one spent.


Why then did the Great Smog and the dramatic air pollution lead rapidly to legislation against polluters in developed nations, whereas the nascent evidence against tobacco smoke would take decades more to see any meaningful legislation?There are, of course, a number of reasons — the media-savvy strategies of tobacco companies, libertarian and anti-fascist public opinion that was loathe to restrict something enjoyable, and the economic concentration of a single industry. But I’d argue that perhaps even more fundamentally was a real debate about causality and epistemology — it’s not hard to determine that pollution exposure causes an emergency room visit the next day, or a heart attack death the next week. But how do you tell that a single exposure causes a disease 10, 20, 30 years down the line? How can we really determine what causes chronic diseases?

That’s it for part 1. But I want you to mull that question — because the answer, and the implications of that answer, are still being debated today .And to tell parts 2 and 3 about Richard Doll, Austin Bradford Hill, and their attempts to answer this question about lung cancer and cigarette smoking, I’m going to be joined again by my favorite internist-turned-epidemiologist, and the smartest person I know, Dr. Shoshana Herzig. So tune in next month!


But wait, now it’s time for a #AdamAnswers!


And that’s right — in honor of Game of Thrones coming back for its final season, we have a Westeros-themed #AdamAnswers — the segment on the show where I answer whatever questions you might have about medicine, or in this case, find someone a lot smarter than me to do it!


Fun fact about the Game of Thrones theme song — Game of Thrones started when I was a wee medical student starting on my surgery rotation, so I set my alarm to be the ringtone to wake me up at 4:00 in the morning, thinking that it would pump me up for my day. Instead, it just made me associate the theme with a 12-day of retracting. With that med school nostalgia, it’s appropriate that I have a question from one of my medical school mentors, Ben Rothwell, who asks, “In honor of Game of Thrones coming back what do you think is the pathogen responsible for Greyscale?”


Ben — and it’s still weird to call you that instead of Dr. Rothwell — instead of my opinion, I called up the global expert greyscale:




So there you have it Ben — epidermodysplasia verruciformis, likely caused by an HPV-like virus! Or a literary take on medieval leprosy — inspired possibly by psoriasis!


In any event, I had a wonderful time chatting with Jules — and hope to see you again soon! You can and should follow him on Twitter @juleslipoff for more dermatology goodness.


Now that’s really it for the show! Let me know what you thought! This was originally going to be a single episode, but when I looked at a 20-page draft with some 40 references, I realized I had a monster on my hands. A couple of announcements — Tony Breu and I are doing a live podcast at the ACP National Meeting on April 11th at 11:15 AM. We can’t wait to see you there! And there is also going to be a meet up later that day! The Internal Medicine Podcasters Unite, hosted by Human Diagnosis, will be at McGillin’s Olde Ale House in downtown Philly, with the Curbsiders, Annals on Call, CoreIM, CPSolvers, and myself! Tickets are $15 I believe and include light fare and an open bar. The Curbsiders have done all the work in setting this up — so head over their way! And finally, to act like a realish podcaster who’s interested in self-promotion, I hired the talented medical student/artist Ryoko Hamaguchi to produce an awesome Bedside Rounds sticker showing Leuwenhoek’s animalcules. Come find me in Philly and I’ll have them on hand! Ryoko’s not only Twitter, but her amazing artwork in on her website at ryokohamguchi.carbonmade.com. And finally, I was interviewed in Mark Shapiro’s excellent healthcare interview podcast Explore the Space this month. Give it a listen — and a subscribe, since Mark’s a wonderful interviewer with amazing guests!


All of the episodes are on the website at www.bedside-rounds.org, or on Apple Podcasts, Spotify, Stitcher, or the podcast retrieval method of your preference. I’m on facebook at /BedsideRounds, and on Twitter @AdamRodmanMD, where I occasionally make Tweetorials and tweet about medical history. Come say hi! I will be posting a thread with images from this episode.


All of the sources are in the shownotes.


And finally, while I am actually a doctor and I don’t just play one on the internet, this podcast is intended to be purely for entertainment and informational purposes, and should not be construed as medical advice. If you have any medical concerns, please see your primary care provider.