In October of 1846, at Massachusetts General Hospital in Boston, a dentist named William Morton gave the first public demonstration of the use of ether as an anesthetic. Word quickly spread across the Atlantic, and by mid-December, a London dentist, James Robinson, had begun using ether on his patients, usually with a small audience of amazed medical men in attendance. On December 28, he performed another successful extraction. In the room, watching, with his usual quiet and observant manner, was John Snow.
By the turn of the new year, the excitement over ether had spilled beyond the medical community and into the popular press. Punch was running mock editorials advocating its use on difficult wives. But the miracle anesthetic was unreliable in practice. Some applications would work flawlessly: the patient would nod off for the length of the surgery, and then awaken minutes later with no memory of the procedure, and a greatly minimized feeling of pain. But other patients would fail to go under, or return to consciousness abruptly in the middle of a particularly delicate operation. More than a few patients never woke up at all.
Snow quickly hypothesized that the unreliability of ether was likely a problem of dosage, and embarked on a series of interlinked experiments to determine the best mechanism for delivering the miracle gas. From his earlier studies, Snow knew the concentration of any gas varied dramatically with temperature, and yet the early adopters of etherization had failed to take room temperature into account in their procedures. A patient etherized in a chilly room would end up with a significantly lower dose than one etherized in a room warmed by a roaring fire. By mid-January, Snow had compiled a “Table for Calculating the Strength of Ether Vapour.” Increasing the temperature by twenty degrees Fahrenheit would nearly double the dosage. The Medical Times published Snow’s table at the end of January.
While compiling the data for his numerical breakdown of ether’s properties, Snow had begun collaborating with a surgeon’s instrument maker named Daniel Ferguson in making an inhaler that would allow maximum control of the dosage. Snow’s idea was to adapt the well-known Julius Jeffrey vaporizer for the purposes of delivering ether, forcing it through a metal spiral at the center of the device, thus maximizing the surface area of metal exposed to the gas as it traveled to the patient’s mouth. The unit would be placed in a vat of heated water that would transmit its warmth to the metal contraption, where it would raise the temperature of the ether. All the doctor needed to control was the temperature of the water; the device would do the rest. Once the doctor had a reliable fix on the ether’s temperature, he could determine the proper dose with little variation. Snow first presented his device to the Westminster Society on January 23, 1847.
Snow’s productivity during this period is truly astounding, when you think that the very concept of etherization simply hadn’t existed three months before. Not only had Snow detected one of the fundamental properties of the gas within two weeks of first seeing it applied, he had also engineered a state-of-the-art medical device to deliver it. And his research had only begun: in the following months, he explored the biology of etherization: everything from the initial intake of the gas in the lungs, to its circulation through the bloodstream, all the way to its psychological effects. When the medical community shifted its focus to the rival anesthetic chloroform later in 1847, Snow immersed himself in its properties as well. By the end of 1848 he had published a seminal monograph on the theory and practice of anesthesia: On the Inhalation of the Vapour of Ether in Surgical Operations.
Snow managed to build his mastery of this embryonic field almost entirely through research conducted in his own home. He maintained a small menagerie in his Frith Street quarters—birds, frogs, mice, fish—where he spent countless hours watching the creatures’ response to various dosages of ether and chloroform. He also used his medical practice as a source of experimental data, but was not above using himself as a test subject. There is something wonderful—and more than a little ironic—in this image of Snow the teetotaler, arguably the finest medical mind of his generation, performing his research. He sits alone in his cluttered flat, frogs croaking around him, illuminated only by candlelight. After a few minutes tinkering with his latest experimental inhaler, he fastens the mouthpiece over his face and releases the gas. Within seconds, his head hits the desk. Then, minutes later, he wakes, consults his watch through blurred vision. He reaches for his pen, and starts recording the data.
SNOW’S MASTERY OF ETHER AND CHLOROFORM RAISED HIM to a new echelon in the London medical world. He became the most sought-after anesthesiologist in the city, assisting with hundreds of operations a year. By the 1850s, a growing number of doctors were recommending chloroform as a palliative for the discomfort of childbirth. As the birth of her eighth child approached in the spring of 1853, Queen Victoria decided to give chloroform a try, encouraged by the scientifically astute Prince Albert. Her choice of an anesthesiologist was an obvious one. Snow gave the episode a few more words than usual in his casebooks, though his tone did not betray the magnitude of the professional honor that had been bestowed upon him:
Thursday 7 April: Administered Chloroform to the Queen in her confinement. Slight pains had been experienced since Sunday. Dr. Locock was sent for about nine o’clock this morning, stronger pains having commenced, and he found the os uteri had commenced to dilate a very little. I received a note from Sir James Clark a little after ten asking me to go to the Palace. I remained in an apartment near that of the Queen, along with Sir J. Clark, Dr. Ferguson and (for the most part of the time) Dr. Locock till a little a [sic] twelve. At a twenty minutes past twelve by a clock in the Queen’s apartment I commenced to give a little chloroform with each pain, by pouring about 15 minims [0.9 ml] by measure on a folded handkerchief. The first stage of labour was nearly over when the chloroform was commenced. Her Majesty expressed great relief from the application, the pains being very trifling during the uterine contractions, and whilst between the periods of contraction there was complete ease. The effect of the chloroform was not at any time carried to the extent of quite removing consciousness. Dr. Locock thought that the chloroform prolonged the intervals between the pains, and retarded the labour somewhat. The infant was born at 13 minutes past one by the clock in the room (which was 3 minutes before the right time); consequently the chloroform was inhaled for 53 minutes. The placenta was expelled in a very few minutes, and the Queen appeared very cheerful and well, expressing herself much gratified with the effect of the chloroform.
Snow’s research into anesthesia had elevated him from a surgeon of humble origins to the very apogee of Victorian London. But, in a way, the most impressive thing about his research was not the levels of social class that he traversed but rather the intellectual strata, the different scales of experience that his mind crossed so effortlessly. Snow was a truly consilient thinker, in the sense of the term as it was originally formulated by the Cambridge philosopher William Whewell in the 1840s (and recently popularized by the Harvard biologist E. O. Wilson). “The Consilience of Inductions,” Whewell wrote, “takes place when an Induction, obtained from one class of facts, coincides with an Induction obtained from another different class. Thus Consilience is a test of the truth of the Theory in which it occurs.” Snow’s work was constantly building bridges between different disciplines, some of which barely existed as functional sciences in his day, using data on one scale of investigation to make predictions about behavior on other scales. In studying ether and chloroform, he had moved from the molecular properties of the gas itself, to its interactions with the cells of the lungs and the bloodstream, to the circulation of those properties through the body’s overall system, to the psychological effects produced by these biological changes. He even ventured beyond the natural world into the design of technology that would best reflect our understanding of the anesthetics. Snow was not interested in individual, isolated phenomena; he was interested in chains and networks, in the movement from scale to scale. His mind tripped happily from molecules to cells to brains to machines, and it
was precisely that consilient study that helped Snow uncover so much about this nascent field in such a shockingly short amount of time.
And yet, there was a ceiling to his intellectual pursuit of ether and chloroform: his research stopped at the scale of the individual subject. The next step up the chain—the larger, connected world of cities and societies, of groups, not individuals—did not factor into his anesthesia investigations. He might have attended on the queen’s body, but the body politic remained outside Snow’s frame of reference.
Cholera would change all that.
WE DON’T KNOW EXACTLY WHAT SEQUENCE OF EVENTS turned John Snow’s interest toward cholera in the late 1840s. For this working physician and researcher, of course, the disease would have been a constant presence in his life. There may in fact have been a direct link to his practice as an anesthesiologist, since chloroform had been (wrongly) championed as a potential cure for cholera by some early adopters who were less rigorous in their empiricism than Snow. Certainly, the outbreak of 1848–1849, the most severe British outbreak in more than a decade, made cholera one of the most urgent medical riddles of its time. For a man like Snow, obsessed with both the practice of medicine and the intellectual challenge of science, cholera would have been the ultimate quarry.
There were practically as many theories about cholera as there were cases of the disease. But in 1848, the dispute was largely divided between two camps: the contagionists and the miasmatists. Either cholera was some kind of agent that passed from person to person, like the flu, or it somehow lingered in the “miasma” of unsanitary spaces. The contagion theory had attracted some followers when the disease first reached British soil in the early 1830s. “We can only suppose the existence of a poison which progresses independently of the wind, of the soil, of all conditions of the air, and of the barrier of the sea,” The Lancet editorialized in 1831. “In short, one that makes mankind the chief agent for its dissemination.” But most physicians and scientists believed that cholera was disease spread via poisoned atmosphere, not personal contact. One survey of published statements from U.S. physicians during the period found that less than five percent believed the disease was primarily contagious.
By the late 1840s the miasma theory had established a far more prestigious following: the sanitation commissioner, Edwin Chadwick; the city’s main demographer, William Farr; along with many other public officials and members of Parliament. Folklore and superstition were also on the side of the miasmatists: the foul inner-city air was widely believed to be the source of most disease. While no clear orthodoxy existed regarding the question of cholera’s transmission, the miasma theory had far more adherents than any other explanatory model. Remarkably, in all the discussion of cholera that had percolated through the popular and scientific press since the disease had arrived on British soil in 1832, almost no one suggested that the disease might be transmitted by means of contaminated water. Even the contagionists—who embraced the idea that the disease was transmitted from person to person—failed to see merit in the waterborne scenario.
Snow’s detective work into cholera began when he noticed a telling detail in the published accounts of the 1848 epidemic. Asiatic cholera had been absent from Britain for several years, but it had recently broken out on the Continent, including the city of Hamburg. In September of that year, the German steamer Elbe docked in London, having left port at Hamburg a few days earlier. A crewman named John Harnold checked into a lodging house in Horsleydown. On September 22, he came down with cholera and died within a matter of hours. A few days later, a man named Blenkinsopp took over the room; he was seized by the disease on September 30. Within a week, the cholera began to spread through the surrounding neighborhood, and eventually through the entire nation. By the time the epidemic wound down, two years later, 50,000 people were dead.
Snow recognized immediately that this sequence of events posed a severe challenge to the opponents of the contagion model. The coincidence was simply too much for the miasma theory to bear. Two cases of cholera in a single room in the space of a week might be compatible with the miasma model, if one believed that the room itself contained some kind of noxious agent that poisoned its inhabitants. But it was stretching matters beyond belief to suggest that the room should suddenly become prone to those poisonous vapors the very day it was occupied by a sailor traveling from a city besieged by the disease. As Snow would later write: “Who can doubt that the case of John Harnold, the seaman from Hamburgh, mentioned above, was the true cause of the malady in Blenkinsopp, who came, and lodged, and slept, in the only room in all London in which there had been a case of true Asiatic cholera for a number of years? And if cholera be communicated in some instances, is there not the strongest probability that it is so in the others—in short, that similar effects depend on similar causes?”
But Snow also recognized the weakness of the contagionist argument. The same doctor attended both Harnold and Blenkinsopp, spending multiple hours in the room with them during the rice-water phase of the disease. And yet he remained free of the disease. Clearly, the cholera was not communicated through sheer proximity. In fact, the most puzzling element of the disease was that it seemed capable of traveling across city blocks, skipping entire houses in the process. The subsequent cases in Horsleydown erupted a few doors down from Harnold’s original lodging house. You could be in the same room with a patient near death and emerge unscathed. But, somehow, you could avoid direct contact altogether with the infected person and yet still be seized with the cholera, simply because you lived in the same neighborhood. Snow grasped that solving the mystery of cholera would lie in reconciling these two seemingly contradictory facts.
We do not know if Snow hit upon the solution to this riddle sometime in the months that followed the initial 1848 outbreak, or if perhaps the solution had long lingered in the back of his mind, a hunch that had first taken shape more than a decade before, as he tended to the dying miners in Killingworth as a young surgeon’s apprentice. We do know that in the weeks after the Horsleydown outbreak, as the cholera began its fatal march through the wider city and beyond, Snow embarked on a torrid stretch of inquiry: consulting with chemists who had studied the rice-water stools of cholera victims, mailing requests for information from the water and sewer authorities in Horsleydown, devouring accounts of the great epidemic of 1832. By the middle of 1849, he felt confident enough to go public with his theory. Cholera, Snow argued, was caused by some as-yet-unidentified agent that victims ingested, either through direct contact with the waste matter of other sufferers or, more likely, through drinking water that had been contaminated with that waste matter. Cholera was contagious, yes, but not in the way smallpox was contagious. Sanitary conditions were crucial to fighting the disease, but foul air had nothing to do with its transmission. Cholera wasn’t something you inhaled. It was something you swallowed.
Snow built his argument for the waterborne theory around two primary studies, both of which showcased talents that would prove to be crucial five years later, during the Broad Street outbreak. In late July of 1849, an outbreak of cholera killed about twelve people living in slum conditions on Thomas Street in Horsleydown. Snow made an exhaustive inspection of the site and found ample evidence to support his developing theory. All twelve lived in a row of connected cottages called the Surrey building, which shared a single well in the courtyard they faced. A drainage channel for dirty water ran alongside the front of the houses, connecting to an open sewer at the end of the courtyard. Several large cracks in the drain allowed water to flow directly into the well, and during summer storms, the entire courtyard would flood with fetid water. And so a single case of cholera would quickly spread through the entire Surrey building population.
The layout of the Thomas Street flats provided Snow with an ingenious control study for his inquiry. The Surrey building backed onto a set of houses that faced another courtyard known as Truscott’s Court. These abodes were every bit as squalid as the Surrey building, with the exact same de
mographic makeup of poor working families living within them. For all intents and purposes, they shared the same environment, save one crucial difference: they got their water from different sources. During the two-week period that saw the deaths of a dozen residents in the Surrey building, only one person perished in Truscott’s Court, despite the fact that both groups lived within yards of each other. If the miasma were responsible for the outbreak, why would one squalid, impoverished group suffer ten times the loss of the one living next door?
The Thomas Street outbreak showcased Snow’s on-the-ground investigative skills, his eye for the details of transmission patterns, sanitary habits, even architecture. But Snow also surveyed the outbreak from the bird’s-eye view of citywide statistics. During his research, Snow had amassed an archive of information about the various companies that supplied water to the city, and that study had revealed a striking fact: that Londoners living south of the Thames were far more likely to drink water that had originated in the river as it passed through Central London. Londoners living north of the river drank from a variety of sources: some companies piped in water from the Thames above Hammersmith, far from the urban core; some drew from the New River in Hertfordshire to the north; others from the River Lea. But the South London Water Works drew its supply from the very stretch of the river where most of the city’s sewers emptied. Anything that was multiplying in the city’s intestinal tracts would be more likely to find its way into the drinking water of South London. If Snow’s theory of cholera was on the mark, Londoners living below the Thames should have been significantly more prone to the disease than those living above.
Snow next surveyed the tables of cholera death that had been compiled by William Farr, London’s registrar-general. What he found there followed the pattern that the water-supply routes predicted: of the 7,466 deaths in the metropolitan area during the 1848–1849 epidemic, 4,001 were located south of the Thames. That meant that the per capita casualty rate was near eight per thousand—three times that of the central city. In the growing suburbs of West and North London, the death rate was just above one per thousand. For the miasmatists, who were inclined to blame those death rates on the foul air of the working-class neighborhoods south of the river, Snow could point to the neighborhoods of the East End, which were probably the most destitute and overcrowded of any in the city. And yet their death rate was exactly half that of the area south of the Thames.
The Ghost Map Page 7
