There is a lovely symmetry that comes from telling the story this way, because a city and a bacterium are each situated at the very extreme boundaries of the shapes that life takes on earth. Viewed from space, the only recurring evidence of man’s presence on this planet are the cities we build. And in the night view of the planet, cities are the only thing going at all, geologic or biologic. (Think of those pulsing clusters of streetlights, arranged in the chaotic, but still recognizable patterns of real human settlement patterns, and not the clean, imperial geometry of political borders.) With the exception of the earth’s atmosphere, the city is life’s largest footprint. And microbes are its smallest. As you zoom in past the scale of the bacterium and the virus, you travel from the regime of biology to the regime of chemistry: from organisms with a pattern of growth and development, life and death, to mere molecules. It is a great testimony to the connectedness of life on earth that the fates of the largest and the tiniest life should be so closely dependent on each other. In a city like Victorian London, unchallenged by military threats and bursting with new forms of capital and energy, microbes were the primary force reigning in the city’s otherwise runaway growth, precisely because London had offered Vibrio cholerae (not to mention countless other species of bacterium) precisely what it had offered stockbrokers and coffeehouse proprietors and sewer-hunters: a whole new way of making a living.
So the macro-growth of the urban superorganism and the microscopic subtleties of the bacterium are both essential to the events of September 1854. In some cases, the chains of cause and effect are obvious ones. Without the population densities and the global connectivity of industrialization, cholera might not have been as devastating in England, and thus might not have attracted Snow’s investigative skills in the first place. But in other places, the causal chains are more subtle, though no less important to the story. The bird’s-eye view of the city, the sense of the urban universe as a system, as a mass phenomenon—this imaginative breakthrough is as crucial to the eventual outcome of the Broad Street epidemic as any other factor. To solve the riddle of cholera you had to zoom out, look for broader patterns in the disease’s itinerary through the city. When health matters are at stake, we now call this wide view epidemiology, and we have entire university departments devoted to it. But for the Victorians, the perspective was an elusive one; it was a way of thinking about patterns of social behavior that they had trouble intuitively grasping. The London Epidemiological Society had been formed only four years before, with Snow as a founding member. The basic technique of population statistics—measuring the incidence of a given phenomenon (disease, crime, poverty) as a percentage of overall population size—had entered the mainstream of scientific and medical thought only in the previous two decades. Epidemiology as a science was still in its infancy, and many of its basic principles had yet to be established.
At the same time, the scientific method rarely intersected with the development and testing of new treatments and medicines. When you read through that endless stream of quack cholera cures published in the daily papers, what strikes you most is not that they are all, almost without exception, based on anecdotal evidence. What’s striking is that they never apologize for this shortcoming. They never pause to say, “Of course, this is all based on anecdotal evidence, but hear me out.” There’s no shame in these letters, no awareness of the imperfection of the method, precisely because it seemed eminently reasonable that local observation of a handful of cases might serve up the cure for cholera, if you looked hard enough.
But cholera couldn’t be studied in isolation. It was as much a product of the urban explosion as the newspapers and coffeehouses where it was so uselessly anatomized. To understand the beast, you needed to think on the scale of the city, from the bird’s-eye view. You needed to look at the problem from the perspective of Henry Mayhew’s balloon. And you needed a way to persuade others to join you there.
THAT WIDER PERSPECTIVE IS WHAT JOHN SNOW FOUND himself searching for by noon on Monday. He had reexamined his samples from the Soho wells in the light of day and found nothing suspicious in the Broad Street water. As he delivered chloroform to a patient of a nearby dentist who was performing a tooth extraction, he pondered the outbreak still raging a few blocks away. The more he thought about it, the more convinced he became that the water supply must have been contaminated somehow. But how to prove it? The water alone might not be sufficient, since he didn’t even know what he was looking for. He had a theory about cholera’s routes of transmission and its effects on the body. But he had no idea what the agent that caused cholera was exactly, much less how to identify it.
Ironically, just a few days before Snow had unsuccessfully attempted to see any telltale signs of cholera in the water, an Italian scientist at the University of Florence had discovered a small, comma-shaped organism in the intestinal mucosa of a cholera victim. It was the first recorded sighting of Vibrio cholerae, and Filippo Pacini published a paper that year describing his findings, under the title “Microscopical Observations and Pathological Deductions on Cholera.” But it was the wrong time for such a discovery: the germ theory of disease had not yet entered mainstream scientific thought, and cholera itself was largely assumed by the miasmatists to be some kind of atmospheric pollution, not a living creature. Pacini’s paper was ignored, and V. cholerae retreated back into the invisible kingdom of microbes for another thirty years. John Snow would go to his grave never learning that the cholera agent he had spent so many years pursuing had been identified during his lifetime.
The fact that Snow had no idea what cholera looked like under the microscope didn’t stop him from doing further tests on the water. After his appointment with the dentist, he returned to draw more samples from the Broad Street pump. This time he saw small white particles in the water. Back in his lab, he ran a quick chemistry experiment, which reported an unusually high presence of chlorides. Encouraged, he took the sample to a colleague, Dr. Arthur Hassall, whose skill with the microscope Snow had long admired. Hassall reported that the particles had no “organized structure,” which led him to believe they were the remnants of decomposed organic matter. He also saw a host of oval-shaped life-forms—Hassall called them “animalculae”—presumably feeding on the organic substances.
So the Broad Street water was not as pure as he had originally thought. But still, there was nothing in Hassall’s analysis that pointed definitively to the presence of cholera. If he was going to crack this case, the solution wouldn’t be found under the microscope, on the scale of particles and animalculae. He needed to approach the problem from the bird’s-eye view, on the scale of neighborhoods. He would try to find the killer through an indirect route: by looking at patterns of lives and deaths on the streets of Golden Square.
As it turned out, Snow had already spent much of the past year thinking about cholera from this perspective. After his first publications at end of the 1840s had failed to persuade the medical authorities of his waterborne theory, Snow had continued looking for evidence supporting this theory. He followed outbreaks in Exeter, Hull, and York from afar. He read William Farr’s Weekly Returns of Birth and Deaths the way the rest of the population devoured the installments of Bleak House and Hard Times. Each outbreak of the disease offered a new configuration of variables, a new pattern—and thus the possibility for a new kind of experiment, one that would unfold in the streets and cemeteries rather than in Snow’s crowded flat. In this, Snow developed a strangely symbiotic relationship with V. cholerae: he needed the disease to flourish to have a shot at conquering it. The quiet years between 1850 and 1853, during which the cholera was largely dormant in England, were good years for the health of the nation. But they were unproductive ones for Snow the investigator. When the cholera returned with a vengeance in 1853, he threw himself into Farr’s Weekly Returns with extra zeal, scanning the charts and tables for clues.
In Farr, Snow had the closest thing to an ally in the existing medical establishment. In many ways their lives had f
ollowed parallel paths. Born to poor Shropshire laborers five years before Snow, Farr had trained as a doctor in the 1830s but went on to revolutionize the use of statistics in public health in the following decade. He had joined the newly created Registrar-General’s Office in 1838, a few months after his first wife had died of that other nineteenth-century killer, tuberculosis. Farr had been hired to track the most elemental of demographic trends: the number of births, deaths, and marriages in England and Wales. Over time, though, he had refined the statistics to track more subtle patterns in the population. “Bills of Mortality” dated back to the plague years of the 1600s, when clerks first began recording the names and parishes of the dead. But Farr recognized that these surveys could be far more valuable to science if they included additional variables. He waged a long campaign to persuade physicians and surgeons to report a cause of death wherever possible, drawing upon a list of twenty-seven fatal diseases. By the mid-1840s, his reports tallied deaths not only by disease, but also by parish, age, and occupation. For the first time, doctors and scientists and health authorities had a reliable vantage point from which to survey the broad patterns of disease in British society. Without Farr’s Weekly Returns, Snow would have been stuck in the street-level view of anecdote, hearsay, and direct observation. He might still have been able to build a theory of cholera on his own, but it would have been almost impossible to persuade anyone else of its validity.
Farr was a man of science, and shared Snow’s belief in the power of statistics to shed light on medical riddles. But he also shared many assumptions with the miasma camp, and he used the number-crunching of the Weekly Returns to reinforce those beliefs. Farr thought that the single most reliable predictor of environmental contamination was elevation: the population living in the putrid fog that hung along the riverbanks were more likely to be seized by the cholera than those living in the rarefied air of, say, Hampstead. And so, after the 1849 outbreak, Farr began tabulating cholera deaths by elevation, and indeed the numbers seemed to show that higher ground was safer ground. This would prove to be a classic case of correlation being mistaken for causation: the communities at the higher elevations tended to be less densely settled than the crowded streets around the Thames, and their distance from the river made them less likely to drink its contaminated water. Higher elevations were safer, but not because they were free of miasma. They were safer because they tended to have cleaner water.
Farr was not entirely opposed to Snow’s theory. He seems to have entertained the idea that the cholera was somehow originating in the murky waters of the Thames, and then rising into the smoggy air above the river as some kind of poisonous vapor. He had clearly followed Snow’s publications and presentations closely over the years, and engaged the theory on occasion in the editorials that would sometimes accompany the Weekly Returns. But he remained unconvinced by the purely waterborne theory. He also suspected that Snow would have a difficult time proving his theory. “To measure the effects of good or bad water supply,” Farr editorialized in November of 1853, “it is requisite to find two classes of inhabitants living at the same level, moving in equal space, enjoying an equal share of the means of subsistence, engaged in the same pursuits, but differing in this respect,—that one drinks water from Battersea, the other from Kew.… But of such experimenta crucis the circumstances of London do not admit.”
Snow must have taken that last line as a slap in the face, having heard the exact same Latinate phrase used against him after the publication of his original cholera monograph four years before. Yet despite his skepticism, Farr had been intrigued enough by Snow’s waterborne theory to add a new category to his Weekly Returns. In addition to tracking the age and sex and elevation of the cholera victims, Farr would now track one additional variable: where they got their water.
THE SEARCH FOR UNPOLLUTED DRINKING WATER IS AS OLD as civilization itself. As soon as there were mass human settlements, waterborne diseases like dysentery became a crucial population bottleneck. For much of human history, the solution to this chronic public-health issue was not purifying the water supply. The solution was to drink alcohol. In a community lacking pure-water supplies, the closest thing to “pure” fluid was alcohol. Whatever health risks were posed by beer (and later wine) in the early days of agrarian settlements were more than offset by alcohol’s antibacterial properties. Dying of cirrhosis of the liver in your forties was better than dying of dysentery in your twenties. Many genetically minded historians believe that the confluence of urban living and the discovery of alcohol created a massive selection pressure on the genes of all humans who abandoned the hunter-gatherer lifestyle. Alcohol, after all, is a deadly poison and notoriously addictive. To digest large quantities of it, you need to be able to boost production of enzymes called alcohol dehydrogenases, a trait regulated by a set of genes on chromosome four in human DNA. Many early agrarians lacked that trait, and thus were genetically incapable of “holding their liquor.” Consequently, many of them died childless at an early age, either from alcohol abuse or from waterborne diseases. Over generations, the gene pool of the first farmers became increasingly dominated by individuals who could drink beer on a regular basis. Most of the world’s population today is made up of descendants of those early beer drinkers, and we have largely inherited their genetic tolerance for alcohol. (The same is true of lactose tolerance, which went from a rare genetic trait to the mainstream among the descendants of the herders, thanks to the domestication of livestock.) The descendants of hunter-gatherers—like many Native Americans or Australian Aborigines—were never forced through this genetic bottleneck, and so today they show disproportionate rates of alcoholism. The chronic drinking problem in Native American populations has been blamed on everything from the weak “Indian constitution” to the humiliating abuses of the U.S. reservation system. But their alcohol intolerance mostly likely has another explanation: their ancestors didn’t live in towns.
Ironically, the antibacterial properties of beer—and all fermented spirits—originate in the labor of other microbes, thanks to the ancient metabolic strategy of fermentation. Fermenting organisms, like the unicellular yeast fungus used in brewing beer, survive by converting sugars and carbohydrates into ATP, the energy currency of all life. But the process is not entirely clean. In breaking down the molecules, the yeast cells discharge two waste products—carbon dioxide and ethanol. One provides the fizz, the other the buzz. And so in battling the health crisis posed by faulty waste-recycling in human settlements, the proto-farmers unknowingly stumbled across the strategy of consuming the microscopic waste products generated by the fermenters. They drank the waste discharged by yeasts so that they could drink their own waste without dying in mass numbers. They weren’t aware of it, of course, but in effect they had domesticated one microbial life-form in order to counter the threat posed by other microbes. The strategy persisted for millennia, as the world’s civilizations discovered beer, then wine, then spirits—until tea and coffee arrived to offer comparable protection against disease without employing the services of fermenting microbes.
But by the middle of the nineteenth century, in England at least, water was finding a role for itself in the urban diet. Starting in the mid-1700s, a growing patchwork of privately owned water pipes began snaking their way through the city, supplying the wealthiest Londoners with running water in their homes (or, in some cases, depositing the water in a cistern near their house). It is difficult to overestimate the revolutionary impact of this advance. So many of the household conveniences of modern life—the dishwashers and washing machines and toilets and showers—depend on a reliable supply of water. Just being able to pour yourself a glass from a faucet in your home would have been miraculous to the Londoners who first experienced it.
By the mid-1800s, the loose assortment of small firms running the water pipes had consolidated into roughly ten major firms, each with its own protected turf in the city. The New River Water Company supplied the city proper, while the Chelsea Water Company piped
to the West End. South of the Thames, two companies controlled the area: Southwark and Vauxhall (otherwise known as S&V), and Lambeth. Many of these companies—including S&V and Lambeth—had intake pipes within the tidal reach of the Thames. The water they supplied their customers was therefore contaminated by the raw waste of the city, thanks to the growing network of sewers that emptied into the increasingly foul river. Even the most ardent miasmatist could find something offensive in that arrangement, and so in the early 1850s, Parliament passed legislation ordering that all London’s water companies had to move their intake pipes above the tidewater mark by August 1855. S&V chose to delay its move to the very last minute, continuing to draw from Battersea, but Lambeth switched its waterworks to the far cleaner supply at Thames Ditton in 1852.
Snow had been following the water companies since his early investigation of 1849 and had already been tracking the results of Lambeth’s move. But the real breakthrough came in the form of a footnote in the November 26 edition of the Weekly Returns. Below the cholera deaths for South London, Farr had appended this seemingly innocuous line: “In three cases… the same districts are supplied by two companies.”
That minor bit of infrastructure trivia would have immediately struck Snow as a tremendous opportunity. A population all living in the same space, at the same elevation, divided between two water supplies, one rank with the sewage of the city, the other comparatively pure. Farr’s footnote had inadvertently supplied Snow with his experimenta crucis.
The Ghost Map Page 10
