Commentary: Snow on rickets

Nigel Paneth

College of Human Medicine, Michigan State University, Department of Epidemiology, Suite 600, 4660 S Hagadorn Road, East Lansing, MI 48823, USA. E-mail: paneth{at}msu.edu

John Snow’s little piece on rickets,1 written less than a year before his death, illustrates in miniature the integrative thought processes that made him a founding figure of both epidemiology and scientific anaesthesiology. Snow was one of those rare medical scientists who move effortlessly across conceptual categories usually kept distinct. In studying cholera, anaesthesia, and rickets, he investigated the distribution of molecules in solution and the distribution of diseases in populations. Snow’s great contribution to epidemiology—unravelling the mode of transmission of cholera decades before germ theory—was an exercise in the blending of ideas operating at molecular, pathological, clinical, and epidemiological levels. His understanding of molecular forces in living things led him to hypothesize a minuscule, reproducing agent of disease. His view of the intestinal nature of cholera pathophysiology led him to hypothesize fecal–oral transmission. And his observations of the geographical and temporal features of acute outbreaks led him to hypothesize that municipal water supplies maintained urban cholera epidemics.

Snow turned the administration of anaesthesia from a parlour game, a hit-and-miss medical oddity, into a medical technology of supreme importance because of his insight into the chemistry of vaporizing gases, including the influences of temperature, humidity, and dosage. But Snow also recognized the need for systems of care to monitor anaesthetic safety (he was the first to insist that the anaesthetist not be the surgeon), and was virtually unique in compiling careful comparative records of the rate of anaesthetic accidents with different agents. His scientific work was nearly always accompanied by specific suggestions for improving clinical practice or maintaining public health.

In his paper on rickets, Snow’s first observation is epidemiological, his second chemical. His chemical knowledge taught him that the underlying problem in rickets is undermineralized bones, deficient in phosphate of lime. Nearly 70 years later, the pathophysiology of rickets would be described in virtually identical terms.2 From chemistry, Snow reasoned that deficiency of milk —which he knew to be rich in calcium phosphate—might lead to rickets. But the epidemiology was unsupportive—few cases of rickets were seen in Snow’s early practice in the less-industrial corners of northern England (he was apprenticed in Newcastle, and in the Yorkshire villages of Pateley Bridge and Burnop Field), but many poor children in the north were without milk in their diets. Searching for a cultural or behavioural difference that would explain the excess of rickets in London, and focusing especially on diet, Snow hit upon bread, which northerners baked themselves, but Londoners bought from stores.

What Londoners bought to eat, as Snow’s friend Arthur Hill Hassall showed repeatedly during the 1850s, was hardly what they thought it was. Hassall made a career of buying foods in London shops, testing them chemically, examining them microscopically, and publishing his usually shocking findings in the Lancet or in his several books. The level of deliberate adulteration of foods in London then was truly astonishing. Additives, frequently quite poisonous, were put in foods to add weight, to add colour, or to cover offensive odours. Of 42 samples of mustard tested by Hassall, not one was free of flour colored with turmeric.3 Not only were 90% of coffee samples adulterated with chicory, but the chicory was itself adulterated with flour, corn, ground acorn, or even sawdust. Black tea was coloured with black lead, green tea with Prussian blue (ferric cyanide). Bread was, as Snow found, contaminated with alum, but you were a lucky Londoner indeed if your bread did not also contain mashed potatoes, water, or rice flour.

Hassall reports that alum (potassium aluminum phosphate) contamination of bread was a cottage industry for London bakers. The compound is most stable with water molecules attached, making it excellent for adding weight, and it makes flour look whiter. Still a component of some baking powders today, it also helps bread rise. Virtually every baker in London had a druggist who supplied him with what was called ‘hards’ or ‘stuff’ in the trade, a mixture of rock alum and salt, added, so Hassall estimates, at about half a pound per sack of flour. The loaves Snow tested, with 500–600 grains of alum per 4 lb loaf, were even more densely contaminated.

Was Snow right that alum could precipitate out dietary calcium phosphate and thereby contribute to rickets? While such a process has not been reported for alum, other aluminum salts, such as are found in antacids, have been found to interfere with intestinal phosphate absorption by competitive binding, even producing rickets on occasion.4

In Snow’s time, rickets was just another part of the vast spectrum of disease that was the special plague of the poor. The social distribution of disease implicated the evils of the industrial world—close living quarters, bad hygiene, bad ventilation. To many public health reformers of 19th century England, distinguishing one ‘miasmatic’ disease from another was hardly worth the effort. Edwin Chadwick put it thus:

The various forms of epidemic, endemic and other disease caused, or aggravated, or propagated chiefly among the laboring classes by atmospheric impurities produced by decomposing animal and vegetable substances, by damp and filth and close and overcrowded dwellings prevail amongst the population in every part of the kingdom.5

To the modern ear, Chadwick’s failure to implicate nutrition among the list of disease-inducing evils seems a curious omission, but, as Christopher Hamlin has shown, it was not accidental.6 To Chadwick, and to many in the sanitary reform movement, criticizing drains and housing removed the onus of ill-health away from factories and their near slave-labour conditions.7

Snow saw things differently. The son of a Yorkshire labourer and of a mother born out of wedlock, he knew the distinction between filth and disease, and sought the specific elements of the social environment that facilitated the development and spread of specific diseases. An experimentalist at heart, he sought out the ‘natural’ (but usually man-made) experiments that could test his disease hypotheses. The Thames water that supplied South London houses came from two sources—one far above, the other just below, London’s sewer outlets—a circumstance which Snow exploited to show the impact of fecalized water on cholera mortality. He searched for an analogous contrast to test his bread–rickets hypothesis, but could not find comparable settings supplied with different kinds of bread.

Having concluded that cholera was transferred by the fecal–oral route, Snow thought of ways to address the public health problem. The poor suffered more from cholera, not, as many sanitarians held, because of their immoral behaviour, but, said Snow, because they had less light in their homes to notice fecal contamination, and fewer washing facilities to avert it. Miners—a special concern for Snow since his youthful experience managing a cholera epidemic in a coal mine—needed shorter shifts so they would not have to bring their meals to the running sewers in which they worked, inevitably contaminating their food. His recommendations on keeping urban water supplies free of fecal matter, not widely implemented until a decade after his death, did more to control cholera than did the liming of streets and the abolition of cesspools recommended by London sanitary authorities. Indeed, since cesspools were replaced by sewer lines that fed raw sewage directly to the Thames, and thereby to the water supply, this sanitary ‘improvement’ surely increased cholera mortality, as Snow quietly pointed out.8

In rickets too, Snow sought aetiological uniqueness within the broader theme of poverty and disease. He missed perhaps the chief culprit, the lack of sunlight which shone more on the ruddy village poor of Yorkshire than on the denizens of London’s dark alleys, but his approach to the problem—a blend of astute social observation and up-to-date chemistry—has much to recommend it to the modern epidemiologist. And in proposing that the authorities ‘oblige’ bakers to supply institutions for the sick and poor with unadulterated bread, he emphasized another useful message—the importance of translating science into public policy.


    References
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 References
 
1 Snow J. On the adulteration of bread as a cause of rickets. Lancet 1857;ii:4–5. (Reprinted in Int J Epidemiol 2003;32:336–37.)

2 Vaughan Victor C. Epidemiology and Public Health. Vol. 2. Nutritional Disorders, Alimentary Infections, Percutaneous Infections. St Louis: CV Mosby, 1923, p. 106.

3 Hassall AH. Food and its Adulterations. London: Longman, Brown, Green and Longmans 1855. pp. ix; xiii; xv–xvi; 159–60.

4 Pivnick EK, Kerr NC, Kaufman RA et al. Rickets secondary to phosphate depletion. A sequela of antacid use in infancy. Clin Pediatr 1995;34: 73–78.[ISI][Medline]

5 Chadwick E. Report to Her Majesty’s Principal Secretary of State for the Home Department, from the Poor Law Commissioners on an Inquiry into the Sanitary Condition of the Labouring Population of Great Britain; with Appendices. London: HMSO, 1842, p. 369.

6 Hamlin C. Could you starve to death in England in 1839? The Chadwick-Farr controversy and the loss of ‘social’ in public health. Am J Public Health 1995;85:856–66.[Abstract]

7 Hamlin C. Public Health and Social Justice in the Age of Chadwick: Britain, 1800–1854. Cambridge: Cambridge University Press, 1998.

8 Snow J. On the communication of cholera by Thames water. Medical Times and Gazette 1854;366:Oct. 7.





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