Commentary: John Snow and alum-induced rickets from adulterated London bread: an overlooked contribution to metabolic bone disease

M Dunnigan

Department of Human Nutrition, University of Glasgow, Glasgow Royal Infirmiary, Glasgow G31 2ER, UK.

Dr John Snow (1813–1858) is remembered for his hypothesis that cholera was communicated by contaminated drinking water. On the Mode of Communication of Cholera, published in 1849, was validated on 2 September 1854 when he persuaded the Soho parish Board of Guardians to disconnect the handle of the Broad Street pump.1 The number of cases of cholera in the parish plummeted and Snow’s fame was assured.

In contrast, Snow’s Lancet paper of 4 July 18572 suggesting that the adulteration of bread with alum might be a cause of rickets has been forgotten. At first sight, scepticism seems justified since infantile rickets had been endemic in Northern Europe since at least the 17th century when the first clear descriptions of the disease appeared.3,4 To an audience uninformed by chemical insight, Snow’s hypothesis must have seemed eccentric. To a 21st century eye, aware of the potential interactions of aluminium salts with calcium and phosphorus metabolism, Snow’s hypothesis is astonishingly prescient.

Snow observes that rachitic deformity is prevalent in areas where baker’s bread adulterated with alum (aluminium potassium phosphate) is consumed (principally London and the south of England), while children in areas where home-baked bread, made from unadulterated flour, is consumed are rarely affected. He also observes that rachitic deformity is equally prevalent in children consuming adulterated bread in villages around London (where fresh air and sunlight are unrestricted), and in urban children of the more affluent middle classes. The absence of an urban–rural and socioeconomic gradient is not typical of classical Glissonian infantile rickets determined by restricted exposure to ultra-violet radiation and adherence to a strict lactovegetarian diet (predominantly bread and milk [saps] with added sugar in the first 2 years).5

Snow then proposes a hypothesis to explain the link between rickets and the consumption of alum which predates modern evidence by 70 years.6 Utilizing the findings of the distinguished German chemist Leibig (1803–1883), that aluminium salts react with phosphorus-containing compounds to form insoluble aluminium phosphate, he suggests that this reaction may inhibit the absorption of dietary phosphorus required for the formation of skeletal ‘phosphate of lime’. Finally, Snow proposes a case-control study of the prevalence of rachitic deformity in children under 4 years in ‘towns where respectively the people buy chiefly flour or ready made bread ... to decide the question’.

This hitherto neglected paper is clearly the product of astute clinical and epidemiological observation combined with scientific insight, resulting in what appears to be the first paper in the medical literature to raise the issue of the potential toxicity of ingested aluminium compounds in man.

The unrecognized implications of Snow’s observations for the public health of Londoners in the 19th century are sobering. Snow states that London bakers would add about 11/2 ounces of alum per 4 lb loaf (42 g per 1800 g bread). Given that a manual labourer might consume 70% of his energy requirements as bread, he could ingest 20 g of alum daily [AlK(SO4)2 + 12H2O], equivalent to the aluminium content of 4 g aluminium hydroxide [Al(OH)3]. This is the maximum recommended daily dose of this compound as an antacid and alum in equivalent quantities may have been consumed continuously in adulterated bread by a substantial proportion of the capital’s population.

Long-term intakes of aluminium salts of this order may induce hypophosphataemic osteomalacia.7 A phosphorus depletion syndrome has been described in which prolonged intakes of aluminium-containing antacids resulted in hypophosphataemia, hypercalciuria with calcium resorption from bone, and general malaise, debility, anorexia, and muscle weakness.8 In children subsisting on bread as a basic food following weaning, at a period of peak growth velocity, the effects of chronic aluminium ingestion may have been severe, resulting in rachitic deformity. In subjects with impaired renal function, unable to excrete the small proportion of aluminium absorbed from the gut, the potential benefits of a reduction in high serum phosphate levels may have been offset by an accumulating body burden of aluminium leading to worsening renal osteodystrophy and deteriorating cognitive function, well illustrated by aluminium-induced dialysis encephalopathy and dementia.9

Analogous to its present day use as a decolourant in water treatment plants, alum appears to have been added to bread as a whitener (as was chalk and bone-meal). A statute to prevent the adulteration of bread which specifically mentions alum was passed in the reign of King George II in 1757 and widely ignored, as Snow notes. I have been unable to discover when the practice was discontinued.

It would be of interest to verify Snow’s hypothesis. Spectrophotometric analysis of bone samples from the skeletons of mid-19th century Londoners, presumably available in the city’s many anatomy and pathology collections, would detect the presence of abnormal quantities of aluminium. This investigation might belatedly vindicate (or rebut) Snow’s perception of a major toxicological hazard to which London’s population were unwittingly exposed as they consumed their daily bread.


    References
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 References
 
1 Porter R. The Greatest Benefit to Mankind: A Medical History of Humanity from Antiquity to the Present. London: Harper Collins, 1997, pp. 412–13.

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

3 Glisson F. De Rachitide sive Morbo Pueri, qui Vulgo. The Rickets dicitur. London, 1650.

4 Whistler D. De Morbo Pueri Anglorum Quem Patrio Idiomate Indigenae Vocant. The Rickets. University of Leyden. MD Thesis, 1645.

5 Dunnigan MG, Henderson JB. An epidemiological model of privational rickets and osteomalacia. Proc Nutr Soc 1997;56:939–56.[ISI][Medline]

6 Schaeffer G et al. The dangers of certain mineral baking powders based on alum, when used for human nutrition. J Hyg 1928;28:92–99.

7 Bloom WL, Flinchum D. Osteomalacia with pseudofractures caused by the ingestion of aluminium hydroxide. JAMA 1960;174: 1327–30.[ISI]

8 Lotz M, Zisman E, Bartter FC. Evidence for a phosphorus-depletion syndrome in man. New Engl J Med 1968;278:409–15.[ISI][Medline]

9 Alfrey AC, Le Gendre GR, Kaehny WD. The dialysis encephalopathy syndrome. Possible aluminium intoxication. New Engl J Med 1976; 294:184.[Abstract]





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