American Journal of Epidemiology Advance Access originally published online on June 12, 2006
American Journal of Epidemiology 2006 164(2):194-195; doi:10.1093/aje/kwj197
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Letter to the Editor |
RE: "ARSENIC EXPOSURE AND CARDIOVASCULAR DISEASE: A SYSTEMATIC REVIEW OF THE EPIDEMIOLOGIC EVIDENCE"
1 Division of Cardiology, Department of Medicine, Kaiser Permanente Medical Care Program, Oakland, CA 94611
2 Division of Research, Kaiser Permanente Medical Care Program, Oakland, CA 94611
(e-mail: arthur.klatsky{at}kp.org)
For their systematic review of arsenic and cardiovascular disease, Navas-Acien et al. (1
) thoroughly searched and rigorously reviewed reports from 1966 through April 2005. This methodology, exemplary in a modern context, could not have uncovered citations pertinent to a documented episode of arsenic-mediated cardiotoxicity that happened in the United Kingdom long before 1966. That epidemic, here called "arsenic-beer drinkers' disease," warrants attention for both historical interest and possible insights into the pathogenesis of cardiac myocyte disorders.
In 1900, in and near Manchester, England, an epidemic occurred of a multisystem disease with over 6,000 cases with more than 70 deaths. With replicated testing, the proved culprit was accidental contamination of beer by arsenic (2). The syndrome included the usual signs and symptoms of arsenic poisoning, with skin, nervous system, and gastrointestinal manifestations. Unusual in arsenic poisoning, but especially prominent in this epidemic, were cardiovascular aspects. In a superb clinical description, Dr. Ernest Reynolds wrote the following: 1) "cases were associated with so much heart failure and so little pigmentation that they were diagnosed as beri-beri ..."; 2) "so great has been the cardiac muscle failure that—undoubtedly the principal cause of death has been cardiac failure"; and 3) "at the post-mortem examinations the only prominent signs were the interstitial nephritis and the dilated flabby heart ..." (3, p. 169).
For several years, there were lively relevant entries in The Lancet (3–7). It was determined that the source of the arsenic was contaminated sulfuric acid used to treat cane sugar. The result in the affected beer was 2–4 parts per million of arsenic (approximately 0.2–0.4 mg/liter), an amount not believed, by itself, likely to cause serious toxicity (4, 7). For example, Gowers reflected that 10 times the amount of arsenic involved was prescribed for epilepsy over substantial periods of time without toxicity; thus, "the amount of arsenic ... was not sufficient to explain the poisoning" (4, p. 99).
It was observed that some seemed to have a "peculiar idiosyncrasy" (5, p. 218), and that "many persons became ill who drank less beer than others who were not affected" (6, p. 673). The governmental investigative body (Royal Commission Appointed to Inquire into Arsenical Poisoning) suggested that "alcohol predisposed people to arsenic poisoning" (2, p. 673). A more probable and more modern view would be the converse, that arsenic predisposed susceptible persons to alcoholic cardiomyopathy.
Recognized 65 years after the arsenic-beer episode, a condition known as "Quebec-beer drinkers' cardiomyopathy" (8) was eerily similar in some respects. Heart failure epidemics among chronically heavy beer drinkers in Omaha, Nebraska, Minneapolis, Minnesota, and Quebec, Canada (9), included rapidly developing symptoms. Deaths were common, but those who recovered did well despite return, by many, to previous beer habits. Quebec investigators (8) tracked down the etiology, which proved to be the addition of small amounts of cobalt chloride by certain breweries to improve the foaming qualities of beer. Removal of the cobalt additive ended the epidemic in all locations; biochemical mechanisms were not established. As with the arsenic-beer episode, there must have been other factors, since most exposed persons did not develop the condition.
Viewing, in 1969, the arsenic and cobalt episodes, Alexander commented: "This is the second known metal induced cardiotoxic syndrome produced by contaminated beer" (9, p. 413). Cobalt or arsenic, substantial amounts of alcohol, and other predisposing factors were needed to produce these syndromes. It is unclear whether they represented synergistic or additive myocardial toxicity by the respective contaminants plus alcohol. What is clear is the reminder that most clinical entities are pluricausal in nature.
ACKNOWLEDGMENTS
Conflict of interest: none declared.
References
- Navas-Acien A, Sharrett AR, Silbergeld EK, et al. Arsenic exposure and cardiovascular disease: a systematic review of the epidemiologic evidence. Am J Epidemiol 2005;162:1037–49.
[Abstract/Free Full Text] - Royal Commission Appointed to Inquire into Arsenical Poisoning from the consumption of beer and other articles of food or drink. Final report. Part I. London, England: Wyman and Sons, 1903.
- Reynolds ES. An account of the epidemic outbreak of arsenical poisoning occurring in beer drinkers in the north of England and the midland counties in 1900. Lancet 1901;i:166–70.
- Gowers WR. 1901. In: Epidemic of arsenical poisoning in beer-drinkers in the north of England during the year 1900. Royal Medical and Chiururgical Society. Lancet 1901;i:98–100.
- Royal Commission on Arsenical Poisoning. First report. Lancet 1901;ii:218.
- Royal Commission on Arsenical Poisoning. Lancet 1901;i:672–3.
- Tunnicliffe FW, Rosenheim O. Selenium compounds as factors in the recent beer poisoning epidemic. Lancet 1901;i:318.
- Morin Y, Daniel P. Quebec beer-drinkers' cardiomyopathy: etiologic considerations. Can Med Assoc J 1967;97:926–8.[Medline]
- Alexander CS. Cobalt and the heart. Ann Intern Med 1969;70:411–13.
[Abstract/Free Full Text]
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  A. Navas-Acien, A. R. Sharrett, and E. Guallar THREE AUTHORS REPLY Am. J. Epidemiol., July 15, 2006; 164(2): 195 - 196. [Full Text] [PDF]
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