Nationality swapping in the Olympic field: towards the marketization of citizenship?

Nationality swapping in sports is commonly assumed to be a rapidly expanding practice that is indicative of the marketization of citizenship. Sports are said to have become wholesale markets in which talent is being traded for citizenship. In this article, we seek to empirically explore such claims by analysing 167 athletes who have competed for two different countries in the Summer Olympic Games. It seems that most switches occurred after the 1990s. Then, following a citizenship as a claims-making approach, we introduce the work of Bourdieu so as to connect citizenship as both legal status and practice with normative claims. The analysis reveals that the practice of nationality switching is shaped by structural conditions of the Olympic field. First, a complex realm of citizenship laws and regulations produces conditions under which athletes make legitimate claims to citizenship. Second, through a mechanism of reverberative causation, prior migrations are often echoed in contemporary nationality swapping . Only a limited number of athletes acquired citizenship via the explicit market principle we call jus talenti. Claiming that instrumental nationality swapping is indicative of the marketization of citizenship obscures the complex interplay between structures of and practices within the Olympic field.     

Subacute fatal aluminum poisoning in dialyzed patients: post-mortem toxicological findings

The population of Cura?ao, Netherlands Antilles (133,000) shows a very high prevalence of end-stage renal disease (approximately 1 per 1,000). These patients are often treated chronically with haemodialysis. As the drinking water on the island is prepared by distillation of sea water, the haemodialysis fluid used to be prepared with tap water without further treatment. In 1996, the 27 patients of one of the dialysis centers on the island presented with nausea, vomiting, and hypercalcaemia in a short time span, which was initially diagnosed as 'hard water syndrome'. In spite of treatment with low-calcium dialysate, microcytic anaemia and neurological symptoms developed. Ten patients died of convulsions, sepsis, and coma. As aluminum (Al) intoxication was suspected, Al in serum (AlS) was measured. Ante mortem AlS was 808 microg/l (n = 7; range 359-1189); in the survivors AlS was 255 microg/l (n = 17; range 113-490). Normal AlS is < 10 microg/l, and <50 microg/l in asymptomatic dialyzed patients. The court requested post-mortem toxicological analysis of four patients. Al concentrations in liver, bone, and cerebral cortex were significantly increased as compared with background levels. Al intoxication was, therefore, considered to be the most likely cause of death in these patients. Investigations of the tap water supply revealed that a few weeks before the onset of the symptoms, a water conduit pipe to the dialysis unit had been replaced, which was lined with Al- and Ca-rich cement mortar. These ions leached into the distilled water and caused both Ca- and Al-intoxication through uptake from the dialysate into the patients' circulation. The symptoms of the latter were initially not recognized as they were masked by the symptoms of hypercalcaemia.