Effects of fluoridation of community water supplies for people with chronic kidney disease.

Research on the effects of fluorides on oral health has been in existence for almost a century. Following the observation that communities with naturally fluoridated drinking water had a lower incidence of tooth decay, many developed countries initiated artificial water fluoridation programmes, whereby fluoride is added to the reticulated water supply, such that it reaches approximately one part fluoride per million parts water (ppm) or 1mg fluoride per litre of water (mg/l). Recent reviews [1–5] summarizing the extensive fluoride literature have concluded that water fluoridation reduces the prevalence of dental decay, and it is estimated that a median of six people need to receive fluoridated water for one extra person to be caries-free [2]. Compared with other methods of systemic fluoridation (including fluoridated sugar, milk or salt, fluoride toothpastes, fluoride supplements), water fluoridation is argued to be the most cost-effective, equitable and safe means to provide community-wide protection against tooth decay [6]. As a result, artificial fluoridation of community water supplies is currently supported by numerous international health and dental organizations, including the World Health Organization and the International Association for Dental Research. However, while access to fluoridated drinking water has positive effects on dental health, the characteristics of fluoride metabolism mean that fluoride consumption may have implications for the kidney. The calcified tissues in the human body contain 99% of the body burden of fluoride and most of this is non-exchangeable. Absorption of fluoride is rapid and extensive, with about 50% of the absorbed fluoride becoming associated with calcified tissues within 24 h and the remainder being excreted in the urine. In infants and young children, the amount of fluoride retained in calcified tissues is >50% of the ingested daily amount. The renal clearance of fluoride is high, around 30–40ml/min in healthy adults [7]. Fluoride is freely filtered by the glomerulus and then undergoes a variable amount of tubular reabsorption. Fluoride excretion falls markedly in the presence of an acid urine and is increased with higher rates of urine flow [8–10]. Considering the pivotal role of the kidney in the body’s ability to metabolize fluoride, there have been surprisingly few attempts to synthesize studies relating to the relationship between fluoride consumption and kidney function. The most recent literature reviews on the health effects of fluoride intake have contained limited discussion on the potential impact on the kidneys [1–5]. Recently there has been a resurgence of interest in the artificial fluoridation of drinking water in Australia, with efforts to expand the fluoridation of public water supplies to the one remaining unfluoridated capital city (Brisbane) and several unfluoridated regional areas. With the renewed debate in Australia regarding water fluoridation, questions have been raised concerning the impact of fluoride consumption for the large proportion of the Australian population affected by chronic kidney disease (CKD). In the general Australian community over age 25, there is evidence of at least one indicator of CKD (proteinuria or reduced kidney function) in !16% of individuals [11]. However, CKD is frequently asymptomatic, and many afflicted individuals will have significant reduction of kidney function but no overt signs or symptoms, and hence will be unaware they have the condition. The United States National Kidney Foundation published a brief position statement on fluoridation of drinking water in the early 1980s [12], and concluded that there was insufficient evidence to recommend the use of fluoride-free drinking water for all people with CKD. This position statement was reaffirmed in 1998, but no new research or discussion was added. Correspondence to: Dr Marie Ludlow, Kidney Health Australia, GPO Box 9993, Adelaide, South Australia 5001. Email: [email protected] Nephrol Dial Transplant (2007) 22: 2763–2767 doi:10.1093/ndt/gfm477 Advance Access publication 27 July 2007