By Karen Blakey and Richard J. Q. McNally
Since their introduction in the United States in the 1940s, artificial fluoridation programmes have been credited with reducing tooth decay, particularly in deprived areas. They are acknowledged by the US Centers for Disease Control and Prevention as one of the ten great public health achievements of the 20th century (alongside vaccination and the recognition of tobacco use as a health hazard). Such plaudits however, have only gone on to fuel what is an extremely polarised ‘water fight’. Those opposed to artificial fluoridation continue to claim it causes a range of health conditions and diseases such as reduced IQ in children, reduced thyroid function, and increased risk of bone cancer. Regardless of the controversy, the one thing that everyone agrees upon is that little or no high quality research is available to confirm or refute any public concerns. The York systematic review of water fluoridation has previously highlighted the weakness of the evidence base by acknowledging the quality of the research included in the review was low to moderate.
Fluoride changes the structure of tooth enamel making it more resistant to acid attack and can reduce the incidence of tooth decay. This is why it is added to drinking water as part of artificial fluoridation programmes. The aim is to dose naturally occurring fluoride to a level that provides optimum benefit for the prevention of dental caries. The optimum range can depend on temperature but falls within the range of 0.7-1.2 parts per million (ppm) for Great Britain. Levels lower than 0.7ppm are considered to provide little or no benefit. Drinking water standards are set so that the level of fluoride must not exceed 1.5ppm in accordance with national regulations that come directly from EU law.
Severn Trent Water, Northumbrian Water, South Staffordshire Water, United Utilities, and Anglian Water are the only water companies in Great Britain that artificially fluoridate their water supply to a target level of 1 ppm. The legal agreements to fluoridate currently sit with the Secretary of State, acting through Public Health England, although local authorities are the ultimate decision makers when it comes to establishing, maintaining, adjusting or terminating artificial fluoridation programmes. As a programme dedicated to improving oral health, all of the associated costs come from the public health budget. Therefore, it is important to know that the money is being spent in the most effective way.
Our study has, for the first time, enabled an in-depth examination of the relationship between the incidence of two of the most common types of bone cancer that are found in children and young adults, osteosarcoma and Ewing sarcoma, and fluoride levels in drinking water across the whole of Great Britain. We have combined case data from population based cancer registries, fluoride monitoring data from water companies and census data within a computerised geographic information system, to enable us to carry out sophisticated geo-statistical analyses.
The study found no evidence of an association between fluoride in drinking water and osteosarcoma or Ewing sarcoma. The study also found no evidence that those who lived in an area of Great Britain with artificially fluoridated drinking water, or who were supplied with drinking water containing naturally occurring fluoride at a level within the optimal range, were at an increased risk of osteosarcoma or Ewing sarcoma.
It is important to note that finding no evidence of an association between the geographical occurrences of osteosarcoma or Ewing sarcoma and fluoride levels in drinking water, does not necessarily mean there is no association. Indeed, intake of fluids and food products that contain fluoride will not be the same for everyone and not taking this variation into consideration is one of the limitations of our study. Nevertheless, the methodologies we have developed could be used in the future to examine fluoride exposure over time and take other risk factors into consideration at an individual level. Such an approach could help the controversy surrounding artificial fluoridation ebb rather than flow.
Another important, although unexpected, finding arose from our use of fluoride monitoring data. We found that the fluoridation levels of approximately one third of the artificially fluoridated water supply zones were below 0.7ppm (the minimum limit of the optimum range). This finding reinforces that it is incorrect to assume an artificially fluoridated area is dosed up to 1ppm. In reality, it may be a lot less. A number of previous studies have mistakenly made this assumption making their conclusions unreliable. Our study shows that you cannot guarantee that fluoride levels in all artificially fluoridated water supply zones are close to the target level of 1ppm. Assuming that water fluoridation is a safe practice and evidence surrounding calculation of recommended dosage is reliable, this finding has economic implications in terms of public health. If public money is paying for artificial fluoridation shouldn’t the water supply zones be dosed up to a level that will provide the greatest benefit? If they aren’t then could it be that public money is merely being thrown down the drain?
Karen Blakey is a Research Assistant at the Institute of Health & Society, Newcastle University. She is interested in geographical information systems and the spatial analysis of disease registry data. Richard J.Q. McNally is a Reader in Epidemiology at the Institute of Health & Society, Newcastle University. He is interested in spatial epidemiology, the epidemiology of chronic diseases and the statistical analysis of registry data. They are authors of the paper ‘Is fluoride a risk factor for bone cancer? Small area analysis of osteosarcoma and Ewing sarcoma diagnosed among 0-49-year-olds in Great Britain, 1980-2005’, which is published in the International Journal of Epidemiology.
The International Journal of Epidemiology is an essential requirement for anyone who needs to keep up to date with epidemiological advances and new developments throughout the world. It encourages communication among those engaged in the research, teaching, and application of epidemiology of both communicable and non-communicable disease, including research into health services and medical care.
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by Caroline Relton
Epidemiology, a well established cornerstone of medical research, is a group level discipline that aims to decipher the distribution and causes of diseases in populations. Epigenetics, perceived by many as the most fashionable research arena in which to be involved, is a mechanism of gene regulation. What brings these perhaps unlikely partners together?
Epigenetic processes are key features in gene regulation. Epigenetic patterns are laid down in early development and are moulded through in utero and early postnatal life and continue to show some degree of plasticity across the lifecourse. Many environmental, behavioural, nutritional and lifestyle factors are believed to influence epigenetic patterns and in some case the evidence base is substantial. What is less clear is the role of this environmentally modifiable ‘epigenome’ on disease risk in populations. This is where epidemiology can help. A good starting point for an epidemiological engagement with epigenetics is clearly identified by Nessa Carey, in her recent popular science book The Epigenetics Revolution:
“The majority of non-infectious diseases that afflict most people take a long time to develop, and then remain as a problem for many years if there is no cure available. The stimuli from the environment could theoretically be acting on the genes all the time in the cells that are acting abnormally, leading to disease. But this seems unlikely, especially because most of the chronic diseases probably involve the interaction of multiple stimuli with multiple genes. It’s hard to imagine that all these stimuli would be present for decades at a time. The alternative is that there is a mechanism that keeps the disease-associated cells in an abnormal state, i.e. expressing genes inappropriately. In the absence of any substantial evidence for a role for somatic mutation, epigenetics seems like a strong candidate for this mechanism”.
Recent literature points to a role for epigenetic variation in a range of diseases including neurological disease, cardiovascular disease, osteoarthritis and obesity but in most instances these are correlations without robust evidence of causality. Indeed, epigenetics is often proffered as the answer to many unresolved causes of disease. The enthusiasm for establishing whether epigenetic mechanisms link the environment with disease development must be tempered by the knowledge that the epigenome is dynamic and has as much potential to respond to disease as respond to the environment. Therefore it is very difficult to disentangle cause from consequence when studying epigenetic variation and disease.
This is just one of the many challenges that face researchers interested in understanding the role of epigenetics in common complex disease. Other challenges include the differences in interpretation of the term ‘epigenetics’ itself – in a field that attracts cell, developmental and evolutionary biologists, epidemiologists and bioinformaticians, amongst others, it is unsurprising that epigenetics means different things to different people and discussions of its relevance to disease can sometimes suffer misinterpretation.
The methods at our disposal to accurately measure epigenetic variation and in turn assess the impact this has upon disease risk are still being developed and there is much to do in this arena with respect to when, where and how to look at the epigenome. The complexity and interplay of multiple factors in determining d
By David A. Leon
Making a difference to the health of populations, however small, is what most people in public health hope they are doing. Epidemiologists are no exception. But often caught up in the minutiae of our day-to-day work, it is easy to lose sight of the bigger picture. Is health improving, mortality declining, are things moving in a positive direction? Getting out and taking in the view (metaphorically as well as literally) can have a salutary effect. It broadens our perspectives and challenges our assumptions. Looking at recent trends in European life expectancy is a case in point.
Since 1950 estimated life expectancy at birth of the world’s population has been increasing. Initially, this was accompanied by a convergence in mortality experience across the globe—with gains in all regions. However, in the final 15 years of the 20th century, convergence was replaced with divergence, in part due to declines in life expectancy in sub-Saharan Africa. However, this global divergence was also the result of declining life expectancy in Europe. Home to 1 in 10 of the world’s population, and mainly comprised of industrialized, high-income countries, Europe has over 50 states. These include Sweden and Iceland that have consistently been ranked among the countries with the highest life expectancies in the world. But while for the past 60 years all Western European countries have shown increases in life expectancy, the countries of Central and Eastern Europe (CEE), Russia and other parts of the former Soviet Union have had a very different, and altogether more negative experience.
Trends in life expectancy between 1970 and the latest year available are shown in the Figure 1 for an illustrative selection of countries. These data were taken from one of two open sources : (i) the WHO Health for All Database or (ii) the Human Mortality Database, depending on which one had the longest time series. Differences between the sources are minimal for the purposes of this editorial. It is important to emphasize at the outset, that with one exception (discussed below), the trends shown in the Figure 1 are overwhelmingly driven by changes in mortality in adult life, not in infancy or childhood and are not the result of artefact.
Former communist countries of Eastern Europe
Between 1970 and the end of the 1980s, life expectancy at birth in the former communist countries of CEE (Czech Republic, Hungary, Poland and Slovakia), Russia and the Baltic states (Estonia, Latvia and Lithuania) stagnated or declined (Figure 1). This led to an increasing gap between them and Western European countries as the latter steadily improved. However, within a few years of the collapse of the Berlin wall in 1989, life expectancy started to steadily increase in the countries of CEE. This vividly illustrates that mortality can decline rapidly in response to political, social and economic change. Interestingly, once underway, the post-1989 increase in life expectancy in these countries has continued at a steady rate that is very similar to Western Europe. These parallel trajectories mean that the East–West gap, measured in terms of absolute differences in years of life expectancy, is proving very difficult to eliminate, despite earnest hopes to the contrary.
The trajectories of Russia and other Soviet countries, including the three Baltic States in the Figure 1, were strikingly different to those of the CEE countries. The anti-alcohol
