A Paradigm for Solving the Mystery of Declining Tooth Decay

by
Daniel A. Montgomery

Abstract. The prevalence of caries declined in the developed countries in the last half of the twentieth century. This trend could not be explained by the ubiquitousness of fluoridation. The concentration of blood cadmium has declined during the same time span that caries prevalence declined and fluoride ingestion increased. Cadmium is associated with more caries. Cadmium impairs vitamin D metabolism. The distributions of cadmium and caries are skewed. This hypothesis predicts that individuals with the most caries will be lowest in vitamin D and highest in cadmium. Iron may be a confounding factor in cadmium toxicity. Epidemiological studies of caries should relate cadmium, vitamin D and fluoride status of the individual for greater discriminant power.


There have been large reductions in the prevalence of caries in the developed countries which could not be attributed to fluoridation. These large reductions were a general trend in both the fluoridated and unfluoridated areas over a span of about 30 years at the time Diesendorf reviewed the statistics.(1)

Cadmium has been associated with the promotion of caries. Gingivitis, tooth loss and caries attributable to cadmium were found in nickel-cadmium battery production workers.(2) Cadmium injections during molar tooth development strongly promoted caries in female rats. Cadmium partially negated the cariostatic effect of fluoridated drinking water in both male and female rats.(3)

Cadmium alters vitamin D metabolism. Chalkley, et al.(4) investigated the effects of lead and cadmium on the pathway of vitamin D3, in 59 smelter workers occupationally exposed to lead and cadmium. In 19 of the workers, the plasma vitamin D3 metabolites and blood lead were measured. Concentrations for 24R,25(OH)2D3 were depressed below the normal range as blood and urinary cadmium increased independent of lead concentrations. Exposure to cadmium alone decreased the concentrations of 1 alpha,25(OH)2D3 and 24R,25(OH)2D3, whereas exposure to both cadmium and lead increased the concentrations of 1 alpha,25(OH)2D3. The effect of cadmium on the vitamin D metabolic pathway can lead to osteoporosis or osteomalacia. These risks are possibly increased in the presence of lead.

There is a weak association between children's lead exposure and caries prevalence.(5)

In rats, cadmium exposure caused an imbalance of minerals stored in the liver. Depletion of iron was the strongest effect of cadmium. Depleted iron stores may increase the risk of cadmium induced osteoporosis.(6)

Cadmium exposure from industrial sources declined in the developed countries during the last half of the twentieth century. This was due to stricter standards for industrial pollution.(7) Atmospheric cadmium pollution from industry point source emissions declined 87 percent from 1970 to 1988 in the Rhine Basin countries.(8) Declining levels of cadmium pollution caused significant reductions in blood cadmium concentrations.(9,10)

Blood cadmium concentration is most strongly associated with smoking status.(11, 12) In a British epidemiological survey, blood cadmium concentrations were highly skewed. The strongest association was with smoking, but there was substantial geographic variation.(13)

Smoking declined and became more skewed in the last half of the twentieth century. The annual per capita consumption of cigarrettes in the United States was 4345 in 1963 and 2261 in 1998. The prevalence of smoking in people aged 18 and older was 42.4% in 1965 and 24.7% in 1997. The percentage of adults who never smoked was 44% in the mid-1960s and 55% in 1997.(14)

The prevalence of caries has decreased, but the distribution has become skewed. Anderson found that 20% of the population had 60% of the caries.(15)

Mansfield (16) studied urinary fluoride in the U.K. In the artificially fluoridated population, 60% were excreting 1 ppm F or more and 18% were excreting 2 ppm F or more. For the non-fluoridated group, 39% excreted 1 ppm or more and 8% excreted 2 ppm F or more. F levels of 4 ppm or higher were found in 2% of the samples from the fluoridated areas. When comparing populations for the effects of fluoride, Epidemiological studies of the fluoridation status of the drinking water of a population have a lower discriminant power than could be achieved with measurements of individual fluoride status.

Epidemiological studies of caries should relate cadmium, vitamin D and fluoride status of the individual for greater discriminant power.


References

1. Diesendorf M. The mystery of declining tooth decay. Nature 1986 Jul 10;322:125-9.

2. Bar-Sela S, Levy M, Westin JB, Laster R, Richter ED. Medical findings in nickel-cadmium battery workers. Isr J Med Sci 1992 Aug-Sep;28(8-9):578-83.

3. Shearer TR, Britton JL, DeSart DJ, Johnson JR, Influence of cadmium on caries and the cariostatic properties of fluoride in rats, Arch Environ Health 1980 May-Jun;35(3):176-80.

4. Chalkley SR, Richmond J, Barltrop D. Measurement of vitamin D3 metabolites in smelter workers exposed to lead and cadmium. Occup Environ Med 1998 Jul;55(7):446-52. Comment in: Occup Environ Med. 1999 Nov;56(11):788.

5. Gemmel A, Tavares M, Alperin S, Soncini J, Daniel D, Dunn J, Crawford S, Braveman N, Clarkson TW, McKinlay S, Bellinger DC. Blood lead level and dental caries in school-age children Environ Health Perspect 2002 Oct;110(10):A625-30.

6. Noël L, Guérin T, Kolf-Clauw M. Subchronic dietary exposure of rats to cadmium alters the metabolism of metals essential to bone health. Food Chem Toxicol 2004 Aug;42(8):1203-10.

7. Van Assche, F. The relative contribution of different environmental sources to human cadmium exposure and the EU risk assessment, Proceedings of the 8th International Nickel cadmium conference, Prague, 21-22 Sept 1998; publ.: International Cadmium Association, Brussels, Belguim.

8. Anderberg S, Prieler S, Olendrzynski K, de Bruyn S. Old Sins: Industrial Metabolism, Heavy Metal Pollution, and Environmental Transition in Central Europe. Tokyo: United Nations University Press. 2000. www.unu.edu/unupress/unubooks/80841EOc.htm.

9. Ducoffre G, Claeys F, Sartor F. Decrease in blood cadmium levels over time in Belgium, Arch Environ Health 1992 Sep-Oct;47(5):354-6.

10. Benes B, Spĕvácková V, Cejchanová M, Smíd J, Svandová E. Retrospective study of concentration levels of Pb, Cd, Cu and Se in serum of the Czech population in time period 1970-1999. Cent Eur J Public Health 2001 Nov;9(4):190-5.

11. McKelvey W, Gwynn C, Jeffery N, Kass D, Thorpe LE, Garg RK, Palmer CD, Parsons PJ. A Biomonitoring Study of Lead, Cadmium, and Mercury in the Blood of New York City Adults. Environ Health Perspect 2007 Oct;115(10):1435-41.

12. Paschal1 DC, Burt V, Caudill SP, Gunter EW, Pirkle JL, Sampson EJ, Miller DT, Jackson RJ. Exposure of the U.S. Population Aged 6 Years and Older to Cadmium: 1988-1994. Arch Environ Contam and Toxicol 2000 Apr;38(3):377-383.

13. Pocock SJ, Delves HT, Ashby D, Shaper AG, Clayton BE, Blood cadmium concentrations in the general population of British middle-aged men, Hum Toxicol 1988 Mar;7(2):95-103.

14. Office on Smoking and Health, National Center for Chronic Disease Prevention and Health Promotion, CDC, Achievements in Public Health, 1900-1999: Tobacco Use -- United States, 1900-1999, Morb Mortal Wkly Rep 1999 Nov 5;48(43):986-93.

15. Anderson MH. Changing paradigms in caries management. Curr Opin Dent 1992 Mar;2:157-62.

16. Mansfield, P. The Distribution of Urinary Fluoride Concentration in the UK. Fluoride 1999, 32(1):27-32.