Regarding Dietary Calcium to Reduce Lead Toxicity

Bogden, John D.; Louria, Donald B.; Oleske, James M.

Regarding Dietary Calcium to Reduce Lead Toxicity

James Oleske

2009, Nutrition Reviews

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zy zyxw zyx zyxwvutsrqpo zyxwvutsrqp Letters to the Editor September 2001: 307-310 Regarding Dietary Calcium to Reduce Lead Toxicity To the editor: In a recently published review, Ballew and Bowman’ conclude that scientific evidence does not support the conclusion that increased dietary calcium is warranted as a specific prophylaxis against lead toxicity. By contrast, we believe it is a scientifically plausible and very promising strategy that must be rigorously tested. In addition, it seems to us that their review of the literature is inordinately negative. A few examples should suffice to illustrate the imbalance of their position: 1. A consistent theme in their review is the between- and within-study variability of the effects of dietary calcium on lead absorption and toxicity in human or animal studies. Variability of data, of course, is hardly unique to lead-calcium interactions. It has long been known that increased dietary calcium reduces lead absorption in some adults substantially more than in others.* Because of the physiologic and molecular complexity of leaddietary calcium interactions, a point acknowledged by Ballew and Bowman, it is quite possible that an increase in dietary calcium may better protect a subset of children from lead. Further studies are needed to define that possibility.However, even if increased calcium does not protect 100% of the children, but only 20%, 40%, 6O%, or 8O%, it is still a worthwhile strategy. 2. Ballew and Bowman suggest that the numerous studies in experimental animals that demonstrate a protective effect of dietary calcium against lead toxicity need to be extrapolated to the human situation with caution. We agree, but the fact is that, despite typical variability among studies, in every animal species investigated, including rats, chicks, dogs, lambs, and horses, increased dietary calcium protects against lead absorption and/or toxicity. 3. Ballew and Bowman assert “Many of the animal study protocols used high doses of lead and extreme variations in calcium.” Some did, others did not. For example, in one of our investigations in the rat,3 we found that, compared with a diet containing 1 mg Cdg, a diet containing 5 mg C d g fed for 1 year reduced lead concentrations by approximately twofold for blood, but by approximately six- to twentyfold in critical target organs, such as the brain, skeleton, and kidneys. The dose of calcium that we used, 1 mg C d g of diet, is approximately 50 m a g for a 0.3-kg rat. This is identical to the dose of a 10-kg child ingesting 500 mg c a l c i d d a y . Ten kilograms is the median body weight of a child approximately 1.5 years old within the age range of greatest risk for lead poisoning. Thus, the dose of calcium we used does not represent an “extreme” protocol. In addition, mean blood lead concentrations of the rats were in the range of 5-50 pg/dL, which is typical of those of many children. Similarly, doses used by other investigators cited by Ballew and Bowman are also not “extreme.” 4. Ballew and Bowman note that the protective effect of increased calcium varied “from organ to organ” in reported studies, as if this were unexpected. However, target organs that accumulate lead, such as the kidney and skeleton, may show larger reductions with increased calcium than blood and other organs. Ballew and Bowman focus excessively only on changes in blood lead, ignoring the more profound changes in target organ lead that occur simultaneously, as shown in the above and other studies. 5. Their assertion that “no single dietary manipulation is likely to have a very profound effect on lead status” ignores the rich history of evidence that single nutrients can markedly influence health. Ballew and Bowman then segue from the literature analysis to policy implications and those suggestions should be examined very carefully. Screening can detect already-poisoned children for the overwhelming majority of whom there is no treatment other than no additional e x p o s ~ r eThe . ~ number of children so designated is likely to increase dramatically as evidence accumulates that our current 10 pg/dL boundary between acceptable and unacceptable blood lead concentrations should be lowered to perhaps 3-5 pg/dL to avoid demonstrable brain damage. Education is presumably valuable, but in actuality, there are no adequate data documenting its effectiveness. Abatement is a slow, expensive process that can be of limited value to already-poisoned ~ h i l d r e nand , ~ could be primary prevention only if we abated houses before the children living in them developed excessive lead burdens. The long history of good intentions but little abatement in many communities demonstrates that this is not likely to happen. Besides, no matter how much housing abatement we did, we could not solve the problem given the wide dispersion of lead in the environment. Although all the other efforts are laudable and should be vigorously supported, perhaps the best hope for effective primary prevention is nutritional, primarily through increases in calcium intake. Surely the evidence is strong enough to virtually mandate trials with careful evaluation that will tell us in a reasonably brief period of time whether increasing calcium intake does, indeed, decrease the incidence of low level, but potentially very dangerous lead zyxwvu zyxwvuts Nutrition Reviews@,Vol. 59, No. 9 307 zyxwvuts zyxwvut intoxication.As Ballew and Bowman indicate, getting children to have adequate dietary calcium intake is not nutritionally controversial, and an added health benefit may be the avoidance of lead poisoning. That hypothesis needs to be tested and should not be ignored because of the argument presented by Ballew and Bowman that such actions might undercut screening, abatement, and educational approaches to lead poisoning. Increasing calcium intake is an adjunct to these other measures, not a replacement. The World Health Organization, Centers for Disease Control and Prevention, and U.S. Environmental Protection Agency each issued recent recommendations about increased dietary calcium as a means to reduce lead absorption and toxicity. Retraction of this advice in the absence of solid evidence for doing so will confuse parents and health care providers, and be a large step backward in our efforts to address this major public health problem. In fact, we should further emphasize the potential role of dietary calcium in protecting against lead toxicity while also improving our efforts in the areas of environmental abatement and behavioral change. The current effort we are undertaking in Newark, New Jersey, to increase calcium intake is good for children’s health and is based on substantial experimental data and enough human evidence to justify, as part of this campaign, determining whether that increased calcium intake reduces lead poisoning. Ballew and Bowman support adequate calcium intake for young children. How in the world can they then be against also assessing its role in primary prevention of lead poisoning? As carefully documented in a recent Government Accounting Office r e p ~ r t lead ,~ poisoning remains a substantial problem among young urban children despite a general decline in blood lead concentrations. We should do all we can to solve this problem, including abatement, behavioral change, and dietary recommendations. Our goal should be to reduce blood lead concentrations as much as possible, not just to below 10 pg/dL, a convenient round number that is not sufficiently protective against lead toxicity. If Ballew and Bowman are arguing for a status quo approach to lead poisoning or not conducting the ongoing calcium campaign and relevant studies on lead-calcium relationships, we believe their position would be untenable. On the other hand, if they are arguing that the value of increasing calcium intake must be rigorously evaluated and that a campaign to increase calcium intake must be careful not to undercut screening, abatement, and education efforts, we are in full agreement. Authors ’ response: We sympathize with and, indeed we share the hope that dietary adequacy might reduce the impact of lead exposure among young children, given the insidious nature of lead toxicity, the difficulty and expense of abatement, and the ongoing risk among the most vulnerable strata of our population. We urge rigorous testing of the hypothesis that appropriate calcium intake might reduce lead absorption or toxicity in children. However, recommendations and policy must be based on evidence rather than conviction. These were the central points of our review. Bogden et al. have evidently misunderstood our position. Their statements about our article are simply wrong, as a dispassionate reading of our article will reveal. We disagree with their assertion that our review was inordinately negative and imbalanced. On the contrary, our review was exhaustive, balanced, and gave full weight to all the evidence, both positive and negative. We did not deny the positive evidence but we did caution against inappropriate interpretation of and extrapolation from the positive studies. Further, we did not ignore the negative evidence. Bogden et al.’s letter reflects a more selective view ofthe literature in the field. 308 zyxw John D. Bogden, Ph.D., Donald B. Louria, M.D., James M. Oleske, M.D. UMDNJ-New Jersey Medical School Department of Preventive Medicine and Community Health Department of Pediatrics Newark,NJ 07103-2714 1. 2. 3. 4. 5. Ballew C, Bowman B. Recommending calcium to reduce lead toxicity in children: a critical review. Nutr Rev 2001;59:71-9 Blake DC, Mann M. Effect of calcium and phosphorus on gastrointestinalabsorption at 203 Pb in man. Environ Res 1983;30:188-94 Bogden JD, Gertner SB, Christakos S, et at. Dietary calcium modifies concentrations of lead and other metals and renal calbindin in rats. J Nutr 1992; 122:1351-60 Rogan WJ, Dietrich KN, Ware JH, et al. The effect of chelation therapy with succimer on neuropsychological development in children exposed to lead. N Engl J Med 2001;344:1421-6 United States General Accounting Office. Lead poisoning. Federal health care programs are not effectively reaching at-risk children. Washington, DC: US. General Accounting Office, 1999 Carol Ballew, Ph.D. Formerly: Epidemiologist, Division ofNutrition and Physical Activity Centers for Disease Control and Prevention Currently: Director, Epidemiology Center Alaska Native Health Board zyxwv zy zyx zy BarbaraBowman, Ph.D. Associate Director for Policy Studies Division of Diabetes Translation Centers for Disease Control and Prevention Nutrition Reviewsa, Vol. 59, No. 9

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