Magnesium 4: 5-15 (1985)
Key Words. Magnesium · Drinking water · Cardiovascular mortality
Abstract. Water hardness can no longer be considered as the most reliable ‘water factor’ with regard to the cardiovascular risk observed in epidemiologic studies. Only two out of three studies have shown a reverse correlation between cardiovascular mortality and water hardness. But studies carried out on the water Mg level alone, as opposed to those on water hardness (Ca + Mg) have all shown a reverse correlation between cardiovascular mortality and the Mg level.
In developed countries, the Mg intake is often marginal and the Mg intake coming from drinking water represents the critical factor through which the intake is deficient or satisfactory. Thus, Mg deficiency, either experimental or in man facilitates cardiovascular pathology.
The importance of the Mg intake in drinking water is both quantitative and qualitative. Water containing Mg is better and more quickly absorbed than dietary Mg. This particular availability might help to understand why an adequate water Mg level may determine a better state of health, even without any Mg deficiency. Epidemiological data in man and experimental data in rats have demonstrated that the intake of water containing a sufficient amount of Mg may prevent arterial hypertension and correlated ionic and nervous disturbances.
Indirectly the water Mg level also interferes in the leakage of food-borne Mg during cooking. There is an inverse correlation between the Mg loss in the cooked food and the Mg level of the cooking water itself. Mg appears to be an antagonist of noxious polluting agents (e.g. in the human amnion, Mg is a competitive inhibitor of Pb and Cd). It is not advisable to enrich water in Mg in the course of the processing since its corrosivity index would also increase. The best pathway is probably to neutralize corrosive water by filtration on calibrated grains of earth-alkaline metal (Neutralite or Magno or Akdolit) to ensure the highest possible Mg/Ca ratio, with the best anticorrosive power.
In 1957, Kobayashi  pointed out the possible relationship between the composition of drinking water and cardiovascular diseases after observing a geographical correlation between stroke mortality and the water acidity of the rivers. Schroeder  statistically checked the validity, of the Japanese data, and then examined the epidemiological implications of this phenomenon in the United States. He suggested an inverse correlation between various types of heart diseases and total drinking water hardness: drinking soft water increases the cardiovascular risk which is reciprocally reduced by hard water consumption.
In all continents, numerous studies have been devoted to this inverse correlation through a large number of statistical units of.observations (states, towns, districts) diversification of the causes of mortality (general, cardiac, vascular) and multiplication of observed parameters (analytical data on water, climatic and geological factors) [27, 49, 54, 71-78, 86]. The inverse correlation has been confirmed in the majority of the studies and, in particular, when the geographical scale of the epidemiological study is larger, i.e. when the cultural, climatic and professional parameters vary widely. However, the inverse relationship between the hardness of the water and cardiovascular mortality is not always found [26, 27, 51]. Consequently, the water parameter cannot be considered a major risk since it may be completely missing; but studies on the water factor have shown the frequency of the relationship between cardiovascular diseases and drinking water. Other etiological and atmospheric cofactors, associated with hardness (i.e. pluviosity  or salt-consumption ) might have possible roles, but the main question concerns the relationship between drinking water and a satisfactory condition of the cardiovascular apparatus. Two types of research have attempted to determine either the cardiovascular protecting factors in protective water, or the cardiovascular toxic factors in noxious water. These water factors are only to be taken into consideration when they represent a notable part of the recommended dietary allowances or qualitatively, if they constitute a higher bioavailability intake.
A significant inverse correlation has been irregularly found between cardiovascular mortality and natural water elements: K+ , Ca2+ , Li+ , CO3H- , F- , I- [77, 78], Ni , Cr, Fe, Zn, Cu, Se [41, 77, 78, 80], perhaps Va [44, 96], Si  and As . It is obvious that if the importance of dietary K intake (particularly the K/Na ratio [69, 85, 105] is critical, the quantitative part of water K is rarely important. This observation is identical with that made on Ca. Its dietary intake has an important cardiovascular protective role [10, 12, 68, 89, 94], but Ca in drinking water, which is often poorly assimilated, represents a negligible element of the Ca intake. The importance of the Ca level in drinking water can be presented to the consumer as an anticorrosive substrate of the protective coating deposited on the pipes by nonaggressive waters. The inverse correlation between Li+ and mortality is low and becomes inverse when the partial correlations are calculated . Nevertheless, the lowered bicarbonate and carbonate levels are essential elements of the corrosivity [7, 8, 99]. The water contribution of various trace elements, the minimum requirements of which are known (F, I, Cr, Fe, Zn, Cu), may be important, but it is difficult to appreciate this contribution when the requirements have not yet been defined (As, Si ...).
Of all the factors studied in drinking water, the highest inverse correlation has been observed between Mg and cardiovascular mortality [2-4, 54, 71-76 100, 108a, 109] Moreover, in Canada, the myocardial level is significantly lower in soft water districts than in hard-water districts. The same is found in the hearts of the subjects who died from sudden heart attacks or myocardial infarcts (even outside necrosed tissue areas where the leak also depends on tissue lysis [3, 5, 6, 23-25, 71-75, 106]). Quantitatively, the water Mg contribution may represent the amount of Mg required to bring an insufficient dietary Mg level to a correct level [3, 42, 54, 71-75, 77, 78, 102, 109]. In fact, in developed countries, the adult Mg intake is marginal as to the ‘recommendable’dietary allowance [6 mg/kg/day; 36, 100, 101] and even to the slightly lower recommended dietary allowance (5 mg/kg/day) proposed by the US National Academy of Sciences in adults. The inadequacy of the Mg intake is even worse in anabolic phases such as growth, pregnancy, lactation...
According to its Mg content (from 10 to 100 mg/l), 2 liters of water. (drinking water, tea, coffee, soups) increase the Mg intake from 20 to 200 mg/day. A higher water Mg intake is even observed with some bottled mineral waters, i.e. Vittel Hépar: 130 mg/l .
The Mg level of cooking water also interferes in the Mg dietary intake. A nutrient in the cooking water, always loses an important part of its Mg , but the Mg loss is lower when the food is cooked in a water with high Mg content. There is an inverse correlation between the Mg loss in the cooked food and the Mg level of the cooking water [28, 36, 47, 77]. Nowadays, housewives often cook with softened water. They would do better to use unsoftened drinking water.
Thus, quantitatively, the magnesium of drinking water represents an appreciable part of the dietary intake. As a risk index, the Mg level in water is more satisfactory than hardness. According to a number of reports its participation in hardness ranges from 10 to 89% [75, 76]. One should distinguish between hard water content in Great Britain  France [29, 108], uncorrelated with cardiovascular mortality and the US hard waters with high Mg contents [75, 76] and reversely correlated with cardiac diseases . It is to be hoped that in water, as well as in-the overall diet , the Mg/Ca ratio is not too low. As a matter of fact, in France and Great Britain, the Mg/Ca ratio amounts on the average to a. few hundredths, while in the US, it ranges from 1 to 5.
The water Mg intake may quantitatively represent the critical contribution allowing the control of an Mg deficiency whose physiological effects on the cardiovascular apparatus are perfectly well known [2-4, 11, 100].
But, the contribution of Mg in drinking water is also interesting qualitatively.
Studies conducted by Lowik et al.  and Binnerts et al.  with diets. poor, normal and rich in Mg show that with an absolute. equivalent Mg intake, Mg in drinking water is much better absorbed than dietary Mg. This particular bioavailability of water Mg can be proven experimentally. The mortality rate of mice in which Mg deficiency had been induced by a diet with a very low Mg content could be controlled by the mere intake of water containing 30 mg Mg/l [54, 109]. This Mg level is found in various hard waters of the distribution system. The boiling of water, decreases the Ca level, but has little effect on the Mg level.
Breakfast should provide an intake of water Mg since the Mg requirements increase when people resume their activities. Suppressing breakfast and/or the coffee break induces massive reduction of magnesuria [13, 66].
Accordingly, the urinary Mg/Ca ratio is higher than it is in the ingested water [61, 62]
These particular absorption qualities of water Mg  suggest an interpretation of the investigations of Novikov et al. . The study of various cardiovascular, nervous and, ionic parameters in, Siberian populations, comparable in all respects except for the hardness of their drinking water, shows an inverse correlation between soft water with a low Mg content and arterial hypertension as well as K-Na, P-Ca and neuroendocrine alterations which may cause vascular pathology.
Rats were administered a balanced diet, namely with an adequate Mg level: blood and tissue Mg was normal in all these animals. But the Mg and Ca levels of their drinking water were different in each group. The results showed similar correlations between the Mg water level and vascular impairments with similar ionic and neuroendocrine disorders in the rats and the Siberian populations. This suggests that an insufficient Mg level in drinking water can induce hypertension together with neuroendocrine and humoral disorders in both animals and man. Recently, Altura and Altura [3a] have indeed demonstrated that alterations in dietary and waterborne Mg intake can produce hypertension in rats; they found an inverse correlation between serum Mg level and elevation in arterial blood pressure which was linked to microvascular changes.
The effect of Mg contained in drinking water could be explained by its particular bioavailability. In awakening periods, when the metabolic Mg requirements are increased, an adequate intake of quickly and well-absorbed water Mg would avoid solicitation of the neuroendocrine controls of the Mg homeostasis (vegetative, adrenal, thyroparathyroid and pancreatic [34, 35]) When the water Mg intake is too low the necessity of maintaining the Mg homeostasis might induce, in the long run, a dysfunction of these regulations . Since the diverse regulatory mechanisms of Mg homeostasis are the same as those which control the K-Na and P-Ca balance [34, 35], it is conceivable that their dysfunction might induce nervous hyperexcitability and arterial hypertension.
Drinking water containing Mg as a specific element of Mg intake, qualitatively and quantitatively, is particularly beneficial to the cardiovascular and nervous functions. This is probably due to the fact that dietary Mg intake acts as an antagonist of certain noxious factors of the water.
The noxious effects of Na on blood vessels have been known for over 4,500 years . The industrial civilization consumes too much Na  and not enough K [41, 69, 81, 85, 93, 105]. Numerous studies have considered Na as a major risk factor in drinking water [14, 20, 21, 112]. In the majority of the epidemiological studies , a direct correlation between hypertension and the Na level in drinking water has been observed. However, this relation is not consistent [39, 98]. It is obvious that the Na of drinking water is not a major element of the Na intake, but it can easily be modified. It is difficult to cut down by 50% the Na intake which is provided in meat and dairy products! People are more reluctant to reduce their usual consumption of salt. But one should avoid the consumption and use of cooking water which is very rich in Na such as artificially softened waters , whose Na levels can be as high as 500 mg/l. It should be mentioned that the use of soft waters seems to involve an increased consumption of salt, as demonstrated by a direct correlation with natriuria .
Water intake represents only a small part of the total Na level and of the Na/K ratio in the general intake. Still, its importance should not be overlooked in cases of specific backgrounds such as hypertension and of consumption of soft waters with high Na contents which result in increased consumption of salt.
As early as 1974, Schroeder and Kraemer  thought that the noxious cardiovascular effects of certain soft waters might be due to the presence of toxic metals solubilized in the geological layers or in the pipes.
Kobayashi [cited by Schroeder, 96] gives a prominent position to the direct correlation between the ratio-related to the water acidity (X 3-5) and diseases such as hypertension and strokes in Japan.
Water alkalinity (bicarbonate CO3H  and level [7, 8]) might be a protective factor. One should distinguish between two physical factors of water: aggressivity towards Ca carbonate and corrosivity to metals. A nonaggressive water may be corrosive. These two notions can, however, be connected because of the occurrence of a calcium deposit which protects the pipes from corrosion. Corrosivity decreases together with aggressivity [30, 56]. The Langelier index  determines whether a water is encrusting (IL > 0) or aggressive (IL < 0); a positive response of IL is a sign of anti-aggressivity.
Ryznar  has proposed an empirical index (IR), which appears to be more representative of the corrosive or scaling characteristics of the water: IR < 6: scaling water; 6 < IR < 7: balanced water; IR > 7: corrosive water.
The Ryznar index should be systematically used in epidemiological studies on the relationship between drinking water and health. It is obvious that a very corrosive water can be contaminated by metals classified into ‘essential’ elements and ‘toxic’ polluting factors. But this classification is unsatisfactory since high levels of ‘essential’ elements become toxic and conversely low levels of ‘toxic’ elements appear to be essential . For example, a negative correlation is found between cardiovascular mortality and low levels of Fe, Cu, Cr, Mn, Zn, As intake, but high levels of Ca [67, 70, 71, 88, 99, 102], Cr [71, 99], Mn [70, 71, 99], V , Zn (57), and As  have polluting, toxic effects. The noxiousness of corrosive waters. is mainly due to two toxic heavy metals: Pb and Cd [17, 18, 39, 102]. Water Pb does not have a geological origin. Unlike Cd, it has a pseudocolloidal form which, in the course of further processing, easily flocculates and is eventually absorbed. The lead loading occurs in the distribution system [17, 18, 39, 102]. A short portion of lead water pipe, lead solders, stagnation in the pipes (therefore high Pb levels in the early morning, heating of the water, earth plugging of an electrical appliance) make the problem even worse and can bring about elevated levels of Pb in the water [32, 33, 114]. Attempts have been made to replace lead pipes with galvanized iron pipes. However, Zn which is used for galvanization always contains Cd, which is released when corrosive water stagnates in the pipes [17, 18]. The use of polyvinyl chloride (PVC) pipes does not always solve the water pollution problem, as PVC may contain lead salts as stabilizing agents and may contaminate the water .
The effects of water-polluting agents cumulated with those from digestive and pulmonary sources are greatly to be feared, because cation absorption is increased when the cations are water soluble . Besides, even low levels [59, 107] of Cd and Pb have detrimental cumulative effects on the cardiovascular system [80, 90], as they increase tissue Na and Ca levels and decrease the K and Mg levels. These effects, which are comparable to those of Mg deficiency, can be controlled by Mg intake. Indeed, Cd intoxication decreases the Mg level in bone, teeth and soft tissues [52, 53, 59, 113]. Conversely, Mg reduces Cd absorption [109, 110] and is a competitive inhibitor of Cd in the isolated amnion (unpublished data). Mg, partly, antagonizes the carcinogenic effects of Cd  and antagonizes the uncoupling of oxidative phosphorylation induced by Cd in hepatic mitochondria but not in renal mitochondria . The increase in Mg intake reduces Pb retention and increases Pb excretion [79, 104]. But a decrease of Pb absorption due to the described Mg intake  has not been confirmed [109, 110], and is ancillary because the increase in the urinary Pb level observed in the course of parenteral Mg loading cannot be easily explained through this mechanism . Conversely, Mg deficiency increases Pb retention, both in the mother and in the fetus . Also, all the available studies [except for two: ref. 40, 82] show an antagonism between Mg and Pb. For example, Pb and Cd cross animal [1, 31, 89] and human [19, 50, 64] placental barriers, and Mg is a competitive inhibitor of Pb and Cd in the isolated human amnion [9, 43, 44].
Drinking water containing Mg is, qualitatively and quantitatively, useful, and therefore drinking and cooking water should not be softened. In the case of Mg-poor water, the problem of the best processing technique can be discussed. It is tempting to have it enriched in order to get 30 mg/l Mg.
Simpson  suggests that one should increase the Mg level of tap water after it has been collected from the tap. Marier et al.  and Anderson et al.  do not agree with the idea of adding Mg to the water in processing stations. This increase in the Mg level, in processing stations, might impair the balance due to super saturation of CO3Ca and increase corrosivity.
Two methods have been proposed to reduce the corrosivity: Richards and Moore  increase the pH and precipitate the metals by adjunction of lime, but this method is inadequate because the decrease of Pb is insufficient; besides, Na orthophosphate which is used as a corrosivity inhibitor increases the already excessive intake of P in our diet.
Neutralization by filtration on calibrated grains of earth-alkaline metals reduces the Pb level in water. Marble has long been used, but the reaction is too low. Neutralite (CO3Ca + CO3Mg) or Magno or Akdolit (CO3Ca + MgO) [15, 30] have also been used. With the best anticorrosive power the best filter should induce the highest Mg/Ca ratio.
La dureté de l’eau ne peut représenter la caractéristique correspondant fidèélement avec la donnée épidémiologique définissant un <<facteur eau>> de risque cardiovasculaire. La notion selon laquelle la mortalité cardiovasculaire est en relation inverse avec la dureté de l’eau ne se retrouve que dans 2 enquêtes sur 3. Par contre, la correlation inverse se retrouve toujours lorsqu’on remplace l’étude de la dureté (somme de taux de Ca et Mg) par celle du taux isolé de Mg. La ration alimentaire des pays développés étant très souvent marginale, l’apport du Mg de l’eau de boisson constitue le facteur critique laissant la ration déficiente si l’eau est pauvre en Mg et la faisant passer à un taux non carencé lorsqu’elle est riche en Mg. Or la carence magnésique expérimentale et clinique favorise la pathologie cardiovasculaire. L’importance de l’apport du Mg de l’eau de boisson ne se reduit pas à cette donnée quantitative directe. Elle est aussi qualitative car le Mg de l’eau semble être absorbé mieux et plus rapidement que celui des aliments. Cette particularité pourrait peut-être permettre de comprendre que — même avec un apport magnésique suffisant — une eau riche en Mg soit plus saine: des données épidémiologiques et expérimentales vérifient en effet que méme en l’absence de carence magnésique, la prise d’une eau riche en Mg prévient l’hypertension artérielle, les troubles sodopotassiques, phosphocalciques et nerveux observés tant chez l’homme que chez l’animal d’experience. Le taux de Mg de l’eau intervient aussi indirectement sur 1es apports en Mg par ses effets au cours de la cuisson des aliments: une eau douce appauvrit les aliments en Mg tandis qu’une eau dure les enrichit. Le taux de Mg de la ration intervient enfin pour antagoniser les polluants cardiovasculo-nocifs (par exemple, dans l’amnios humain, Mg est un inhibiteur compétitif de Pb et Cd). Aux effets propres du Mg sur l’appareil cardiovasculaire, il convient donc d’adjoindre ses propriétés antagonistes des métaux cardiovasculotoxiques dont les eaux corrosives favorisent l’apport. Comme il ne paraît pas possible d’enrichir artificiellement en Mg les eaux de boisson sans en accroître <<l’indice de cor rosivité>>, cette pratique apparemment séduisante, ne semble donc pas recommandable dans les stations de traitement des eaux. Il convient d’y neutraliser les eaux corrosives par filtration sur des grains calibrés d’alcalino-terreux (Neutralite, Magno ou Akdolit), en s’efforçant d’obtenir a pouvoir anti-corrosif égal le rapport Mg/Ca hydrique le plus élevé.
1 Ahokas, R.A.; Dilts, P.V., Jr.: Cd uptake by the rat embryo as a function of gestational age. Am. J. Obstet. Gynec. 135: 2 19-222 (1979).
1a Altura, B.M.: Sudden death ischemic heart disease and dietary magnesium intake: is the target site coronary vascular smooth muscle? Med. Hypotheses 5: 843-849 (1979).
2 Altura, B.M.; Altura, B.T.: Role of Mg ions in contractility of blood vessels and skeletal muscles. Magnesium-Bull. 3: suppl. 1A, pp: 102-114 (1981).
3 Altura, B.M.; Altura, B.T.: Mg, Na and K interactions and coronary heart diseases. Magnesium 1: 241-265 (1982).
3a Altura, B.M.; Altura, B.T.; Gebrewold, A.; Ising, H.; Günther, T.: Mg deficiency and hypertension: correlation between magnesium deficient diets and microcirculatory changes in situ Science 223: 1315-1317 (1984).
4 Altura, B.T.; Altura, B.M.: The role of Mg in etiology of strokes and cerebrovasospasm. Magnesium 1:277-291 (1982).
5 Anderson, T.W.; Neri, L.C.; Schreiber, G.; Talbot, F.D.F.; Zdrejewski, A.: Ischemic heart disease, water hardness and myocardial Mg. Can. med. Ass. J. 113: 199-202 (1975).
6 Anderson, T.W.: Water hardness, Mg and ischemic heart disease: Nova Scotia med. Bull. April: 58-61 (1977).
7 Arden, T.V.: Soft water and heart disease.. Water Services 80: 250-252 (1976).
8 Arden, T.V.: Cardiovascular mortality an analysis of the water effect (Aqua Europa Publ, Henley on Thames (1977).
9 Bara, M.; Guiet-Bara, A.: Magnesium effect on the permeability of the amniotic membrane as a whole and of the epithelial cells, Magnesium-Bull. 3: 145-150 (1981).
10 Belizan, J.M.; Vilar, J.; Pineda, O.; Gonzalez, A.E.; Sainz, E.; Garrera, G.; Sibrian; R.: Reduction of blood pressure with Ca supplementation in young adults. J. Am. med. Ass 249: 1161-1165 (1983)
11 Berthelot,A.; Esposito,J.: Effects of dietary.Mg on.the development of hypertension in the spontaneously hypertensive rat. J..Am.Coll. Nutr. 4: 343-353 (1983).
12 Berthelot, A.; Gairard, A.: PTH- and DOCA-induced hypertension in the rat. Clin. Sci. 58: 365-371 (1980).
13 Binnerts W.T.; Lowik M.R.H.; Groot, E M.: On the importance of Mg in drinking water, in trace element. Analyt. Chem. Med. Biol. vol. 2, pp 87-93 (De Gruyter, Berlin 1983).
14 Blaustein, M.P.; Hamlyn, J.M.: Role of natriuertic factor in essential hypertension: an hypothesis. Ann. intern. Med. 98: 785-792 (1983).
15 Bonnefoy, X.; Certain, R.; Kisfaludi, G.: Essais de neutralisation des eaux agressives d'un massif greseux et granitique. Techniques Sci. municip. 79: 131-136 (1984).
16 Bonnefoy, X.; Huel, G.; Gueguen, R.: Variation of the blood lead level as a function of lead contamination of the subjects drinking water. Water Res.(in press 1984).
17 Boudene, C.; Food contamination by metals; in Di Ferrante, Trace metal exposure and health effects, pp. 163-183 (Pergamon Press, Oxford 1979).
18 Boudene, C.; Arsac, F.: Les métaux présents dans notre alimentation quotidienne. Gaz. méd. 88: 2103-2121 (1981).
19 Buchet, J.P.; Roels, H.; Hubermont, G.; Lauwerys, R.: Placental transfer of lead, mercury, cadmium and carbon monoxide in women. II. Influence of some epidemiological factors on the frequency distributions of the biological indices in maternal cord blood. Environ. Res. 15: 494-503 (1978).
20 Calabrese, E.J.; Tuthill, R.W.: Elevated blood pressure level and community drinking water characteristics. J. environ. Sci. Health A13: 781-802 (1978).
21 Calabrese, E.J., Tuthill, R.W.: The influence of elevated levels of Na in drinking water on elementary and high school students in Massachusssetts. Sci. tot. Environ. 18: 117-133 (1981).
22 Cerklewsli, F.L.: Influence of maternal magnesium deficiency on tissue lead content of rats. J. Nutr. 113: 1443-1447 (1983).
23 Chipperfield, B.: Chipperfield, J.R.: Heart muscle Mg, K and Zn concentrations after sudden death from heart disease. Lancet ii: 293-296 (1973).
24 Chipperfield, B.; Chipperfield, J.R.: Behr, G.; Burton, P.: Mg in heart muscle. Lancet i: 1354-1355 (1976).
25 Chipperfield, B.; Chipperfield, J.R.: Cot deaths and mineral salts. Lancet ii: 220 (1979).
26 Comstock, G.W.: Water hardness and cardiovascular diseases. Am. J. Epidem. 110: 375-400 (1979).
27 Cottet, J.; Cristol, R.; Hydrotimétrie (ou dureté de l'eau) et maladies cardiovasculaires. Bull. Acad. natn. Méd. 166: 421-431. (1982).
28 Dauncey, M.J.; Widdowson, E.M.: Urinary excretion of Ca, Mg, Na and K in hard and soft water areas. Lancet i: 711-714 (1972).
29 De Fulvio, S; Olori, L.: Definitions and classification of naturally soft and naturally hard waters. Proc. Symp. Hardness.of.Drinking Water and Public Health, Luxembourg, pp 95-122 (Pergamon Press, Oxford 1975).
30 Degremont, G.: Mémento technique de l’eau (Technique et Documentation, Paris, 1978).
31 Dilts, P.V., Jr.; Ahokas, R.A.: Effects of dietary Pb and Zn on fetal organ growth. Am. J. Obstet. Gynec. 136: 889-896 (1980).
32 Duc, M.; Abensur, R.: L’inquiétante persistance du saturnisme hydrique. Concours méd. 104: 6659-6672 (1982).
33 Duc, M.; Abensur, R.; Barbier, P.; Chaput, C.: Les aspects actuels du saturnisme hydrique. J. Toxicol. Med. 3: 323-339 (1983).
34 Durlach, J.: Les contrôles neurohormonaux du métabolisme du Mg et leurs conséquences cliniques. Revue fr. Endocr. clin. 21: 507-524 (1980).
35 Durlach, J.; Durlach, V.: Speculations on hormonal controls of Mg homeostasis: a hypothesis. Magnesium 3:109-131 (1984).
36 Durlach, J.; Rayssiguier, Y.; Laguitton, A.: Le besoin en Mg et son apport dans la ration. Méd. Nutr. 16: 15-21 (1980).
37 Dyckner, T.; Wester, P.O.: Effect of Mg on blood pressure. Br. med. J. 286: 1847-1849 (1983).
38 Fine, B.P.; Barth, A.; Sheffet, A.; Lavenhar, M.A.: Influence of magnesium on the intestinal absorption of lead. Environ. Res. 12: 224-227 (1976).
39 Folsom, A.R.; Prineas, R.J.: Drinking water composition and blood pressure: a review of the epidemiology. Am. J. Epidem. 115: 818-832 (1982).
40 Galt, R.M.; MacCreary, P.A.; Laing, G.H.; Hass, G.M.: Lead vs. magnesium in dietary induction of rat tumors; in Hemphill, Trace substances in environmental health, 189-194 (1980).
41 Guang-Sheng, Z.; Shang-Da, C.: An epidemiological study on the relationship of urinary Na and K excretion to blood pressure in China. Magnesium 1: 139-143 (1982).
42 Gueux, E.; Poenaru, S.; Duchene-Marullaz, P.: Electromyographic changes associated with high level of magnesium in drinking water. Magnesium-Bull. 4: 154-156 (1982).
43 Guiet-Bara, A.; Bara, M.: Transfert des cations monovalents à travers la membrane amniotique humaine isolée. C.r. Séanc. Soc. Biol. 173: 875-880 (1979).
44 Guiet-Bara, A.; Bara, M Durlach, J.: Magnesium: a competitive inhibitor of lead. Study on the isolated human amnion; in Halpern, Durlach, Magnesium deficiency. 1st Eur. Congr. Magnesium, Lisbon 1983, pp. 38-45 (Karger Basel 1985).
45 Hackett,. P.L.; Kelman, B.J.: Availability of toxic trace metals to the conceptus. Sci. total Environ. 28: 433-442 (1983).
46 Hankin, J.H.; Margen, S.; Goldsmith, N.F.: Contribution of hard water to calcium and magnesium intakes of adults. J. Am. diet. Ass. 56: 212-224 (1970).
47 Haring, B.S.A.; van Delft, W.: Changes in the mineral composition of food as a result of cooking in ‘hard’ and ‘soft’ water. Archs envir. Hlth 36: 33-35 (1981).
48 Hasegawa, T.: Phosphorylation oxydative de mitochondries de foie et de rein du rat après intoxication par le Cd et effet préventif du Mg. Okoyama Igakai. Zasshi 91: 1447-1454 (1979).
49 Huel, G.; Derrienic, F.; Ducimetière, P.; Lazar, P.Dureté de l’eau et mortalité cardiovasculaire. Analyse critique des arguments de pathologie géograpique. Revue- Epidém. Santé publ. 26: 349-359 (1978).
50 Huel, G.; Ibrahim, M.A.; Boudéne,. C.: Cd and Pb content of maternal and newborn hair relationship to parity, birth weight and hypertension. Archs. envir. Hlth 36: 221-227 (1981).
51 Huel, G.; Thomazeau, R.; Derriennic, F.; Lazar, P.: Dureté de l’eau et mortalité cardiovasculaire. Analyse portant sur 947 communes alsaciennes. Revue Epidém. Santé publ. 26: 381-390 (1978).
52 Itokawa, Y.; Abe, T.; Tanaka, S.: Bone changes in experimental chronic Cd poisoning. Archs Envir. Hlth 25: 241-244 (1973).
53 Itokawa, Y.; Abe, T.; Tanaka, S.: Renal and skeletal lesions in experimental Cd poisoning in rats. Histology and renal function. Environ. Res. 15: 206-217 (1978).
54 Kalkman, C.: Mg, hart vaatziekten en de waterfactor; thesis No. 7430, Amsterdam (Huisdrukkerij, Faculteit der Geneeskunde, Amsterdam 1979).
55 Karppanen, H.: Epidemiological studies on the relationship between Mg intake and cardiovascular disease. Artery 9: 190-199 (1981).
56 Kemmer, F.N.: The NALCO water book (McGraw-Hill, Maidenhead 1979).
57 Klevay, L.M.: Mg, Ca, Cu and Zn in meals: correlations related to the epidemiology of ischemic heart disease. Biol. Trace Elements Res. 4:95-104 (1982).
58 Kobayashi, J.A.: Geographical relationship between the chemical nature of river water and death rate from apoplexy; Ber. Ohara Inst. Lansw. Biol. 11: 12-21 (1957).
59 Kopp, S.V.; Perry, H.M.; Perry, E.F.; Erlanger, M.: Cardiac physiologic and tissue metabolic changes following chronic low level Cd and Cd plus lead ingestion in the rat. Toxicol appl. Pharmacol. 69: 149-160 (1983).
60 Krall, A.R.; MacLean, W.S.; Gamble, H.F.; Rogers, E.W.; Reigart, J.R.; Collawn, S.S.: Effects of magnesium infusions on the metabolism of calcium and lead; in Cantin, Seelig, Magnesium in health and disease, pp. 941-948 (1980).
61 Krizek, V.; Sadilek, L.; Stepanek, P.: Die Trinkkur bei Patienten mit Normo- und Hyperkalziurie. II.- Eine Studie über die Marienbader Karolinenquelle. Balneol. Bohem. 11: 91-104 (1982).
62 Labeeuw, M.; Gerbaulet, C.; Pozet N.; Zech, P.; Traeger, J.; Dissociation of Mg and Ca urinary excretions following water ingestion. Magnesium 2: 156-163 (1983).
63 Lange1ier,W.F.:The analytical control of anti-corrosion water treatment. J. Am. Water Works Ass. 28: 1500-1521 (1936).
64 Lauwerys R.; Buchet, J.P.; Roels H; Hubermont, G.: Placental transfer of lead, mercury, cadmium and carbon monoxide in women. I. Comparison of the frequency distributions of the biological indices in maternal and umbilical cord blood. Environ. Res. 15: 278-289 (1978).
65 Levin A.I.; Novikov, Y.V.; Plitman, S.I.; Noarov, .Y.A.; Lastochkina, K.O.: Effect of water of varying degrees of hardness on the cardiovascular system. Gig. Sanit. 10: 16-19 (1981).
66 Lowik, M.R.H.; Groot, E.M.; Binnerts, W.T.: Mg and public health: the impact of drinking water; in Hemphill, Trace substances in environmental health vol. 16, pp. 189-195 (1982).
67 Luoma, H.; Kivilvoto, L,; Punsar, S.; Knekt, P.; Risk of myocardial infarction in Finnish men in relation to fluoride magnesium and calcium concentration in drinking water. Acta med. scand. 213: 171-176 (1983).
68 MacCarron, D.A.: Ca, Mg and P balance in human and experimental hypertension. J Am. med. Ass. 4: suppl, III, pp. III27-III33 (1982).
69 Mantel, O.; Marcel, G.A.; Lagrue, G.: Hypertension artérielle, potassium et vaisseaux. Médecine act. 10: 219-229 (1983).
70 Manthey, J.; Stoeppler, L.; Morgenstern, W.; Nussel, E.; Opherk, D.; Weintraut, A.; Wesch, H.; Kubler, W.: Magnesium and trace metals: risk factor for coronary heart disease? Circulation 64: 722-729 (1981).
71 Marier, J.R.; Neri, L.C.; Anderson, .T.W.: Dureté de l’eau, santé et importance du magnesium. NRCC/CNRC No. 17582 (Ottawa 1980).
72 Marier, J.R.: Role du Mg dans la cardio-protection des eaux dures. Méd. Nutr. 16: 23-29 (1980).
73 Marier, J.R.: Nutritional and myocardial aspects of Mg in drinking water. Magnesium-Bull. 3: suppl. 1A, pp. 48-54 (1981).
74 Marier, J.R.: Quantitative factors regarding Mg status in the modern-day world. Magnesium 1: 3-15 (1982).
75 Marier, J.R.: Role of environmental Mg in cardiovascular diseases. Magnesium 1: 266-276 (1982).
76 Marier, J.R.: Le Mg provenant de l’eau potable. Gaz. méd. Fr. 90: 1993 (1983).
77 Masironi, R.: Valeur des oligoéléments de l’eau pour la santé. Chron. OMS 32: 413-417 (1978).
78 Masironi, R.; Shaper, A.G.: Epidemiological studies of health effects of water from different sources. A. Rev. Nutr. 1: 375-380 (1981).
79 Maugeri, S.; Santi, C.: Calcio e magnesio nella pro filas del saturnismo sperimentale. Medna Lav. 24: 1-14 (1938).
80 Merz, W.; Trace minerals and atherosclerosis. Fed. Proc. 41: 2807-2812 (1982)
81 Meyer, P.: Hypertension artérielle humaine génétique environnement (Na). Med. Nutr. 19: 284 (1983).
82 Mylroie, A.A.; Hickmon, T.; Hill, G.: Effects of supplemental magnesium on blood and tissue lead levels and toxicity of ingested lead in the rat; in Hemphill, Trace substances in environmental health, pp. 178-183 (l981).
83 Ninard, B.: Analyse des eaux minérales françaises les plus riches en magnésium (au dessus de 75 mg/l). Méd. Nutr. 13: 53 (1977).
84 Novikov, Y.V.; Plitman, S.I.; Levin, A.I.; Noarov, Y.: Fixation de normes hygiéniques pour le taux minimal du Mg dans l'eau potable. Gig. Sanit. No. 9, pp. 7-11 (1983).
85 Pitkanen, H.: Industrial possibilities to interfere with the salt problem: dietary Na/ (K+Mg) ratio. Magnesium 1: 298-303 (1982).
86. Pocock, S.J.; Shaper, A.G.; Cook, D.G.; Packham, R.F.; Lacey, R.F.; Powell, P.; Russel, P.F.: British Regional Heart Study: geographic variations in cardiovascular mortality and the role of water quality. Br. med. J. 280: 1243-1249 (1980).
87 Poirier, L.A.; Kasprzak, K.S.; Hoover, K.L.; Wenk, M.L.: Effects of Ca and Mg acetates on the carcinogenicity of Cd chloride in Wistar rats. Cancer Res. 43: 4575-4582 (1983).
88 Punsar, S.; Karvonen, M.J.: Drinking water quality and sudden death: observations from West and East Finland. Cardiology 64: 24-34 (1979).
89 Renaud, S.; Ciavatti, M.; Thevenon, C.; Ripoll, J.P.: Protective effects of dietary Ca and Mg on platelet function and atherosclerosis in rabbits fed saturated fat. Atherosclerosis 47: 187-198 (1983).
90 Revis, N.W.; Major, T.C.; Horton, C.Y.: The effects of calcium, magnesium, lead or cadmium on lipoprotein metabolism and atherosclerosis in the pigeon. J. environ. Path. Toxic. 4: 293-304 (1980).
91 Richards, W.N.; Moore, M.R.: Plumbosolvency in Scotland: the problem, remedial action taken and health benefit observed. Proc. Conf. Am. Water Works Ass., Miami, pp. 901-918 (1982).
92 Ryznar, J.W.: A new index for determining amount of calcium carbonate scale formed by a water. J. Am. Water Works Ass. 36: 472-473 (1944).
93 Sasaki, N.: Na and K intake of the Japanese. Magnesium 1: 151-155 (1981).
94 Schleiffer, R.; Berthelot, A.; Pernot, F.; Gairard, A.: Parathyroids, thyroid and development of hypertension in SHR. Jap. Circul. J. 45: 1272- 1279 (1981).
95 Schlettwein-Gsell, D.; Mommsen-Straub, S.: Übersicht Spurenelemente in Lebensmitteln: VII: Mg. Z. Vitam.-Horm.-Fermentforsch. 42: 324-352 (1972).
96 Schroeder, H.A.: Degenerative cardiovascular disease in the Orient. II. Hypertension. J. chron. Dis. 8:312-333 (1958).
97 Schroeder, H.A.: Relation between mortality from cardiovascular disease and treated water supplies. Variations in states and 163 largest municipalities in US. J. Am. med. Ass. 172: 1902-1908 (1960).
98 Schroeder, H.A.: Municipal drinking waters and cardiovascular death rates. J. Am. med. Ass. 195: 125-129 (1966).
99 Schroeder, H.A.; Kraemer, L.A.: Cardiovascular mortality, municipal water and corrosion. Archs envir. Hlth 28:302-311 (1974).
100 Seelig, M.S.: Mg in the pathogenesis of disease. Early roots cardiovascular skeletal and renal abnormalities, p. 488 (Plenum Press, New York 1980).
101 Seelig, M.S.: Mg requirements in human nutrition. Magnesium-Bull. 3:suppl. lA, 26-47(1981).
102 Sharrett, A.R.: The role of chemical constituents of drinking water in diseases. Am. J. Epidemiol: 110: 401-418 (1979).
103 Simpson, D.J.: Mg supplementation in drinking water. Vet. Rec. 71: 174 (1971).
104 Singh, N.P.; Thind, I.S.; Vitale, L.F.; Pawlow, M.: Intake of magnesium and toxicity of lead: an experimental model. Archs envir; Hlth 34: 168-173 (1979).
105 Skrabal, J.; Hörtnagl, H.; Auböck, J.A.: The role of the sodium pump in the control of vascular tone on the rat. Lancet I: 463-470 (1980).
106 Speich, M.; Bousquet, B.; Nicolas, G.: Intéret physio pathologique de l'étude des rapports Mg/Ca et K/Na dans les ventricules cardiaques de sujets témoins et de malades décédes après un infarctus du myocarde. Revue fr. Endocr. clin. 20: 545-549 (1979).
107 Speich, M.; Metayer, C.; Arnaud, P.; Nguyen, V.G.; Boitea, H.C.: Concentrations of Pb, Mg, Ca, Zn and Cd in 20 rabbit tissues after exposure to low lead doses and atherogenic diet. Ann. Nutr. Metab. 27: 531-541 (1983).
108 Thomas,J.; Gaultier. J.; Thomas, E.; Desgrez, P.: Sur la teneur en Mg des eaux de boisson. Revue fr. Endocr. clin. 19: 151-153 (1978).
108a Turlapaty, P.D.M.V.; Altura, B.M.: Magnesium deficiency produces spasms of coronary arteries: relationship to etiology of sudden death ischemic heart disease. Science 208: 198-200 (1980).
109 Van Barneveld, A.A.: Trace element absorption and retention in mice. The role of experimental conditions and the influence of Ca and Mg, p. 215 (Fotodruck J. Mainz, Aachen 1983).
110 Van Barneveld, A.A.; Van den Hamer, C.S.A.; Houtman, J.P.V.: Drinking water hardness, trace elements and cardiovascular diseases: influence of Ca and Mg on metabolism of Cd, Ca, Cu, Zn and Se in mice;in Hemphill Trace substances in environmental health, vol. 16, pp. 196-204 (1982).
111 Wanger, P.D.; Weswig, P.H.; Stoner, J.C.: Arsenic levels in Oregon waters. Environ. Hlth Perspect. 19: 139-143 (1977).
112 Wardener, H.E. de; MacGregor, G.A.: The role of a circulating inhibitor of Na+-K+ATPase in essential hypertension. Am. J. Nephrol. 3: 88-91(1983).
113 Wesenberg, G.B.M.: Effect of Cd. on Ca, Mg and P content of rat molars. Scand. J. dent. Res. 90: 95-101(1982).
114 Wong, C.S.; Berrang, P.: Contamination of tap water by lead pipe and solder. Bull. env. Contam. Toxicol. 15: 530-534 (1976).
115 Zaversnik, H.; Ozim, V; Ozim, V.: Magnesium in our drinking water. Zdrav. Vestn. 52: 179-182 (1983).
Received: July 16, 1984
Accepted: October 2, 1984
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