They really are counting the manganese weight, not the total weight counting the chelate, based on their also giving the percent Daily Value number (2500%.)
Yes, by all means stop it immediately.
Freeland-Graves, J.H., C.W. Bales and F. Behmardi. 1987. Manganese requirements of humans. In: Nutritional Bioavailability of Manganese, C. Kies, ed. American Chemical Society, Washington, DC. p. 90-104.
NRC (National Research Council). 1989. Recommended Dietary Allowances, 10th ed. Food and Nutrition Board, National Research Council, National Academy Press, Washington, DC. p. 230-235.
WHO (World Health Organization). 1973. Trace Elements in Human Nutrition: Manganese. Report of a WHO Expert Committee. Technical Report Service, 532, WHO, Geneva, Switzerland. p. 34-36.
Manganese is a ubiquitous element that is essential for normal physiologic functioning in all animal species. Several disease states in humans have been associated with both deficiencies and excess intakes of manganese. Thus any quantitative risk assessment for manganese must take into account aspects of both the essentiality and the toxicity of manganese. In humans, many data are available providing information about the range of essentiality for manganese… The reference dose is estimated to be an intake for the general population that is not associated with adverse health effects; this is not meant to imply that intakes above the reference dose are necessarily associated with toxicity. Some individuals may, in fact, consume a diet that contributes more than 10 mg Mn/day without any cause for concern.
The Food and Nutrition Board of the National Research Council (NRC, 1989) determined an “estimated safe and adequate daily dietary intake” (ESADDI) of manganese to be 2-5 mg/day for adults. The lower end of this range was based on a study by McLeod and Robinson (1972), who reported equilibrium or positive balances at intakes of 2.5 mg Mn/day or higher. The range of the ESADDI also includes an “extra margin of safety” from the level of 10 mg/day, which the NRC considered to be safe for an occasional intake.
While the NRC determined an ESADDI for manganese of 2-5 mg/day, some nutritionists feel that this level may be too low. Freeland-Graves et al. (1987) have suggested a range of 3.5-7 mg/day for adults based on a review of human studies. It is noted that dietary habits have evolved in recent years to include a larger proportion of meats and refined foods in conjunction with a lower intake of whole grains. The net result of such dietary changes includes a lower intake of manganese such that many individuals may have suboptimal manganese status.
The World Health Organization (WHO, 1973) reviewed several investigations of adult diets and reported the average daily consumption of manganese to range from 2.0-8.8 mg Mn/day. Higher manganese intakes are associated with diets high in whole-grain cereals, nuts, green leafy vegetables, and tea. From manganese balance studies, the WHO concluded that 2-3 mg/day is adequate for adults and 8-9 mg/day is “perfectly safe.”
Evaluations of standard diets from the United States, England, and Holland reveal average daily intakes of 2.3-8.8 mg Mn/day. Depending on individual diets, however, a normal intake may be well over 10 mg Mn/day, especially from a vegetarian diet. While the actual intake is higher, the bioavailability of manganese from a vegetarian diet is lower, thereby decreasing the actual absorbed dose. This is discussed in more detail in the Additional Studies / Comments Section.
From this information taken together, EPA concludes that an appropriate reference dose for manganese is 10 mg/day (0.14 mg/kg-day). In applying the reference dose for manganese to a risk assessment, it is important that the assessor consider the ubiquitous nature of manganese, specifically that most individuals will be consuming about 2-5 mg Mn/day in their diet. This is particularly important when one is using the reference dose to determine acceptable concentrations of manganese in water and soils.
There is one epidemiologic study of manganese in drinking water, performed by Kondakis et al. (1989). Three areas in northwest Greece were chosen for this study, with manganese concentrations in natural well water of 3.6-14.6 ug/L in area A, 81.6-252.6 ug/L in area B, and 1600-2300 ug/L in area C. The total population of the three areas studied ranged from 3200 to 4350 people… The individuals chosen were submitted to a neurologic examination, the score of which represents a composite of the presence and severity of 33 symptoms (e.g., weakness/fatigue, gait disturbances, tremors, dystonia)… The mean (x) and range (r) of neurologic scores were as follows: Area A (males: x=2.4, r=0-21; females: x=3.0, r=0-18; both x=2.7, r=0-21); Area B (males x=1.6, r=0-6; females: x=5.7 r=0-43; both: x=3.9, r=0-43); and Area C (males: x=4.9, r=0-29; females: x=5.5, r=0-21; both x=5.2, r=0-29). The authors indicate that the difference in mean scores for area C versus A was significantly increased (Mann-Whitney z=3.16, p=0.002 for both sexes combined). In a subsequent analysis, logistic regression indicated that there is a significant difference between areas A and C even when both age and sex are taken into account (Kondakis, 1990).
… This study, nevertheless, raises significant concerns about possible adverse neurological effects at doses not far from the range of essentially.
… Second, the study by Kondakis et al. (1989) raises some concern for possible adverse health effects associated with a lifetime consumption of drinking water containing about 2 mg/L of manganese.
… While an outright manganese deficiency has not been observed in the general human population, suboptimal manganese status may be more of a concern. As reviewed by Freeland-Graves and Llanes (1994), several disease states have been associated with low levels of serum manganese. These include epilepsy, exocrine pancreatic insufficiency, multiple sclerosis, cataracts, and osteoporosis. In addition, several inborn errors of metabolism have been associated with poor manganese status (e.g., phenylketonuria, maple syrup urine disease). While a correlation has been shown for low levels of serum manganese and these disease states, a causal relationship has not been demonstrated, and this remains an area in which additional research is needed.
… A report by Kawamura et al. (1941) is the only epidemiologic study describing toxicologic responses in humans consuming large amounts of manganese dissolved in drinking water. The manganese came from about 400 dry- cell batteries buried near a drinking water well, resulting in high levels of both manganese and zinc in the water. Twenty-five cases of manganese poisoning were reported, with symptoms including lethargy, increased muscle tonus, tremor and mental disturbances… The well water was not analyzed until 1 month after the outbreak, at which time it was found to contain approximately 14 mg Mn/L. When re-analyzed 1 month later, however, the levels were decreased by about half. Therefore, by retrospective extrapolation, the concentration of manganese at the time of exposure may have been as high as 28 mg Mn/L…
A few case studies have also pointed to the potential for manganese poisoning by routes other than inhalation. One involved a 59-year-old male who was admitted to the hospital with symptoms of classical manganese poisoning, including dementia and a generalized extrapyramidal syndrome (Banta and Markesbery, 1977). The patient’s serum, hair, urine, feces and brain were found to have manganese “elevated beyond toxic levels,” perhaps a result of his consumption of “large doses of vitamins and minerals for 4 to 5 years.” Unfortunately, no quantitative data were reported.
Another case study of manganese intoxication involved a 62-year-old male who had been receiving total parenteral nutrition that provided 2.2 mg of manganese (form not stated) daily for 23 months (Ejima et al., 1992). The patient’s whole blood manganese was found to be elevated, and he was diagnosed as having parkinsonism, with dysarthria, mild rigidity, hypokinesia with masked face, a halting gait and severely impaired postural reflexes. To be able to compare the manganese load in this individual with that corresponding to an oral intake, the difference between the direct intravenous exposure and the relatively low level of absorption of manganese from the GI tract must be taken into account. Assuming an average absorption of roughly 5% of an oral dose, the intravenous dose of 2.2 mg Mn/day would be approximately equivalent to an oral intake of 40 mg Mn/day.
… Although conclusive evidence is lacking, some investigators have also linked increased intakes of manganese with violent behavior. Gottschalk et al. (1991) found statistically significant elevated levels of manganese in the hair of convicted felons (1.62 +/- 0.173 ppm in prisoners compared with 0.35 +/- 0.020 ppm in controls). The authors suggest that “a combination of cofactors, such as the abuse of alcohol or other chemical substances, as well as psychosocial factors, acting in concert with mild manganese toxicity may promote violent behavior.” Caution should be exercised to prevent reading too much into these data, but support for this hypothesis is provided by studies of a population of Aborigines in Groote Eylandt. Several clinical symptoms consistent with manganese intoxication are present in about 1% of the inhabitants of this Australian island, and it may not be coincidental that the proportion of arrests in this native population is the highest in Australia (Cawte and Florence, 1989; Kilburn, 1987). The soil in this region is very high in manganese (40,000-50,000 ppm), and the fruits and vegetables grown in the region also are reported to be high in manganese. Quantitative data on oral intakes have not been reported, but elevated concentrations of manganese have been determined in the blood and hair of the Aborigines (Stauber et al., 1987). In addition to the high levels of environmental manganese, other factors common to this population may further increase the propensity for manganism: high alcohol intake, anemia, and a diet deficient in zinc and several vitamins (Florence and Stauber, 1989).
… Another issue of great importance to consider in the risk assessment for manganese concerns the bioavailability of different forms of manganese consumed under different exposure conditions. Various dietary factors as well as the form of manganese can have a significant bearing on the dose absorbed from the GI tract. Many constituents of a vegetarian diet (e.g., tannins, oxalates, phytates, fiber) have been found to inhibit manganese absorption presumably by forming insoluble complexes in the gut.
So this company is not only providing a dose which is 5 times the amount generally considered safe in the US, and an even greater multiple relative to the EU, but is doing it in a chelate form for, perhaps, greater absorption than usual! Yes, I would stop, indeed. It will clear out in reasonable time after doing so.