Rev/1: Revisions indicated with a vertical line in the left margin. 

WHO/SDE/WSH/03.04/104/Rev/1 

 

Manganese in Drinking-water 

Background document for development of 

WHO Guidelines for Drinking-water Quality
Manganese in Drinking-water 

Background document for development of WHO Guidelines for Drinking-water 

Quality

© World Health Organization 2011 

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imply that they are endorsed or recommended by the World Health Organization in 

preference to others of a similar nature that are not mentioned. Errors and omissions 

excepted, the names of proprietary products are distinguished by initial capital letters. 

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responsibility for the interpretation and use of the material lies with the reader. In no 

event shall the World Health Organization be liable for damages arising from its use. 

The named authors alone are responsible for the views expressed in this publication. 
Preface 

One of the primary goals of the World Health Organization (WHO) and its Member 

States is that “all people, whatever their stage of development and their social and 

economic conditions, have the right to have access to an adequate supply of safe 

drinking water.” A major WHO function to achieve such goals is the responsibility 

“to propose ... regulations, and to make recommendations with respect to international 

health matters ....” 

The first WHO document dealing specifically with public drinking-water quality was 

published in 1958 as International Standards for Drinking-water. It was subsequently 

revised in 1963 and in 1971 under the same title. In 1984–1985, the first edition of the 

WHO Guidelines for Drinking-water Quality (GDWQ) was published in three 

volumes: Volume 1, Recommendations; Volume 2, Health criteria and other 

supporting information; and Volume 3, Surveillance and control of community 

supplies. Second editions of these volumes were published in 1993, 1996 and 1997, 

respectively. Addenda to Volumes 1 and 2 of the second edition were published in 

1998, addressing selected chemicals. An addendum on microbiological aspects 

reviewing selected microorganisms was published in 2002. The third edition of the 

GDWQ was published in 2004, the first addendum to the third edition was published 

in 2006 and the second addendum to the third edition was published in 2008. The 

fourth edition will be published in 2011. 

The GDWQ are subject to a rolling revision process. Through this process, microbial, 

chemical and radiological aspects of drinking-water are subject to periodic review, 

and documentation related to aspects of protection and control of public drinkingwater quality is accordingly prepared and updated. 

Since the first edition of the GDWQ, WHO has published information on health 

criteria and other supporting information to the GDWQ, describing the approaches 

used in deriving guideline values and presenting critical reviews and evaluations of 

the effects on human health of the substances or contaminants of potential health 

concern in drinking-water. In the first and second editions, these constituted Volume 2 

of the GDWQ. Since publication of the third edition, they comprise a series of freestanding monographs, including this one. 

For each chemical contaminant or substance considered, a lead institution prepared a 

background document evaluating the risks for human health from exposure to the 

particular chemical in drinking-water. Institutions from Canada, Japan, the United 

Kingdom and the United States of America (USA) prepared the documents for the 

fourth edition. 

Under the oversight of a group of coordinators, each of whom was responsible for a 

group of chemicals considered in the GDWQ, the draft health criteria documents were 

submitted to a number of scientific institutions and selected experts for peer review. 

Comments were taken into consideration by the coordinators and authors. The draft 

documents were also released to the public domain for comment and submitted for 

final evaluation by expert meetings. 
During the preparation of background documents and at expert meetings, careful 

consideration was given to information available in previous risk assessments carried 

out by the International Programme on Chemical Safety, in its Environmental Health 

Criteria monographs and Concise International Chemical Assessment Documents, the 

International Agency for Research on Cancer, the Joint FAO/WHO Meetings on 

Pesticide Residues and the Joint FAO/WHO Expert Committee on Food Additives 

(which evaluates contaminants such as lead, cadmium, nitrate and nitrite, in addition 

to food additives). 

Further up-to-date information on the GDWQ and the process of their development is 

available on the WHO Internet site and in the current edition of the GDWQ. 
Acknowledgements 

The current version of Manganese in Drinking-water, Background document for 

development of WHO Guidelines for Drinking-water Quality, is a revision of the 

background document prepared for an earlier edition of the Guidelines by Dr J. Du, 

United States Environmental Protection Agency. 

The work of the following working group coordinators was crucial in the 

development of this document and others contributing to the fourth edition: 

Dr J. Cotruvo, J. Cotruvo & Associates, USA (Materials and chemicals) 

Mr J.K. Fawell, United Kingdom (Naturally occurring and industrial 

contaminants and Pesticides) 

Ms M. Giddings, Health Canada (Disinfectants and disinfection by-products) 

Mr P. Jackson, WRc-NSF, United Kingdom (Chemicals – practical aspects) 

Professor Y. Magara, Hokkaido University, Japan (Analytical achievability) 

Dr A.V. Festo Ngowi, Muhimbili University of Health and Allied Sciences, 

United Republic of Tanzania (Pesticides) 

Dr E. Ohanian, Environmental Protection Agency, USA (Disinfectants and 

disinfection by-products) 

The draft text was discussed at the Expert Consultation for the fourth edition of the 

GDWQ, held in December 2011. The final version of the document takes into 

consideration comments from both peer reviewers and the public. The input of those 

who provided comments and of participants at the meeting is gratefully 

acknowledged.

The WHO coordinators were Mr R. Bos and Mr B. Gordon, WHO Headquarters. Ms 

C. Vickers provided a liaison with the International Programme on Chemical Safety, 

WHO Headquarters. Mr M. Zaim, Public Health and the Environment Programme, 

WHO Headquarters, provided input on pesticides added to drinking-water for public 

health purposes. 

Ms P. Ward provided invaluable administrative support at the Expert Consultation 

and throughout the review and publication process. Ms M. Sheffer of Ottawa, Canada, 

was responsible for the scientific editing of the document. 

Many individuals from various countries contributed to the development of the 

GDWQ. The efforts of all who contributed to the preparation of this document and in 

particular those who provided peer or public domain review comments are greatly 

appreciated. 
Acronyms and abbreviations used in the text 

IOM Institute of Medicine (USA) 

LD50 median lethal dose 

MMT methylcyclopentadienyl manganese tricarbonyl 

NOAEL no-observed-adverse-effect level 

TDI tolerable daily intake 

USA United States of America 
Table of contents 

1. GENERAL DESCRIPTION......................................................................................1 

1.1 Identity .................................................................................................................1 

1.2 Physicochemical properties .................................................................................1 

1.3 Organoleptic properties........................................................................................1 

1.4 Major uses............................................................................................................2 

1.5 Environmental fate...............................................................................................2 

2. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE..................................2 

2.1 Air ........................................................................................................................2 

2.2 Water....................................................................................................................3 

2.3 Food .....................................................................................................................4 

2.4 Estimated total exposure and relative contribution of drinking-water.................6 

3. KINETICS AND METABOLISM IN LABORATORY ANIMALS AND 

HUMANS ......................................................................................................................6 

4. EFFECTS ON LABORATORY ANIMALS AND IN VITRO TEST SYSTEMS...8 

4.1 Acute exposure.....................................................................................................8 

4.2 Short-term exposure.............................................................................................8 

4.3 Long-term exposure.............................................................................................9 

4.4 Reproductive and developmental toxicity ...........................................................9 

4.5 Mutagenicity and related end-points..................................................................10 

4.6 Carcinogenicity..................................................................................................10 

5. EFFECTS ON HUMANS........................................................................................11 

6. PRACTICAL CONSIDERATIONS........................................................................14 

6.1 Analytical methods ............................................................................................14 

6.2 Treatment methods and performance.................................................................14 

7. CONCLUSION........................................................................................................14 

8. REFERENCES ........................................................................................................15 

1 

1. GENERAL DESCRIPTION 

1.1 Identity 

Compound Chemical Abstracts Service No. Molecular formula

Manganese 7439-96-5 Mn 

Manganese(II) chloride 7773-01-5 MnCl2

Manganese(II, III) oxide 1317-35-7 Mn3O4

Manganese dioxide 1313-13-9 MnO2

Potassium permanganate 7722-64-7 KMnO4

Manganese sulfate 7785-87-7 MnSO4

Source: ATSDR (2000). 

Manganese is one of the most abundant metals in Earth’s crust, usually occurring with 

iron. It is a component of over 100 minerals but is not found naturally in its pure 

(elemental) form (ATSDR, 2000). Manganese is an element essential to the proper 

functioning of both humans and animals, as it is required for the functioning of many 

cellular enzymes (e.g. manganese superoxide dismutase, pyruvate carboxylase) and 

can serve to activate many others (e.g. kinases, decarboxylases, transferases, 

hydrolases) (IPCS, 2002). Manganese can exist in 11 oxidative states; the most 

environmentally and biologically important manganese compounds are those that 

contain Mn2+, Mn4+ or Mn7+ (USEPA, 1994). 

1.2 Physicochemical properties

The physical and chemical properties of different manganese compounds vary 

substantially. These characteristics in turn determine the environmental behaviour and 

fate, exposure potential and subsequent toxicological potential of each compound. 

Property Mn MnCl2 Mn3O4 MnO2 KMnO4 MnSO4

Melting point 

(°C) 

1244 650 1564 Loses 

oxygen at 

535 °C 

Decomposes 

at <240 °C 

700 

Boiling point 

(°C) 

1962 1190 No data No data No data Decomposes 

at 850 °C 

Density 

(g/cm3) 

7.21–

7.44 

2.98 4.86 5.03 2.70 3.25 

Water 

solubility (g/l) 

Decomposes 723 

(25 °C) 

Insoluble Insoluble 63.8 (20 °C) 520 (5 °C) 

700 (70 °C) 

Source: ATSDR (2000) 

1.3 Organoleptic properties 

At concentrations exceeding 0.1 mg/l, the manganese ion imparts an undesirable taste 

to beverages and stains plumbing fixtures and laundry (Griffin, 1960). When 

manganese(II) compounds in solution undergo oxidation, manganese is precipitated, 
MANGANESE IN DRINKING-WATER 

2 

resulting in encrustation problems. At concentrations as low as 0.02 mg/l, manganese 

can form coatings on water pipes that may later slough off as a black precipitate 

(Bean, 1974). A number of countries have set standards for manganese of 0.05 mg/l, 

above which problems with discoloration may occur. 

1.4 Major uses 

Manganese is used principally in the manufacture of iron and steel alloys and 

manganese compounds and as an ingredient in various products (IPCS, 1999; 

ATSDR, 2000). Manganese dioxide and other manganese compounds are used in 

products such as batteries, glass and fireworks. Potassium permanganate is used as an 

oxidant for cleaning, bleaching and disinfection purposes (ATSDR, 2000; HSDB, 

2001). Manganese greensands are used in some locations for potable water treatment 

(ATSDR, 2000). An organic manganese compound, methylcyclopentadienyl 

manganese tricarbonyl (MMT), is used as an octane-enhancing agent in unleaded 

petrol in Canada, the United States of America (USA), Europe, Asia and South 

America (Lynam et al., 1999). Other manganese compounds are used in fertilizers, 

varnish and fungicides and as livestock feeding supplements (HSDB, 2001). 

1.5 Environmental fate 

Manganese compounds may be present in the atmosphere as suspended particulates 

resulting from industrial emissions, soil erosion, volcanic emissions and the burning 

of MMT-containing petrol (IPCS, 1999). In surface waters, manganese occurs in both 

dissolved and suspended forms, depending on such factors as pH, anions present and 

oxidation–reduction potential (ATSDR, 2000). Anaerobic groundwater often contains 

elevated levels of dissolved manganese. The divalent form (Mn2+) predominates in 

most water at pH 4–7, but more highly oxidized forms may occur at higher pH values 

or result from microbial oxidation (ATSDR, 2000). Manganese can be adsorbed onto 

soil, the extent of adsorption depending on the organic content and cation exchange 

capacity of the soil. It can bioaccumulate in lower organisms (e.g. phytoplankton, 

algae, molluscs and some fish) but not in higher organisms; biomagnification in foodchains is not expected to be very significant (ATSDR, 2000). 

2. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE 

2.1 Air 

Levels of manganese compounds in air vary widely depending on the proximity of 

point sources, such as ferroalloy production facilities, coke ovens and power plants. 

Average manganese levels in ambient air near industrial sources have been reported 

to range from 220 to 300 ng/m3, whereas manganese levels in urban and rural areas 

without point sources have been reported to range from 10 to 70 ng/m3 (Barceloux, 

1999). Existing data indicate that little difference is found between manganese levels 

in ambient air in areas where MMT is used in the petrol and air levels in areas where 

MMT is not used (Lynam et al., 1999). The United States Environmental Protection 

Agency (USEPA, 1990) estimated the average annual background concentration of 
MANGANESE IN DRINKING-WATER 

3 

manganese in urban areas to be 40 ng/m3

, based on measurements in 102 cities in the 

USA. 

2.2 Water 

Manganese occurs naturally in many surface water and groundwater sources and in 

soils that may erode into these waters. However, human activities are also responsible 

for much of the manganese contamination in water in some areas. 

A survey of snow samples near an urban expressway in Montreal, Canada (where 

MMT is used in petrol), was unable to establish an association between automobile 

emissions and manganese concentrations in the snow (Loranger et al., 1996). 

Loranger et al. (1994) found ambient manganese concentrations to be significantly 

correlated with traffic density. Areas of intermediate and high traffic densities in 

Montreal had ambient manganese concentrations above the natural background level 

of 40 ng/m3 (Loranger & Zayed, 1994; Loranger et al., 1994). 

Ambient manganese concentrations in seawater have been reported to range from 0.4 

to 10 μg/l (ATSDR, 2000), with an average of about 2 μg/l (Barceloux, 1999). Levels 

in fresh water typically range from 1 to 200 μg/l (Barceloux, 1999). ATSDR (2000) 

reported that a river water survey in the USA found dissolved manganese levels 

ranging from <11 to >51 μg/l. The United States Geological Survey’s National Water 

Quality Assessment Program has gathered limited data since 1991 on representative 

study basins around the USA. These data indicate a median manganese level of 16 

μg/l in surface waters, with 99th-percentile concentrations of 400–800 μg/l (Leahy & 

Thompson, 1994; USGS, 2001). Higher levels in aerobic waters are usually 

associated with industrial pollution. 

The reducing conditions found in groundwater and some lakes and reservoirs favour 

high manganese levels; concentrations up to 1300 μg/l in neutral groundwater and 

9600 μg/l in acidic groundwater have been reported (ATSDR, 2000). The National 

Water Quality Assessment Program data indicate that the 99th-percentile level of 

manganese in groundwater (5600 μg/l) is generally higher than that in surface waters, 

but the median level in groundwater (5 μg/l) is lower than that in surface water 

(USGS, 2001). 

Overall, the detection frequency of manganese in groundwater in the USA is high 

(approximately 70% of sites) due to the ubiquity of manganese in soil and rock, but 

the levels detected in groundwater are generally below levels of public health concern 

(USEPA, 2002). Similarly, manganese is detected in about 97% of surface water sites 

(at levels far below those likely to cause health effects) and universally in sediments 

and tissues of aquatic biota (at levels that suggest that manganese does not 

bioaccumulate) (USEPA, 2002). 

In the USA, the National Inorganic and Radionuclide Survey collected data from 989 

community public water systems served by groundwater in 49 states between 1984 

and 1986 and found that manganese was detected in 68% of the groundwater systems, 
MANGANESE IN DRINKING-WATER 

4 

with a median concentration of 10 μg/l. Supplemental survey data from public water 

systems supplied by surface water in five states reported occurrence ranges similar to 

those of groundwater. In Germany, the drinking-water supplied to 90% of all 

households contained less than 20 μg of manganese per litre (Bundesgesundheitsamt, 

1991). 

2.3 Food 

Manganese occurs naturally in many food sources, such as leafy vegetables, nuts, 

grains and animal products (IOM, 2002). Food is the most important source of 

manganese exposure in the general population (ATSDR, 2000; USEPA, 2002). 

Typical ranges of manganese concentrations in common foods are shown below: 

Type of food Range of mean concentrations (mg/kg) 

Nuts and nut products 18.21–46.83 

Grains and grain products 0.42–40.70 

Legumes 2.24–6.73 

Fruits 0.20–10.38 

Fruit juices and drinks 0.05–11.47 

Vegetables and vegetable products 0.42–6.64 

Desserts 0.04–7.98 

Infant foods 0.17–4.83 

Meat, poultry, fish and eggs 0.10–3.99 

Mixed dishes 0.69–2.98 

Condiments, fats and sweeteners 0.04–1.45 

Beverages (including tea) 0.00–2.09 

Soups 0.19–0.65 

Milk and milk products 0.02–0.49 

Source: ATSDR (2000). 

Heavy tea drinkers may have a higher manganese intake than the general population. 

An average cup of tea may contain 0.4–1.3 mg of manganese (ATSDR, 2000). In 

addition to dietary sources, approximately 12% of the adult population of the USA 

consumed manganese supplements in 1986 (Moss et al., 1989). The median intake of 

manganese in these dietary supplements was determined to be 2.4 mg/day, similar to 

the amount of the element consumed in the diet (based on information from the Third 

National Health and Nutrition Estimation Survey, held in 2001). 

The hazard posed by overexposure to manganese must be weighed against the 

necessity for some minimum amount of manganese in the diet, because manganese is 

an essential nutrient, acting as a component of several enzymes and a participant in a 

number of important physiological processes. Freeland-Graves et al. (1987) suggested 

a range of 3.5–7 mg/day for adults based on a review of human studies. After 
MANGANESE IN DRINKING-WATER 

5 

reviewing dietary surveys, Greger (1999) presented a range for average intakes from 

adult Western and vegetarian diets of 0.7–10.9 mg of manganese per day. 

Infant formulas contain 50–300 μg of manganese per litre (Collipp et al., 1983), 

whereas human milk contains approximately 3.5–15 μg/l (USEPA, 1997; ATSDR, 

2000). Assuming an intake of 742 ml of breast milk per day (USEPA, 1996), a 

breastfed infant would have an estimated daily manganese intake of 2.6–11.1 μg. An 

infant consuming the same volume of infant formula would have an estimated daily 

manganese intake of 37.1–223 μg. Assuming an average weight of 6 kg for an infant 

aged 6 months, the weight-adjusted average daily intake would range from 0.4 to 1.9 

μg/kg of body weight per day for breastfed infants. The corresponding weightadjusted intake for a formula-fed infant would be 6.2–37.2 μg/kg of body weight per 

day. Regarding the high manganese content of milk-based formula, the 

underexposure of infants to manganese appears less probable than their overexposure 

(Keen et al., 1986; Dörner et al., 1987; Davidsson et al., 1989a). Once solid foods are 

introduced, however, the contribution of manganese intake from milk becomes less 

significant. 

In addition to manganese concentrations in food, an important consideration for 

determining human exposure to manganese in food is bioavailability. Several factors 

can influence the degree to which manganese in foods is absorbed upon ingestion. 

These include intake of dietary fibre, oxalic acids, tannins and phytic acids, which 

tend to decrease manganese absorption (Gibson, 1994; USEPA, 2002), as well as 

possibly sex-specific iron status (low iron can result in increased manganese 

absorption; Finley, 1999). 

 

The Food and Nutrition Board of the Institute of Medicine (IOM, 2002) set adequate 

intake levels for manganese at 2.3 mg/day for men and 1.8 mg/day for women. 

Adequate intake levels for manganese were also set for other age groups; the values 

were 0.003 mg/day for infants from birth to 6 months, 0.6 mg/day for infants from 7 

months to 1 year, 1.2 mg/day for children aged 1–3 years, 1.5–1.9 mg/day for 

children aged 4–13 years and 1.6–2.3 mg/day for adolescents and adults (IOM, 2002). 

The adequate intake for infants (newborn to 6 months) was set based on an average 

manganese concentration of 0.0035 mg/l in human milk and an average milk 

consumption of 0.78 litres/day. The manganese concentration in human milk varies. 

For example, manganese concentrations in human milk have been found to range 

from 0.003 to 0.01 mg/l (ATSDR, 2000) and from 0.007 to 0.015 mg/l (USEPA, 

1997). Assuming an intake of 0.78 litres of milk per day and concentrations in human 

milk ranging from 0.003 to 0.015 mg/l, an infant (0–6 months) would ingest 0.002–

0.012 mg of manganese per day from human milk, the upper limit of which is higher 

than the adequate intake set by IOM (2002) (i.e. 0.003 mg/day). 

The IOM also set a tolerable upper intake level at 11 mg/day for adults, based on a 

recent review (Greger, 1999; IOM, 2002) that stated that the average manganese 

intake for adults eating typical Western and vegetarian diets in various surveys ranged 

from 0.7 to 10.9 mg of manganese per day. Davis & Greger (1992) reported that 

women given daily supplements of 15 mg of manganese (as an amino acid–chelated 
MANGANESE IN DRINKING-WATER 

6 

manganese supplement) for 90 days experienced no adverse effects other than a 

significant increase in lymphocyte manganese-dependent superoxide dismutase, a 

biomarker that increases in direct relation to manganese exposure (Greger, 1998, 

1999). 

WHO (1973) reviewed several investigations of adult diets and reported that the 

average daily consumption of manganese ranged from 2.0 to 8.8 mg/day. Higher 

manganese intakes were associated with diets high in whole-grain cereals, nuts, green 

leafy vegetables and tea. From manganese balance studies, WHO (1973) concluded 

that 2–3 mg of manganese per day is adequate for adults and 8–9 mg/day is “perfectly 

safe.” 

Evaluations of standard diets from the USA, the United Kingdom and the Netherlands 

reveal average daily intakes of 2.3–8.8 mg of manganese per day. Depending on 

individual diets, however, a normal intake may be well over 10 mg of manganese per 

day (Schroeder et al., 1966), especially for vegetarian diets. 

2.4 Estimated total exposure and relative contribution of drinking-water 

The greatest exposure to manganese is usually from food. Adults consume between 

0.7 and 10.9 mg/day in the diet (Greger, 1999), with even higher intakes reportedly 

being associated with some vegetarian diets (Schroeder et al., 1966; Freeland-Graves 

et al., 1987). 

Manganese intake from drinking-water is normally substantially lower than intake 

from food. At the median drinking-water level of 10 μg/l determined in the National 

Inorganic and Radionuclide Survey described above, the intake of manganese would 

be 20 μg/day for an adult, assuming a daily water intake of 2 litres. Drinking mineral 

water regularly can add significantly to manganese intake (Dieter et al., 1992). 

Exposure to manganese from air is generally several orders of magnitude less than 

that from the diet, typically around 0.04 ng/day on average (USEPA, 1990), although 

this can vary substantially depending on proximity to a manganese source. 

3. KINETICS AND METABOLISM IN LABORATORY ANIMALS AND 

HUMANS

Absorption of manganese across the gastrointestinal tract is regulated by normal 

physiological processes to help maintain manganese homeostasis. A 7-week study in 

which seven adult male volunteers ingested high-fibre diets containing 12.0–17.7 mg 

of manganese per day (0.17–0.25 mg/kg of body weight per day) found that an 

average of 7.7% ± 6.3% of the manganese was absorbed during weeks 5–7, with no 

measurable net retention of manganese (Schwartz et al., 1986). Similarly, an average 

absorption of 8.4% ± 4.7% was observed in seven adults ingesting infant formula 

containing manganese (Sandström et al., 1986). Johnson et al. (1991) studied the 

absorption of radiolabelled manganese from various plant foods in adult men and 

women and reported that the absorption ranged from 1.4% to 5.5% and was 

significantly lower than the mean values of 7.8–10.2% from controls (manganese(II) 
MANGANESE IN DRINKING-WATER 

7 

chloride dissolved in water). Manganese absorption may be higher in young animals 

and infants (Keen et al., 1986). 

As mentioned above, several factors can influence the degree to which manganese in 

foods is absorbed upon ingestion. These include intake of dietary fibre, oxalic acids 

and phytic acids, which tend to decrease manganese absorption (Gibson, 1994; 

USEPA, 2002). The absorption of manganese is also closely linked to iron 

absorption; iron-deficient diets lead to an increased absorption of both iron and 

manganese (Thomson et al., 1971; Sandström et al., 1986; Finley, 1999). Absorption 

is also related inversely to the level of calcium in the diet (Schroeder et al., 1966; 

McDermott & Kies, 1987; Lutz et al., 1993). Certain constituents of tea, such as 

tannins, can result in reduced manganese absorption (Freeland-Graves & Llanes, 

1994).

Some constituents of both infant formula and breast milk may also affect manganese 

bioavailability. Formula made from soy protein contains high levels of phytic acids 

and vegetable proteins, which probably decrease manganese bioavailability. Data 

from Keen et al. (1986) indicate that overall uptake of manganese from soy formula 

in rat pups was much greater than that from human milk or cow’s milk, even though 

fractional manganese absorption was lowest in the soy formula, because formula 

contains much more manganese than human milk does. If the formula is also ironfortified, manganese bioavailability may be further decreased, although studies on the 

inhibitory influences of iron have produced conflicting results (Freeland-Graves, 

1994). Davidsson et al. (1989a) reported that the fractional absorption of manganese 

in adult humans given human milk (8.2%) was significantly higher than absorption 

from cow’s milk (2.4%) and soy formula (0.7%). Manganese in infant formula is in 

the divalent state (Mn2+), the absorption of which cannot be regulated by the 

lactoferrin receptors in the gut; breast milk manganese is in the trivalent form bound 

to lactoferrin, and its absorption is thus regulated (USEPA, 1997). Davidsson et al. 

(1989a) suggested that the lactoferrin in human milk as well as the higher calcium 

content in cow’s milk contributed to the difference in absorption. Therefore, many 

factors probably control manganese absorption from infant formula, and firm 

conclusions are difficult to make in the absence of further data. 

It should be noted that Davidsson et al. (1989a) performed their studies in adults; 

manganese body burden in infants may be influenced by the fact that the biliary 

excretion system, which is the primary route of manganese excretion, is not 

completely developed in human infants (Lönnerdal, 1994). Dörner et al. (1989) 

reported high retention of manganese in infants ingesting both human milk and cow’s 

milk formulas. Studies in rats have demonstrated that young animals absorb 

significantly more manganese in the gut than do mature animals (Lönnerdal et al., 

1987). Also, experimental animal studies have shown that manganese crosses the 

blood–brain barrier in neonates at a rate 4 times higher than that in adults (Mena, 

1974). The relevance of these studies to humans is unknown, however, and few direct 

absorption data for manganese in human infants are available. Evidence exists, 

however, to indicate that infants are less well protected than adults against manganese 

overload. The manganese contents of erythrocytes in infants up to the age of 6 weeks 
MANGANESE IN DRINKING-WATER 

8 

are higher by about 7–9% than those in adults (Hatano et al., 1985). Collipp et al. 

(1983) reported manganese levels in hair that increased significantly from birth (0.19 

μg/g) to 6 weeks (0.865 μg/g) and 4 months (0.685 μg/g) of age in infants given 

formula, whereas infants given breast milk exhibited no significant increase (0.330 

μg/g at 4 months). This study also reported that the average manganese level in hair 

in children exhibiting learning disabilities was significantly increased (0.434 μg/g) 

compared with that in children who exhibited normal learning ability (0.268 μg/g). It 

should be noted that the Collipp et al. (1983) study did not indicate that the increased 

manganese level in hair was from ingested manganese. 

Manganese is present in all tissues of the body, the highest levels usually being found 

in the liver, kidney, pancreas and adrenals (Tipton & Cook, 1963; Sumino et al., 

1975). It accumulates preferentially in certain regions of the brain in infants and 

young animals (Zlotkin & Buchanan, 1986; Kontur & Fechter, 1988). 

Manganese is almost entirely excreted in the faeces, only a small proportion (0.1–2%) 

being eliminated in the urine (Davis & Greger, 1992). Faecal manganese is composed 

of unabsorbed dietary manganese plus manganese excreted in bile. In humans, 

elimination is biphasic, with half-lives of 13 and 37 days (Sandström et al., 1986; 

Davidsson et al., 1989b). Sweat, hair and the milk of lactating mothers also contribute 

to excretion (Roels et al., 1992). 

Possible indicators of manganese exposure are the blood, with background levels 

ranging from 6.7 to 7.6 μg/ml (Roels et al., 1992; Mergler et al., 1994; Loranger & 

Zayed, 1995), and perhaps the hair (Fergusson et al., 1983; Chutsch & Krause, 1987). 

Manganese levels in blood do not provide data on long-term exposure. However, the 

blood platelet monoamine oxidase should be taken into consideration as an early 

biochemical indicator for adverse oxidative effects of manganese (Benedetti & 

Dostert, 1989; Humfrey et al., 1990). 

4. EFFECTS ON LABORATORY ANIMALS AND IN VITRO TEST SYSTEMS

4.1 Acute exposure 

ATSDR (2000) noted that the acute lethality of manganese in animals appears to vary 

depending on the chemical species and whether exposure is via gavage or dietary 

ingestion. Single-dose oral median lethal dose (LD50) values in adult rats exposed by 

gavage ranged from 331 mg of manganese per kilogram of body weight per day (as 

manganese chloride) (Kostial et al., 1989) to 1082 mg of manganese per kilogram of 

body weight per day (as manganese acetate) (Smyth et al., 1969), whereas 14-day 

exposure of rats to 1300 mg of manganese per kilogram of body weight per day (as 

manganese sulfate) in feed resulted in no deaths (NTP, 1993). 

4.2 Short-term exposure 

The central nervous system is the chief target of manganese toxicity. Oral doses 

ranging from 1 to 150 mg/kg of body weight per day produced a number of 
MANGANESE IN DRINKING-WATER 

9 

neurological effects in rats and mice, mainly involving alterations in neurotransmitter 

and enzyme levels in the brain. These changes were sometimes accompanied by 

clinical signs, such as incoordination and changes in activity level (ATSDR, 2000). 

Deskin et al. (1980) reported an increase in monoamine oxidase activity in the 

hypothalamus in rats intubated with a daily dose of 20 mg of manganese per kilogram 

of body weight per day from birth to 24 days of age. Gastric irritation in the form of 

patchy necrosis of the epithelium was observed in guinea-pigs administered 10 mg of 

manganese per kilogram of body weight per day via gavage for 30 days (Chandra & 

Imam, 1973); the method of administration might have contributed to the observed 

effects, however. Male mice fed high doses of manganese in food for 13 weeks 

exhibited mild hyperplasia and hyperkeratosis of the forestomach; no effects were 

seen in female mice or male and female rats (NTP, 1993). 

4.3 Long-term exposure 

Chronic ingestion of 1–2 mg of manganese per kilogram of body weight per day 

produced changes in appetite and reduction in haemoglobin synthesis in rabbits, pigs 

and cattle (Hurley & Keen, 1987). Transient effects on biogenic amine levels and 

activities of dopamine β-hydroxylase and monoamine oxidase in rat brain have been 

noted with long-term exposures to manganese (Lai et al., 1984; Eriksson et al., 1987; 

Subhash & Padmashree, 1990). An increase in physical activity level and a transient 

increase in dopaminergic function were observed in rats given 40 mg of manganese 

per kilogram of body weight per day for 65 weeks (Nachtman et al., 1986). Two-year 

oral exposures to extremely high doses (1800–2250 mg/kg of body weight per day as 

manganese(II) sulfate) in male and female mice resulted in hyperplasia, erosion and 

inflammation of the forestomach; no effects were seen in rats (NTP, 1993). 

Neurotoxicity is a known effect of long-term exposure to inhaled manganese in 

humans and animals, but the potential for neurotoxicity resulting from oral exposure 

is less well characterized. Muscular weakness and lower limb rigidity were observed 

in four male rhesus monkeys given oral doses of 6.9 mg of manganese per kilogram 

of body weight per day (as manganese chloride) for 18 months (Gupta et al., 1980). 

Degenerated neurons in the substantia nigra were observed at autopsy. 

4.4 Reproductive and developmental toxicity 

The results of several studies in rats and mice indicate that the ingestion of 

manganese can delay reproductive maturation in male animals (ATSDR, 2000). 

Testosterone levels were reduced in male rats given an oral dose of 13 mg of 

manganese per kilogram of body weight per day for 100–224 days (Laskey et al., 

1982), whereas delayed growth of the testes was observed in young rats ingesting 140 

mg of manganese per kilogram of body weight per day for 90 days (Gray & Laskey, 

1980). These effects do not appear to be severe enough to affect male reproductive 

function (ATSDR, 2000). Several studies that found effects on male reproductive 

organs, however, did not assess reproductive performance (IPCS, 1999). 
MANGANESE IN DRINKING-WATER 

10 

The results of most studies indicate that oral exposure to manganese does not result in 

reproductive toxicity in the female rodent (e.g. rats and mice) and rabbit (ATSDR, 

2000), although increased post-implantation loss was observed in female rats in at 

least one study (Szakmáry et al., 1995). Results from several developmental studies in 

rodents and rabbits are equivocal. Data from the majority of these studies indicate that 

manganese exposure during part or all of gestation results in increased manganese 

levels in the pups (Järvinen & Ahlström, 1975; Kontur & Fechter, 1988) but generally 

causes 1) no measurable effect (Grant et al., 1997), 2) transient effects such as weight 

decreases and hyperactivity (Pappas et al., 1997) or 3) self-correcting effects on 

skeletal and organ development (Szakmáry et al., 1995). Studies involving oral 

exposures to manganese in drinking-water or by gavage in neonatal pups have 

reported changes in brain neurochemistry but generally do not show effects on 

neurological development (ATSDR, 2000). The data from one recent study indicate 

that rodent pups administered 22 mg of manganese per kilogram of body weight per 

day in drinking-water from birth to weaning (21 days) resulted in changes in brain 

neurochemistry and evoked sensory response (Dorman et al., 2000). 

4.5 Mutagenicity and related end-points 

The genotoxic potential of manganese in humans is not known (IPCS, 1999). 

Laboratory evidence for the mutagenicity and genotoxicity of manganese is 

equivocal. In vitro bacterial gene mutation tests have yielded both positive and 

negative results, whereas in vitro tests with fungi and mammalian cells have been 

predominantly positive. In vivo rat studies have been negative, and in vivo mouse 

studies have been positive (ATSDR, 2000). Manganese chloride produced an 

increased frequency of mutations in Salmonella typhimurium strain TA1537, but 

negative results in other strains; manganese sulfate was reported to be both positive 

and negative in separate studies in Salmonella strain TA97, but negative in other 

strains (IPCS, 1999). Positive results were obtained with various manganese 

compounds in Photobacterium fischeri and Escherichia coli, as well as in 

Saccharomyces cerevisiae, mouse lymphoma cells and hamster embryo cells 

(ATSDR, 2000). Manganese sulfate and potassium permanganate have been shown to 

increase sperm head abnormalities in vivo and increased the number of chromosomal 

aberrations and micronuclei in rat bone marrow (ATSDR, 2000). In spite of these 

results, the genotoxic potential of manganese in humans is not known (IPCS, 1999). 

4.6 Carcinogenicity 

No studies are available on the potential carcinogenicity of manganese following 

inhalation or dermal exposure in humans or experimental animals (ATSDR, 2000). A 

2-year oral study of manganese sulfate in rats and mice produced equivocal evidence 

of carcinogenicity (NTP, 1993). In rats fed manganese sulfate (30–331 mg of 

manganese per kilogram of body weight per day in males, 26–270 mg of manganese 

per kilogram of body weight per day in females), no treatment-related increases in 

tumour incidence were reported. In mice fed manganese sulfate (63–722 mg of 

manganese per kilogram of body weight per day in males, 77–905 mg of manganese 

per kilogram of body weight per day in females), the incidence of follicular cell 
MANGANESE IN DRINKING-WATER 

11 

adenoma of the thyroid was increased slightly in high-dose animals compared with 

controls. These increases were not statistically significant, and the tumours were 

observed at the end of the study only. However, follicular cell adenoma of the thyroid 

appears with low frequency in historical control male mice of this strain. Thus, the 

significance of these results and their relevance to normal human exposure to 

manganese are questionable. 

5. EFFECTS ON HUMANS 

Manganese is an essential element for many living organisms, including humans. For 

example, some enzymes require manganese (e.g. manganese superoxide dismutase), 

and some are activated by the element (e.g. kinases, decarboxylases). Adverse health 

effects can be caused by inadequate intake or overexposure. Manganese deficiency in 

humans appears to be rare, because manganese is present in many common foods. 

Animals experimentally maintained on manganese-deficient diets exhibit impaired 

growth, skeletal abnormalities, reproductive deficits, ataxia of the newborn and 

defects in lipid and carbohydrate metabolism (USEPA, 1984; Hurley & Keen, 1987). 

The neurological effects of inhaled manganese have been well documented in humans 

chronically exposed to elevated levels in the workplace (Canavan et al., 1934; Cook 

et al., 1974; Roels et al., 1999; ATSDR, 2000). The syndrome known as 

“manganism” is caused by exposure to very high levels of manganese dusts or fumes 

and is characterized by a “Parkinson-like syndrome”, including weakness, anorexia, 

muscle pain, apathy, slow speech, monotonous tone of voice, emotionless “masklike” facial expression and slow, clumsy movement of the limbs. In general, these 

effects are irreversible. Some motor functions may already be affected following 

chronic exposure to levels of manganese of ≤1 mg/m3 (if the inhaled manganese is 

respirable), but individuals in these situations have not shown the overt, clinical 

symptoms of those exposed to much higher levels (Roels et al., 1992; Mergler et al., 

1994). 

From animal experiments, it is known that inhaled manganese (even the insoluble 

manganese dioxide) is transported in a retrograde direction from the olfactory 

epithelium to the striatum of the brain (Gianutsos et al., 1997; Roels et al., 1997). 

During its uptake through the olfactory nerve endings (Tjälve et al., 1996; Brenneman 

et al., 2000; Vitarella et al., 2000; Bench et al., 2001), it may damage the astrocytes 

(Henriksson & Tjälve, 2000). After peroral uptake, manganese, like all other metals, 

is filtered from the blood by the choroid plexus (Zheng et al., 1991; Ingersoll et al., 

1995). The retrograde transport of manganese through the olfactory epithelium 

directly into certain regions of the central nervous system or the brain could explain 

why the safe dose is much lower following inhalation exposure than after oral 

ingestion (Wang et al., 1989). 

By the oral route, manganese is often regarded as one of the least toxic elements, 

although there is some controversy as to whether the neurological effects observed 

with inhalation exposure also occur with oral exposure. Several case reports of oral 

exposure to high doses of manganese have described neurological impairment as an 
MANGANESE IN DRINKING-WATER 

12 

effect, but the quantitative and qualitative details of exposure necessary to establish 

direct causation are lacking. An individual who took large mineral supplements over 

several years displayed symptoms of manganism (Banta & Markesbery, 1977). 

Another individual who ingested 1.8 mg of potassium permanganate per kilogram of 

body weight per day for 4 weeks developed symptoms similar to Parkinson disease 9 

months later (Holzgraefe et al., 1986; Bleich et al., 1999). 

An epidemiological study in Japan described adverse effects in humans consuming 

manganese dissolved in drinking-water, probably at a concentration close to 28 mg/l 

(Kawamura et al., 1941). The manganese was derived from 400 dry-cell batteries 

buried near a drinking-water well. Fifteen cases of poisoning were reported among 25 

persons examined, with symptoms including lethargy, increased muscle tone, tremor 

and mental disturbances. The most severe effects were seen in elderly people; less 

severe effects were seen in younger people, and effects were absent in children aged 

1–6 years. However, the level of exposure to manganese was poorly quantified, and 

the people were also exposed to high levels of zinc. The rapid onset and progression 

of the symptoms and the recovery of some patients prior to mitigation of the 

manganese-contaminated well water suggest that exposure to other chemicals may 

also have been a factor in the presentation of symptoms. 

An epidemiological study was conducted in Greece to investigate the possible 

correlation between long-term (i.e. more than 10 years) manganese exposure from 

water and neurological effects in elderly people (Kondakis et al., 1989). The levels of 

manganese in the drinking-water of three different geographical areas were 3.6–14.6 

μg/l in the control area and 81–253 μg/l and 1800–2300 μg/l in the test areas. The 

authors concluded that progressive increases in the manganese concentration in 

drinking-water are associated with a progressively higher prevalence of neurological 

signs of chronic manganese poisoning and higher manganese concentrations in the 

hair of older persons. However, no data were given on exposure from other sources 

such as food and dust, and little information was provided on nutritional status and 

other possible confounding variables. 

The individuals examined in the Kondakis et al. (1989) study also had exposure to 

manganese in their diet. This was originally estimated to be 10–15 mg/day because of 

the high intake of vegetables (X.G. Kondakis, personal communication, 1990). This 

estimate was subsequently lowered to 5–6 mg/day (X.G. Kondakis, personal 

communication, 1993). Because of the uncertainty in the amount of manganese in the 

diet and the amount of water consumed, it is impossible to estimate the total oral 

intake of manganese in this study. These limitations preclude the use of this study to 

determine a quantitative dose–response relationship for the toxicity of manganese in 

humans. 

Contrary to the above study, another long-term drinking-water study in a northern 

rural area of Germany (Vieregge et al., 1995) found no neurological effects of 

manganese at a level of at least 0.3 mg/l. No significant differences in neurological 

tests were found in older people (41 subjects older than 40 years with a mean age of 

57.5 years) consuming well water containing at least 0.3 mg of manganese per litre 
MANGANESE IN DRINKING-WATER 

13 

(0.3–2.16 mg/l) for 10–40 years. The control group (74 subjects, mean age 56.9 

years) was exposed to water containing less than 0.05 mg of manganese per litre. 

Subjects of both groups were randomly selected and matched with respect to age, sex, 

nutritional habits and drug intake. However, like the Kondakis et al. (1989) study, this 

study lacks exposure data from other routes and sources, and the manganese 

concentration range in the water is very wide. 

In one area of Japan, a manganese concentration of 0.75 mg/l in the drinking-water 

supply had no apparent adverse effects on the health of consumers (Suzuki, 1970). No 

signs of toxicity were observed in patients given 30 mg of manganese citrate (9 mg of 

manganese) per day for many months (Schroeder et al., 1966). The incidence of 

motor neuron disease in a small Japanese town was positively correlated with a 

significantly increased manganese concentration in local rice and a low magnesium 

concentration in the drinking-water (Iwami et al., 1994). The study did not provide 

good estimates of overall exposure to manganese in either the control population or 

the population with motor neuron disease; therefore, development of the disease 

could not be conclusively attributed to manganese exposure. The simultaneous 

exposure to manganese and the deficiency of other essential minerals were possibly 

the reasons for the enhanced incidence of neurotoxicological symptoms in Japan and 

in another population in Guam (Yoshida et al., 1988; Florence & Stauber, 1989). 

There was also some speculation on a link between mineral deficiency, enhanced oral 

manganese uptake and manganese-catalysed denaturation of copper-free prion protein 

to the pathogenic prion protein (Brown et al., 2000), which could contribute to the 

enhanced occurrence of some prion diseases in certain world regions (Purdey, 2000). 

Adverse neurological effects (decreased performance in school and in 

neurobehavioural examinations of the World Health Organization core test battery) 

were reported in 11- to 13-year-old children who were exposed to excess manganese 

through ingestion of contaminated water and from wheat fertilized with sewage water 

(He et al., 1994; Zhang et al., 1995). The exposed and control groups were both from 

farming communities and were matched for age, sex, grade, family income level and 

parental education level. The average manganese concentration of the drinking-water 

of the exposed group was 0.241 mg/l compared with the control level of 0.04 mg/l. 

The total exposure data, including manganese exposure from food, water and air, 

exposure duration, the nutritional status of the children and other confounding factors 

were not well characterized. Therefore, it was not possible to establish a cause–effect 

link between ingestion of excess manganese and preclinical neurological effects in 

children. Oral uptake of environmental manganese together with a deficiency of other 

minerals was suggested as a possible contributory factor to explain the enhanced 

incidence of neurological symptoms in isolated populations on Guam and the Kii 

Peninsula in East Asia (Yoshida et al., 1988; Florence & Stauber, 1989; Iwami et al., 

1994). 
MANGANESE IN DRINKING-WATER 

14 

6. PRACTICAL CONSIDERATIONS 

6.1 Analytical methods 

Sensitive methods exist for measuring total manganese in biological and 

environmental samples, although distinguishing between different oxidation states of 

manganese is not possible (IPCS, 1999). Atomic absorption spectroscopy is used for 

determining manganese concentrations in biological samples (e.g. urine, faeces and 

hair) at a detection limit as low as 1 μg/l for urine and 0.2 μg/g for hair. The 

technique has also been used to analyse manganese concentrations in water samples 

at levels as low as 0.01 μg/l (ATSDR, 2000). Inductively coupled argon–plasma 

optical emission spectrometry has also been used to measure manganese 

concentrations in biological fluids, water, waste products and air and has a detection 

limit of around 1–2 μg/l for liquids and 5 μg/m3 for air (ATSDR, 2000). Colorimetric 

methods are also used in water analysis and have detection limits of about 10 μg/l 

(ISO, 1986). 

6.2 Treatment methods and performance 

Manganese concentrations in drinking-water are easily lowered using common 

treatment methods. Oxidation and filtration are usually adequate to achieve a 

manganese concentration of 0.05 mg/l in drinking-water.

7. CONCLUSION 

Experimental animal data, especially rodent data, are not desirable for human risk 

assessment, because the physiological requirements for manganese vary among 

different species. Further, rodents are of limited value in assessing neurobehavioural 

effects, because the neurological effects (e.g. tremor, gait disorders) seen in primates 

are often preceded or accompanied by psychological symptoms (e.g. irritability, 

emotional lability), which are not apparent in rodents. The only primate study (Gupta 

et al., 1980) is of limited use in a quantitative risk assessment, because only one dose 

group was studied in a small number of animals, and information on the manganese 

content in the basal diet was not provided. 

While several studies have determined average levels of manganese in various diets, 

no quantitative information is available to indicate toxic levels of manganese in the 

diet of humans. Because of the homeostatic control that humans maintain over 

manganese, manganese is generally not considered to be very toxic when ingested 

with the diet.

A review of typical Western and vegetarian diets found average adult manganese 

intakes ranging from 0.7 to 10.9 mg/day (Greger, 1999; IOM, 2002). The upper range 

manganese intake value of 11 mg/day from dietary studies is considered a noobserved-adverse effect level (NOAEL). It is not believed that this amount of 

manganese in the diet represents an overexposure to the element (IOM, 2002). 
MANGANESE IN DRINKING-WATER 

15 

A health-based value can be calculated using this upper range value. A tolerable daily 

intake (TDI) of 0.06 mg/kg of body weight can be calculated by dividing the NOAEL 

of 11 mg/day by an uncertainty factor of 3 (to allow for the possible increased 

bioavailability of manganese from water) and an adult body weight of 60 kg. The 

guideline value of 0.4 mg/l is then derived from the TDI by assuming an allocation of 

20% of the TDI to drinking-water and consumption of 2 litres of drinking-water per 

day by a 60 kg adult. However, as this health-based value is well above 

concentrations of manganese normally found in drinking-water, it is not considered 

necessary to derive a formal guideline value.

It should be noted that the presence of manganese in drinking-water will be 

objectionable to consumers if the manganese is deposited in water mains and causes 

water discoloration. Concentrations below 0.05 mg/l are usually acceptable to 

consumers, although this may vary with local circumstances. 

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