Barium

(endorsed 2011)

Guideline

Based on health considerations, the concentration of barium in drinking water should not exceed 2 mg/L.

General description

Barium makes up approximately 0.04 per cent of the Earth’s crust, and is the 16th most abundant non-gaseous element. Barium in drinking water is primarily from natural sources. Some barium salts such as the chloride and nitrate are soluble in water; others, including the carbonate, fluoride, phosphate and sulfate, are insoluble. Barium is not considered to be an essential nutrient for humans.

Barium compounds have a wide variety of industrial applications. They are used in the plastics, rubber, electronics, steel, optical, and textile industries. They are also used in ceramic glazes and enamels, in glass and paper making, as a lubricant additive, in pharmaceuticals and cosmetics, and as a rodenticide.

The concentration of barium in drinking water overseas is usually low, typically less than 0.02 mg/L.

Most foods contain small quantities of barium. The major dietary sources are milk, potatoes and flour. Some cereal products and nuts can contain large amounts. It has been estimated that average dietary intake is approximately 1 mg per day.

Typical values in Australian drinking water

In Australian drinking water supplies, typical concentrations of barium range from <0.002 mg/L to 1.1 mg/L.

Treatment of drinking water

Conventional water treatment using alum or ferric coagulation is not effective in removing barium from drinking water. Lime softening can remove more than 90%.

Measurement

The barium concentration in drinking water can be determined using inductively coupled plasma emission spectroscopy (APHA Method 3500-Ba Part C 1992), or atomic absorption spectroscopy (APHA Method 3500-Ba Part B 1992). For both methods the limit of determination is approximately 0.01 mg/L.

Health considerations

Reviews of the human and animal toxicity data for barium are available (IPCS 2001, OEHHA 2003, WHO 2004a, USEPA 2005, ATSDR 2007).

The degree of absorption from the gastrointestinal tract depends on the solubility of the barium compound, and on other factors including age, study duration, species, and fasting status of the animals. The presence of food in the gastrointestinal tract appears to decrease barium absorption, and absorption appears to be higher in young animals than in older ones. The range of reported oral absorption in animal studies was 0.7–85.0%; a default value of 20% gastrointestinal absorption of dissolved barium in drinking water is assumed by the Safe Drinking Water Committee of the National Research Council of the USA (IPCS 2001, OEHHA 2003). After absorption, barium is deposited in bone and teeth.

Barium toxicity is caused by the free cation, and highly soluble barium compounds are more toxic than insoluble compounds. In rodents, kidney toxicity appears to be the most sensitive effect, whereas in humans, cardiovascular (hypertension) effects have been of prime concern.

The identification of hypertension as a health end-point of concern for humans is supported by findings of hypertensive effects in humans who ingested acutely high doses of barium compounds, in workers who inhaled dusts of barium ores and barium carbonate, in experimental animals given barium intravenously, and in rats exposed to barium in drinking water while on calcium-restricted diets (IPCS 2001).

A number of epidemiological studies have been carried out on the effects of barium in drinking water on cardiovascular disease. Wones et al. (1990) exposed eleven normotensive volunteers to barium in drinking water for 10 weeks at concentrations up to 10 mg/L. No cardiovascular effects were observed at the maximum estimated dose of 0.21 mg per kg bodyweight per day (mg/kg bw/day). Between 1976 and 1977, Brenniman and Levy (1985) studied two populations (n = 1175 and 1203) in the United States where water softeners were not used and mean barium concentrations were 0.1 mg/L or 7.3 mg/L (range 2–10 mg/L for the latter). No differences were observed in blood pressure or incidence of kidney disease between the two communities. Assuming 70 kg body weight and 2 L/day drinking water consumption, the mean doses of barium were 0.003 mg/kg bw/day and 0.21 mg/kg bw/day. Thus, 0.21 mg/kg bw/day is a no-observed-adverse-effect level (NOAEL) in this study, however because no adverse effects were found, the NOAEL is likely to be higher than this value.

Chronic toxicity studies of barium chloride in drinking water of rats and mice caused kidney effects at the higher doses used. Relevant NOAELs in these studies were 45 mg/kg bw/day for female rats and 75 mg/kg bw/day in male mice (NTP 1994)

There is no evidence from chronic rodent studies that barium causes cancer. The weight of evidence indicates barium is not mutagenic in tests with bacteria and does not damage DNA.

Derivation of guideline

A drinking water guideline of 2 mg/L has been set after considering the following.

Using animal data:

Based on the chronic male mouse-study data of the National Toxicology Program (NTP 1994), the United States Environmental Protection Agency (USEPA 2005) and Agency for Toxic Substances and Disease Registry (ATSDR 2007), the lower confidence limit for the benchmark dose at 5% incidence ($\text{BMDL}_{05}$) of renal effects was determined to be 63 and 61 mg/kg bw/day. A drinking-water guideline value of 6 mg/L (rounded) can be derived following the standard procedure:

$$\text{5.6 mg/L} = \frac{\text{60 mg/kg bw/day x 70kg x 0.8}}{\text{300 x 2L/day}}$$

Where:

• 60 mg/kg bw/day is the $\text{BMDL}_{05}$ for kidney effects determined from a long-term drinking water study in mice.

• 70 kg is taken as the average weight of an adult.

• 0.8 is a proportionality factor based on the assumption that 80% of daily intake attributable to drinking water.

• 2 L/day is the estimated maximum amount of water consumed by an adult.

• 300 is the safety factor applied to the $\text{BMDL}_{05}$ derived from animal studies (10 for interspecies variations, 10 for intraspecies variations and 3 for database inadequacies).

The lowest NOAEL of 45 mg/kg bw/day from the chronic rat and mouse studies can also be used in the above equation to give a guideline value of 4 mg/L (rounded).

Using human data:

The NOAEL of 0.2 mg/kg bw/day from the Brenniman and Levy (1985) epidemiological study gives a drinking water guideline of 2 mg/L (rounded) as follows:

$$\text{ 1.87 mg/L } = \dfrac{\text{ 0.2 mg/kg bodyweight/day x 70 kg x 0.8 }}{\text{ 2 L/day x 3 }}$$

Where:

• 0.2 mg/kg/day is the NOAEL in humans identified by Brenniman and Levy (1985).

• 3 is the safety factor applied to account for potential variability in response between humans. Justified on the grounds the study population was randomly selected from all people above the age of 18 years and therefore inherently included sensitive sub-populations. Furthermore, as the highest mean barium water concentrations in the study did not cause an adverse effect, the NOEL is likely to be higher than the one used to derive the drinking water guideline.

The World Health Organization (WHO 2004) established a guideline of 0.7 mg/L by dividing the mean barium water concentration of 7.3 mg/L in the Brenniman and Levy (1985) study by an uncertainty factor of 10 to account for human intraspecies variation. WHO (2006) acknowledges that this may be highly conservative.

The United States Environmental Protection Agency (USEPA 2006) indicates that 2 mg/L is the lowest level to which present technology and resources can reasonably be required to remove barium should it occur in drinking water.

References

APHA Method 3500-Ba Part B, (1992). Barium: Atomic Absorption Spectrophotometric method. Standard Methods for the Examination of Water and Wastewater, 18th edition. American Public Health Association, Washington.

APHA Method 3500-Ba Part C, (1992). Barium: Inductively Coupled Plasma method. Standard Methods for the Examination of Water and Wastewater, 18th edition. American Public Health Association, Washington.

ATSDR (Agency for Toxic Substances and Disease Registry) (2007). Toxicological Profile for Barium and Barium Compounds. ATSDR, US Department Of Health And Human Services. PB2008-100003.

Brenniman GR, Levy PS (1985). Epidemiological study of barium in Illinois drinking water supplies. Advances in Modern Environmental Toxicology, Princeton Publishing Co, New Jersey, 9:231–249.

IPCS (International Programme on Chemical Safety) (2001). Barium and barium compounds. Concise International Chemical Assessment Document 33. IPCS, World Health Organization.

NTP (National Toxicology Program) (1994). Technical report on the toxicology and carcinogenesis studies of barium chloride dihydrate (CAS No. 10326-27-9) in F344/N rats and B6C3F1 mice. NTP, Washington, DC.

OEHHA (Office of Environmental Health Hazard Assessment) (2003). Public Health Goal for Barium in Drinking Water. OEHHA, California Environmental Protection Agency.

USEPA (United States Environmental Protection Agency) (2005). Toxicological Review of Barium and Compounds. USEPA, EPA/635/R-05/001.

USEPA (United States Environmental Protection Agency) (2006). Consumer Factsheet on: Barium. USEPA.

WHO (World Health Organization) (2004a). Barium in Drinking-Water, Background document for development of WHO Guidelines for Drinking-water Quality, World Health Organization. WHO/SDE/WSH/03.04/76

WHO (World Health Organization) (2006). Guidelines for Drinking-water Quality. 3rd Edition, First Addendum, WHO, Geneva, Switzerland.

Wones RG, Stadler BL, Frohman LA (1990). Lack of effect of drinking water barium on cardiovascular risk factors. Environmental Health Perspectives, 85:355-359.