Appendix A

A Review of Risks Associated to Arsenic, Cadmium, Lead, Mercury and Zinc

Mikael Johannesson Kalmar University, Sweden

The Market Implication of Integrated Management of Heavy Metals Flows for Bioenergy use in the European Union Thermie STR/1881/98-SE

Published 2002 by Kalmar University Department of Biology and Environmental Science Environmental Science Section SE-391 82 Kalmar, SWEDEN http://www.bom.hik.se/ess ISBN 91-89584-07-4 (This report, appendix A) ISBN 91-89584-06-6 (The main report)

This report is an appendix to the report The Market Implication of Integrated Management for Heavy Metals Flows for Bioenergy use in the European Union. The correct citation of this report is: Johannesson, M.: A Review of Risks Associated to Arsenic, Cadmium, Lead, Mercury and Zinc, p. 62. Appendix A in Johannesson, M. (ed.) et al.: 2002, The Market Implication of Integrated Management for Heavy Metals Flows for Bioenergy use in the European Union. Kalmar University, Department of Biology and Environmental Science, Kalmar, Sweden, p. 115.

Table of contents
1. Summary ...................................................................................................................5
1.1 Introduction ....................................................................................................................5 1.2 Production, emission, concentration.............................................................................6 1.3 Accumulation, biomagnification, mobility, availability..............................................6 1.4 Current load compared to toxicity and essentiality ....................................................7 1.5 Concluding remarks .......................................................................................................8

2. Arsenic (As) .........................................................................................................11

2.1 General information .....................................................................................................11 2.2 Use ..................................................................................................................................12 2.3 Production .....................................................................................................................12 2.4 Emission and deposition...............................................................................................13 2.5 Concentrations (in nature and human) ......................................................................13 2.6 Limit values ...................................................................................................................15 2.7 Risk assessments, exposure and harmful effects .......................................................15 3.

Cadmium (Cd) .....................................................................................................21

3.1 General information .....................................................................................................21 3.2 Use ..................................................................................................................................22 3.3 Production .....................................................................................................................22 3.4 Emission and deposition...............................................................................................23 3.5 Concentrations (in nature and human) ......................................................................24 3.6 Limit values ...................................................................................................................26 3.7 Risk assessments, exposure and harmful effects .......................................................27

4. Lead (Pb) ................................................................................................................30

4.1 General information .....................................................................................................30 4.2 Use ..................................................................................................................................31 4.3 Production .....................................................................................................................31 4.4 Emissions and deposition .............................................................................................32 4.5 Concentrations (in nature and human) ......................................................................33 4.6 Limit values ...................................................................................................................34 4.7 Risk assessments, exposure and harmful effects .......................................................35

5. Mercury (Hg)..................................................................................................... 38
5.1 General information .................................................................................................... 38 5.2 Use ................................................................................................................................. 38 5.3 Production..................................................................................................................... 39 5.4 Emissions and deposition............................................................................................. 39 5.5 Concentrations (in nature and human)...................................................................... 41 5.6 Limit values .................................................................................................................. 43 5.7 Risk assessments, exposure and harmful effects ....................................................... 43

6. Zinc (Zn) ................................................................................................................ 48

6.1 General information .................................................................................................... 48 6.2 Use ................................................................................................................................. 48 6.3 Production..................................................................................................................... 49 6.4 Emissions and deposition............................................................................................. 49 6.5 Concentrations (in nature and human)...................................................................... 50 6.6 Limit values .................................................................................................................. 52 6.7 Risk assessments, exposure and harmful effects ....................................................... 53

7. References............................................................................................................. 58

1. Summary
1.1 Introduction1
The environmental and health risk associated to heavy metals and how to reduce the risks has been discussed on the scientific and political agenda for decades. Several efforts have been made by national and international bodies such as WHO, FAO, EU, OECD, and UN-ECE in order to survey the risks and decide on measures to reduce the risks. This first chapter includes a summary and conclusions made from the following review of the risks associated to the heavy metals cadmium, mercury, lead and zinc. Arsenic, although classified as a metalloid, is also included in that study. Among the data that has been reviewed and put together for each element are: use and production, concentrations in human and nature, emissions and deposition, trends, limit values, harmful effects. There are two aims putting all these data together: 1) Make an overall risk analysis of the elements in question including all relevant environmental and human aspects, 2) analyse to what extent biofuel have a relevance for the risks associated to these elements. If we shall reduce the use of fossil fuel in order to avoid the threat of an anthropogenic climate change, and partly replace the fossil fuel use by increased use of biofuel, we have to analyse the risks associated to a significant increase of bioenergy. One important risk to analyse is then the risks of a changed flow and exposure of heavy metals in the society and environment. Data mainly from review reports that summarizes the knowledge from different areas has been put together for each element. Reports from international bodies such as WHO, OECD, EU, and FAO has preferably been used but also reports from national authorities and scientific books that deals with a specific area of interest. The use of review reports compared to a deep review of the specialized literature saves a lot of time, especially in this kind of study that include so many different aspects. When using review reports the data will inevitable be some years old. However, in this case we are most interested in the right magnitude of the figures and of qualitative data. The picture given here describe in particular the general situation in the western world, which is regarding to most aspects investigated quite similar in most of these countries. However, in order to be cautious and not underestimate the risks, emphasize has when possible been put on those data that indicate the biggest risks. In this context it is important to note that the harmful effects of a substance is a combination of the substance inherent properties and the exposure of the substance. Thus, also small concentrations/flows might constitute a significant risk to human and nature. Although small, these concentrations/flows must be taken into consideration. It is also important to note that these elements occur in many different forms, which have various properties and constitute different levels of risks. Further, they change form and availability due to chemical and physical conditions in the surrounding medium, and due to biological activity. Due to lack of data and the fact that the elements/compounds undergoes transformation during the flows in the nature and the society it is not possible to make separate risk analysis for each possible compound that could include these elements. However, we have to bear in mind that a comparatively harmless compound might undergo a transformation to a much more potentially harmful compound during specific conditions. This means that it is wise to use a
1 It should be observed that this report was written in 1999 and some data concerning limit values, emissions etc have not updated. In the main report there may be more recent data available. However, most kinds of data are relevant and do not get old in a couple of years. From the source it is also possible to identify the age of the data.

precautionary approach when identifying flows/concentrations of importance for the risk humans and nature are exposed to.

1.2 Production, emission, concentration

The production of arsenic has gone up and down during the last 1015 years and it is hard to say anything about the trend. The production of cadmium has been stable since 1985, while the zinc primary production has increased. The world primary production of lead has since the beginning of 1980s remained on about the same level, while the secondary produced lead has increased. Only the production of mercury has decreased substantially during the last 1015 years. For all studied elements the emissions are decreasing and are expected to continue to decrease. However, large quantities are stored in products in the society and will gradually reach the environment unless they are taken care of safely. Some uses, for instance the use of lead for ammunition, will inevitably end up in the environment. This means that the elements flow from society to the environment will not stop even if the emissions from production etc. are stopped. Further, large quantities of the lead, cadmium and mercury are stored in the nature. For instance, the very large amounts of mercury in soil constitute a chemical time bomb that can cause severe pollution of aquatic ecosystems if it should be mobilized. However, the concentration in air and watercourses of the elements has in general decreased substantially due to the decreased emissions. But the response is much slower in soils, sediments, big lakes etc. were the turn overtime is much longer. In spite of the decreased emissions to air is the balance of the elements in soils still in many areas positive (increasing) since the input via fertilizer, sewage sludge and air deposition together is greater than the generally slow removal of the elements.

1.3 Accumulation2, biomagnification3, mobility, availability

The elements tendency to accumulate or biomagnify in organisms is dependent both on which form the element is present and on the organisms. Relative differences in the uptake of metal ions between plant and cultivars are controlled genetically and by various factors, including surface area of the root, root CEC (cation exchange capacity), root exudates and the rate of evatranspiration. The transfer coefficient (the metal conc. in plant tissue above ground divided by the total metal concentration in the soil) differs between metals. It is in general considerable higher for cadmium and zinc, 110, than for arsenic, mercury and lead 0.010.1. However, since a numerous soil and plant factors can affect the accumulation of metals in plants the transfer figures are not precise values but can indicate accumulation differences. Arsenic is subject to bioaccumulation but not to biomagnification. Arsenic concentration is elevated in marine biota. Plants take up arsenic in proportion to the soil concentration. However, some crops and mushrooms may accumulate high levels of arsenic even at relatively low soil arsenic levels. Arsenic in soils is highly mobile, resulting in possible groundwater contamination, but retention and accumulation by biota should remain low. Of all toxic metals released in large quantities into the environment, cadmium is generally regarded as the one most likely to accumulate in the human food chain. In certain situations, cadmium displays a propensity for marked bioaccumulation. Shellfish (e.g. crab and lobster), filter feeding molluscs and fungi can accumulate cadmium to considerable high levels. Plant species differ widely in their ability to accumulate cadmium. Leafy crops are capable of
2 Bioacumulation means that the concentration is considerably higher in the organisms than in their environment or food. 3 Biomagnification means that the concentration increases along food chains.

accumulating cadmium to relatively high levels. The most important factors influencing plant cadmium accumulation are soil pH and cadmium concentration. The uptake of lead differs a lot between species and the accumulation of lead in different tissues differs also a lot. Most plants seams to have a root barrier that prevents lead to reach the sprout. In general there is a positive relationship between the concentration of lead in the soil and the plant. However, only a small proportion of the lead in soil is in general available for uptake by plants. The lead concentration is in general higher in plants than in animals and higher in herbivore animals than in predators. Thus, there is in general no biomagnification in the lead case. When lead is released into the environment it has a long residence time compared with most other pollutants. The proportion of bio-available lead is higher if the pH, content of organic matter and concentration of iron-hydroxide is low compared to the opposite condition. This is essentially also true for the water environment. Mercury is involved in a whole chain of environmental transformations where the physical and chemical properties of mercury are changed. It is more mobile than most other heavy metals. Once released in the environment, mercury may be redistributed between and within environmental compartments. Inorganic mercury may be methylated to more toxic organic forms. Mercury is accumulated in soil invertebrates, aquatic invertebrates, and insects. Fish also take up mercury and retain it in tissues, principally methylmercury. Due to bioaccumulation and biomagnification the mercury concentration could be comparatively high in fresh and marine fish especially for fish of prey. Accumulation of mercury in plants increases with increasing soil mercury concentration. However, plant takes up only a small portion of the total mercury in soils. Generally, the highest concentrations of mercury are like in the lead case found in the roots. Besides the species of mercury, the toxicity and uptake of mercury to aquatic organisms is also dependent on for instance pH, organic matter, salinity, temperature, presence of selenium and sulphide ion, and water hardness. Zinc is under special circumstance bioaccumulated in organisms but is not subject to biomagnification in terrestrial or aquatic food chains. When the surrounding value is elevated the organisms on the lowest trophic level accumulate zinc (show higher concentration compared to the environment), while organisms on higher trophic levels (e.g. birds and mammals) accumulates zinc when the surrounding level of zinc is lower than normal. The uptake/excretion of zinc is regulated by organisms on all trophic levels but to a higher degree by organisms on the higher trophic levels.

1.4 Current load compared to toxicity and essentiality

The toxicity of the studied elements is strongly dependent on in which form they occur. All investigated elements may occur in forms that are toxic to very toxic for living organisms. Zinc and possibly also arsenic are the only ones that are observed to be essential for living organisms in such amounts that there may be a risk for deficiency also in situations that could not be characterized as extreme. Zinc is essential for all living organisms and in comparatively large quantities. Arsenic is observed to be essential for animals, possibly essential for humans but probably not for plants. Cadmium and lead is normally counted as non-essential metals although there are studies that indicate that they may have a positive effect on growth for some organism at very low levels. Mercury has as far as we know no necessary function in any living organism. Most of the arsenic exposure is of natural origin. Humans may in special areas, due to hydrogeological conditions, be exposed to harmful levels of arsenic via drinking water. The other important rout of exposure is via seafood. However, the bulk of the arsenic found in seafood exist in organic forms which are regarded as less toxic compared to the inorganic forms. Inorganic arsenic is classified as carcinogenic and there exist as far as we know no safe level of exposure.

The major human exposure of cadmium for non-smokers is food and drinking water, which amounts to about 80 % of the total intake. The critical effect for humans is probably tubular damage. Even if the population average kidney concentration is relatively low for the general population, a certain proportion may have values exceeding the value where renal tubular damage can occur. It has been estimated that, at present average daily intake of cadmium in Sweden, about 1 % of women with low body iron stores and smokers may experience adverse renal effects related to cadmium. If the average daily intake of cadmium would increase to 30 g/day, about 1 % of the entire population would have cadmium-induced tubular damage. For women with low iron stores up to 5 % would have tubular damage. Some population groups in Europe already exceed this intake and the margin is very narrow for large groups. The major exposure of lead for the non-smoking exposed adult population is food and water. For infants older than about 5 month and young children dust/soil may also be a major source of exposure. Young children and foetus are more sensitive to lead exposure than older children and adults. The toxic effects of lead have now been demonstrated at very low levels, and there is some suggestion that there may be no level of exposure below which lead is harmless. Lead is known to cause proximal renal tubular damage. For lead levels in blood less than 1.2 mol/l (25 g/dl) decrements in intelligence quotient (IQ) has been observed and reduction in human peripheral nerve conduction velocity may occur with levels as low as 1.44 mol/l (30 g/dl). Recent studies made by Bringmark and Bringmark at the Swedish university of agricultural science (SLU) indicate that lead and mercury may distinctly affect microbiological soil processes at lower levels than previously found. Effects were observed at levels that could be found in forest soils in the south of Sweden. The general population is primarily exposed to mercury through diet (organic mercury from fish and inorganic mercury from non-fish food) and dental amalgam (inorganic mercury). The clinical and epidemiological evidence indicates that prenatal life is more sensitive to the toxic effects of methylmercury than is adult life. The inhibition of protein synthesis is one of the earliest detectable biochemical effects in the adult brain. The kidney is the critical organ following the ingestion of inorganic divalent mercury salts. The central nervous system is the critical organ for mercury vapour exposure. It is not possible to set a level for mercury (e.g. in blood or urine) below which (in individual cases) mercury-related symptoms would not occur. Human hypersensitive reactions (dermatitis) to metallic mercury have also been identified. Certain groups with high fish consumption may attain a blood concentration of about 200 g litre/litre, (corresponding to 50 g/g of hair) associated with a 5 % risk of neurological damage to adults. Microorganisms responsible for decomposition of cellulose are usually very sensitive to heavy metals, especially mercury. There are indications that the regional enhanced concentrations of mercury in central Europe and southern Scandinavia may have an adverse effect on microbiological life processes, and indirectly on the recycling of important nutrients and on the tree vitality. Except for occupational exposure and point sources zinc do not probably occur in such elevated concentrations that negative effects should be expected. On the contrary, if zinc supply is not given, there is a risk of zinc deficiency in arable soils and for humans with certain needs. However, some aquatic organisms are very sensitive to zinc and elevated concentrations could be found downstream a zinc mine even long time after the mining is ceased.

1.5 Concluding remarks

Table 1.5b summarizes important information regarding arsenic, cadmium, lead, mercury and zinc with respect to environmental and health risk analyses. Further, the following 5 important concluding remarks could be made:

1) In the environment commonly found concentrations of arsenic, cadmium, lead and mercury constitute a risk for living organisms and may cause distinct negative effects on sensitive organisms and humans during specific conditions. At least for zinc and possible also for arsenic there may also be a risk for deficiency during specific conditions. 2) Although the emissions of cadmium, mercury and lead has decreased significantly during the last decades and probably will continue to decrease, the concentrations of these elements in for example forest soils and arable soils will continue to increase or decrease very slowly during the coming decades. 3) The plant uptake of zinc and cadmium ions is in general considerably larger than it is for arsenic, lead and mercury. 4) In order to eliminate or significantly reduce the risk and negative effects on organisms and humans that are not occupationally exposed or exposed by point sources, the diffuse emissions of especially cadmium, lead and mercury have to be reduced significantly. However, the exposure from point sources may be of significant and crucial importance for individuals and for the environment situated near them. This includes also zinc and arsenic. Point sources contribute also significantly to the overall load. 5) It is possible divide the five elements into four groups based on both the overall risk they constitute and on their relevance in the context of bio energy use. See table 1.5a below.
Table 1.5a Grouping of As, Cd, Hg, Pb and Zn with respect to risk and biofuel relevance

High risk and high relevance Cadmium High risk and moderate relevance Lead, Mercury

Moderate risk and high relevance Zinc Moderate risk and moderate relevance Arsenic

1) High general risk and high relevance Cadmium: The current load constitutes a risk to human and the environment. The load will continue to be high for several decades. Cadmium is taken up in comparatively high amounts by plants. 2) High general risk moderate relevance Lead and mercury: The current load constitutes a risk to human and the environment. The load will continue to be high for several decades. The uptake by plants is moderate. 3) Moderate general risk and moderate/high relevance Arsenic and Zinc: The current load constitutes a moderate risk to human and the environment except for occupationally exposed and exposure near point sources. Elevated arsenic exposure via drinking water should be identified and eliminated. Zinc is taken up in comparatively high amounts by plants. But it constitutes in general no problem. The uptake of arsenic by plants is moderate.

Table 1.5b Summary of some qualitative data of importance for the assessment of human and environmental risks associated to arsenic, cadmium, lead, mercury and zinc in relation to an increased use of biofuel.
Arsenic
Primary production. No trend last 15 years.

Cadmium
Constant last 15 years. Decreasing. Increasing/constant. Decreasing in the upper part of some European forest soils. Some species, varieties or clones accumulate high concentrations. High. Human renal tubular damage and osteoporosis (risk groups). Probably effects on sensitive organisms. High.

Lead
Constant last 15 years. Decreasing. Increasing/constant.

Mercury
Significant decrease the last decades. Decreasing. Increasing/constant.

Zinc
Significant increase last 15 years. Decreasing. Constant. Decreasing if not using farmyard manure or additives. High uptake.

Emissions to air & water. Decreasing. Change of concentration ? in soil.

Soil uptake by plants.

Low uptake by root.

Low uptake by root.

Low uptake by root.

Current load to human and the environment compared to toxicity.

In general low. High human exposure via drinking water in some areas.

High. No safe limit. Probably effects on risk groups and sensitive organisms.

High. No safe limit. Probably effects on risk groups and sensitive organisms.

In general low. Some compounds may constitute a risk. Risk for deficiency in specific cases. High.

The importance of terrestrial plants for element exposure and circulation. Accumulation and biomagnification.

Moderate.

Relatively high source of Moderate. exposure. Moderate importance for circulation. In general no bioaccumulation or biomagnification. Bioaccumulation and bio-magnification, yes. Especially organic mercury in aquatic organisms. Non-essential.

Bioaccumulation, yes. Especially in the marine environment. Biomagnification no. Essential for animals. Possibly also for humans.

Bioaccumulation, yes. Both in the terrestrial and in the marine environment. Non-essential. Possibly essential for some species.

Accumulation occurs at low trophic level. Biomagnification in deficient environments. Essential.

Essential for living organisms?

Non-essential. Possibly essential for some species.

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2. Arsenic (As)
2.1 General information
Arsenic is a grey element with a metallic lustre. Arsenic is classified as a metalloid and exhibits both metallic and non-metallic properties. Its chemical properties are similar to those of phosphorus and belong to the same group (Va) in the periodic table. Arsenic is present in valency -3, 0, +3, and +5. The valence 0 is unusual, and is not absorbed, while the -3 form (arsine) is a gas and would not account for any significant exposure under most environment settings. Elemental arsenic is insoluble in water but soluble in HNO3. The average concentration of arsenic in the earth crust has been estimated to 1.52 mg/kg. It is the 20th most abundant element in the crust, fourteenth in the seawater, and twelfth in the human body. Arsenic occurs naturally in more than 200 mineral species: from the native element or alloys to arsenides, sulphides and oxidation products (oxides, arsenites, and arsenates). Arsenic is present in many mineral deposits and in particular those containing sulphide minerals. The most common mineral is arsenopyrites (FeSAs). Arsenic is in normal seawater conditions present as HAsO42-. Arsenic has a rich and complex organic chemistry and this is reflected to some extent in its environmental behaviour. Complex organic arsenic compounds such as tetramethylarsonium salts, arsenocholine, arsenobetaine, dimethyl (ribosyl) arsine oxides, and arsenic containing lipids have been identified in the marine environment. A variety of complex organoarsenic compounds may be present at sites containing wastes from coal utilisation or oil production (WHO 1992:10; Park Ridge 1993:60; WHO 1986:17; Thornton & Farago 1997:2; North et al. 1997:407; Azcue & Nriagu 1994; Naqvi et al. 1994:56). Arsenic has been known for about 4 000 years and first gained notoriety as a poison. In 1885, it accounted for nearly one-third of the homicide poisonings in France (North et al. 1997:406). Arsenic differs from many of the common heavy metals in that the majority of organic compounds are less toxic than inorganic arsenic compounds. Whilst having many chemical similarities to phosphorus, the soil chemistry of arsenic is much more diverse because it can exist in more than one oxidation state under the normal range of soil conditions, and arsenic can form bounds with sulphur and carbon much ore readily than does phosphorus (ONeill 1995:105, 110). Arsenic compounds are often unstable, and in many cases not well defined materials. For example, the arsenites (+3) of the alkali metals are slowly converted in solution to arsenates (+5), by atmospheric oxygen. Arsenic trisulphide reacts vigorously with oxidizing agents, and hydrogen sulphide is generated on contact with strong acids. Arsenic trichloride is highly reactive with water, strong oxidants, ammonia, and some alkalis; the reaction results in the generation of hydrogen chloride and chloride gas. Inorganic arsenic compounds may generate highly toxic (and flammable) arsine gas when in contact with acids plus reducing metals (e.g., zinc or iron), or with sodium hydroxide plus aluminium (WHO 1992:9-10). As a result of the presence of arsenic in the parent rock, arsenic is present naturally in soils in various quantities. Inorganic arsenic is found chiefly in the form of its compounds with metals (arsenides), which usually occur in isomorphous mixture with sulphides (WHO 1992:13). Arsenic in soils is highly mobile, resulting in possible groundwater contamination, but retention and accumulation by biota should remain low. Any retention of arsenic by soils would occur by adsorption especially if the soils contained iron or aluminium oxides (Bhumbla & Keefer 1994:73). Arsenic is subject to bioaccumulation in marine organisms but in general not to biomagnification. There is substantial evidence in animals that arsenic is an essential trace

element, but only a little data on its potential essentially in humans. Arsenic is not essential for plants (WHO 1986:51-52; North et al. 1997:407; Alloway 1995:3031).

2.2 Use
Metallic arsenic is used in alloys, in combination with lead and copper, in semiconductor devices, and in glasses. The most important use of arsenic(As3+)oxide is in the manufacture of a variety of insecticides, herbicides, fungicides, algicides, sheep dips, and pharmaceutical products. Arsenic sulphide is used for dehairing skins intanning, in the manufacture of pyrotechnics and semiconductors, and in the manufacture of special optical glass. Calcium and lead arsenates have been used as insecticides but have largely been replaced. About on third of the world arsenic production is used for wood preservation. They usually consist of chromated copper arsenate. Other examples where arsenic compounds are used are solar-cells, light emitting diodes, paints, dyes, ceramics, algaecides and feed additives (for instance prevention of swine dysentery) (WHO 1992:12; North et al. 1997:406; Azcue & Nriagu 1994:12). The addition of up to 3 % of arsenic hardens lead and minimizes the softening of lead-base bearing alloys used in internal combustion engines. Automotive body solders usually contain 0.5 % of arsenic. The addition of arsenic (0.52 %) improves the sphericity of lead ammunition (Azcue & Nriagu 1994:13). From the 1860s until the introduction of DDT and other organic pesticides in the 1940s, inorganic compounds of arsenic remained the dominant insecticides available to farmers and fruit growers (Azcue & Nriagu 1994:12). Arsenic compounds have been used in medicine since the time of Hippocrates ca. 400 B.C.E. Inorganic arsenicals have been used for centuries, and organoarsenicals have been used for at least a century in the treatment of syphylis, yaws, amoebic dysentery and trypanosomiasis (Eisler 1994:188).

2.3 Production
The world production of white arsenic (arsenic trioxide) was in 1994 (estimate) about 43 000 tonnes. In 1985 the world production was about 53 000 tonnes, and in 1989 it was 61 000 tonnes. According to Chapman et al. (1999) the world production of arsenic trioxide was about 50 million tonnes in 1997 from the countries listed. However, in addition to the countries listed eight more countries were believed to produce arsenic trioxide. It is from these date hard to say anything about the trend during the last ten years (Chapman et al. 1999:21; Knight-Ridder financial/commodity research bureau 1996:7). China and Chile was the worlds largest producer of arsenic and contributed to about half of the world production in 1997. In 1997 France and Belgium produced most arsenic among the EU-countries listed by Chapman et al. (Chapman et al. 1999:21). Arsenic is recovered as a by-product of processing certain complex ores that are mainly for copper, cobalt, lead, zinc, gold and silver, and its supply is dependent to a large extent on the demand for these metals. Arsenic trioxide is the most important commercial compound. The United States was the worlds largest consumer of arsenic in 1994, accounting for about onehalf of the total world demand (Azcue & Nriagu 1994:58; Knight-Ridder financial/commodity research bureau 1996:7).

12

2.4 Emission and deposition

The greatest amount of flux of arsenic has been estimated to occur from land (3 000 x 108 g/yr.) and atmosphere (2 000 x 108 g/yr.) to oceans, followed by oceans to sediments (2 500 x 108 g/yr.) and sediments to land (2 400 x 108 g/yr.). The amount of flux from oceans is fairly high to sediments, biota (1.300 x 108 g/yr.) and dissolved phases (1 000 x 108 g/yr.). On the other hand, the amounts of flux from land to biota (300 x 108 g/yr.), or terrestrial biota to land (300 x 108 g/yr.) is medium to low, and less than from mining and smelting (tot 500 x 108 g/yr.). Very low flux has been estimated to take place from volcanoes to land (54 x 108 g/yr.), to sediments (40 x 108 g/yr.) and to atmosphere (3 x 108 g/yr) (Bhumbla & Keefer 1994:54). Sources of arsenic into drinking/irrigation waters into soils, dust and the food chain may be derived from (a) naturally occurring arsenic-rich minerals and rocks, (b) from sulphide mineralization and waste materials resulting from mining and smeltering activities, and from the burning of arsenic-rich coal (Thornton & Farago 1997:7). One example of previous emission from a plant in Slovakia burning coal is mentioned by Bencko. The plant burned low-grade coal with an arsenic content ranging from 800 to 1 500 g arsenic/ton dry weight and emitted about half a ton arsenic every day around 1960 despite the use of electrostatic eliminators (Bencko 1997:84). The roasting of arsenic-containing (sulphide) ores and burning of arsenic rich coal releases arsenic trioxide, which may react in air with basic oxides, to form arsenates, which can then be deposited to soils. For example, in mineralised areas of Cornwall, concentrations of arsenic in surface soils range up to 2 500 mg/kg, and in the vicinity of old roasting ovens and smelter stacks it may range from 0.1 to 1.0 % or more (Thornton & Farago 1997:3). Estimates for 32 countries in Europe of past and likely future air emission of arsenic, cadmium, lead, and zinc have been made by European Environmental Agency (EEA). The emissions of arsenic to air has decreased from about 2 000 tonnes in 1975 to about 1 000 tonnes in 1991, and it is expected to continue to decrease (EEA 1998:112). In 1990 the air emissions of arsenic in EU-15 has been estimated to 575 tonnes of which 202 came from Italy, 166 from UK, and 122 from Germany (Eurostat 1998:78). Arsenic has been added to soils in many ways. In 1988, the major portion about 40 % was from commercial products and about 25 % was from coal fly ash and bottom ash, 14 % from atmospheric fallout, 10 % from mine tailings, 7 % from smelters, 3 % from agriculture, and 2 % from manufacturing, urban and forestry wastes (Bhumbla & Keefer 1994:55, Nriagu & Pacyna 1988).

2.5 Concentrations (in nature and human)

More than 99 % of the total arsenic in the environment is present in rocks. Almost all the rest are found in the oceans and in the soil, while biota and atmosphere contain very little compared to the other reservoirs (Bhumbla & Keefer 1994:5354). The average concentration of arsenic in the earths crust has been estimated to be about 1.8 mg/kg. The average concentrations of arsenic in igneous rocks, limestone, sandstone and shale are 1.5, 2.6, 4.1 and 14.5 mg/kg respectively. Arsenic is concentrated in some reducing marine sediments which may contain up to 3 000 mg/kg. Soils overlaying sulphide-ore deposits may contain several hundred mg/kg (WHO 1992:13). Uncontaminated soils usually contain 140 mg arsenic /kg, with the lowest concentrations in sandy soils and those derived from granites. However, there are also reports of high concentrations in soils from granites and quartzite (up to 250 mg/kg for soils derived from granite). Higher concentrations are found in alluvial soils and in organic soils. The estimated mean value of arsenic in uncontaminated soils is 56 mg arsenic/kg, although divergent values (both higher and lower concentrations) could be found in specific countries or regions (WHO 1986:17; Thornton & Farago 1997:2-3; Huang YanChu 1994:18, 21; Bhumbla & Keefer 1994:5354, 62). 13

High levels of arsenic may be present in some sulphide-rich coals (up to 1 500 mg/kg). Arsenic is present in much larger amounts in fly ash than in bottom ash. Average arsenic concentrations in coal ashes have been reported to vary from 56 mg/kg and 128 mg/kg to 156 mg/kg, but some samples may exceed 1 000 mg/kg. Arsenic can be present in sewage sludge. Some researchers have reported concentrations from 3 to 46 mg of As/kg in sludge from the United States and the Netherlands (Bhumbla & Keefer 1994:56; 62). The airborne concentration of arsenic in unpolluted areas is generally less than a few nanograms per m3, while as much as 1 g/m3, or more, has been recorded near point sources (WHO 1986:47). The concentration of arsenic in fresh water varies greatly. The concentrations in unpolluted fresh waters typically ranges from 110 g/litre, rising to 1005 000 g/litre in areas of sulphide mineralization and mining. Natural high concentrations of arsenic in drinking water constitute a serious health problem in several regions around the world (see chapter 2.7) (Thornton & Farago 1997:2). Arsenic in aquatic systems is preferentially distributed to the sediment. Arsenic associated with soils particles can be a major source of arsenic contamination when soil particles are detached and carried as sediments during erosion. Sediments can contain substantial (100300 mg/kg) amounts of total arsenic. In addition to the particle-bound arsenic originating from land, new suspended solids with large amounts of arsenic are generated within bodies of water due to precipitation of salts (WHO 1992:13; Bhumbla & Keefer 1994:70). Typically reported Arsenic concentrations in the open sea lies in the range of 1.3 g to 2.4 g/litre of which arsenate is the dominant species, although arsenit, due to biological activity, occurs at concentrations greater than those expected from purely thermodynamic considerations. Only a very minor fraction of total arsenic in the oceans remains in solution in seawater, as the majority is sorbed on to suspended particulate material. The concentration in uncontaminated sea sediments varies considerable from less than 1 mg/kg d.w. to over 100 mg/kg, with an average for world oceans of about 40 mg/kg and in the range of 3 to 15 mg/kg for coastal regions and estuaries. The concentration in uncontaminated sediments in the coastal areas is in general lower than in the deep-sea sediments Sediment (WHO 1986:24, Thornton & Farago 1997:2; Francesconi & Edmonds 1994:223224). There is a significant difference in the level and chemical forms of arsenic in terrestrial and marine organisms. In terrestrial flora and fauna, and fresh water biota the background levels of arsenic are usually less than 1 mg As/kg (dry weight) whereas marine organisms contain from 1 mg As/kg to more than 100 mg (dry weight). Arsenic concentrations in the tissues in marine biota show a wide range of values, being highest in lipids, liver, and muscle tissues, and varying with age of the organism, geographic locale. Arsenic appears to be elevated in marine biota because of their ability to accumulate arsenic from seawater and food sources, not because of localized pollution (Maeda 1994:156; Eisler 1994:201, 213214). Marine algae can accumulate high concentrations of arsenic of which a significant part may be inorganic arsenic. Most of the arsenic in algae is present as arsenic-containing ribosides (both water-soluble and lipid-soluble). In general, brown algae contain considerable amounts of arsenic, typically in the range 10 to 100 mg/kg d. w. while green and red algae contains 1 to 20 mg/kg d. w. Generally, the arsenic content in freshwater algae is lower than in marine algae. However, some fresh water algae accumulate arsenic to a large degree (WHO 1986:25; Maeda 1994:166168; Francesconi & Edmonds 1994:253; Phillips 1994:265266). Arsenic levels in human food products, with exception of seafood, are generally low (less than 0.25 mg As/kg). The concentration in edible plants is generally low even when the crops are grown on contaminated land. Seafood commonly contains 120 mg arsenic/kg mainly as organic arsenic on a wet weight basis, although higher values have been reported (up to 50 100 mg/kg). Highest values are found in bottom-feeding fish and crustacean. Freshwater fish and pelagic marine fish have in general total arsenic concentration around or below 1 mg/kg. Elevated arsenic levels have been found in wine (WHO 1992:14; WHO 1986:25-30, 47-48; Phillips 1994, ONeill 1995:115). 14

The level of arsenic in terrestrial plants is generally well below the concentrations in soil. In general roots contain higher levels than stems, leaves or fruit (ONeill 1995:115). Human hair and nails show the highest arsenic concentrations, while fairly high concentrations are found in skin and lungs. Examples of reported median concentrations: blood (whole) 38 g/kg, bone 57 g/kg, brain 13 g/kg, hair 460 g/kg, kidney 33 g/kg, liver 28 g/kg, lung 82 g/kg, and nail 300 g/kg The high concentrations in nails and hair has been explained by the high content in these tissues of keratin, the SH-groups of which may bind trivalent inorganic arsenic. The methylated metabolites of inorganic arsenic and the seafood arsenic are not accumulated in hair (WHO 1986:40, 42). The average concentration of total arsenic in urine is general in the range of 15-30 g/litre. Intake of seafood meal may give rise to arsenic concentrations of more than 1 000 g/litre within 24 hours. After 23 days, the concentrations have decreased to almost normal values. The concentration of inorganic metabolites is generally less than 10 g/litre urine in the European countries (WHO 1986:43-45). Eisler (1994) has put together an extensive list of arsenic concentrations found in both nonbiological and biological materials.

2.6 Limit values

In 1993 the WHO made a provisional guideline recommendation of 10 g/litre for arsenic in drinking water (North et al. 1997:416). The EU has (1998) adopted 10 g/litre as limit value for inorganic arsenic in drinking water. The limit value should be met within five years (European Union 1998). Before 1993, the WHO drinkingwater guideline value for arsenic (total) was 50 g/litre which corresponds to a daily intake of 100-200 g (WHO 1992:14; WHO 1986:50). In the WHO air quality guidelines for Europe it was concluded that, because inorganic arsenic is carcinogenic and there is no safe threshold, no safe level for arsenic can be recommended (WHO 1992:25). The WHO has estimated the human lifetime risk of getting lung cancer from arsenic in air as 0.0015 per g/m3. WHO has recommended that the daily oral intake of inorganic arsenic should not exceed 2 g arsenic/kg body weight. The Joint FAO/WHO Expert Committee on Food Additives assigned a provisional tolerable weekly intake (PTWI) of 15 g inorganic arsenic/kg body weight, but stressed that there is a narrow margin between the PTWI and intakes reported in epidemiological studies to have toxic effects (WHO 1992:19, 25). There are indications that arsenic may be essential, at least for some animals. If it is essential also for humans, the human requirement for arsenic is probably close to 20 g/day (WHO 1996:219). The PTWI value (15 g) corresponds to maximum daily intake of 150 g for a human weighing 70 kg. Yamane reported in 1979 that the maximum allowable limit of arsenic residue at 15 mg/kg, as determined by the 1 N HCl extraction method. It has been estimated that rice yield decreases by 10 % at 25 mg arsenic/kg (Huang YanChu 1994:40). Eisler has put together a list of criteria for arsenic that has been proposed by authorities and experts from different countries in order to protect natural resources and human health (Eisler 1994:245251).

2.7 Risk assessments, exposure and harmful effects

As a result of its natural occurrence, humans are universally exposed to arsenic in various forms. The various naturally occurring inorganic and organic arsenic compounds are interlinked through complex biotic and abiotic transformations in the environment. Inorganic 15

arsenic can be converted to methylated species in soil and water by a number of microorganisms (e.g. fungi and bacteria in soils, algae in water) under aerobic, as well as anaerobic, conditions. In anoxic parts of the soil layer, arsenic can be immobilized as the sulphide. In water at moderate or high redox potentials arsenic can be stabilized as a series of pentavalent (arsenate) oxyanions. However, under most reducing conditions, the trivalent arsenite species dominates. The reduced form of inorganic arsenic, arsenite (As3+), is considered to be much more toxic, more soluble and mobile than the oxidised form, arsenate (As5+). Soluble arsenic concentrations are usually controlled by redox conditions, pH, biologically activity and adsorption reactions but not by solubility equilibria. In general the toxicity effects of arsenic on plants increases as soils becomes more acid (WHO 1992:13; Thornton & Farago 1997:2; Bhumbla & Keefer 1994:6364; ONeill 1995:116). The main sources of arsenic in soils are the parent materials from which they are derived. However, arsenic may also originate from industrial waste discharges or agricultural use (fertilizers, lime and pesticides). In many regions of long agricultural use, soils have accumulated residues of arsenic. Under the ranges of Eh and pH in soils, arsenic may be present as either As5+ arsenate or As3+ arsenit, with microbial activity causing methylation, demethylation and/or change in oxidation state. Arsenates of iron and aluminium are the dominant phases in acid soils and are less soluble than calcium arsenate, which is the main chemical form in many calcareous soils. Arsenic sulphide minerals may form if sulphur species are present and if redox potential is low enough (Thornton & Farago 1997:3; Huang YanChu 1994:1819; Alloway 1995:24-25). Arsenic adsorption in soils is related to the pH, chemical and physical properties, and cation exchange capacity. In one study it was found that the maximum adsorption of arsenite took place at pH interval 68. The adsorption of arsenate is dependent on the ratio of (CaO + MgO) to (Al2O3 + Fe2O3. Arsenic and phosphate in soil exhibit similar behaviour; both are for instance strongly adsorbed by amorphous iron oxide. Phosphate substantially suppresses arsenic adsorption by soils and the extent of suppression varies from soil to soil. Arsenic is more strongly bound to soils that have a high clay or high organic matter content. In these circumstances arsenic is less available to plants. Plants take up arsenic in proportion to the soil concentration (passive uptake), except at very high soil concentrations. In order for plant levels to reach 1 mg As/kg on fresh weight bases, soil levels must in general exceed 200 to 300 mg As/kg. However, some crops may accumulate high levels of arsenic even at much lower soil arsenic levels. For instance, arsenic concentrations in crops grown on soils containing 25 to 50 mg As/kg were 6 to 12 mg As/kg on a fresh weight bases for alfalfa and pasture grass. Also some mushrooms can accumulate high concentrations of arsenic (WHO 1992:13; Thornton & Farago 1997:4; Huang YanChu 1994:30, 3235; Bhumbla & Keefer 1994:73; Maeda 1994:162). In a study where vegetables (beetroot, lettuce, onion, pea, carrot and bean) concentrations of arsenic were compared with the arsenic in soils (range 144-892 mg/kg) it was found that the concentration in the plant increased with the soil concentration except for carrots and beans. However, only lettuce exceeded 1 mg/kg dry weight. A positive correlation between extractable arsenic in soil and the content of arsenic in rise and wheat has also been found. The distribution of arsenic in plants, in general, is in descending order from root to stem and leaf to edible parts. It has been suggested that low levels of phosphates displace arsenic from soil particles which increases the uptake and phytotoxicity, whereas, larger amount of phosphates compete with arsenic at root surfaces to decrease uptake and phytotoxicity. Arsenic concentrations in leaves may also be elevated if arsenic pesticides have been used (Thornton & Farago 1997:4; Huang YanChu 1994:3839). Arsenic is subject to bioaccumulation but not to biomagnification. Rather the arsenic level decreases successively in freshwater organisms and marine organisms with elevation in the tropic level. Algae actively take up naturally occurring arsenate, and transform inorganic arsenic into a variety of organic arsenic compounds. The concentration of arsenic in unicellular algae has been reported to reach up to 3 000 times the concentration in the surrounding water. This is a major source of arsenic for higher organisms. Fish and 16

crustaceans accumulate arsenic compounds via the food-chain. The accumulation direct via seawater is low. A number of studies have demonstrated positive relation between size of marine animals and their arsenic concentration. Arsenic is in general not biomagnified in marine food-chains. Arsenobetaine (CH3)3As+CH2COO-, has been found to be the major form of arsenic in marine animals contributing to the human diet. In general organoarsenic species are dimethylarsenic compounds in aqueous plants such as algae, and trimethylarsenic compounds in molluscs, crustaceans and fish, among marine organism (WHO 1992:14; WHO 1986:21- 23, 51-52; Maeda 1994:180181). Arsenobetaine has also been found in higher organisms in brackish water but not in fresh water environments, except in shrimp. In fresh water organisms several other organic compounds than arsenobetaine has been found. While relatively high proportion of arsenic may be present in algaes in the more toxic inorganic form the organic form is predominant (more than 80 %) in for instance crustaceans and fish (WHO 1986:25, 28; Maeda 1994:181). Exposure of the general population occurs mainly through arsenic present in food and drinking water. Seafood is in general the dominant source of arsenic to humans. People that often consumes seafood may reach several thousands g of total arsenic per day. However, 8595 % of the arsenic in marine products is in general present as the much less toxic, organic arsenic compounds. In some areas, the natural high arsenic content of the drinkingwater has caused endemic, chronic arsenic poisoning. South-west Taiwan, West Bengal India, Langunera northern Mexico, Northern Chile, South-east Argentine, Inner Mongolia are examples of areas where naturally elevated concentration of arsenic in drinking water and irrigation water has caused chronic arsenic poisoning resulting in for instance, hyperkeratosis, hyperpigmentation and skin cancer. Millions of people in these areas are exposed to arsenic levels that lies above the present WHO drinkingwater guideline value for arsenic of 50 g/litre. The drinking water used in these areas often contain 100 g As/l or more, and sometimes up to twenty times more (Thornton & Farago 1997:7-10; Luo et al. 1997:55-68; Chowdhury et al. 1997:93-111). Excluding such areas the daily intake of arsenic through drinking normally contributes to less than 10 g As/day (WHO 1992:14; WHO 1986:47, 49, 52). Soil and dust ingestion may in arsenic contaminated areas significant contribute to the overall exposure of arsenic for young children. However, to assess the risk from that source one have to examine the bioavailibilty which may be much less for the arsenic species found in soil than those in water (Farago et al. 1997:221-223). It has been estimated that the normally daily intake of inorganic arsenic is less than 50 g in Europe and USA and more than 100 g in Japan. Although most of the arsenic in seafood is present in organic form, the contribution of inorganic arsenic from seafood may be significant. A daily consumption of 150 g seafood would give rise to an intake of about 15-75 g inorganic arsenic per day, the higher figure relating to a daily intake of flatfish, crustacean and molluscs. The daily intake of seaweed in Japan is about 5 g. With an assumed average arsenic concentration of about 100 mg As/kg dry weight, or about 20 mg As/kg wet weight, this means that the daily intake of arsenic from seaweed might exceed 100 g, out of which 60-80 % probably is in the form of inorganic arsenic. Daily consumption of seafood would give rise to an intake of about 135 1 500 g organic arsenic. However, it can be estimated that the world average daily intake of organic arsenic from seafood (most of which is arsenobetaine) is 15-20 g (WHO 1986:49, 52). In the working environment high inhalation exposures may be associated with the smelting of non-ferrous sulphide ores, glass manufacturing, wood preservation plants, and the agricultural application of arsenic-containing pesticides (WHO 1992:14). Studies on experimental animals, as well as on humans, have shown that over 90 % on an ingested dose of dissolved inorganic trivalent or pentavalent arsenic is absorbed from the gastrointestinal tract. In 15 human subjects, each ingesting about 10 mg of arsenic (mostly arsenobetaine) with witch flounder, less than 1 % was recovered in the faces within 8 days 17

indicating a high absorption. In the lungs, water-soluble arsenic compounds are rapidly absorbed (WHO 1992:14; WHO 1986:37-38). Although high levels of arsenic are maintained for long periods of time in the bone, hair, and nails of exposed individuals, most inorganic arsenic is eliminated at much higher rate with the urine, manly as dimethyl-arsenic acid and methane-arsonic acid. Depending on the administrated dose, the half-life in man, after short-term exposure, is in the range of 13 days. There is no long-term accumulation of arsenic in soft tissues. With increasing arsenic intake, the proportion of arsenic detoxified (methylated) is reduced. Increases in the inorganic arsenic body burden may be expected at daily intakes exceeding about 200 g/person. In persons with a low (stable) dietary arsenic intake, the urinary levels may be used to monitor exposure to inorganic arsenic. Since the elimination of arsenic takes place mainly via the kidneys, the concentration of arsenic in the urine is a good indication of exposure to inorganic arsenic (WHO 1992:14). Arsenic is a common, for human, toxic substance with exceedingly diverse manifestations of poisoning. Different species of arsenic have different degrees of toxicity, with arsine and trivalent (arsenite) causing the most damage. The bodys toxic response depends on the route and dose of exposure plus individual and local tissue susceptibilities. Eisler has put together an extensive list of at what level lethal and sublethal effects of arsenic have been found in different organisms (Morton & Dunette 1994:29; Eisler 1994). According to Eisler (1994) most experts agree on 10 points: (1) inorganic arsenicals are more toxic than organic arsenicals, and trivalent forms are more toxic than pentavalent forms; (2) episodes of arsenic poisoning are either acute or subacute; cases of chronic arsenosis are rarely encountered, except in humans; (3) sensitivity to arsenic is greatest during the early developmental stages; (4) arsenic can traverse placental barriers; as little as 1.7 mg As+5/kg body weight at critical stages of hamster embryogenesis, for example, can produce foetal death and malformation; (5) biomethylation is the preferred detoxification mechanism for inorganic arsenicals; (6) arsenic is bioconcentrated by organisms, but not biomagnified in the food chain; (7) in soils, depressed crop yields were recorded at 3 to 28 mg water-soluble As/L, or about 25 to 85 mg total As/kg soil; adverse effects on vegetation were recorded at concentrations in Air > 3.9 g As/m3; (8) some aquatic species were adversely affected at water concentrations of 19 to 48 g As/L, or 120 mg As/kg in the diet, or tissue residues of 1.3 to 5 mg As/kg fresh weight; (9) sensitive species of birds died following single oral doses of 17.4 to 47.6 mg As/kg body weight; and (10) adverse effects were noted in mammals at single oral doses of 2.5 to 33 mg As/kg body weight, and at feeding levels of 50 mg, and sometimes only 5 mg, As/kg in the diet (Eisler 1994:214215). In man, the smallest recorded fatal dose of inorganic arsenic is in the range of 70180 mg, but recovery has been reported after much larger doses. Common acute symptoms include: nausea, vomiting, abdominal pain, rice-water diarrhoea, progressive general weakness, and severe dehydration leading to collapse and heart failure. If the patient survives, hepatic and renal impairment and central nervous and peripheral nervous system damage may become evident (WHO 1992:16). With long-term exposure of inorganic arsenic, significant toxic effects in humans can be expected to occur above a daily oral intake of 100-200 g. Tolerance to arsenic can develop after repeated exposure. The chronic signs of toxicity are insidious and may be difficult to diagnose. They are chiefly related to the skin, gastrointestinal tract, respiratory tract and nervous system, but also to the mucous membranes, blood, heart and liver. Inorganic arsenic is a proven human carcinogen (skin cancer, bladder cancer and other internal cancers) after long-term oral intake, as well as after inhalation. Arsenic is a unique carcinogen. It is the only known human carcinogen for which there is adequate evidence of carcinogenic risk by both inhalation and ingestion. Oral exposure of arsenic to human beings is usually not the result of anthropogenic activity as it is with many carcinogens, but the result of natural contamination of well-water supplies by arsenic-rich geologic strata. Furthermore, the evidence for carcinogenity of arsenic is very strong in humans, but weak in animals, a different scenario 18

found with most carcinogens. A daily lifetime intake of 0.4 mg inorganic arsenic via drinking water has been found to correspond to a 5 % prevalence of skin cancer. Correlations, between elevated atmospheric arsenic levels and mortalities from cancer, bronchitis, and pneumonia were established in an epidemiological study in England and Wales, where death from respiratory cancer increased at air concentrations > 3g As/m3 (WHO 1992:1618, 25; WHO 1986:44, 46, 50, 53; Abernathy et al. 1997; North et al. 1997:410, 41417; Eisler 1994:186; Guha Mazumber et al. 1997:112123). In general, the toxic action of arsenic in experimental animals resembles that seen in man. However, animals are in general not as sensitive to arsenic as humans, which can be partially attributed to differences in gastrointestinal absorption. The oral LD50 of arsenic ranges from 15 to 293 mg/kg body weight in rats, and from 11 to 150 mg/kg body weight in other animals. Inorganic arsenic is in general considerably more toxic than organic arsenic compounds which are the dominant species found in seafood. And trivalent arsenics are, in general, more toxic than pentavalent arsenic. However, the relative difference in toxicity between the two inorganic forms is reasonably small (2- to 3-fold). Different forms of arsenic may be interconverted, both in the environment and in the vertebrate body (WHO 1992:1516; Naqvi et al. 1994:5758). There are increasing evidence that arsenic may be essential, at least for some species. Low doses (< 2 g/day) have been found to stimulate the growth and metamorphosis in tadpoles and increased viability and cocoon yield in silkworm caterpillars. Arsenic deficiency has been observed in rats, goats and pigs, the latter fed on a diet containing less than 0.05 mg As/kg. In these animals, reproductive performance was impaired, neonatal mortality was increased, birth weight was lower and weight gain in second-generation animals was decreased. Several biochemical changes accompanying the signs of arsenic deficiency have been described, but the fundamental mode and site of action of the element are not yet known. Extrapolation from animal experiments suggest that human adult intakes in the range 1215 g/day are probable adequate to meet any possible requirement. A substantial number of organic arsenicals, most of them derivatives of phenylarsonic acid, are used as feed additives in poultry and swine production. Inorganic selenium and inorganic arsenic are antagonistic in several animal species. In rats, dogs, swine, cattle and poultry, the arsenic protects against selenium poisoning if arsenic is administrated in the drinking water and the selenium in the diet. However, the toxicity of naturally methylated selenium compounds is markedly enhanced by inorganic arsenic (WHO 1996:218; Eisler 1994:194). For most aquatic animal species, the acute toxicity of inorganic arsenic compounds is moderate to low (LC50 10100 mg/litre). However, long-term exposure of immature fish populations to sublethal doses may result in toxic effects at about 4 mg/litre, and exposure of Daphnia may lead to slightly impaired reproduction at 0.5 mg/litre. In aquatic ecosystems, algal communities seem to suffer most from exposure to arsenic. The growth of some species of unicellular algae is inhibited at arsenate concentrations as low as 75 g/litre. Communities of some species of marine algae (seaweed) may be eliminated at exposures of about 10 g/litre. The growth of some marine phytoplankton is inhibited by concentrations of arsenate at, or little above, ambient levels when phosphate concentration is low (WHO 1992:14; WHO 1986:31). Arsenic is also toxic to terrestrial plants. Although arsenic is commonly not regarded as an essential element for plants, small yield increases have sometimes been observed at low soilarsenic levels, especially for tolerant crops such as potatoes, corn, rye and wheat. Arsenic is chemically similar to phosphorus, an essential plant nutrient; it behaves very much like phosphate in the plantsoil system. Arsenate can enter into reactions in place of phosphorus, thereby becoming a toxicant. Their is strong evidence that arsenate is normally absorbed in a manner similar to the phosphate uptake mechanism (Bhumbla & Keefer 1994:73; Eisler 1994:195). The relationship between soil arsenic and growth of plants depends on the form and availability of the arsenic. The toxicity of arsenic to plants varies (as i does for animals an 19

humans) with its form and valence, its toxic order being AsH3 > As3+ > As5+ > organic As. Phytotoxicity studies have shown that 1 ppm soluble arsenic causes injury to cowpeas, 2 ppm causes injury to barley, 7 ppm causes injury to rice and 9 ppm to peas, and beans. The yield of oat was found to be reduced when 20 ppm arsenic in soil was applied (Huang YanChu 1994:36-38, 40). Plants growing on mine or smelter waste have developed resistance to arsenic toxicity. For instance, Cynodon dactylon was found to grew on a mine waste with 1 980 mg As/kg present. Plants growing on contaminated soils sometimes have concentrations of arsenic (6 000 mg/kg has been found) that may be toxic to animals eating the plants (WHO 1992:13; Bhumbla & Keefer 1994:73). Environmental contamination with arsenic emitted from coal burning power stations has been reported from several countries, including Slovakia, China and India. The implications of these arsenic emissions to human health have still to be fully assessed. One example of ecological effects from burning arsenic-rich coal is the mass extinction of honeybees that took place within 30 km of a power plant in Slovakia when local coal containing 900 to 1 500 mg/kg of arsenic was burned. In a province in China endemic arsenosis caused by burning arsenic-rich coal has been reported (Thornton & Farago 1997:12; Bencko 1997:85).

20

3. Cadmium

(Cd)

3.1 General information

Cadmium is a metal that belongs, together with zinc and mercury, to group IIb in the Periodic Table. It is a relatively rare element (being 67th in order of element abundance) and is not found in the pure state in the nature. Cadmium minerals (principally greenockite, CdS) do not occur in concentrations and quantities sufficient to justify mining them in their own right. Cadmium is mainly associated with sulphide ores of zinc, lead and copper. Residual levels of cadmium in lead refining are much lower than in zinc, and still lower in copper refining. It is not possible to produce refined zinc metal without generating cadmium as a by product (WHO 1992a:36; OECD 1994:35; Alloway 1995b:122). Cadmium can form a number of salts but there are no evidence that organocadmium compounds occur in nature (WHO 1992b:16). Cadmium has a relatively high vapour pressure and volatilises at a comparatively low temperature. Its vapour is oxidized rapidly in air to produce cadmium oxide. When reactive gases or vapour, such as carbon dioxide, water vapour, sulphur dioxide, sulphur trioxide or hydrogen chloride are present, cadmium vapour reacts to form cadmium carbonate, hydroxide, sulphite, sulphate or chloride, respectively. These compounds may be formed in stacks and emitted to the environment (WHO 1992a:24). Cadmium is highly toxic to plants and animals and is normally counted as a non-essential metal for biological functions, even though it can probably be essential for certain mushrooms, according to recent findings. There are also studies on rats and goats that indicate that to low intake of cadmium have negative effects on the growth. However, further evidence, accompanied by adequate statistical verification of the data, is needed before cadmium according to WHO can be regarded as physiologically essential (Landner & Lindestrm 1998:98; WHO 1992a:36; Alloway 1995b:122; WHO 1996:210211). The mobility of cadmium in the environment and the effects on the ecosystem depends to a large extent on the nature of its compounds. Further, the speciation of cadmium in soil, plants animal tissues, and foodstuffs may be of importance for the evaluation of the health hazards associated with areas of cadmium contamination or high cadmium intake. However, very few data on the occurrence and speciation of cadmium compounds in nature are available (WHO 1992a:24-25). Relative differences in the uptake of metal ions between plant and cultivars are controlled genetically and by various factors, including surface area of the root, root CEC (cation exchange capacity), root exudates and the rate of evatranspiration. The transfer coefficient (the metal conc. in plant tissue above ground divided by the total metal concentration in the soil) differs between metals. It is in general considerable higher for cadmium and zinc, 110, than for arsenic, mercury and lead 0.010.1. However, since a numerous soil and plant factors can affect the accumulation of metals in plants the transfer figures are not precise values but can indicate accumulation differences (Alloway 1995:27). The cadmium content of crops is depending on farming practices and can be reduced by liming and maintaining a high organic matter content in the soil, and by reducing the input of cadmium into soils via phosphorus fertilizer, sewage sludge and atmospheric deposition (Tahvonen & Kumpulainen 1993:253). However, there are reasons to be cautious with liming. One Swedish study has demonstrated that liming more than what is generally recommended may increase the cadmium uptake (Andersson & Simn 1991). Several studies have reported that the concentration of cadmium in soils and crops have increased during the last century as an effect of atmospheric cadmium deposition and input 21

via phosphate fertilizers. With the estimated half-life for cadmium in soils varying between 15 and 1 100 years this is obviously a longterm problem and pollution needs to be prevented or minimised wherever possible (WHO 1992a:49; KemI 1995:22; Alloway 1995b:122). The pattern of cadmium consumption has changed in recent years with significant decreases in electroplating and increases in batteries and specialized electronic uses. Between 1981 and 1989 the production and consumption of refined cadmium metal in the western world (not Central and Eastern European countries) showed a general increase. However, during the first years of 1990s it decreased slightly (WHO 1992a:17, OECD 1994:23).

3.2 Use
Unlike lead, mercury and copper, which have been utilised for centuries, cadmium has only been widely used this century. Cadmium has a limited number of applications but within this range the metal is used in a large variety of consumer and industrial materials. The principal applications of cadmium fall into five categories: protective plating on steel; stabilizers for poly vinyl chloride (PVC); pigments in plastics and glasses; electrode material in nickel cadmium batteries; and as a component of various alloys. The production of rechargeable nickel-cadmium batteries accounted for about 60 % of the consumption of cadmium in the beginning of 1990s. The patterns of use vary considerably from country to country, among other things due to restrictions in use (WHO 1992a:38; OECD 1994:15; Alloway 1995b:122). In 1990 the estimated use of cadmium for different applications in the Western world was: Ni-Cd batteries 55 %, pigments 20 %, stabilizers 10 %, coatings 8 %, alloys 3 %, and miscellaneous uses 4 % (OECD 1994:25-32). Although the amount of cadmium used in batteries is much greater than that used in pigments, stabilizers and plating, the latter uses cause the major part of the cadmium flow to waste deposits at present due to differences in product life span, degree of recycling etc. (OECD 1994:35).

3.3 Production
The world production of cadmium was in 1997 19 800 tonnes. The world production has been about the same during the last ten years and was in 1985 about 19 000 tonnes. Estimated world resources of cadmium are about six million tonnes (Knight-Ridder financial/commodity research bureau 1996:16; Chapman et al. 1999:43). Commercial cadmium production started at the beginning of this century (WHO 1992a:17). The most abundant sources of cadmium are the ZnS minerals sphalerite and wurtzite and secondary minerals, such as ZnCO3 (smithsonite) which typically contain 0.20.4 % cadmium although concentrations of up to 5 % cadmium can be found Alloway 1995b:123). Cadmium is a by-product of zinc production and the amount produced is more dependent on zinc refining than on market demand. As a result, the level of cadmium output has closely followed the pattern of zinc production. The percentage of cadmium in zinc concentrates varies from mine to mine, ranging from 0.07 to 0.83 per cent with an average of 0.23 per cent. Since the average zinc content of these concentrates is 55 per cent, approximately 3 kg of cadmium will be produced for every tonnes of refined zinc (WHO 1992a:38; OECD 1994:15, 23). The production in the western world (Central and Eastern Europe excluded) in 1993 was about 15 000 tonnes. Over 10 % of the production is from secondary production i.e. recovery and recycling. Cadmium recycling has been practical only from nickel-cadmium batteries, some alloys, and dust from electric arc furnaces operated by the steel industry. Cadmium can in these cases be separated from other materials in a comparatively uncomplicated fashion, with fairly low expenditure. However, cadmium in the form of compounds that are present at low concentrations constrains the recycling of cadmium. The production in countries with economies in transition was estimated to be around 4 500 tonnes in 1990, but fell to 3 000 22

tonnes more recently with more than half produced in countries that were formerly part of the Soviet Union (OECD 1994:2327, WHO 1992a:17; Knight-Ridder financial/commodity research bureau 1996:16).

3.4 Emission and deposition

Volcanic activity is a major natural source of cadmium release to the atmosphere. The global yearly flux from this source has been estimated to 820 tonnes. Deep-sea volcanisms contribute to the flux of cadmium to the sea but it is difficult to estimate to what extent. In the first half of the 1980s about 1015 % of total airborne cadmium emissions arise from natural processes, the major source being volcanic action. Weathering results in a global riverine transport of cadmium to the sea in an estimated order of 15 000 tonnes/year (WHO 1992a:3640; OECD 1994:33). The atmospheric deposition of cadmium to fresh and marine waters represents a major input of cadmium at the global level (WHO 1992a:43). Cadmium is released to the air, land and water by human activities. In general, the two major sources of contamination are the production and consumption of cadmium and other nonferrous metals and the disposal of wastes containing cadmium (WHO 1992a:17). The global anthropogenic emissions of cadmium to air was for the year 1983 estimated to lie in the range of 3 100 to 12 000 tonnes (Nriagu & Pacyna 1988). The replacement of thermal melting by electrolyte refining as method of zinc production has considerable reduced the cadmium emission to air. Emissions of cadmium to air also arise from, iron production, fossil fuel combustion, cement manufacture, and incineration of waste. (WHO 1992a:4041). The production of iron and steel may contribute to significant cadmium emissions. Although the concentration of cadmium is low in both secondary and primary steel-making the volumes of materials handled are very high. The cadmium content of coal varies from 1 g/g (lignite) to 2 g/g. However, also in this case it is a question of huge quantities. Most of the cadmium from combustion of fossil fuels will be found in the fly ash and will be captured by emission control devices (OECD 1994:36). Non-ferrous metal mines represent a major source of cadmium release to the aquatic environment. Cadmium release are not restricted to active mine sites, and mines disused for many years can still be responsible for continuing water contamination. At the global level, the smelting of non-ferrous metal ores has been estimated to be the largest human source of cadmium release to the aquatic environment (WHO 1992a:42). Although the contribution of emissions from point sources in Europe are of importance, cadmium emissions comes mainly from diffuse sources. Point sources are generally less important than for other heavy metals. A European map of the cadmium concentrations in mosses during the early 1990s shows however, that the concentration varies considerably over Europe and is elevated around point sources (EEA 1998:112114; EEA 1995:45, 159). Worldwide, between 15 000 and 17 000 tonnes of cadmium per year is transformed into products belongings. The products have a potential of releasing cadmium to the environment. The significance of releases during manufacture is dependent upon the processes utilized and the emission control techniques. Releases from these processes may mainly occur to both air and water, but solid manufacturing wastes may also be generated (OECD 1994:34). Solid wastes from variety of human activities (e.g. ashes from fossil fuel combustion, waste from cement manufacture, municipal refuse, sewage sludge, solid wastes from non-ferrous production and from the manufacture of cadmium-containing articles and, ashes from refuse incineration) resulting in large cadmium inputs at the national and regional levels. The three latest mentioned sources probably constitute the greatest risk (WHO 1992a:43). Phosphate fertilizers and atmospheric deposition are significant sources of cadmium input to arable soils in some parts of the world; sewage sludge can also be an important source at the 23

local level. Plants take up cadmium and cadmium is removed by harvest. Cadmium is a natural constituent of rock phosphates and deposits from some regions of the world contain markedly elevated levels of the metal. Continuous application of phosphate fertilizers has been shown to cause increased soil cadmium concentrations. The total input of cadmium in European arable land has during several decades in general been significantly larger than the output. Thus, the concentration of cadmium in the arable soils has increased. Also the concentration of cadmium in crops has increased during the same period (WHO 1992a:18, 42, 44; Statistiska centralbyrn 1995:31). The cadmium input to agriculture soil from P fertilizers has in UK been estimated to 4.3 g/ha/y and in the former West Germany to 3.5 g/ha/y. In the EU, fertilizer inputs are estimated to be around 300 tonnes cadmium per year (Alloway 1995b:127). Animal manure has a very heterogeneous composition. The concentration of cadmium in sewage sludge varies considerably. However there are examples where the use of sewage sludge has lead to inputs as high as 80 grams of cadmium/hectare. At normal rates of application of animal manure, up to 3 grams of cadmium per hectare may be added per year. Some cadmium will be subject to recirculation on the farm, although additional cadmium can be introduced through imported feeding stuffs (OECD 1994:36-38; Alloway 1995b:128). According to the European Environment Agency, the air emissions of cadmium was in Europe about 12 000 tonnes in 1965 and less than 3 000 tonnes in 1991 (EEA 1998:112). However, according to Eurostat the total air emissions of cadmium in 38 European countries was in 1990 only 613 tonnes. In EU-15 the air emission was about 200 tonnes 1990 of which more than half came from Italy, Spain, and Germany (Eurostat 1998:78; UN/ECE 2000). The cadmium emissions from 12 EU-countries (no figures available for Greece, Ireland and Spain) has decreased by 40-50 % from 1990 to the mid 1990-ties (UN/ECE/ 2000). The air emissions of cadmium are expected to continue to decrease (EEA 1998:112). Cadmium is removed from the atmosphere by dry and wet deposition. Annual deposition rates in rural areas in Scandinavia ranged from 0.4 to 0.9 g/ha during the 70s. It was estimated that 3 g/ha/year was a representative value of the deposition of cadmium to agricultural soils in rural areas of the EEC around 1980. This could be compared with a corresponding estimated input of 5 g/ha per year for these areas from the application of phosphate fertilizers (WHO 1992a:46). At present, it is not possible to determine whether human activities have caused a historic increase in cadmium levels in the polar ice caps. However, samples from the Arctic contain on average more than ten times higher value (5 pg/g respectively 0.3 pg/g) possible indicating an suspected greater anthropogenic influence in the Arctic compared to Antarctic (WHO 1992a:17, 37).

3.5 Concentrations (in nature and human)

Cadmium is widely distributed in the earths crust at average concentration of about 0.1 0.2 mg/kg. However, higher levels may accumulate in sedimentary rocks, and marine phosphates often contain about 15 mg cadmium /kg. Cadmium is strongly associated to zinc minerals. High soil concentrations are more commonly found in areas containing deposits of zinc, lead and copper ores. Some black shale also contains elevated cadmium levels leading to high soil cadmium concentrations. Naturally elevated concentrations of over 22 mg/kg have been found in soils from shales in California and in the Pennine Hills, UK (WHO 1992a:36; OECD 1994:33). Typically concentrations of cadmium in soils range between 0.1 and 0.4 mg/kg, while fresh water contains < 0.010.06 ng/litre. The concentration of lead, cadmium and mercury in the humus layer of forest soils in 50 % of Sweden has increased by a factor between three and ten since the pre-industrial era; concentrations fall from south to north. However, for some 24

Swedish forest podzol soils the cadmium balance is now negative in the upper organic rich layer (the cadmium concentration is decreasing). The average cadmium content of seawater is about 5-20 ng/litre in open seas, while concentrations in European unpolluted rivers roughly varied from 20 to 100 ng/litre. Average cadmium concentrations for the period 1991 to 1993 were about 50 times higher in polluted European rivers than in clean rivers. However, in general the concentrations in European rivers have decreased since 1985. Cadmium levels of up to 5 mg/kg have been reported in river and lake sediments, and from 0.03 to 1 mg/kg in marine sediments. Atmospheric concentrations in remote areas are typically in the range of 0.010.04 ng/m3, while the concentrations in European rural areas vary from 0.1 to 0.5 ng/m3 according to measurements reported in 1992 (WHO 1992a:36-37; OECD 1994:3334; EEA 1998:112, 114115; Bergbck & Johansson 1996:46-48). Phosphate fertilizers are widely regarded as being the most ubiquitous source of cadmium contamination of agricultural soils. It has been estimated that for individual western countries the relative contribution from the major anthropogenic sources was for phosphate fertilizers 5458 %, atmospheric deposition 3941 %, and sewage sludge 25 % (Alloway 1995b:131). A survey of agricultural soils in the USA comprising 3 045 samples representing 307 different soil series collected from sites remote from obvious sources of metal contamination gave a mean topsoil cadmium concentration of 0.265 mg/kg, a median of 0.2 mg/kg and a range of <0.0012.0 mg/kg. In a Swedish study comprising 3 067 samples from Swedish agricultural top soils the mean value was 0.23 mg/kg and the median value was 0.20 mg/kg (Naturvrdsverket 1997:20). The input of cadmium to agricultural soils are in generally higher than the loss by harvesting etc. In Sweden, where the input of cadmium compared to most other European countries is low, the cadmium concentration is increasing by about 0.1 % per year in 1997 (Alloway 1995b:139140; Naturvrdsverket 1997:6). The cadmium content of phosphate fertilizers varies widely and depends on the origin of the rock phosphate. It has been estimated that fertilizers of West African origin contain 4590 ppm of cadmium, while those derived from the USA contain 5100 ppm. Cd/P2O5 ratios vary from 1 to 5 for Kola or Palabora rocks to over 200 for Naru, Senegal or the state of Idaho in the US. The cadmium content of animal manure varies from 0.3 to 1.8 mg/kg of dry matter. However, as mentioned above some cadmium will be subject to recirculation on the farm (OECD 1994:3637; Alloway 1995b:126128). Human urinary excretion of cadmium is related to body burden, recent exposure and renal damage. The level of cadmium in faeces is a good indicator of recent daily intake from food in the absence of inhalation exposure. There are at least two compartments in blood, one related to recent exposure with a half-time of about 23 months, and one which is probably related to body burden with half-time of several years (WHO 1992a:19-20). Smokers have about 45 times higher blood cadmium concentrations (about 1.5 g/l), and twice as high kidney cortex cadmium concentrations (about 2030 g/g wet weight) as non-smokers (Jrup et al. 1998:7). In general, cadmium concentrations in terrestrial and aquatic biota from uncontaminated localities are low. However, in certain situations, cadmium displays a propensity for marked bioaccumulation. Shellfish (e.g. crab and lobster), filter feeding molluscs and fungi can accumulate cadmium and show sometimes considerable high levels. Phytoplankton in areas of oceanic upwelling contains raised cadmium levels. Oysters are well known cadmium accumulators, 8 mg/ kg wet weight have been recorded. It can be concluded that marine organisms generally contain higher cadmium residues than their freshwater and terrestrial counterparts (WHO 1992a:18, 49; WHO 1992b:30). Bioconcentrations factors (the ratio between the cadmium concentrations in the organism and the concentration in the medium) have been studied for several organisms. The result range from 16 (Water hyacinth) to 130 000 (Red maple roots) and do not seam to show any consistent pattern. However, microorganisms generally exhibit a high capacity to take up cadmium from water and retain the metal in their cells. Cadmium concentrations are generally 25

higher in older organisms. Invertebrates it is especially accumulated in the liver and kidneys. Due to the lack of concentration data on nutrient such as calcium or, zinc it is not possible to calculate any purification factors for the studies examined in the 1992 WHO report (WHO 1992b:30, 52-58). Concentrations of cadmium have been measured in mussels, fish and sediments from sites located in both clean and contaminated areas in Europe. Cadmium concentrations in mussels ranged from 10 to 1 700 g/kg wet weight. Concentrations up to about 300 g/kg can occur even far from known discharge points. Concentrations in fish ranged from very low, up to 15 g/kg wet weight in the Gulf of Finland, the Gulf of Bothnia and the open waters of Central Mediterranean, to 560 g in samples from the Greek coast. Concentrations in sediments varied between 10 and 9 000 g/kg dry weight. Excluding some samples collected very close to point sources, the highest concentrations were measured near the mouth of the Rhine. Generally, concentrations below 200 g/kg can be considered as background levels (EEA 1998:215219). Meat, fish and fruit generally contain similar cadmium levels and values of 510 g/kg fresh weight are representative for these food classes. Most plantbased foodstuffs contain higher cadmium concentrations and a value of 25 g/kg fresh weight is considered representative for the staple items, cereals and root vegetables. Although, cadmium residues in plants are normally less than 1 mg/kg, plants growing in soils amended with cadmium (e.g. from sewage sludge) may contain significantly higher levels (WHO 1992a:56; WHO 1992b:31). A great deal (35-65 % of heavy metals is in the outer layer of the seed, e.g. in the germ and bran, and can be removed from the caryopsis by certain methods of cereal technology. Whole grain flours contain higher cadmium levels than lower extraction flours (Tahvonen & Kumpulainen 1993:251). High content of Cadmium have been found in wheat and products made of wheat for instance pasta. Finland: pasta 117 g/kg (mean), 182 g/g (max) in 1990, 104 g/kg (mean) 145 g/kg (max) in 1991. High values in durum wheat have also been found in Italy (Tahvonen & Kumpulainen 1993:251). In early 1990s the production of dry sludge from wastewater was about 6.3 million tonnes in the whole European community (Alloway 1995a:45). High maximum levels of cadmium have been measured in sewage sludge. Levels of cadmium in dry sludge reported in the literature range from less than 1 mg/kg to about 3 400 mg/kg. In UK the median cadmium value of sludge used in 1990/91 was 3.2 mg/kg (Alloway 1995a:46; Alloway 1995b:129).

3.6 Limit values

The present PTWI (provisional tolerable weekly intake) for cadmium recommended by JEFCA (Joint Expert Committee on Food Additives) is 7 g/kg body weight. For a 65kg man this corresponds to a dietary intake of 65 g/day. The PTWI does not include a safety factor and there is only a relatively small safety margin between exposure in the normal diet and exposure that produces deleterious effects (WHO 1996:206; Tahvonen 1995:15; FAO/WHO 1993). At an average daily intake of 70 g/day, corresponding to the present PTWI, 7 % of the adult general population would be expected to develop cadmium-induced kidney lesions. For highrisk groups the percentage would be even higher (up to 17 %). This has made a Swedish group of cadmium-health experts to claim that the current PTWI value is unacceptable and needs to be lowered (Jrup et al. 1998:8). The WHO air quality guideline for cadmium is (1999) 5 ng/m3 (year average). The WHO guideline for drinking water is 3 g/l (WHO 1996:206). The EU has (1998) adopted 5 g/litre as limit value for cadmium in drinking water. The limit values should be met within five years (European Union 1998). The limit value for cereals is on EU-level 0.1 mg/kg except for

26

wheat, bran, germs and rice for which it is 0.2 mg/kg. The limit values for vegetables and fruits on the EU-level vary between 0.05 and 0.2 mg Cd/kg (European Communities 2001). The maximal allowable cadmium concentrations in sewage sludge in some countries listed by Alloway was in 1995: Denmark 0.8 mg/kg, Finland 1.5 mg/kg, and Sweden 2.0 mg/kg, while USA (1993) allowed 8.5 mg cadmium/kg. The great differences of the accepted values depend on different risk management approaches. While the Nordic countries are unwilling to accept an increase of the cadmium concentration in the arable soil in the long run, the US EPA has made an analysis of the extra risk the input of sewage sludge cadmium constitute taking into account how much additional cadmium in the soils that will be bioavailable to plants (Alloway 1995b:130).

3.7 Risk assessments, exposure and harmful effects

Of all toxic metals released in large quantities into the environment, cadmium is generally regarded as the one most likely to accumulate in the human food chain (Tahvonen 1995:13). It has been shown repeatedly that an increase in soils cadmium result in an increased plant uptake of the metal. It is this basic relationship that makes the soil-crop pathway of human exposure susceptible to increased levels of soil cadmium (WHO 1992a:47-48). A study comprising 30 countries in different parts of the world showed a good correlation between the extractable content of cadmium in soil and the cadmium content in plants. The level of cadmium in cultivated soils and the concentration of cadmium in plants varied a lot between countries and areas in a country. The sample with the highest cadmium content in plants exceeded the lowest about 1 500-times (6 037 g/kg respectively 4 g/kg, median value 61 g/kg) while the extractable soil cadmium maximum value was 125 times higher than the lowest value (FAO 1992:15). The most important factors influencing plant cadmium accumulation are soil pH and cadmium concentration. Increases in soil cadmium content result in an increase in the uptake of cadmium by plants: the pathway of human exposure from agricultural crops is thus susceptible to increase in soil cadmium. Cadmium is rather immobile in soil. However, a decreased soil pH increases the availability of cadmium in the soil, since it affects all adsorption mechanisms and the speciation of metals in the soil solution. Acidification of soils and lakes may result in enhanced mobilization of cadmium from soils and sediments and lead to increased levels in surface and ground water. An other important factor that influences the uptake is the redox conditions. The uptake decreases with increased content of organic matter, clay, and the hydrous oxides of manganese and iron. Zinc has been found to have an antagonistic effect on cadmium uptake in soils with low cadmium concentrations (WHO 1992a:17, 43, 48; OECD 1994:17, Alloway 1995b:137-139). Plant species differ widely in their ability to absorb, accumulate and tolerate cadmium. Leafy crops are capable of accumulating cadmium to relatively high levels. The cadmium concentrations in plants can arise from the uptake from soils and direct deposition on leaves. In general, cadmium concentrations are lower in seed, tuber and fruit tissues relative to leafy tissue. Cadmium are together with Zn and some other elements recognised as being the trace elements which are readily translocated to plant tops after absorption through roots. However, for some species are the concentrations of cadmium higher in root than in other organs (OECD 1994:17, Alloway 1995b:139140). Cadmium entering fresh water is rapidly adsorbed on particulate matter. Although sediment is the ultimate sink for cadmium, natural or man-induced changes in the physio-chemical conditions in water can result in remobilisation of cadmium (OECD 1994:16). Concern over the long-term implications of cadmium inputs to European arable soils has led to modelling studies of the future cadmium exposure for the general population. It was estimated that the atmospheric deposition and input via fertilizers at the level of 1980 would result in an annual increase of the concentration in the Danish arable soil of about 0.6 %/year. 27

The corresponding increase in crop cadmium concentrations would lead to about a 70 % increase in the Danish dietary cadmium intake 100 years hence. Similar soils and dietary cadmium increases have been predicted for the EEC as a whole (WHO 1992a:49). The major route of exposure for the non-smoking general population is via food; the contribution from other sources is comparatively small. Food and drinking water amounts to about 80 % of the total intake for non-smokers (WHO 1992a:23; WHO 1996:195). The cadmium content of food depends upon the food type, the major sources of dietary intake being leafy vegetables, grains and cereals (OECD 1994:17). Cereals and vegetables normally account for about 50 % of the cadmium intake (WHO 1996:199). Average daily intake from food in most areas not polluted with cadmium is for adults between 1040 g. In polluted areas it has been found to be several hundred g per day. A survey of dietary intakes of cadmium in 24 countries indicated that adult intakes varied from 0.9 to 7 g/kg per week. The corresponding range for infants or children from 10 countries was 1.9 9.9 g/kg per week. Tobacco is an important source of cadmium uptake in smokers. Occupational exposure to cadmium is mainly by inhalation but includes additional intakes through food and tobacco (WHO 1992a:23; WHO 1996:206). The absorption of cadmium in the lungs is 10 50 % depending on chemical speciation, particle size, and solubility in biological fluids, while the absorption in the gastrointestinal tract is only a few per cent (Jrup et al. 1998:7). The gastrointestinal absorption shows large individual variations depending on the type of diet and nutritional status. Diets low in calcium promote significant increases in the absorption and retention of both cadmium and lead. There are clear indications that iron deficiency promotes cadmium retention and may thus decrease the tolerance of high environmental or dietary cadmium concentrations (WHO 1992a:18; WHO 1996:40). Cadmium absorbed from the lungs or the gastrointestinal tract is mainly stored in the liver and kidneys, where more than half of the body burden will be deposited. Excretion is normally slow, and the biological half-time is very long (decades) in the muscles, kidneys, liver, and whole body of humans (WHO 1992a:19). The blood cadmium concentrations are substantially elevated in persons with low body iron stores, indicating increased gastrointestinal absorption. About 1040 % of Swedish women of childbearing age are reported to have empty iron stores (S-ferritin < 12 g/l). The population groups at highest risk are probably smokers, women with low body iron stores, and people habitually eating a diet rich in cadmium (Jrup et al. 1998:7). High inhalation exposure to cadmium oxide fume results in acute pneumonitis with pulmonary oedema, which may be lethal. High ingestion exposure of soluble cadmium salts causes acute gastro-enteritis (WHO 1992a:21). The accumulation of cadmium in the renal cortex leads to renal tubular dysfunction with impaired reabsorption of, for instance, proteins, glucose, and amino acids. A characteristic sign of tubular dysfunction is an increased excretion of low molecular weight proteins in urine (WHO 1992a:21). Renal tubular damage is probably the critical health effect of cadmium exposure, both in the general population and in occupationally exposed workers. Both human and animal studies indicate that skeletal damage (osteoporosis) may be a critical effect of cadmium exposure. However, the present evidence is not sufficient to make such a conclusion for humans. The International Agency for Research on Cancer (IARC) decided in 1993 to classify cadmium as a human carcinogen (category I). Recent evaluation of old data and new data indicate that a classification of cadmium as a probable human carcinogen, group 2A would be more appropriate (Jrup et al. 1998:7). Data from several recent reports from different countries indicate that an average urinary cadmium excretion of 2.5 g/g creatinine is related to an excess prevalence of renal tubular damage of 4 %. An average urinary excretion 2.5 g/g creatinine corresponds to an average 28

concentration of cadmium in renal cortex of 50 g/g, which would be the result of long-term (decades) intake of 50 g per day (Jrup et al. 1998:7). It is important to bear in mind that even if the population average kidney concentration is relatively low for the general population, a certain proportion may have values exceeding the value where renal tubular damage can occur. It has been estimated that, at present average daily intake of cadmium in Sweden, about 1 % of women with low body iron stores and smokers may experience adverse renal effects related to cadmium. If the average daily intake of cadmium would increase to 30 g/day, about 1 % of the entire population would have cadmium-induced tubular damage. For women with low iron stores up to 5 % would have tubular damage. Some population groups in Europe already exceed this intake and the margin is very narrow for large groups (Jrup et al. 1998:78). Cadmium is toxic to a wide range of microorganisms. However, the presence of sediment, organic matter or high concentrations of dissolved salts reduces the availability of cadmium to microorganisms and, therefore, reduces the toxic impact. The growth of freshwater algaes are affected at 50 g/litre, while at least 100 g/litre and often 1 000 g/litre, is required to reduce growth in marine species. The available results indicate that the embryonic and larval stages of aquatic organisms are more sensitive than the adult stage. The lowest recorded 96-h LC50 in a flow system is 16 g cadmium/litre for the adult shrimp Mysidopsis bahia. A nominal no-observed effect level (NOEL) of 0.6 g cadmium/litre was found for Daphnia magna, reproductive rate being the most sensitive parameter. A nominal NOEL has been noted at a similar level (1.7 to 3.4 g cadmium per litre) with respect to the reproductive effects on brook trout (WHO 1992b:59, 66, 95). Field studies in Sweden showed that perch from a cadmium-contaminated river (0.1 to 0.2 g cadmium/litre) had physiological abnormalities similar to those shown in laboratory experiments (WHO 1992b:112). Certain marine birds and mammals contain markedly elevated kidney and liver cadmium concentrations. Although this high cadmium concentration is considered to be of natural origin, they have been linked to signs of kidney damage in pelagic seabirds. The birds appear to cope with this damage to the kidney and suffer no effects on survival or breeding success. Also certain long-lived terrestrial mammals such as horse and moose show considerable cadmium accumulation in the kidney and liver (WHO 1992a:18, 50; WHO 1992b:113). Cadmium has adverse effects on hydroponically grown plants at concentrations in the mg/litre range, whereas plants grown in soil only show reduced growth in contaminated soils with hundreds of mg cadmium/kg. Terrestrial invertebrates are relatively insensitive to cadmiuminduced toxic effect (WHO 1992b:102). In order to reduce the risks associated to cadmium, varying measures are planned and have been taken by organizations and individual countries. Among the OECD countries there exist a mostly comparable baseline including environmental quality criteria, and permissible levels, to limit emissions to air, water soil and food. Many OECD countries control the input of cadmium to the environment from contaminated products, e.g. fertilizers, sludge and manure. Measures to reduce or ban the use of cadmium in products show considerable variability between countries. In many countries, regulations or voluntary programmes are aimed at the labelling, collection and recycling of NiCd batteries (OECD 1994:18). The interaction between zinc and cadmium has been investigated particularly intensively in recent years. In lettuce and spinach, for example, cadmium concentrations were found to decrease with increased zinc concentration in the nutrient solutions in which they were grown. Several studies are reported where it was possible to reduce cadmium uptake in a crop by application of zinc to the soil. Significant reductions of the cadmium concentration in a crop (wheat and potatoes) were for instance found in experiments in Australia, where application of zinc to agricultural land in various quantities has been practised (Landner & Lindestrm 1998:138).

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4. Lead (Pb)
4.1 General information
Lead is a soft grey metal, melting at 327 C and boiling at 1 744 C. It has two oxidations states Pb2+ and Pb4+, but the environmental chemistry is dominated by the plumbous ion, Pb2+. Lead is highly resistant to corrosion, but is soluble in nitric and hot sulphuric acids. Lead sulphide and lead oxides are poorly soluble and the nitrate, chlorate and chloride salts are reasonable soluble in cold water. Lead also forms salts with such organic acids as lactic and acetic, and stable organic compounds such as tetraethyllead and tetramethyllead (WHO 1995:25; Davies 1995:206). Lead has a strong affinity for sulphur. Therefore it concentrates in S phases in rocks and the major or mineral is galena (PbS). However, primary lead from mining is often produced as a by-product with other metals such as zinc, silver copper and cadmium. Lead is believed to have been mined as early as 5000 BC and was used in ancient times in making pottery glazes, art objects, coins and water piping (Davies 1995:207; OECD 1993:11). Lead has as far as we know no necessary function in any living organism. It is commonly counted as a non-essential metal. However, there are studies that indicate that lead may have a positive effect on growth for some organism at very low levels. It is well known for being poisonous for mammals and there are fears that human body burden below those at which clinical symptoms of lead toxicity appears may cause mental impairment in young children. It has been suggested that there may be no level of exposure below which lead is harmless (Landner & Lindestrm 1998:98; Davies 1995:206; WHO 1996:209210). When lead is released into the environment it has a long residence time compared with most other pollutants. Lead and its compounds tend to accumulate in soils and sediments where, due to their low solubility and relative freedom from microbial degradation, they will remain bioavailable far into the future. There is little evidence that lead is readily lost from soil profiles by leaching and soils have a rather large capacities for immobilisation of lead. Organic matter plays in important role in the fixation of lead in soils. (OECD 1993:13; Davies 1995:213214). Plant species differ widely in their ability to absorb, accumulate and tolerate lead. In general there is a positive relationship between the concentration of lead in the soil and the plant. However, in general only a small proportion of the lead in soil is available for uptake by plants. Low pH increases the solubility of lead in soils although there are studies that reports no or low effect on the uptake. The uptake of lead in carrots, beetroots and rhubarbs has for instance been observed to not only be related to the concentration of the lead in the soil but also the pH. However, if organic matter is present, leads high affinity to organic matter makes lead immobilized. This is to a minor extent also true if iron-hydroxide is present. Thus, one should expect a higher proportion of bioavailable lead if the pH, content of organic matter and concentration of iron-hydroxide is low compared to the opposite condition. This is essentially also true for the water environment. The toxicity of lead in water depends strongly on the water condition. High water hardness, high pH, high content of dissolved humus, salts and mineral particles (e.g. clay) reduce the bioavailability. Besides the chemical conditions the uptake of lead by plants and other organisms depends on temperature, season, gender and species (Bergbck & Lindestrm 1998:65, 67, 71; WHO 1995:63; OECD 1993:74, 80; Davies 1995:217219). Although the decreased use of lead in gasoline have resulted in lower concentrations of in air, lead may still represent a pollution problem near roads with intense traffic in the countries which still have a relatively high lead content in gasoline (Jol et al. 1997:15).

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4.2 Use
OECD countries accounted for 63 per cent of the total world demand of 5 627 thousand tonnes in 1990 and the Central and Eastern European countries and Asias demand was 21 per cent and 9 per cent respectively (OECD 1993:12). The lead consumption in Europe was about 1 500 thousand tonnes in 1994 (International lead and zinc study group 1996). Lead and lead compounds are used for a wide diversity of purposes (e.g. Ponsaing & Hansen 1995b). Metallic lead has a combination of physical and chemical properties that have made it extremely useful industrially, i.e. high density, high opacity to gamma and X-ray energies, low sound conductance, a low melting point, exceptional malleability, high corrosion resistance, and stability (WHO 1995:53). Metallic lead is for instance used for, ammunition, battery, for cable sheeting, as weights, protection against radiation and in electric equipments. The use of lead compounds are in several countries restricted for instance lead in paints, in gasoline, plastic and rubber (OECD 1993:46-58; International lead and zinc study group 1996). Lead arsenate (PbHAsO4) has been applied to orchard trees to control insect pests and orchard soils may therefore contain elevated concentrations of Pb. However, commercial use of lead compounds to control insects is now infrequent since they have been replaced by organic pesticides (Davies 1995:207). The use of lead was in EU in 1994 distributed on: batteries (52 %), rolled and extruded products (15 %), pigments and other compounds (14 %), shot/ammunition (4 %), others (4 %), alloys (3 %), and gasoline additives (Eurostat 1997).

4.3 Production
Lead is produced from ores, concentrates and/or from recycling in over 50 countries. USA, Australia and Canada are the greatest producer of lead from mines while USA, Japan, Germany and Great Britain, are the greatest producer of refined lead (Bergbck & Lindestrm 1998:7). In 1997 the world mine production of lead was 3.1 million tonnes and the total production of refined (primary and secondary) lead was in 1997 6.0 million tonnes. The world smelter production (primary and secondary) was sable, about 5.4 million tonnes during 1987 to 1994. The worlds five greatest producer of mine lead was in order China, Australia, USA, Peru, and Canada contributing to about 2/3 of the global production. In 1997 the EU countries together produced 211 thousand tonnes of lead from mines of which about half was produced in Sweden. The five greatest producer of refined lead was in 1997 (in order) USA, China, UK, Germany, and Japan contributing to about half of the global production. The EU countries produced in 1997 about 1.6 million tonnes refined lead. The EU production and consumption of lead was about the same in 1994 (Chapman et al. 1999: 147149; OECD 1993:11-12; Eurostat 1997). Lead is one of the most recycled metals. In 1994 about half of the EU production of lead was based on recycling. Batteries are in EU recycled with more than 90 % efficiency. In USA the corresponding figure was 72 % (Eurostat 1997). The world total production of lead (primary and secondary) has slightly increased (about 7 %) during the last ten years. The world primary production of lead has since the beginning of 1980-ies remained on about the same level, 3 millions of tonnes annually, while the secondary produced lead has increased (Chapman et al. 1999:147149; United Nations 1995:347348; Knight-Ridder financial/commodity research bureau 1996:154).

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4.4 Emissions and deposition

The natural releases of lead principally through crustal weathering, volcanism and sea spray etc. has worldwide been estimated to 19 000 tonnes, whereas the anthropogenic emissions to air from sources related to industrial activity, power generation (coal and oil burning), and incineration of wastes has been estimated to be around 100 000 tonnes (WHO 1995:25, 48; OECD 1993:13). The total current air emissions of lead in 32 countries in Europe are about 65 % below the peak levels of 1965 and has decreased from about 100 000 tonnes in 1965 to about 35 000 tonnes in 1991. The total air emissions of lead from EU-15 has been estimated to about 19 250 tonnes in 1990 of which 4 674 came from Spain, 4 414 from France, and 2 703 from UK (Eurostat 1998:78). The air emissions of lead are expected to continue to decrease (EEA 1998:112). The emission from products are much more difficult to calculate than water and air emissions. Some emissions from products such as ammunition and gasoline lead are relatively easy to estimate while it is more complicated to estimate how much of the lead used for cables will reach the environment within a certain time. Different emissions factors have been suggested and used for different products. The emission factor specifies how large proportion of the lead in a certain type of product that is judged to be released to nature sooner or later (Bergbck & Lindestrm 1998:18). If lead-containing industrial solid wastes and post-consumer products are not recycled or reused, they are generally sent to landfills for disposal or are incinerated. However, it has been observed in some countries that the volume of lead in municipal waste is declining. For properly managed landfills with runoff and leakage controls and for incinerators with proper technology (efficiency 99 %) the health concerns are minimal (OECD 1993:13). The risk reduction efforts have in the past to a great extent been focused on the emissions from chimneys and sewage pipes. The relatively importance of the emissions from consumer products has increased (Bergbck & Lindestrm 1998:5). Even for products where there are efficient recycling systems, as for batteries in many countries, some part will never be collected and thus end up in the nature where it constitute a risk. Consequently, recycling systems are not enough reason for not phasing out lead if safe and cost-effective options exist. Alternatives exist for many lead uses/products (Ponsaing & Hansen 1995a; Ponsaing & Hansen 1995b). In specific areas point sources may be a significant source of lead to the environment, but on a global scale, is the combustion of alkyllead in petrol the dominant source to the increased lead in all compartments of the environment (WHO 1995:56). Unleaded petrol is about 2 % more expensive to produce than leaded, but some countries have introduced fiscal incentives to encourage its use. These, together with the requirement to introduce catalysts (which can not run with leaded petrol), have resulted in a fall in the road transport emissions of lead in for instance the EU-countries (EEA 1998:8889, 112). The transport and distribution of lead from fixed, mobile and natural sources are primarily via air. Most lead emissions are deposited near the source, although some particulate matter (< 2 m in diameter) is transported over long distances, thousands of kilometres (WHO 1995:26, WHO 1993:72). From measurement of heavy metals in mosses in Scandinavia it possible to identify a decreasing lead gradient with relatively high values in the south and low values in the north. The deposition pattern is a combination of local sources and long-range transport (EEA 1995:159). Air deposition of lead plays an important role in the lead polluting of coastal seas. About 35 per cent of all the lead deposited annually in the North Sea came around 1990 from air deposition. For cadmium and zinc the corresponding figures was 14 respectively 5 per cent (EEA 1995:45). The deposition of lead in rural areas in Europe and North America was in the beginning of 1990s in the range of 20-80 g/m2/day and about 1.5-10 times higher in large 32

cities. In Greenland and the Antarctic, values below 1 g/m2/day have been recorded (OECD 1993:72).

4.5 Concentrations (in nature and human)

The average level of lead in the earths crust is 10-20 mg/kg. The average lead content has been estimated to be for gabbro 1.9 mg/kg, andesite 8.3 mg/kg, sandstone 10 mg/kg, granite 22.7 mg/kg, shales and mudstones 23 mg/kg, and limestones and dolomites 71 mg/kg (WHO 1995:48; Davies 1995:207). Atmospheric deposition (wet and dry) is a major source of lead in soil and sediment General background levels of lead in soil range between 10 and 70 mg/kg although it may be higher depending on the nature of the parent material. Much of the observed lead in soils in many areas has originated from anthropogenic emissions. The concentration of lead, cadmium and mercury in the humus layer of forest soils in 50 % of Sweden has increased by a factor between three and ten since the pre-industrial era; concentrations fall from south to north. Industrialized countries and areas with high population density have in general higher soil lead values and especially high concentration of lead in soils could be found in cities, near roads, point sources and shooting-ranges (OECD 1993:13; WHO 1995:26, Wixon & Davies 1993:26-27, 33; FAO 1992:25; Davies 1995:207; EEA 1998:114). The levels of lead in soils along highways decrease rapidly with distance (OECD 1993:78). Extremely high levels of lead (mean values of thousands of mg/kg) in garden soils and agricultural soils have been found in mining/smelter villages (OECD 1993:76; Davies 1995:211-212). Atmospheric lead concentrations of 50 pg/m3 have been found in remote areas (WHO 1995:25). Lead concentrations in the air in cities in some OECD countries did in 1970s range from 0.5 g/m3 up to 10 g/m3 in densely travelled inner city areas due to lead in gasoline. However, restriction on lead in gasoline have resulted in marked decrease city air concentrations and was in the beginning of the 1990s in the range of 0.2-0.8 g/m3 in many European and North American cities (OECD 1993:13). However, lead concentrations in a few Central and Eastern European cities (e.g. Katowice, Vilnius) have slightly increased during 1990-95, due to the increase in traffic and the continuing use of leaded fuels (EEA 1998:254 255). Pre industrial levels of lead in air have been estimated to be in the range of 0.01-0.1 g/m3. In general the lead concentration decreases from rainwater, to freshwater, to seawater (OECD 1993:73). The natural concentration of lead in surface water has been estimated to be 0.02 g/l. Present levels of lead in surface water rarely exceed a few micrograms/litre. Average lead concentrations for the period 1991 to 1993 were about 11 times higher in polluted European rivers than in clean rivers. However, in general the concentrations in European rivers have decreased since 1985 (WHO 1995:26; EEA 1998:112, 115). The lead concentration in food and water varies widely. In drinking water the lead concentration is usually below 5 g/l. However, water taken from taps (faucets) in homes where lead is present in the plumbing can contain levels in excess of 100 g/litre (WHO 1995:26-27). Representative levels of lead in food are for cereals 60 g/kg, for roots, tubers, fruits, vegetables and meat 50 g/kg and for fish 100 g/kg. The presence of lead in cereal products does not seem to be a problem in most industrialized countries (Tahvonen & Kumpulainen 1994:628; WHO 1995:79). Food packed in lead soldered cans may have levels as high as 100 to 400 g/kg (OECD 1993:89). High maximum levels of lead have been measured in sewage sludge. Levels of lead in dry sludge reported in the literature range from about 30 mg/kg to about 3 600 mg/kg. A median content of 121 mg/kg has been reported from a non-industrial area. The typical concentration in human faeces is about 11 mg/kg. Extra lead comes from road run of and water pipes etc. Because of the similarity of the ionic sizes of Pb2+ and Ca2+ the former may proxy for the latter in calcite and lead may be added to the soil by liming materials. (Alloway 1995:46, 33

Davies 1995:213). However, the concentration of lead in sludge has decreases with decreased use of lead in petrol and pipes. Soils receiving heavy sludge applications over a long period were found to contain 425 mg/kg compared with 47 mg/kg in an unsludged soil (OECD 1993:78). However, the level of lead in sludge is due to recycling systems etc. in most cases decreasing. In early 1990s the production of dry sludge from wastewater was about 6.3 million tonnes in the whole European community (Alloway 1995:45). The lead concentration is in general higher in plants than in animals and higher in herbivore animals than in predators. Thus, there is no biomagnification in the lead case (Bergbck & Lindestrm 1998:68). Concentrations of lead have been measured in mussels, fish and sediments from sites located in both clean and contaminated areas in Europe. Lead concentrations in mussels varied considerably, from the extremely low value of 15 g/kg wet weight in Iceland to 1 200 g/kg at the mouth of the Rhine and up to 3 300 g/kg on the Mediterranean Spanish coast. Background levels are typically below 500 g/kg. Generally, concentrations of lead in marine biota are falling by about 5 % per year, consistent with reductions in the use of leaded petrol. Lead concentrations in sediments varied between 1 700 and 167 000 g/kg dry weight. The natural concentration of lead in sediments is generally 30 000 g/kg or lower (EEA 1998:215219).

4.6 Limit values

The WHO guideline for lead in air is since 1993 0.5 g/m3 (year average) (EEA 1998:250, 254). The EU has adopted the same value as air limit value for lead. The limit value is to be met 1 January 2005, or 1 January 2010 in the immediate vicinity of specific industrial sources (European Union 1999). The FAO/WHO Expert Committee on Food Additives and Food Contaminants has recommended a provisional tolerable weakly intake (PTWI) of 25 g/kg body weight for adults, children and infants (WHO 1995:233; WHO 1996:203). The World Health organization (WHO) has for acceptable blood lead concentration, recommended that no more than 2 % of the population should have a PbB greater than 20 g/dl (Wixon & Davies 1993:60). To protect workers from the adverse effects of lead on haem synthesis and on the peripheral and central nervous system, an exposure limit of 1.92 mol/litre (40 g/dl) was recommended by a WHO Study Group. It was further recommended that blood lead levels in women within the reproductive age range should not exceed 1.44 mol/litre (30 g/dl). Depending upon the background levels of Pb levels in blood in the workers population, air lead levels should not exceed 30-60 g/m3 (WHO 1995:233). The European community has issued directives regulating lead in products, and across different environmental media and environmental sources. In 1987 the EC limited the permitted lead content in leaded petrol to 0.15 and to 0.013 for unleaded petrol. In 1993, the EC prohibited the use of lead capsules for over-corking wine bottles (OECD 1993:22). The WHO drinking guideline for lead was in 1993 revised to 10 g/l (WHO 1995:233). The EU has (1998) adopted 10 g/litre as limit value for lead in drinking water. The limit value should be met within five years (European Union 1998). The EU lead limit value for cereals including buckwheat, legumes and pulses is 0.2 mg/kg (European Communities 2001). Based on a literature survey it was concluded that the concentration of lead has to be at least 87 g/g dry weight in soil before any effects on basic soil processes (mineralization, microbiological biomass, nitrogen fixation, etc.) at all could be observed, while effects surely appears when the concentration is 790 g/g or higher. However, recent studies made by Bringmark and Bringmark at Swedish university of agricultural science (SLU) indicate that lead may distinctly affect microbiological soil processes at lower levels than previously found. Effects were observed at levels that could be found in forest soils in the south of Sweden. Inorganic lead compounds have been observed to be in general less toxic for microorganisms and fish. De maximum acceptable concentration of inorganic lead for fish 34

has been decided for several species. It varies between 40 and 200 g/l with the lowest value referring to soft water. In another literature survey it was suggested that a concentration of 100-200 g/g should be the upper limit for lead in forest soils avoiding harmful effect on invertebrates. However, there are reports of effects on invertebrates in water concentrations between 19 and 30 g/l and on specific fish species in real soft water with lead concentration between 5-10 g/l (Bergbck & Lindestrm 1998:74-75, Bringmark & Bringmark 2001a; Bringmark & Bringmark 2001b).

4.7 Risk assessments, exposure and harmful effects

Industrialization has vastly accelerated the transport of lead into human environmental pathways. Substantial human exposure to lead can occur in all environmental media (OECD 1993:13). The contribution from natural sources of lead to human exposure is small (WHO 1995:50). Airborne lead can be deposited on soil and water, thus reaching humans through the food chain and in drinking water. Atmospheric lead is also a major source of lead in household dust (WHO 1995:26). Inhalation and ingestion (of water, food, paint, soil and dust) are the primary routes of human exposure to lead. The relatively importance of a single source of exposure vary with geographic location, climate and local chemistry (OECD 1993:14). However, the major exposure for the non-smoking and non-occupationally exposed adult population is food and water (WHO 1995:72). For infants older than about 5 month and young children dust/soil may also be a major source of exposure. The level of dietary exposure to lead depends upon many lifestyle factors including foodstuffs consumed, processing technology, use of lead solder, lead levels in water and use of lead-glazed ceramics. Up to 50 % of the inhaled lead compounds may be absorbed while about 10 % of the dietary lead may be absorbed. However, in infants and young children as much as 50 % of dietary lead may be absorbed (WHO 1995:27-28). About 90 % of the total amount of lead in humans is found in the bone tissue. The amount of lead absorbed by the body varies depending on factors such as the concentration and composition (for example particle size, chemical form), and nutritional factors. Diets low in calcium promote significant increase in the absorption and retention of both lead and cadmium. Highcalcium, highphytate diets appear to restrict lead uptake. Evidence from a variety of experiments on animals suggests that iron deficiency promotes lead uptake and retention. The evidence for humans is conflicting, but in some studies substantial increases in lead uptake are said to have occurred when dietary iron and iron status were low (OECD 1993:14; Wixon & Davies 1993:40-41; WHO 1996:40). Depending on the source, the concentration of lead and its bioavailability, the relative contribution of each source of lead exposure to humans may vary considerably (WHO 1995:66). The intensity of exposure experienced by an individual can vary for example as a function of age, sex, occupation, socio-economic status, diet and cultural practices. Lead intake from air can for example very from less than 4 g/day to more than 200 g/day depending on the air concentration (WHO 1995:27). Lead in drinking water may also constitute a considerable contribution to the overall lead exposure. The combination of acid or aggressive water and lead in plumbing results in very high concentrations of lead in drinking water, in many cases over 100 g/litre (WHO 1995:72). Bread, cereals and beverages account, typically, for about 35 % of the daily intake of lead, the remainder being derived from a variety of food types. Data from 26 countries indicated that the dietary intake of adults was in the range 264 g/kg body weight per week; for infants and children in 14 countries, the corresponding figure was 224 g/kg body weight per week (WHO 1996:199, 203). In order to illustrate the possible total amount of absorbed lead for adults and children from air, dust, food and water, a calculation has been made by using absorption factors and making 35

assumptions of lead intake from different sources. The absorbed amount of lead in these calculations ranges from about 14 g/day (with a mean air concentration of 0.3 g/m3) to about 28 g/day (with an air concentration of 2.0 g/m3). About 10 g of the absorbed lead is estimated to come from food, 2 g from water and the rest from air exposure. For children (15 years) the total amount of absorbed lead was higher and ranged from 30.6 g/day to 132 g/day, mainly due to higher absorption factors and for the higher values a considerable contribution from dust intake (WHO 1995:92). Additional intake of lead will take place in certain groups from the use of tobacco and alcoholic beverages (WHO 1995:91). In a study made on the lead content in table wines in USA about five per cent of the samples contained more than 250 g lead per litre (WHO 1995:87). The uptake of lead differs a lot between species and the accumulation of lead in different tissues differs also a lot. Most plants seams to have a root barrier that prevents lead to reach the sprout. For most species is the concentration of lead, with the origin from the soil, higher in the root than in the rest of the plant (Bergbck & Lindestrm 1998:67; Davies 1995:217). Most of the lead measured in plants is in general derived from direct deposition (Bergbck & Lindestrm 1998:69-70; Tahvonen & Kumpulainen 1993). For plants where the edible parts are exposed to deposition of pollution, the direct deposition of lead will in general be conclusive for the degree of human exposure. However, it is sometimes possible to wash off most of the lead. (Bergbck & Lindestrm 1998:72; OECD 1993:80). Several studies of adults daily intake of lead via food have been performed in different countries. The group of USA, Finland Sweden, Switzerland, Australia and Denmark showed a relatively low intake (a weekly intake of around 5 g/kg body weight or less). The corresponding result from UK was around 8 g/kg, Germany 14 g/kg, France 20 g/kg, Belgium 21 g/kg and Italy 60 g/kg (WHO 1995:81). The investigations were made during 1980s and it is probable that the intake since then have decreased with decreased emissions of lead. It has been estimated (1990) that from harvest to packing, lead concentrations in food increase by a factor of 2 to 12! Most of the total lead occurring in the diet of children in the United States is lead present in drinking water and lead in dust inadvertently incorporated into food during processing and preparation (Thavonen & Kumpulainen 1993:251). Lead has in all species of experimental animal studied, including non-human primates, shown to cause adverse effects in several organ systems, including haematopoietic, nervous, renal, cardiovascular, reproductive and immune systems. Lead also effects bone and has been shown to be carcinogenic in rats and mice (WHO 1995:29). In humans, lead can result in a wide range of biological effects depending upon the level and duration of exposure. It affects several organs and organic systems, with sub cellular changes and neurodevelopmental effects appearing to be the most sensitive. Some effects are not reversible. Young children and foetus are more sensitive to lead exposure than older children and adults. Effects of lead on the haemopoitic system result in decreased haemoglobin synthesis, and anaemia has been observed in children at blood concentrations above 1.92 mol/litre (40 g/dl). Lead has also been shown to be associated with impaired neurobehavioral functioning in children and after long-term exposure of workers. Further, lead is known to cause proximal renal tubular damage. For lead levels in blood less than 1.2 mol/l (25 g/dl) decrements in intelligence quotient (IQ) has been observed and reduction in human peripheral nerve conduction velocity may occur with levels as low as 1.44 mol/l (30 g/dl). There is no evidence of a threshold level and studies indicate that there might be effects even under the level of 0.48-0.72 mol/l (10-15 g/dl). Reduction in gestational age and in birth weight has also been reported (WHO 1995:30-32, Wixon & Davis 1993:51-74). In OECD countries which monitor lead levels, data indicate that while the demand for lead products have increased, the average levels of lead in air, food and blood have due to regulations declined below levels of national concern. However, in some countries there are portions of people that are exposed to levels that execs those of national concern (OECD 36

1993:14). The view of what risk present exposure and use of lead constitute and if it is acceptable or not may vary. In all the Nordic countries lead is regarded as a high priority hazardous substance and considerably efforts have been invested into reducing the lead exposure of humans and the environment. It is the goal of all the Nordic countries to reduce the exposure of lead to the environment and humans to the extent possible. Substitution of lead is a primary part of the strategy employed to achieve this goal. Despite this significant releases can be expected due to huge amounts of lead and lead waste accumulated and still accumulating in the society. In parts of the environment (soil) the levels of lead are still increasing. Thus, the amount of lead being released to the environment is still not to a level that may be regarded as sustainable (Ponsaing & Hansen 1995a). There are several ways of reducing the risk for exposure of lead including reduction of the emission to air and water, restriction in the use of lead products (e.g. lead in pesticides, paints, soldered food cans, in drinking water systems, petrol), controlling the pH in water supply systems in order to reduce the solubility of lead (OECD 1993:14). The available data on the daily intake of lead by adults and children indicate a general decrease in those areas where the level of lead in petrol has decreased and a concerted effort made to avoid lead soldered cans for food storage (WHO 1995:89; OECD 1993:23, 177273, 276).

37

5. Mercury (Hg)
5.1 General information
Mercury is a naturally occurring element in the earths crust. The most important primary Hg minerals are cinnabar (HgS) and livinstonite (HgSb4S7). Mercury has been used by humans for at least 3 500 years. Mercury can exist in a wide variety of physical and chemical states which all have their inherent toxic properties and different applications in industry and agriculture. Metallic mercury is a heavy silvery liquid at normal temperatures and pressures. There are three states of inorganic mercury: Hg0 (metallic), Hg22+ (mercurous), and Hg2+ (mercuric) mercury. Besides elementary mercury, mercury forms salts such as mercury chloride, mercury nitrate, mercurysulphate and organometallic compounds with organic groups such as methyl, ethyl and propyl. The carbon mercury bond is chemically stable (Steinnes 1995:245; Rundgren et al. 1992:4; WHO 1989: 9; WHO 1991: 22; OECD 1994:27). Mercury is involved in a whole chain of environmental transformations where the physical and chemical properties of mercury is changed, which makes it exceedingly difficult to follow the pathways of mercury from emission source to ultimate sinks. Once released in the environment, mercury may be redistributed between and within environmental compartments. It is more mobile than other heavy metals. Inorganic mercury may be methylated to more toxic organic forms. Environmental methylmercury arises largely, if not solely, from the methylation of inorganic mercury. Methylation can occur non-enzymically or through microbial action. However, some studies have found no clear relation between methylation of mercury in soil/water and the microbial activity indicates that that the process may be of chemical nature. It is possible that formation of methylmercury also occur in the atmosphere. Methyl Iodide has been suggested as an atmospheric methyl group donor since it is photolytically cleaved into methyl radicals and iodine atoms. Once methylmercury is released, it enters the food chain by rapid diffusion and tight binding to proteins giving rise to bioaccumulation and biomagnification in living organisms. Aquatic sediments are major sinks for mercury. However, because several biogeochemical processes lead to element enrichment in surface sediments, mercury can be released to both water and the atmosphere (Munthe 1993:2,15, 21; OECD 1994: 17-18; WHO 1991:34; WHO 1990:11-13). Mercury has as far as we know no necessary function in any living organism. It is a nonessential metal. On the contrary, mercury is among the most toxic elements to man and many higher animals (Landner & Lindestrm 1998:98; Steinnes 1995:246). A number of studies have indicated that selenium, vitamin E and other substances may in several cases play a protecting role against the toxicity of mercury (WHO 1989:35; WHO 1990:65-67). However, a study has shown that selenium may increase the toxicity of mercury to fish eggs at high (> 5 g/litre) concentrations of mercury. At low concentrations selenium seams to be antagonistic (WHO 1989:68-71).

5.2 Use
Mercury has been used by humans for at least 3 500 years. Mercury was early used in China and India (sixth century BC) in medicine and by the Romans for production of red pigment. The invention of scientific instruments such as the barometer in 1643 by Torricelli and the Hg thermometer in 1720 by Fahrenheit involved the introduction of Hg into scientific research (Steinnes 1995:245). Mercury and mercury compounds are and have been used for a number of applications. The uses in the chloralkali industry (cathode in the electrolysis of sodium chloride), batteries, electrical equipments, paints, tooth filling are some of the main areas. However, there are a 38

wide variety of other uses in industry, agriculture, military application, medicine, cosmetic (for lighter skin and mascara) and gold mining (WHO 1989:13; OECD 1994:32-35; WHO 1991:30-33; Maxon et al. 1991). In some areas for instance concerning batteries, the substitution of mercury has accelerated during the second half of 1980s and 1990s. The OECD-countries have reduced their use of mercury substantially since the 1970s (OECD 1994:32, 48). The total amount of mercury in the yearly consumption of batteries has been estimated to be about 100 tonnes for 1995 in whole Europe: the corresponding figure in 1989 has been estimated to 380 tonnes, i.e. a reduction in the order of 75 % (KemI 1997:15).

5.3 Production
Although more than 20 principal mercury minerals are known in nature, commercial production of mercury is made almost entirely from cinnabar. Mercury also occurs in the Earths crust as complex with zinc, iron and other metals, but only to a small extent as the native metal (Steinnes 1995:247). Primary production of mercury decreased worldwide from about 10 000 tonnes in 1970 to about 5 500 tonnes 1990 (OECD 1994:15). The world production of mercury was in 1997 about 2 200 tonnes. It is believed that several countries have an unrecorded production of mercury from copper electrowinning processes. The annually world mine production of mercury decreased substantially, with about 25 %, during the period 1986 to 1994 (from 7 200 tonnes to 1 800 tonnes). Kyrgyzstan, China, Algeria and Spain were in 1997 the worlds greatest producer and contributed to more than 90 % of the worlds production in 1997 (Knight-Ridder financial/commodity research bureau 1996:170; Chapman et al. 1997:170). Secondary production (recycling, recovery and industrial reprocessing) accounts for a significant supplementary amount of mercury. However, in several cases the recycling of products are not economical and the products are then stored as hazardous waste or ends up in landfills, or are burned in incinerators (OECD 1994:15, 28, 45).

5.4 Emissions and deposition

Naturally emissions of mercury arise from degassing of the earths crust, through volcanic activities, weathering from geological deposits, by evaporation from the oceans, lakes and soils. Main anthropogenic sources are industrial activities, energy production (principally coal combustion), solid waste incineration, crematory and the use and disposal of consumer products (OECD 1994:16; Munthe 1993:4, 6-7). The global anthropogenic emission 1983 was estimated to be 3 600 tonnes to air, 4 600 tonnes to water (including atmospheric fall-out) and 8 300 tonnes to soil (including atmospheric fallout) (OECD 1994: 16). Comparing the estimations of the natural and anthropogenic sources it is obvious that the natural sources are not negligible but rather could in a global perspective be of the same order or exceed the anthropogenic emissions. However, in industrialised areas the anthropogenic source is in general of much more importance (Maxon et al. 1991:31, 8990). OECD cites four estimations of the total global anthropogenic mercury emission to air. They all are in the range from about 1 000 tonnes to less than 10 000 tonnes, three of them with a best guess between 2 000 and 4 500 tonnes. The total natural emissions lies according to the same sources in the range of 100 tonnes to < 15 000 tonnes. Three of them with a best guess between 2 500 and 4 000 tonnes (OECD 1994:38; WHO 1991:15). The total anthropogenic emissions of mercury to air in Europe during 1988-1990 was according to several studies in the range of about 460 to 800 tonnes per year, while the 39

deposition of mercury in Europe is estimated at 120 to 300 tonnes per year. The deposition of metals in Europe is in general much less than the emissions, indicating that Europe contributes to deposition outside its borders (KemI 1997:13; EEA 1995:42; Munthe et al. 1998:5). From the change in deposition of mercury in the Swedish west coast the anthropogenic emissions of mercury to air in Europe has been estimated to have decreased with about 40 % from 1989/1990 to the mid 1990s (KemI 1997:36). The total emission of mercury to air in Europe (the EMEP area) was estimated at 462 tonnes in 1990, of which half came from energy generation and 38 % from industrial sources. Sources in Western Europe generated slightly over half the total (EEA 1998:112113). The emission of mercury within the European community was in 1989 estimated to be 760 tonnes. The immediate destinations of the emissions were 26 % to air, 5 % to water and 69 % to land (Maxon et al. 1991:96). In 1990 the EU-15 air emission of mercury has been estimated to 245 tonnes of which 113 came from Germany, 33 from France, and 26 from UK (Eurostat 1998:78). Product related emissions (during use and after disposal) of mercury contribute significantly to the total and transboundary emissions of mercury in Europe. It has been estimated that in the mid 1990s 4 % of the total emission in Europe came from batteries, 3 % from measuring and control instruments and 11 % from lighting and electrical equipments. According to the same study these product categories accounts for 10-14 % of the total deposition in Scandinavia (KemI 1997:38). The formation of the elemental mercury is expected to be due to both biotic and abiotic processes. Elemental mercury and dimethylmercury are the principal candidates for volatilisation (emission and/or re-emission) into the atmosphere from natural waters and soil surfaces. Total vapour phase mercury fluxes from agricultural and forest soils are substantially smaller (by a factor of six) than those from the surface of a lake. The emissions from Swedish soils had been measured to 1.1 0.4 ng mercury/m2/hectare and from Swedish lakes 6.3 3.6 ng mercury/m2/hectare (OECD 1994:52, 54). The greatest part of atmospheric mercury is generally assumed to be in the form of elemental mercury vapour which has a long atmospheric residence time, possible as much as one year. Due to the long residence time elemental mercury can be transported globally, while Hg2+ compounds such as HgCl2 and particulate mercury have shorter residence times and are generally distributed over local to regional scales. However, ozone oxidises elemental mercury and elevated ozone concentrations in industrial areas may significantly influence the residence time of Hg0. The concentration of MeHg are usually less than 0.5 % of the total gaseous mercury in air and about 1 to 5 % in precipitation. Methylation of inorganic mercury may occur in sediments ore elsewhere in the aquatic environment but the contribution from atmospheric deposition has been shown to be significant if not dominant. Mercury is removed from the atmosphere by both wet and dry deposition (OECD 1994:17; KemI 1997:37; Munthe 1993:3; Munthe et al. 1998:6; Steinnes 1995:249-250). The long-range transport and increased deposition of anthropogenic mercury have markedly increased the mercury content, by about five to ten times, in organic rich top soil layers in central Europe and southern Scandinavia (OECD 1994:57). Current or recent Hg deposition rates over large parts of Europe, including Scandinavia, will slowly increase the amounts of Hg present in soils of most ecosystems. Mechanisms of this accumulation are the very high affinity of Hg2+ to soil organic matter and the low turnover or leaching losses of humic matter. It is estimated that total input to soils has to be reduced to 10 30 % of the recent deposition rates for equilibrium to be attained in the entire profile of both cultivated and forest soils. Future concentrations of Hg in mor horizons are difficult to prognosticate because of their dependence on future changes in primary productivity, organic matter decomposition, and vertical transport rates of soluble humic substances. However, some additional increase in the

40

Hg concentration of mor will most likely occur at the current deposition rate in northern Europe (Rundgren et al. 1992:3, 68). One investigation of coastal wet deposition of total mercury in Sweden estimated the deposition to 7-27 g/m2/year and the wet deposition of mercury in the southern Baltic Sea has been measured to 5.914.8 g/m2/year. The total deposition of total mercury in Germany has in remote area been measured to 22 g/m2/year and 740 g/m2/year in an industrial area (OECD 1994:55; Munthe 1993:17). Considerable amounts of mercury may be added to agricultural soils with fertilisers, lime, manure, and sewage sludge. The annual Hg quantity introduced to cultivated soils in Europe as a result of fertilization was in the end of 70s calculated to 0.05 0.3 g/hectare. Fertilization may add about the same amount of Hg to soil as wet deposition with a typical Hg content of 25 ng/l in remote to more polluted sites. However, organic fertilizers of municipal origin, such as sewage sludge and compost from organic waste, may have far higher Hg contents. Mercury containing fungicides did in particular during the period 19451970 contribute to a considerably input of mercury to agricultural soils. However, the use of organic mercurials as seed disinfectant did not always increase the mercury contents of agricultural soils (Rundgren et al. 1992:6; Steinnes 1995:250251).

5.5 Concentrations (in nature and human)

The crustal average of mercury is of the order of 20 g/kg or perhaps less. Some mean values reported for different types of rock are: basalt 3.9 g/kg, granite 3.5 g/kg, sandstone 12 g/kg, limestone 9 g/kg and shale 23 g/kg. Typical value in agricultural soils lies in the range of 30150 g/kg d.w. while the concentration in contaminated soils may be 10 to 100 times higher (OECD 1994:53, 147; Steinnes 1995:247249). Due to strong binding of mercury to soil particles, including organic matter, only small amounts of the metal are present in soil solution. European cultivated topsoils have a mean total Hg concentration of ca. 0.10 g/g dry weight, or ca. 200 g/hectare in the 020 cm layer. With the exception of soils developed from parent materials naturally high in Hg (which occur very locally) and soils polluted by local industry, by the use of sewage sludge etc., cultivated soils are expected to fall within the range of 0.030.15 g/g corresponding to ca. 60 300 g/ha in the 20 cm top layer. Lower concentrations sometimes reported are probably not total Hg. The natural share of total Hg is not well known but probably within 0.010.03 g/g on average. With exception of mor horizons of podzolic soils and of peat soils, both very high in organic matter, the concentration ranges reported for natural, mainly forest soils are almost identical to those of cultivated soils (much higher concentrations occur locally). Mor and peat have often 24 times higher concentrations of organic matter calculated on a dry weight basis. Calculated per organic dry weight or hectare of the ground, however, such soils seem to have less Hg accumulated (Rundgren et al. 1992:1, 28-36, 66; Steinnes 1995:254). The concentration of lead, cadmium and mercury in the humus layer of forest soils in 50 % of Sweden has increased by a factor between three and ten since the pre-industrial era; concentrations fall from south to north (EEA 1998:114). Typical values for mercury in air for remote areas are 14 ng/m3 and for industrial areas 450 ng/m3. More than 90 % of total Hg in air is volatile species and Hg0 is assumed to be the predominant form. Typical background concentrations of mercury in rain and snow are in the range of 1 25 ng/l, depending on the distance to industrial activities emitting mercury, with occasional values of around 100 ng/l during pollution events. For groundwater the concentration of mercury in general lies in the range 0.515 ng/l, for lake water 2-12 ng/l, and open ocean water (dissolved) 0.053 ng/l. It is usually assumed that Hg(OH)2 and HgCl2 are the predominant species in surface water. However, organic mercury has been reported to represent 2237 % of the total mercury in lake, river and tap water from Ottawa, Canada area. The concentration in drinking water is in the same order as in rain, with average of about 25 41

ng/litre. The concentrations in sediments vary from about 0.05 mg/kg d.w. (dry weight) in uncontaminated sediments, to the normal sediment with concentrations of 0.20.4 mg/kg d.w. and contaminated sediments 1 >20 mg/kg d.w. In plants the concentration is in general lower than 0.1 mg/kg f.w. (fresh weight). In the case of cereals the content in grain is reported to be 310 times lower than that of the. Even at very low levels it may be assumed that foliar uptake of Hg0 from air plays a significant role. Due to bioaccumulation and biomagnification the mercury concentration could be much higher in fresh and marine fish especially for fish of prey. Typical values for freshwater fish are 0.27 mg/kg f.w., marine fish 0.011.5 mg/kg f.w., tuna and swordfish 0.37 mg/kg f.w., and shellfish 0.011mg/kg f.w. (OECD 1994:53, 59, 147; Munthe 1993:16-18; Rundgren et al. 1992:4; WHO 1989:14-15; WHO 1990:35-36; Steinnes 1995:256). Concentrations of mercury have been measured in mussels, fish and sediments from sites located in both clean and contaminated areas in Europe. Concentrations of mercury in mussels ranged from 7 to about 900 g/kg wet weigh, with background levels typically below 3040 g/kg. Concentrations were around the background level at most sites, with 120 g/kg found on the Atlantic coast of Spain, up to 420 g/kg in the east Adriatic and up to 910 in the north western Mediterranean. Concentrations in fish were in general 20 to 100 g/kg wet weight, with 135 g/kg recorded at the mouth of the Rhine and up to 200 g/kg in the Mediterranean. High concentrations of mercury, 4 300 g/kg, has been found in Mediterranean bluefin tuna, 45 times higher than in the Atlantic bluefin tuna. Mercury concentrations in sediments in Europe varied between 10 and 1 180 g/kg dry weight. Background levels are generally lower than 100 g/kg. The highest concentrations were found in the inner of Oslofjord, the Rhine, the Thames and the German Bight (EEA 1998:215219). Concentrations of mercury in fish, especially in Scandinavia, are higher than acceptable from a health point of view. About 40 000 Swedish lakes are estimated to contain pike in which the concentration of mercury exceeds the consumer health-related target value of 0.5 mg/kg. The levels of mercury in fish are not decreasing, in spite of the dramatic decrease of domestic emissions in Sweden, probably as a result of the transport of mercury from elsewhere and local leaching (EEA 1998:115). Measurement of mercury in Swedish freshwater sediments have indicated a five-fold increase in mercury concentration, as compared with background conditions in southern Sweden, and approximately a doubling in the northernmost part of the country. Sediments from the deep basins in the Baltic Sea show a three-fold increase over the concentrations in pre 1850 samples (OECD 1994:56). Hg0 and Hg2+ are the states of mercury normally encountered in soils. Besides the redox potential, pH and the Cl concentration are key parameters in determining the speciation of mercury in the soil solution. In addition to chemical reactions, transformations may also be mediated by microbial activity. An other important property of mercury is the ability to bind strongly to sulphide ion. Only a small fraction of Hg2+ occurs in the soil solution, the major fraction being either bound in soil minerals or adsorbed on solid surfaces, inorganic and organic (Steinnes 1995:251). Coal contains mercury as a natural component in trace amounts (0.04-0.7 mg/kg). Given the large amount of coal burned considerably amounts of mercury are released. Depending on the flue gas cleaning process for combustion sources, mercury will be released to the atmosphere or become a waste product to water and soil (OECD 1994:41-42). The concentration of mercury in coal varies. Figures of the mercury concentration in coal of nine different origin listed by Munthe range from 0.04 mg/kg to 3.3 mg/kg. The concentration of mercury in waste can be higher, around 5 mg/kg, but is substantially decreased if products containing mercury, such as batteries and thermometers, are removed. Another potential important fuel is peat, which contains less mercury than coal or waste, 0.01 to 0.2 mg/kg. The mean concentration of total mercury in whole blood (in absence of consumption of fish with high concentrations of methylmercury) is probably of the order of 5-10 g/litre and in hair about 1-2 mg/kg. The average mercury concentration in urine is about 4 g/litre and in placenta about 10 mg/kg wet weight (WHO 1991:60). Limited information from deceased 42

miners shows mercury concentrations in the brain, years after cessation of exposure, of several mg/kg. I seems that a moderate number (about 25) of amalgam surfaces may on average increase the brain mercury concentration by about 10 g/kg and in the kidney with about 300-400 g/kg. However, the individual variation is considerable (WHO 1991:18-19). In one study the amalgam-free subjects had a mean mercury level in kidneys of 49 g/kg (21105), whereas subjects with amalgam fillings had a corresponding level of 433 g/kg (48810) (WHO 1991:38). Most commercial fertilisers have mercury contents below 50 g/kg, but considerably higher values occur. Manure typically exhibits mercury levels in the order of 100 g/kg, while typically values for sewage sludge are 5 000 to 10 000 g/kg (Steinnes 1995:250251).

5.6 Limit values

The FAO/WHO expert committee on food additives (JEFCA), has recommended a permissible weekly intake (PTWI) for methylmercury in adults of 200 g corresponding to 3.3 g/kg body weight. For total mercury, the PTWI value recommended by JEFCA is 5 g/kg body weight. In a review of 26 national dietary surveys none showed a mean dietary intake approaching these figures (WHO 1996:209; WHO 1996:209). However, the intake varies considerably among individuals depending on the diet and amalgams present. The WHO air quality guideline for inorganic mercury is (1999) 1 g/m3 (year average). The LOAEL (lowest observed adverse effect level) for humans is 0.02 mg/m3 (renal tubular effect). The recommended health-based occupational exposure limit for metallic mercury vapour (WHO 1980) is 25 g/m3 air (TWA long-term exposure) and 500 g/m3 air (peaks, short-term exposure). The equivalent value for long-term exposure to inorganic mercury compounds is 50 g/m3 air. A maximum individual urine mercury concentration of 50 g/g creatine has also been recommended. The exposure of women of childbearing age to mercury vapour should be as low as possible (WHO 1991:112, 116). The EU-limit value for mercury in fish is 0.5 mg/kg fresh weight. However, for mercury in some fish species (for instance pike, eel and tuna) the limit value is 1 mg/kg (European Communities 1993). The EU has (1998) adopted 1.0 g/litre as limit value for mercury in drinking water. The limit value should be met within five years (European Union 1998). The European Union has regulated by different directives the environmental pollution from mercury and the use of several mercury-containing products. Some examples are giving below. EEC Directive 79/117, amended in 1991 by EEC Directive 91/188, for phasing out of the use of mercury in seed dressing in a few years. EEC Directive 82/176 defines the limit values and quality objectives for mercury discharges from the chlor-alkali industry. EEC Directive 89/369 set limits on emission to the atmosphere from new municipal waste incinerators as follows: 0.2 mg Cd+Hg/m3. EEC Directive 89/677 bans from ultimo 1991 the use of mercury in antifouling paint, preservation of wood, impregnation of heavy-duty industrial textiles and yarn intended for their manufacture, and in treatment of industrial waters (OECD 1994:123).

5.7 Risk assessments, exposure and harmful effects

In a survey of risk reduction activities in the OECD-countries it was noticed that all OECDcountries got national legislation/regulations for mercury emissions to air, water and soil. Most OECD-countries had forbidden the use of mercury in paints, for seed dressing (nearly all uses) and established guidelines or standards for mercury in fish. Most countries had also taken measures to reduce risks from occupational exposure. Several countries had restricted or banned the use of mercury in thermometers. Some countries had established national or regional databases to identify areas of elevated metal levels and some had also guidelines or standards for mercury in sewage sludge applied to agricultural land. A few 43

countries had a general ban on the use of mercury, with exemptions. A few countries had also decided to prohibit the use of mercury in dental fillings in the near future (OECD 1994:19). The general population is primarily exposed to mercury through diet (organic mercury from fish and inorganic mercury from non-fish food) and dental amalgam (inorganic mercury) but significant contributions may also arise from for instance air, water and pharmaceuticals. It has been estimated that humans have a daily intake of about 2.4 g methylmercury from al sources, and a daily uptake of approximately 2.3 g. The total daily intake of all forms of mercury from all sources (principally food) has been estimated to be 6.7 g, with an added burden of 3.8 to 21 g of mercury vapour from dental amalgams, if present (WHO 1990:13; OECD 1994:60). Typical total dietary intakes reported is in the range of 26 g of mercury/day for children and 2140 g/day for adults, the contribution from fish and foods of marine origin accounting for about 40 % and fruit and vegetables 20 % (WHO 1996:199). Fish is a dominant source of human exposure to methylmercury. Methylmercury is converted to inorganic mercury in humans and experimental animals. A weekly consumption of only 200 g of fish having 0.5 mg/kg will result in an intake of 0.1 mg mercury (predominantly methylmercury, which is one-half of the tolerable recommended weekly intakes. However in most foodstuffs, the mercury concentration is usually below 20 g mercury/kg fresh weight (WHO 1990:14; WHO 1991:35). The uptake and accumulated mercury from amalgam show substantial individual variations but increases with chewing and number of dental amalgam fillings. Use of soaps and creams containing mercury can give rise to substantial mercury exposure. High occupational exposure to inorganic mercury has been observed in the chloralkali industry (e.g. workers with average urine mercury 50-100 g/litre creatinine), dental clinics, mercury-mines and where products containing mercury are produced (WHO 1991:16-17, 43-46, 86). According to studies on human and animals, about 80 % of inhaled mercury vapour is retained by the body, whereas less than 1 % (some data on rats indicate less than 0.01 %) of liquid metallic mercury is absorbed by the body. Inorganic mercury is probably absorbed by the gastrointestinal tract to a level less than 10 % (probably on average around 6 %) but there are considerable individual variations. Absorption in young children may be considerably greater (WHO 1991:17, 48-49). Due to the complicated pattern of metabolisms for different mercury compounds there are no suitable indicator media that will reflects concentrations of inorganic mercury in the critical organs, the brain and kidney, under different exposure situations (WHO 1991:61). The kidney is the main depository of mercury after the administration of elemental mercury vapour or inorganic mercury compounds (5090 % of the body burden of animals). It also accumulates in for instance the thyroid, pituitary, liver, pancreas, testes, ovaries, prostate, and brain. Significantly more mercury is transported to the brain of mice and monkeys after inhalation of elemental mercury than after intravenous injection of equivalent doses of the mercuric (Hg2+) form. The metallic mercury vapour crosses the blood-brain barrier, the placenta and other tissues. Oxidation in these tissues serves as a trap to hold the mercury and leads to accumulation in brain and foetal tissues. The oxidation of elemental mercury vapour in the body can be reduced considerable by moderate amounts of alcohol leading to higher concentrations in liver and lower in brain. The faecal and urinary routes are the main pathways for the elimination of inorganic mercury in humans, although some elemental mercury is exhaled. The faecal pathway accounts for about 90 % of the total elimination of mercury in man and other mammals after exposure to methylmercury. The ultimate fate of the absorbed mercury will depend on their chemical transformation in the body as well as the kinetics. The biological half-time which only lasts days or weeks for most of the absorbed mercury, is very long probably years, for a fraction of mercury. The half-time is longer in the brain than in other organs. The long biological half-time mercury may be biochemically inactive mercury selenide (WHO 1991:17-18, 47, 50, 52, 59-60; WHO 1990:13-14, 46).

44

Acute inhalation exposure to mercury vapour may be followed by chest pains, dyspnoea, coughing, haemoptysis and sometimes interstitial pneumonitis leading to death. The ingestion of mercuric compounds, in particular mercuric chloride, has caused ulcerative gastroenteritis and acute tubular necrosis causing death from anuria where dialysis was not available (WHO 1991:19). The clinical and epidemiological evidence indicates that prenatal life is more sensitive to the toxic effects of methylmercury than is adult life. The inhibition of protein synthesis is one of the earliest detectable biochemical effects in the adult brain. It can also react directly with important receptors in the nervous system. In the case of prenatal exposure, the effects of methylmercury seem to be quite different and of much more general nature (WHO 1990:1516). The kidney is the critical organ following the ingestion of inorganic divalent mercury salts. Experimental studies on animals have shown that inorganic mercury may induce autoimmune glomerulonephritis in all species tested, but not in all strains, indicating a genetic predisposition. It is not possible to set a level for mercury (e.g. in blood or urine) below which (in individual cases) mercury-related symptoms would not occur. Human hypersensitive reactions (dermatitis) to metallic mercury have also been identified (WHO 1991:21, 97-98). The central nervous system is the critical organ for mercury vapour exposure. Sub acute exposure has given rise to decreased verbal intelligence and memory, and psychotic reactions characterized by delirium, hallucinations, and suicidal tendency. Occupational exposure has resulted in erethisms as the principal feature of a broad ranging functional disturbance. With continuing exposure a fine tremor develops, initially involving the hands. Decreased nerve conduction velocity has also been demonstrated in mercury-exposed workers. At a urinary mercury excretion level of 100 g/g creatin, the probability of developing the classical neurological signs of mercurial intoxication (tremor, erethisms) and proteinuria is high. An exposure corresponding to 30 to 100 g mercury/g creatinine increases the incidence of toxic effects. Changes in EEG were found in one study comprising 40 workers that have been exposed to metallic vapour level of 25 g/m3, corresponding to a urine mercury level of about 20 g/litre (WHO 1991:19-20, 90-91). The general population does not face a significant health risk from methylmercury. Certain groups with high fish consumption may attain a blood concentration of about 200 g methylmercury/litre, (corresponding to 50 g/g of hair) associated with a 5 % risk of neurological damage to adults. However, foetus is more sensitive and faces a greater risk. Evidence shows that at peak maternal hair mercury levels above 70 g/g there is a high risk (more than 30 %) of neurological disorder in the offspring. Data also indicate that a 5 % risk may be associated with a peak mercury level of 10-20 g/g in maternal hair (WHO 1990:17). The very large amounts of mercury in soil constitute a chemical time bomb that can cause severe pollution of aquatic ecosystems if should be mobilized. Clearly, these pools will to a large extent delay the effects of new abatement strategies aimed at reducing the mercury load to ecosystems. In one study it was found that the mercury run-off from a catchment area was 3.4 g/km2/year while the total amount of mercury stored was 8.8 kg/km2 (Munthe 1993:20). Besides the species of mercury, the toxicity and uptake of mercury to aquatic organisms is also dependent on for instance pH, organic matter, salinity, temperature, presence of selenium and sulphide ion, and water hardness (WHO 1989:48-49; WHO 1990:31-34). There are indications that zinc may reduce the uptake of mercury in fish. Exceptionally low level of mercury in fish has been found in en environments where the zinc concentrations are high. Outside most of Swedens sulphide ore mines, the mercury concentration in pike flesh is lower than in most unpolluted mountain lakes (Landner & Lindestrm 1998:139). There is a dynamic exchange of volatile Hg compounds between atmosphere and soil, mainly in the form of Hg0, which is easily absorbed by soil organic matter though available for reemission of Hg from certain soils. Microbial and biochemical processes are important for 45

the exchange rates. The sorption of Hg0 vapour to soils varies according to organic matter, the mineralogical properties, soil moisture, duration of exposure and size of contact surface. Soils with a high content of clay, as well as sandy soils and dry soils sorbs little Hg0 vapour compared to moistly soils rich in organic matter. Humic acids in soil organic matter seem to play the major role in the sorption of Hg, in particular Hg2+ (Rundgren et al. 1992:1, 5, 17; Steinnes 1995:249). Field measurements of mercury in open field rain and throughfall have shown that the passage through the forest canopy increases the concentrations of mercury in rainwater during summer months. This effect was attributed to dry deposition of mercury compounds on the needle surfaces, followed by wash-off by the rain falling through canopy. Furthermore, the amount of mercury reaching the forest floor with litterfall is of the same order of magnitude, or higher, as the total deposition via throughfall. Dry deposition may be of equal importance compared to direct wet deposition in forest. Additionally, there is according to Munthe no evidence of an internal redistribution of mercury or methylmercury from the roots to the green parts of the trees (Munthe 1993:18). However, according to Rundgren et al. litter produced in forest carries Hg to the forest floor. The origin of this Hg is both dry deposition and plant uptake from the soil. Therefore, the uppermost soil horizons are usually enriched in Hg compared to the underlying layers (Rundgren et al.1992:16). Mercury deposited in forest soils becomes mobile in increasing amounts by association with organic matter and is transported via run-offs from the drainage areas to surface waters. The affinity to organic matter makes the transport of mercury in freshwater closely related to the transport of humic matter. However, the annual transport of mercury on humus colloids from forest soils to lakes in Sweden is estimated to be less than 1 % of the amount stored in the humus layer of the soil. The residence time of mercury in soil is very long and may be in the order of 1 000 years. Sediments are major sinks for mercury. However, because of the dynamic exchange with the overlaying water column and methylation of mercury in sediments by microorganisms, mercury can be released again to both water and the atmosphere. There is also an exchange of volatile elemental mercury and mercury compounds between the atmosphere and the soil (OECD 1994:56-57; Steinnes 1995:253, 257). Because of the very high affinity of several mercury compounds to soil organic matter, leaching losses to subsoil horizons, groundwater or surface water are thought to be small for normal soils. In nearly neutral soils, sometimes low in organic matter, iron and clay minerals may be important absorption sites. In acid soils, transport of the carrier organic matter constituents is almost a prerequisite for mercury mobility, as the stability of complexes of organic matter is high at low pH values (pH 3-5). No indications of an increased Hg transport as a result of soil acidification, except possible from sandy soils poor in organic matter, have been reported. This might be due to the presence of sufficient humic matter. It seems that acidification of soils and waters does not have the same major importance in regulating the output of Hg from forest soils as for many other metals. However, although the increased acidity will not directly affect the chemistry of mercury in soil, lake water and sediments, a correlation exists between low pH and high concentrations in fish. The explanation may be a combination of several factors such as a lowered productivity and biomass, which increases the biomagnification in the aquatic food chain, and an increased net methylation rate in the lake. Liming might during specific conditions increase the transport and mobility of soil mercury (Rundgren et al. 1992:23-24; Munthe 1993:21). Mercury accumulates in soil invertebrates starting at only slightly elevated concentrations in the soil. Plant takes up only little Hg, also from soils treated with mercury compounds. Indications were found that plant roots act as a barrier against Hg uptake and therefore sometimes accumulate high amounts of Hg. Accumulation of mercury in plants increases with increasing soil mercury concentration. Soil types have considerable influence of this process. Generally, the highest concentrations of mercury have been found in the roots; but translocation to other organs, for instance leaves, has also been identified. However, for most studies mercury has been administrated as a solution in hydroponic culture, which makes it

46

difficult to determine their relevance to natural conditions (OECD 1994:57; Rundgren et al. 1992:26; WHO 1989:78). Organisms in water and soil readily take up organic mercury and mercuric salts. Soil invertebrates, aquatic invertebrates, and insects, accumulate mercury to high concentrations. Fish also take up mercury and retain it in tissues, principally methylmercury. Elimination of methylmercury is slow from fish, with half times of months or years. Terrestrial organisms are also contaminated by mercury. Sea birds and those feeding in estuaries are most contaminated (Rundgren 1992:2; WHO 1989:9-11). Inorganic and organic mercury is toxic to microorganisms (WHO 1989:92-93). Impeded litter decomposition and reduced soil respiration rate usually characterize heavy metal polluted soil. Microorganisms responsible for decomposition of cellulose are usually very sensitive to heavy metals, including Hg2+, and are probably less able to develop resistance even to moderate Hg concentrations in soils. Hg2+ is one of the metal ions, which are most toxic to biota, only surpassed by Ag2+ (Rundgren et al. 1992:1-2). There are indications that the regional enhanced concentrations of mercury in central Europe and southern Scandinavia may have an adverse effect on microbiological life processes, and indirectly on the recycling of important nutrients and on the tree vitality (OECD 1994:57). According to one study soils enzymes activity may be inhibited by as little as 0.2 g HgCl2/g d.w. However, there are only a few sources of information about effects on the enzyme activity at low level mercury concentrations (Rundgren et al. 1992:45). Inorganic mercury is reported to have effects (for instance on phytoplankton growth) in concentrations of 5 g/litre, whereas organomercury compounds have effects at least 10 times lower concentrations. The toxicity of organic forms are generally much more toxic to aquatic organisms and birds too. For Daphnia magna, the NOTEL (no-observed-toxic-effect-level) for reproductive impairment is 3 g/l for inorganic mercury and < 0.04 g/litre for methylmercury. Freshwater fish show lethal responses to inorganic mercury in acute nominal concentrations from approximately 30 g/litre but are approximately 10 times more sensitive to oragnomercury compounds. Larvae are 10 times more sensitive than adults. The NOTEL for most sensitive parameters may be well below 0.01 g/l. The use of orgnomercury fungicides as seed dressing in Europe led to the deaths of large numbers of granivorous birds, together with birds of prey. Some effects on survival in earthworms are reported from concentrations of added Hg2+ of one order of magnitude above the baseline of the soil. Plants are in comparison generally insensitive to mercury compounds. Terrestrial plants, mammals and birds are, except from those that eat food from lakes or seas and those that are exposed to mercury fungicides (directly or indirectly), in general exposed to low levels of mercury and acute effect should not be expected (WHO 1989:44, 92-93; WHO 1991:65-67).

47

6. Zinc (Zn)
6.1 General information
Zinc is together with cadmium and mercury a member of group IIB in the periodic table. In pure form it is a pale greyishblue, malleable metal. It occurs in a number of compounds that range from readily soluble to completely insoluble in water. Zinc normally occurs in the environment in an oxidation state of Zn2+. The (Zn,Fe)S minerals sphalerite and wurtzit is by far the most predominant zinc ore minerals (Kiekens 1995:285; Landner & Lindestrm 1998:1415). Zinc is an essential trace metal for terrestrial as well as aquatic organisms. It is necessary for the function of various enzymes. It is one of the less toxic heavy metals, but also one of the most widely occurring. However, at excessive uptakes, zinc can be toxic. Zinc is mobilized by acidification. It is under special circumstance bioaccumulated in organisms but is not subject to biomagnification. When the surrounding value is elevated the organisms on the lowest trophic level accumulate zinc (show higher concentration compared to the environment), while organisms on higher trophic levels (e.g. birds and mammals) accumulates zinc when the surrounding level of zinc is lower than normal. The uptake/excretion of zinc is regulated by organisms on all trophic levels but to a higher degree by organisms on the higher trophic levels (Landner & Lindestrm 1998:104-105; KemI 1995:971; Kiekens 1995:284). Zinc may be considered, together with cadmium as very mobile a bioavailable metal. Mobility of zinc varies with concentration of adsorbing material, pH, dissolved and particulate iron and manganese concentration of complexing ligands, cation exchange capacity, organic content, concentration of zinc and redox potential (indirectly). Zinc is due to mobilization by acidification transported downwards in the soil profile. Zinc adsorption is not anticipated below pH 6.0. However, above pH 7.0 metal oxides, clay and apatite are efficient adsorbents capable of binding 90100 % of the zinc (KemI 1995:971; 984, 988; Kiekens 1995:302, WHO 1996:72). In theory and according to certain laboratory experiments, there are examples of both synergistic and antagonistic interaction between zinc and other metals. When an organism is exposed to cadmium, for example, the addition of zinc usually mitigates the adverse effect of cadmium and reduces the uptake of cadmium by the organism (Landner & Lindestrm 1998:131). This ability to mitigate the effect of other metals such as the non-essential metals cadmium, lead and mercury is due to the fact that the toxic effect of these metals is largely exerted by their substitution for zinc in enzymes and other vital proteins in the organism. If the occurrence of zinc in the environment increases, zinc can retake its place and displace the other metals in the process of uptake in the organism in question. There are numerous examples of this for lead and cadmium in particular in both plants and animals. However, an excessive input of zinc can lead to a corresponding deficiency of other essential metals such as copper and iron (Landner & Lindestrm 1998:132). It has been estimated that the concentration of zinc in Swedish agricultural soils have increased by 10 % during 19001990. The Swedish releases of zinc to air and water have decreased considerably during the last two decades. The deposition of zinc in mosses has decreased in Sweden by 21 % between 1975 and 1985 (KemI 1995:976-978).

6.2 Use
Pure zinc is used mainly for protecting steel from rust (galvanization). Other important fields of application are Zinc-base alloys, brass and bronze, zinc semi-manufactures and chemicals. Zinc oxide is used mainly for rubber processing products, pigment, and as intermediate for 48

zinc chemicals. Zinc chloride is used as wood preserver, in soldering fluxes, for galvanization, and as dry battery filler. Zinc phosphate is used as corrosion-inhibitive pigment and material for dental cements (International lead and study group 1996; KemI 1995:974). In general, zinc compounds are used for various purposes: pesticides, fungicides, insecticides, wood preservatives, drugs, animal feed additives, astringents, catalysts, dietary supplements, chemical reagents, metal plating agents, tanning agents, intermediates for zinc chemicals, oil additives, flame retardants, pharmaceuticals, ointments, in rubber processing (activators, accelerators and vulcanizing agents) etc. (KemI 1995:974; Landner & Lindestrm 1998:21). The use of zinc was in EU in 1994 distributed on: galvanizing (39.8 %), brass and bronze (24.6 %), zinc semis (12.4 %), zinc base alloys (11.3 %), chemicals (8.3 %), zinc dust powders (2.5 %), and other uses (1.1 %) (Eurostat 1997).

6.3 Production
The world total mine production of zinc was in 1997 about 7.4 million tonnes, in 1987 the primary production of zinc was about 6.6 million tonnes, and in 1982 the production was about 5.7 million tonnes. Thus, the production has increased significantly during the last fifteen years. Figures from the world smelter production of zinc indicate that the smelter production of zinc was stable ( 7.3 million tonnes) during the period 1989 to 1994 (Chapman et al. 1999:269; United Nations 1995:405; Knight-Ridder financial/commodity research bureau 1996:316; Eurostat 1997). Both the production (primary and secondary) and consumption of zinc was in 1994 about 1.7 million tonnes in EU. This constituted about 25 % of the world production and consumption (Eurostat 1997). The zinc consumption in Europe was about 2.3 million tonnes in 1994 (International lead and study group 1996). The use of zinc as corrosion protection and in various alloys, as well as its use in batteries, permits recovery of a substantial portion of the used zinc. However, when it comes to the use of zinc in chemicals, paint pigment, rubber products, sacrificially anodes etc. its practically or technically in most cases not feasible. The potential recovery rate of zinc in galvanized steel scrap is believed to be around 6080 %, while the actual global recovery rate in 1990 has been estimated to around 29 % (Landner & Lindestrm 1998:25; Eurostat 1997). According to Eurostat, metal production from secondary sources accounted for more than 8 % of the total EU refined zinc output in 1994 (Eurostat 1997). The zinc ores often occur together with ores containing other metals, usually lead, copper, silver and cadmium. The cadmium production is closely linked to the production of zinc. It is difficult to determine whether resource availability in itself is a limiting factor for the future use of a metal. However, zinc is reported to be one of the metals for which ore reserves appear to be scarcest. Estimations on how long the reserves will last with current exploitation varies from 25 years to 480 years. It is among other thing dependent on if the estimation is based on economically exploitable zinc reserves or technically extractable reserves. However, concerning another important resource utilisation aspect, the energy consumed in primary production, zinc shows the lowest value for all base metals except iron. In this context it is important to bear in mind that one of the principal applications for zinc is as corrosionprotection coating for iron steel, i.e. an application whose purpose is to reduce resource withdrawal and consumption of another base metal (Landner & Lindestrm 1998:910, 17 19).

6.4 Emissions and deposition

Important releases of zinc to the environment are for instance discharges of smelter slags and wastes, mine tailing, coal and bottom fly ash, municipal and industrial effluents, and the use of commercial products such as fertilizers and wood preservative that contain zinc. Important 49

emission to air comes from zinc production and other metals production where zinc is present, fuel combustion and incineration. Weathering of rocks and soil particles are other important natural sources of zinc (KemI 1995:976-977). Estimates for 32 countries in Europe of past and likely future air emission of arsenic, cadmium, lead, and zinc have been made by European Environmental Agency (EEA). The emissions of zinc to air has decreased from about 160 000 tonnes in 1975 to about 60 000 tonnes in 1991 (EEA 1998:112). However, according to Eurostat the total air emissions of zinc in 38 European countries was in 1990 only about 26 000 tonnes. In EU-15 the air emission of zinc from EU-15 has been estimated to 11 115 tonnes in 1990, of which 3 400 came from Spain, 1 800 from France, and 1 600 from Germany (Eurostat 1998:78). The air emission of zinc is expected to continue to decrease (EEA 1998:112). Manure and atmospheric deposition are the main sources of zinc inputs to agricultural soil. For Swedish conditions it has been estimated that the removal of zinc from the soil with the harvest amounts to approximately 200 g/ha/year, and the removal by weathering and leaching amounts to about 10 g/ha/year. Approximately 60 g/ha/year is returned to the soil by the atmospheric deposition in southern Sweden, and only 15 g/ha/year in cases of commercial fertilizers is used. This means that the soils are slowly being depleted of zinc, with a risk of deficiency. This depletion can be counteracted by the use of farmyard manure, which contains much more zinc than commercial fertilizer. A large portion of the zinc in manure comes from zinc added to animal feed to prevent deficiency symptoms in the livestock (Landner & Lindestrm 1998:32). The deposition of zinc in southern Sweden has been estimated to be roughly twice as high as the natural value and near the natural value in the interior of Norrland in the northern part of Sweden. Zinc deposition over Sweden decreased between 1975 and 1985 by more than 20 % on average. A halving of zinc emission to air from Swedish sources is expected during the period 1990-2000. At the same time, a reduction of zinc emissions in Europe is being accomplished by various emission control measures, and due to production cutbacks in Eastern Europe. This should lead to a continued evening-out of zinc deposition over Sweden towards a level defined by the natural cycle of zinc (Landner & Lindestrm 1998:62). Zinc is found in the atmosphere at the highest concentrations in the smallest particles. Particles with small diameters and low densities may travel long distances from emissions sources. The possibility of long range transport indicates that lifetime in air is at least on the order of days. Zinc is removed from the atmosphere by dry and wet deposition. The average annual deposition of zinc in southern parts of Sweden is 6-7 mg/m2 and in the north about 2 mg/m2 (KemI 1995:978, 986987).

6.5 Concentrations (in nature and human)

Zinc is the 24th most abundant element in the earths crust. Its average concentration is estimated to 70 mg/kg. Volcanic rock contains around 70 mg/kg and sedimentary rocks 15 100 mg/kg. High zinc concentrations are found in shales and clay sediments 80120 mg/kg. Zinc also occurs in phosphate rocks. The average zinc concentration in 91 % of the phosphate reserves has been estimated to 239 mg/kg (Landner & Lindestrm 1998:16; Kiekens 1995:285). The total zinc concentration in soils is largely dependent on the composition of the parent rock materials. The common concentration in soils is 10300 mg/kg with an average of around 50 mg/kg dry weight kg. The concentration of zinc in solution is, however, compared to the total concentration in general very low. The zinc concentrations in most soils in Western Europe are consistent with the levels considered as background values, with exception for mined areas (Landner & Lindestrm 1998:16; Kiekens 1995:285, 289). Sewage sludge exhibit a wide range of zinc concentrations, which are generally higher than the background levels, found in soils. Mean concentrations in the range of 1 5004 100 mg/kg dry weight has been reported. All fertilisers, mineral as well as organic, and soil amendments 50

contain zinc, most often as impurities. Zinc concentrations in inorganic phosphate fertiliser range from 501 450 mg/kg, in limestones from 10450 mg/kg, while manure values from 15250 mg/kg have been reported. Together with atmospheric deposition these sources may cause a positive zinc balance (enrichment of zinc) in soils (Kiekens 1995:287). Zinc has accumulated in the technosphere to a high degree compared with the naturally occurring quantities. However, mercury, lead and copper show an even higher degree of accumulation in the society (Landner & Lindestrm 1998:89). The mean concentration of zinc in the soils mor layer is roughly the same in all parts of Sweden, with an average concentration of 55 g/g, although there are local variation due to local anthropogenic sources and geological conditions. The concentration of zinc in the mor layer in Swedish forest soils does not appear to be elevated. Zinc is more weakly bound to organic matter in the mor layer than most other metals. In parts of southern and central Sweden, where the soil is acidified, leaching of zinc from forest soils has been measured to be in the order of 12 % per year. With this trend, there is a clear risk that zinc deficiency will occur in certain forest soils (Landner & Lindestrm 1998:54, 66-67). The mean concentration of zinc in Swedish agricultural soil, 57 g/g d. w., is close to the level in forest soil (Notter 1994:70). Typically zinc concentrations for river water are 4 g/l, ground water 10 g/l, rainwater 10 g/l. In the Baltic seawater the average zinc value is 1 g/l (Landner & Lindestrm 1998:105). In most waters, zinc concentration is higher in the sediment than in the water column and the concentration in water decreases when the salinity increases (KemI 1995:978). The zinc concentrations in Swedish lakes and watercourses are largely determined by the nature of soils within the associated drainage basins. Acidification is the leading cause of high zinc concentrations in certain smaller drainage basins in southern Sweden. It has been suggested that 1 g/l is a general natural value for small watercourses, while 3 g/l has been suggested for larger bodies of water. The concentration of zinc in ground water is also highly affected by low pH value but for samples with pH higher than 6, the median concentration is 3 g/l (Landner & Lindestrm 1998:54, 76). The vegetation in zinc-contaminated environments generally has higher zinc concentrations than normal. The concentration elevation varies considerably both between species and between different parts of the plant. But the degree of enrichment in plants is never in proportion to the concentration elevation in the soil. On a contaminated site with 23 times higher zinc concentration in the raw humus than on an unaffected site, the corresponding concentration elevation in grass and woody plants and in spruce needles was 4-5 times, and in bark and thick roots only 2-3 times (Landner & Lindestrm 1998:103). Zinc plays a central role in ensuring proper structure and function of a number of proteins in living organisms. It participates in many vital reactions such as detoxification, maintenance of the genetic code in DNA and RNA, protein synthesis etc. Zinc is found in most, if not all, tissues in organisms (Landner & Lindestrm 1998:96). Zinc is present in all the tissues and fluids of the human body. The total body content has been estimated to be approximately 2 g. The zinc concentration of lean body mass is approximately 30 g/g. Skeletal muscle accounts for approximately 60 % of the total body content, and bone, with a zinc concentration of 100200 g/g, for about 30 %. High concentrations of zinc are found in the choroids of the eye, 274 g/g, and in prostatic fluids, 300500 g/ml. Some typically concentrations of zinc in man are for muscle 220 g/g d.w., liver 210 g/g, brain 70 g/g, whole blood 7 000 g/l, mothers milk 2 000 g/l, perspiration 1 100 g/l, sperm 150 000 g/l (WHO 1996:75; Landner & Lindestrm 1998:105). The zinc concentration in the human environment and in various foods is in general lower than in human tissues. The zinc concentration in human muscles, for example, is 10 times 51

higher than in potatoes, and it is about 2 000 times higher in blood than in Swedish lakes and watercourses (Landner & Lindestrm 1998:96-97). Typically zinc values in some foods are for potatoes 20 g/g (d.w.), rice (polished) corn 10 12 g/g (w.w.), wheat flour 8 g/g (d.w.), cod 22 g/g (d.w.), pikes from Swedish lakes 70300 g/g (d.w.), red meat (beef) 170 g/g (d.w.), pork (lean) 20-30 g/g (w.w), chicken 720 g/g (w.w), cheese 3040 g/g (w.w) and milk 35 g/kg (WHO 1996:78; Landner & Lindestrm 1998:105; KemI 1995:982).

6.6 Limit values

The normative physiological requirement for absorbed zinc has by WHO been set to 1.4 mg/day for adult male and 1.0 mg/day for adult females (i.e. the need before adaptation). (Pregnant women and lactating women needs more zinc.) This corresponds to 21.6 g/kg body weight respectively 17.8 g/kg body weight. Infants, children and youths needs more zinc per body weight than adults do. As an example, infants in the age of 0.5 year to 1 year needs according to the WHO estimates at least 93.2 g/kg body weight (WHO 1996:8081, 83, 8586). Thus, if 50 % of the intake is absorbed the total intake has to be at least 2.8 mg/day for adult males and 2.0 mg/day for adult females. If the absorption is only 20 %, the intake consequently has to be at least 7.0 mg/day respectively 5.0 mg/day. However, the zinc intake should be lower than 50 mg/day since such level has been shown to influence copper status, as indicated by a decline in erythrocyte copperzinc superoxide dismutase activity. The upper limit of zinc intake recommended by WHO is 45 mg/day for adult male (65 kg), 35 mg/day for adult female (55 kg), and higher or about the same counted per body weight for infants, children and youths (WHO 1996:73, 99). WHO has recommended a daily zinc intake of 8 mg for girls in the age of 19, 13 mg for girls 10-13 years, 11 mg for adult women, 13-15 mg for pregnant women and, 27 mg for breast feeding women (Landner & Lindestrm 1998:125). Occupational exposure limit values set for zinc oxide (fume) by US, German and Swedish authorities is 5 mg/m3, for zinc chloride a limit value of 1 mg/m3 has been set by Swedish and US authorities (KemI 1995:973).The Swedish limit value for zinc in drinking water is 300 g/l at water works or taps after letting the water run, and 1 000 g/l at taps without letting the water run (Landner & Lindestrm 1998:126). To obtain a 95 % protection level for species and functions in freshwater ecosystems, an upper limit of 25 g Zn/l (dissolved, bioavailable zinc) would according to Landner and Lindestrm be applicable to Swedish inland waters. To achieve more or less 100 % protection the level have to be lowered to 15 g/l as regards dissolved bioavailable zinc. However, there are many examples of water areas where the total concentration of zinc is high or very high (up to 300 g/l) without any signs of adverse impact on the aquatic organisms. In these cases, the bioavailable portion of the total zinc concentration is presumable small (Landner & Lindestrm 1998:113, 121). Landner & Lindestrm suggest a limit value for protecting marine ecosystems in the Swedish west coast of 10 g Zn/l. It is significantly lower than the corresponding water quality criteria in USA 86 g Zn/l and in UK 40 g Zn/l (Landner & Lindestrm 1998:114). The SEPA (Swedish environmental protection agency) has suggested preliminary guideline values for soils. For sensitive soil use (use for housing, cultivation, animal husbandry and groundwater protection as well as parkland) the suggested value is 400 g/g dry weight. For less sensitive soil use with groundwater protection (industrial areas, roads etc.) the suggested value is 700 g/g. A zinc concentration of 400 g/g is about 78 times higher than the median value for Swedens agricultural and forest soil (Landner & Lindestrm 1998:116). However, an other way of determine a limit value could be the degree of increase in zinc content compared to a natural background value rather than the absolute concentration level. 52

According to SEPA (Swedish Environmental Protection Agency) for most metals studied, the minimum known effect levels are 3-5 times higher than the initial concentration (quoted from Notter 1994:24). If that better determines whether or not adverse effects will occur in the soil ecosystem then limit values given as absolute concentration levels may in some cases cause an over-protection while the same value may in other cases not provide a sufficient protection of sensitive ecosystems (Landner & Lindestrm 1998:116-117). However, the bioavailability is a crucial factor. Perhaps it would be more accurate (although more complicated) to relate a limit value to the amount of bioavailable zinc in different environment rather than to use absolute values or degree of increase values. Based on the assumption that one should not expect severe regional effects unless the regional background level is increased by more than three times the critical concentration of zinc in agricultural land in Sweden has been estimated to 170 mg/kg d.w. (Notter 1994:26). Without a good knowledge of several other soil properties, which affect the solubility, and bioavailability of zinc, it is not considered possible to specify any reliable critical limit values for toxic zinc concentrations in the soil (Landner & Lindestrm 1998:115). Limit values for sewage sludge that are used on agricultural land are for most countries in the range of 1 0005 000 mg zinc/kg (Kiekens 1995).

6.7 Risk assessments, exposure and harmful effects

Environmental authorities in various countries have shown a growing interest in zinc in resent years. Various activities and policies are now aimed at reducing or regulating the use of zinc and zinc compounds (Landner & Lindestrm 1998:7). The Dutch National Institute of Public Health and Environmental Protection has in their criteria document on zinc from 1991 drawn following conclusion: The risks associated with the current concentration of zinc in the environment appears to be nil for man, and limited and localised for animals and plants. For humans, especially lactating women, the possibility of too low zinc intake is greater than that of excessive intake (quoted in Landner & Lindestrm 1998:8). The Swedish National Chemicals Inspectorate (KemI) did 1994 selected zinc as a candidate for risk reduction with the following reasons: Serious aspects of zinc are its wide distribution and relatively high mobility, and as shown in the laboratory its high to very high toxicity to several aquatic organisms and its moderate to very high bioaccumulation potential. Regarding health, serious aspects of some zinc compounds are their genotoxic effects and the fact that zinc chromate probably has carcinogenic effects (KemI 1995:972). The general population is mainly exposed to zinc via food. Drinking water and atmospheric dust may also contribute to the total exposure. In an investigation in the U.S. the mean intake of zinc via drinkingwater was estimated to be 0.4 mg/day with a maximum value of 26 mg/day. Exposure via dermal sorption of soil and dust are relevant for children (KemI 1995:982983). The proportion of the ingested zinc (or other trace elements) that is available is governed by a wide range of variables. They include: (i) the physicochemical characteristics of trace element sources in the diet; (ii) the biochemical interactions of these elements with synergistics or antagonists either in the gut lumen or in tissues; and (iii) physiological variables which, in response to changing relationships between element and supply and demand, influence the efficiency of element absorption, storage or incorporation into functional sites (WHO 1996:22). The zinc absorption is poorly regulated in infants and is declining by senility. It is further related inversely to both the current intake of zinc and the existing zinc status. Uptake and retention of orally administrated zinc is strongly dependent on pre-existing zinc status. In one study were the subjects were given 7, 15, 30 mg Zn/day it was found that the absorption was 47, 32 and 21 % respectively (WHO 1996:25). The systemic availability of tissues zinc is profoundly influenced by the balance of anabolic and 53

catabolic process governing the turnover of soft tissues and the skeleton. Studies on non human species also suggest that skeletal zinc can be redistributed and utilized if skeletal resorption is induced by a low calcium intake (WHO 1996:29). Zinc absorption is concentrationdependent and takes place throughout the small intestine. Isotopic studies with human subjects have identified three principal dietary factors influencing zinc absorption and utilization, namely the content of inositol hexaphophate (phytate), the level and source of protein, and the total zinc content of the diet. The principal route of excretion of ingested zinc in humans is through intestine (WHO 1996:7677; KemI 1995:994). The jejunum appears to be the site of maximum absorption, the colon not playing a significant role. Intestinal perfusion studies in humans suggest that zinc absorption is a carriermediated transport process, which is not saturated under normal physiological conditions. However, recent isotopic studies of zinc absorption from single meals indicate that saturation of absorption is approached if the intake of available forms of zinc by adults exceeds approximately 4 or 5 mg per meal. Zinc administrated in aqueous solution to fasting subjects is absorbed very efficiently (6070 %) and there is no indication of saturation up to doses of 1015 mg. Absorption from solid diets is much less efficient and, depending on the content of zinc in meals otherwise identical in composition, can vary widely (WHO 1996:76). Requirements for dietary zinc are determined partly by the physiological processes governing tissue demands for zinc and its rate of loss from the body, and partly by the intrinsic characteristics of the diet, which influence the release of potentially absorbable forms of the element during digestion. Except in young rapidly growing subjects or those in whom zinc losses are enhanced as a consequence of stress or other challenges, it is notable that the activity of zincdependent processes can be maintained for several weeks after both the intake and the total absorption of zinc have declined. This is achieved by a means of a substantial reduction in endogenous losses. The total losses of zinc in faeces and urine and from skin during zinc depletion can decrease by approximately 40 % if subjects have had a previous opportunity to adapt to the low zinc intake (WHO 1996:79, 81). The tentative estimates of zinc losses suggest that the average physiological requirement for absorbed zinc to ensure the maintenance of a metabolically available bodyzinc pool in the fully adapted adult is approximately 1 mg/day for men and 0.7 mg/day for women. The normative physiological requirement for absorbed zinc has by WHO been set to 1.4 mg/day for adult male and 1.0 mg/day for adult females (i.e. the need before adaptation). Growing individuals, lactating women and pregnant women have a particularly high zinc requirement (WHO 1996:8081, 83, 8586, 97; see chapter 6.6 above). WHO has recommended a daily zinc intake of 8 mg for girls in the age of 19, 13 mg for girls 10-13 years, 11 mg for adult women, 13-15 mg for pregnant women and, 27 mg for breast feeding women (Landner & Lindestrm 1998:125). However, the amount that is absorbed differs a lot between different food and due to other factors as mentioned above. For instance has the abortion of zinc from maternal milk been estimated to be about 80 %, while the abortion for wheyadjusted cows milk has been estimated to be only 3035 % (WHO 1996:9293 About 90 % of the Swedish women have a daily intake below 11.6 mg/day. The median value was in one study 8.7 mg/day while the Swedish and international recommendations are 12 respectively 11 mg/day. Studies of zinc intake suggest that zinc deficiency can occur in pregnant and lactating women (where the recommended intake are higher) in Sweden unless zinc supplements are taken (Landner & Lindestrm 1998:113, 125). There is a general risk for zinc deficiency for infants older than 6 months if their only zinc source is maternal milk (WHO 1996:94). The dietary intake of zinc of an average teenage male in US has been estimated to 18.6 mg/day. For adults in United Kingdom the zinc intake has been estimated to 9.7 3.3 (SD) mg/day and to 7.518 mg for adults in the Netherlands (KemI 1995:983, WHO 1996:79).

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The principal clinical features of severe zinc deficiency in humans are growth retardation, a delay in sexual and skeletal maturation, the development of orificial and acral dermatitis, diarrhoea, alopecia, a failure of appetite and the appearance of behavioural changes. An increased susceptibility to infections reflects the development of defects in the immune system. The effects of marginal or mild zinc deficiency are less obvious and can readily be overlooked. A reduced growth rate and impaired resistance to infection are frequently the only manifestations of mild deficiency in humans. Children need more zinc per body weight than adult do and male children are particularly susceptible to zinc deficiency (WHO 1996:72, 74, 83). Few instances of acute zinc poisoning have been reported; its manifestations include nausea, vomiting, diarrhoea, fever and lethargy and have been observed, typically after ingestion of 48 g of zinc (WHO 1996:73). A lethal oral dose in humans is reported to be 28 g zinc. A dose of 12 g is described as an emetic and 12 gram of metallic zinc caused severe intoxication symptoms (KemI 1995:997; Landner & Lindestrm 1998:120). Metal fume fever is the most prevalent effect, due to inhalation of zinc oxide dust. However, most authorities agree that metal fume fever itself is a relatively innocuous condition. Occupational exposure to zinc chromate has been associated with an increased risk for lung cancer. IARC has classified zinc chromate as probably carcinogenic to humans (group 2A). Oral exposure to high levels of zinc has caused anaemia, decreased levels of HDL cholesterol, and pancreatic damage in humans and in animals. Several cases of gastrointestinal disturbances have been reported after ingestion of large amounts of zinc sulphate. Studies on experimental animals indicate that the acute oral toxicity of zinc compounds is generally medium to moderate. Some zinc compounds are irritating to the skin. Of all zinc compounds examined, zinc chloride clearly possessed the most potent irritancy and the highest mitogenic activity in skin. Genotoxic, immunological and reproductive effects, caused by zinc compounds, have been observed in experimental tests (KemI 1995:971, 994-998, 1000-1001). Longterm exposure to high zinc intakes substantially in excess of requirements has been shown to result in interference with the metabolism of other trace elements. Copper utilization is especially sensitive to an excess of zinc. This copper/zinc interaction has been responsible for the inadvertent induction of copper accumulation in Wilson disease. A zinc intake of as little as 50 mg/day has been shown to influence copper status, as indicated by a decline in erythrocyte copperzinc superoxide dismutase activity (WHO 1996:73). Zinc is bioaccumulated in aquatic organism. The bioconcentration factors vary from moderate to very high between different taxa. Higher concentrations are found in crustaceans, marine algae, and in benthic insects than in fish. Zinc does not concentrate in terrestrial plants. Zinc does not biomagnify through terrestrial or aquatic food chains (KemI 1995:987) Zinc does not volatilise from soil but adsorbs strongly to soil particles. However, zinc in soluble form, such as zinc sulphate, is fairly mobile in most soils. In most unpolluted waters, zinc exists primarily as the free (hydrated) divalent cation. Zinc is readily transported in most natural waters and is one of the most mobile of the heavy metals. Most zinc is considered to be partitioned to sediments through adsorption and precipitation, although a large fraction will remain dissolved in the water phase, especially at low pH values (KemI 1995:984985). Higher plants predominantly absorb Zn as a divalent cation (Zn2+), which acts either as a metal component of enzymes or as a functional, structural, or regulatory cofactor of a large number of enzymes. The uptake of zinc by plants and animals can vary depending on age and gender of the individuals, zinc in the surrounding environment and in the food. Furthermore, there are considerably differences between different species and trophic levels. Only 13 % of total zinc in soils has been reported to be available to plants. The most important soil components contributing to adsorption of zinc are clay minerals, hydrated metal oxides and organic matter (Kiekens 1995:284, 292, 297; Landner & Lindestrm 1998 102-103; KemI 1995:988).

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The bioavailability of zinc is dependent on a variety of environmental factors, among which hardness and acidity together with the total zinc content are the most important. Other important factors are: organic matter, microbial activity, adsorption site and moisture regime. A high concentration of organic matter and phosphorus also reduces the bioavailability in water. Liming normally reduces the uptake of zinc in plants. The uptake of zinc in plants is largely an active (energy-demanding) process. Plants seem to be capable of storing a large excess of zinc for possible later use without suffering visible harm. The higher an organisms is in the food chain, the grater its ability to regulate zinc uptake. In mammals and birds, zinc uptake regulation is so effective that no abnormally high accumulation of zinc occurs in tissues even in environments with much higher concentration of zinc than normal. Man actively takes up zinc from his environment to satisfy the bodys need of zinc. This is evidenced by the fact that the zinc concentration in various human tissues is generally higher than in the human environment and food (Kiekens 1995:298; Landner & Lindestrm 1998:9698, 102-103). Many cultivated plants are known to prone to developing symptoms of zinc deficiency relatively easily such as, maize and sorghum, flax, hops, cotton beans, onions, potatoes, wheat and certain species of fruit trees. Zinc deficiency can also occur in wild plant species. In the sea, there are examples of the fact that zinc can be a limiting factor for algal production, although only at very low levels. The symptoms of zinc deficiency in higher plants are chlorophyll defects and reduced growth in biomass and length (Kiekens 1995:284; Landner & Lindestrm 1998:97, 107). Zinc deficiency has occurred in wheat and barley grown in soil containing 3.56.6 mg/kg (KemI 1995:989). Zinc deficiency causes a variety of symptoms in animals, among which skin changes in pigs are among the better known. The earliest symptoms on animals are reduced food intake, followed by reduced growth, feebleness, diminished immune defences, poor wound healing and reduced fur growth. Skin changes are a well-known symptom on deficiency for fastgrowing pigs. Other effects of zinc deficiency are reproductive disturbances and foetal damages, abnormal feather formation and reduced egg production in birds, and hoof and horn changes in sheep and goats. Most effects of zinc deficiency in animals are reversible and disappear when the zinc intake increase (Landner & Lindestrm 1998:107108). An increased incidence of congenital malformations in infants has been associated with zinc deficiency in the mothers (KemI 1995:996). Of primary importance to zinc toxicity are the physical (i.e. suspended/dissolved) and chemical state of zinc. Laboratory data on toxicity of zinc to aquatic organisms indicate that acute toxicity of zinc is moderate to a few of the tested organisms, but high to very high to most of the tested species. The risk of effect on freshwater organisms varies with a number of environmental factors, such as hardness, phosphorus and humus content, and salinity. Among these, the hardness of the water (e.g. measured as concentration of CaCO3) is generally considered to be the dominant factor determining the bioavailability of zinc in most European surface waters. For phytoplankton, zooplankton, common sea mussel, and crab the chronic toxicity begins at 1020 g/l, whereas early life stages of rainbow trout and fathead minnow are affected at concentrations of 3070 g/l. However, laboratory data may not reflect the true toxicity of zinc in any realistic situation in the environment (KemI 1995:989990; Landner & Lindestrm 1998:123-124, 133). If the zinc intake of an organism is so great that the normal mechanisms for transport and excretion cannot keep up with the uptake, the zinc concentration in the tissues can increase so much that the zinc becomes toxic. The toxic effects of zinc in living organisms seems mainly to be associated with the fact that it competes with other metals, e.g. copper, iron, and calcium for their binding sites. The usual result is that the organism shows symptoms of a deficiency in the displaced metals. The scientific literature contains few or no examples of adverse effects in terrestrial plants and animals, including man, of a moderately elevated zinc exposure. The zinc concentration in the superficial, organic soil layer must be more than five times, and probably ten times, greater than the natural background levels before any adverse impact on soil biology or vegetation can be expected. Local elevation of zinc concentrations 56

by a factor of 10-15 above the background level have been recorded in the mor layer in coniferous forest, without any inhibition of microbial soil processes or damage to sensitive plants species having been detected (Landner & Lindestrm 1998:112, 124). Toxic effects of zinc begin to appear at soil concentrations of 50 g/g (KemI 1995:989). In experiments where plants of certain sensitive tree species have been cultivated in nutrient solutions, an excess of zinc has resulted in reduced root growth at a zinc concentration of about 100 g/l. Organism that are exposed to elevated zinc concentrations can gradually develop a higher tolerance. However, an increased tolerance of fish to zinc has been found to be associated to an increased sensitivity to other stress (Landner & Lindestrm 1998:117, 134, 136). As far as Swedish agricultural soil is concerned, there are no observations of negative effects of zinc excess. The only apprehension that has cropped up recently concerns a somewhat paradoxical consequence of the use of zinc for veterinary purposes. Zinc oxide is added to piglet feed for weaning purposes in such quantities (up to 70 tonnes per year) that the local soils fertilized with excrement from piglets risk receiving zinc inputs that exceed current norms (0.8 kg Zn/ha/year (Landner & Lindestrm 1998:125). The zinc concentration in Swedens soils, water, plants and animals lies at a level that does not give rise to the risk of adverse effects. However, elevated zinc concentrations in the vicinity of point sources may cause adverse effects on terrestrial flora and fauna. Local effects on aquatic organisms may also occur at sites with elevated zinc concentrations. Generally speaking, zinc deficiency in animals appears to be a greater problem than zinc excess (KemI 1995:989, 99; Landner & Lindestrm 1998:120, 143).

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