Cadmium (Cd) is a naturally occurring chemical element that is normally present in our bodies at low concentrations. Most of the Cd that we take in each day is delivered in food. With the exception of smokers and occupationally exposed groups, food usually accounts for over 90 percent of the Cd absorbed by members of the general population.
Cd is both non-essential and highly toxic in mammals. At a biochemical level it appears that we could live without Cd, if that were possible to arrange. The high toxicity of Cd refers to its capacity as an effective poison at low dose. Exposure to a sufficient dose of Cd over a short time period is capable of causing acute poisoning with or without subsequent fatality. The acute lethal dose to humans can be as little as 0.35 grams by ingestion. Death from this cause is not rapid, occurring between 24 hours to two weeks later. However, food safety risks of Cd are in another category entirely. Here doses are measured in millionths of a gram per day, and the risks are not immediate but rather relate to the long-term consequence of cumulative exposure.
Cd is one of the best examples that we have of a biologically cumulative substance. With food as a constant daily source, and loss of each daily dose taking between 20 to 40 years, the amount of Cd retained in a person’s body gradually increases with age, from an estimated 1 millionth of a gram at birth to perhaps 15 to 80 milligrams (mg) by age 50, depending on personal history. About half (47 percent) of this accumulated Cd is retained in the liver and kidneys due to the presence of a metal-binding protein called metallothionein; a further three percent is shared between the lungs and pancreas, and the remaining 50 percent becomes more or less evenly distributed among the other tissues.
Unsurprisingly, the first reliable toxic effect of Cd accumulation in the body is the point where the burden of Cd in kidneys is sufficient to induce a change in kidney function. This toxicological endpoint is the focus of tolerable intake limits promulgated by the World Health Organization (0.025 mg of Cd per kilogram (kg) of body weight per month), and its science advisory body European Food Safety Authority (EFSA) (equivalent to 0.0108 mg/kg of body weight/month). The limits essentially represent the point at which the earliest onset of a change in kidney function may be starting to occur in post-50 year olds.
For contaminants that do not primarily act as carcinogens, regulatory bodies set tolerable intake limits by first determining the most sensitive toxicological consequence and then working backwards. It is unclear whether Cd should be treated in this way because some evidence exists that Cd may increase rates of breast and testicular cancers. The kidney is currently regarded the primary target organ of Cd toxicity with tolerable intake limits based on changes to kidney function, but a future change in approach may result in still lower recommended limits.
Another, much harder, problem exists that is likely to prevent tolerable intake limits from being reduced any further than the EFSA-recommended current figure. This is that at ordinary levels of Cd in foods, we are already hitting against the kidney-function threshold. The preferred toxicological approach for residues and contaminants in the diet is to apply an uncertainty (“safety”) factor to the lowest observed effects level to allow for inter-species and individual human variability, of perhaps 100. For Cd there is no such safety factor: The first onset of apparently toxic effects does appear to occur at the upper end of the usual intake range.
Recently, EFSA has released a set of “risk-based” food standards for Cd that, if adhered to and averaged across typical diets, would help achieve compliance with their recommended tolerable intake limit for Cd. The shift to risk-based food standards in recent decades has been a welcome development because many of older food standards were not overtly linked to tolerable intakes (toxicity is defined by the dose), or if they had been derived on this basis, the process was obscure. For food producers, these and other pre-existing food standards for Cd primarily represent a product compliance and trade risk. With a new set of food standards, it is likely that European regulators and markets will be placing a heavier emphasis on food compliance monitoring for Cd in the future.
Most dietary Cd comes from foods with elevated Cd concentrations that are consumed in significant amounts. These include cereals, vegetables, nuts, starchy roots or potatoes, and some meat products. Vegetarians have higher dietary exposures, as do regular consumers of bivalve mollusks and wild mushrooms. Smokers double their overall exposure, because tobacco contains significant Cd and the lungs are efficient at absorbing it. Together, ensuring compliance with tolerable intake limits and food standards will ensure the risk from Cd exposure from food is tolerably low.
There is Only One Problem
Most Cd in food comes from the soil where crops are grown and animals are raised. As a chemical element, Cd is present at low concentrations in all soils. However, human activities are causing soil Cd concentrations to increase, which results in increased Cd concentrations in food. While industrial activity, waste disposal, and mining can result in localized soil contamination, fertilizers and soil conditioners are the most important source of Cd in food-producing soils.
Elevated Cd concentrations are often associated with sources of phosphorus (P), an essential plant nutrient. Humanity needs to add P to soil to maintain productivity and feed an ever-growing population. P is added to soil via fertilizers, effluents, and sludge. These materials can contain Cd as an unwanted passenger that cannot easily be removed. The ultimate source of P is phosphate rock, a non-renewable resource that is mined and processed to give fertilizers (for example, superphosphate fertilizer). Geologically, Cd is co-deposited with P and phosphate rock can have over 500 mg of Cd for every kg of P. While the Cd concentration of phosphate rock varies, low-Cd sources of this mineral are mined preferentially, command a premium price, and will eventually be exhausted. In many countries like New Zealand, current P and Cd levels in many agricultural soils are now four to six times higher than their natural concentrations. Just as the majority of P in our diets could now be traced back to agricultural use of phosphate fertilizers, it is likely that most dietary Cd now also originates from this same source.
Municipal effluents and biosolids (sewage sludge) can be used effectively as P-containing soil conditioners. However, these materials also contain elevated Cd concentrations, along with other potential soil contaminants, particularly if there are industrial inflows into the sewage treatment plant.
Once added to soil, Cd binds strongly to soil particles, causing this toxic element to accumulate with each fertilizer application. Only small amounts of Cd are lost from the soil via surface runoff (with fertilizer runoff) and leaching, which is not significant until very high soil Cd concentrations are reached. The rate of Cd accumulation in soil depends on the concentration of Cd in the fertilizer. Low-cost fertilizers and effluents used by poor countries often have higher Cd concentrations, resulting in a more rapid buildup of this toxic metal in soil.
Plant roots can cause soil particles to release bound Cd, resulting in Cd entering the root and then the shoots of the plant. Grazing animals may consume the Cd-containing plant or, in some cases, ingest small amounts of soil directly. As with humans, the highest Cd concentrations in grazing animals are found in the kidneys and liver. Fortunately, there are no reports of muscle or milk products containing concerning Cd concentrations.
There is a large variation in the ability of plants to take up Cd from soil. Leafy greens such as lettuce and spinach have the highest Cd concentrations, while grains tend to have the lowest. That said, Cd concentrations in grains are of concern because they can represent a large proportion of the diet.
Managing Cd Concentrations in Food
Reducing or reversing the accumulation of Cd in soil requires the reduction of Cd applied with phosphate fertilizers. Removing Cd from phosphate fertilizers would halt further increases in the Cd concentrations of most agricultural soils. Unfortunately, there is no cheap way of removing Cd during fertilizer production.
In most cases, reducing the amount of phosphate fertilizer applied would result in an unacceptable drop in productivity. A characteristic of phosphate in soil is that it becomes immobilized and unavailable for plants, thus requiring additional fertilizer applications and further Cd accumulation. One line of research to reduce the reliance on phosphate fertilizers is investigating methods of liberating immobilized phosphate by using selected crop varieties or other soil amendments.
Sourcing phosphate rock with a lower Cd concentration reduces the amount of Cd added to soil. For example, most Cd in New Zealand’s pastoral soils come from the application of superphosphate made from Nauru phosphate rock, which contained ca. 550 mg of Cd for each kg of P. Subsequently, the fertilizer industry has reduced the Cd concentration in fertilizers to less than 280 mg Cd/kg P by using phosphate rock from other locations. To avoid the accumulation of Cd in soil, phosphate fertilizers would need to contain less than 50 mg Cd/kg P. Further exploration and innovation in mining may yield fertilizers with even lower Cd concentrations. An example is the potential source of low-Cd phosphate in the Chatham Rise, off the cost of New Zealand. Accessing this resource has the technical and environmental challenges associated with undersea mining.
Most Cd in agricultural soil is bound within the top 10 centimeters. Therefore, plowing the soil will dilute the Cd within the soil profile. Plowing can reduce plant Cd uptake by moving the Cd to a zone of lower root density. This dilution effect increases at greater plough depths. However, continued application of Cd-laden fertilizers will eventually increase the Cd concentration in the entire soil profile.
Cd-contaminated soil cannot easily be cleansed. There are no commercially available techniques to remove Cd from contaminated soil at a cost that is less than the value of the agricultural land. Extracting the Cd using fast-growing plants such as willow may work in principle, but it is unclear whether this will ever be a commercially viable technology for farmers.
The amount of Cd that is taken up by plants and subsequently enter food products is dependent not only on the total Cd in the soil, but also on a plethora of other soil factors and plant factors. Some of these factors can be managed to reduce Cd concentrations in food. There is considerable variation in the Cd uptake among plant varieties. Selective breeding or genetic manipulation can be used to obtain plant varieties that take up low concentrations of Cd.
Plants in acid soils, soils with low organic matter, or soils that are high in chloride more readily take up Cd. Liming to reduce soil acidity can effectively reduce Cd uptake in some soils, but not others. However, liming is a blunt instrument: Over-liming can induce deficiencies of essential nutrients.
Adding some types of organic matter to soil can effectively reduce plant-Cd uptake. There is variation in the effectiveness of various types of organic matter in reducing plant-Cd uptake. Elucidating the critical factors for such Cd immobilization is an ongoing area of research. Plants take up more Cd from soils that are deficient in the essential micronutrient zinc (Zn). Alleviating Zn deficiency in soil may reduce plant Cd uptake and increase the Zn concentration in foods. This has the double benefit of alleviating Zn deficiency in people (which affects some two billion worldwide) and reducing the toxicity of Cd in Zn-deficient people.
Managing such plant and soil factors can reduce the Cd concentrations in food over the short term. While these measures do not stop the accumulation of Cd in the soil, they can extend the time that food production can safely occur on Cd-contaminated soils. This gives additional time for the development of low Cd fertilizers, or new soil cleansing techniques.
While Cd concentrations in agricultural soils are increasing and Cd concentrations in some foods are nearing food standards, there are no reports of widespread Cd intoxication in the general population. In many agricultural lands, food production can probably continue apace without a widespread health calamity. However, over the medium term, continued accumulation Cd of agricultural soils is unsustainable because the upper end of current dietary Cd intakes are already commensurate with tolerable intake limits, and regulators will be moving to ensure that Cd in foods stay as low as reasonably achievable. Modifications to soil and plant factors can soften the impact of Cd accumulation in soils, and potentially work to reduce Cd in both individual foods and the whole diets, but the benefits of this work will ultimately be lost if Cd continues to strongly accumulate in growing soils. Therefore, a primary goal for agriculturalists should be to move to a steady-state condition, where annual inputs of new Cd to soils are no larger than losses.
The immediate issues for food producing countries are that food exports may be blocked if food standards are exceeded and the image of the country as a safe food producer may be tarnished. For countries with protectionist governments, Cd concentrations in foods may be a useful means of circumventing the World Trade Organization and imposing non-tariff trade barriers to protect local producers, even if the local produce also contains high Cd concentrations.
Any management decisions or regulations that are designed to reduce Cd concentrations in food need to be balanced against the cost of food production and the need to feed a growing population.
In the meantime, the clandestine threat that Cd poses to food safety will inexorably increase.
Dr. Kim is an analytical environmental chemist who works at Massey University in Wellington, New Zealand. Reach him at N.Kim@massey.ac.nz. Dr. Robinson is a professor of soil and physical sciences at Lincoln University in New Zealand. Reach him at Brett.Robinson@lincoln.ac.nz.
References Furnished Upon Request
One serious case of environmental Cd poisoning first focused scientific and regulatory attention on the possibility that long-term accumulation of Cd could cause serious harm. Between 1910 and the late 1940s, several hundred people from villages on the banks of the Jinzu River, Toyama Prefecture, Japan suffered from chronic Cd poisoning. Among other sources, Cd fumes and particulate matter emitted from a nearby mining company caused an excessive accumulation of Cd in soils of a farming community. Rice and soybeans grown in these soils contained high concentrations of Cd (1 to 3 mg/kg). Cd was not recognized as the cause until the mid-1950s. It was typically 30 to 40 years before the onset of symptoms, the most prominent of which was that the victim’s bones fractured under slight pressure due to their decalcification and subsequent softening. The disease was extremely painful, and the sickness became known as Itai-itai disease, variously translated “it hurts-it hurts” or “ouch-ouch.” By the end of 1965, some 100 deaths had resulted from disease.—N.K. & B.R.