Cadmium exposure and human health
It has been well established that excess cadmium exposure produces adverse health effects on human beings. For virtually all chemicals, adverse health effects are noted at sufficiently high total exposures. For certain elements such as copper and zinc which are essential to human life, a deficiency as well as an excess can cause adverse health effects. Cadmium is not regarded as essential to human life. The relevant questions with regard to cadmium exposure are the total exposure levels and the principal factors which determine the levels of cadmium exposure and the adsorption rate of the ingested/inhaled cadmium by the individual, in other words, the pathways by which cadmium enters the food chain, the principal pathway of cadmium exposure for most human beings.
4.1 Principal Factors Which Determine Levels of Human Exposure
Humans normally absorb cadmium into the body either by ingestion or inhalation Dermal exposure (uptake through the skin) is generally not regarded to be of significance (Lauwerys 1988). It is widely accepted (WHO 1992, ATSDR 1997) that approximately 2% to 6% of the cadmium ingested is actually taken up into the body. Factors influencing cadmium absorption are the form in which cadmium is present in the food, and the iron status of the exposed individual. In contrast, from 30% to 64% of inhaled cadmium is absorbed by the body, with some variation as a function of chemical form, solubility and particle size of the material inhaled. Thus, a greater proportion of inhaled cadmium is retained by the body than when cadmium is taken in by ingestion. For the non-occupationally exposed individual, inhalation exposure to cadmium does not usually contribute significantly to overall body burden. The exception to this generalisation is the cigarette smoker. One model for human cadmium intake (Van Assche 1998) has estimated that ingestion accounts for 95% of total cadmium intake in a non-smoker. For a smoker, this model estimates that roughly 50% of their cadmium intake arises from cigarettes with the balance due to ingestion and the low levels of cadmium naturally present in ambient air. In the past, occupational exposure was also a significant contributor to total cadmium intake, but with very stringent occupational standards in place today, occupational cadmium intake is much less of a consideration than it was 20 years ago. Thus, the principal determinants of human cadmium exposure today are smoking habits, diet, and, to a certain extent, occupational exposure.
4.2 Human Intake of Cadmium
Much of the cadmium which enters the body by ingestion comes from terrestrial foods. This is to say, from plants grown in soil or meat from animals which have ingested plants grown in soil. Thus, directly or indirectly, it is the cadmium present in the soil and the transfer of this cadmium to food plants together with the cadmium deposited out of the atmosphere on edible plant parts which establishes the vast majority of human cadmium intake, Some have estimated that 98% of the ingested cadmium comes from terrestrial foods, while only 1% comes from aquatic foods such as fish and shellfish, and 1% arises from cadmium in drinking water (Van Assche 1998).
As noted earlier, the cadmium content of terrestrial foods varies significantly as a function of the type of food crop grown, the agricultural practices pursued, and the atmospheric deposition of cadmium onto exposed plant parts. Cadmium levels in the soil, principally derived from natural sources, phosphate fertilisers and sewage sludge will naturally impact upon this cadmium uptake. However, this effect is secondary to the type of crop grown and the agricultural practices followed with respect to tillage, Aiming and crop rotation.
Cadmium Intake From Foods
Many studies have attempted to establish the average daily cadmium intake resulting from foods, In general, these studies show that the average daily diet for non-smokers living in uncontaminated areas is at present at the low end of the range of 10 to 25 µg of cadmium (Elinder 1985, OECD 1994, ATSDR 1997). This general trend is confirmed by decreasing blood cadmium levels in the general population in several countries during this time period (Ducoffre 1992, MURL 1989). In a rather recent evaluation, the International Programme on Chemical Safety (IPCS) assessed the average daily intake at the lower end of this range (WHO 1992).
The World Health Organisation (WHO) has established a provisional tolerable weekly intake (PTWI) for cadmium at 7 µg/kg of body weight This PTWI weekly value corresponds to a daily tolerable intake level of 70 µg of cadmium for the average 70-kg man and 60 µg of cadmium per day for the average 60-kg woman. Clearly, the daily cadmium intake for the general population from food, which is by far the dominant source of cadmium, is well below the guidelines established by the World Health Organisation. The average daily cadmium intake for the general population in the Western World has shown a distinct downward trend from 1970 through 1992 (Van Assche and Ciarletta 1992), a reduction presumed to be due to the marked decreases in direct atmospheric deposition of cadmium onto crops and soils. Other studies have suggested that, over the timeframe of 1980 - 1985, levels of cadmium intake have been relatively constant (OECD 1994). At an absorption rate of 5% from ingestion, the average person is believed to retain about 0.5 to 1.0 µg of cadmium per day from food.
There is considerable information in the literature regarding the cadmium contents of foods grown in contaminated areas (Elinder 1985, WHO 1992, OECD 1994). Detailed studies have indicated that only a small percentage of these contaminated areas were actually utilised for growing foods which were subsequently consumed with the exception of rice fields in Japan where considerable cadmium did find its way into the average person's diet through rice grown on contaminated rice fields (Elinder 1985). In specific cases, management measures to reduce the transfer of cadmium from historically contaminated soils into the local food chain have proven successful (Staessen et al. 1991).
Cadmium inhalation is a far smaller contributor to total cadmium body burden except, as previously noted, in the cases of smokers or some highly exposed workers of the past. Today, the inhalation route is well controlled in the occupational setting, and is well-controlled from point sources such as those which directly pertain to the non-ferrous, cadmium or cadmium products industries. Ambient air emissions from fossil fuel power generation plants, the iron and steel industry and other major industries where cadmium may be present as a low concentration impurity, on the other hand, may be substantial because the volumes of the waste gases generated are substantial.
Cadmium Intake From Cigarette Smoking - Smokers absorb amounts of cadmium comparable to those from food, about 1 to 3 µg of cadmium per day, from the smoking of cigarettes. It has been reported that one cigarette contains about 1 - 2 µg of cadmium and that about 10% of the cadmium content is inhaled when the cigarette is smoked (WHO 1992). Cigarette construction, the use of filters and variations in the cadmium contents of tobaccos could decrease cadmium exposure by this route, but in general cigarette smoking is a habit which can more than double the average person's daily cadmium intake. Cigarette smokers WHO are also occupationally exposed may increase their total cadmium intake even further.
Cadmium Intake From Occupational Exposure - Up to the l960s, very elevated cadmium in air exposure levels were measured in some workplaces, sometimes as high as 1 mg/m³. Since that time, workplace exposures and standards have decreased markedly so that most occupational exposure standards today are in the range from 2 to 50 µg/m³. The result has been that occupational exposures today are generally below 5 µg/m³, and most cadmium workers are exposed at levels which are considered to be safe (ATSDR 1997). In rare cases where cadmium air levels are higher, the use of personal protective equipment is obligatory. Extensive preventative hygiene programs and medical follow-up programs have been developed to control the risk related to cadmium exposure at the workplace (ACGIH 1996, OSHA 1992, Lauwerys 1986, Cadmium Council 1986). Considering present levels of occupational exposure cadmium intake, general dietary intake, and cigarette smoking intake, it still would appear, however, that the average daily cadmium intake is well below the values recommended by the World Health Organisation.
4.3 Human Health Effects of Cadmium
The kidney is the critical target organ for the general population as well as for occupationally exposed populations. Cadmium is known to accumulate in the human kidney for a relatively long time, from 20 to 30 years, and, at high doses, is also known to produce health effects on the respiratory system and has been associated with bone disease. Most of the available epidemiological information on cadmium has been obtained from occupationally exposed workers or on Japanese populations in highly contaminated areas.
Most studies have centred on the detection of early signs of kidney dysfunction and lung impairment in the occupational setting, and, in Japan, on the detection and screening for bone disease in general populations exposed to cadmium-contaminated rice. More recently, the possible role of cadmium in human carcinogenesis has also been studied in some detail.
4.3.1 General Population
Ingestion of cadmium in food is the major source of cadmium for non-smokers. Average daily intakes from food in non-contaminated areas is at the lower end of the 10 to 25 µg range of which approximately 0.5 to 1.0 µg is actually retained in the body. Uptake of cadmium from smoking could more than double that amount.
The actual level of intake which results from food ingestion varies as a function of multiple factors. For example, certain crops (e.g., sunflowers) and shellfish contain naturally elevated amounts of cadmium. Individuals WHO consume large amounts of these materials might thus at first seem to be at increased risk. However, recent studies have demonstrated that foods which are naturally enriched in cadmium are also enriched in substances which inhibit the uptake of cadmium into the body. Thus, individuals WHO ingest large amounts of sunflower seeds may ingest up to 1 00 µg cadmium per day, yet these individuals do not have levels of cadmium in blood or urine which are higher than individuals with far lower levels of cadmium intake (Reeves et al. 1997). Similarly, consumption of a diet rich in shellfish can double the intake of dietary cadmium without producing significant impacts upon blood cadmium (Vahter et al. 1996) These studies illustrate that the cadmium content of food is just one of a number of factors which determines the actual uptake of cadmium into the body. Indeed, recent studies (Vahter et al. 1996) have suggested that overall nutritional status is a more important determinant of cadmium uptake into the body than is the actual amount of cadmium ingested. For example, women subsisting upon a vegetarian diet and with reduced iron stores have increased uptake of ingested cadmium. For these women, iron deficiency is a more important determinant of cadmium uptake than is the actual amount of cadmium ingested.
The present levels of cadmium intake in most European countries are far below the PTWI recommended by WHO. Indeed, as a result of numerous public health policies implemented over the past several decades, the cadmium body burden of the general population appears to be rapidly declining (Friis et al. 1998). Present exposure levels in many European countries are now comparable to, or lower than, those which characterise 'unacculturated populations' residing in the jungles of South America (Hecker et al. 1974).
Present levels of general population exposure to cadmium have no known adverse health consequences. Existing standards such as the PTWI are based upon biological models which associate cadmium exposure and increased urinary excretion of low molecular weight proteins. This has been estimated to occur in humans with a life-long daily intake of approximately 200 µg. Only in highly contaminated agricultural areas, and only if the cadmium levels in the food grown there were significantly increased, can levels of exposure be sufficient so as to produce kidney dysfunction. Such a situation did occur in the 1950s and 1960s in Japan where heavy cadmium contamination of rice fields, along with nutritional deficiencies for iron, zinc and other minerals, led to renal impairment and bone disease (Itai Itai disease) in exposed populations. Studies utilising very sophisticated biomarkers have detected mild alterations in kidney functions at lower levels of exposure (Buchet et al. 1990). However, more recent studies in the occupational setting have suggested that such alterations have no actual clinical consequences (Roels et al. 1997).
4.3.2 Occupationally Exposed Populations
Occupational exposure to cadmium is mainly by inhalation but also may include additional intakes through food, tobacco, and poor personal hygiene practices. In the past, the total cadmium in air level in the workplace has varied according to the type of industry, type of workplace, and industrial hygiene programs in place. Depending upon the level and duration of cadmium exposure, a wide variety of effects have been observed in occupationally exposed groups. For acute exposure by ingestion, the principal effects are gastrointestinal disturbances such as nausea, vomiting, abdominal cramps and diarrhoea. Acute poisoning by inhalation may lead to respiratory manifestations such as severe bronchial and pulmonary irritation, subacute pneumonitis, lung emphysema, and, in the most severe situations, death from pulmonary oedema may occur (Lauwerys, 1986). Chronic obstructive airway disease has been associated with long-term high-level occupational exposure by inhalation (WHO 1992, OECD 1994). While there have been suggestions in past studies that such exposure may cause lung or prostate cancer, more recent epidemiological analyses of cadmium-exposed cohorts have dismissed the prostate cancer association and indicate that arsenic rather cadmium may be responsible for the observed increase in lung cancer mortality rates (Sorahan et al. 1995, Sorahan et al. 1997). In addition, most of the other data cited as evidence for the carcinogenicity of cadmium (OSHA 1992) relies on studies which are confounded by the presence of other carcinogenic substances such as nickel, asbestos or tobacco smoke as well as arsenic.
For chronic cadmium exposure, effects occur mainly on the kidneys, lungs, and bones. A relationship has been established between cadmium air exposure and proteinuria (an increase in the presence of low molecular weight proteins in the urine and an indication of kidney dysfunction) (WHO 1992, OECD 1994). Cadmium is known to accumulate in the renal cortex, and there is evidence that the level of cadmium in the renal cortex associated with increased urinary excretion is about 200 to 250 µg/g (wet weight). Depending upon exposure level and other sources of cadmium, this level might be reached after 20 years occupational exposure. However, recent work has demonstrated that these effects are reversible at low exposure levels once the cadmium exposure has been removed or reduced (Roels et al. 1997). With today's low occupational exposure standards, coupled with required biological monitoring of cadmium exposure levels (e.g. cadmium-in-blood and cadmium-in-urine) and kidney function parameters (e.g. B-2 microglobulin, a low molecular weight protein), there is every assurance that kidney dysfunction or other effects YAII not develop in occupationally exposed workers as they did in the past.
4.4 Sources of Human Cadmium Exposure
While sources of cadmium emissions to the environment have been listed in some detail in this report and others (Cook and Morrow 1995, WHO 1992, OECD 1994, Nriagu 1989, ERL 1990, Jackson and MacGillivray 1993, Jensen and Bro-Rasmussen 1992, Jones et al. 1993, Van Assche and Ciarletta 1992, Nriagu and Pacyna 1988), there have been very few attempts to partition human cadmium exposure to its various sources. Van Assche (Van Assche and Ciarletta 1992, Van Assche 1998) has developed a model for cadmium exposure for human beings and allocated this exposure to the various sources. Some of the assumptions and the data inputs for the model have been based in large part on actual data from Belgium and the European Community, and, in particular, on the Environmental Resources Limited Report on the sources of human and environmental contamination in Europe (ERL 1990) and the updated data on cadmium emissions contained in the OECD Monograph on Cadmium (OECD 1994).
The analysis acknowledges that most human cadmium exposure comes from ingestion of food, and most of that arises from the uptake of cadmium by plants from fertilisers, sewage sludge, manure and atmospheric deposition, Specifically, the model estimated that the relative importance of various cadmium sources to human exposure is as follows (Van Assche 1998):
|Fossil Fuel Combustion
|Iron & Steel Production
Clearly, of the anthropogenic sources of cadmium, phosphate fertilisers, fossil fuel combustion, and some industrial activities contribute far more to human cadmium exposure than production, use and disposal of cadmium products and incineration of all cadmium-containing materials. However, as shown earlier, this observation should be put in the perspective of average daily cadmium intakes well below those necessary to ensure human health. Thus no action seems required to reduce cadmium from its existing levels.