The main threats to human health from heavy metals are associated with exposure to lead, cadmium, mercury and arsenic. These metals have been extensively studied and their effects on human health regularly reviewed by international bodies such as the WHO. Heavy metals have been used by humans for thousands of years. Although several adverse health effects of heavy metals have been known for a long time, exposure to heavy metals continues, and is even increasing in some parts of the world, in particular in less developed countries, though emissions have declined in most developed countries over the last 100 years. Cadmium compounds are currently mainly used in re-chargeable nickel-cadmium batteries. Cadmium emissions have increased dramatically during the 20th century, one reason being that cadmium-containing products are rarely re-cycled, but often dumped together with household waste. Cigarette smoking is a major source of cadmium exposure. In non-smokers, food is the most important source of cadmium exposure. Recent data indicate that adverse health effects of cadmium exposure may occur at lower exposure levels than previously anticipated, primarily in the form of kidney damage but possibly also bone effects and fractures. Many individuals in Europe already exceed these exposure levels and the margin is very narrow for large groups. Therefore, measures should be taken to reduce cadmium exposure in the general population in order to minimize the risk of adverse health effects. The general population is primarily exposed to mercury via food, fish being a major source of methyl mercury exposure, and dental amalgam. The general population does not face a significant health risk from methyl mercury, although certain groups with high fish consumption may attain blood levels associated with a low risk of neurological damage to adults. Since there is a risk to the fetus in particular, pregnant women should avoid a high intake of certain fish, such as shark, swordfish and tuna; fish (such as pike, walleye and bass) taken from polluted fresh waters should especially be avoided. There has been a debate on the safety of dental amalgams and claims have been made that mercury from amalgam may cause a variety of diseases. However, there are no studies so far that have been able to show any associations between amalgam fillings and ill health. The general population is exposed to lead from air and food in roughly equal proportions. During the last century, lead emissions to ambient air have caused considerable pollution, mainly due to lead emissions from petrol. Children are particularly susceptible to lead exposure due to high gastrointestinal uptake and the permeable blood-brain barrier. Blood levels in children should be reduced below the levels so far considered acceptable, recent data indicating that there may be neurotoxic effects of lead at lower levels of exposure than previously anticipated. Although lead in petrol has dramatically decreased over the last decades, thereby reducing environmental exposure, phasing out any remaining uses of lead additives in motor fuels should be encouraged. The use of lead-based paints should be abandoned, and lead should not be used in food containers. In particular, the public should be aware of glazed food containers, which may leach lead into food. Exposure to arsenic is mainly via intake of food and drinking water, food being the most important source in most populations. Long-term exposure to arsenic in drinking-water is mainly related to increased risks of skin cancer, but also some other cancers, as well as other skin lesions such as hyperkeratosis and pigmentation changes. Occupational exposure to arsenic, primarily by inhalation, is causally associated with lung cancer. Clear exposure-response relationships and high risks have been observed.

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Hazards of heavy metal contamination.

Presented and described in detail is a clinical technique called subjective global assessment (SGA), which assesses nutritional status based on features of the history and physical examination. Illustrative cases are presented. To clarify further the nature of the SGA, the method was applied before gastrointestinal surgery to 202 hospitalized patients. The primary aim of the study was to determine the extent to which our clinician's SGA ratings were influenced by the individual clinical variables on which the clinicians were taught to base their assessments. Virtually all of these variables were significantly related to SGA class. Multivariate analysis showed that ratings were most affected by loss of subcutaneous tissue, muscle wasting, and weight loss. A high degree of interobserver agreement was found (kappa = 0.78, 95% confidence interval 0.624 to 0.944, p less than 0.001). We conclude that SGA can easily be taught to a variety of clinicians (residents, nurses), and that this technique is reproducible.

http://www.nutricionclinica.sld.cu/Editoriales/DetskyASArticleOnSGA.pdf

What is subjective global assessment of nutritional status

Essentiality Toxicity Carcinogenicity Lead(Pb) Exposure Toxicokinetics Toxicity Neurologic, Neurobehavioral, and Developmental Effects in Children Mechanisms of Effects on the Developing Nervous System Peripheral Neuropathy Hematologic Effects Renal Toxicity Lead and Gout Effects on Cardiovascular System Immunotoxicity Bone Effects Reproductive Effects Birth Outcomes Carcinogenicity Other Effects Dose Response Treatment Organic Lead Compounds Mercury (Hg) Exposure Disposition and Toxicokinetics Metabolic Transformation Cellular Metabolism Toxicology Biological Indicators Treatment Nickel (Ni) Exposure Toxicokinetics Essentiality Toxicity Nickel Carbonyl Poisoning Dermatitis Indicators of Nickel Toxicity

/pdf/toxic-effects-of-metals-2t2btb1i7f.pdf

Toxic effects of metals

Chapter 1: Overview of Zinc Nutrition ............................................................................................................... S99 1.1 Biological functions of zinc ............................................................................................................................. S99 1.2 Tissue zinc distribution and reserves .............................................................................................................. S99 1.3 Zinc metabolism ........................................................................................................................................... S100 1.4 Importance of zinc for human health........................................................................................................... S101 1.5 Human zinc requirements............................................................................................................................. S105 1.5.1 Adult men ............................................................................................................................................. S106 1.5.2 Adult women......................................................................................................................................... S109 1.5.3 Children ................................................................................................................................................ S110 1.5.4 Pregnancy.............................................................................................................................................. S111 1.5.5 Lactation ............................................................................................................................................... S112 1.6 Dietary sources of zinc and suggested revisions of Recommended Daily Intakes .................................... S112 1.6.1 Dietary sources of zinc and factors affecting the proportion of zinc available for absorption ........ S112 1.6.2 Revised estimates of dietary requirements and recommended intakes for zinc ............................... S114 1.7 Zinc toxicity.................................................................................................................................................... S118 1.8 Causes of zinc deficiency and groups at high risk ....................................................................................... S121 1.9 Summary ........................................................................................................................................................ S123

International Zinc Nutrition Consultative Group (IZiNCG) technical document #1. Assessment of the risk of zinc deficiency in populations and options for its control.

This report provides a review of the cadmium exposure situation in Sweden and updates the information on health risk assessment according to recent studies on the health effects of cadmium. The report focuses on the health effects of low cadmium doses and the identification of high-risk groups. The diet is the main source of cadmium exposure in the Swedish nonsmoking general population. The average daily dietary intake is about 15 micrograms/day, but there are great individual variations due to differences in energy intake and dietary habits. It has been shown that a high fiber diet and a diet rich in shellfish increase the dietary cadmium intake substantially. Cadmium concentrations in agricultural soil and wheat have increased continuously during the last century. At present, soil cadmium concentrations increase by about 0.2% per year. Cadmium accumulates in the kidneys. Human kidney concentrations of cadmium have increased several fold during the last century. Cadmium in pig kidney has been shown to have increased by about 2% per year from 1984-1992. There is no tendency towards decreasing cadmium exposure among the general nonsmoking population. The absorption of cadmium in the lungs is 10-50%, while the absorption in the gastrointestinal tract is only a few percent. Smokers have about 4-5 times higher blood cadmium concentrations (about 1.5 micrograms/l), and twice as high kidney cortex cadmium concentrations (about 20-30 micrograms/g wet weight) as nonsmokers. Similarly, the blood cadmium concentrations are substantially elevated in persons with low body iron stores, indicating increased gastrointestinal absorption. About 10-40% of Swedish women of child-bearing age are reported to have empty iron stores (S-ferritin < 12 micrograms/l). In general, women have higher concentrations of cadmium in blood, urine, and kidney than men. The population groups at highest risk are probably smokers, women with low body iron stores, and people habitually eating a diet rich in cadmium. According to current knowledge, renal tubular damage is probably the critical health effect of cadmium exposure, both in the general population and in occupationally exposed workers. Tubular damage may develop at much lower levels than previously estimated, as shown in this report. Data from several recent reports from different countries indicate that an average urinary cadmium excretion of 2.5 micrograms/g creatinine is related to an excess prevalence of renal tubular damage of 4%. An average urinary excretion of 2.5 micrograms/g creatinine corresponds to an average concentration of cadmium in renal cortex of 50 micrograms/g, which would be the result of long-term (decades) intake of 50 micrograms per day. When the critical concentrations for adverse effects due to cadmium accumulation are being evaluated, it is crucial to consider both the individual variation in kidney cadmium concentrations and the variations in sensitivity within the general population. Even if the population average kidney concentration is relatively low for the general population, a certain proportion will have values exceeding the concentration where renal tubular damage can occur. It can be estimated that, at the 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 micrograms/day, about 1% of the entire population would have cadmium-induced tubular damage. In risk groups, for example, women with low iron stores, the percentage would be higher, up to 5%. Both human and animal studies indicate that skeletal damage (osteoporosis) may be a critical effect of cadmium exposure. We conclude, however, that the present evidence is not sufficient to permit such a conclusion for humans. We would like to stress, however, that osteoporosis is a very important public health problem worldwide, but especially in the Scandinav

Health effects of cadmium exposure - a review of the literature and a risk estimate

Increased dietary cadmium absorption in mice and human subjects with iron deficiency

Effects of iron, tin, and copper on zinc absorption in humans.

The relationship between iron and lead absorption in humans.

Total body counting was used to determine cadmium absorption in 14 healthy subjects and in 1 patient with an ileostomy. Breakfast was extrinsically tagged with 115mCdCl2, and a poorly absorbed marker, 51CrCl3, was added to determine the point of complete elimination of unabsorbed radiocadmium from the gastrointestinal tract. The 51Cr was not an ideal marker: fecal excretion of radiocadmium continued beyond the point at which chromium was completely eliminated from the body, Nevertheless, it was helpful in six subjects in identifying the presence of unabsorbed radiocadmium still in transit in the lumen of the gastrointestinal tract 3--5 wk after the test meal. The average body retention of radiocadmium determined between 7 and 14 d after the disappearance of the chromium marker from the body was 4.6 +/- 4.0% (SD), with a range of 0.7--15.6%. The biological half-time of absorbed radiocadmium in one of the subjects was 100 d.

Measurement of dietary cadmium absorption in humans

We performed 38 cerebral perfusion studies in 33 patients with brain death or with severe central nervous system injury using technetium-99m hexamethyl-propyleneamine oxime [( 99mTc]HM-PAO). Uptake by the cerebrum and/or cerebellium was present in all patients who were not clinically brain dead (ten studies) although the study was often abnormal. In those patients who were brain dead, 16/17 studies demonstrated no uptake in either the cerebrum or cerebellum. In patients suspected of brain death, but who had conditions interfering with the diagnosis the test demonstrated no uptake in 9/11 studies, confirming brain death. A radionuclide angiogram (RNA) of the head was also performed in 33/38 studies and showed complete agreement with the [99mTc]HM-PAO uptake, except in one case. We conclude that cerebral perfusion imaging with [99mTc]HM-PAO is a simple, noninvasive and reliable test to confirm brain death. By comparison with conventional technetium agents, [99mTc]HM-PAO is not dependent on the quality of the bolus injection, is easier to interpret and allows evaluation of posterior fossa blood flow.

https://jnm.snmjournals.org/content/jnumed/30/10/1627.full.pdf

M J Chamberlain

Papers

Increased dietary cadmium absorption in mice and human subjects with iron deficiency

Effects of iron, tin, and copper on zinc absorption in humans.

The relationship between iron and lead absorption in humans.

Measurement of dietary cadmium absorption in humans

Cerebral perfusion imaging with technetium-99m HM-PAO in brain death and severe central nervous system injury.