This study was carried out on the evaluation of cadmium in chicken meat and offal in Bodija, Sango and Ojoo markets in Ibadan between July and October, 2015. The appraisal was aimed at assessing the cadmium that can be accumulated in the kidney, liver, intestine, blood, muscle and the feathers. Ten mature chickens were bought and dissected to remove the chicken meat and offal samples. This samples were oven-dried separately and pulverised into powdered form through grinding with a mortar and pestle. These were acid-digested for cadmium analyses using Buck Scientific 210 VGP Atomic Absorption Spectrophotometer. The results showed varying mean concentrations in the intestine (0.713±0.024 ppm), feather (0.702±0.035 ppm) and muscle (0.592±0.019 ppm) with low mean concentrations in the blood (0.426±0.032 ppm), liver (0.432±0.021 ppm) and kidney (0.352±0.027 ppm). Most of the chicken meat and offal samples were above the WHO guideline limit of 0.05 ppm. The Target Hazard Quotient (THQ) from the study was below 1 which is indicative that the general populace in this study area is not at risk. It is therefore recommended that regular biomonitoring should be carried out on chicken meat and offal locally and globally for the purpose of food safety.
TABLE OF CONTENTS
DEDICATION
LIST OF FIGURES PAGE
LIST OF TABLES PAGE
ABSTRACT
CHAPTER ONE - INTRODUCTION
1.1 TOXIC METALS
1.2 CADMIUM
1.3 END USES OF CADMIUM
1.4 AIM
1.5 OBJECTIVES
CHAPTER TWO - LITERATURE REVIEW
2.1 CADMIUM: PROPERTIES AND SOURCES
2.2 CADMIUM AS AN ENVIRONMENTAL POLLUTANT
2.2.1 NATURAL CADMIUM EMISSIONS
2.2.2 ANTHROPOGENIC CADMIUM EMISSIONS
2.2.3 FACTORS IN ANTHROPOGENIC EMISSIONS ANALYSES
2.3 CADMIUM IN THE HUMAN BODY
2.4 GUIDELINES FOR CADMIUM
2.4.1 AMBIENT STANDARDS AND GUIDELINES
2.4.2 PERMISSIBLE LIMITS OF CADMIUM
2.5 CADMIUM UPTAKE: UPTAKE THROUGH FOOD
2.6 TRANSPORT AND STORAGE OF CADMIUM
2.7 CADMIUM EXCRETION
2.8 CADMIUM TOXICITY IN HUMANS
2.8.1 TOXICITY AT ORGAN SYSTEM LEVEL
2.8.2 KIDNEY AND BONE
2.8.3 LUNG
2.8.4 PERIODONTAL TISSUES
2.8.5 MAMMARY GLAND
2.8.6 BLOOD VESSELS AND THE HEART
2.8.7 GASTROINTESTINAL TRACT
2.8.8 REPRODUCTIVE SYSTEM
2.9.9 IMMUNE SYSTEM
2.9 MECHANISM OF CADMIUM TOXICITY
2.9.1 INTERFERENCE WITH ESSENTIAL METALS
2.9.2 DISRUPTION OF SIGNALING AND BIOMOLECULES
2.9.3 CHANGES IN METHYLATION
2.10 CADMIUM AND CARCINOGENESIS
2.10.1 ABERRANT GENE EXPRESSION
2.11 CADMIUM AND APOPTOSIS
2.12 CADMIUM AND OXIDATIVE STRESS
2.13. PREVIOUS WORKS ON HEAVY METALS IN CHICKEN MEAT AND OFFAL IN NIGERIA.
CHAPTER THREE – MATERIALS AND METHODOLOGY
3.1 STUDY SITE
3.2 SAMPLE COLLECTION AND PROCESSING
3.3 SAMPLE ANALYSES
3.4 DATA ANALYSES
3.5 HEALTH RISK ASSESSMENT
CHAPTER FOUR - RESULTS
4.1 CADMIUM LEVEL IN THE CHICKEN MEAT AND OFFALS IN IBADAN
4.2 VARIATIONS IN THE CADMIUM LEVELS IN CHICKEN AT THE SAMPLING SITES
4.3 HEALTH RISK ASSESSMENT
CHAPTER FIVE- DISCUSSION
5.1 CADMIUM LEVEL IN THE CHICKEN MEAT AND OFFALS IN IBADAN
5.2 VARIATIONS IN THE CADMIUM LEVELS IN CHICKEN AT THE SAMPLING SITES
5.3. HEALTH RISK ASSOCIATED WITH CADMIUM LEVELS IN THE CHICKEN MEAT AND OFFAL IN IBADAN
5.4. RECOMMENDATION
REFERENCES
DEDICATION
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LIST OF FIGURES PAGE
Figure 1 Cadmium levels in organs and tissues of Sample A
Figure 2 Cadmium levels in organs and tissues of Sample B
Figure 3 Cadmium levels in organs and tissues of Sample C
Figure 4 Cadmium levels in organs and tissues of Sample D
Figure 5 Cadmium levels in organs and tissues of Sample E
Figure 6 Cadmium levels in organs and tissues of Sample F
Figure 7 Cadmium levels in organs and tissues of Sample G
Figure 8 Cadmium levels in organs and tissues of Sample H
Figure 9 Cadmium levels in organs and tissues of Sample I
Figure 10 Cadmium levels in organs and tissues of Sample J
LIST OF TABLES PAGE
Table 1 Cadmium consumption by end-users in Western World 1990
Table 2 Global emission of cadmium to air in mid-1990s
Table 3 EU, USEPA and WHO reference standard and guidelines
Table 4 Mean cadmium levels, standard deviation and Min-Max values
ABSTRACT
This study was carried out on the evaluation of cadmium in chicken meat and offal in Bodija, Sango and Ojoo markets in Ibadan between July and October, 2015. The appraisal was aimed at assessing the cadmium that can be accumulated in the kidney, liver, intestine, blood, muscle and the feathers. Ten mature chickens were bought and dissected to remove the chicken meat and offal samples. This samples were oven-dried separately and pulverised into powdered form through grinding with a mortar and pestle. These were acid-digested for cadmium analyses using Buck Scientific 210 VGP Atomic Absorption Spectrophotometer. The results showed varying mean concentrations in the intestine (0.713±0.024 ppm), feather (0.702±0.035 ppm) and muscle (0.592±0.019 ppm) with low mean concentrations in the blood (0.426±0.032 ppm), liver (0.432±0.021 ppm) and kidney (0.352±0.027 ppm). Most of the chicken meat and offal samples were above the WHO guideline limit of 0.05 ppm. The Target Hazard Quotient (THQ) from the study was below 1 which is indicative that the general populace in this study area is not at risk.
CHAPTER ONE - INTRODUCTION
1.1 TOXIC METALS
All minerals can cause toxicosis in animals, when consumed in fairly significant quantities (Pondet al., 1995). The margin of safety between the minimum amounts required to feed animals and the amount that causes adverse effects varies for different minerals, depending on prevailing conditions. However, there are many minerals that do not participate in any known function of the animal body and, in fact, are harmful or toxic. Today, environment, plants, animals and humans are exposed to high levels of these toxic minerals, and even higher than ever historically recorded. This is due to their industrial use, and to the limitless burning of coal, gas and oil, but also to the incineration of waste materials that takes place around the world. Thus, the toxic minerals are now everywhere, participating in a perpetual food chain and affect "everyone and everything" on the planet, thus being a major cause of disease, aging, and even birth defects. Among existing toxic mineral elements, the most important are arsenic, cadmium, lead and mercury, which are harmful to animals’ health (Suttle, 2010).
1.2 CADMIUM
Cadmium is a heavy metal with a high toxicity. Cadmium is toxic at very low exposure levels and has acute and chronic effects on health and environment. Cadmium is not degradable in nature and will thus, once released to the environment, stay in circulation. New releases add to the already existing deposits of cadmium in the environment. Cadmium and cadmium compounds are, compared to other heavy metals, relatively water soluble. They are therefore also more mobile in e.g. soil, generally more bioavailable and tend to bioaccumulate. Chronic cadmium exposure produces a wide variety of acute and chronic effects in humans. Cadmium accumulates in the human body and especially in the kidneys. According to the current knowledge kidney damage (renal tubular damage) is probably the critical health effect. Other effects of cadmium exposure are disturbances of calcium metabolism, hypercalciuria and formation of stones in the kidney. High exposure can lead to lung cancer and prostate cancer. The major issues of concern related to cadmium may be summarised as follows:
Atmospheric deposition seems continuously to cause the content of cadmium in agricultural top soil to increase, which by time will be reflected in an increased human intake by foodstuffs and therefore in an increased human risk of kidney damages and other effects related to cadmium.
In the marine environment levels of cadmium may significantly exceed background levels causing a potential for serious effects on marine animals and in particular birds and mammals.
Significant quantities of cadmium are continuously stockpiled in landfills and other deposits and represent a significant potential for future releases to the environment.
The dominant sources of atmospheric emission will vary depending on the region or country considered. Non-ferrous metal production as well as combustion of coal and oil and waste incineration should be considered important sources. Important sources of cadmium input to the marine environment include atmospheric deposition, domestic waste water and industrial discharges. Emissions to air as well as water on an international scale seem to be lowering due to improved flue gas and waste water treatment.
1.3 END USES OF CADMIUM
The general trend in the global cadmium consumption over the last two decades has been a steep increase in the use of cadmium for batteries and a decrease in the use for nearly all other applications. Batteries accounted in 1990 for 55% of the total Western World consumption and for about 73% of the estimated EU consumption in 2000 (table 3.3). Although the use of cadmium for pigments, Polyvinylchloride stabilisers and plating in some countries by and large has been phased out, these applications at the EU level still account for a significant part of the total cadmium consumption in 2000.
Table 1. Cadmium consumption by end-users in Western World 1990 (derived from OECD 1993) and the EU about 2000.
illustration not visible in this excerpt
(Source: Scoulloset al., 2001)
1) The figures in tonnes are calculated from the distribution represented in percentages in the reference.
2) The figures for consumption are derived from a diagram showing the Cd flows in EU. The flow diagram is indicated as a preliminary draft. The report text states that Ni-Cd batteries account for 78% of the total consumption of end products. The consumption is here calculated from the flow diagrams indication of consumption, import and export of cadmium with batteries.
Table 2. Global emission of cadmium to air in mid-1990s.
illustration not visible in this excerpt
The significant decrease in air emissions noted in table 2 is mainly caused by improved flue gas cleaning, which has partly changed a problem of direct release to the environment to an issue of how to control cadmium being stockpiled in landfills and other deposits in the long time perspective.
1.4 AIM
The aim of this study is to evaluate organ and tissue concentration of cadmium in domestic chicken as an indicator on the composition of tissues and its consequences when consumed by man.
1.5 OBJECTIVES
1. To evaluate the bioavailability of cadmium in chicken meat and offals in Ibadan.
2. To assess the differences in tissues and organ levels of cadmium from different markets in Ibadan.
3. To compare the mean cadmium concentration in chicken meat and offals with World Health Organisation (WHO) and Food and Agricultural Organisation (FAO) guideline standards.
CHAPTER TWO - LITERATURE REVIEW
2.1 CADMIUM: PROPERTIES AND SOURCES
Cadmium (CAS registry number 7440-43-9) is a naturally occurring element of relatively poor abundance (64th amongst elements) in the earth's crust (0.1-0.5 ppm) with the symbol Cd and atomic number 48. While it occurs in air, water, soil as well as in tissues of plants and animals, it is not found in free state. Cadmium is present primarily in ores of zinc, copper or lead, the extraction and processing of which releases large quantities of cadmium into the atmosphere, hydrosphere and soil thereby contaminating the human environment. It is toxic, nonessential and classified as a human carcinogen by the North Carolina National Toxicology Program (NTP, 2000).
The physical and chemical properties of cadmium namely corrosion resistance (particularly in alkaline and seawater environments), low melting temperature, rapid ion electrical exchange activity, high electrical and thermal conductivity (in both alloy and oxide forms) make it suitable for incorporation into batteries, alloys and for electroplating, welding, electrical, and nuclear fission applications (Schroeder, 1965). Mainly, cadmium is used to produce colorants, stabilizers of plastics and electroplating protective coatings, solders and alloys, cadmium rods. It is also used for the production of alkaline nickel-cadmium batteries, fireworks and fluorescent paints (Carroll, 1969) .Moreover, as pigments cadmium compounds with stand high temperatures and disperse well in polymers producing strong colours with high opacity and good tinting strength.
Cadmium compounds known as chalcogenides by virtue of their optical properties have found applications in plastics, paintings, enamels, inks, display devices, photovoltaic cells and more recently, quantum dots. The worldwide production of Cadmium in 2005 was estimated to be 20,000 metric tons.
2.2 CADMIUM AS AN ENVIRONMENTAL POLLUTANT
Cadmium emissions arise from two major source categories, natural sources and man-made (anthropogenic sources). Emissions enter in to the three major compartments of the environment - air, water and soil. Emissions to air are considered faster than that to water which in turn are considered faster than that to soil.
2.2.1 NATURAL CADMIUM EMISSIONS
Cadmium is distributed throughout the environment from natural sources as well as processes such as the abrasion of rocks, erosion of soil, transportation of contaminated soil particles by wind and from singular events such as forest fires and volcanic eruptions. Average cadmium concentration in the earth's crust ranges from 0.1 to 0.5 ppm, although much higher levels may accumulate in sedimentary rocks. Marine phosphates and phosphorites have been reported to contain levels as high as 500 ppm. Major natural activities that emit cadmium include weathering and erosion of parent rocks and transportation to oceans [15,000 metric tonnes (mt) per annum] (Pondet al., 1972; Bakeret al., 1977), volcanic activity into the atmosphere (as high as 820 mt per year) (Pondet al, 1972; Baker et al, 1977; EFSA, 2009) and to a lesser extent, forest fires (1 to 70 mt per year) (EFSA, 2009).
2.2.2 ANTHROPOGENIC CADMIUM EMISSIONS
Anthropogenic activities contribute 3–10 times more Cadmium to the environment than natural activities (NRC, 2001). Since Cadmium cannot be degraded, the risk of environmental exposure is constantly increasing because of accumulation via the food chain (Bloodet al., 1992). Man-made cadmium emissions can be from products intentionally incorporating cadmium (Nickel- Cadmium Batteries ,Cadmium Pigmented Plastics, Ceramics, Glasses, Paints and Enamels, Cadmium Stabilized Polyvinylchloride (PVC) Products, Cadmium Coated Ferrous and Non-ferrous Products, Cadmium Alloys and Cadmium Electronic Compounds) or those in which cadmium is an impurity (Non-ferrous Metals and Alloys of Zinc, Lead and Copper, Iron and Steel, Fossil fuels like Coal, Oil, Gas, Peat and Wood, Cement and Phosphate fertilizers ). Moreover cadmium is a by-product of the extraction, smelting and refining of the nonferrous metals – zinc, lead and copper and improper collection or disposal methods can lead to cadmium contamination of environment.
2.2.3 FACTORS IN ANTHROPOGENIC EMISSIONS ANALYSES
Several studies (Pondet al., 1972; Bakeret al., 1977; EFSA, 2008) have identified four factors of primary importance in determining the levels of cadmium emissions. The first one, cadmium emission factors (amounts of cadmium emitted to the environment per unit of cadmium processed) tend to be lower in more technologically advanced regions of the world such as North America, Western Europe and Japan than in other regions (Pondet al., 1972; NRC, 2008). Second, data submitted by many countries are rather incomplete and lack information about cadmium release from unintended cadmium addition or use. Third, while cadmium levels in the environment has rapidly increased between the years 1800-1960 owing to industrialization and huge amount of fossil fuel combustion, the period post 1960 has seen drastic decrease in environmental cadmium levels due to improved emission control for fossil fuel combustion as well as improved technology for the production, use and disposal of cadmium and cadmium-containing products and tighter controls as well as stricter regulations (Pageet al., 1972). Fourth, in many of its deliberate applications, cadmium or cadmium compounds are embedded in the product’s matrix, do not readily leach from the product, and are therefore not readily available. A notable example is products colour by cadmium sulphide pigments that are encased in plastics, glasses, ceramics or enamels, and which are therefore completely insoluble. Finally, many cadmium-containing products such as batteries, coatings and alloys are recyclable, (although at present recycling of only Ni-Cd batteries is commercially and economically viable). Success in the recycling largely depends on appropriate collection systems which seem to be limited to the developed world.
Cadmium (Cd) occurs naturally in the environment in its inorganic form as a result of volcanic emissions and weathering of rocks. In addition, anthropogenic sources have increased the background levels of cadmium in soil, water and living organisms. It is used in many technological applications and released into the environment via the smelting of other metals, the burning of fossil fuels, the incineration of waste materials, and the use of phosphate and sewage sludge fertilizers. Both natural processes (such as volcanic emissions and weathering of rocks) and anthropogenic activities can contribute to the contamination by cadmium of the environment and consequently of the food chain (EFSA, 2004; EFSA, 2009).
Increases in cadmium levels in soil result in an increase in the uptake of cadmium by plants, although the extent to which this happens will depend on the soil pH, plant species and the part of the plant, as well as other soil characteristics. Moreover, edible free-living food such as shellfish, crustaceans and fungi are natural accumulators of cadmium. However, the US NRC (NRC, 2007) reported that cadmium is a necessary element for the animal organization, when received in minimal doses.
The intoxication of animals by cadmium is rare (EFSA, 2008). However, when that happens, cadmium is toxic to all animal species, and is accumulated in the kidney and to a lesser extent in liver. Subsequently, large differences exist between the effects of a single exposure to a high concentration of cadmium, and chronic exposures to lower doses (EFSA, 2004). The maximum content of cadmium in complete feed has been set by the European Union at 0.5 mg/kg feed (with 12% moisture) for all animal species.
Cadmium occurs as a trace constituent of most ecosystems. Because the effects of a single, large dose are often quite different from those produced by repeated, small doses (Eaton and Klaasen 1996), studies of acute toxicity are only marginally useful in assessing risk to natural populations. In addition, most studies of metals toxicity among natural populations have been done in aquatic ecosystems. Few investigators have explored the effects of chronic metals exposure on terrestrial organisms or populations.
2.3 CADMIUM IN THE HUMAN BODY
Cadmium has been known as a toxic element for some time. Man’s extensive use of cadmium in many industrial processes has enhanced the potential exposure to human population (Friberget al., 1971). It has been proposed that low level exposure to humans might be associated with cardiovascular disease, emphysema and hypertension (Schroeder, 1965; Carroll, 1969; Hirst et al., 1973).
One possible route of cadmium to the human body is through the food chain. Although most soils are relatively low in cadmium, increases in the amount of this element can occur through the application of waste materials such as sewage sludge to the land (Bakeret al., 1977; Chaneyet al., 1977). It is becoming apparent that there is considerable variation among plant species in their ability to accumulate cadmium from the soil (Pageet al., 1972).
Cadmium has no known biological function in animals and humans, but mimics other divalent metals that are essential to diverse biological functions (EFSA, 2004; EFSA, 2009). Cadmium was found to be competitive with zinc and copper and to a lesser extent to iron (Pond et al., 1995; NRC, 2001). It can cross the various biological membranes by different mechanisms (e.g. metal transporters) and once inside the cells binds to ligands with exceptional affinity (e.g. metallothioneins) (EFSA, 2004), thereby reducing the absorption of copper and, to a lesser extent, of zinc (NRC, 2001). Especially, the liver and kidneys contain metallothioneins, which accumulate cadmium throughout the animal life. However, cadmium is not easily cleared by the cells and the poor efficiency of cellular export systems explains the long residence time of this element in storage tissues such as the intestine, the liver and the kidneys (EFSA, 2004). Cadmium absorbed into the body (0.5-7% of ingested amount, depending on the animal species) is eliminated very slowly, with a biological half-life estimated to be 10-30 years (EFSA, 2004; EFSA, 2009). Perturbation of calcium, zinc or iron homeostasis plays a key role in the toxicological action of cadmium that involves a general threat to basic cellular functions (EFSA, 2009).
Cadmium exposure has been associated with nephrotoxicity, osteoporosis, neurotoxicity, carcinogenicity and genotoxicity, teratogenicity, and endocrine and reproductive effects (EFSA, 2004; EFSA, 2009). In general, clinical symptoms of cadmium toxicity in animals include kidney and liver damage, anaemia, retarded testicular development or degeneration, enlarged joints, scaly skin, and reduced growth and increased mortality (Pond et al., 1995; Blood et al., 1992; EFSA, 2004). Manifestation of toxicity varies considerably, as depending on dose and time of exposure, species, gender, and environmental and nutritional factors.
Cadmium alters a number of parameters of the host’s immune system and increased its susceptibility to infections, autoimmune diseases and allergic manifestations. A number of studies documented that heavy metals are not only toxic for the organism but also may modulate immune responses (Fujimakiet al., 1983 and Krocovaet al., 2000).
Cadmium inhibits growth and has toxic effects on the kidneys, liver, lung, testes, placenta and the erythropoietic system. It may pass placental barriers and accumulate in fetal brain, liver and heart (Trottieret al., 2002), and it has a teratogenic effect to the growing embryo.
Chronic cadmium intoxication is characterized by renal proximal tubular dysfunction, general osteomalacia with severe pains and anaemia (Horiguchiet al., 1996).
2.4 GUIDELINES FOR CADMIUM
Ingestion through food, especially plant-based foodstuffs, is the major route by which cadmium enters the human body from the environment.
Average human daily intake of cadmium from food has been estimated at around 10–50 μg. This may increase to several hundred micrograms per day in polluted areas. The intake of cadmium through inhalation is generally less than half that through ingestion, while daily intake from drinking water ranges from below 1 μg to over 10 μg (WHO 1987). The kidney, especially the renal tract, is the critical organ of intoxication after exposure to cadmium. Excretion is slow, and renal accumulation of cadmium may result in irreversible impairment in the reabsorption capacity of renal tubules.
Only a small proportion (5–10%) of ingested cadmium is absorbed by humans (FAO and WHO, 1972), and large variations exist among individuals. Severe renal dysfunction and damage to the bone structure, a syndrome termed itai-itai disease, have been associated with long-term exposure to cadmium in food (mainly rice) and water in Japan.
WHO (1987) estimated that long-term daily ingestion of 200 μg of cadmium via food can be connected with 10% prevalence of adverse health effects. Deficiencies of iron, zinc, and calcium in the human body generally facilitate cadmium absorption.
Less than 50% of inhaled cadmium is absorbed from the lungs. Acute and chronic exposure to cadmium dust and fumes, occurring mainly under working conditions, can result in cadmium poisoning. Acute respiratory effects can be expected at cadmium fume concentrations above 1 mg/m3.
Chronic effects occur at exposures to 20 μg/m3 cadmium concentrations after about 20 years. Because of the cadmium content of tobacco, heavy smokers have elevated absorption of airborne cadmium. Cigarettes containing 0.5–3 μg cadmium per gram of tobacco can result in up to 3 μg daily cadmium absorption via the lungs, assuming a 25% absorption factor (WHO 1987). Considering various sources of exposure and applying a safety factor, WHO (1987) estimated that 0.2 μg/m3 was a safe level of atmospheric cadmium concentrations with regard to renal effects through inhalation.
Animal studies have yielded sufficient evidence of the carcinogenicity of cadmium in animals (IARC 1976). Limited evidence of human carcinogenicity is also available in studies (reviewed in WHO 1992a, b) linking long-term occupational exposure to cadmium to increased occurrence of prostate and lung cancer cases. USEPA (1985) estimated the incremental cancer risk from continuous lifetime exposure to 1 μg/m3 concentrations to be 0.0018.
2.4.1 AMBIENT STANDARDS AND GUIDELINES
Ambient environmental standards and guidelines are meant to protect human health and natural resources by limiting exposure.
Table 3. Presents EU, USEPA, and WHO reference standards and guidelines.
This image has been removed due to copyright issues.
The WHO ambient air quality guidelines take into account the impact of atmospheric cadmium on deposition and accumulation in soil used for agricultural production and set different acceptable levels in urban and rural areas. Ambient water quality guidelines focus on drinking water and other water resources intended for drinking, to protect human health.
Stationary sources that contribute to the increase of cadmium in the environment should not exceed the cadmium emissions referred to in the relevant industry section of this guideline. These emissions are normally achievable through good industrial practices. In addition, the impacts of new sources on ambient concentrations of cadmium should be considered. When the use of certain fuels results in emissions that contributes to a significant increase in ambient cadmium concentrations, or in areas where agricultural crops affected by such emissions are a main dietary source of the population, the environmental assessment should ensure that cadmium emissions are properly abated, taking into consideration alternative fuels, technologies, and control measures. Intermittent monitoring of the surrounding soil and plants should ensure that cadmium concentrations do not pose an increased health threat to the population in the vicinity of the industrial plant.
2.4.2 PERMISSIBLE LIMITS OF CADMIUM
Daily intake of cadmium from food by a person in different countries is at the level of 10-35μg per person (WHO guideline). The content of cadmium in food affects its concentration in the blood. Placenta protects the foetus from cadmium compounds. The content of cadmium in adult body (at 50 years of age) is about 15-30 mg and increases with age (The Ministry of Environment, 2005). This is due to the extremely long half-life of cadmium, which is estimated at 10-30 human years, an average of about 20 years (Martelliet al, 2005). A safe intake limit of 7 μg cadmium/week/kg body weight or 25 μg cadmium/kg body weight per month (mg/kg bw-mo) or 0.4- 0.5 mg /week, and the maximum dose of 60-70 μg per day was set based on the critical renal cadmium concentration of between 100 and 200 μg/g wet weight that corresponds to a urinary threshold limit of 5–10μg/g creatinine (WHO, 1989).
Provisional tolerable weekly intake (PTWI) for a chemical with no intended function is an estimate of the amount of the chemical that can be ingested weekly over a lifetime without appreciable health risk (WHO, 1989). The PTWI value initially set for cadmium was 400–500 μg/person/week (WHO, 1989). These levels were based on a critical renal concentration of 100–200 μg cadmium/g wet kidney cortex weight, attained after a cadmium intake of 140–260 μg/day for > 50 years or 2,000 mg over a lifetime (WHO, 1989).The PTWI model incorporates an oral absorption rate of 5 % (retention about 0.5 to 1.0 μg of cadmium per day from food) and a daily excretion rate of 0.005% of total body burden. A toxicokinetic model predicts, based on similar assumptions, that the renal cortical cadmium level of 50 μg/g wet weight could be attained at the cadmium intake of 1 μg/kg body weight/day over 50 years (Sataruget al,2003; Sataruget al, 2000).
Investigations around the world have shown that, for the general population, the average cadmium intake is low compared to the World Health Organization’s (WHO) standard for tolerable cadmium intake and that cadmium intake levels have in fact been decreasing over the past 20 years. Average cadmium intakes in 1960 were about 15 μg/kg bodyweight per month but by 2000 had decreased to about 5 μg/kg body weight per month, well below the current WHO JECFA (Joint FAO/WHO Expert Committee on Food Additives) standard established in 2010 ( 25 μg/kg body weight per month).
2.5 CADMIUM UPTAKE: UPTAKE THROUGH FOOD
Because of its high rates of soil-to-plant transfer (via cation exchange in cell membranes and intracellular transport), the diet is the main source of environmental cadmium exposure (95%) in non-smokers in most parts of the world (McLaughlin et al, 2006) although the uptake is inefficient (6%) (Elinder, 1985). Atmospheric deposition of airborne cadmium, mining activities and the application of cadmium-containing fertilizers and sewage sludge on farm land may lead to the contamination of soils and increased cadmium uptake by crops and vegetables grown for human consumption. High concentrations of cadmium are present in mollusks and crustaceans. As mentioned previously, certain foods contain high levels of cadmium. Based on estimation of cadmium intake, more than 80% of the food-cadmium comes from cereals, vegetables and potato. The average cadmium intake from food generally varies between 8 and 25 μg per day of which approximately 0.5 to 1.0 μg is actually retained in the body (Berglund et al, 1994). Factors influencing this mode of uptake are dose, exposure time, and chemical components of the diet, the body's nutritional status, age and gender.
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- Quote paper
- Emmanuel Tyokumbur (Author), 2015, Assessment of Cadmium in Chicken Meat and Offal. Food Safety and Food Poisoning, Munich, GRIN Verlag, https://www.grin.com/document/1363523
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