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INTRODUCTION ABSORPTION, TRANSPORT and EXCRETION ALUMINUM crytstalline ductilemetal abundant metal in the crust found combined other elements such as: Oxygen Silicon Fluorine to its good conductivity of heat and electricity, ease of welding, tensile strength, light weight, and oxide coat, aluminum i...

Description

INTRODUCTION

ABSORPTION, TRANSPORT and EXCRETION

ALUMINUM silver-white hite -a crytstalline silver-w ductilemetal -most most abundant metal in the earth’s ccrust rust -always found combined w/ other elements such as:  Oxygen  Silicon  Fluorine -Due to its good conductivity of heat and electricity, ease of welding, tensile strength, light weight, and corrosion-resistant oxide coat, aluminum is applicable to a wide variety of industrial and household uses. - used for beverage cans, pots and pans, airplanes, siding and roofing, and foil. - often mixed with small amounts of other metals to form aluminum alloys, which are stronger and harder than aluminum alone. - water treatment and alumina in abrasives and furnace linings. - are also found in consumer products such as :  antacids  astringents  buffered aspirin  food additives  cosmetics  antiperspirants -average adult in the United States ingests about 7 to 9 mg aluminum per day in their food. -The human organism can absorb aluminum and its compounds orally, by inhaling, and parenterally. - no indication of dermal absorption. - inhaled inhaled:1.5% to 2% - absorbed: 0.01% to 5% -The absorption efficiency is dependent on chemical form, particle size (inhalation), and concurrent dietary exposure to chelators such as citric acid or lactic acid. -After a relatively quick uptake of aluminum into the intestinal walls, its passage into the blood is much slower. -In plasma is bound to carrier proteins such as transferrin. -binds to various ligands in the blood and distributes to every organ -highest concentrations ultimately found:  bone (~50% of the body burden)  lung tissues (~25% of the body burden) - levels in lungs increase with age. –Urine: Urine:  Excretion: 95%  Elimination in bile: 2%

ARSENIC -ubiquitous element displaying both metallic and non-metallic properties. - content in the earth’s crust : estimated at 1.5 to 2.0 mg/kg. -For most people, food is the largest source of arsenic exposure (about about 25 to 50 µg/d µg/d) - lower amounts coming from drinking water and air. -Anthropogenic sources of arsenic:  production of metals  burning of coil  fossil fuels  timber  its use in agriculture -release three times more of arsenic than natural sources. preservative tive : the main current - wood preserva use of arsenic -Other current and past uses of arsenic :  Pesticides  pigments  poison gases  ammunition manufacturing  semiconductor processing  medicines

Acute arsenic exposure -gastrointestinal (nausea, emesis, abdominal pain, and rice water diarrhea) -bone marrow (pancytopenia, anemia, and basophilic stippling) -cardiovascular (ECG changes) - central nervous system (encephalopathy and polyneuropathy) - renal (renal insufficiency and renal failure) hepatic (hepatitis) systems.

Chronic arsenic exposure -dermatologic (Mees’ lines, hyperkeratosis, hyperpigmentation, and alopecia) -hepatic (cirrhosis and hepatomegaly) -cardiovascular (hypertension and peripheral vascular disease [PVD]) -central nervous system (“socks and glove” neuropathy and tremor) - malignancies (squamous cell, hepatocellular, skin, bladder, lung, and renal carcinomas). -blackfoot blackfoot disease -a severe form of PVD(peripheral vascular disease) which leads to gangrenous changes -The white powder of arsenic trioxide: odorless, tasteless, and one of the most common poisons in human history.

CADMIUM - a soft, bluish-white metal, which is easily cut with a knife. -Principal industrial uses of cadmium:  manufacture of pigments and batteries  in the metal-plating and plastics industries. - In the United States, the burning of fossil fuel fuelss such as coal and oil and the incineration of municipal waste materials constitute the largest sources of airborne cadmium exposure, along with zinc, lead, and copper smelters in some locations. -Cadmium-containing waste products and soil contamination, primarily as a result of human activity activity, are becoming of concern - the US Environmental Protection Agency (EPA) has established loading rates of 20 kg/ha for high cation exchange capacity soils with a pH of 6.5 and a lower rate of 5 kg/ha for acid soils

-0.0005 mg/kg/d: reference dose for cadmium in drinking water based on renal function (development of proteinuria) -Absorption is higher in females due in iron storage. - is 0.001 mg/kg/d : dose for dietary exposure to cadmium -10% to 50% : absorption of inhaled cadmium in air - 5% : gastrointestinal absorption of cadmium -10% to 50% : absorption in cigarette smoke - smokers of tobacco products have about twice the cadmium abundance in their bodies as nonsmokers. - For nonsmokers, the primary exposure to cadmium is through ingested food. - 90%: instead cadmium excreted in the feces

-0.01 to 0.05 g dose: toxic symptoms

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HEALTH EFFECTS , DEFICIENCY and TOXICITY

LABORA LABORATORY TORY EV EVALUA ALUA ALUATION TION

-has been shown to interfere with a variety of enzymatic processes - encephalopathy similar to that seen in Alzheimer disease : administration of aluminum to experimental animals -Although aluminum-containing over-the-counter oral products are considered safe in healthy individuals at recommended doses -Workers who breathe large amounts of aluminum dusts can have lung problems -Signs and symptoms of aluminum toxicity:  encephalopathy (stuttering, gait disturbance, myoclonic jerks, seizures, coma, and abnormal EEG);  osteomalacia or aplastic bone disease (painful spontaneous fractures, hypercalcemia, and tumorous calcinosis);  proximal myopathy;  increased risk of infection  ; microcytic anemia;  increased left ventricular mass  decreased myocardial function. -Aluminum toxicity occurs in people with renal insufficiencies who are treated by dialysis with aluminumcontaminated solutions or oral agents that contain aluminum. -The clinical manifestations of aluminum toxicity include:  anemia,  bone disease  progressive dementia with increased concentrations of aluminum in the brain. -Prolonged intravenous feeding of preterm infants with solutions containing aluminum is associated with impaired neurologic development. -primarily measured using ICPMS or GF GFAAS AAS -Urine and serum levels are useful in determining toxic exposures, monitoring exposure over time, and monitoring chelation therapy.

-0.12 and 0.3 g :lethal dose - The most effective antidotes for arsenic poisoning are the following chelating agents:  dimercaprol (a.k.a British antiLewisite)  penicillamine  succimer The main routes of exposure:  ingestion of arsenic containing foods, water, and beverages  inhalation of contaminated air -Arsenocholine and Arsenobetaine - Organic forms of arsenic that are commonly found in fish and seafood - are considered relatively nontoxic, and are cleared rapidly -Inorganic species of arsenic are highly toxic and occur naturally in rocks, soil, and groundwater. -also found in many synthetic products, poisons, and industrial processes. -Methylated species are intermediate in toxicity and arise primarily from metabolism of inorganic species, but small amounts may arise directly from food. Organic Inorganic methylated arsenic methylated arsenic -considered less monomethylarsonic toxic than As(3+) and acid (MMA) and As(5+) dimethylarsenic they are acid (DMA) are eliminated formed by hepatic slowly (1 to 3 metabolism of wk). As(3+) and -the sum of As(5+). inorganic and methylated metabolites of arsenic in urine is 35 µg/L. -clinical symptoms may not be evident at 35 µg/L.

-primarily measured using ICP-MS, GFAAS, or HG-AAS. - best detected by urine due to the short half-life of arsenic in blood

-no known role in normal human physiology. -Toxicity is believed to be a result of protein-Cd adducts causing denaturation of the associated proteins, resulting in a loss of function - Ingestion of high amounts of cadmium :  rapid onset with severe nausea,  vomiting  abdominal pain. dysfunction nction is a common - Renal dysfu presentation for chronic cadmium exposure, often resulting in slowonset proteinuria. - Acute effects of inhalation of fumes containing cadmium include respiratory distress due to chemical pneumonitis and edema and can cause death. -Breathing of cadmium vapors can also result in nasal epithelial damage and lung damage similar to emphysema. -Cadmium exposure can affect the liver, bone, immune, blood, and nervous systems. EDTA A can be used as a chelating - EDT agent in cadmium poisoning.

-quantified by GFAAS and ICPMS; ICP-AES -70% in blood (RBCS) -Urinary excretion is about 0.001% and 0.01% of the body burden per 24 hours.

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CHROMIUM

COPPER

LEAD

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INTRODUCTION

-(Cr), from the Greek word chroma (“color”) emeralds alds - makes rubies red and emer green green.. -21st 21st most abundant element in the earth’s ccrust rust -is used in the manufacturing of stainless steel -Occupational exposure: occurs in wood treatment, stainless steel welding, chrome plating, the leather tanning industry, and the use of lead chromate or strontium chromate paints. -Chromium exists in two main valency states: Trivalent & hexavalent 

ugh - (Cu) is a relatively soft yet to tough metal with excellent electrical and heat conducting properties. - widely distributed in nature both in its elemental form and in compounds. -forms alloys with:  zinc (brass)  tin (bronze)  nickel (cupronickel, widely used in coins) -an essential trace element found in four oxidation states , Cu(0), Cu(1+), Cu(2+), and Cu(3+), with Cu(2+) the most stable of all oxidation states. - Copper is an important cofactor for several metalloenzymes and is critical for the reduction of iiron ron in heme synthesis.

ABSORPTION, TRANSPOR TRANSPORT T and EXCRETION

-Cr(6+) is better absorbed and much more toxic than Cr(3+). - transferrin and albumin involved in chromium absorption and transport. -T Transferrin binds the newly absorbed chromium at site B, -Albumin Albumin acts as an acceptor and transporter of chromium if the transferrin sites are saturated. -Other plasma proteins bind chromium:  β- and γ-globulins  lipoproteins

HEAL HEALTH TH EFF EFFECTS, ECTS, DEFICIENCY and T TOXICIT OXICIT OXICITY Y

-Cr(3+) is an essential dietary element and plays a role in maintaining normal metabolism of glucose, fat, and choleste cholesterol. rol. -50 to 200 µg/d: safe and adequate daily intake of chromium for adults -Chromium deficiency is characterized by:  glucose intolerance  glycosuria  hypercholesterolemia  decreased longevity

- 50 to 120 mg: copper content in the normal human adult -is distributed through the body with the highest concentrations found in liver, brain, heart, and kidneys. -Hepatic copper accounts for about 10% of the total copper in the body. -also found in the cornea, spleen, intestine, and lung. -50% to 80%: amount of ingested copper absorbed from the intestine -10 mg or more: average daily intake of copper. -transported to the liver and bounds to albumin, transcuprein, and low-molecular-weight components in the portal system. -Liver Liver Liver:incorporated into ceruloplasmin. -Ceruloplasmin: α2-globulin, and each 132,000 Da molecular weight -98%: excreted in normal physiological state, through the bile -with copper losses in the urine and sweat comprising approximately 2% of dietary intake. -a component of several metalloenzymes -Copper deficiency:premature infants -Copper absorption: severe diffuse diseases of small bowel, lymphosarcoma, and scleroderma. -Copper deficiency:malnutrition, malabsorption, chronic diarrhea, hyperalimentation, and prolonged feeding with low copper, total-milk diets. -Signs of copper deficiency: (1)

-(Pb) is soft, bluish white, highly malleable, and ductile. -a poor conductor of electricity and heat and is resistant to corrosion . --widely distributed in the earth’s crust -the main lead ores are galena, cerrusite, and anglesite anglesite. -used in the production of storage batteries, ammunition, solder, and foils. -Tetraethyl lead was once used extensively as an additive in gasoline (petrol) for its ability to increase the fuel’s octane rating -Toxic concentrations of lead can be found in areas adjacent to homes painted with lead-based paints and around highways where it has accumulated from the past use of leaded gasoline. - In recent years, there have been massive recalls of toys and costume jewelry produced in China, due to concerns over elevated lead content. -Lead plays no known role in normal human physiology. -Exposure leads primarily respiratory or gastrointestinal. -Inhalation results in 30% to 40% of absorption efficiency. -Gut absorption depends on a variety of factors (age and nutritional status, with enhanced gastrointestinal absorption occurring in children younger than 6 years of age) -About 99% of absorbed lead is taken up by erythrocytes where it interferes with heme synthesis. -distributes to soft tissues , such as liver, kidneys, and brain - greater than 90% : skeletal lead concentrations. -Absorbed lead is excreted in: urine (76%) and feces (16%), and the remaining 8% is excreted in hair, sweat, nails, and others.

60 µg/dL or higher with 45 µg/dL - blood levels of children where symptons seen - typical threshold for acute, clinical intervention. 10 µg/ dL or higher - blood lead levels (BLLs) of IQ declines seen in children o -Other conditions may include acute nephropathy and anemia. -The US Centers for Disease Control and Prevention (CDC)

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 decreased sperm counts  impaired fertility. -Cr(6+) compounds are powerful oxidizing agents and are more toxic systemically than Cr(3+) -At physiological pH, Cr(6+) forms CrO42- and readily passes through cell membranes due to its similarity to essential phosphate and sulfate oxyanions. -Intracellularly, Cr(6+) is reduced to reactive intermediates, producing free radicals and oxidizing deoxyribonucleic acid (DNA), both potentially inducing cell death. -Severe dermatitis and skin ulcers can result from contact with Cr(6+) salts. -Up to 20% of chromium workers develop contact dermatitis. - Allergic dermatitis with eczema has been reported in printers, cement workers, metal workers, painters, and leather

LABORA LABORATOR TOR TORY Y EVALU EVALUA ATION

GFAAS, AAS, NAA, or -determined by GF ICP-MS ICP-MS. -Plasma, serum, and urine do not indicate the total body status of the individual -urine levels may be useful for metabolic studies. -In the setting of suspected failure of MoM hip implants that use a cobalt– chrome alloy femoral head, serum is the preferred specimen type for both chromium and cobalt analysis.

neutropenia and hypochromic anemia (2) osteoporosis and various bone and joint abnormalities (3) decreased pigmentation of the skin and general pallor, and (4), possible neurologic abnormalities (hypotonia, apnea, and psychomotor retardation). -Menkes Menkes disease disease: extreme form of copper deficiency Symptoms: -appear: at age 3 months and death: age of 5. -fatal, progressive brain disease is characterized by peculiar hair, called kinky or steely, and retardation of growth. -Clinical signs include progressive mental deterioration, coarse feces, disturbance of muscle tone, seizures, and episodes of severe hypothermia. -Copper toxicity : living near copper-producing facilities, using water from copper pipes or cooking with copper-lined vessels or exposure to algaecides, herbicides, pyrotechnics, ceramic glazes, electrical wiring, or welding supplies. -Because of its redox potential, copper is an irritant to epithelia and mucous membr membranes anes and can cause hepatic and renal damage with hemolysis. -has a characteristic blue-green color. -Wilson’s disease: genetically determined copper accumulation -present ages of 6 and 40 years. -Clinical findings include neurologic disorders, liver dysfunction, and Kayser-Fleischer rings (green-brown discolor discolorati ati ation) on) in the cornea caused by copper deposition. -the disease can be halted with the use of zinc acetate or chelation therapy . -Serum ceruloplasmin levels and the direct measurement of free copper are key diagnostic steps in the diagnosis of Wilson’s disease. -measured by flame AAS, ICP-MS, ICP-AES ICP-AES,, and ASV ASV.. -Serum copper and urine copper: used to monitor for nutritional adequacy and subacute management of copper toxicity.

estimates an incidence of more than 450,000 for children with BLLs higher than 10 µg/dL. - In adults, the following symptoms may be observed: peripheral neuropathies, motor weakness, chronic renal insufficiency and systolic hypertension, and anemia. Lead exposure primarily arises in two settings:  childhood exposure  adult occupational.

whole venous blood -whole : most common specimen type; result of which is commonly referred to as the BLL. : preferred over plasma and serum as circulating lead is predominantly associated with RBCs. -Urine lead may be useful for detecting recent exposures to lead or to monitor chelation therapy. -Noninvasive measurements of lead in bone may be available radiographically. -ICP-MS ICP-MS is a preferred method of

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analysis, although ICP-AES and GFAAS are also used.

INTRODUCTION

ABSORPTION, TRANSPORT a and nd EXCRETION

HEAL HEALTH TH EFFECTS, DEFICIENCY and EXCRETION

LABORA LABORATORY TORY EVALU EVALUA ATION

IRON -(Fe) is the fourth most abundant element in the earth’ earth’ss crust -the most abundant tran transition sition metal. Methods of extracting iron from ore have been known for centuries. physical properties of iron alloys can be varied over an enormous range by appropriate alloying and heat treating  methods, giving a range of strength, hardness, toughness, corrosion resistance (in the form of stainless steels)  magnetic properties and ability to take and hold a sharp edge - Iron ions are able to participate in redox chemistry in both the ferrous [Fe(2+)] and ferric [Fe(3+)] states Absorption of iron from the intestine -is the primary means of regulating the amount of iron within the body. -10% of the 1 g/d of dietary iron is absorbed. -To be absorbed by intestinal cells, iron must be in the ferrous ox oxidation idation state and bound to protein. -In the intestinal mucosal cell, Fe(2+) can be bound by ferritin for storage and eliminated after sloughing off or be exported to the basolateral side. - From there, iron is oxidized to Fe(3+) and bound by apotransferrin for transport throughout the body. -The peptide hormone hepcidin regulates iron absorption in the upper gastrointestinal tract by modulating the export of iron from cells by ferroportin . -After about 120 da days ys in circulation, red cells are degraded by the spleen, liver, and macrophages, which return Fe to the circulation for reuse. -Absorption and transport capacity can be increased in conditions such as iron deficiency, anemia, or hypoxia. - Iron is lost primarily by desquamatio desquamation n and red cell loss to urine and feces. o 40 mg of iron. -With each menstrual cycle, women lose approximately 20 tto -Of the 3 to 5 g of iron in the body -2 to 2.5 g of iron is in hemoglobin, mostly in RBCs and red cell precursors. - ~130 mg is in myoglobin, the oxygen-carrying protein of muscle. -8 mg extremely important pool is bound in tissue to enzymes that require iron for full activity. - also stored as ferritin and hemosiderin, primarily in the bone marrow, spleen, and liver. -3 to 5 mg of iron is found in plasma - Increased blood loss, decreased dietary iron intake, or decreased release from ferritin may result in iron deficiency. - as demonstrated by a decreased RBC count, mean corpuscular hemoglobin concentr concentration, ation, and microcytic RBCs RBCs. - hereditary hemochromatosis (HH). Primary Fe o overload verload verload:most frequently associated with HH is a single-gene homozygous recessive disorder -Primary - HH causes tissue accumulatio...