Perfluorooctaic Acid (PFOA):
PFOA chemical properties:
Molecular Formula: C8HF15O2, Melting point: 52 – 54 °C, Color: white to off-white powder, pKa range: -0.5 to 4.2
PFOA sources of exposure
PFOA and some similar compounds can be found at low levels in some foods, drinking water, and in household dust. Although PFOA levels in drinking water are usually low, they can be higher in certain areas, such as near chemical plants that use PFOA. PFOA has been detected in the blood of almost all US residents.
Leaked documents exposed that DuPont hid studies showing the risks of a Teflon related chemical, Zonyl which breaks down into PFOA. Zonyl is used to line microwave popcorn bags, candy wrappers, pizza boxes and hundreds of other food containers. The documents describe “laboratory tests showing [Zonyl] came off paper coatings and leached into foods at levels three times higher than the FDA limit set in 1967.”
PFOA health concerns
Studies have looked at people exposed to PFOA from living near or working in chemical plants. Some of these studies have suggested an increased risk of testicular cancer with increased PFOA exposure. Studies have also suggested possible links to kidney cancer and thyroid cancer. Other studies have suggested possible links to other cancers, including prostate, bladder, and ovarian cancer. Data taken from over 69,000 people in West Virginia – an area that has endured PFOA emissions from a nearby work site since the 1950s – revealed links from PFOA to testicular and kidney cancer, liver malfunction, hormonal changes, thyroid disruption, high cholesterol, obesity, ulcerative colitis, lower birth weight and size.
The International Agency for Research on Cancer (IARC) has classified PFOA as “possibly carcinogenic to humans” (Group 2B), based on limited evidence in humans that it can cause testicular and kidney cancer, and limited evidence in lab animals.
PFOA body excretion capabilities
Biological half-life: 0.5 – 11 (mean: 3.5 years)
Polytetrafluoroethylene (PTFE)
Polytetrafluoroethylene (PTFE) chemical properties:
Molecular Formula: Cn+F2n+2. PTFE is composed of at least 20,000 C2F4 monomer units linked into very long unbranched chains
The melting point of PTFE is quoted as 327°C, but its mechanical properties degrade above 260 °C. PTFE boiling point: 400 °C
Fluorine is so electronegative that it holds the electrons in the carbon-fluorine bonds close to itself. The extreme electronegativity of the Fluorine atoms is what causes Teflon to be so chemically resistant.
PTFE sources of exposure
Major source of exposure of PTFE is food consumption and food packaging. More than 1000 products contain PTFE. From fast food fries wrappers to GORE-Tex clothes, PTFE is frequently used in the manufacturing industry. Avoid using protective sprays for leather and shoes and non organic paint or cleaning products
Teflon is added to many products to make them resistant to water and stains. These include carpets, fabrics, clothing, and paint as well as cookware. Other brands that use PTFE include Silverstone, Stationmaster, and Gore-Tex. Teflon, and the chemicals used in its production have grown into an industry which profits $2 billion a year.
According to 2017 VCRP data, PTFE is reported to be used in 377 cosmetic products (355 leave-on and 22 rinse-off products). PTFE is included on the list of resinous and polymeric coatings that FDA has determined may be safely used as the food-contact surface of articles intended for use in producing, manufacturing, packing, processing, preparing, treating, packaging, transporting, or holding food. The increased use of synthetic polymeric materials (e.g., PTFE) as construction materials for homes, in furniture, carpeting, and draperies, as packaging material and in aircraft or automobiles has increased the probability for inhalation exposure to the thermal decomposition products of these materials.
However, major source of exposure for a large portion of the population remains cooking with non-stick Teflon pans. Not only PTFE can leak into your foods but you are also exposed to PTFE when breathing air that contains contaminated dust from hot skillet, carpets, upholstery, clothing, etc.
if you’re located close to a manufacturing facility, PTFE can be found in large quantity in drinking water. Inhalation of PTFE may be important in area close to waste recycling centers.
Perfluoroalkyls (PFA) contaminate food, water, wildlife, consumer products, and have been detected in every corner of the globe. They have been found in the blood of virtually all Americans tested over the last decade. In the human body, these chemicals are persistent, bioaccumulative and toxic to numerous organs.
464°F/ 240°C
Ultrafine particulate matter These particles have caused extreme lung damage to rats within 10 minutes of exposure. Longer exposures cause death.
680°F/ 360°C
Difluoroacetic acid Largely unstudied, although kidney toxicity has been reported in rats.
Hexafluoropropene Produces decreased immunity and chromosomal abnormalities in animals. In people, it can lead to eye, nose and throat irritation, heart palpitations, irregular heart rate, headaches, light-headedness, and decreased motor speed, memory and learning.
Monofluoroacetic acid Can kill people even in extremely low doses. Low doses provoke nervous system symptoms. Higher exposures can lead to irregular heart rate, heart attacks and respiratory failure.
Perfluorooctanoic acid Causes four types of tumours in rats – in the liver, pancreas, mammary gland (breast) and testes. Similar effects have also been noted in humans. It has also been linked to hypothyroidism and raised cholesterol.
Tetrafluoroethylene A potential kidney and liver carcinogen known to cause cancer in laboratory animals.
Trifluoroacetic acid Causes bone abnormalities and birth defects in animals.
878°F/ 470°C
Silicon tetrafluoride A highly
toxic, corrosive gas that can cause eye and throat irritation, difficult
breathing, bluish skin colour from lack of oxygen, lung damage and lung
oedema. Long-term exposure can cause weight loss, decreased numbers of
red and white blood cells, discoloration of the teeth and abnormal
thickening of the bone.
887°F/ 475°C
Perfluoroisobutene A highly toxic
corrosive chemical warfare agent. Symptoms in people include bad taste
in mouth, nausea and weakness. Lung oedema occurs about one to four
hours after exposure.
932°F/ 500°C
Carbonyl fluoride A fluoridated
version of a WWI chemical warfare agent. Fumes can irritate eyes, ears
and nose. More serious symptoms of exposure include chest pains,
breathing difficulty, fluid accumulation in the lungs, liver damage and
increased glucose levels.
Hydrogen fluoride A toxic corrosive gas that can cause death to any tissue it comes into contact with, including the lungs.
1,112°F/ 600°C
Octafluorocyclobutane Can cause
heartbeat irregularities, unconsciousness and death. People with
pre-existing heart conditions may be extra vulnerable.
Perfluorobutane A global warming chemical. Untested for long-term effects in humans.
Trifluoroacetic acid fluoride Largely unstudied, but can cause foetal bone abnormalities and neural tube defects in rats.
1,202°F/ 650°C
Carbon tetrafluoride A
refrigerant and potent greenhouse gas. Can cause eye, ear and nose
irritation, heart palpitations, irregular heart rate, headaches,
confusion, lung irritation, tremors and, occasionally, coma.
PTFE health concerns
In 2003, an EWG-commissioned test showed that in just two to five minutes on a conventional stove top, cookware coated with Teflon and other non-stick surfaces could exceed temperatures at which the coating breaks apart and emits toxic particles and gases.
PTFE is most notorious for its toxicity to birds. This has been referred to as “Teflon toxicosis” where the lungs of exposed birds hemorrhage, filling up with fluid and leading to suffocation.
In humans, Teflon toxicity causes polymer fume fever, a temporary, intense, though not very serious influenza-like syndrome. Only a few cases have been reported of people going to the hospital from overheated Teflon. Since the fever mimics the flu, it is likely doctors would not realize the origin of the illness coming from overheated Teflon. Polymer fume fever is only caused from exposure to PTFE breakdown products. Further alarm comes as PTFE residuals, known as perfluorocarbons (PFC’s) were found in breast milk from all 45 nursing mothers tested in this study.
Contaminated water with PTFE has been linked to developmental problems, cancer, liver damage, immune effects AND THYROID PROBLEMS.
The following toxic effects are included: pulmonary edema, labored or rapid breathing, intraalveolar hemorrhage, alveolar edema and hemorrhage, airway damage and lung congestion, pulmonary inflammatory responses, pulmonary edema and hemorrhage, increased lung weight, lung congestion and unspecified gross changes in liver, kidney tubule necrosis, emphysema and alveolitis
PTFE body excretion capabilities
PTFE biological half life in humans in approximately 900 days. As FRD-902 is used as a replacement of PFOA and its ammonium salt (APFO) for the production of Teflon, a comparison of the toxicological properties of both ammonium salts (FRD-902 and APFD) is considered relevant. Biological half life of APFO in humans is 1378 days.
Cadmium (Cd)
Cadmium (Cd) chemical properties:
Cadmium is a lustrous, silver-white, ductile, very malleable metal. Its surface has a bluish tinge and the metal is soft enough to be cut with a knife, but it tarnishes in air. It is soluble in acids but not in alkalis. This soft, bluish-white metal is chemically similar to the two other stable metals in group 12, zinc and mercury. Like zinc, it demonstrates oxidation state +2 in most of its compounds Cadmium makes up about 0.1 ppm of Earth’s crust. It is much rarer than zinc, which makes up about 65 ppm. The only cadmium mineral of importance, greenockite (CdS), is nearly always associated with sphalerite (ZnS). This association is caused by geochemical similarity between zinc and cadmium, with no geological process likely to separate them. Thus, cadmium is produced mainly as a byproduct of mining, smelting, and refining sulfidic ores of zinc, and, to a lesser degree, lead and copper. Small amounts of cadmium, about 10% of consumption, are produced from secondary sources, mainly from dust generated by recycling iron and steel scrap.
Melting point : 321 °C, Boiling point : 767 °C
Cd sources of exposure
About three-fourths of cadmium is used in Ni-Cd batteries, most of the remaining one-fourth is used mainly for pigments, coatings and plating, and as stabilizers for plastics.
One of the most important use of cadmium in the United States is in the production of nicad (Nickel Cadimum alloy).
Cadium has been used particularly to electroplate steel where a film of cadmium only 0.05 mm thick will provide complete protection against the sea. Cadmium has the ability to absorb neutrons, so it is used as a barrier to control nuclear fission.
Cadmium can mainly be found in the earth’s crust. It always occurs in combination with zinc. Cadmium also consists in the industries as an inevitable by-product of zinc, lead and copper extraction. After being applied it enters the environment mainly through the ground, because it is found in manures and pesticides.
It ranks in the lower 25 percent of the elements in terms of abundance in the earth
Naturally a very large amount of cadmium is released into the environment, about 25,000 tons a year. About half of this cadmium is released into rivers through weathering of rocks and some cadmium is released into air through forest fires and volcanoes. The rest of the cadmium is released through human activities, such as manufacturing.
Another important source of cadmium emission is the production of artificial phosphate fertilizers. Part of the cadmium ends up in the soil after the fertilizer is applied on farmland and the rest of the cadmium ends up in surface waters when waste from fertilizer productions is dumped by production companies.
Food is the primary source of Cadmium exposure among general population as a consequence of the bio-concentration of Cadmium from soil.
Foodstuffs that are rich in cadmium include liver (and sweatmeat in general), mushrooms, shellfish, mussels, cocoa powder, dried seaweed and cereals (especially rice). From the soil, certain plants (tobacco, rice, other cereal grains, potatoes, and other vegetables) take up cadmium more avidly than they do other heavy metals such as lead and mercury. Cadmium is also found in meat, especially sweetmeats such as liver and kidney. In certain areas, cadmium concentrations are elevated in shellfish and mushrooms.
In the [Kim, K., Melough, M., Vance, T., Noh, H., Koo, S., & Chun, O. (2019). Dietary Cadmium Intake and Sources in the US. Nutrients, 11(1), 2] study, it was concluded that the foods that contributed most to total Cd intake were lettuce (14%), spaghetti (8%), bread (7%), and potatoes (6%).
For its report, ConsumerLab.com analyzed 21 cocoa products, mostly cocoa powders and dark chocolate bars, but also several cocoa supplements. All seven dark chocolate bars fell below the WHO limits for cadmium though one exceeded California’s daily cadmium limit. However, of eight cocoa powders, six failed because of excessive cadmium levels, with most having three to five times the WHO limit. Two had more than three times the California limit and one had five times the limit. And one cocoa powder that fell below the cadmium limit contained a small amount of lead, as did two other powders.
A 2006 study from the Slovak Republic, of non-smokers, found vegans to have significantly higher blood levels of cadmium than non-vegans
Cadmium can also enter the food chain from water. In Japan, zinc mining operations contaminated the local water supplies with cadmium. Local farmers used that water for irrigation of their fields. The soil became contaminated with cadmium which led to the uptake of cadmium into their rice.
An exposure to significantly higher cadmium levels occurs when people smoke. Other high exposures can occur with people who live near hazardous waste sites or factories that release cadmium into the air and people that work in the metal refinery industry.
Colored glass and children’s products found to contain large quantities of cadmium include jewelry and toys
Cd health concerns
Chronic Cadmium exposure has been reported to be associated with chronic kidney disease, osteoporosis, diabetes, cardiovascular disease and cancer.
Because of the sufficient evidences in humans for the carcinogenicity of Cadmium and its compounds, International Agency for Research on Cancer re-evaluated and classified Cadmium and its compounds as carcinogens to humans (Group 1). Cadmium and Cadmium compounds cause cancer of the lung and are positively associated with kidney and prostate cancer.
Recent studies also suggest that cadmium exposure may produce other adverse health effects at lower exposure levels than previously predicted, including increased risk of hormonal cancers. For example, researchers on Long Island estimated that as much as a third of breast cancer in the U.S. might be associated with elevated cadmium levels.
Cadmium is first transported to the liver through the blood. There, it is bond to proteins to form complexes that are transported to the kidneys. Cadmium accumulates in kidneys, where it damages filtering mechanisms. This causes the excretion of essential proteins and sugars from the body and further kidney damage.
CANCEROGENICITY SLOPE FACTOR FOR Cd: 6.1 (mg/kg/day)-1
The population-based study in Flemish women living in districts with low to moderate environmental Cadmium pollution showed the association between osteoporosis and environmental Cadmium exposure.
Animals eating or drinking cadmium sometimes get high blood-pressures, liver disease and nerve or brain damage. Cadmium initiates atherosclerosis and promotes progression as shown by induction of endothelial dysfunction in vitro and acceleration of atherosclerotic plaque formation in vivo.
Cd toxicologic data
Actual cadmium absorption via inhalation exposure has been estimated to be 30 to 60% in humans. Absorption of cadmium from the gastrointestinal tract appears to be a saturable process with the fraction absorbed decreasing at high doses (btween 2% – 10%).
Although cadmium is widely distributed throughout the body, most (50 to 70% of the body burden) accumulates in the kidneys and liver.
In 2009, the Panel on Contaminants in the Food Chain of European Food Safety Authority (EFSA) issued an opinion in which the PTWI should be reduced to a tolerable weekly intake (TWI) of 2.5 μg/kg body weightNo Significant Risk Level (NSRL) through inhalation of 0.05 µg/day and a Maximum Allowable Dose Level (MADL) through oral absorption of 4.1 µg/day. This level is far above the recommendations of Californian Office of Environmental Health Hazard Assessment, which recommends a
Cd body excretion capabilities
The principal route of excretion is via the urine, with average daily excretion for humans being about 2 to 3 µg. Daily excretion represents only a small percentage of the total body burden, which accounts for the 25 (between 17 to 30) years half-life of cadmium in the body. Unabsorbed cadmium is removed from the gastrointestinal tract by fecal excretion. Typical daily cadmium excretion has been reported to be about 0.01% of the total body burden. There is some evidence for biliary excretion of cadmium
Lead (Pb)
Lead (Pb) chemical properties:
Melting point : 327 °C, Boiling point : 1755 °C
Lead is a bluish-white lustrous metal. It is very soft, highly malleable, ductile, and a relatively poor conductor of electricity. It is very resistant to corrosion but tarnishes upon exposure to air. Lead isotopes are the end products of each of the three series of naturally occurring radioactive elements.
Despite the fact that lead has four electrons on its valence shell, its typical oxidation state is +2 rather than +4, since only two of the four electrons ionize easily. Apart from nitrate, chlorate and, to a much lesser degree, chloride, most of the inorganic salts of lead (II) have poor solubility in water.
Pb sources of exposure
Native lead is rare in nature. Currently lead is usually found in ore with zinc, silver and copper and it is extracted together with these metals. The main lead mineral in Galena (PbS) and there are also deposits of cerrussite and anglesite which are mined. Galena is mined in Australia, which produces 19% of the world’s new lead, followed by the USA, China, Peru’ and Canada. Some is also mined in Mexico and West Germany. World production of new lead is 6 million tonnes a year, and workable reserves total are estimated 85 million tonnes, which is less than 15 year’s supply.
Lead occurs naturally in the environment. However, most lead concentrations that are found in the environment are a result of human activities. Due to the application of lead in gasoline an unnatural lead-cycle has consisted. In car engines lead is burned, so that lead salts (chlorines, bromines, oxides) will originate. These lead salts enter the environment through the exhausts of cars. The larger particles will drop to the ground immediately and pollute soils or surface waters, the smaller particles will travel long distances through air and remain in the atmosphere. Part of this lead will fall back on earth when it is raining. This lead-cycle caused by human production is much more extended than the natural lead-cycle. It has caused lead pollution to be a worldwide issue.
Lead is a soft metal that has known many applications over the years. It has been used widely since 5000 BC for application in metal products, cables and pipelines, but also in paints and pesticides.
Lead can enter (drinking) water through corrosion of pipes. This is more likely to happen when the water is slightly acidic. That is why public water treatment systems are now required to carry out pH-adjustments in water that will serve drinking purposes.
Lead has been found in inexpensive children’s jewelry sold in vending machines and large volume discount stores across the country. It also has been found in inexpensive metal amulets worn for good luck or protection. Some costume jewelry designed for adults has also been found to contain lead. It is important to make sure that children don’t handle or mouth any jewelry. People exposed to lead at work may bring lead home on their clothes, shoes, hair, or skin. Some jobs that expose people to lead include: home improvement; painting and refinishing; car or radiator repair; plumbing; construction; welding and cutting; electronics; municipal waste incineration; lead compound manufacturing; manufacturing of rubber products, batteries, and plastics; lead smelting and refining; working in brass or bronze foundries; demolition; and working with scrap metal. Some hobbies also use lead. These hobbies include making pottery, stained glass, or refinishing furniture.
Spot measurements in five French and four United States cities in 1984–1985 reported air lead levels ranging from 0.005 μg/m3 to 0.44 μg/m3, the highest value being from Paris. Air lead concentrations in industrial areas and in urban areas with high traffic density have decreased steadily over the past 15 years, subsequent to abatement of industrial emissions and to reductions in the lead content of petrol or to the increasing use of lead-free petrol. A typical example are annual means of air lead concentrations reported for the industrialized urban Rhine–Ruhr region in Germany. Whereas annual means were 0.81–1.37 μg/m3 in 1974, they were only 0.17–0.19 μg/m3 in 1988; for traffic-dominated cities (Cologne and Düsseldorf) the decrease was from 0.81 and 0.96 μg/m3 to 0.17 and 0.18 μg/m3, respectively, whereas for more industrialized areas (Essen and Dortmund) it was from 1.30 and 1.37 μg/m3 to 0.17 and 0.19 μg/m3, respectively. Even more pronounced downward trends from above 3 μg/m3 in 1974 to about 0.5 μg/m3 in 1988 have been reported for areas with high traffic density in Belgium. Higher air lead concentrations may still be found in the vicinity of primary or secondary lead smelters. Most of the lead in the air is in the form of fine particles with a mass median equivalent diameter of less than 1 μm. The fraction of organic lead (predominantly lead alkyls that escaped combustion) is generally below 10% of the total atmospheric lead, the majority (>90%) of lead from leaded petrol emissions being inorganic particles such as PbBrCl. In the immediate vicinity of smelters, the particle size distribution usually shows a predominance of larger particles. However, these particles settle at distances of a few hundred metres or 1–2 km, so that further away the particle size distribution is indistinguishable from that of other urban sites. Lead is removed from the atmosphere by dry or wet deposition. The residence time of leadcontaining particles in the atmosphere varies according to a number of factors, such as particle size, wind currents, rainfall and height of emission. Soil and water pollution from car emission fallout is predominantly limited to the immediate urban area. Fallout from the emissions of industrial sources, such as smelters, is likewise limited mainly to the immediate vicinity. However, strong evidence indicates that a fraction of airborne lead is transported over long distances. As a result, a long-term global accumulation of lead has occurred in recent decades. This has been demonstrated convincingly by analyses of glacial ace and snow deposits in remote areas, such as the Greenland ice cap, until about 1960; however, subsequent measurements revealed a marked downward trend in the same glacial strata, corresponding to the global fall in the use of alkyl lead additives in petrol.
Lead contamination of food arises as a result of environmental emissions, such as mining and the now diminished use of leaded petrol. Data from the SCOOP report on heavy metals show that levels of lead in most commonly consumed foodstuffs are generally low. However, like mercury, lead can accumulate in fish and shellfish and in addition can be found at higher levels in the offal (liver and kidney) of food animals. Consumers eating diets rich in these foods may therefore be exposed to an unacceptable level of lead.
A further source of lead in the diet is from food containers containing lead, e.g. storage in lead-soldered cans, ceramic vessels with lead glazes and leaded crystal glass. The first of these has now been largely discontinued, at least in the EU, and the second is also strictly regulated under EU legislation related to food contact materials. However, there are repeated instances of food dishes, utensils or other materials manufactured outside the EU that release lead into food at levels above those permitted in the EU.
Results from the USD FDA Total Diet Study, raised special concern regarding the concentration of lead in the following foods: liver (10 mg/kg), Tuna (7 mg/kg), Schrimp (7 mg/kg), Spinach (4 mg/kg), Dill cucumber pickles (7mg/kg), Margarine (4 mg/kg), Honey (6 mg/kg), Chocolate cake (6mg/kg), Candy bar (11 mg/kg), Chocolate (12 mg/kg), Brownies (11 mg/kg), Cookies (12 mg/kg) Wine (7 mg/kg), Corn flakes cereals (5 mg/kg), Crisped rice cereal (4 mg/kg), Raisin bran cereal (3 mg/kg), Oat ring cereal (4 mg/kg), Canned apricots (11 mg/ kg), Canned Swet potatoes (12 mg/kg), Fruit cocktail (10 mg/kg), Pineapple juice (4 mg/kg), Prune juice (4 mg/kg), Canned peache (12 mg/kg)
nIt is very apparent from that list that foods with major lead contamination are ones that are stored in can for long time. Additionally, due to industrial processses, chocolate and wine contain very elevated lead concentration. On the other hand, food contaminated through environmental lead pollution are fishes, sweetmeats and certain types of vegetables such as spinach, strawberries and lettuce. It is also worring to notice that because of land pesticide contamination, honey starts to be produced from cities bees swam. This may explain the significant concetration of lead in honey samples
Lead is one out of four metals that have the most damaging effects on human health. It can enter the human body through uptake of food (65%), water (20%) and air (15%).
Pb health concerns
For as far as we know, lead fulfils no essential function in the human body, it can merely do harm after uptake from food, air or water. The toxic effects of lead, like those of mercury, have been principally established in studies on people exposed to lead in the course of their work. Short-term exposure to high levels of lead can cause brain damage, paralysis (lead palsy), anaemia and gastrointestinal symptoms. Longer-term exposure can cause damage to the kidneys, reproductive and immune systems in addition to effects on the nervous system. The most critical effect of low-level lead exposure is on intellectual development in young children. Infants and young children are more vulnerable than adults to the toxic effects of lead, and they also absorb lead more readily. Even shorttem, low-level exposures of young children to lead is considered to have an effect on neurobehavioural development.
Lead can cause other several unwanted effects, such as: disruption of the biosynthesis of haemoglobin and anaemia, a rise in blood pressure, declined fertility of men through sperm damage, behavioural disruptions, such as aggression, impulsive behavior and hyperactivity.
Lead can enter a foetus through the placenta of the mother. Because of this it can cause serious damage to the nervous system and the brains of unborn children, miscarriages and subtle abortions.
Lead has also been associated to lung cancer, stomach cancer, and gliomas, hepatobiliary cancer. Renal tumours have been reported to be associated with lead exposure. In all of the available studies renal carcinogenicity has been found in rats at high dietary doses of lead and long exposure times on a background of cell hyperplasia, cytomegaly and cellular dysplasia
Pb body excretion capabilities
Depending upon chemical speciation, particle size, and solubility in body fluids, up to 50% of inhaled lead in lead compounds may be absorbed. Absorption of lead from the gastrointestinal tract after ingestion can range from 3 to 80% and is influenced by the physico-chemical nature of the ingested material, nutritional status, and type of diet consumed. Absorption is predominantly influenced by food intake with much higher absorption occurring after fasting than when lead is ingested with a meal.
Nonabsorbed lead passes through the gastrointestinal tract and is excreted in the faeces. Of the absorbed fraction, 50–60% is removed by renal and biliary excretion. Intestinal clearance is about 50% of the renal clearance.
Absorbed lead is distributed among soft tissues (blood, liver, kidney, brain etc) and mineralizing systems (bone, teeth). Bone is the body’s major storage site. Lead accumulates in bones over the lifetime. About 95% of the body burden in adults is located in the bones, compared with about 70% in children. Knowledge of the kinetics is important because of the possibility of the release of stored lead under appropriate conditions. Biokinetic movements of lead in the body, based on tracer and balance data, have been characterized by a three-compartment model. Lead within these three compartments, namely blood, bone and soft tissues, was found to have different half-times, with blood being the most labile pool (half-time about 36 days), bone the most stable (half-time about 17 – 27 years) and the soft tissues also labile (half-time about 40 days).
Aluminum (Al)
Aluminum (Al) chemical properties:
Aluminum is the third most abundant element on the Earth’s crust. it is believed to be contained in a percentage from 7.5% to 8.1%. Aluminum is very rare in its free form. Aluminium occurs principally in bauxite. Aluminum contribute greatly to the properties of soil, where it is present mainly as insoluble aluminum hydroxide.
Melting point: 660.4 °C
Boiling point: 2467 °C
Aluminum is a shiny, silvery white colored metal that is light in weight and strong. The density of aluminum is 2.7 g/mL, which means the metal will sink in water, but is still relatively light.
When it comes in contact with oxygen, aluminum forms an oxide skin called aluminum oxide. This skin helps to protect aluminum from corrosion. Aluminum is among the most difficult metals on earth to refine, the reason is that aluminum is oxidized very rapidly and that its oxide is an extremely stable compound that, unlike rust on iron, does not flake off.
Aluminum catches fire easily if exposed to flame when it is in powdered form. It is also reactive with both acids and alkalis.
Aluminum (Al) sources of exposure
An average adult in the United States eats about 7–9 mg of aluminum per day in their food.
The main source of exposure to aluminium for the general population is food, which contributed to more than 95% of total exposure, particularly through foods added with aluminium-containing food additives, but the intake can be increased 10 to 100 times through the use of aluminium-containing medicinal products such as antacids. Generally, the intake of aluminium from foods is less than 1% of that consumed by individuals using aluminium-containing pharmaceuticals such as astringents and buffered aspirin. Although the absorption of Aluminum through skin is reduced compared to other absorption types, Aluminim contamination could also arise from antiperspirants and cosmetics because of their very elevated Aluminium amount.
A number of medications and supplements contain aluminum either as an active ingredient or a contaminant.Drugs that contain aluminum as an active ingredient include certain antacids, such as Mylanta, and buffered aspirin, both of which can cause aluminum toxicity when taken regularly. Drug and supplement additives that have been shown to be contaminated with aluminum include magnesium stearate, microcrystalline cellulose, and talcum. Some calcium, iron, and B-complex tablets have been found to contain high levels of aluminum, presumably because of these contaminated additives.
Dietary sources of exposures to aluminium include drinking water, natural food sources, migration from food-contact material and food additives. Unprocessed foods like fresh fruits, vegetables, and meat contain very little aluminum, whereas aluminum compounds may be added during processing of foods, such as: flour, baking powder, coloring agents, anticaking agents
The highest predicted contribution to aluminium in the Irish diet is from tea (high levels are naturally present in tea leaves), along with cereal crops and cereal based foods such as breads and certain cakes and pastries, either from the natural presence in grains or from the use of certain food additives. In addition some vegetables, fruit, meat and dairy products may naturally contain aluminium. In addition, elvated concentration of Aluminum are often reported in cocoa powder and chocolate candy bars. In another study, the only foods that contained more than 1 µgAl/g food after being cooked in stainless steel utensils were green beans, peas, unpeeled potatoes, pudding, rice and ham. In addition cooking with an aluminum cookwares may increse by 50 the aluminum content of raw food for certain food types such as eggs and ham.
Food related uses of aluminium compounds include preservatives, fillers, colouring agents, anti-caking agents, emulsifiers and baking powders; soy-based infant formula can contain aluminium. In a study analyzing the Aliminum content of foods consummed in Hong Kong, high levels of aluminium were found in the ten powder mix samples for bakery/fried food, ranged from 180 to 16000 mg/kg. Except a baking powder sample which was found to have the highest level of aluminium (16000 mg/kg), the aluminium levels of remaining powder mix samples ranged from 180 to 1900 mg/kg. Aluminium-containing food additives have been used in food processing for over a century, as firming agent, raising agent, stabiliser, anticaking agent and colouring matter, etc.1,7 and some are permitted to be used in food in many countries such as the United States (US), the European Union (EU), Australia, New Zealand, Japan and Mainland China, etc. Some aluminium-containing food additives have been included in the Codex General Standard for Food Additives
The Previsional Tolerable Weekly Intake is likely to be exceeded to a large extent by some population groups, particularly children, who regularly consume foods added with aluminium-containing food additives. Overseas report revealed that high levels of aluminium were found in soya-based formulae and dietary exposure to aluminium was expected to bevery high, up to 1 mg/kg bw/day, for infants fed on soya-based formula.
Another significant route of exposure to aluminium in infants is through immunization with Al-adjuvanted vaccines where the addition to the body burden might be as high as from breast milk or formula feeding.3 Indeed, the first encounter a newborn (at day 0) has with aluminium is not through colostrum but through a large parenteral load of Al(OH)3 from the Hepatitis B vaccine (HBV) as an adjuvant. Indeed, neonates (<24 h and weighing > 2000 g) may receive an Al (250 mg) exposure from HBV that is far in excess of that absorbed from breast milk taken during the entire six months of lactation.
The largest markets for aluminium metal and its alloys are in transportation, building and construction, packaging and in electrical equipment. Transportation uses are one of the fastest growing areas for aluminium use. Aluminium powders are used in pigments and paints, fuel additives, explosives and propellants. Aluminium oxides are used as food additives and in the manufacture of, for example, abrasives, refractories, ceramics, electrical insulators, catalysts, paper, spark plugs, light bulbs, artificial gems, alloys, glass and heat resistant fibres. Aluminium hydroxide is used widely in pharmaceutical and personal care products. Natural aluminium minerals especially bentonite and zeolite are used in water purification, sugar refining, brewing, paper industries and sometimes in kitchen utenils. Aluminum is also used to make beverage cans, pots and pans.
Aluminum is added to lipsticks to keep colors from bleeding. Almost all lipstick applied gets ingested. It has been estimated that heavy lipstick users can ingest potentially hazardous amounts of aluminum.[ Choose your cosmetics wisely and incorporate make-up-free days into your routine.
People generally consume little aluminum from drinking water. Water is sometimes treated with aluminum salts while it is processed to become drinking water. But even then, aluminum levels generally do not exceed 0.1 mg/L. Several cities have reported concentrations as high as 0.4–1 mg/L of aluminum in their drinking water. Aluminum (Al) salts are used as a coagulant for purification of drinking water.
Most people take in very little aluminum from breathing. Levels of aluminum in the air generally range from 0.005 to 0.18 micrograms per cubic meter (ìg/m3), depending on location, weather conditions, and type and level of industrial activity in the area. Most of the aluminum in the air is in the form of small suspended particles of soil (dust). Aluminum levels in urban and industrial areas may be higher and can range from 0.4 to 8.0 ìg/m3.
Aluminum (Al) health concerns
Long lasting uptakes of significant concentrations of aluminum can lead to serious health effects, such as: damage to the central nervous system, dementia, loss of memory, listlessness, severe trembling.
Osteomalacia has been reported in humans following daily intake of several grams of aluminium-containing antacids for several months and in patients with chronic renal failure after exposed to aluminium in dialysis fluids
Inhalation of finely divided aluminum and aluminum oxide powder has been reported as a cause of pulmonary fibrosis and lung damage. This effect, know as Shaver’s Disease, is complicated by the presence in the inhaled air of silica and oxides of iron.
Aluminium is the cause of dialysis encephalopathy, nor by decades of animal experimentation demonstrating intoxication.
Exposure of human populations to toxic metals can result in damage to a variety of organ systems. One of the most commonly toxic metals studied, aluminum, is implicated in many diseases. Al3+ can pass the blood-brain barrier by receptor-mediated endocytosis of the Fe-carrier protein and in rats approximately 0.005% of the metal complexes enter the brain. Al toxicity is caused by disruption of homeostasis of metals such as magnesium, calcium, and iron (Fe): in fact, Al mimics these metals in their biological functions and triggers many biochemical alterations. Al is considered as a major neurotoxin. In particular, Al both exerts direct genotoxicity in primary human neural cells and induces neurodegeneration, through an increase in Fe accumulation and oxygen reactive species (ROS) production. Soluble aluminum salts can be absorbed from the stomach and the metal is deposited in the gray matter in the brain. Following exposure to aluminum, aggregates of neurofilaments accumulate in neurons. Aluminum influences a number of neuronal processes, such as increasing protein synthesis and neurotransmitter breakdown, to decreasing neurotransmitter reuptake and slow axonal transport. The neurotoxicity potential for aluminium has received particular attention due to a speculated association with Alzheimer’s disease. An increasing number of epidemiological reports relate the aluminum content of drinking water with increasing incidence of neurological disease. Another study correlated the risk of developing Alzheimer’s disease with residing in areas where aluminum concentrations in the municipal drinking water are 100 μg/L or greater. A dose-response correlation between an increasing concentration of Al in the drinking water and a higher risk of developing Alzheimer’s disease (AD) was found. Another study, looking at elderly populations exposed to Al3+ in drinking water (100 μg/L), also reported a similar link between exposure and the prevalence of AD.
The removal of toxic metal from human body can represent a useful tool to avoid the beginning or progression of many diseases related to metal intoxication. In 1991, treatment with low dose intramuscular desferrioxamine (DFO), a trivalent chelator that can remove excessive iron and/or aluminium from the body, was reported to slow the progression of Alzheimer’s disease.
There is evidence relating aluminum exposure to Parkinson’s disease. An epidemiological study has found a correlation between this disorder and Al exposure (Altschuler, 1999). Al concentrations are elevated in dopamine-related brain regions of PD patients and occupational exposure to aluminum may constitute a risk factor for PD.
Effects of Al on autoimmunity, oral tolerance, CD4+ and CD8+ expression, hypersensitivity, and erythrocyte immune function are suggestive of its immunotoxicologic activity. It has been suggested that many of the features of Al-induced neurotoxicity may arise in part from autoimmune reactions.
Aluminium has been recognised as a mutagen for many years. Research seems to indicate a link between aluminium accumulation and breast cancer. Tests which had been carried out on women who had mastectomies found high levels of aluminium, an ingredient found in some deodorants, in their breast tissue. The evidence linking aluminum to breast cancer has now grown so strong that a diverse group of European researchers recently called for the urgent reduction of this metal in antiperspirants.
Among workers first employed in Quebec aluminum smelters, chronic obstructive pulmonary disease and respiratory cancer (one cohort each) mortality were statistically in excess. In the combined cohorts, standardized mortality ratios exceeded 110 for cancers of esophagus, rectum, and rectosigmoid junction, pancreas, larynx, lung, non-Hodgkin lymphoma, cerebrovascular disease, and asthma. These findings essentially mirrored the experience of pre-1950 workers. There was a significant downward trend in mortality from all causes, lung and bladder cancer.
In another cohort study, from January 1970 through June 1986, 79 cases of bladder cancer were identified in this cohort of aluminum workers aged 65 years or younger. Although, occupational exposure to certain aromatic amines also causes bladder cancer, many occupational groups including dye workers, rubber workers, leather workers, painters, truck drivers, and aluminum workers have increased bladder cancer risk.
In a study reviewing the epidemiologic evidence of cancer risks among workers in aluminum reduction plants with emphasis on associations with specific work areas and exposures, it was concluded that work in potrooms with Söderberg electrolytic cells was associated with increased risk of bladder cancer, and the increase was correlated to duration of tar exposure. There was a suggestion of increased risk of leukemias and pancreatic cancers in potroom workers, and of kidney and brain cancers without any clear association with specific exposures or work areas.
In another cohort study of aluminum reduction plant workers, all men with three or more years at an aluminum reduction plant in British Columbia (BC), Canada between the years 1954 and 1997 were included (a total of 6,423 workers). Among them a total of 662 men were diagnosed with cancer, representing a 400% increase from the original study (14 years back in time). Standardized mortality and incidence ratios were used to compare the cancer mortality and incidence of the cohort to that of the BC population. The risk for bladder cancer was related to cumulative exposure to CTPV measured as BSM and BaP (p trends <0.001), and the risk for stomach cancer was related to exposure measured by BaP (p trend BaP <0.05).
In a Swedish cohort of workers (n = 6,454) from seven aluminum foundries and three secondary aluminum (scrap) smelters there was no overall excess risk of cancer among male or female workers less than 85 years of age (males: 325 observed cases, standardized incidence ratio (SIR) 1.02, 95% confidence interval (CI) 0.91–1.13; females: 22 cases, SIR = 0.95, 95% CI = 0.60–1.44). In male workers, however, significantly elevated risk estimates were observed for cancer of the lung (51 cases; SIR = 1.49, 95%CI = 1.11–1.96), anorectal cancer (33 cases; SIR 2.13, 95%CI = 1.47–2.99), and sinonasal cancer (4 cases; SIR = 4.70, 95%CI = 1.28–12.01). There was no increase of urinary bladder or liver cancer.Occupational exposure to certain aromatic amines also causes bladder cancer. Many occupational groups including dye workers, rubber workers, leather workers, painters, truck drivers, and aluminum workers have increased bladder cancer risk.
Analysis of mortality by job-exposure category in workers at a northwestern United States prebake-type aluminum reduction plant, suggests that some of the lymphatic and hematopoietic cancers (especially malignant lymphoma), lung cancers and pulmonary emphysema may be of occupational origin in this worker population.
Aluminum (Al) body excretion capabilities
The biological half life of Aluminum is very dependent of the tissue. In soft tissues including liver, biological half life is of 1.43 days. In extracellular fluids and blood, the biological half life is very short (10 min), whereas in Cortical Bone Mineral, the biological half-life is of 28 years.
A small increase in brain aluminum seems sufficient to produce neurotoxicity. Once aluminum enters the brain it persists there for a very long time; estimates of the half-life range from 20% of the lifespan to greater than the lifespan. Al persistence in bone, which maintains the majority of the body burden, may influence brain Al, due to equilibrium among the body’s organs.
Nickel (Ni)
Nickel (Ni) chemical properties:
Nickel is silvery-white. hard, malleable, and ductile metal. It is of the iron group and it takes on a high polish. It is a fairly good conductor of heat and electricity. In its familiar compounds nickel is bivalent, although it assumes other valences. It also forms a number of complex compounds. Most nickel compounds are blue or green. Nickel dissolves slowly in dilute acids but, like iron, becomes passive when treated with nitric acid. Finely divided nickel adsorbs hydrogen. Nickel exhibits magnetic properties below 345°C. Nickel is highly resistant to rusting and corrosion, it does not react with air under ambient conditions (metal nickel) but in the finely dispersed state nickel it ignites spontaneously in air.
Melting point: 1453 °C
Boiling point: 2913 °C
Naturally occurring nickel (28Ni) is composed of five stable isotopes; 58Ni, 60Ni, 61Ni, 62Ni and 64Ni with 58Ni being the most abundant (68.077% natural abundance). 26 radioisotopes have been characterised with the most stable being 59Ni with a half-life of 76,000 years, 63Ni with a half-life of 100.1 years, and 56Ni with a half-life of 6.077 days. All of the remaining radioactive isotopes have half-lives that are less than 60 hours and the majority of these have half-lives that are less than 30 seconds. This element also has 1 meta state. Although 58Ni is an isotope stable, it is suspected to desintegrate by double radiation β+ in 58Fe2, with a very long radioactive half-life (greater than 700×1018 years). The majority of radioactive isotopes of Nickel with an atomic mass from 47 to 82 are of artificial origin.
The major use of nickel is in the preparation of alloys. Nickel alloys are characterized by strength, ductility, and resistance to corrosion and heat. About 65 % of the nickel consumed in the Western World is used to make stainless steel, whose composition can vary but is typically iron with around 18% chromium and 8% nickel. 12 % of all the nickel consumed goes into super alloys. The remaining 23% of consumption is divided between alloy steels, rechargeable batteries, catalysts and other chemicals, coinage, foundry products, and plating. Nickel is used to make coins.
Nickel is easy to work and can be drawn into wire. It resist corrosion even at high temperatures and for this reason it is used in gas turbines and rocket engines. Monel is an alloy of nickel and copper (e.g. 70% nickel, 30% copper with traces of iron, manganese and silicon), which is not only hard but can resist corrosion by sea water, so that it is ideal for propeller shaft in boats and desalination plants.
Nickel occurs combined with sulphur in millerite, with arsenic in the mineral niccolite, and with arsenic and sulphur in nickel glance. Most ores from which nickel is extracted are iron-nickel sulphides, such as pentlandite. The metal is mined in Russia, Australia, New Caledonia, Cuba, Canada and South Africa. Annual production exceeds 500.000 tons and easily workable reserves will last at least 150 years.
Ni sources of exposure
Humans may be exposed to nickel by breathing air, drinking water, eating food or smoking cigarettes. Skin contact with nickel-contaminated soil or water may also result in nickel exposure. Food remains the major source of exposure to nickel
Soil usually contains between 4 and 80 parts of nickel in a million parts of soil (ppm; 1 ppm=1,000 ppb). The highest soil concentrations (up to 9,000 ppm) are found near industries that extract nickel from ore. High concentrations of nickel occur as dust that is released into air from stacks during processing and settles on the ground. You may be exposed to nickel in soil by skin contact. Children may also be exposed to nickel by eating soil.
Scattered studies indicate a highly variable dietary intake of nickel, but most averages are about 200-300 micrograms/day. Vegetables usually contain more nickel than do other food items; high levels have been found in legumes, dried beans, peas, spinach, lettuce, nuts, salted cashews, almonds, licorice, whole wheat, soybeans, oatmeals and coffee. Nickel occurs in some beans where it is an essential component of some enzymes. Another relatively rich source of nickel is tea which has 7.6 mg/kg of dried leaves. Consumption of these products in larger amounts may increase the nickel intake to 900 μg/person/day or more. In France, the estimated weekly intake for the general population of nickel from wine consumption was, on the basis of 66 l/year/resident, 30.6 μg/ week (4.37 μg/day). Nickel amount are also very elevated in canned foods and gelatin. Animal tissues generally contain less nickel in comparison to plant tissues. Meat, poultry and eggs are suitable for low nickel diet. Except for a few varieties of fishes that show high concentration of nickel such as tuna, herring, shellfish, salmon and mackerel, other fishes can be used for low nickel diet.
In most food products, the nickel content is less than 0.5 mg/kg fresh weight. Cacao products and nuts may, however, contain as much as 10 and 3 mg/kg, respectively. Certain products, such as baking powder and cocoa powder, have been found to contain excessive amounts of nickel, perhaps related to nickel leaching during the manufacturing process. Recovery studies indicate an absorption rate of less than 15% from the gastrointestinal tract.
Vitamin supplements can also contain very large amount of Nickel.
Nickel concentrations in drinking-water in European countries of 2–13 μg/litre have been reported. An average value of 9 μg/litre and a maximum of 34 μg/litre were recorded in Germany. Nickel may, however, be leached from nickel-containing plumbing fittings, and levels of up to 500 μg/litre have been recorded in water left overnight in such fittings. In areas with nickel mining, levels of up to 200 μg/litre have been recorded in drinking-water. The average level of nickel in drinking-water in public water supply systems in the United States was 4.8 μg/litre in 1969. Assuming a concentration of 5–10 μg/litre, a daily consumption of 2 litres of drinking-water would result in a daily nickel intake of 10–20 μg.
Nickel is released into the air by power plants and trash incinerators. It will than settle to the ground or fall down after reactions with raindrops. It usually takes a long time for nickel to be removed from air. Nickel can also end up in surface water when it is a part of wastewater streams. Nickel in air is attached to small particles. Over a 6-year period (1977-1982) in the United States, average nickel concentrations in cities and in the country ranged from 7 to 12 nanograms per cubic meter (ng/m3; 1 ng/m3 is equivalent to 1 billionth of a gram in a cubic meter of air). In another study, concentrations of 18–42 ng/m3 were recorded in 8 United States cities. These values correspond to the average value of 37 ng/m3 for 30 United States Urban Air National Surveillance Network Stations for the period 1957–1968. Ranges of 10–50 ng/m3 and 9–60 ng/m3 have been reported in European cities. Higher values (110–180 ng/m3) have been reported from heavily industrialized areas. Assuming a daily respiratory rate of 20 m3, the amount of airborne nickel entering the respiratory tract is in the range 0.1–0.8 μg/day when concentrations are 5–40 ng/m3 in ambient air. A total deposition of about 50% of the inhaled dose was estimated for particles with an MMD of 2.0 μm, while deposition was about 10% for those of 0.5 μm. For larger particles, more than 50% of the deposited dose was in the nasopharyngeal part of the respiratory tract as against less than 10% for
the smaller particles. Tobacco smoke also contain preoccupying amount of Nickel. About 0.04–0.58 μg of nickel is released with the mainstream smoke of one cigarette (6). Smoking 40 cigarettes per day may thus lead to inhalation of 2–23 μg of nickel.
Skin contact with soil, bath or shower water, or metals containing nickel, as well as, metals plated with nickel can also result in exposure. Stainless steel and coins contain nickel. Some jewelry is plated with nickel or made from nickel alloys. Patients may be exposed to nickel in artificial body parts made from nickel-containing alloys. Population exposure to Nickel also occurs through coins handling and touching other metals containing Nickel. Ear-piercing, however, increases the probability of nickel sensitization
Exposure of an unborn child to nickel is through the transfer of nickel from the mother’s blood to fetal blood. Likewise, nursing infants are exposed to nickel through the transfer of nickel from the mother to breast milk. However, the concentration of nickel in breast milk is either similar or less than the concentration of nickel in infant formulas and cow’s milk.
Nickel alloys are often used in nails and prostheses for orthopaedic surgery, and various sources may contaminate intravenous fluids. Iatrogenic exposure to nickel may occur as a result of dialysis treatment, prostheses and implants, and medication.
Ni health concerns
The soluble compounds, such as nickel acetate, were the most toxic, and the insoluble forms, such as nickel powder, were the least toxic.
Nickel fumes are respiratory irritants and may cause pneumonitis. Nickel exposure may also cause lung embolism, respiratory failure, asthma and chronic bronchitis
Nickel absorption may also provoke birth defects. Animal studies have reported reproductive and developmental effects, such as a decreased number of live pups per litter, increased pup mortality, and reduction in fetal body weight, and effects to the dam from oral exposure to soluble salts of nickel. Sperm abnormalities and decreased sperm count have been reported in animals exposed to nickel nitrate orally and nickel oxide by inhalation, respectively.
Nickel exposure may also be particularly damaging for the heart. Gastrointestinal distress (e.g., nausea, vomiting, diarrhea) and neurological effects were reported in workers who drank water on one shift that was contaminated with nickel as nickel sulfate and nickel chloride. Renal edema were reported in humans and animals following acute (short-term) exposure to nickel carbonyl.
Exposure to nickel and its compounds may result in the development of a dermatitis known as “nickel itch” in sensitized individuals. The first symptom is usually itching, which occurs up to 7 days before skin eruption occurs. The primary skin eruption is erythematous, or follicular, which may be followed by skin ulceration. Nickel sensitivity, once acquired, appears to persist indefinitely.
Too large quantities of Nickel intake leads to higher chances of development of lung cancer, nose cancer, larynx cancer and prostate cancer.
Nickel and certain nickel compounds have been listed by the National Toxicology Program (NTP) as being reasonably anticipated to be carcinogens. The International Agency for Research on Cancer (IARC) has listed nickel compounds within group 1 (there is sufficient evidence for carcinogenicity in humans) and nickel within group 2B (agents which are possibly carcinogenic to humans). Nickel is on the ACGIH Notice of Intended Changes as a Category A1, confirmed human carcinogen.
Ni body excretion capabilities
In animal studies, between 60 and 90% of intravenously injected nickel was excreted within 24 hours. It may be assumed that 2% of 63Ni uptake transfers to the kidney where it is retained with a biological half-life of 2 days; 68% is directly excreted; and 30% is uniformly distributed throughout all organs and tissues of the body including the kidneys, and retained there with a biological half-life of 300 (particle size 1.2µm) – 700 days (particle size 4µm).
Chromium (Cr)
Chromium (Cr) chemical properties:
Chromium is found in the center of the periodic table. Elements in Groups 3 through 12 are known as the transition metals. These elements all have similar physical and chemical properties. They have a bright, shiny surface and high melting points.
Chromium is a lustrous, brittle, hard metal. Its colour is silver-gray and it can be highly polished. It does not tarnish in air, when heated it borns and forms the green chromic oxide. Chromium is unstable in oxygen, it immediately produces a thin oxide layer that is impermeable to oxygen and protects the metal below
Melting point: 1907 °C
Boiling point: 2672 °C
Chromium main uses are in alloys such as stainless steel, in chrome plating and in metal ceramics. Chromium plating was once widely used to give steel a polished silvery mirror coating. Chromium is used in metallurgy to impart corrosion resistance and a shiny finish; as dyes and paints, its salts colour glass an emerald green and it is used to produce synthetic rubies; as a catalyst in dyeing and in the tanning of leather; to make molds for the firing of bricks. Chromium (IV) oxide (CrO2) is used to manufacture magnetic tape.
The main human activities that increase the concentrations of chromium (III) are steal, leather and textile manufacturing. The main human activities that increase chromium(VI) concentrations are chemical, leather and textile manufacturing, electro painting and other chromium(VI) applications in the industry. These applications will mainly increase concentrations of chromium in water. Through coal combustion chromium will also end up in air and through waste disposal chromium will end up in soils.
Chromium compounds have many different uses. Some include:
• chromic fluoride (CrF 3 ): printing, dyeing, and mothproofing woolen cloth
• chromic oxide (Cr 2 O 3 ): a green pigment (coloring agent) in paint, asphalt roofing, and ceramic materials; refractory bricks; abrasive
• chromic sulfate (Cr 2 (SO 4 ) 3 ): a green pigment in paint, ceramics, glazes, varnishes, and inks; chrome plating
• chromium boride (CrB): refractory; high-temperature electrical conductor
• chromium dioxide (CrO 2 ): covering for magnetic tapes (“chromium” tapes)
• chromium hexacarbonyl (Cr(CO) 6 ): catalyst; gasoline additive
Environmental sources of chromium include: airborne emissions from chemical plants and incineration facilities, cement dust, contaminated landfill, effluents from chemical plants, asbestos lining erosion, road dust from catalytic converter erosion and asbestos brakes, tobacco smoke, and topsoil and rocks.
Occupational sources of chromium include: anti-algae agents, antifreeze, cement, chrome alloy production, chrome electroplating (soluble Cr[VI]), copier servicing, glassmaking, leather tanning (soluble Cr[III]), paints/pigments (insoluble Cr[VI]), photoengraving, porcelain and ceramics manufacturing, production of high-fidelity magnetic audio tapes, tattooing, textile manufacturing, welding of alloys or steel, and wood preservatives, i.e. Acid Copper Chromate.
Most of the chromium in air will eventually settle and end up in waters or soils. Chromium in soils strongly attaches to soil particles and as a result it will not move towards groundwater. In water chromium will absorb on sediment and become immobile. Only a small part of the chromium that ends up in water will eventually dissolve.
One radioactive isotope of chromium is used in medical research, chromium-51. A common use of chromium-51 is in studies of red blood cells. The isotope can be used to find out how many blood cells are present in a person’s body. It can be used to measure how long the blood cells survive in the body. The isotope can also be used to study the flow of blood into and out of a fetus (an unborn child).
Cr sources of exposure
Electroplating, leather tanning, and textile industries release relatively large amounts of chromium in surface waters. Leaching from topsoil and rocks is the most important natural source of chromium entry into bodies of water. Solid wastes from chromate-processing facilities, when disposed of improperly in landfills, can be sources of contamination for groundwater, where the chromium residence time might be several years. The general population is exposed to chromium by eating food or food supplements, drinking water, and inhaling air that contain chromium. The mean daily dietary intake of chromium from air, water, and food is estimated to be <0.2-0.4, 2.0, and 60 micrograms, respectively [ATSDR 2000]. According to another study, food was also considered as a major source of exposure to chromium, and estimated daily oral intakes for infants (1 yr), children (11 yr), and adults are 33-45, 123-171, and 246-343 micrograms/person/d, respectively.
Some of the best sources of chromium are broccoli, liver, brewer’s yeast and red wine. Potatoes, oat, barley, seafood, green beans, and meats (turkey breast, beef, …) also contain chromium.
A recent cross-sectional survey indicated that 19% of the US population uses chromium-containing dietary supplements (i.e., single-nutrient supplements and multiple ingredient supplements), with the highest proportion of users (29%) found in adults aged over 50 years (52). Trivalent chromium is available as a supplement in several forms, including chromium chloride, chromium nicotinate, chromium picolinate, and high-chromium yeast. These are available as stand-alone supplements or in combination products. Doses typically range from 50 to 200 μg of elemental chromium.
A survey conducted from 1974 to 1975 provides estimates of chromium concentrations in U.S. drinking water. The survey reported the concentration of chromium in tap water in U.S. households was from 0.4 to 8.0 micrograms per liter (µg/L). [ATSDR 2000] (EPA’s maximum contaminant level for chromium in drinking water is 100 µg/L.)
You can be exposed to trace levels of chromium by breathing air containing it. Releases of chromium into the air can occur from: industries using or manufacturing chromium, living near a hazardous waste facility that contains chromium, fuel combustion and cigarette smoke
Rural or suburban air generally contains lower concentrations of chromium than urban air: <10 ng/m3 in rural areas, 0-30 ng/m3 in urban areas as a result of smoking, indoor air contaminated with chromium can be 10-400 times greater than outdoor air concentrations.
Based on reports, Chromium levels in mainstream cigarette smoke ranges from 0.0002 – 0.5 mg per cigarette. It is known that Cr accumulates in tissue, especially in the lung. Concentrations of about 4.3 mg/kg (dry weight) are found in smokers compared to 1.3 mg/kg in non smokers, increasing with age and smoking time.
Cr health concerns
For most people eating food that contains chromium(III) is the main route of chromium uptake, as chromium(III) occurs naturally in many vegetables, fruits, meats, yeasts and grains. Various ways of food preparation and storage may alter the chromium contents of food. When food in stores in steel tanks or cans chromium concentrations may rise.
Chromium(III) is an essential nutrient for humans and shortages may cause heart conditions, disruptions of metabolisms and diabetes. But the uptake of too much chromium(III) can cause health effects as well, for instance skin rashes. Chromium(III) is an essential element for organisms that can disrupt the sugar metabolism and cause heart conditions, when the daily dose is too low. Trivalent chromium has been proposed to be the cofactor for an oligopeptide called chromodulin. Chromodulin may be able to potentiate the action of insulin, hence improving tissue sensitivity to insulin and facilitating glucose transport into cells.
Chromium(III) seems to play a role in helping the body use sugar. Chromium III may also be hazardous since some research shows that constant exposure to it would equally destroy lymphocyte DNA. It can also lead to an inability to metabolize iron and hence the occurrence of iron deficiency anemia.
The health hazards associated with exposure to chromium are dependent on its oxidation state. The metal form (chromium as it exists in this product) is of low toxicity. The hexavalent form is toxic. Adverse effects of the hexavalent form on the skin may include ulcerations, dermatitis, and allergic skin reactions. Inhalation of hexavalent chromium compounds can result in ulceration and perforation of the mucous membranes of the nasal septum, irritation of the pharynx and larynx, asthmatic bronchitis, bronchospasms and edema. Respiratory symptoms may include coughing and wheezing, shortness of breath, and nasal itch.
Chromium(VI) is mainly toxic to organisms. It can alter genetic materials and cause cancer. Epidemiological evidence and animal experiments indicate that the slightly soluble hexavalent salts are one of the most potent carcinogens. The most serious health effect associated with Chromium(VI) is lung cancer, which has been associated with some occupational exposure scenarios. In most cases, Chromium (IV) causes respiratory cancer due to its exposure through inhalation. According to the World Health Organization, more than 8,000 tannery workers in India are suffering from problems related to stomach and intestines, as well as skin related diseases. A large number of these people, of up to 90%, die before 50 years of age.
Although chromium-exposed workers were exposed to both chromium (III) and chromium (VI) compounds, only chromium (VI) has been found to be carcinogenic in animal studies, so EPA has concluded that only chromium (VI) should be classified as a human carcinogen. Animal studies have shown chromium (VI) to cause lung tumors via inhalation exposure. EPA has classified chromium (VI) as a Group A, known human carcinogen by the inhalation route of exposure.
A report by the Industrial Injuries Advisory Council (IIAC) considers the association of chromium and sino-nasal cancer with certain occupations and whether sino-nasal cancer should be included the list of prescribed diseases for which Industrial Injuries Benefit is payable.
Excessive consumption of the widely available supplement chromium could cause cancer, according to an australian study.
Oral studies have reported severe developmental effects in mice such as gross abnormalities and reproductive effects including decreased litter size, reduced sperm count, and degeneration of the outer cellular layer of the seminiferous tubules.
Cr body excretion capabilities
The study shows that exposure to airborne dust and fumes containing chromium may cause accumulation of chromium in the body, and that when exposure ends, elimination of chromium is very slow.
In a 8 years study measuring chromium in serum and urine in a former plasma cutter of stainless steel who was exposed to airborne dust and fumes containing chromium during this work. After the first examination for serum chromium the exposure ended. Serum chromium concentration has been measured seven times during the period and was initially very high and has subsequently dropped slowly. The half life was 40 months in serum. Urinary chromium has been measured five times. The half life was 129 months in urine.
Antimony (Sn)
Antimony (Sn) chemical properties:
Antimony is a semimetallic chemical element (or metalloid element which has both the properties of metals and non metals). Because it is semimetallic, it can exist in two forms: the metallic form is bright, silvery, hard and brittle; the non metallic form is a grey powder. Antimony is a poor conductor of heat and electricity, it is stable in dry air and is not attacked by dilute acids or alkalis. Antimony and some of its alloys expand on cooling. The electronic structure of antimony is closely related to that of arsenic, and consists of three half-filled orbitals in the last shell. It is thus able to form covalent bonding and exhibits -3 and +3 oxidation states. Antimony acts as an oxidizing agent and readily reacts with many metals to form antimonides. All antimonides, in general, resemble phosphides, nitrides and arsenides but are somehow more metallic.
It has a scaly surface and is hard and brittle like a non-metal. It can also be prepared as a black powder with a shiny brilliance to it. Antimony has been known since ancient times. It is sometimes found free in nature, but is usually obtained from the ores stibnite (Sb2S3) and valentinite (Sb2O3).
Melting point : 631 °C
Boiling point : 1587 °C
Sn sources of exposure
Very pure antimony is used to make certain types of semiconductor devices, such as diodes and infrared detectors. Antimony is alloyed with lead to increase lead’s durability. Antimony alloys are also used in batteries, low friction metals, type metal and cable sheathing, among other products.
Antimony compounds are used to make flame-proofing materials and paints. Other minor uses of antimony include the manufacture of glass and ceramics and the production of plastics. In glass and ceramics, a small amount of antimony insures that the final product will be clear and colorless. In the production of plastics, antimony is used as a catalyst. A catalyst is a substance used to speed up or slow down a chemical reaction. The catalyst does not undergo any change itself during the reaction.
Human exposure to antimony can take place by breathing air, drinking water and eating foods that contain it, but also by skin contact with soil, water and other substances that contain it. Breathing in antimony that is bound to hydrogen in the gaseous phase, is what mainly causes the health effects.
Antimony accumulation in marine and freshwater species is considered to be low so exposure to naturally occurring antimony through food is usually considered to be low.According to the UK diet study, the principle source of antimony in foods is through milk. The occurene of antimony in milk may arise from for milk bottles, of rubber nipples containing antimony. Recently unexpected possibilities of harm have been detected in some of the enameled cooking utensils. Other foods containing concerning quantities of antimony are fruit gelatins, lemonades, puch, popsickes. Other sources of antimony is through fish and seafoods. Juices and wines, products and processed foods, spices and seasoning products, and dietary supplements may contain a preoccupying level of antimony, possibly because their are stored in packaging materials containg elevated levels of antimony. Level of antimony absorbed per days through food is comprised between 4-7 µg/days.Antimony does not bio-accumulate so exposure to naturally occurring antimony through food is very low.According to the UK diet study, the principle source of antimony in foods is through milk. The occurene of antimony in milk may arise from for milk bottles, of rubber nipples containing antimony. Recently unexpected possibilities of harm have been detected in some of the enameled cooking utensils. Other foods containing concerning quantities of antimony are fruit gelatins, lemonades, puch, popsickes. Other sources of antimony is through fish and seafoods. Juices and wines, products and processed foods, spices and seasoning products, and dietary supplements may contain a preoccupying level of antimony, possibly because their are stored in packaging materials containg elevated levels of antimony. Level of antimony absorbed per days through food is comprised between 4-7 µg/days.
Antimony poses both acute and chronic health effects in drinking water. Antimony concentrations in bottled waters ranged from 0.095 to 0.521 ppb. Summertime temperatures inside of cars, garages, and enclosed storage areas can promote antimony leaching from polyethylene terephthalate (PET) bottled waters. Antimony levels as high as 9.7 µg/L have been reported in drinking water. Water in PET bottles may contain higher levels of antimony.
Microwave and conventional oven cooking caused a distinct increase in the concentration of antimony in food and ready meals of 0–17 and 8–38 µg/kg, respectively.
Organotin compounds reach humans primarily through the diet (in particular fish and fish products). These compounds are widely diffused in the aquatic environment as a result of their use as antifouling agents and biocides in agricultural practices. Organotins occur mainly in aquatic organisms and intake of seafood may be an important source of human exposure. Tin is used in canned foods to protect the steel base from corrosion both externally (aerobic conditions) and internally when in contact with foods (anaerobic). Acidic foods are more aggressive to the tin coating in metal cans and canned acidic foods have higher tin contents. Tomato-based products tend to have high levels of tin as nitrate in the food accelerates corrosion of the tin. Tin concentrations of canned foods increase with storage time and temperature.
The use of lacquers in can linings has enabled different types of food products to be satisfactorily packed. For example, some highly pigmented foods (beetroot, berry fruits) have their colours bleached by tin dissolution and are best protected from contact with tin by use of linings.
Airborne concentrations of antimony average < 1–170 ng/m3 air depending on proximities to smelters or mines, which make it >1,000 ng/m3 air. The Occupational Safety and Health Administration in the USA and UK have set a limit of 0.5 mg/m3 of antimony in workroom air, assuming that workers complete an 8-h shift and 40-h working week. The antimony emission factors originating from automobiles were ca. 32 µg Sb/braking/car for PM10 (emission factors of brake abrasion dusts of 5.8 mg/braking/car) and 22 µg Sb/braking/car for PM2.5 (emission factors of brake abrasion dusts of 3.9 mg/braking/car).
Antimony and its compounds are also used in the field of medical sciences. Antimony trioxide is used in the preparation of certain medicines called antimonials, which are used as emetics. Selected antimony compounds are used in the treatment of protozoans. Tarter emetic (Potassium antimonyl tartrate) was once used as a leading anti-schistosomal drug but has been replaced by praziquantel. Antimony can be toxic depending on its chemical state. Generally, metallic antimony is inert but stibunite is very toxic. When handling antimony and its compounds, proper ventilation should be used to avoid contamination. Notable cases of dermatitis and other skin conditions have been reported in facilities handling antimony
Sn health concerns
Antimony and its compounds are dangerous to human health. In low levels, these materials can irritate the eyes and lungs. They may also cause stomach pain, diarrhea, vomiting, and stomach ulcers. At higher doses, antimony and its compounds can cause lung, heart, liver, and kidney damage. At very high doses, they can cause death.
Stibine is a hemolytic agent. In some cases, cardiac arrhythmias and mild jaundice may occur necessitating treatment with intramuscular dimercaprol.
Skin exposure can produce “antimony spots” or rashes which resemble chicken pox. Certain molds can produce the highlyneurotoxic stibine gas from Antimony; stibine inhibits acetylcholinestelase activity.
The primary effects from chronic exposure to antimony in humans are respiratory effects that include antimony pneumoconiosis (inflammation of the lungs due to irritation caused by the inhalation of dust), alterations in pulmonary function, chronic bronchitis, chronic emphysema, inactive tuberculosis, pleural adhesions, and irritation. Other effects noted in humans chronically exposed to antimony by inhalation are cardiovascular effects (increased blood pressure, altered EKG readings and heart muscle damage) and gastrointestinal disorders.
Animal studies have reported effects on the respiratory and cardiovascular systems and kidney from chronic inhalation exposure. Oral animal studies have reported effects on the blood, liver, central nervous system (CNS), and gastrointestinal effects. A National Toxicology Program (NTP) 14-day drinking water study of potassium antimony tartrate reported an increase in relative liver and kidney weights in the high dose group (females only). A 13-week intraperitoneal injection study, also by the NTP, reported inflammation and/or fibrosis of the liver in mice dosed with potassium antimony tartrate.
McCallum describes the effect of antimony in potentiating antimony spots, heart disease, pneumoconiosis, and lung cancer. Other authors suggest an increased mortality from lung cancer and associated non-malignant respiratory heart diseases in workers exposed to antimony. Antimony in conjunction with other metals may biologically alter several cellular defence mechanisms thus potentiating carcinogenesis. Lung cancer has been observed in some studies of workers, and mice breathing high concentrations of antimony (Antimony (III) oxide (by inhalation) has been shown to cause lung cancer in female rats). The International Agency for Research on Cancer has determined that antimony trioxide is possibly carcinogenic to humans (group 2B) .
Reproductive disorders and chromosome damage may be associated with chronic antimony exposure with consequent mutagenic and oncogenic potential and should be avoided in pregnancy and in patients with hepatic, renal, or cardiovascular disease. An increased incidence of spontaneous abortions, as compared with a control group, was reported in women working at an antimony plant. Disturbances in the menstrual cycle were reported in women exposed to various antimony compounds in a metallurgical plant. However, the study that reported these findings was unclear about concurrent exposure to other chemicals, nor did it provide the characteristics of the controls used. Animal studies have reported a decrease in the number of offspring born to rats exposed to antimony prior to conception and throughout gestation. Reproductive effects, including metaplasia in the uterus and disturbances in the ovum-maturing process, were reported in a rat study, following inhalation exposure.
Sn body excretion capabilities
The absorption, distribution, and excretion of antimony vary depending on its oxidation state. Urinary excretion appears to be greater for pentavalent antimony than for trivalent compounds. An elimination half-life of approximately 95 hours has been estimated after occupational exposures. This biological half life of excretion often relates to the biological half life of serum although other tissues may have a far different biological half life. A small fraction of the assimilated antimony appears to have a much longer half‐life. For lung tissue there was no tendency towards decreased antimony concentrations with time (up to 20 years) after the cessation of exposure, and this result indicates a long biological half-time
Copper (Cu)
Copper (Cu) chemical properties:
The abundance of copper in the Earth’s crust is estimated to be about 70 parts per million. It ranks in the upper quarter among elements present in the Earth’s crust. Small amounts (about 1 part per billion) also occur in seawater.
At one time, it was not unusual to find copper lying on the ground. However, this is no longer true. Today, copper is obtained from minerals such as azurite, or basic copper carbonate (Cu 2 (OH) 2 CO 3 ); chalcocite, or copper glance or copper sulfide (Cu 2 S); chalcopyrite, or copper pyrites or copper iron sulfide (CuFeS 2 ); cuprite, or copper oxide (Cu 2 O); and malachite, or basic copper carbonate (Cu 2 (OH) 2 CO 3 )
Copper is a reddish metal with a face-centered cubic crystalline structure. It reflects red and orange light and absorbs other frequencies in the visible spectrum, due to its band structure, so it as a nice reddish color. It is malleable, ductile, and an extremely good conductor of both heat and electricity. It is softer than zinc and can be polished to a bright finish. It is found in group Ib of the periodic table, together with silver and gold. Copper has low chemical reactivity. In moist air it slowly forms a greenish surface film called patina; this coating protects the metal from further attack.In most of its compounds it can have the valency (oxidation state) of +I or the valency state +II. The aqueous solutions of copper ions in the oxidation state +II have a blue colour, whereas copper ions in the oxidation state +I are colourless. Copper and copper compounds give a greenish color to a flame.
All common metals and alloys react with a moist atmosphere and corrode. Only in hot/dry (deserts) and cold/dry environments do metals resist corrosion. However, due to the chemical properties of copper, the corrosion process is very slow. The corrosion resistance of copper and copper alloys is based on their ability to form stable compounds that provide some protection from corrosive attack. When exposed to the atmosphere, protective layers of oxides and poorly soluble basic salts form on the surface of copper and copper alloys. Suitable alloying elements can positively influence the formation of these coatings.
The people who lived in that historical period combined copper with iron or tin to produce an alloy called bronze. Another alloy of copper is brass. Brass and bronze are stronger than copper; hence, they are used to make weapons, such as spear tips, hammers, axes, and so on.
Melting point: 1083 °C
Boiling point: 2595 °C
Most copper is used for electrical equipment (60%); construction, such as roofing and plumbing (20%); industrial machinery, such as heat exchangers (15%) and alloys (5%). The main long established copper alloys are bronze, brass (a copper-zinc alloy), copper-tin-zinc, which was strong enough to make guns and cannons, and was known as gun metal, copper and nickel, known as cupronickel, which was the preferred metal for low-denomination coins.
Copper is ideal for electrical wiring because it is easily worked, can be drawn into fine wire and has a high electrical conductivity.
Copper is a very common substance that occurs naturally in the environment and spreads through the environment through natural phenomena. Humans widely use copper. For instance it is applied in the industries and in agriculture. The production of copper has lifted over the last decades. Due to this, copper quantities in the environment have increased.
The world’s copper production is still rising. This basically means that more and more copper ends up in the environment. Rivers are depositing sludge on their banks that is contaminated with copper, due to the disposal of copper-containing wastewater. Copper enters the air, mainly through release during the combustion of fossil fuels. Copper in air will remain there for an eminent period of time, before it settles when it starts to rain. It will then end up mainly in soils. As a result soils may also contain large quantities of copper after copper from the air has settled.
Copper can be released into the environment by both natural sources and human activities. Examples of natural sources are wind-blown dust, decaying vegetation, forest fires and sea spray. A few examples of human activities that contribute to copper release have already been named. Other examples are mining, metal production, wood production and phosphate fertilizer production. Because copper is released both naturally and through human activity it is very widespread in the environment. Copper is often found near mines, industrial settings, landfills and waste disposals.
Most copper compounds will settle and be bound to either water sediment or soil particles. Usually water-soluble copper compounds occur in the environment after release through application in agriculture.
Cu sources of exposure
Copper concentrations in air are usually quite low, so that exposure to copper through breathing is negligible. But people that live near smelters that process copper ore into metal, do experience this kind of exposure.
People that live in houses that still have copper plumbing are exposed to higher levels of copper than most people, because copper is released into their drinking water through corrosion of pipes.
A number of copper compounds are used as pesticides, chemicals that kill insects and rodents like rats and mice:
• basic copper acetate (Cu 2 O(C 2 H 3 O 2 ) 2 ): insecticide (kills insects) and fungicide (kills fungi)
• copper chromate (CuCrO 4 ○ 2CuO): fungicide for the treatment of seeds
• copper fluorosilicate (CuSiF 6 ): grapevine fungicide
• copper methane arsenate (CuCH 3 AsO 3 ): algicide (kills algae)
• copper-8-quinolinolate (Cu(C 9 H 6 ON) 2 ): protects fabric from mildew
• copper oxalate (CuC 2 O 4 ): seed coating to repel rats
• copper oxychloride (3CuO ○ CuCl 2 ): grapevine fungicide
• tribasic copper sulfate (CuSO 4 ○ 3Cu(OH) 2 ): fungicide, used as a spray or dust on crops
Other copper compounds are found in battery fluid; fabric dye; fire retardants; food additives for farm animals; fireworks (bright emerald color); manufacture of ceramics and enamels; photographic film; pigments (coloring agents) in paints, metal preservatives, and marine paints; water purification; and wood preservatives.
Turquoise and malachite are semi-precious gemstones made up of copper compounds. Turquoise ranges in color from green to blue.
Most diets contain enough Cu (1-5 mg) to prevent a deficiency and not enough to cause toxicity. In the United States, the dietary or nutrient reference (recommended) intakes for Cu are based on the Food and Nutrition Board, Institute of Medicine recommendations of 0.9 mg/d for adults of both genders, 19-70 years.
The best dietary sources include seafood (especially shellfish such as lobsters or oysters), baker’s yeast, mushrooms, spirulina, organ meats (e.g., liver), sesame seeds, whole grains, legumes (e.g., beans and lentils), potatoes and chocolate. Nuts, including brazil nuts, peanuts and pecans, are especially rich in copper, as are grains such as wheat and rye, and several fruits including lemons and raisins.
Soil generally contains between 2 and 250 ppm copper, although concentrations close to 17,000 ppm have been found near copper and brass production facilities. High concentrations of copper may be found in soil because dust from these industries settles out of the air, or wastes from mining and other copper industries are disposed of on the soil. Another common source of copper in soil results from spreading sludge from sewage treatment plants. This copper generally stays strongly attached to the surface layer of soil.
The concentration of copper in air ranges from a few nanograms (1 nanogram equals 1/1,000,000,000 of a gram or 4/100,000,000,000 of an ounce) in a cubic meter of air (ng/m³) to about 200 ng/m³. A cubic meter (m³) is approximately 25% larger than a cubic yard. Near smelters, which process copper ore into metal, concentrations may reach 5,000 ng/m³. You may breathe high levels of copper-containing dust if you live or work near copper mines or processing facilities. Cocoa, wheat, yeast, seafoods, liver, peepers, ceratin mushrooms are foods very elevated in copper.
Exposure to high levels of soluble copper may occur when drinking water that are above the acceptable drinking water standard of 1,300 parts copper per billion parts of water (ppb), especially if your water is corrosive and you have copper plumbing and brass water fixtures. The average concentration of copper in tap water ranges from 20 to 75 ppb. However, many households have copper concentrations of over 1,000 ppb. That is more than 1 milligram per liter of water. This is because copper is dissolved from copper pipes and brass faucets when the water sits in the pipes overnight. After the water is allowed to run for 15-30 seconds, the concentration of copper in the water decreases below the acceptable drinking water standard. The greatest potential source of copper exposure is therefore through drinking water.
Cu health concerns
Copper is an important mineral because it benefits the health of our bones, nerves and skeletal system. It’s also essential for the production of hemoglobin and red blood cells, and it’s needed for the proper utilization of iron and oxygen within our blood. Copper is an essential micronutrient for both plants and animals. A healthy human has no more than about 2 milligrams of copper for every kilogram of body weight. Copper is critical to enzyme production. An enzyme is a substance that stimulates certain chemical reactions in the body. Without enzymes, the reactions would be too slow. Copper enzymes function in the production of blood vessels, tendons, bones, and nerves. Animals seldom become ill from a lack of copper, but copper-deficiency disorders (problems because of lack of copper) can occur with animals who live on land that lacks copper.
Wilson disease is an inherited disorder in which excessive amounts of copper accumulate in the body, particularly in the liver, brain, and eyes. The signs and symptoms of Wilson disease usually first appear between the ages of 6 and 45, but they most often begin during the teenage years. The features of this condition include a combination of liver disease and neurological and psychiatric problems. Liver disease is typically the initial feature of Wilson disease in affected children and young adults; individuals diagnosed at an older age usually do not have symptoms of liver problems, although they may have very mild liver disease. The signs and symptoms of liver disease include yellowing of the skin or whites of the eyes (jaundice), fatigue, loss of appetite, and abdominal swelling.Nervous system or psychiatric problems are often the initial features in individuals diagnosed in adulthood and commonly occur in young adults with Wilson disease. Signs and symptoms of these problems can include clumsiness, tremors, difficulty walking, speech problems, impaired thinking ability, depression, anxiety, and mood swings. In many individuals with Wilson disease, copper deposits in the front surface of the eye (the cornea) form a green-to-brownish ring, called the Kayser-Fleischer ring, that surrounds the colored part of the eye. Abnormalities in eye movements, such as a restricted ability to gaze upwards, may also occur.
Wilson’s disease is also suspected to cause hypoparathyroidism (failure of the parathyroid glands leading to low calcium levels), infertility, and habitual abortion.
Long-term exposure to copper can cause irritation of the nose, mouth and eyes and it causes headaches, stomachaches, dizziness, vomiting and diarrhea. Intentionally high uptakes of copper may cause liver and kidney damage and even death.
There are scientific articles that indicate a link between long-term exposure to high concentrations of copper and a decline in intelligence with young adolescents.
Blood color
In humans, the blood that comes from the lungs to the cells is bright red. The red color is caused by oxyhemoglobin (the compound hemoglobin combined with oxygen). Hemoglobin carries oxygen through the blood and is red because of the iron it carries. Compounds of iron are often red or reddish-brown. Blood returning from cells to the lungs (which flows through the veins) is purplish-red because the hemoglobin has lost its oxygen.
Some animals, however, do not have hemoglobin to carry oxygen through the blood. For example, crustaceans (shellfish like lobsters, shrimps, and crabs) use a compound called hemocyanin. Hemocyanin is similar to hemoglobin but contains copper instead of iron. Many copper compounds, including hemocyanin, are blue. Therefore, the blood of a crustacean is blue, not red.
Cu body excretion capabilities
The elimination of copper in the urine may be greatlyenhanced in the copper-poisoned patient if the body storage sites are saturated. Thus Walsh et al. (1977) reported the case of a child intoxicated following the ingestion of 3 g ofcopper sulphate. A two hour sample of urine contained 500microgram/100 mL Cu (normal range 5 to 25 microgram/24hours). Urinary copper levels were maximal (2.8 to 3.0 mg/L)between the second and third week, and fell to 0.95 mg/L bythe end of the third week. In another case report, Cross et al. (1979) measured a urine copper concentration of 1.5 mg/L as compared with a suggested normal value of 0.12 mg/L in a patient who had ingested a solution containing copper, chromium and arsenic.
Copper biological half life may be of 33 – 40 days (although this fraction may represent the amount of copper (exploitation) in the slow compartment (such as serum). It is also very probable that the copper absorbed may reach other organs (bones, liver, …) which are represented in mathematical modeling by another compartment.
Iron (Fe)
Iron (Fe) chemical properties:
Iron is believed to be the tenth most abundant element in the universe. Iron is also the most abundant (by mass, 34.6%) element making up the Earth; the concentration of iron in the various layers of the Earth ranges from high at the inner core to about 5% in the outer crust. Most of this iron is found in various iron oxides, such as the minerals hematite, magnetite, and taconite. The earth’s core is believed to consist largely of a metallic iron-nickel alloy.
Iron is a lustrous, ductile, malleable, silver-gray metal (group VIII of the periodic table). It is known to exist in four distinct crystalline forms. Iron rusts in damp air, but not in dry air. It dissolves readily in dilute acids. Iron is chemically active and forms two major series of chemical compounds, the bivalent iron (II), or ferrous, compounds and the trivalent iron (III), or ferric, compounds. Iron has a good transmission of heat or electricity. It is easily magnetized. It can stretch without breaking.
Melting point: 1536 °C
Boiling point: 2861 °C
Iron is the most used of all the metals, including 95 % of all the metal tonnage produced worldwide. Thanks to the combination of low cost and high strength it is indispensable. Its applications go from food containers to family cars, from scredrivers to washing machines, from cargo ships to paper staples.
Steel is the best known alloy of iron, and some of the forms that iron takes include: pig iron, cast iron, carbon steel, wrought iron, alloy steels, iron oxides.
Fe sources of exposure
Diet is the major source of iron intake. Animal products, such as meat contain heme iron which is better absorbed by the body (20-25% of iron intake) than non-heme iron contain in vegetables (5-10% of iron intake).
Dietary iron is present in food in 2 forms: heme and nonheme iron. As a component of hemoglobin, heme iron is found in animal food sources such as meat, organ meats (beef, pork, poultry, lamb, duck, venison), fish (mackerel, trout, bass, tuna, sardines), seafood (oysters, shrimp, octopus, clams, scallops, crab), and poultry. Heme iron is efficiently absorbed from the diet, with an approximate absorption of 25%. Nonheme iron is present in plant-based foods (dried beans, peas, lentils, spinach, tomatoe puree, oatmeal) as well as iron-enriched o\r iron-fortified foods (i.e., iron-fortified cereals). Multiple dietary and individual factors influence the degree of dietary nonheme iron absorption, with a mean absorption estimated to be ∼7% in the United States. Individuals with adequate body iron stores will absorb less dietary nonheme iron compared with individuals with insufficient body iron stores. Other factors that influence dietary nonheme iron absorption include enhancing factors found in animal muscle tissue and foods containing vitamin C. Food factors that inhibit dietary nonheme absorption include phytates, tannins, calcium, polyphenols, and soybean proteins or possibly other soy components.
The best source of iron is animal-based foods, especially red meat and offal (such as liver). Chicken, duck, pork, turkey, eggs and fish (sardines) also have iron.Iron is also found in many plant-based foods such as: green vegetables, for example spinach, silverbeet and broccoli, lentils and beans, nuts and seeds, grains, for example whole wheat, brown rice and fortified breakfast cereals and dried fruits (cashews, apricots), tomatoes.
Cast Iron cookware may not only contain Iron. Heavy metals may also be found in Cast Iron skillets. It is best to consult the chemial composition of cast iron cookware if available. It should be further mentionned that three heavy metals chemicals are often in much lower proportion in cast iron than in other type of metal made cookware (for instance inox and copper cookware).
In drinking-water supplies, iron(II) salts are unstable and are precipitated as insoluble iron(III) hydroxide, which settles out as a rust-coloured silt. Anaerobic groundwaters may contain iron(II) at concentrations of up to several milligrams per litre without discoloration or turbidity in the water when directly pumped from a well, although turbidity and colour may develop in piped systems at iron levels above 0.05–0.1 mg/litre. Staining of laundry and plumbing may occur at concentrations above 0.3 mg/litre
Fe health concerns
Iron is essential to almost living things, from micro-organisms to humans.
Iron, as a component of hemoglobin in erythrocytes (red blood cells), is required for transporting oxygen around the body and, in the form of myoglobin, for the storage and use of oxygen in muscles. The oxygen released in the tissues from hemoglobin is used in oxidative metabolism. Hemoglobin binds carbon dioxide in the tissues and carries it to the lungs where it is exhaled. In adults, most body iron is present in hemoglobin (60–70%) in circulating erythrocytes where it is essential for oxygen transport, and in muscle myoglobin (10%). The remaining body iron (20–30%) is found primarily in storage pools located in the liver and reticulo-endothelial (macrophage) system as ferritin and hemosiderin. Only about 1% of body iron is incorporated in the range of iron-containing enzymes and less than 0.2% of body iron is in the plasma transport pool where it is bound to transferrin.Iron, as a component of hemoglobin in erythrocytes (red blood cells), is required for transporting oxygen around the body and, in the form of myoglobin, for the storage and use of oxygen in muscles. The oxygen released in the tissues from hemoglobin is used in oxidative metabolism. Hemoglobin binds carbon dioxide in the tissues and carries it to the lungs where it is exhaled.
A common problem for humans is iron deficency, which leads to anaemia. A man needs an average daily intake pf 7 mg of iron and a woman 11 mg; a normal diet will generally provided all that is needed. Iron is an essential part of hemoglobin; the red colouring agent of the blood that transports oxygen through our bodies.
Genetic disorders such as sickle cell disease and thalassemia can lead to increased body iron loads as a result of the frequent need for blood transfusions as part of the clinical care of these disorders. Iron overdose with acute iron toxicity is possible from the accidental consumption of iron supplements
Iron excess may cause conjunctivitis, choroiditis, and retinitis if it contacts and remains in the tissues. Chronic inhalation of excessive concentrations of iron oxide fumes or dusts may result in development of a benign pneumoconiosis, called siderosis, which is observable as an x-ray change. No physical impairment of lung function has been associated with siderosis. Inhalation of excessive concentrations of iron oxide may enhance the risk of lung cancer development in workers exposed to pulmonary carcinogens. LD50 (oral, rat) =30 gm/kg. (LD50: Lethal dose 50. Single dose of a substance that causes the death of 50% of an animal population from exposure to the substance by any route other than inhalation. Usually expressed as milligrams or grams of material per kilogram of animal weight (mg/kg or g/kg).)
There is a limited amount of epidemiological data on the association between iron intakes and high iron depots on colorectal cancer risk. The available data suggest that: increased dietary intakes of total or heme iron might be associated with increased colorectal cancer risk
There is a limited amount of epidemiological data on the association between iron intakes and high iron depots on colorectal cancer risk. The available data suggest that: increased dietary intakes of total or heme iron might be associated with increased colorectal cancer risk
High iron intake or high iron depots increase the risk of diabetes mellitus and rheumatoid arthritis in the general population. Significant dietary iron may be associated with neurodegenerative diseases, especially Parkinson’s disease. Excess iron gets deposited in the liver, heart and pancreas, where it can cause cirrhosis, liver cancer, cardiac arrhythmias and diabetes.
Fe body excretion capabilities
Results from a study with radioiron in man (to estamte the iron biological half life) biological half-life for iron in the blood and blood-forming organs of 65 days. This result is probably based on early data obtained with animals and would appear to be considerably too low for the adult man.
Other studies, indicate that in tissues (not in the serum) iron is retained in organs and tissues with a biological half–life of 2000 days.
Once absorbed, iton circulates in the serum and is also taken by specific cells with very long storage time. Therefore from a mathematical point of view, iron metabolism may be estimated using at least a two compartement model (with a rapidly variating iron concentration compartment and a slow compartment which stores iron for a much longer time period).
References
PFOA related documents:
[https://pubchem.ncbi.nlm.nih.gov/compound/Pentadecafluorooctanoic_acid] [Li Y, Fletcher T, Mucs D, et al, “Half-lives of PFOS, PFHxS and PFOA after end of exposure to contaminated drinking water” , Occup Environ Med 2018;75:46-51] [Biomonitoring of perfluoroalkyl acids in human urine and estimates of biological half-life. Zhang Y1, Beesoon S, Zhu L, Martin JW.] [ Olsen GW, Burris JM, Ehresman DJ, et al. Half-life of serum elimination of perfluorooctanesulfonate,perfluorohexanesulfonate, and perfluorooctanoate in retired fluorochemical production workers. Environ Health Perspect. 2007;115(9):1298-305] [Occurrence, temporal trends, and half-lives of perfluoroalkyl acids (PFAAs) in occupational workers in China Jianjie Fu, Yan Gao, Lin Cui, Thanh Wang, Yong Liang, Guangbo Qu, Bo Yuan, Yawei Wang, Aiqian Zhang & Guibin Jiang] [Per- and polyfluoroalkyl substances in human serum and urine samples from a residentially exposed community, Rachel Rogers Worleya,*, Susan McAfee Moorea, Bruce C. Tierneya, Xiaoyun Yeb, Antonia M. Calafatb, Sean Campbellc, Million B. Woudnehc, and Jeffrey Fisherd] [https://www.mass.gov/files/documents/2018/06/11/pfas-ors-ucmr3-recs_0.pdf]
PTFE related documents:
[http://www.essentialchemicalindustry.org/polymers/polytetrafluoroethene.html https://www.prodeflon.it/en/processing/ptfe-properties https://teflonashleybonin.weebly.com/chemical-properties.html] [http://www.polymer-search.com/teflon.html https://www.researchgate.net/post/Why_polytetrafluoroethylene_PTFE_is_hydrophobic_in_nature] [http://www.chemspider.com/Chemical-Structure.8000.html?rid=35e96b28-01be-48c9-86ee-509781126a2b https://www.engineeringtoolbox.com/melting-freezing-point-molar-mass-molecular-weight-hydrocarbon-aromatics-alkanes-cycloalkanes-paraffins-naphthenes-estimate-predict-calculate-d_1963.html] [https://www.chemicalbook.com/ChemicalProductProperty_EN_CB4392561.htm] [https://www.worldofmolecules.com/materials/teflon.htm]
[Philipson, K., Falk, R., Gustafsson, J., & Camner, P. (1996). Long-term lung clearance of 195Au-labeled teflon particles in humans. Experimental lung research, 22(1), 65-83] [The Facts Behind Teflon®, Elizabeth Walterscheid, Kathleen Esquibel, Kelly Morgese, Jonathan Lucero] [PFOS/PFOA in People, Mike LaScuola, Spokane Regional Health District] [Long-Chain Perfluorinated Chemicals (PFCs), Action Plan] [Evaluation of substances used in the GenX, technology by Chemours, Dordrecht, RIVM Letter report 2016-0174, M. Beekman et al.] [Potential human health effects of perfluorinated chemicals (PFCs), Glenys Webster] [Safety Assessment of Fluoropolymers as Used in Cosmetics, Scientific Literature Review for Public Comment] [DECOMPOSITION PRODUCTS of FLUOROCARBON POLYMERS, NIOSH] [Refining Human Risk Assessment through Comparisons of Human and Animal Internal Dosimetry: PFOA as a Case Example, Hugh A. Barton, National Center for Computational Toxicology, US EPA, Presentation for Toxicology Forum, July 13, 2006] [https://www.ewg.org/key-issues/consumer-products/cookware] [http://www.nbcnews.com/id/8404384/ns/health-cancer/t/teflon-chemical-cancer-risks-downplayed/#.XF9kGJeWV8E] [https://harvesthealthfoods.com/news/testtflmagcom/your-cookware-poisoning-you] [https://www.salon.com/2018/02/04/the-chemical-industry-doesnt-want-you-to-be-afraid-of-teflon-pans-you-should-be/] [https://www.nrdc.org/experts/anna-reade/epa-finds-replacements-toxic-teflon-chemicals-are-also] [https://www.business-humanrights.org/en/epa-steps-up-study-of-teflon-chemical-risk-to-humans-usa-0] [https://www.propublica.org/article/how-the-epa-and-the-pentagon-downplayed-toxic-pfas-chemicals%C2%A0] [https://planetark.org/news/ https://wellnessmama.com/77396/ditch-the-teflon/] [https://www.telegraph.co.uk/foodanddrink/foodanddrinkadvice/11643213/Are-we-really-being-poisoned-by-non-stick-pans.html] [https://www.nontoxicliving.tips/blog/teflon-coating-cookware-health-risks] [https://www.stonefryingpans.com/non-stick-frying-pan-health-risks/] [https://www.theguardian.com/lifeandstyle/2015/jan/25/are-my-non-stick-pans-a-health-hazard-teflon] [https://articles.mercola.com/sites/articles/archive/2015/06/03/non-stick-cookware-dangers.aspx] [https://mightynest.com/learn/make-your-nest-mighty/for-your-home/dangers-of-teflon] [https://greenlivingideas.com/2012/06/13/how-toxic-is-teflon/] [www.abc.net.au/health/thepulse/stories/2006/02/23/1576391.htm] [https://homeguides.sfgate.com/dangers-scratched-teflon-cookware-85350.html] [https://wellnessmama.com/77396/ditch-the-teflon/] [https://www.webmd.com/cancer/features/teflon-pans] [https://www.webmd.com/a-to-z-guides/features/what-is-pfoa#1] [https://www.scientificamerican.com/article/are-nonstick-pans-safe/] [www.berkeleywellness.com/healthy-eating/food-safety/article/should-you-stick-teflon]
Cadmium related documents
][https://www.lenntech.com/periodic/elements/cd.htm#ixzz5fvu752Jt] [https://en.wikipedia.org/wiki/Cadmium]
[http://www.chemistryexplained.com/elements/A-C/Cadmium.html] [https://www.livescience.com/10683-cadmium-dangerous.html] [https://en.m.wikipedia.org/wiki/Cadmium_poisoning] [https://nutritionfacts.org/2015/10/15/how-to-reduce-your-dietary-cadmium-absorption/] [https://rais.ornl.gov/tox/profiles/cadmium.html] [https://www.livescience.com/10683-cadmium-dangerous.html] [https://www.who.int/ifcs/documents/forums/forum5/nmr_cadmium.pdf] [Barberá, R., Farré, R., & Mesado, D. (1993). Oral intake of cadmium, cobalt, copper, iron, lead, nickel, manganese and zinc in the University student’s diet. Food/Nahrung, 37(3), 241-245] [Schäfer, S. G., & Forth, W. (1983). The influence of tin, nickel, and cadmium on the intestinal absorption of iron. Ecotoxicology and environmental safety, 7(1), 87-95] [Satarug, S., & Moore, M. R. (2004). Adverse health effects of chronic exposure to low-level cadmium in foodstuffs and cigarette smoke. Environmental health perspectives, 112(10), 1099-1103] [Hutton, M. (1983). Sources of cadmium in the environment. Ecotoxicology and environmental safety, 7(1), 9-24] [Murthy, G. K., Rhea, U., & Peeler, J. T. (1971). Levels of antimony, cadmium, chromium, cobalt, manganese, and zinc in institutional total diets. Environmental Science & Technology, 5(5), 436-442] [https://ec.europa.eu/food/safety/chemical_safety/contaminants/catalogue/cadmium_en] [Li, Z., Gu, J. Y., Wang, X. W., Fan, Q. H., Geng, Y. X., Jiao, Z. X., … & Wu, W. S. (2010). Effects of cadmium on absorption, excretion, and distribution of nickel in rats. Biological trace element research, 135(1-3), 211-219] [https://www.atsdr.cdc.gov/csem/csem.asp?csem=6&po=9] [Chunhabundit, R. (2016). Cadmium exposure and potential health risk from foods in contaminated area, Thailand. Toxicological research, 32(1), 65] [Song, Y., Wang, Y., Mao, W., Sui, H., Yong, L., Yang, D., … & Gong, Y. (2017). Dietary cadmium exposure assessment among the Chinese population. PloS one, 12(5), e0177978] [https://www.atsdr.cdc.gov/phs/phs.asp?id=46&tid=15] [https://cfpub.epa.gov/ncea/iris2/chemicalLanding.cfm?substance_nmbr=141] [https://veganhealth.org/cadmium/]
Lead related documents:
[Steenland, K., & Boffetta, P. (2000). Lead and cancer in humans: where are we now?. American journal of industrial medicine, 38(3), 295-299] [Juberg, D. R., Kleiman, C. F., & Kwon, S. C. (1997). Position paper of the American Council on Science and Health: lead and human health. Ecotoxicology and environmental safety, 38(3), 162-180]
[Chapter 6.7 Lead – WHO/Europe – World Health Organization]
[Lead and inorganic lead compounds, Evaluation of health hazards and estimation of a quality criterion in soil, Environmental Project No. 1518, 2013] [http://www.cancer-environnement.fr/537-Cancer-de-la-vesicule-biliaire.ce.aspx] [http://theconversation.com/is-lead-in-the-us-food-supply-decreasing-our-iq-79481] [https://www.health.ny.gov/environmental/lead/sources.htm] [https://www.atsdr.cdc.gov/csem/csem.asp?csem=34&po=5] [https://www.fda.gov/Food/FoodScienceResearch/TotalDietStudy/ucm184293.htm] [https://www.lenntech.com/periodic/elements/pb.htm#ixzz5giu56GAW][Toxicology Fact Sheet Series, Mercury, Lead, Cadmium, Tin and Arsenic in Food]
Aluminum related documents:
[https://www.alunorf.de/alunorf/alunorf.nsf/id/physical-and-chemical-properties-en?open&setprintmode=1&nowebedit=1] [https://melscience.com/en/articles/aluminum-its-chemical-properties-and-ability-enter/] [http://chemistry.elmhurst.edu/vchembook/102aluminum.html] [http://www.elementalmatter.info/aluminum-properties.htm] [https://www.lenntech.com/periodic/elements/al.htm] [https://sciencing.com/physical-chemical-properties-aluminum-element-6785380.html] [https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0089715] [https://www.fsai.ie/faq/aluminium.html] [http://www.winchesterhospital.org/health-library/article?id=164929] [https://www.greenfacts.org/en/aluminium-alzheimer-cancer/index.htm] [https://wellnessmama.com/91772/aluminum-safe/] [https://www.researchgate.net/publication/269114736_The_meaning_of_aluminium_exposure_on_human_health_and_aluminium-related_diseases] [https://www.ccohs.ca/oshanswers/diseases/alzheime.html] [http://www.vancouversun.com/health/health+myths+unmasking+sources+aluminum+diets/8090675/story.html] [http://dietgrail.com/aluminum-content-of-foods/] [https://www.healthcastle.com/aluminum-in-food-should-you-worry/] [A Yokel, R. (2012). The pharmacokinetics and toxicology of aluminum in the brain. Current Inorganic Chemistry, 2(1), 54-63] [Priest, N. D. (2004). The biological behaviour and bioavailability of aluminium in man, with special reference to studies employing aluminium-26 as a tracer: review and study update. Journal of Environmental Monitoring, 6(5), 375-403] [Greger, J. L., Goetz, W., & Sullivan, D. (1985). Aluminum levels in foods cooked and stored in aluminum pans, trays and foil. Journal of Food Protection, 48(9), 772-777] [Risk Assessment Studies, Report No. 35, Chemical Hazard Evaluation, ALUMINIUM IN FOOD, May 2009, Centre for Food Safety, Food and Environmental Hygiene Department, The Government of the Hong Kong Special Administrative Region] [Dórea, J. G. (2014). Aluminium concentrations in human milk: Additional comments on exposure issues in the neonate. Pediatrics & Neonatology, 55(2), 81-82] [Stahl, T., Taschan, H., & Brunn, H. (2011). Aluminium content of selected foods and food products. Environmental Sciences Europe, 23(1), 37] [Stahl, T., Taschan, H., & Brunn, H. (2011). Aluminium content of selected foods and food products. Environmental Sciences Europe, 23(1), 37] [Greger, J. L. (1992). Dietary and other sources of aluminium intake. Aluminium Biol Med, 169, 26-9] [Klotz, K., Weistenhöfer, W., Neff, F., Hartwig, A., van Thriel, C., & Drexler, H. (2017). The health effects of aluminum exposure. Deutsches Ärzteblatt International, 114(39), 653] [Krewski, D., Yokel, R. A., Nieboer, E., Borchelt, D., Cohen, J., Harry, J., … & Rondeau, V. (2007). Human health risk assessment for aluminium, aluminium oxide, and aluminium hydroxide. Journal of Toxicology and Environmental Health, Part B, 10(S1), 1-269] [Crisponi, G., Fanni, D., Gerosa, C., Nemolato, S., Nurchi, V. M., Crespo-Alonso, M., … & Faa, G. (2013). The meaning of aluminium exposure on human health and aluminium-related diseases. Biomolecular concepts, 4(1), 77-87] [Niu, Q., Zhang, Q., Li, H., Wang, L., & Lu, X. (2018). 1708b The immunotoxicity and neurotoxicity of aluminium] [Fulgenzi, A., Vietti, D., & Ferrero, M. E. (2014). Aluminium involvement in neurotoxicity. BioMed research international, 2014] [Bondy, S. C. (2010). The neurotoxicity of environmental aluminum is still an issue. Neurotoxicology, 31(5), 575-581] [Harsha, S. N., & Anilakumar, K. R. (2013). Protection against aluminium neurotoxicity: A repertoire of lettuce antioxidants. Biomedicine & Aging Pathology, 3(4), 179-184] [Exley, C. (2014). What is the risk of aluminium as a neurotoxin?] [Kumar, V., & Gill, K. D. (2009). Aluminium neurotoxicity: neurobehavioural and oxidative aspects. Archives of toxicology, 83(11), 965-978] [Fulgenzi, A., Vietti, D., & Ferrero, M. E. (2014). Aluminium involvement in neurotoxicity. BioMed research international, 2014] [Kumar, V., & Gill, K. D. (2009). Aluminium neurotoxicity: neurobehavioural and oxidative aspects. Archives of toxicology, 83(11), 965-978] [https://www.nhs.uk/news/cancer/are-deodorants-linked-with-breast-cancer/] [https://www.breastcanceruk.org.uk/science-and-research/background-briefings/aluminium-salts/] [https://universityhealthnews.com/daily/cancer/does-antiperspirant-cause-cancer-heres-why-you-should-be-concerned-about-aluminum-toxicity/] [https://www.cancer.gov/about-cancer/causes-prevention/risk/myths/antiperspirants-fact-sheet] [https://scholar.google.fr/scholar?start=40&q=aluminum+cancer&hl=fr&as_sdt=0,5] [Milham, S. (1976). Cancer mortality patterns associated with exposure to metals. Annals of the New York academy of sciences, 271(1), 243-249] [Kaehny, W. D., Hegg, A. P., & Alfrey, A. C. (1977). Gastrointestinal absorption of aluminum from aluminum-containing antacids. New England Journal of Medicine, 296(24), 1389-1390] [Kaehny, W. D., Hegg, A. P., & Alfrey, A. C. (1977). Gastrointestinal absorption of aluminum from aluminum-containing antacids. New England Journal of Medicine, 296(24), 1389-1390] [Gibbs, G. W., & Labreche, F. (2014). Cancer risks in aluminum reduction plant workers: a review. Journal of occupational and environmental medicine, 56(5 Suppl), S40] [Seldén, A. I., Westberg, H. B., & Axelson, O. (1997). Cancer morbidity in workers at aluminum foundries and secondary aluminum smelters. American journal of industrial medicine, 32(5), 467-477] [Abramson, M. J., Wlodarczyk, J. H., Saunders, N. A., & Hensley, M. J. (1989). Does aluminum smelting cause lung disease?. American Review of Respiratory Disease, 139(4), 1042-1057] [Thériault, G. P., Tremblay, C. G., & Armstrong, B. G. (1990). Bladder cancer screening among primary aluminum production workers in Quebec. Journal of occupational medicine.: official publication of the Industrial Medical Association, 32(9), 869-872] [Rönneberg, A., & Langmark, F. (1992). Epidemiologic evidence of cancer in aluminum reduction plant workers. American journal of industrial medicine, 22(4), 573-590] [Rönneberg, A., & Langmark, F. (1992). Epidemiologic evidence of cancer in aluminum reduction plant workers. American journal of industrial medicine, 22(4), 573-590] [Romundstad, P., Andersen, A., & Haldorsen, T. (2000). Cancer incidence among workers in six Norwegian aluminum plants. Scandinavian journal of work, environment & health, 26(6), 461-469] [Milham, J. S. (1979). Mortality in aluminum reduction plant workers. Journal of occupational medicine.: official publication of the Industrial Medical Association, 21(7), 475-480] [Gibbs, G. W., & Horowitz, I. (1979). Lung cancer mortality in aluminum reduction plant workers. Journal of occupational medicine.: official publication of the Industrial Medical Association, 21(5), 347-353] [Spinelli, J. J., Band, P. R., Svirchev, L. M., & Gallagher, R. P. (1991). Mortality and cancer incidence in aluminum reduction plant workers. Journal of occupational medicine.: official publication of the Industrial Medical Association, 33(11), 1150-1155] [Armstrong, B., Tremblay, C., Baris, D., & Thériault, G. (1994). Lung cancer mortality and polynuclear aromatic hydrocarbons: a case-cohort study of aluminum production workers in Arvida, Quebec, Canada. American journal of epidemiology, 139(3), 250-262] [Theriault, G., De Guire, L., & Cordier, S. (1981). Reducing aluminum: an occupation possibly associated with bladder cancer. Canadian Medical Association Journal, 124(4), 419] [Estimating the relationship between exposure to tar volatiles and the incidence of bladder cancer in aluminum smelter workers, Armstrong BG, Tremblay CG, Cyr D, Theriault GP]
Nickel related documents:
[PerkinElmer, Nickel-63 Handling Precautions] [PennState Hershely, Low Nickel Diet] [Systemic nickel hypersensitivity and diet: myth or
reality?, S. Pizzutelli] [Toxicological Review of Soluble Nickel Salts, U. S. Environmental Protection Agency, and Health Canada] [Cempel, M., & Nikel, G. (2006). Nickel: A review of its sources and environmental toxicology. Polish Journal of Environmental Studies, 15(3)] [6.10-Nickel, Esther Christenhuis] [FICHE RADIONUCLÉIDE, 1LFNHO et environnement, IRSN] [Wilson, H. W. (1951). Radioactivity of nickel. Physical Review, 82(4), 548] [https://rais.ornl.gov/tox/profiles/nickel_and_nickel_compounds_f_V1.html] [https://www.nap.edu/read/11537/chapter/47] [Barberá, R., Farré, R., & Mesado, D. (1993). Oral intake of cadmium, cobalt, copper, iron, lead, nickel, manganese and zinc in the University student’s diet. Food/Nahrung, 37(3), 241-245] [https://toxnet.nlm.nih.gov/cgi-bin/sis/search/a?dbs+hsdb:@term+@DOCNO+1096] [Edelman, D. A., & Roggli, V. L. (1989). The accumulation of nickel in human lungs. Environmental health perspectives, 81, 221-224] [Kuehn, K., & Sunderman Jr, F. W. (1982). Dissolution half-times of nickel compounds in water, rat serum, and renal cytosol. Journal of inorganic biochemistry, 17(1), 29-39] [Biliary excretion of nickel in rats, AbubakrMarzouk, F.William SundermanJr] [Low Nickel Diet in Dermatology, Ashimav D Sharma] [https://toxnet.nlm.nih.gov/cgi-bin/sis/search/a?dbs+hsdb:@term+@DOCNO+1096] [Handbook on Metals in Clinical and Analytical Chemistry, Hans Seiler, Astrid Sigel, Helmut Sigel] [Dissolution half-times of nickel compounds in water, rat serum, and renal cytosol, Kuehn K, Sunderman FW Jr] [In vivo determination of aluminum, cobalt, chromium, copper, nickel, titanium and vanadium in oral mucosa cells from orthodontic patients with mini-implants by Inductively coupled plasma-mass spectrometry (ICP-MS), Ana Martín-Cameán, Angeles Jos, Maria Puerto, Ana Calleja, Alejandro Iglesias-Linares, Enrique Solano, Ana M.Cameán]
Chromium related documents:
Antimony related documents:[https://www.azom.com/article.aspx?ArticleID=9075] [https://medium.com/sable-university-writing-tips/chemistry-properties-and-application-of-sb-antimony-89973956d47a] [https://oehha.ca.gov/water/crnr/final-technical-support-document-updated-public-health-goal-antimony-drinking-water] [http://earthresources.vic.gov.au/earth-resources-regulation/information-for-community-and-landholders/antimony/reducing-exposure-faqs?SQ_DESIGN_NAME=mobile&SQ_ACTION=set_design_name] [https://www.cfs.gov.hk/english/whatsnew/whatsnew_fstr/whatsnew_fstr_dietary_exposure_to_antimony.html] [https://www.tandfonline.com/doi/abs/10.1080/10643381003608227?journalCode=best20] [https://www.atsdr.cdc.gov/phs/phs.asp?id=330&tid=58] [familywellnesshq.com/heavy-metals-sources-toxicity/] [http://www.fia.usv.ro/fiajournal/index.php/FENS/article/view/302] [https://pubchem.ncbi.nlm.nih.gov/compound/antimony#section=Chemical-Vendors] [https://www.cdc.gov/biomonitoring/Antimony_BiomonitoringSummary.html] [https://chemicalwatch.com/54585/study-finds-antimony-in-food-contact-articles] [TOXICITY SUMMARY FOR ANTIMONY, DECEMBER 1992, Robert A. Young, Chemical Hazard Evaluation and Communication Group, Biomedical and Environmental Information Analysis Section] [WHO/SDE/WSH/03.04/74, Antimony in Drinking-water, Background document for development of WHO Guidelines for Drinking-water Quality]
Antimony related documents
[https://chemicalwatch.com/54585/study-finds-antimony-in-food-contact-articles] [https://www.cdc.gov/biomonitoring/Antimony_BiomonitoringSummary.html] [https://pubchem.ncbi.nlm.nih.gov/compound/antimony#section=Chemical-Vendors] [Gerhardsson, L., Brune, D., Nordberg, G. F., & Wester, P. O. (1982). Antimony in lung, liver and kidney tissue from deceased smelter workers. Scandinavian journal of work, environment & health, 201-208] [Bencze, K. (2002). Antimony [Biomonitoring Methods, 1988]. The MAK‐Collection for Occupational Health and Safety: Annual Thresholds and Classifications for the Workplace, 31-46] [Young, R. A. (1992). Toxicity Summary for Antimony] [Djurić, D., Thomas, R. G., & Lie, R. (1962). The distribution and excretion of trivalent antimony in the rat following inhalation. Internationales Archiv für Gewerbepathologie und Gewerbehygiene, 19(5), 529-545] [Cruz, A., Rainey, P. M., Herwaldt, B. L., Stagni, G., Palacios, R., Trujillo, R., & Saravia, N. G. (2007). Pharmacokinetics of antimony in children treated for leishmaniasis with meglumine antimoniate. The Journal of infectious diseases, 195(4), 602-608] [ANTIMONY IN FOODS, JAMA. 1916;LXVII(12):883-884. doi:10.1001/jama.1916.02590120039017] [Belzile, N., Chen, Y. W., & Filella, M. (2011). Human exposure to antimony: I. Sources and intake. Critical reviews in environmental science and technology, 41(14), 1309-1373] [BARLOKOVÁ, D., ILAVSKÝ, J., & KUNŠTEK, M. (2017). Removal of antimony from water by coagulation. Food and Environment Safety Journal, 11(4)] [Butterman, W. C., & Carlin Jr, J. F. (2004). Mineral commodity profiles: Antimony (No. 2003-19)] [Welle, F., & Franz, R. (2011). Migration of antimony from PET bottles into beverages: determination of the activation energy of diffusion and migration modelling compared with literature data. Food Additives & Contaminants: Part A, 28(1), 115-126] [Emsley, A. M., & Stevens, G. C. (2008). The risks and benefits of flame retardants in consumer products. In Advances in Fire Retardant Materials (pp. 363-397). Woodhead Publishing] [http://familywellnesshq.com/heavy-metals-sources-toxicity/] [Cooper, R. G., & Harrison, A. P. (2009). The exposure to and health effects of antimony. Indian journal of occupational and environmental medicine, 13(1), 3] [Agency for Toxic Substances and Disease Registry (ATSDR), Public Health Statement for Antimony] [Belzile, N., Chen, Y. W., & Filella, M. (2011). Human exposure to antimony: I. Sources and intake. Critical reviews in environmental science and technology, 41(14), 1309-1373] [https://www.cfs.gov.hk/english/whatsnew/whatsnew_fstr/whatsnew_fstr_dietary_exposure_to_antimony.html] [http://earthresources.vic.gov.au/earth-resources-regulation/information-for-community-and-landholders/antimony/reducing-exposure-faqs?SQ_DESIGN_NAME=mobile&SQ_ACTION=set_design_name] [http://www.npi.gov.au/resource/antimony-and-compounds] [https://oehha.ca.gov/water/crnr/final-technical-support-document-updated-public-health-goal-antimony-drinking-water] [https://medium.com/sable-university-writing-tips/chemistry-properties-and-application-of-sb-antimony-89973956d47a] [https://www.azom.com/article.aspx?ArticleID=9075] [
Copper related documents:
[http://mysite.du.edu/~jcalvert/phys/copper.htmWazir, S. M., & Ghobrial, I. (2017). Copper deficiency, a new triad: anemia, leucopenia, and myeloneuropathy. Journal of community hospital internal medicine perspectives, 7(4), 265-268] [Huff, J. D., Keung, Y. K., Thakuri, M. C., Beaty, M. W., Owen, J., & Molnar, I. (2005). Copper Deficiency Anemia Is Not Uncommon in a Hematology Practice] [https://en.wikipedia.org/wiki/Copper_deficiency] [Considine, D. M. (2012). Foods and food production encyclopedia. Springer Science & Business Media] [Nordberg, G. F., Fowler, B. A., & Nordberg, M. (Eds.). (2014). Handbook on the Toxicology of Metals. Academic press] [https://en.wikipedia.org/wiki/Copper_in_health#Food_sources] [http://apjcn.nhri.org.tw/server../INFO/BOOKS-PHDS/BOOKS/FOODFACTS/html/data/data5i.html] [http://mysite.du.edu/~jcalvert/phys/copper.htm] [http://www.chemistryexplained.com/elements/C-K/Copper.html] [https://www.atsdr.cdc.gov/phs/phs.asp?id=204&tid=37] [Gaetke, L. M., Chow-Johnson, H. S., & Chow, C. K. (2014). Copper: toxicological relevance and mechanisms. Archives of toxicology, 88(11), 1929-1938] [G. Georgopoulos, A. Roy, MJ Yonone-Lioy, RE Opiekun, PJ Lioy, P. (2001). Environmental copper: its dynamics and human exposure issues. Journal of Toxicology and Environmental Health Part B: Critical Reviews, 4(4), 341-394] [https://www.health.state.mn.us/communities/environment/water/factsheet/copper.html] [Gamakaranage, C. (2018). Clinical Features of Acute Copper Sulphate Poisoning. ARCHIVOS DE MEDICINA, 3(1), 2] [https://www.grahamreiddesign.com/portfolio/half-life-of-copper/] [THE ROLE OF COPPER IN ERYTHROPOIESIS, GEORGE E.CARTWRIGHT, CLARK J.GUBLER AND MAXWELL M.WINTROBE] [https://www.nadis.org.uk/disease-a-z/sheep/copper-poisoning-in-sheep/] [https://sevenfigurepublishing.com/2015/09/09/the-link-between-copper-and-cancer/] [https://www.sciencedaily.com/releases/2013/11/131114102526.htm] [http://www.mensahmedical.com/copperandbreastcancer/] [Denoyer, D., Masaldan, S., La Fontaine, S., & Cater, M. A. (2015). Targeting copper in cancer therapy:‘Copper That Cancer’. Metallomics, 7(11), 1459-1476] [https://www.medicalnewstoday.com/articles/256470.php] [Copper and Zinc, Biological Role and Significance of Copper/Zinc Imbalance, Josko Osredkar, Natasa Sustar] [https://medlineplus.gov/ency/article/002419.htm] [https://www.gicare.com/gi-health-resources/copper-restriction/] [https://en.wikipedia.org/wiki/Copper_in_health#Food_sources] [Ma, J., & Betts, N. M. (2000). Zinc and copper intakes and their major food sources for older adults in the 1994–96 continuing survey of food intakes by individuals (CSFII). The Journal of nutrition, 130(11), 2838-2843] [https://blog.radiantlifecatalog.com/bid/65561/Nutrient-Dense-Foods-and-the-Copper-Zinc-Connection] [http://dietgrail.com/copper/] [https://www.lenntech.com/periodic/elements/cu.htm] [https://copperalliance.eu/about-copper/copper-and-its-alloys/properties/] [https://sciencestruck.com/chemical-properties-of-copper] [https://www.curejoy.com/content/foods-rich-in-copper/] [Bost, M., Houdart, S., Oberli, M., Kalonji, E., Huneau, J. F., & Margaritis, I. (2016). Dietary copper and human health: Current evidence and unresolved issues. Journal of Trace Elements in Medicine and Biology, 35, 107-115] [https://vegfaqs.com/vegan-food-sources-of-copper/] [Bilirubin, Copper-Porphyrins, and the Bronze-Baby Syndrome, Antony F. McDonagh] [http://apjcn.nhri.org.tw/server../INFO/BOOKS-PHDS/BOOKS/FOODFACTS/html/data/data5i.html]
Iron related documents:
[https://www.everydayhealth.com/pictures/foods-high-in-iron/] [https://my.clevelandclinic.org/health/diseases/14621-iron-rich-foods-and-anemia/management-and-treatment] [http://www.unlockfood.ca/en/Articles/Vitamins-and-Minerals/How-to-get-more-iron.aspx] [https://www.medicalnewstoday.com/articles/322272.php] [https://www.rd.com/food/best-sources-of-iron-youre-missing/] [https://www.healthdirect.gov.au/foods-high-in-iron] [https://nutritionfacts.org/2017/06/15/plant-versus-animal-iron/] [https://well.blogs.nytimes.com/2012/08/13/a-host-of-ills-when-irons-out-of-balance/] [Iron, Meat and Health, Catherine Geissler, Mamta Singh] [https://www.lenntech.com/periodic/elements/fe.htm] [Biological Half-Life of Radioiron in Man, R. OLIVER, L. G. LAJTHA] [https://www.cdc.gov/nutrition/infantandtoddlernutrition/vitamins-minerals/iron.html] [https://www.verywellfamily.com/iron-rich-foods-to-battle-anemia-in-pregnancy-2757517] [https://truweight.in/blog/food-and-nutrition/iron-rich-fruits.html] [FUNDAMENTALS OF INDUSTRIAL HYGIENE, 6TH ED.HOMEWORK #6 INDIVIDUAL MEASUREMENT OF RADIOACTIVITY] [Korchinski, D. J., Taha, M., Yang, R., Nathoo, N., & Dunn, J. F. (2015). Iron oxide as an Mri contrast agent for cell tracking: supplementary issue. Magnetic resonance insights, 8, MRI-S23557] [https://www.imoa.info/HSE/environmental_data/human_health/molybdenum_uptake.php] [Oxidative Stress and Neurodegenerative Disorders, G. Ali Qureshi, S. Hasan Parvez]