Liver Function Test / Liver Profile

Liver Function Test:

Liver function tests are blood tests used to help diagnose and monitor liver disease or damage. The tests measure the levels of certain enzymes and proteins in blood.

Liver function tests can be used to:

• Screen for liver infections, such as hepatitis.
• Monitor the progression of a disease, such as viral or alcoholic hepatitis, and determine the treatment.
• Measure the severity of a disease, particularly scarring of the liver (cirrhosis).
• Monitor possible side effects of medications.

General symptoms of liver problems include: Lack of appetite, Nausea or vomiting, Weakness or feeling very tired, Yellowish eyes or skin (jaundice).

Some common liver function tests include:

1. ALTL - Alanine Aminotransferase (ALT)
2. ASTL-  Aspartate Aminotransferase (AST)
3. ALB2 - Albumin Blood Test
4. BIL - Bilirubin
5. ALP2L-  (Alkaline phosphatase)
6. TP- Total Protein
7. Gamma-glutamyltransferase (GGT)
8. L-lactate dehydrogenase (LD)
9. Prothrombin time (PT)

ALTL - Alanine Aminotransferase (ALT) / (Normal Range: 7 to 55 units per liter (U/L)

                Alanine aminotransferase is an enzyme that is concentrated primarily in the liver. ALT levels can increase when liver cells are damaged, so the test can be used to evaluate the condition of the liver. ALT testing may be useful in diagnosis of symptoms that can be tied to liver problems like nausea and vomiting, abdominal pain, itching, jaundice, fatigue, and appetite loss.

                High levels of ALT can be a result of damage or injury to cells. Because ALT is most concentrated in the liver, abnormal ALT test results are generally associated with conditions affecting the liver, such as inflammation (hepatitis) and scarring (cirrhosis).

ASTL- Aspartate Aminotransferase (AST) / (Normal Range: 5 to 40 units per liter (U/L)

                Aspartate aminotransferase (AST) is an enzyme AST exists mostly in the liver, but it is found in numerous tissues in the body.AST may be measured if you have had jaundice, fatigue, swelling, unexplained weight loss, itching, nausea and vomiting, or other symptoms that are associated with liver problems.

                AST levels in the blood can rise when cells are damaged, elevated AST can reflect health conditions, including liver diseases like cirrhosis or hepatitis.Very high levels of AST often reflect short-term liver damage while smaller but persistent elevations in AST over time can be tied to chronic conditions.

ALB2 - Albumin Blood Test / (Normal Range: 3.5 to 5.5 grams per deciliter g/dL)

                Albumin is a protein.Test used forMeasure the potential liver disease such as jaundice or fatigue or symptoms of possible kidney disease such as abnormal urination or unexplained swelling, particularly of the feet and legs.

                Abnormally low albumin levels can also be tied to kidney conditions, malnutrition, inflammation, infection, thyroid disease, and gastrointestinal problems

                Abnormally high levels of albumin most often occur as a result of dehydration, which may be caused by other conditions such as severe diarrhoea.

BIL – Bilirubin / (Normal Range: 0.3 and 1.2 milligrams per deciliter (mg/dL)

                To screen for or monitor liver disorders or hemolytic anemia; to monitor neonatal jaundice. Bilirubin is an orange-yellow pigment Heme is a component of hemoglobin, which is found in red blood cells (RBCs) Bilirubin is ultimately processed by the liver.Test measures the amount of bilirubin in the blood to evaluate a person’s liver function or to help diagnose anemias caused by RBC destruction (hemolytic anemia).

Unconjugated (indirect) bilirubin, there typically is a problem associated with decreased elimination of bilirubin by the liver cells.Some conditions that may cause this include: Viral hepatitis (hepatitis A, hepatitis B, hepatitis C), Drug reactions, and Alcoholic liver disease.Conjugated (direct) bilirubin is also elevated more than unconjugated (indirect) bilirubin when the liver is able to process bilirubin but there is blockage of the bile ducts.This may occur, for example, with: Gallstones present in the bile ducts, Tumors, Scarring of the bile ducts.

Increased bilirubin levels may result from the accelerated breakdown of red blood cells due to: Blood type incompatibility between the mother and her newborn, causing hemolytic disease of the newborn (HDN), certain congenital infections, Lack of oxygen (hypoxia), Diseases that can affect the liver.

ALP2L- (Alkaline phosphatase) / (Normal Range: 40 to 129 units per liter (U/L)

Alkaline phosphatase, or ALP, is another liver enzyme that is measured in a standard liver panel or comprehensive metabolic panel. ALP is produced and found in the liver. But it is also present in a number of other tissues in the body, including the bones.

Test results that are below normal are sometimes found in people with malnutrition or anaemia.

Higher-than-normal levels of ALP indicates liver damage or disease, a blocked bile duct, or bone disease.

TP Total Protein / (Normal Range: 6 to 8.3 g/dL)

                Albumin and globulin are two types of protein in your body. The total protein test measures the total amount albumin and globulin in your body. It’s used as part of your routine health checkup.It may also be used if you have unexpected weight loss, fatigue, or the symptoms of a kidney or liver disease. Albumin proteins keep fluid from leaking out of your blood vessels. Globulin proteins play an important role in your immune system.

                Low total protein may indicate: bleeding, liver disorder, kidney disorder, such as a nephrotic disorder or glomerulonephritis, malnutrition, malabsorption conditions, such as celiac disease or inflammatory bowel disease, extensive burns, agammaglobulinemia,which is an inherited condition in which your blood doesn’t have enough of a type of globulin, affecting the strength of your immune system, inflammatory conditions, delayed post-surgery recovery.

                Elevated total protein may indicate: inflammation or infections, such as viral hepatitis B or C, or HIV, bone marrow disorders, such as multiple myeloma or Waldenstrom’s disease.

Gamma-glutamyltransferase (GGT) / (Normal Range: 8 to 61 units per liter (U/L)

GGT is an enzyme in the blood. Higher-than-normal levels may indicate liver or bile duct damage.

L-lactate dehydrogenase (LD) / (Normal Range: 122 to 222 units per liter (U/L)

LD is an enzyme found in the liver. Elevated levels may indicate liver damage but can be elevated in many other disorders.

Prothrombin time (PT) / (Normal Range: 9.4 to 12.5 seconds)

PT is the time it takes your blood to clot. Increased PT may indicate liver damage Medications that thin your blood, such as warfarin (Coumadin), can also lead to a longer PT. 

Sample Analysis:

Sample types:  Serum, plasma, urine, CSF, hemolysate and whole blood (HbA1c).

Instrumentation: Cobas Integra 400 Plus

LFT are performed by Cobas Integra 400+ system. The COBAS INTEGRA 400 plus system has up to 36 different on-board assays.All types of sample matrices are measured with one of 4 different measuring technologies – absorbance photometry, turbidimetry, fluorescence polarisation and ion selective potentiometry

Mycotoxins - Chemical Hazard in Food

Mycotoxins

 

Mycotoxins are a chemically diverse range of secondary metabolites and are produced by various fungal species (Aspergillus, Penicillium, Fusarium, and Claviceps). Several hundred different mycotoxins have been identified, but the most commonly observed mycotoxins that present a concern to human health and livestock include aflatoxins, ochratoxin A, patulin, fumonisins and zearalenone.

They are toxic to humans and most are chemically stable and survive prolonged heat processing.

Aflatoxins are difuranocoumarin derivatives produced by a polyketide pathway

A.flavus and A. parasiticus, which produce aflatoxins in maize, groundnuts, tree nuts, and, less frequently, other commodities

A.ochraceus and A. carbonarius, which produce ochratoxin A commonly occur in grapes, dried vine fruits, wine, and coffee.

Penicillium verrucosum also produces ochratoxin A but occurs only in cool temperate climates, where it infects small grains. Ochratoxin A is a nephrotoxin to all animal species studied to date and is most likely toxic to humans. ochratoxin A is a liver toxin, an immune suppressant, a potent teratogen, and a carcinogen (2).

Aspergillus niger also produces fumonisins.

F. graminearum is the major producer of deoxynivalenol and zearalenone, is pathogenic on maize, wheat, and barley 

Claviceps purpurea produces sclerotia among the seeds in grasses, including wheat, barley, and triticale.

Fusarium fungi are common to the soil and produce a range of different toxins, including trichothecenes such as deoxynivalenol (DON), nivalenol (NIV) and T-2 and HT-2 toxins, as well as zearalenone (ZEN) and fumonisins.

Patulin is a toxic fungal metabolite produced by certain moulds of the Penicillium, Aspergillus and Byssochlamys.

Occurrence in Foods:

They commonly enter the food chain through contaminated food and feed crops, mainly cereals.

Other occurrence in foods include nuts, spices, dried fruits, apples and coffee beans, often under warm and humid conditions.

Animals consuming mycotoxin-contaminated feeds can produce meat and milk that contain toxic residues and biotransformation products. Thus, aflatoxins in cattle feed can be metabolized by cows into aflatoxin M1, which is then secreted in milk (1).

Ochratoxin in pig feed can accumulate in porcine tissues (2)

Effects on Health:

The toxic effects of mycotoxins can be significant and varied depending on the toxin, dose, host and food matrix involved.

These effects include: Carcinogenicity (cancer causing) especially in the liver, Hepatotoxicity (liver damage), Mutagenicity (changes to DNA), Other toxic effects include kidney disease, immuno-suppression and disturbance to the nervous and hormone systems.

Aflatoxin is associated with both toxicity and carcinogenicity in human and animal populations. The diseases caused by aflatoxin consumption are loosely called aflatoxicoses. Acute aflatoxicosis results in death; chronic aflatoxicosis results in cancer, immune suppression, and other “slow” pathological conditions (3, 4).

Control and Preventive Measures:

Good Agricultural Practice:

Proper preparation of the land, crop rotation, use of fungus and/or pest resistant cultivars, control of insect damage to the growing crop, control of fungal infection, prevention of stress to the growing crop, e.g. drought, weeds, harvesting at the appropriate time, and correct handling and storage after harvesting.

Monitoring Programs:

Inspection and sampling of commodities intended for introduction into the food supply chain. Maximum levels are defined and often legally controlled in specific legislation. Rejection and removal of failed batches is a common control measure

Pest Control Program:

Pest damage may result in heating and moisture generation, leading to fungal growth and mycotoxin production in localised “hot spots”. Therefore, it is important to have adequate pest control programs in place.

Inactivation of Toxins:

This can be achieved through roasting of peanuts, heat and moisture control, chemical control, e.g. acids, H2O2, NH3, hypochlorites.

Testing

Monitoring using analytical methods have been developed based on HPLC, TLC and ELISA.

Bioterrorism

Mycotoxins can be used as chemical warfare agents (5). There is considerable evidence that Iraqi scientists developed aflatoxins as part of their bioweapons program during the 1980s. Toxigenic strains of Aspergillus flavus and Aspergillus parasiticus were cultured, and aflatoxins were extracted to produce over 2,300 liters of concentrated toxin (5). The majority of this aflatoxin was used to fill warheads; the remainder was stockpiled. Aflatoxins seem a curious choice for chemical warfare because the induction of liver cancer is “hardly a knockout punch on the battlefield” (6).

Reference

1. Van Egmond, H. P. 1989. Aflatoxin M1: occurrence, toxicity, regulation, p. 11-55. In H. P. Van Egmond (ed.), Mycotoxins in dairy products. Elsevier Applied Science, London.
2. Rutqvist, L., N.-E. Bjorklund, K. Hult, E. Hockby, and B. Carlsson. 1978. Ochratoxin A as the cause of spontaneous nephropathy in fattening pigs. Appl. Environ. Microbiol. 36:920-925.
3. Hsieh, D. 1988. Potential human health hazards of mycotoxins, p. 69-80. In S. Natori, K. Hashimoto, and Y. Ueno (ed.), Mycotoxins and phytotoxins. Third Joint Food and Agriculture Organization/W.H.O./United Nations E? Program International Conference of Mycotoxins. Elsevier, Amsterdam, The Netherlands.
4. Beardall, J. M., and J. D. Miller. 1994. Disease in humans with mycotoxins as possible causes, p. 487-539. In J. D. Miller and H. L. Trenholm (ed.), Mycotoxins in grains. Compounds other than aflatoxin. Eagan Press, St. Paul, Minn.
5. Ciegler, A. 1986. Mycotoxins: a new class of chemical weapons. NBC Defense & Technol. Int., April 1986, p. 52-57.
6. Stone, R. 2002. Peering into the shadows: Iraq's bioweapons program. Science 297:1110-1112.

Overview of Pathogenic Bacteria: Bacillus cereus

  Pathogenic Bacteria: Bacillus cereus

Industrial Microbiology Techniques based on International Standards ISO/ BAM, etc...

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Bacillus cereus (B. cereus) is a Gram-positive, facultatively anaerobic, endospore-forming, large rod and has colonial morphology of about 2-7 mm in diameter, with a white granular texture.

The optimal growth temperature is 28°C to 35°C, with a minimum growth temperature of 4°C and a maximum of 48°C. Growth can occur in pH ranges from 4.9 to 9.

Pathogenicity: It causes two kinds of food-borne disease:

1. Intoxication due to a toxin performed in the food
2. Infection is due to the ingestion of cells that produce enterotoxins in the small intestine.

Sources: Widespread in the environment being found in soil, water, air, and vegetable matter.

 Rice products, pasta, vegetables, herbs, spices, milk, and meat.

Illness, Symptoms, and Complications:

B. cereus food poisoning is caused by toxins produced during the growth of the bacteria (emetic toxin (ETE)) and three different enterotoxins: Hemolysin (HBL), Nhe, and EntK. These toxins cause two distinctly different forms of food poisoning – the emetic/vomiting type or diarrhoeal type. Symptoms usually last around 24 hours. EntK ( Not involved in food poisoning).

Emetic-type symptoms include nausea, vomiting, and abdominal cramps.

Diarrhoeal-type symptoms include watery diarrhea, abdominal cramps, and pain with occasional nausea and vomiting.

Although both forms are self-limiting more severe cases have been reported which included complications such as pyogenic infections, gangrene, septic meningitis, lung abscesses, and infant death.

Controls to reduce the risk:

Foods should be cooked to a core temperature of 75°C (167°F) e.g. 70°C (158°F) for 2 minutes which will destroy the cells however in order to prevent the spores from germinating it is essential that rapid cooling takes place. It may be beneficial to implement or install rapid chilling equipment to speed up the cooling process.

Hot food should be maintained at a temperature greater than or equal to 63°C (145.4°F) and chilled food should ideally be maintained at a temperature less than or equal to 4°C (39.2°F).

Testing Method

ISO 7932:2004/AMD 1:2020 Microbiology of food and animal feeding stuff — Horizontal method for the enumeration of presumptive Bacillus cereus — Colony-count technique at 30 degrees.

BAM Chapter 14: Bacillus cereus; Authors: Sandra M. Tallent, Ann Knolhoff, E. Jeffery Rhodehamel (ret.), Stanley M. Harmon (ret.), and Reginald W. Bennett (ret.)

Lead Toxicity / Poisoning

Lead is the most important toxic heavy element in the environment. Due to its important physico-chemical properties, its use can be retraced to historical times. Globally it is an abundantly distributed, important yet dangerous environmental chemical (8).

Human exposure

Occupational exposure is a major source for lead poisoning in adults.

Exposed to lead through occupational and environmental sources.

This mainly results from:

Inhalation of lead particles generated by burning materials containing lead, for example, during smelting, recycling, stripping leaded paint, and using leaded gasoline or leaded aviation fuel; and

Ingestion of lead-contaminated dust, water (from leaded pipes), and food (from lead-glazed or lead-soldered containers).

Once lead enters the body, it is distributed to organs such as the brain, kidneys, liver and bones. The body stores lead in the teeth and bones where it accumulates over time. Lead stored in bone may be re-mobilized into the blood during pregnancy, thus exposing the fetus.

• Lead in the soil can settle on or be absorbed by plants grown for fruits or vegetables or plants used as ingredients in food, including dietary supplements.
• Lead in plants or water may also be ingested and absorbed by the animals we eat, which is then passed on to us.
• Lead in some pottery and other food contact surfaces containing lead can pass or leach lead into food or drinks when food is prepared, served, or stored in them

Lead toxicity: a review (ncbi)

Effects on Health:

Lead is a highly poisonous metal affecting almost every organ in the body. Of all the organs, the nervous system is the mostly affected target in lead toxicity, both in children and adults. The toxicity in children is however of a greater impact than in adults. This is because their tissues, internal as well as external, are softer than in adults. Long-term exposure of adults can result in decreased performance in some tests of cognitive performance that measure functions of the nervous system. Infants and young children are especially sensitive to even low levels of lead, which may contribute to behavioural problems, learning deficits and lowered IQ (9). 

Types of lead Poisoning.

	Exposure	Lead levels (µg/dl)	Clinical symptoms
Acute poisoning	Intense exposure of short duration	100–120	Muscle pain, fatigue, abdominal pain, headache, vomiting, seizures and coma
Chronic poisoning	Repeated low-level exposure over a prolonged period	40–60	Persistent vomiting, encephalopathy, lethargy, delirium, convulsions and coma

Toxicity of lead: A review

After absorption, Pb is distributed in the body through red blood cells (RBC). Pb is mostly bound to hemoglobin rather than RBC membrane after entering the cell [2]. The hematopoietic is a sensitive system for critical Pb toxicity and may lead to anemia [1].

Histopathological observations confirmed that Pb ions are transported to the liver, where they can induce chronic damage to the liver.

Pb toxicity also increases blood enzyme levels and reduces protein synthesis [3-5].

Pb imposes toxic effects on kidneys through structural damage and changes in the excretory function [3-5].

The other organ and tissue systems affected due to lead toxicity are the nervous, cardiovascular, and reproductive systems [1,2,6].

Pb toxicity imposes mineralizing of bones and teeth, which is a major body burden.

The International Agency for Research on Cancer (IARC) stated that inorganic Pb is probably carcinogenic to humans (Group 2A) based on limited evidence in humans and sufficient evidence in animals. (1, 2-7)

Centers for Disease Control and Prevention (USA) have set the standard elevated blood lead level for adults to be 10 μg/dL and for children 5 μg/dL of the whole blood (CDC, 2012, 10).

Prevention & Control

Lead poisoning causes severe effects and is a matter of serious concern, yet importantly, it is preventable. The best approach is to avoid exposure to lead (11). It is recommended to frequently wash the children´s hands and also to increase their intake of calcium and iron. It is also recommended to discourage children from putting their hands, which can be contaminated, in their mouth habitually, thus increasing the chances of getting poisoned by lead.

Vacuuming frequently and eliminating the use and or presence of lead containing objects like blinds and jewellery in the house can also help to prevent exposures. House pipes containing lead or plumbing solder fitted in old houses should be replaced to avoid lead contamination through drinking water. 

Bottled Water

The FDA, through its regulatory authority under the Federal Food, Drug, & cosmetic Act, limits levels of lead (as well as other contaminants) in bottled water by establishing allowable levels in the quality standard for bottled water. For lead, this level is set at 5 ppb. This level is below the 15 ppb allowed by the U.S. Environmental Protection Agency for lead in public drinking water, as the tap water standard takes into account lead that can leach from pipes.

Juice and Candy

The FDA has issued recommended guidelines to industry on specific foods and drinks more likely to be consumed by small children, including limiting lead in candy to a maximum level of 0.1 ppm and in juice to 50 ppb.

Reference:

1. Flora S.J.S. Nutritional components modify metal absorption, toxic response and chelation therapy. J. Nutr. Environ. Med. 2002; 12:53–67. doi: 10.1080/13590840220123361. 

2. Abadin H., Ashizawa A., Stevens Y.W., Llados F., Diamond G., Sage G., Quinones A., Bosch S.J., Swarts S.G. Toxicological Profile for Lead, Atlanta (GA): Agency for Toxic Substances and Disease Registry (US) Lewis Publishers; Boca Raton, FL, USA: 2007. 

3. Yuan G., Dai S., Yin Z., Lu H., Jia R., Xu J., Song X., Li L., Shu Y., Zhao X. Toxicological assessment of combined lead and cadmium: Acute and sub-chronic toxicity study in rats. Food Chem. Toxicol. 2014;65:260–268. doi: 10.1016/j.fct.2013.12.041. 

4. Cobbina S.J., Chen Y., Zhou Z., Wu X., Zhao T., Zhang Z., Feng W., Wang W., Li Q., Wu X., et al. Toxicity assessment due to sub-chronic exposure to individual and mixtures of four toxic heavy metals. J. Hazard. Mater. 2015;294:109–120. doi: 10.1016/j.jhazmat.2015.03.057. 

5. Shaban El-Neweshy M., Said El-Sayed Y. Influence of vitamin C supplementation on lead-induced histopathological alterations in male rats. Exp. Toxicol. Pathol. 2011;63:221–227. doi: 10.1016/j.etp.2009.12.003. 

6. Abdou H.M., Hassan M.A. Protective role of omega-3 polyunsaturated fatty acid against lead acetate-induced toxicity in liver and kidney of female rats. BioMed Res. Int. 2014;2014:435857. doi: 10.1155/2014/435857.

7. Carocci A., Catalano A., Lauria G., Sinicropi M.S., Genchi G. Lead toxicity, antioxidant defense and environment. Rev. Environ. Contam. Toxicol. 2016; 238: 45–67.

8. Mahaffey KR. Environmental lead toxicity: nutrition as a component of intervention. Environ Health Perspect. 1990;89:75–78.

9. Rubin R, Strayer DS. Rubins pathology; Clinicopathologic Foundations of Medicine. 5th ed. Lippincot Williams & Wilkins; 2008. Environmental and Nutritional pathology.

10. Advisory Committee on Childhood Lead Poisoning Prevention (ACCLPP)”. CDC. 2012 Retrieved 19 sept. 2014.

11. Rossi E. Low Level Environmental Lead Exposure - A Continuing Challenge. Clin Biochem Rev. 2008;29:63–70.

Copper Toxicity In Food

 

Copper 

            Copper is a metallic element that occurs naturally as the free metal, or associated with other elements in compounds that comprise various minerals. Most copper compounds occur in +1 Cu(I) and +2 Cu(II) valence states. Copper is primarily used as a metal or an alloy (e.g., brass, bronze, gun metal). Copper sulfate is used as a fungicide, algicide, and nutritional supplement.

Sources of exposure

          Copper particulates are released into the atmosphere by windblown dust; volcanic eruptions; and anthropogenic sources, primarily copper smelters and ore processing facilities. Copper particles in the atmosphere will settle out or be removed by precipitation, but can be resuspended into the atmosphere in the form of dust.

Copper is released into waterways by natural weathering of soil and rocks, disturbances of soil, or anthropogenic sources (e.g., effluent from sewage treatment plants).

The general population is exposed to copper through inhalation, consumption of food and water, and dermal contact with air, water, and soil that contains copper. The estimated daily intake of copper from food is 1.0–1.3 mg/day for adults.

Drinking water is the primary source of excess copper. Populations living near sources of copper emissions, such as copper smelters and refineries and workers in these and other industries may also be exposed to high levels of copper in dust by inhalation. Copper concentrations in soils near copper emission sources could be sufficiently high to result in significantly high intakes of copper in young children who ingest soil. For example, copper concentrations of 2,480–6,912 ppm have been measured near copper smelters. These levels of copper in soils would result in the intake of 0.74– 2.1 mg copper per day in a child ingesting 300 mg of soil.

Health effects

          Copper is an essential nutrient that is incorporated into a number of metalloenzymes involved in hemoglobin formation, drug/xenobiotic metabolism, carbohydrate metabolism, catecholamine biosynthesis, the cross-linking of collagen, elastin, and hair keratin, and the antioxidant defence mechanism.

            Copper-dependent enzymes, such as cytochrome c oxidase, superoxide dismutase, ferroxidases, monoamine oxidase, and dopamine β-monooxygenase, function to reduce activated oxygen species or molecular oxygen. Symptoms associated with copper deficiency in humans include normocytic, hypochromic anemia, leukopenia, and osteoporosis.

            Copper homeostasis plays an important role in the prevention of copper toxicity, exposure to excessive levels of copper can result in a number of adverse health effects including liver and kidney damage, anemia, immunotoxicity, and developmental toxicity. Many of these effects are consistent with oxidative damage to membranes or macromolecules. Copper can bind to the sulfhydryl groups of several enzymes, such as glucose-6-phosphatase and glutathione reductase, thus interfering with their protection of cells from free radical damage.

One of the most commonly reported adverse health effect of copper is gastrointestinal distress. Nausea, vomiting, and/or abdominal pain in humans ingesting beverages contaminated with copper or water containing copper sulfate.

Copper is also irritating to the respiratory tract. Coughing, sneezing, runny nose, pulmonary fibrosis, and increased vascularity of the nasal mucosa have been reported in workers exposed to copper dust.

The liver is also a sensitive target of toxicity. Liver damage (necrosis, fibrosis, abnormal biomarkers of liver damage) have been reported in individuals ingesting lethal doses of copper sulfate. Liver effects have also been observed in individuals diagnosed with Wilson’s disease, Indian childhood cirrhosis, or idiopathic copper toxicosis (which includes Tyrollean infantile cirrhosis). These syndromes are genetic disorders that result in an accumulation of copper in the liver; the latter two syndromes are associated with excessive copper exposure.

There is some evidence from animal studies to suggest that exposure to airborne copper or high levels of copper in drinking water can damage the immune system. Impaired cell-mediated and humoral-mediated immune function have been observed in mice. Studies in rats, mice, and mink suggest that exposure to high levels of copper in the diet can result in decreased embryo and fetal growth.

Prevention and control

People can prevent copper toxicity by:           

Limiting exposure to copper from contaminated food and drinks, avoiding the use of corroded or rusted copper cookware, dishes, and utensils.

Installing filters in the house that remove unwanted minerals from water sources

 Reference:

1. Mason KE. A conspectus of research on copper metabolism and requirements of man. J Nutr. 1979 Nov; 109(11):1979-2066.
2. Tapiero H, Townsend DM, Tew KD. Trace elements in human physiology and pathology. Copper. Biomed Pharmacother. 2003 Nov; 57(9):386-98.
3. Gamakaranage CS, Rodrigo C, Weerasinghe S, Gnanathasan A, Puvanaraj V, Fernando H. Complications and management of acute copper sulphate poisoning; a case discussion. J Occup Med Toxicol. 2011 Dec 19; 6(1): 34.
4. Fuentealba IC, Aburto EM. Animal models of copper-associated liver disease. Comp Hepatol. 2003 Apr 03; 2(1):5.
5. Sinkovic A, Strdin A, Svensek F. Severe acute copper sulphate poisoning: a case report. Arh Hig Rada Toksikol. 2008 Mar; 59(1): 31-5

Food Fraud - Chemical Hazard: Melamine

Food Fraud - Chemical Hazard: Melamine

 

Melamine

Melamine is a synthetic triazine compound and an organic base with the chemical name 2,4,6-triamino-1,3,5-triazine and is high in nitrogen (C3N6H6).

Melamine is widely used in plastics, adhesives, countertops, dishware and whiteboards.

Sources and Occurrence in Foods: Melamine contamination in food first became a food safety issue when the chemical was detected in pet foods. An investigation showed that melamine was found in wheat gluten and protein concentrate exported from China and was used as a thickening and binding agent within the pet food.

It has also been found in animal feed samples, orange juice and coffee. In 2008 it was also found in dairy products from China, an example being powdered milk to make infant formula.

Melamine is illegally added to inflate the apparent protein content of food products. Because it is high in nitrogen, the addition of melamine to a food artificially increases the apparent protein content as measured with standard tests. This would give a falsely high result in tests designed to determine protein content and cause the material to be assigned a higher quality rating and commercial value (food fraud). It has been estimated that the addition of 1 g of melamine to 1 litre of milk would raise the apparent protein content by approximately 0.4%.

It may also come from other sources especially plastic packaging or processing equipment but usually only at levels not harmful to health.

Effects on Health: Data from animal studies can be used to predict adverse health effects. Melamine alone causes bladder stones in animal tests. When combined with cyanuric acid, which may also be present in melamine powder, melamine can form crystals that can give rise to kidney stones. Acute renal failure or confirmed renal stones

These small crystals can also block the small tubes in the kidney potentially stopping the production of urine, causing kidney failure and, in some cases, death. Melamine has also been shown to have carcinogenic effects in animals in certain circumstances, but there is insufficient evidence to make a judgement on carcinogenic risk in humans.

Symptoms and signs of melamine poisoning include irritability, blood in urine, little or no urine, signs of kidney infection and high blood pressure.

Melamine being recognized as a contaminant, Codex has specified the following maximum limits for melamine in various foods:

Food (other than infant formula) : 2.5 mg/kg  

Powdered infant formula: 1 mg/kg  

Liquid infant formula: 0.15 mg/kg

Control Measures:

Sourcing

Food manufacturers should exercise caution when souring ingredients. Traceability to the point of origin is essential. Materials such as milk powder, dried egg powder and high-protein ingredients should be purchased only from known low-risk sources.

Testing

The only practical control for Melamine in foods at present, other than careful sourcing, is testing analysis of all ingredients that carry a risk of contamination.

Chemical Hazard: Dioxins and PCB’s (Polychlorinated biphenyls)

Chemical Hazard: Dioxins and PCB’s (Polychlorinated biphenyls)

 

Dioxins and PCB’s (Polychlorinated biphenyls)

Dioxins are colorless, odorless organic compounds containing carbon, hydrogen, oxygen and chlorine. Dioxins are ubiquitous environmental contaminants that have been found in soil, surface water, sediment, plants and animal tissue worldwide. They are highly persistent in the environment.

PCB’s or Polychlorinated biphenyls, are chlorinated aromatic hydrocarbons and are produced by the direct chlorination of biphenyls. Like dioxins PCB’s are widespread environmental contaminants and are very persistent in soil and sediments.

Dioxins and PCB’s have a broad range of toxic and biochemical effects and some are classified as human carcinogens.

Occurrence in Foods: Dioxins and PCB’s enter the food chain through a variety of routes. Grazing animals and growing vegetables may be exposed directly or indirectly to these contaminants in the soil.

Leafy vegetables, pasture and roughage can also become contaminated through airborne transport of dioxins and PCB’s.

A significant percentage of paper food packaging materials also contain PCB’s which have the potential to migrate to the packaged food.

Extensive stores of PCB-based waste industrial oils, many with high levels of PCDFs, exist throughout the world. Long-term storage and improper disposal of this material may result in dioxin release into the environment and the contamination of human and animal food supplies.

Dioxins are mainly by-products of industrial processes but can also result from natural processes, such as volcanic eruptions and forest fires. Dioxins are unwanted by-products of a wide range of manufacturing processes including smelting, chlorine bleaching of paper pulp and the manufacturing of some herbicides and pesticides. 

 Effects on Health:

 Humans accumulate dioxins in fatty tissue mostly by eating dioxin contaminated foods. The toxicity of dioxins is related to the amount accumulated in the body during the lifetime.

Once dioxins enter the body, they last a long time because of their chemical stability and their ability to be absorbed by fat tissue, where they are then stored in the body. Their half-life in the body is estimated to be 7 to 11 years. In the environment, dioxins tend to accumulate in the food chain. The higher an animal is in the food chain, the higher the concentration of dioxins.

Short-term exposure of humans to high levels may result in skin lesions, such as chloracne and patchy darkening of the skin and altered liver function.

Dioxins and PCBs are found at low levels in many foods. Longer-term exposure to these substances has been shown to cause a range of adverse effects on the nervous, immune and endocrine systems, and impair reproductive function. They may also cause cancer. Their persistence and the fact that they accumulate in the food chain, notably in animal fat, therefore continues to cause some safety concerns

The developing foetus is the most sensitive to dioxin exposure. New-born with rapidly developing organ systems may also be more vulnerable to certain effects

Prevention and control of dioxin exposure

 Proper incineration of contaminated material is the best available method of preventing and controlling exposure to dioxins. It can also destroy PCB-based waste oils. The incineration process requires high temperatures, over 850°C. For the destruction of large amounts of contaminated material, even higher temperatures - 1000°C or more - are required.

 Prevention or reduction of human exposure is best done via source-directed measures, i.e. strict control of industrial processes to reduce formation of dioxins as much as possible. This is the responsibility of national governments. The Codex Alimentarius Commission adopted a Code of Practice for Source Directed Measures to Reduce Contamination of Foods with Chemicals (CAC/RCP 49-2001) in 2001. Later in 2006 a Code of Practice for the Prevention and Reduction of Dioxin and Dioxin-like PCB Contamination in Food and Feeds (CAC/RCP 62-2006) was adopted.

 Most of human exposure to dioxins is through the food supply, mainly meat, dairy products, fish and shellfish. Protecting the supply chain is one of the most important factors.

Food and feed contamination monitoring systems must be in place to ensure that tolerance levels are not exceeded.

Avoid those areas with increased dioxin contamination due to local emission, accidents or illegal disposal of contaminated materials that are used for grazing or for the production of feed crops. If possible, contaminated soil should be treated and detoxified or removed and stored under environmentally sound conditions.

Limits for dioxins and PCBs set out in EC regulation No. 1881/2006
Foodstuff	Maximum levels (sum of dioxins)	Maximum levels (sum of dioxins and dioxin like PCBs)
Meat from Bovine animals and Sheep	3.0 pg per g of fat	4.5 pg per g of fat
Meat from Poultry	2.0 pg per g of fat	4.0 pg per g of fat
Meat from Pigs	1.0 pg per g of fat	1.5 pg per g of fat
Muscle meat of fish and fishery products	4.0 pg per g of fat	8.0 pg per g of fat
Hen Eggs and Egg products	3.0 pg per g of fat	6.0 pg per g of fat
Vegetable oils and fats	0.75 pg per g of fat	1.5 pg per g of fat