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

ARSENIC - METAL CONTAMINANT IN FOOD

ARSENIC - METAL CONTAMINANT IN FOOD

 

Arsenic is a naturally occurring element in the environment that can enter the food supply through soil, water or air. It has also been known to be used by farmers as a pesticide and a fertilizer.

Arsenic is a widely found contaminant which occurs both naturally and as a result of human activity.

Arsenic is a metalloid that occurs in different inorganic and organic – i.e. containing carbon – forms. These are found in the environment both from natural occurrence and from anthropogenic activity. The inorganic forms of arsenic are more toxic as compared to the organic arsenic.

 Sources of exposure

 Food, particularly grain-based processed products such as wheat bread, rice, milk, dairy products and drinking water are the main sources.

Fish, shellfish, meat and poultry can also be dietary sources of arsenic, although exposure from these foods is generally much lower compared to exposure through contaminated groundwater. In seafood, arsenic is mainly found in its less toxic organic form.

Acceptance level of Natural mineral water is 0.01 mg/L.

 Health effects

Acute effects: The immediate symptoms of acute arsenic poisoning include vomiting, abdominal pain and diarrhoea. These are followed by numbness and tingling of the extremities, muscle cramping and death, in extreme cases.

Long-term effects: The main adverse effects reported to be associated with long term ingestion of inorganic arsenic in humans are: skin lesions, cancer, developmental toxicity, neurotoxicity, cardiovascular diseases, abnormal glucose metabolism and diabetes.

Inorganic arsenic exposure in utero and in the very young is associated with impaired intellectual development, such as decreased performance on certain developmental tests that measure learning. For this reason, the FDA prioritizes monitoring and regulating products that are more likely to be consumed by very young children.

Arsenic is also associated with adverse pregnancy outcomes and infant mortality, with impacts on child health (1), and exposure in utero and in early childhood has been linked to increases in mortality in young adults due to multiple cancers, lung disease, heart attacks, and kidney failure (2). Numerous studies have demonstrated negative impacts of arsenic exposure on cognitive development, intelligence, and memory (3).

 Prevention and control

Substitute high-arsenic sources, such as groundwater, with low-arsenic, microbiologically safe sources such as rain water and treated surface water. Low-arsenic water can be used for drinking, cooking and irrigation purposes, whereas high-arsenic water can be used for other purposes such as bathing and washing clothes.

• Discriminate between high-arsenic and low-arsenic sources. For example, test water for arsenic levels and paint tube wells or hand pumps different colours. This can be an effective and low-cost means to rapidly reduce exposure to arsenic when accompanied by effective education.
• Blend low-arsenic water with higher-arsenic water to achieve an acceptable arsenic concentration level.
• Install arsenic removal systems – either centralized or domestic – and ensure the appropriate disposal of the removed arsenic. Technologies for arsenic removal include oxidation, coagulation-precipitation, absorption, ion exchange, and membrane techniques. There is an increasing number of effective and low-cost options for removing arsenic from small or household supplies, though there is still limited evidence about the extent to which such systems are used effectively over sustained periods of time.

Reference:

1. Association of arsenic with adverse pregnancy outcomes/infant mortality: a systematic review and meta-analysis. Quansah R, Armah FA, Essumang DK, Luginaah I, Clarke E, Marfoh K, et al. Environ Health Perspect. 2015; 123 (5): 412-21.

2.  In utero and early life arsenic exposure in relation to long-term health and disease.
Toxicol Appl Pharmacol. Farzan SF, Karagas MR, Chen Y. 2013; 272 (2):384-90.

3. The developmental neurotoxicity of arsenic: cognitive and behavioral consequences of early life exposure. Tolins M, Ruchirawat M, Landrigan P. Ann Glob Health. 2014; 80 (4):303-14.

4. Food Safety and Standards (Contaminants, toxins and Residues) Regulations, 2011

Chemical Hazard: Ciguatera Toxin

Chemical Hazard: Ciguatera Toxin

 

 

Ciguatera toxin is a heat-stable lipid soluble compound, produced by dinoflagellates and concentrated in fish organs, it is odourless and tasteless.

The dinoflagellates are single-celled eukaryotes constituting the phylum Dinoflagellata. Usually considered algae, dinoflagellates of the genus Gambierdiscus (Gambierdiscus toxicus) are mostly marine plankton, but they also are common in freshwater habitats (1-3).

 

Ciguatera toxin tends to accumulate in large predator fish (weight over 2 Kg or about 4.5 lbs), such as the barracuda and other carnivorous reef fish, because they eat other fish that consume toxin-producing alga, which live in coral reef waters. The toxin has highest concentrations in fish visceral and sex organs. The areas of concern for Ciguatera toxin include the Caribbean Sea, Hawaii and coastal Central America.

Pathogenicity: Eating ciguatera-contaminated tropical or subtropical fish is the main way that humans are exposed to the toxin.

Limits in food: In the EU, legislation covering fishery products states that “fishery products containing biotoxins such as ciguatera toxins” cannot be placed on the market, but no methods of analysis are given. In the USA no action limits have so far been established. However, the FDA has proposed guidance levels of <0.1μg kg -1 C-CTX-1 equivalents and <0.01μg kg -1 P-CTX-1 equivalents.

 Sources: This toxin is found in fish most commonly, barracuda, grouper, red snapper, eel, amberjack, sea bass and Spanish mackerel.

 Illness, Symptoms and Complications: Gastrointestinal symptoms and signs (e.g. vomiting, diarrhea, abdominal pain, nausea) develop within 6–24 hours of eating a reportedly good-tasting reef fish.

Cardiac signs may include hypotension and bradycardia, and may necessitate urgent medical care.

Severe cases of ciguatera poisoning may result in shortness of breath, salivation, tearing, chills, rashes, itching, and paralysis.

Neurologic symptoms vary among patients and include the following: paresthesias (numbness and tingling) in the extremities (feet and hands) and oral region, generalized pruritis (itching), myalgia (muscle pain), arthralgia (joint pain), and fatigue. 

Death due to heart or respiratory failure occurs in rare cases.

 Controls to reduce the risk:

For food manufacturers it can be difficult to control or prevent ciguatera toxin within fish products as it is odourless, tasteless and toxic fish cannot be identified by appearance or behaviour. It is also heat stable so cooking, boiling or any other heat treatment will not destroy it (4).

 Testing

The FDA fish testing procedure is a two-tiered protocol involving: 1) in vitro assay, i.e. a high-throughput screen for toxicity consistent with ciguatoxin’s mode of action; and 2) an analytical chemistry technique known as liquid chromatography-mass spectrometry (LC-MS).

 Reference

1. Yasumoto T, Nakajima I, Bagnis R, Adachi R. Finding of a dinoflagellate as a likely culprit of ciguatera. Jpn Soc Sci Fish. 1977; 43: 1021–1026.
2. Cameron J. Effects of ciguatoxin on nerve excitability in rats (part I) J Neurol Sci. 1991; 101:87–92. 
3. Mattei C, Dechraoui MY, Molgó J, Meunier FA, Legrand AM, Benoit E. Neurotoxins targetting receptor site 5 of voltage-dependent sodium channels increase the nodal volume of myelinated axons. J Neurosci Res. 1999; 55: 666–673.
4. Bagnis R. In: Algal toxins in seafood and drinking water. Falconer I, editor. Academic Press; London: 1993. pp. 105–115.

Chemical Hazard: Acrylamide

Chemical Hazard: Acrylamide

 

Acrylamide

 Acrylamide is a chemical that naturally forms in starchy food products during high-temperature cooking, including frying, baking, roasting and also industrial processing, at 120°C (248°F) and above, and at low moisture.

The main chemical process that causes this is known as the Maillard Reaction; it is the same reaction that ‘browns’ food and affects its taste.

Acrylamide forms from sugars and an amino acid (asparagine) during certain types of high-temperature cooking, such as frying, roasting, and baking (1, 2).

 Occurrence in Foods: Main sources of acrylamide in the diet includes potato products such as fried potatoes, chips and crisps.

Breakfast cereals, bread, biscuits and pastries. Roasted and ground coffee have all also been found to be sources.

Effects on Health: At high levels Acrylamide is a neurotoxin and exposure to these high levels may cause symptoms such as numbness in the hands and feet.

Studies have shown that acrylamide can be carcinogenic in animals (3-5). It may also adversely affect the nervous system, pre-and post-natal development and male reproduction.

Acrylamide caused cancer in animals in studies where animals were exposed to acrylamide at very high doses. In 2010, the Joint Food and Agriculture Organization/World Health Organization Expert Committee on Food Additives (JECFA) concluded that acrylamide is a human health concern, and suggested additional long-term studies.

 Control Measures:

 Processing

Frying, Baking and Roasting at lower temperatures and for shorter times reduce the amount of browning of the product and reduce the amount of acrylamide produced. Some crisp manufacturers have altered frying times and temperature to help with this reduction.

Providing appropriate cooking instructions on frozen French fry packages to guide final preparation by consumers and food service operators may help reduce acrylamide.

Potato Products

Selecting potato varieties that are low in acrylamide precursors, keeping in mind seasonal variation, may help with reduction.

Using treatments to reduce sugar levels may help reduce acrylamide.

Cereal Based Products

Replacing ammonium bicarbonate in cookies and crackers with alternative leavening agents while avoiding overall increases in sodium levels may help to reduce acrylamide levels.

Coffee Products

Manufacturers should identify the critical roast conditions to ensure minimal acrylamide formation within the target flavour profile.

Acceptable Limits/Levels according to Commission Regulation (EU) 2017/2158)
Food	Benchmark Level [μg/kg]
French Fries (Ready to Eat)	500
Potato Crisps from fresh potatoes and from potato dough. Potato based crackers and other potato products from potato dough	750
Soft Bread • Wheat based bread • Soft bread other than wheat based bread	50 100
Breakfast Cereals (excluding porridge) • Bran products and whole grain cereals, gun puffed grain • Wheat and rye based products • Maize, oat, spelt, barley and rice based products	300 300 150
Biscuits and wafers Crackers with the exception of potato based crackers Crispbread Ginger Bread Products similar to the other products in this category	350 400   350 800 300
Roast Coffee	400
Instant Soluble coffee	850
Coffee Substitutes • Coffee substitutes exclusively from cereals • Coffee substitutes from a mixture of cereals and chicory • Coffee substitutes exclusively from chicory	500 (2) 4000
Baby foods, processed cereal based foods for infants and young children excluding biscuits and rusks	40
Biscuits and rusks for infants and young children	150

Reference

1.      Tareke E, Rydberg P, Karlsson P, Eriksson S, Tornqvist M. Analysis of acrylamide, a carcinogen formed in heated foodstuffs. Journal of Agricultural and Food Chemistry 2002; 50(17):4998–5006.

2.      Mojska H, Gielecinska I, Szponar L. Acrylamide content in heat-treated carbohydrate-rich foods in Poland. Roczniki Panstwowego Zakladu Higieny 2007; 58(1):345–349.

3.      Fuhr U, Boettcher MI, Kinzig-Schippers M, et al. Toxicokinetics of acrylamide in humans after ingestion of a defined dose in a test meal to improve risk assessment for acrylamide carcinogenicity. Cancer Epidemiology Biomarkers and Prevention 2006; 15(2):266–271.

4.      Fennell TR, Friedman MA. Comparison of acrylamide metabolism in humans and rodents. Advances in experimental medicine and biology 2005; 561:109-116.

5.      Gargas ML, Kirman CR, Sweeney LM, Tardiff RG. Acrylamide: Consideration of species differences and nonlinear processes in estimating risk and safety for human ingestion. Food and chemical toxicology 2009; 47(4):760-768.