Acrylamide – nothing seems to help

French fries a large contributor to acrylamide exposure (Photo: freephotouk)

Acrylamide is a chemical compound that typically forms in starchy foods during frying, baking, roasting and grilling. It is linked to the browning of food during the so called Maillard reactions. The darker the food the more acrylamide seems to be formed. It was found in food by coincidence in 2002 when examining a leak of the industrial chemical polyacrylamide from a tunnelling project in the south of Sweden. It was first thought to be an environmental contaminant. It has since been shown to actually be a process contaminant formed in food during dry heating, but not boiling.

Acrylamide received a lot of attention among scientists and the popular press over the first years of its discovery. Industry started programs to attempt to reduce its formation and household cooking instructions were issued. The toxicity of the compound was explored in more detail.

Toxic properties

The toxic effects of acrylamide in industrial exposure and in smokers have been known for some time and include damage to the nervous system and to male fertility. However, looking at potential food exposure, the Food and Agriculture Organization of the United Nations and the World Health Organization concluded that the levels required to observe such effects was 500 to 2,000 times higher than the average dietary exposure of acrylamide. From this, they concluded that acrylamide levels in food were safe in terms of neuropathy and infertility, but raised concerns over human carcinogenicity based on known carcinogenicity in laboratory animals.

Checking your consumption patterns (Photo: mikeandanna)

Attempts to confirm a cause and effect relationship in humans between acrylamide exposure and cancer is on-going. A number of epidemiological studies have looked at the correlation between acrylamide intake through food frequency questionnaires and a range of different cancers. Many studies proved negative, but there were indications that dietary acrylamide could be associated with the formation of myeloma, head-neck cancer, oesophageal cancer, endometrial cancer and ovarian cancer.

Now there is documentation of a further effect. A new report published on 23 October 2012 described maternal exposure to acrylamide and birth weight of children. A team led by Marie Pedersen from the Centre for Research in Environmental Epidemiology (CREAL), Spain, measured blood levels of acrylamide and its common metabolite glycidamide and found that dietary exposure to acrylamide while pregnant resulted in reduced birth weight and head circumference in the off-spring. The authors pointed to a potentially substantial public-health implication of their findings since reduced birth head circumference has been associated with delayed neurodevelopment.

Attempts to reduce acrylamide formation

Acrylamide forms from sugars and an amino acid (asparagine) during high-temperature processing of plant foods in particular such as potato crisps, French fries, bread, biscuits and coffee. In a report published by the European Food Safety Authority (EFSA) in 2011, fried potatoes (including French fries), roasted coffee and soft bread were identified as the major contributors to acrylamide exposure in adults, while fried potatoes, potato crisps, biscuits and soft bread were identified as the major contributors to exposure in adolescents and children. The exposure estimates for these different age groups in Europe were comparable to those previously reported in scientific literature and in risk assessments carried out by the Joint FAO/WHO Expert Committee on Food Additives (JECFA).

The food industry has been exploring ways of reducing acrylamide levels in foods without reducing desirability and taste, including using lower cooking temperatures and adding enzymes to reduce the amount of acrylamide that forms during cooking. The industry in Europe developed a “tool box” containing advice on how to reduce acrylamide formation.  Many of the recommendations should have been adopted by now. It seems the process changes have had limited success. An EFSA report published on 23 October 2012 showed only very limited changes in acrylamide levels between 2007 and 2010 in most food groups. With some good will slightly reduced acrylamide levels could be seen in some cereal-based foods for children and non-potato savoury snacks but on the contrary  acrylamide seemed to increase in coffee and coffee substitutes, crisp bread and some types of French fries.

What is the consumer to do?

Coffee – to drink or not to drink? (Photo: arimoore)

If the industry is mainly failing in their attempts to reduce acrylamide levels in food what is the consumer to do? We could of course just give up. A more sensible approach would be to be a bit more careful when heating food since acrylamide formation increases with increased heat. If toasting bread, make it only golden brown. Equally be careful with the French fries. Although coffee might delay the development of Alzheimer’s disease, it is also a major contributor to acrylamide exposure. Not an easy choice.

Up in flames

Flame retardants are supposed to stop fires

On 19 October 2012, the European Food Safety Authority (EFSA) published the last of a series of six opinions covering brominated flame retardants (BFRs). Since 2010, the Panel on Contaminants in the Food Chain (CONTAM) has reviewed the available toxicological data and sparse information in relation to dietary exposure for the BFRs. Three of the BFRs belong to the “nasty nine” chemicals added to the previous “dirty dozen” list of restricted or banned toxic chemicals by a United Nations treaty. They are all persistent organic pollutants or POPs. But first a bit of background.

Collusion to introduce flame retardants

Of course fire should be avoided at all cost, or should it? In an interesting piece of investigative journalism, the Chicago Tribune revealed in mid 2012 how tobacco companies, worried about cigarettes causing fires, championed the treatment of furniture with fire retardants. With couches, chairs and many other products packed with fire retardants, it has been shown that American babies carry the highest levels of flame retardants among infants in the world. But flame retardants can be found all over the world. In 1999, Swedish researchers reported that flame retardant levels in women’s breast milk had increased 60-fold between 1972 and 1997. And some of the chemicals have been linked to cancer, neurological disorders and developmental problems, whilst not even providing effective fire protection according to the Chicago Tribune story.

Since the 1970s manufacturers have repeatedly withdrawn flame retardants amid health concerns. Some have been banned by the United Nations treaty that seeks to eliminate the worst chemicals in the world (the “dirty dozen” and “nasty nine”). Although demand for brominated and chlorinated flame retardants in North America and the European Union is declining, it is still rising in many other regions.

What are flame retardants?

Electronics, furniture and clothes can all be treated with BFRs

There are numerous chemicals that manufacturers use to try to reduce the flammability of all sorts of products, including furniture, textiles, electronics, baby car seats and carpets. Based on their chemical structures, flame retardants can fit into one of several categories, with some categories raising more health concerns than others. Mineral and organophosphate flame retardants have raised less concerns while halogenated compounds, like chlorinated and brominated flame retardants, are the most worrying because they accumulate in human tissues and have a long half-life.

Brominated flame retardants are mixtures of a large range of man-made organobromide compounds that are supposed to inhibit the ignition of combustible materials. Of the commercialised chemical flame retardants, the brominated varieties are the most widely used. They are most effective in plastics and textile applications, e.g. electronics, clothes and furniture.

Actions taken to reduce risks

The earliest flame retardants, polychlorinated biphenyls (PCBs) were banned in 1977 when it was discovered that they were toxic. That’s when industries shifted to using brominated flame retardants instead, but then these started to receive closer scrutiny. Now several brominated flame retardants have been gradually banned in the European Union from 2006 and some have been excluded from the US market by an agreement between the government and industry to be fully implemented by the end of 2013.

Aquatic animals contaminated with BFRs

So has the problem disappeared? The simple answer is no since due to their persistence in the environment there are still concerns about the risks these chemicals can pose to public health. BFR-treated products from the past, whether still in use or discarded, leach BFRs into the environment. At home, house dust can become contaminated by the chemicals from treated foam in furniture and other household objects and pose a particular risk to young children. In nature, contamination of water can lead to accumulation of BFRs in aquatic organisms in particular. Studies have found that these chemicals can be found in fish and other seafood as well as in human blood, urine and breast milk.

Monitoring the situation in Europe

In order to assess the need for further regulatory measures for BFRs, the European Commission asked EFSA to assess the risks related to the presence of brominated bisphenols (PBBs), diphenyl ethers (PBDEs), cyclododecanes (HBCDDs), tetrabromobisphenol A (TBBPA), phenols and phthalic acid derivatives in food.

In October 2010, the CONTAM Panel concluded that the risk to the European population from exposure to PBBs through food was of no concern. Since PBBs are no longer produced or used in Europe and taking into account low and declining environmental concentrations, the CONTAM Panel concluded that PBBs are a low priority for further research or monitoring efforts.

In May 2011, the Panel in assessing the risk related to the presence of PBDEs in food, considered that there might be a potential health concern for young children for one of the compounds in the group. However, other compounds were unlikely to raise health concerns. Nevertheless, since numerous products containing PBDEs are still in use, the Panel recommended that the surveillance of PBDEs should continue.

In July 2011, in its third opinion on BFRs, the Panel concluded that current dietary exposure to HBCDDs in the EU does not raise a health concern. Furthermore, additional exposure, particularly of young children, to HBCDDs from house dust is unlikely to raise a health concern.

In December 2011, the CONTAM Panel published its review of TBBPA and its derivatives in food. These compounds are widely used as flame retardants and can influence thyroid hormone homeostasis. TBBPA is primarily used as reactive flame retardant covalently bound to epoxy and polycarbonate resins. TBBPA derivatives are used as either reactive or additive intermediates in polymer manufacture. Samples tested for TBBPA in fish and other seafood were all negative.  The CONTAM Panel concluded that current dietary exposure to TBBPA in the European Union does not raise a health concern. Equally, other exposure sources for young children like house dust was unlikely to raise a health concern.

In April 2012, the Panel published an opinion on a complex group of compounds called brominated phenols that are used as reactive as well as additive flame retardants in a large range of resins and polyester polymers. The opinion focused on 2,4,6-TBP, but even for this compound there were limitations in the current knowledge. The CONTAM Panel concluded that even for high consumers of fish, molluscs and crustaceans a health concern was unlikely. Due to lack of data a risk assessment of other brominated phenols or their derivatives was not possible.

In October 2012, the Panel finally considered emerging and novel BFRs. Information on 17 emerging and 10 novel BFRs was collected. The information varied widely for these BFRs. Due to the very limited information on occurrence, exposure and toxicity, the CONTAM Panel could not perform a risk characterisation for any of the BFRs considered. Instead, an attempt was made to identify those BFRs that could be a potential health concern and should be considered first for future investigations. There was convincing evidence that tris(2,3-dibromopropyl) phosphate (TDBPP) and dibromoneopentyl glycol (DBNPG) are genotoxic and carcinogenic, warranting further surveillance of their occurrence in the environment and in food. Based on the limited experimental data on environmental behaviour, 1,2-bis(2,4,6-tribromophenoxy)ethane (BTBPE) and hexabromobenzene (HBB) were identified as compounds that could raise a concern for bioaccumulation. A modelling exercise identified ten additional BFRs that should be subjected to further in-depth studies.

What about the rest of the world?

Europe might be a little better off than the rest of the world (Photo: shaire productions)

Although not completely off the hook, the situation in Europe in relation to BFRs seems to be under control. There are some new BFRs that might be a problem, but the current information is insufficient to be able to draw any conclusions. But the rest of the world is much more vulnerable. Some efforts in the USA might improve their situation. The US Environment Protection Agency is concerned that certain PBDE congeners are persistent, bioaccumulative, and toxic to both humans and the environment. They state that the critical endpoint of concern for human health is neurobehavioral effects. Various PBDEs have also been studied for ecotoxicity in mammals, birds, fish, and invertebrates. In some cases, current levels of exposure for wildlife may be at or near adverse effect levels.

Better brainwaves on the loo

Coffee consumption might be beneficial after all (Photo: uzagaku – Flickr)

Apologies for the association, but this post is about a possible diuretic that potentially might improve your brain function according to recent research. We are talking about the assumed effects of consuming coffee and similar beverages. You would have thought that by now the effects of caffeine and related methylxanthine compounds on the human body would be clear. But there are still conflicting opinions in the literature. From mainly negative reporting of gastric ulcers and cardiovascular disease, the situation changed when in 2008 a Harvard-led study reported finding no detrimental effects of consuming up to six cups of coffee a day using 130,000 study subjects.

Coffee consumption

Caffeine, with the full chemical name of 1,3,7-trimethylxanthine, and the related methylxanthines theobromine and theophylline, can be found naturally in the leaves, seeds, and fruits of more than 60 plants, including coffee, tea leaves, kola nuts, guarana, and cocoa beans. Coffee is one of the most widely consumed beverages in the world, and the most commonly consumed psychoactive drug with a production of about 7.4 million tons per year.

The people of Finland are among the biggest coffee consumers in the world. Finns consume an average of 12 kilograms of coffee per capita yearly or 4-5 large cups a day, which is over twice the amount of most other Europeans. Only tiny Luxembourg exceeded this number, with an average consumption of close to 17 kg per year. It might have been expected that countries like Italy or France would be at the top of coffee consumption charts with their famous high quality coffees. However, the French and the Italians only consume an average of 5 kg of coffee per year, slightly higher than the 4 kg in the USA.

Influence on memory

It is clear that caffeine is a psychoactive stimulant drug that influences brain chemistry. It mimics adenosine by binding to adenosine receptors and thus blocking the effects of adenosine, which happens to be to slow down nerve impulses and cause drowsiness. So the brain becomes more alert. Caffeine also increases the levels of dopamine in the brain, which improves the feeling of well-being and mood. But what about memory? Here it is not so clear with studies of short-term and long-term memory showing positive, negative, and no effects at all. The research consensus seems to indicate a slight overall inhibitory effect, reducing the capacity of our short-term memory and working memory. Bad luck!

Improved performance in the elderly (Photo: Lucia Whittaker – Flickr)

However, the situation is much more positive for the elderly. For most older adults, memory performance depends on the time of day, with performance being optimal early in the morning and declining during the late afternoon hours. In a study by Ryan and co-workers from the University of Arizona, adults over the age of 65 who considered themselves “morning types” were tested twice over an interval of 5 to 11 days, once in the morning and once in the late afternoon. Participants consumed either coffee with caffeine or decaffeinated coffee at both sessions. Participants who consumed decaffeinated coffee showed a significant decline in memory performance from morning to afternoon. In contrast, those who consumed caffeine showed no decline in performance from morning to afternoon. The results suggested that time-of-day effects may be mediated by nonspecific changes in the level of arousal.

And the diuretic effects?

review of the available literature suggests that acute consumption of 250-300 mg of caffeine, or 2-3 cups of coffee, results in a short-term stimulation of urine output in individuals who have been deprived of caffeine for a period of days or weeks. However, regular coffee consumption quickly leeds to a tolerance and the diuretic effect is much diminished. But we shouldn’t forget the detrusor muscles in the bladder that help determine capacity limits and outputs and might deteriorate with age. Caffeine happens to relax detrusor muscles causing an urgency to urinate. This indirectly compounds the diuretic effects of caffeine. So it might be that the title is correct after all for the elderly.

But there is more

And in even better news, in 2009 researchers in Finland and Sweden reported results from a study that followed over 1,400 people over 20 years, and found that those who drank 3 to 5 cups of coffee a day in their midlife years had a 65% lower chance of developing dementia and Alzheimer’s disease compared with those who reported drinking no coffee at all or only occasionally. This was supported when researchers from the University of South Florida and the University of Miami, published a paper in June 2012 describing how they monitored the memory and thinking processes of 124 people, aged 65 to 88, and found all those with higher blood levels of caffeine (mostly from drinking coffee) avoided the onset of Alzheimer’s disease in the following four years. The same researchers had previously shown that caffeine consumption could reduce blood levels of the beta-amyloid protein that forms into plaques in the brains of people with Alzheimer’s.

Caffeine can hinder degenerative brain changes (Photo:alles-schlumpf – Flickr)

Further, a research team led by Professor Freund from the University of Illinois suggested that caffeine consumption could help to ease cognitive decline and lower the risks of developing Alzheimer’s disease by blocking inflammation in the brain. The team found that mice given caffeine had lower inflammatory markers and recovered the ability to form memories after hypoxia 33% faster than those not given caffeine.

For Parkinson’s Disease, another neurodegenerative disorder, it appears there is also a link between higher coffee consumption and decreased risk. And like Alzheimer’s, this also seems to be due to caffeine, but it is less clear how it works. One study from the University of North Dakota in the USA, suggested that it might be due to an effect of caffeine that preserves the blood-brain-barrier. The findings were supported by a meta-analysis of 26 studies that suggested an inverse association between tea drinking and the chance of developing Parkinson’s disease. For every increase of 300 mg per day in caffeine intake, they found a drop of 24% in the relative risk of developing Parkinson’s.

Possible health claims

The European Food Safety Authority (EFSA) has received several health claims in relation to products containing caffeine. It has rejected claims that cocoa can enhance mood and that black tea can help focus attention because of insufficient evidence presented. However, claims in relation to what was summarised as alertness and attention after consumption of coffee, guarana or caffeine got the thumbs up by the EFSA Panel on Dietetic Products, Nutrition and Allergies. First the Panel considered that increased alertness and increased attention might both be a beneficial physiological effects. Then, in weighing the evidence, the Panel considered that there was good consensus on the role of caffeine in increasing alertness, measured as speed of reaction times, and increasing attention, measured by a range of psychometric tasks, in healthy individuals of both sexes, at doses of at least 75 mg.

On the basis of the data presented, the Panel concluded that a cause and effect relationship has been established between the consumption of caffeine and increased alertness and attention. In order to bear the claim, a product should contain at least 75 mg caffeine per serving. However, the Panel could not refrain from issuing a warning that for children consumption of a dose of 5 mg/kg body weight could result in transient behavioural changes, such as increased arousal, irritability, nervousness or anxiety. In relation to pregnancy and lactation, they stated that moderation of caffeine intake, from whatever source, is advisable.

So how much coffee do you need?

Two daily cups of coffee might be enough (Photo: antwerpenR – Flickr)

It is quite difficult to figure out how much caffeine is consumed from a regular cup of coffee. Cup sizes differ from country to country. For instance, in the USA, coffee is typically served in a 240 ml cup, which is twice the amount of a typical European serving. The caffeine concentration also varies depending on the beans, how they are roasted, and how the coffee is prepared. A restaurant-style serving of Espresso in a 30ml cup can contain from 40 to 75 mg of caffeine. Even a decaffeinated Espresso can contain up to 15 mg of caffeine.

On the other hand, a 240 ml cup of generic instant coffee can contain any amount from 27 to 173 mg of caffeine, while a Starbucks Pike Place 480 ml cup of brewed coffee contains 330 mg of caffeine. A moderate intake of caffeine is probably around 300 mg per day. This is roughly 3 to 4 cups of ground roasted coffee or 5 cups of instant coffee. So 1-2 cups of coffee a day should easily qualify for the health claim.

By the way, tea has about half as much caffeine as coffee in case you are a tea drinker.

Related articles

Here we go again

Polarised views on GM maize (Illustration: Forbes)

On 19 September 2012, a scientific study was published on-line later to appear in print in the scientific journal Food and Chemical Toxicology. It got an immediate negative response from a large part of the scientific community for using a deficient methodology, but not before receiving strong support from the activist community. The reason for the latter being that it had been circulated to supporters before being published. Sounds intriguing? Here are the facts as much as they can be discerned through the haze of polarised opinion.

The study in question was undertaken by Séralini and co-workers from the universities of Caen and Verona. The French professor Gilles-Éric Séralini is no stranger to controversies and he is well-known for being furiously anti-Monsanto. And here he was, the lead author of a study to test the effects of feeding rats Monsanto’s NK 603 GM maize and the Monsanto herbicide glyphosate separately or in combination. The group set out to prove the need for long-term mammalian toxicity studies before approval of new GM plants. Currently, only 90-day rat feeding trials have been conducted by the biotech industry. The group kept the rats in the trial for two years to prove their point.

The NK 603 GM maize has been genetically modified to be resistant to the herbicide glyphosate sold under the commercial name Roundup. The study claimed that rats fed on GM Maize suffered mammary tumours, and severe liver and kidney damage at double the rate of rats in a matched sample fed non-GM maize – 50% of males and 70% of females died prematurely, compared to 30% and 20% in the control group. The authors concluded that the results could be explained by non linear endocrine-disrupting effects of Roundup, but also by the over expression of the transgene in the GM maize and its metabolic consequences.

The response from anti-GM supporters was immediate. Care2, of which I am a proud member, started a petition to request that the European Union immediately ban all GM food products. There could be many legitimate reasons for not growing GM plants, particularly glyphosate tolerant plants. To all actions there is always a reaction. And to indiscriminately use just one herbicide will meet with a reaction from nature. The weed we’re trying to destroy will fight back and will itself acquire herbicide tolerance. But so far there is very little evidence, if any at all, that GM plants are dangerous if consumed by humans. I was thus very disappointed by the knee-jerk reaction from Care2. I had expected better as a scientist.

The activist response was followed almost immediately after publication of the study by an outcry from many scientists as well. They claimed that you cannot study chronic effects by using so few control animals. The rat strain used was prone to spontaneous cancer development and if left to survive for more than two years might have a 70% cancer incidence in the untreated group. The statistical methods used were not appropriate for this kind of study. And presentation of the findings were selective and impossible to interpret. The European Food Safety Authority was officially asked to provide a comment on the study and wrote an open letter to the authors asking for further information so that they could provide a considered opinion. This was refused by the authors.

So now we have stalemate. The views are extremely polarised. If the authors would have liked to be taken seriously they should have been more careful in their study design. They had previously made clear on what side of the debate they stand and should have expected this reaction from other scientists. Or maybe this was exactly what they were after. They have certainly got enough publicity already and preached for the converted. But will the results contribute to an honest debate? It doesn’t seem so at this stage.

Di…di…dioxins

Dioxins are persistent organic pollutants (Photo: avlxyz – Flickr)

The title might be slightly over the top, as you might not die from poisoning with dioxins. But be aware that dioxins are a group of chemicals belonging to the “dirty dozen” of persistent organic pollutants or POPs for short. Persistent because once they have entered the body they are stored in fat tissue for a long time. Pollutants because they are all but indestructible once released into the environment and can easily spread across the world.

Commonly found at low levels in many foods, dioxins are highly toxic affecting a number of organs and systems. High accidental or intentional short-term exposure may result in skin damage, such as chloracne and patchy darkening of the skin, and altered liver function. This happened to Viktor Yushchenko, President of the Ukraine, whose face was disfigured by chloracne. Long-term exposure is according to the World Health Organization linked to impairment of the immune system, the developing nervous system, the endocrine system, reproductive functions and possibly cancer. But not all dioxins are equal.

What are dioxins?

Bare with me, here is first a little chemistry. Strictly speaking dioxin might refer to a single very toxic substance called TCDD (2,3,7,8- tetrachlorodibenzo para dioxin) and other polychlorinated dibenzo para dioxins (PCDDs). However, the name “dioxins” often includes also the family of structurally and chemically related polychlorinated dibenzofurans (PCDFs). And to confuse the situation even further, certain dioxin-like polychlorinated biphenyls (PCBs) with similar toxic properties might sometimes also be referred to as “dioxins” or dioxin-related compounds.

Of the 419 different dioxin-related compounds that have been identified, only about 30 are considered to have significant toxicity. The good thing is that they all act in a similar way, although to different degrees. Clever scientists thus grouped them together and talk about dioxin toxicity equivalents. It might be important though to discuss a little further about the different origins of dioxins on the one hand and dioxin-like PCBs on the other before lumping them together

origin of dioxins and related compounds

Dioxins (not including the PCBs) are unwanted byproducts of industrial processes, like smelting, chlorine bleaching of paper pulp and incomplete burning in waste incinerators. Natural processes, like volcanic eruptions and forest fires, contribute to dioxin formation.

Dioxins found in Sydney Harbour

Dioxins have also been linked to the manufacturing of some herbicides and pesticides. Remember Agent Orange, the herbicide mixture used during the Vietnam war to defoliate trees? It was contaminated with dioxins during the manufacturing process and caused considerable damage to the next Vietnamese generation. A link to certain types of cancers and also to diabetes is being further investigated.

A Union Carbide plant producing the same herbicide mixture was situated deep in Sydney Harbour. It closed many years ago but its legacy persists on the harbour floor. In 2006, the NSW Government was forced to close parts of Sydney Harbour for commercial fishing because testing found high levels of dioxins in some fish and seafood.

In contrast to dioxins, PCBs had widespread use in numerous industrial applications, due to their physical and chemical properties, such as non-flammability and low heat conductivity. They were produced in high volumes for over four decades until they were banned in the 1980s. The problem now is that long-term storage and improper disposal of PCB-based waste industrial oils may result in their release into the environment contaminating human and animal food supplies.

Dioxins in the food supply

Fish contributes to dioxin exposure

Dioxins in the environment will bio-accumulate in the food chain, that is the higher up in the chain the higher the levels found, with humans the ultimate end point. The European Food Safety Authority (EFSA) in a recent report identified fish, meat and dairy products as the highest contributors to European dietary exposure to the substances. Milk and dairy products were the major contributors for almost all infant and toddler groups, while it was fish and seafood products for the rest of the population. Very low levels are found in plants, water and air.

Comprehensive monitoring programmes conducted worldwide during the past two decades have shown that human exposure to dioxins and PCBs has decreased significantly over time. EFSA noted that over the recent ten-year period dietary exposure to dioxins and PCBs had been reduced by between 20 to 80% depending on dietary habits and European region.

However, accidents or deliberate fraud that still occur can negate the best of intentions.

Recent contamination incidents

Although levels of dioxins and PCBs seems to be falling in the general food supply, the real challenge is to keep contamination incidents from happening. Recent incidents have involved animal feed made from illegal waste industrial oil contaminating pork in Ireland and chicken and eggs in Belgium, the thickener guar gum from India contaminating a range of European processed food products, citrus pulp feed pellets from Brazil contaminating milk in Germany, bentonite clay used in feed production contaminating chickens, eggs and catfish in the USA.

Dioxins found in organic eggs

Equally, localised problem areas cannot be ignored. In a German testing program, high levels of dioxins were recently detected in sheep and deer liver not associated with any specific contamination source. Investigations summarised by EFSA indicated that these high levels were not due to poor husbandry practices or high localised contamination but were much more likely to be associated with the physiology and grazing patterns of the animals. Also in Germany, dioxins at three to six times permitted levels were discovered mid 2012 in eggs by routine tests on an organic farm. How the dioxin came into the eggs was unclear since tests showed no contamination of animal feed at the farm. A Dutch organic egg producer was affected by a similar problem in 2011. Fish from the Baltic Sea are consistently more contaminated with dioxins than fish from most other areas.

Many earlier incidents of food contamination have been reported in other parts of the world. Although all countries can be affected, most contamination cases have been reported in industrialised countries where adequate food contamination monitoring, greater awareness of the hazard and better regulatory controls are available for the detection of dioxin problems.

Continued vigilance is of utmost importance

Continued vigilance to protect food supply (Photo: nemone – Flickr)

Since food contributes to more than 90% of human exposure to dioxins, protecting the food supply is critical. Source-directed measures to reduce overall dioxin emissions were recommended by the Codex Alimentarius Commission to be implemented world-wide.

In the USA, federal agencies have taken a number of actions to reduce dioxin levels in food with quantifiable industrial emissions reduced by more than 75% from their levels in the 1980’s. In Europe, the European Commission produces regular progress reports to measure the effects of their regulatory controls of dioxins. The latest report claimed an overall reduction of industrial emissions of dioxins by about 80% over the past two decades. The Australian Government undertook a range of studies from 2001 to 2004 to measure emissions from sources such as bush fires, and dioxin levels in the environment, food and population claiming that levels were generally low. Health Canada continues to assess the concentrations of dioxin compounds in foods as well as any new research about their health effects.

It is not much we as individuals can do to reduce our exposure to dioxins. But we can pressure governments to continue their vigilance and not become complacent. Regular food monitoring should be in place to ensure that tolerance levels for dioxins are not exceeded. We should never forget that dioxins are among the most potent toxins requiring testing methods maybe more than 1000 times more sensitive than for most other contaminants.