Author: lcoffice

The “swimmer pollution”, up to 14000 tons of sunscreen enter the world’s coral reefs annually

Peggy Orenstein is a regular holidaymaker in Hawaii. For several decades she returned, year after year, to swim at the same bare-bones beach of Big Island. Her recent article in the New York Times is particularly surprising and worrying: … At first I thought it was my imagination, but this summer there was no denying it: I felt, abruptly, like I was snorkeling through an underwater desert. Most of the coral had turned white, a sign that it was in danger of dying. Entire species of fish had vanished, and those that remained — like Hawaii’s tonguetwisting state fish, the humuhumunukunukuapua’a — were sparse, barely a classroom’s worth, let alone a school… [Orenstein 2017].

 

Will this ever definitely be a thing of the past? [photo source: pixabay]

We’ve been told to lavishly apply sunscreen to protect ourselves and our children against the harmful effects of the sun’s UV rays. From now on, eco-conscious beachgoers may want to go easy on sunscreens, as studies evidence that most contemporary sunscreen lotions pose a threat to ocean life [Downs et al. 2016; McCoshum et al. 2016; Corinaldesi et al. 2017; Tsui et al. 2017]. Sunscreens and other personal care products threaten the coral reefs that are most important to people: those that are focal points of tourism as well as the fringing reefs that are critical for protecting coasts from erosion. Moreover, these chemicals significantly reduce the capacity of local subsistence fisherman to access the abundance of food that healthy near-shore reefs once provided. Severe sunscreen pollution does not only affect the survival of these reefs, it also obstructs the recovery and restoration of pre-damaged reefs.

Increased scrutiny and study over the past decades has also raised concern that the products we turn to for UV protection might actually cause harm to the people who put them on their skins [Maipas & Nicolopoulou-Stamati 2015; Lim et al. 2017].

Hundreds of sunscreen products use oxybenzone or benzophenone-3 (BP-3), since this substance provides broad-spectrum ultraviolet coverage. Sunscreens washing off the swimmers ¾ Downs calls this the “swimmer pollution” ¾ threaten coral reefs all over the world, from the Gulf of Aqaba in the Red Sea to the shores of Playa Hermosa, Costa Rica. But besides washing off the swimmers’ skin, sunscreen chemicals can find their way into the sea by other means too. Many raw materials for sunscreen lotions are readily absorbed through the human skin. BP-3 can be detected in the urine within 30 minutes of application. Flushing the toilet or washing off sunscreen in the shower causes plenty of the lotion’s chemicals to enter the sewer. Towns bordering coral reefs that do not have highly efficient sewage treatment  and management systems are particularly exposed to this kind of pollution.

According to Downs et al. [2016], between 6000 and 14000 tons of sunscreen lotion, much of which contains between 1 and 10 % BP-3, annually enter the world’s reefs. So it comes as no surprise that the measured concentrations are sometimes alarmingly high. Research data obtained by Downs et al. [2016] show that early in the morning, before the swimmers even arrive, beaches in Hawaii have BP-3 levels exceeding ~700 parts per trillion ¾ this means ~0.7 mg per litre of seawater. Such high concentrations are ~10 times above the concentrations that trigger ecosystem pathologies. Additional emerging research suggests that BP-3 concentrations on near-shore reefs around the world are commonly between 100 parts per trillion and 100 parts per billion; and this is well within the range of being a significant environmental threat.

There is a great difference between much frequented and quieter beaches. Downs and his team [2016] noticed that bays popular with sunscreen-slathered tourists had dead and sterile coral, while those with very little beachgoers were healthy with lots of coral recruitment and lots of spiny sea urchins. They argue that this remarkable difference confirms that climate change, which was long thought of as the predominant causal factor, is not solely responsible for coral die-offs. Pollutants such as BP-3 (and many others) are able to create sterile, “zombie” reefs.

It was found that BP-3 induces coral bleaching. Moreover, BP-3 is genotoxic, meaning that it damages coral DNA and induces severe and lethal deformities. Even more alarming, however, is the endocrine disrupting activity of BP-3, causing the coral larvae to inappropriately encase themselves in their own “stony” skeleton at a time of their development when they should not even have a skeleton.

And BP-3 is toxic to more than just corals. It is toxic to algae, sea urchins, fish and mammals. It inhibits embryonic development in sea urchins. It can result in gender shifts in fish, whereby male fish take on female attributes, while females have reduced egg production and embryo hatchings. In mammals it has been demonstrated to be a potential mutagen and to exhibit procarcinogenic activity. Studies in both mice and rats have illustrated that exposure to BP-3 increases liver and kidney weights, reduces immunity, increases uterine weights in juveniles and reduces fertility.

Obviously, there is very little published data on the negative human health impact of sustained exposure to BP-3. It is no secret that human couples with higher BP-3 concentrations in their urine may find it harder to procreate. Men with higher BP-3 concentrations had higher levels of diseased sperm. And it can also be assumed that contaminants like BP-3 could be transferred from mothers to their offspring: both dolphin and human mothers were shown to transfer BP-3 via breast milk. The placental and lactation transfer pathways are well known sources of chemical contaminants in infants.

And benzophenone-3 is not the only culprit. This would be particularly illogical. Many other chemicals such as octinoxate, octocrylene, methoxycinnamate, camphors, non-coated nanoparticles (e.g. zinc oxide and titanium dioxide), silicone polymers, cyclic siloxanes such as octamethylcyclotetrasiloxane and decamethylcyclopentasiloxane, and several other “alphabet stews” common to chemical sunscreens have also been found to be toxic to coral reefs. Neither should it be forgotten that many thousands of chemical contaminants resulting from all kinds of anthropogenic activities end up in our watercourses and ultimately in our estuaries and oceans.

Nihil novi sub sole! There is nothing new under the sun! Our planet Earth ¾ our one and only home ¾ is suffering from a treacherous exposure to extremely complex contaminant mixtures. A most insidious aspect of this problem is ever-increasing pollution of the world’s oceans with background levels of pollutants that are becoming a major concern even in the most remote locations. Microplastics, sewage, all types of chemicals, sunscreens etc. add stress that erodes coral reef resilience.

The reefs are weakened and are unable to recover from global events, like bleaching, acidification, increased pollution, and many others.

Whatever some people may think, there is now undeniable evidence that global warming is caused by anthropogenic activities. The Anthropocene is a proposed epoch dating from the commencement of significant human impact on the Earth’s geology and ecosystems, including anthropogenic climate change [Wikipedia]. The coral reefs suffer substantial degradation as  a result of human activities, associated with overexploitation and pollution; a degradation that has dramatically accelerated over the past ~50 years. Especially global warming and ocean acidification are compounding these threats [Wilkinson 2008; Pandolfi et al. 2011].

Applying sunscreen lotions is of course only one of many anthropogenic activities that affect the future of seawater ecosystems, and more particularly the future of coral reefs. As far as coral reefs are concerned, it is carbon dioxide induced ocean acidification and its potential impact on the rate of biogenic calcium carbonate production by the dominant reef calcifiers, i.e. the corals and coralline algae, that poses the most serious threat. On the basis of mathematical models, a 40 to 83 % decline in reef calcification was predicted by 2065 [Langdon & Atkinson 2005; Pandolfi et al. 2011]. Coral reefs are also particularly sensitive to increasing temperatures because the major framework builders, i.e. the scleractinian corals, suffer a serious breakdown in their symbiosis with zooxanthellae when temperatures are abnormally high. The “coral bleaching” phenomenon (so-called because corals become white as zooxanthellae are lost) reduces the performance of the coral host, which receives most of its organic carbon from the symbiont. Mass bleaching events, when most of the coral assemblage bleaches, have become much more frequent and widespread in the past few decades [Baker et al. 2008; Pandolfi 2011].

There is no single solution to the damage sustained through sunscreen lotion pollution. A diversity of approaches could possibly be implemented. All will, however, require further investigation to determine which ingredients are safe and which pose a realistic threat to the marine ecosystem. A useful and efficient approach also requires that the data be duly communicated to consumers, manufacturers, regulators and other stakeholders. And it should be noted that none of these mitigation options requires that sunscreens be completely banned. Sun protection is of course a significant public health issue, and sunscreens play an important role in risk management.

One approach is to ban the use of products that contain threatening ingredients in areas where coral reefs are most susceptible to exposure. This type of regulatory policy has been in place for over 10 years in Mexico’s eco-reserves, including the Xcaret eco-archaeological Park and Xel-Há Park. This sort of policy might be an easy and very cost-effective approach, at least in areas crucial for active reef conservation and restoration, such as coral reef nurseries. A second approach involves a PR campaign to inform both visitors and locals about the environmental impact of sunscreen pollution and recommend they use sun-care products that contain no contaminants. A third strategy is to convince people to reduce the amount of sunscreen they use. Applying lotion to only neck, face, feet and backs of hands can reduce sunscreen loads in the water by 90 %. Also, sun clothes designed to reduce UV exposure have now become much more efficient and fashionable. And finally, a fourth option requires consumers to demand innovation from manufacturers regarding the formulation of their products. We are at a juncture in which industry can either demonstrate leadership by developing environmentally sustainable new products that are popular with consumers or dig in its heels, refusing to adapt and suffering economic and reputational consequences [Downs et al. 2016].

Whatever move is chosen, it should be remembered that the best way to keep marketing practices honest is for the consumer to demand attention to rigorous and unbiased science from industry as well as from governments. Scientific data generated by industry alone are often viewed with suspicion and distrust [Oreskes & Conway 2010]. The relevant science should preferably be conducted by financially neutral parties that follow standardized, validated testing procedures. And governments must play a pivotal role by encouraging third-party testing, standardizing methodologies and moderating dialogue among all interested parties.

Funny how things turn out! Some manufacturers have started to produce sunscreens marketed as “reef friendly”. As for “healthy” and “natural” food labels, the rules that guarantee these designations however are vague or inexistent. Even so, a “reef friendly” lotion sounds like a good idea.

But what role have governments played in all this? It seems as though certification has developed as a private-sector, market-based tool, with little regulatory control by public authorities ¾ which does not mean that decision makers should introduce excessive bureaucracy, seek more control over the behaviour of academics and try to “measure” their scientific output.

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Baker et al. [2008]. Climate change and coral reef bleaching: An ecological assessment of long-term impacts, recovery trends and future outlook, Estuarine, Coastal and Shelf Science 80, 4, 435 – 471

Corinaldesi et al. [2017]. Sunscreen products impair the early developmental stages of the sea urchin Paracentrotus lividus, Scientific Reports 7, 7815, pp. 12

Downs et al. [2016]. Toxicopathological effects of the sunscreen UV filter, Oxybenzone (Benzophenone-3), on coral planulae and cultured primary cells and its environmental contamination in Hawaii and the US Virgin Islands, Archives of environmental contamination and toxicology 70, 2, 265 – 288

Langdon & Atkinson [2005]. Effect of elevated pCO2 on photosynthesis and calcification of corals and interactions with seasonal change in temperature/irradiance and nutrient enrichment, Journal of Geophysical Research 110, pp. 16

Lim et al. [2017]. Current challenges in photoprotection, Journal of the American Academy of Dermatology 76, 3, S91 – S99

Maipas & Nicolopoulou-Stamati [2015]. Sun lotion chemicals as endocrine disruptors, Hormones 14, 1, 32 – 46

McCoshum et al. [2016]. Direct and indirect effects of sunscreen exposure for reef biota, Hydrobiologia 776, 139 – 146

Orenstein [2017]. Is Your Sunscreen Poisoning the Ocean?, The New york Times, August 17

Oreskes % Conway [2010]. Merchants of Doubt, Bloomsbury, pp. 355

Pandolfi et al. [2011]. Projecting Coral Reef Futures Under Global Warming and Ocean Acidification, Science 333, 418 – 422

Tsui et al. [2017]. Occurrence, Distribution, and Fate of Organic UV Filters in Coral Communities, Environmental Science and Technology 51, 4182 – 4190

Wilkinson [2008]. Status of Coral Reefs of the World: 2008, Global Coral Reef Monitoring Network and Reef and Rainforest Research Centre, Townsville, Australia

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Grubs can be eaten raw and when they are cooked they taste like roasted almonds — or so we are told !

… This information will come in handy for those of us following the latest recommendation from the United Nations: Consume more insects … In fact, some two billion people eat a wide variety of insects regularly, both cooked and raw; only in Western countries does the practice retain an “ick” factor among the masses [Holland 2013] 

On the one hand, insects can be slimy, cringe-inducing creatures, very often swatted away by humans or ruthlessly eliminated with insecticides. On the other hand, van Huis et al. [2013] are convinced that beetles, wasps, caterpillars and many more are unexplored nutrition sources that can help reduce global food insecurity. 

Human beings often consider insects as a nuisance; no more than pests that intent on destroying crops and tormenting humans and other animals. Nothing, however, could be further away from the truth. Insects can provide food at low environmental cost, and contribute positively to livelihoods. They play a fundamental role in nature. Yet, many westerners continue to ignore these benefits. Contrary to popular belief, insects are not merely “famine foods” eaten in times of food scarcity. Many people around the world actually choose to eat insects, mainly because of the palatability of insects and their established place in local food cultures. Though insects do not belong to the Western gastronomic tradition, they currently supplement the diets of some 2 billion people and have always been part of the human diet in Asia, Africa and Latin America. Of the ~1 million known insect species, roughly 1900 are consumed by humans. Most consumed insects include beetles, caterpillars, bees, wasps, ants, grasshoppers, locusts and crickets [Holland 2013]. 

As man evolved, the hunter-gatherers collected much more than edible plants. These early people probably hunted for insects too. Insects could be found everywhere and many animals ate them. So why shouldn’t humans eat them? Early humans took their cue from insectivorous animals to decide which insects were edible and tasty. 

 Grotesque and frightening in appearance, cicadas do not bite and are actually harmless to handle
[photo source: pixabay] 

Years later, Romans and Greeks would dine on beetle larvae and locusts. The Greek scientist and philosopher Aristotle even wrote about harvesting tasty cicadas. In the Old Testament book of Leviticus (11, 20 – 23), the authors stated: … All flying insects that walk on all fours are to be regarded as unclean by you. There are, however, some flying insects that walk on all fours that you may eat: those that have jointed legs for hopping on the ground. Of these you may eat any kind of locust, katydid, cricket, or grasshopper. But all other flying insects that have four legs you are to regard as unclean... This “green light” was obviously bad news for locusts and grasshoppers. John the Baptist lived in the desert for months on a diet of locusts and honeycomb ! 

Locusts were also a nutritious, cheap and plentiful source of food for the ancient Algerians. They prepared the insects by boiling them in salt water and drying them in the sun. And the Australian Aborigines made meals of moths. After cooking them in sand, they burned off the wings and legs and sifted the moths through a net to remove their heads, leaving nothing but delectable moth meat. The Aborigines were and continue to be entomophagists. 

Several varieties of ants are also consumed as food in countries like China, Thailand, India and some African countries [van Huis 2013]. Moreover, the Chinese black ant (Polyrhachis dives) has been a traditional edible insect in China for centuries and in addition to its nutritional value the insect has been used in traditional medicine for the treatment of rheumatoid and osteoarthritis, inflammatory diseases, and diabetes [Huang & Xiao 2003]. 

It is difficult to generalizfor all insect species consumed worldwide, but compared to beef, pork and chicken, the insect protein content is, on average, similar. Scientists, decision makers, and business managers are increasingly aware of the importance of new protein sources, which is why it was recommended to consume insects since they are environmentally sustainable and nutritious alternatives to conventional livestock products [Payne et al. 2016]. 

Rhinoceros beetles are very popular pets too, especially in Japan
[photo source: pixabay]  

Moreover, compared to other livestock animals, insects seem to contain more polyunsaturated fatty acids1 and higher levels of minerals, such as iron and zinc, and more vitamins B1, B2, and B3 [van Huis et al. 2013]. Asiatic rhinoceros beetles (Oryctes rhinoceros L.) and winged termites (Macrotermes nigeriensis S.) are real live, crawling and flying stocks of nutrients and minerals [Omosoto et al. 2015]. Both insects are rich sources of proteins, minerals, fibre and fat. Their levels of antinutrient and/or secondary metabolites are lower, when compared to other food sources. Also, these two insects are rich in antioxidants. They can be used to substitute animal proteins like beef and mutton, and inclusion of these insects in the human diet tends to enrich the body with mineral salts. 

Another striking example is that of the people of many ethnic origins living in Manipur — a state in north-eastern India, with the city of Imphal as its capital [Wikipedia] — who capture and consume many insect species living in puddles, ponds, lakes, and rivers. In the valley region of the Manipur state, there are many inland freshwater lakes that act as ideal habitats for aquatic edible insects. They are highly valued and sought after by Malipur locals because of their taste and enhanced availability. The existence of an insect consumption culture in Manipur ensures that the nutritional needs of the indigenous people are met. Although the consumption of edible insects has sometimes been trivialized, they play a major role in food security, health, and environment management [Shantibala et al. 2014]. 

These are just a few illustrations to show that entomophagy is worthy of our attention. The full list of instances of entomophagy is, of course, much longer. Insect consumption is by no means exceptional. It can only grow in importance over the coming years and deserves to be scrutinzed and evaluated. 

The review paper by Testa et al. [2017] also refers to the possible beneficial pharmacological effects of edible insect consumption. Several research teams have studied the possible use of edible ant-lions and edible moths. In developing countries, the number of diabetic patients related to insulin resistance is very high. The main reason for this is that nutrient consumption patterns have shifted from a healthy traditional high-fibre, low-fat, low-calorie diet towards the consumption of calorie-rich foods, containing refined carbohydrates, fats, red meats, and low fibre.  Mujahid et al. [2013] decided to study the hypoglycemic activity of the combination of bitter gourd or bitter melon (Momordica charantia) extract and ant-lion larvae (Myrmeleon sp.) extract in insulin-induced type 2 Diabetes Mellitus. Based on the results obtained in laboratory rat experiments, the authors concluded that the combination of bitter gourd and ant-lion extracts strongly reduced blood glucose levels. 

 
Clanis bilineata, their wingspan is 94 – 150 mm [Sphingidae Taxonomic Inventory] 

Clanis bilineata is an edible and, incidentally, very beautiful moth and its larvae are widely consumed in China. In a study by Xia et al. [2013], chitooligosaccharides2 from larvae skins were prepared and their hypolipidemic activity was determined in rat experiments. The results of this study clearly indicated that chitooligosaccharides could be suitable alterative hypolipidemic sources for humans. 

Another recent study highlights the potential of the desert locust, Schistocerca gregaria, as an unconventional source of dietary and therapeutic sterols3 [Cheseto et al. 2015]. 

Enghoff et al. [2014] suggest that the defensive secretions of millipedes act as potent insect repellents. Whether millipedes will ever become a major human food remains to be seen. Nevertheless, millipedes have been shown to constitute a valuable food source for an ever growing human population, especially in rural Africa. Additionally, the potential of millipede chemicals, such as cyanide and benzoquinones, for deterring (malaria transmitting) mosquitoes and for influencing Plasmodium and other parasites constitutes a promising field of research. Also, Tang et al. [2015] confirmed that Chinese black ants contain chemicals that display anti-inflammatory, immunosuppressive, and renoprotective activities. 

Currently, there is a buzz in the air, and it is all about the human practice of eating insects. Western governments are showing interest as there is huge potential for feeding growing numbers of humans  as well as their livestock and for doing so in a sustainable way. And we are beginning to see restaurants with insects on the menu. 

We should not ignore the expansion of the world population; nor should we be blind to the benefits of entomophagy. The conventional livestock production is land and water thirsty, and this comes at a dramatic cost to our environment. Additional or alternative protein sources with lower environmental impacts should be seen as good news. We still have a lot to learn however. Many authors have already noted the need for ad hoc studies to determine the roles of anti-nutrients and their possible implications for animal health; and one of the most interesting findings is the use of insects as starting points for developing drugs. Potential hypocholesterolemic and hypoglycemic agents, derived from some insects, will definitely require additional efforts to determine their possible uses for human health. Likewise, the antioxidant characteristic exhibited by some insects requires in-depth research to standardize their use in many therapies. 

The review by Testa et al. [2017] shows that the use of insects as food and feed appears to have many positive aspects from the economic, environmental and nutritional points of view — a challenge as well as an opportunity therefore for the 21st century. It is always a good time to invest in the future. It is always a good time to make a significant contribution to sustainability, to environmental quality, and to public health. 

Hopefully, the financing agencies will be sympathetic to these concerns. Deafness and short-sightedness are no recipe for the future. A generous and open-minded attitude is what is needed to stimulate new developments. 

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Cheseto et al. [2015]. Potential of the Desert Locust Schistocerca gregaria (Orthoptera: Acrididae) as an Unconventional Source of Dietary and Therapeutic Sterols, PLoS ONE 10, 5, e0127171 

Enghoff et al. [2014]. Millipedes as Food for Humans: Their Nutritional and Possible Antimalarial Value — A First Report, Evidence-Based Complementary and Alternative Medicine 2014 

Holland [2013]. U.N. Urges Eating Insects; 8 Popular Bugs to Try, National Geographic May 14 

Huang & Xiao [2003]. Study on Polyrhachis vicina, Research and Practice of Chiness Medecines 17, 60 – 62 

Mujahid et al. [2013]. A combination of bitter gourd ethanolic extract with ant lion larvae aqueous extract for a blood glucose-lowering agent, International Food Research Journal 20, 2, 851 – 855 

Omosoto et al. [2015]. Nutrient Composition, Mineral Analysis and  Anti-nutrient Factors of Oryctes rhinoceros L. (Scarabaeidae: Coleoptera) and Winged Termites, Marcrotermes nigeriensis Sjostedt.  (Termitidae: Isoptera), British Journal of Applied Science and Technology 8, 1, 97 – 106 

Payne et al. [2016]. A systematic review of nutrient composition data available for twelve commercially available edible insects, and comparison with reference values, Trends in Food Science & Technology 47, 69 – 77 

Shantibala et al. [2014]. Nutritional and antinutritional composition of the five species of aquatic edible insects consumed in Manipur, India, Journal of Insect Science 14, 14, pp. 10 

Tang et al. [2015]. Constituents from the edible Chinese black ants (Polyrhachis dives) showing protective effect on rat mesangial cells and anti-inflammatory activity, Food Research International 67, 163 – 168 

Testa et al. [2017].  Ugly but tasty: A systematic review of possible human and animal health risks related to entomophagy, Critical Reviews in Food Science and Nutrition 57, 17, 3747 – 3759 

Van Huis et al. [2013]. Edible insects: future prospects for food and feed security, Food and Agriculture Organization of the United Nations, Rome 

Xia et al. [2013]. Hypolipidemic activity of the chitooligosaccharides from Clanis bilineata (Lepidoptera), an edible insect, International journal of biological macromolecules 59, 96 – 98 

 

Frequently occurring hyperthyroidism in pet cats: it is like raising the canary-in-the-coal-mine issue 

… he (the veterinarian) warned, “these cats back here are radioactive.” He meant that literally. The previous day, all five animals received carefully titrated doses of radioactive iodine, designed to destroy the overactive cells that had proliferated in their thyroid glands and flooded their bodies with hormones. These cats are among the millions suffering from hyperthyroidism, one of the most mysterious diseases in veterinary medicine… [Anthes 2017].

Whis it that we are now facing an epidemic of thyroid disease in cats? Dr. Mark Peterson was one of the first to investigate the disorder. When he entered veterinary school in 1972, it seemed that feline hyperthyroidism didn’t even exist. Today, Dr. Peterson treats almost nothing else. The disease was first described in 1979 [Peterson 1979]. Since then its prevalence has increased dramatically [McLean et al. 2014].The state of hyperthyroidism is now accepted as being the most common feline endocrine disorder and an important cause of morbidity in middle-aged cats in the United States, Canada, Europe, Australia, New Zealand and Japan.

Hyperthyroidism is a multi-systemic disorder resulting from excessive circulating concentrations of thyroxine and tri-iodothyronine. In fact, the cats suffer from an overproduction of thyroid hormones. The disease develops in middle-aged and older cats with no obvious breed or gender predilection to be found in most epidemiologic studies [Peterson 2012]. The disease affects many organ systems because of an overall increase in metabolism, weight loss, increased appetite, and poor body condition. Several studies have attempted to identify risk factors involved in the development of hyperthyroidism. The most likely candidates fall into two broad categories: (1) nutritional deficiencies as well as excesses in cat food, leading to metabolic thyroid dysfunction, and (2) the presence of thyroid-disrupting compounds in the cat’s environment, drinking water, or food.

Several epidemiologic studies suggest that cats fed mainly on canned food run a higher risk of developing hyperthyroidism [Peterson 2012]. An accusing finger has been pointed to several flavour additives used in canned food, to plastic linings in easy-open (pop-top) lids, which may contain the thyroid disruptor chemical bisphenol [Edinboro et al. 2004a], and also to goitrogens such as soy isoflavones, generally present in dry cat foods [Bell et al. 2006]. Moreover, a huge variability in iodine intake over time may also contribute to the development of thyroid disease in cats [Edinboro et al. 2004b].

Like polychlorinated biphenyls in the past, polybrominated diphenyl ethers have now become ubiquitous persistent organic pollutants. Polybrominated diphenyl ethers (PBDEs) are synthetic brominated compound that are used as flame retardants in a variety of consumer products such as electronics, furniture and textiles, as well as construction materials. Over the past 30 years, PBDEs have become major global contaminants. They have been detected in human adipose tissue, serum, and breast milk samples [Birnbaum & Staskal 2004; Covaci et al. 2008; Coakley et al. 2012; Marchitti et al. 2017]. Exposure occurs predominantly through the diet and the indoor environment, more particularly indoor dust. Even when the toxicology database is still relatively limited available results in the current literature raise concern.

Since PBDEs are known thyroid disruptors, these chemicals may play a role in the pathogenesis of thyroid tumors and hyperthyroidism in cats. Intensive PBDE production began just before hyperthyroidism was first reported in 1979. This supports the hypothesis that PBDEs might cause the disorder. In a study designed to determine whether the PBDEs body burdens of affected cats were greater than those of non-affected cats, PBDEs were analyzed in serum samples from 11 hyperthyroid and 12 euthyroid house cats. The results support the hypothesis that cats are highly exposed to PBDEs: a variety of PBDE congeners1 was detected in all cats, with overall PBDE levels in cats being 20 to 100 times higher than median levels in US adults [Dye et al. 2007]. However, due to a fairly high variability within each group, no association was detected between hyperthyroid cats and serum PBDE levels. In a follow-up study, investigators measured PBDEs, polychlorinated biphenyls and organo-chlorinated pesticides in serum samples from 16 hyperthyroid and 10 euthyroid Californian household cats [Guo et al. 2012]. Their results indicate that both groups of cats had extremely high serum PBDE levels, with values that were roughly 50 times higher than the levels in human residents living in California. Moreover, PBDE congener patterns in these cats resembled patterns found in house dust, suggesting that house dust, rather than diet, is a very likely route of exposure to PBDEs in domestic cats [Mensching et al. 2012].

 

A small literature survey shows that cats appear to metabolize PBDEs differently to other species thus far studied. Very low levels and even a complete absence of hydroxylated PBDE metabolites were observed in cats. Moreover, statistical data treatments indicate an association between elevated PBDE concentrations in the cats and the occurrence of feline hyperthyroidism [Norrgran et al. 2015], and a correlation between cat serum PBDE levels and household dust PBDE levels. The latter finding confirms the hypothesis that dust is a significant exposure route for cats [Norrgran et al. 2017].

In conclusion, domestic cats can be highly exposed to PBDEs, presumably through the ingestion of household dust during their normal grooming behavior. They revel in the sunshine and roll around in the sand. They like to sleep on our beds, sofas and stuffed chairs; and they like it even better when there is a cat-sized mat, blanket or forgotten shirt or pull-over on top of the furniture. They lick their paws and fur all the time and end up ingesting anything that is present  in the dust. There is also compelling evidence for the possible role of PBDEs in the development of thyroid tumors and feline hyperthyroidism.

However, the role of PBDEs is complex and complicated. Chow et al. [2015] conclude that the aetiopathogenesis2 of feline hyperthyroidism is likely to be multifactorial and includes genetic, nutrional as well as environmental factors rather than one single aetiological agent, whereby PBDEs interact synergistically with other factors. Yet, additional investigation into the role of PBDEs in the development of hyperthyroidism in cats is certainly warranted.

By the mid-2000s, it was clear that PBDEs could alter the thyroid function in rodents, birds and fish. The United States and the European Union have now largely phased out these chemicals. Even so, they remain ubiquitously present. PBDEs take years to degrade, and many people still own products manufactured before they were taken off the market.

Sick animals can be seen as the sentinels that warn us of looming threats to human health. For household chemicals, cats and dogs, which tend to spend nearly all their time in the home and happily hoover up whatever detritus falls on the floor, may be particularly useful sentinels… [Anthes 2017]. Our pets are exposed to many of the same kinds of chemicals that we are. When you observe a health problem in your pet friends, then watch out! All the residents could possibly face the same fate. The results of the by now 10-year-old Dye et al. [2007] study supported the hypothesis that pet cats may serve as sentinels to better assess human exposure and adverse health outcomes related to low-level, but chronic PBDE exposure.

The comparative medicine approach [Rabinowitz et al. 2009 &2010 ], as applied to the study of laboratory animals in order to improve human health, has resulted in significant medical and scientific progress. Much of what is known about the human health risks of many toxic and infectious hazards present in the environment derives from both experimental studies in animals and epidemiological studies of exposed human populations. Yet, there is another, still highly untapped source of in vivo knowledge about host versus environment interactions: the investigation of diseases in naturally occurring animal populations. This approach may signal potential human health threats just as canaries warned coal miners of the risk of toxic gases [Burrell & Seibert 1914]. Animals may serve as sentinels for human environmental health hazards, due to their greater susceptibility, environmental exposure, or shorter life spans.

Rachel Carson’s publication of Silent Spring [Carson 1962] helped launch the environmental movement. Her book evidenced that, like the canaries in the coal mine, dying birds were acting as sentinels. Silent Spring begins with “A Fable for Tomorrow”, a true story using a composite of examples drawn from many real communities, where the use of DDT (and other biocides) had caused damage to wildlife, birds, bees, agricultural animals, domestic pets, and even humans. Carson used it as an introduction to a very complicated and controversial subject [http://www.rachelcarson.org/SilentSpring.aspx]. Through their deaths resulting from higher susceptibility, increased exposure, or recognizable signs of adverse (non-fatal) health events, the animals were warning humans of the health risks associated with a widespread use of chemical pesticides.

The “One Health” approach3 assessing humans, pets, and their common environment will improve our understanding of chronic low-level, largely indoor, exposure to PBDEs and of the effects of exposure in both humans and animals.

And, Dear readers, I am quite sure you will understand that pets can also warn us of the health risks of many other ubiquitous contaminants. For as we are exposed to an extremely complex cocktail of contaminants, so too are our furry friends!

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Anthes [2017], The Mystery of the Wasting House-Cats, The New York Times Magazine, May 16

Bell et al. [2006]. The isoflavone content of commercially-available feline diets in New Zealand,New Zealand Veterinary Journal 54, 3, 103– 108

Birnbaum & Staskal [2004]. Brominated Flame Retardants: Cause for Concern?, Environmental Health Perspectives112, 9–17

Burrell & Seibert [1914]. Experiments with Small Animals and Carbon Monoxide, Industrial and Engineering Chemistry 6, 3, 241–244

Carson [1962]. Silent spring, first published in America by Houghton Mifflin, pp. 323

Chow et al. [2015]. Evaluation of polybrominated diphenyl ethers (PBDEs) in matched cat sera and house dust samples: Investigation of a potential link between PBDEs and spontaneous feline hyperthyroidism, Environmental Research 136, 173–179

Coakley et al. [2012]. Partitioning of persistent organic pollutants (POPs) between human serum and breast milk: a literature review, Chemosphere 89, 8, 911-918

Covaci et al. [2008]. Polybrominated diphenyl ethers (PBDEs) and polychlorinated biphenyls (PCBs) in human liver and adipose tissue samples from Belgium, Chemosphere 73, 2, 170–175

Dye et al. [2007].Elevated PBDE Levels in Pet Cats: Sentinels for Humans?Environmental Science and Technology 41,6350 – 6356

Edinboro et al. [2004]. Epidemiologic study of relationshipsbetween consumption of commercial canned foodand risk of hyperthyroidism in cats, Journal of the American Veterinary Medical Association 224, 6, 879–886

Edinboro et al. [2004b]. Review of iodine recommendations for commercial cat foods and potential impacts of proposed changes,Thyroid 14, 722.

Guo et al. [2012]. High polybrominated diphenyl ether levels in California house cats: house dust a primary source?, Environmental Toxicology and Chemistry 31, 2, 301–306

Marchitti et al. [2017]. Polybrominateddiphenyl ethers in human milk and serum from the U.S. EPA MAMA Study: modeled predictionsof infant exposure and considerations for risk assessment,Environmental Health Perspectives 125, 706–713

McLean et al. [2014].Worldwide prevalence and risk factors for feline hyperthyroidism: A review, Journal of the South African Veterinary Association 85, 1, Art. #1097, 6 pages

Mensching et al. [2012].The Feline Thyroid Gland: A Model for Endocrine Disruption by Polybrominated Diphenyl Ethers (PBDEs)?, Journal of Toxicology and Environmental Health, Part A: Current Issues 75, 4, 201-212

Norrgran et al. [2015]. Higher PBDE Serum Concentrations May Be Associated with Feline Hyperthyroidism in Swedish Cats, Environmental Science and Technology 49,  5107–5114

Norrgran et al. [2017]. Cats’ Internal Exposure to Selected Brominated Flame Retardants and Organochlorines Correlated to House Dust and Cat Food, Environmental Science and Technology 51, 3012−3020

Peterson et al. [1979]. Spontaneous hyperthyroidism in the cat, Proceedings of the American College of Veterinary Internal Medicin, Seattle, WA

Peterson [2012]. Hyperthyroidism in cats – What’s causing this epidemic of thyroid disease and can we prevent it?, Journal of Feline Medicine and Surgery 14, 804–818

Rabinowitz et al. [2009]. Human and Animal Sentinels for Shared Health Risks, Veterinaria Italiana 45, 1, 23 – 24

Rabinowitz et al. [2010]. Animals as sentinels: using comparative medicine to move beyond the laboratory, Institute for Laboratory Animal Research Journal 51, 3, 262-267

Glyphosate has become the world’s most widely used weed killer, which could well be serious cause for concern

Glyphosate has recently been the subject of a number of articles in newspapers and magazines. Three of them in particular caught my attention: “Glyphosate presence in honey raises concerns” in the Canadian weekly The Western Producer [Arnason, 09.03.2017], “Tribunal Monsanto: la firme américaine reconnue coupable d’atteinte aux droits humains (US firm found guilty of human rights abuses)” in the French newspaper Le Monde [Barroux, 19.04.2017], and “Roundup in EU toegestaan omdat Monsanto wetenschappelijke studies beïnvloedde (Roundup allowed in the EU because Monsanto influenced scientific studies)” in the Flemish weekly Knack [Harmsen 25.04.2017].

Glyphosate, the active ingredient in Monsanto’s flagship herbicide Roundup, may have contaminated the honey production because bees forage on corn and soybeans, which are sprayed with the weed killer during the growing season. Glyphosate has been a highly controversial substance since March 2015. The International Agency for Research on Cancer (IARC) classified the herbicide glyphosate and the insecticides malathion and diazinon as probably carcinogenic to humans (Group 2A) — the second worst rating possible[1].

For glyphosate, some evidence of carcinogenicity in humans for non-Hodgkin lymphoma (NHL) is based on several exposure studies, mostly agricultural, since the beginning of the 21st Century [Alexander et al. 2007, and references herein]. In addition, there is convincing proof that glyphosate can cause cancer in laboratory animals [IARC Monograph 112; Guyton et al. 2015]. Not all references of the IARC-report were well received though. For example, Séralini et al. [2012] published a controversial study in Food and Chemical Toxicology, but the paper was eventually retracted by the editor and later republished in Environmental Sciences Europe [Séralini et al. 2014]. The authors evaluated both the effects of feeding laboratory rats with transgenic corn as well as the effects of exposure to the increasingly common herbicide Roundup, and concluded that pathologies cannot be excluded. They observed severe hepatic and renal disturbances. Moreover, Séralini et al. [2014] called into question the earlier conclusions of a Monsanto team [Hammond et al. 2004], claiming that the initial indicators of organ toxicity were not “biologically meaningful”. But the Séralini et al. study suffers from enormous gaps in the number of animals studied and from incorrect statistical interpretation.

Granted, some studies are liable to create controversy. However, in spite of their weaknesses and shortcomings, there is every reason to believe that they will achieve the strategic goal set by the authors, i.e. to endorse the role of whistle-blower.

Monsanto was accused of crimes against humanity and ecocide, and was denounced for the marketing of toxic products that killed people. The “advisory” opinion of the court, under the chairmanship of Françoise Tulkens, former judge of the European Court of Human Rights, was published in The Hague on Tuesday, April 18. The document does not however constitute condemnation in the legal sense of the term as it is not “legally binding”.

Hundreds of internal documents and emails were unsealed by Judge Vince Chhabria, who was presiding over litigation brought by people who claim to have developed NHL as a result of exposure to glyphosate. It would seem that Monsanto has influenced and falsified scientific studies for many years. The documents and internal emails produced in 2015 reveal that Monsanto executives strategise about how to work with academic and independent scientists to convey the company’s message that glyphosate does not increase the risk of cancer. Moreover, the Monsanto documents suggest that company officials “ghost wrote” portions of scientific papers to be submitted to peer-reviewed scientific journals [Cornwall 2017]. One of the emails reveals that the company itself secretly wrote a study, even though it was published in the peer-reviewed journal Regulatory Toxicology and Pharmacology under the authorship of “independent” scientists [Williams et al. 2000].

Approval for Roundup in both the European Union and the United States has been Monsanto’s priority target. The company’s strategy sounds very familiar. Industry has clearly understood that debating the science is much easier and more efficient than debating the policy [Michaels 2008]. Williams et al. [2000] concluded that: … under present and expected conditions of use, Roundup herbicide does not pose health risks to humans… Today, almost 20 years later, this conclusion seems to me highly implausible. Several recent articles on the link between glyphosate and kidney disease, autism, rheumatoid arthritis and pulmonary problems are now available [Jayasumana et al. 2014, 2015; Beecham et al. 2016; Sealy et al. 2016; Parks et al. 2017; Hoppin et al. 2017]. Even when considering that link and causality are significantly different concepts, great care is recommended.

The European Food Safety Authority (EFSA) carried out an additional evaluation and peer review of the toxicity of glyphosate. Its assessment focused on the active substance and considered the weight of evidence of all available information. In contrast to the IARC evaluation, the EU peer review experts, with one exception, concluded that glyphosate is unlikely to pose a carcinogenic hazard to humans and that the evidence does not support classification with regard to its carcinogenic potential [EFSA 2015a].

And again, several references quoted in the report have given rise to a great deal of uneasiness. In their review paper, Kier & Kirkland [2013] concluded that the lack of genotoxic hazard potential, evidenced by core gene mutation and chromosomal effect studies, and coupled with the very low human and environmental species systemic exposure potential, indicates that glyphosate and typical glyphosate-based formulations present negligible genotoxicity risk. Both Kier & Kirkland, however, were paid consultants of the Glyphosate Task Force for the preparation of their review, and Larry Kier was a former employee of Monsanto Company. Employment by a business or research institute whose funding was significantly derived from commercial sources could possibly have been created a conflict of interest [Robinson et al. 2013].

EFSA’s mission is to provide independent scientific advice to risk managers of the European Commission and Member States and to communicate to all interested parties and to the public at large on risks in the food and feed chain. European Member States must act in such a way that they don’t fail to meet their commitments, even when the independent scientific advice is extremely expensive.

The EFSA peer review expert group also concluded [EFSA 2015b] that the toxicity of glyphosate needs to be redefined. Pending the completion of gap-filling research, an acute reference dose (ARfD) of 0.5 mg per kg body weight[2] and an acceptable daily intake of 0.5 mg per kg body weight per day were proposed. Moreover, EFSA proposes that the toxicity of each pesticide formulation and in particular its genotoxic potential should be further considered and addressed by Member State authorities while they re-assess uses of glyphosate-based formulations in their own territories.

Carcinogenic or not carcinogenic: this was a textbook example of the paradoxical situation that affected Europe in 2015/2016. Pending a conclusion by the European Chemicals Agency (ECHA), Europe provisionally authorized glyphosate under certain conditions.

After a great deal of procrastination, ECHA concluded that there were no grounds for classifying the controversial herbicide, glyphosate, as a carcinogen, as a mutagen or as a toxic substance for reproduction. ECHA’s Committee for Risk Assessment (RAC) agreed to maintain its current harmonised classification of glyphosate as a substance causing serious eye damage and being toxic to aquatic life with long-lasting effects, and concluded that the available scientific evidence did not meet the criteria to classify glyphosate as a carcinogen, as a mutagen or as toxic for reproduction [https://echa.europa.eu].

As for EFSA, the classification is based solely on the hazardous properties of the pure substance [EFSA 2015]. Neither does it take into consideration the likelihood of exposure to the substance and so, does not address the risks of exposure.

What chemical substance are we talking about? Glyphosate — its correct IUPAC designation is N-(phosphonomethyl)glycine — is the most heavily-used agricultural chemical in the history of the world. Glyphosate is mainly used as active substance in herbicides or weed killers to prevent unwanted plant growth. It is applied to the leaves of the plants, especially the annual broadleaf weeds and grasses that compete with the crops.

Glyphosate was discovered to be an herbicide by Monsanto chemist John E. Franz in 1970. The company began to market the substance in 1974 under the trade name Roundup [Wikipedia]. Glyphosate is used in agriculture and horticulture to combat weeds before sowing. Moreover, where genetically modified plants with resistance to glyphosate are grown, Glyphosate is sometimes used after sowing to destroy weeds growing among the crops.

The proposed minimum purity of the active substance, as manufactured by the members of the European Glyphosate Task Force, varies between 950 and 983 g per kg. In other words, every kg is “contaminated” with 17 to 50 g of other chemicals, some of them relevant and others not. N-nitroso-glyphosate and formaldehyde are considered relevant impurities [EFSA 2015].

 


Widely used herbicides: also where palm trees grow! [source: PIXABAY – https://pixabay.com/]

Why are the opinions of IARC, EFSA, and ECHA fundamentally different? Or maybe they are not so different? The IARC report looked at both the active substance glyphosate as well as glyphosate-based formulations. The EU assessments, on the other hand, only considered glyphosate. IARC and EU adopted different approaches. It is the distinction between the effects of one single active substance and of pesticide formulations (mixtures of several chemicals) that explains how EFSA and IARC could express different opinions on the basis of the available data. For the EU assessment, studies conducted with glyphosate were more relevant than studies conducted with formulated products containing other constituents, particularly when the other constituents could not be clearly identified.

We know for a fact, however, that humans are chronically exposed to multiple exogenous substances, including environmental pollutants, drugs and dietary components, and we suspect that many among these compounds impact human health and that their combination in complex mixtures could significantly exacerbate their individual harmful effects. Delfosse et al. [2015], for example, clearly demonstrate that a pharmaceutical oestrogen and a persistent organochlorine pesticide, both of which exhibit low efficacy when studied separately, cooperatively bind to the pregnane X receptor, leading to synergistic activation.

Why then focus on the effects of the pure chemical rather than assess pesticide formulations? Many scientists have convincingly evidenced that the effects of mixtures differ from the sums of their individual effects [Pape-Lindstrom & Lydy 1997; Laetz et al. 2002; Gore et al. 2015; Delfosse et al. 2015; Krepker et al. 2017]. Today, the “contaminants’cocktail” remains a broadly misunderstood and insufficiently researched concept with a strong social resonance. Now is the time to invest in studies on the cocktail effects of pollutants.

This is very important, because although some studies suggest that certain glyphosate-based formulations may be genotoxic[3], others that look solely at the active substance glyphosate do not show this effect. It is therefore likely that the genotoxic effects observed in glyphosate-based formulations are caused by exposure to several constituents, such as obligatory ingredients as well as impurities. It also happens that the genotoxic effect of a mixture exceeds the sum of the individual effects since the different compounds work in synergy. It is to be expected that glyphosate-based formulations display higher toxicity than that of the active ingredient, because of the presence of other chemicals.

In its assessment, EFSA suggests that the toxicity of each pesticide formulation and in particular its genotoxic potential should be further investigated and addressed by Member State authorities as they re-assess uses of glyphosate-based formulations in their own territories. This must be done quickly! Inert ingredients can increase the ability of pesticide formulations to affect significant toxicologic end points, including developmental neurotoxicity, genotoxicity, and disruption of hormone function [Cox & Surgan 2006].

It is simply not possible to reach convincing conclusions on the basis of incomplete and poor data, and fabricated or manipulated research results. Professor Jan Tijtgat, a toxicologist at Katholieke Universiteit Leuven, has already suggested starting risk evaluation all over again.

As long as it has not been clearly demonstrated that the product is harmless, large-scale use of glyphosate should be banned by virtue of the precautionary principle that should always be applied by public authorities when managing public health risks. The precautionary principle is relevant in those specific circumstances where risk managers have identified there are reasonable grounds for concern that an unacceptable level of risk to health exists but the supporting information and data may not be sufficiently complete to enable a comprehensive risk assessment to be made. At the end of this year, the European glyphosate license will expire. Hopefully, decision makers will not lend their support to half-baked solutions!

Science moves rapidly and increases our knowledge. New approaches, accounting for chemical similarity and overlaying multiple data sources, will play a future role in risk assesments [Guha et al. 2016]. Moreover, it is now recognized that testing for glyphosate in urine can both help determine the level of exposure to glyphosate and guide towards optimal treatment plans for the patients [Shaw & Pratt-Hyatt 2017].

Premature conclusions have to be avoided, especially since additional analyses are still required by the European Member States [EFSA 2015b].

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[1] This category is used when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals. In some cases, an agent (mixture) may be classified in this category when there is inadequate evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals and strong evidence that the carcinogenesis is mediated by a mechanism that also operates in humans. Exceptionally, an agent, mixture or exposure circumstance may be classified in this category solely on the basis of limited evidence of carcinogenicity in humans (http://ec.europa.eu/health).

[2] The ARfD of a chemical is the estimated amount of a substance in food or drinking water expressed on a body weight basis that can be ingested over a short period of time, usually during one meal or one day, without appreciable health risk to the consumer on the basis of all known facts at the time of evaluation.

[3] In genetics, genotoxicity describes the property of chemical agents that damages the genetic information within a cell causing mutations [Wikipedia].

 

Alexander et al. [2007]. The non-Hodgkin lymphomas: A review of the epidemiologic literature, International Journal of Cancer 120, 1 – 39

Beecham & Seneff [2016]. Is there a link between autism and glyphosate-formulated herbicides? Journal of Autism 3, article 1

Cornwall [2017]. Update: After quick review, medical school says no evidence Monsanto ghostwrote professor’s paper, Science Daily Newsletter, March 23

Cox & Surgan [2006]. Unidentified Inert Ingredients in Pesticides: Implications for Human and Environmental Health, Environmental Health Perspectives 114, 1803 – 1806

Delfosse et al. [2015]. Synergistic activation of human pregnane X receptor by binary cocktails of pharmaceutical and environmental compounds, Nature Communications DOI: 10.1038/ncomms9089

EFSA [2015a]. Conclusion on the peer review of the pesticide risk assessment of the active substance glyphosate, EFSA Journal 13, 11, 4302, pp. 107

EFSA [2015b]. EFSA explains risk assessment – Glyphosate, https://www.efsa.europa.eu/sites/default/files/corporate_publications/files/efsaexplainsglyphosate151112en_1.pdf

Gore et al. [2015]. EDC-2: The Endocrine Society’s Second Scientific Statement on Endocrine-Disrupting Chemicals, Endocrine reviews 36, 6, E1 – E150

Guha et al. [2016]. Prioritizing Chemicals for Risk Assessment Using Chemoinformatics: Examples from the IARC Monographs on Pesticides, Environmental Health Perspectives 124, 1823 – 1829

Guyton et al. [2015]. Carcinogenicity of tetrachlorvinphos, parathion, malathion, diazinon, and glyphosate, Lancet Oncology 16, 5, 490 – 491

Hammond et al. [2004]. Results of a 13 week safety assurance study with rats fed grain from glyphosate tolerant corn, Food and Chemical Toxicology 42, 1003 – 1014

Hoppin et al. [2017]. Pesticides are Associated with Allergic and Non-Allergic Wheeze among Male Farmers, Environmental Health Perspectives 125, 535 – 543

Jayasumana et al. [2014]. Glyphosate, Hard Water and Nephrotoxic Metals: Are They the Culprits Behind the Epidemic of Chronic Kidney Disease of Unknown Etiology in Sri Lanka? International Journal of Environmental Research and Public Health 11, 2125 – 2147

Jayasumana et al. [2015]. Drinking well water and occupational exposure to Herbicides is associated with chronic kidney disease, in Padavi-Sripura, Sri Lanka, Environmental Health 14, 1, pp. 10

Kier & Kirkland [2013]. Review of genotoxicity studies of glyphosate and glyphosate-based formulations, Critical Reviews in Toxicology 43, 4, 283 – 315

Krepker et al. [2017]. Active food packaging films with synergistic antimicrobial activity, Food Control 76, 117 – 126

Laetz et al. [2002]. The Synergistic Toxicity of Pesticide Mixtures: Implications for Risk Assessment and the Conservation of Endangered Pacific Salmon, Environmental Health Perspect 117, 348 – 353

Michaels [2008]. Doubt is their product, Oxford University Press, pp. 372

Pape-Lindstrom & Lydy [1997]. Synergistic toxicity of atrazine and organophosphate insecticides contravenes the response addition method, Environmental Toxicology and Chemistry 16, 11, 2415 – 2420

Parks et al. [2017]. Rheumatoid Arthritis in Agricultural Health Study Spouses: Associations with Pesticides and Other Farm Exposures, Environmental Health Perspectives 124, 1728 – 1734

Robinson et al. [2013]. Conflicts of interest at the European Food Safety Authority erode public confidence, Journal of epidemiology and community health 0, 1 – 4

Sealy et al. [2016]. Environmental factors in the development of autism spectrum disorders, Environment International 88, 288 – 298

Shaw & Pratt-Hyatt [2017]. The importance of testing for glyphosate: the world’s most widely used herbicide, http://www.immh.org/article-source/2017/2/2/the-importance-of-testing-for-glyphosate-the-worlds-most-widely-used-herbicide

Williams et al. [2000]. Safety Evaluation and Risk Assessment of the Herbicide Roundup and Its Active Ingredient, Glyphosate, for Humans, Regulatory Toxicology and Pharmacology 31, 2, 117 – 165

By uncovering its genetic journey,
researchers believe they can restore the flavour of the old-fashioned tomato 

 

What is wrong with the ubiquitous and attractive supermarket tomatoes? For many city dwellers, the delicious taste of a succulent garden tomato is little more than a distant memory. The standard grocery varieties have grown larger and blander. Indeed, the decline in flavour quality of the modern commercial tomato compared to heirloom varieties is often the cause of consumer complaints.


tomatoes-1220774_1280

The colours of a rainbow appear after violent storms [source: PIXABAY – https://pixabay.com/]

 

To address the problem an international research team under the leadership of professor Harry Klee of the University of Florida performed a comprehensive study of the chemistry and genetics of tomato flavour. Tieman et al. [2017] identified the key flavour-enhancing genes that have dwindled or disappeared as the tomato changed over the years. These researchers also believe they are able to return their original taste to today’s fresh market tomatoes.

Flavour is an intricate combination of what the tongue tastes and the nose smells. The flavour of any food item can be regarded as the sum of interactions between taste and olfaction. Taste is one of the five traditional senses that belong to the gustatory system, whereas olfaction is the sense of smell [Wikipedia]. For the tomato, sugars such as glucose and fructose and acids such as citrate and malate activate the taste receptors. On the other hand, a highly diverse set of volatile compounds including alcohols and aldehydes such as 3-methyl-1-butanol, cis-3-hexen-1-ol and hexanal activate the olfactory receptors [Tieman et al. 2012]. Volatiles in particular are essential for good flavour.

For commercial reasons, breeders predominantly focus on yield, disease resistance, and external appearance rather than flavour quality. Also, the fruit and vegetable flavour associated volatiles are present at nano to subnanomolar concentrations. They are difficult to identify and quantify and therefore, have received significantly less attention. Unfortunately, over recent decades, the strong emphasis on production traits has inadvertently led to a decline in flavour quality. Several scientists also refer to the steadily declining nutrient content in cultivated varieties [Davis et al. 2004].

Breeders have selected plants to produce huge amounts of fruit. What they want is larger fruit on the plant. But since the plant cannot cope, what happens is a substantial dilution of the flavour chemicals. Putting tastier sugar back into mainstream tomatoes is simply not feasible with today’s production. That is because growers are not paid for flavour, but per kilo. It costs just as much to have a worker pick a small tomato as it does to pick a huge one, which explains why commercially produced tomatoes are much more massive than their tiny wild ancestors.

Today, however, our first priority is no longer how well tomatoes ship and last on a shelf. The number one priority has now become to substantially increase fruit quality with minimal impact on yield.

Will scientists breed much better tomatoes by focusing on flavour genes? The answer is they soon will.

Step one was to identify the chemical tomato components that most contribute to taste. The researchers studied the alleles, i.e. the variants of a tomato gene located at a specific locus on a chromosome. Alleles induce specific traits. Most genes have two alleles, a dominant and a recessive one. In a certain sense, allele differences can be likened to DNA in humans. We all have the same number of genes in our DNA, but a particular version of each gene determines the specific characteristics, i.e. how heavy we are, how tall, whether we have blue or brown eyes and…

The aim of the study was to uncover why modern tomato varieties are deficient in those flavour chemicals; why they have lost the more desirable alleles of a number of genes. Researchers therefore had to identify the locations of the good alleles in the tomato genome. This required what is called a genome-wide assessment study.

Modern commercial tomato varieties were found to have substantially less flavour than heirloom varieties. To understand and ultimately correct this deficiency, the research team quantified flavour-associated chemicals in 398 modern, heirloom, as well as wild accessions. To include wild accessions and the closest relative of the commercial tomato provided a baseline for its chemical composition before human intervention. A subset of these accessions was evaluated in consumer panels to identify the chemicals that made the most important contributions to flavour and consumer appreciation. It was particularly obvious that modern commercial varieties contain significantly lower amounts of many of these important flavour chemicals than older varieties. The whole-genome sequencing and a genome-wide association study enabled the genetic loci to be identified that affect most of the target flavour chemicals including sugars, acids, and volatiles. Together, these results provide an understanding of the flavour deficiencies in the tomatoes we buy and the information necessary for the recovery of good flavour through molecular breeding [Tieman et al. 2017].

The scientists mapped the genes that control the synthesis of all important chemicals. Once they had found them, they used genetic analysis to replace bad alleles in modern tomato varieties with better ones. So it appears that it is possible to significantly improve our average, ordinary grocery tomatoes. If these tomatoes could be improved, it would be a big gain for consumers, and this study outlines how to do so.

Will the high-taste, high-quality, and inevitably higher-cost tomatoes sell? Because breeding takes time, it may take three or four years before the genetic traits analysed in the present are actually produced in new tomato varieties. This sounds like great news. Let’s not forget, however, that a really tasty tomato is one that ripens on the vine, and that post-harvest practices such as refrigeration can irreversibly damage flavour.

Super tasty tomatoes cannot be produced over long distances and cannot be stored in a grocery store for four weeks without rotting.

Remember also that prime quality comes at a price.

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Davis et al. [2004]. Changes in USDA Food Composition Data for 43 Garden Crops, 1950 to 1999, Journal of the American College of Nutrition 23, 6, 669 – 682

Tieman et al. [2012]. The Chemical Interactions Underlying Tomato Flavor Preferences, Current Biology 22, 1035 – 1039

Tieman et al. [2017]. A chemical genetic roadmap to improved tomato flavor, Science 355, 391 – 394

 

 

Show more determination, please !

Les perturbateurs endocriniens, une menace pour le développement du cerveau (Endocrine disrupters, a threat to brain development) is the striking title of an article by Ludmilla Terres that was published in the French newspaper Le Monde, on March 7th this year. I often ask myself whether exposure to chemical compounds affects our brain development; whether exposure to endocrine disrupting chemicals (EDCs) undermines our intelligence; and whether exposed mothers who are unaware of the threat deliver mentally retarded children.

Brussels is not in the clear yet. Very recently, the EU executive refrained from voting on the criteria for the identification of endocrine disrupters even though criteria are urgently required. Regulatory indecision is probably the last thing we need.

It is general knowledge that omnipresent endocrine disrupting chemicals alter the subtle balance of the hormonal system. Two recently published studies point to endocrine disrupters and their impact on brain growth and development. Fini et al. [2017] conclude that there are multiple impacts on brain development even when exposure times are very short. The authors put forward a twofold, alarming message: (1) obviously, exposures may have several effects (in the plural!) rather than one single effect, and (2) even very short exposures are not safe. Embryos of the species Xenopus laevis, the African clawed frog, were exposed for three days to a chemical cocktail whose concentrations were comparable to those commonly measured in the human amniotic fluid, commonly called a pregnant woman’s water. The age of the embryos was selected according to the onset of the thyroid function, which releases the thyroid hormones essential for good brain development.

As thyroid hormone signalling is strongly conserved across all vertebrates, the results of the study clearly suggest that ubiquitous EDC mixtures exert adverse effects on fœtal human brain development. There can be no doubt that the fœtus can be indirectly exposed to toxic substances. This message had already been clearly expressed in Losing Our Minds, the book published by Prof. Barbara Demeneix [2014].

Granted, Fini et al. [2017] actually use the term “suggest”, meaning they cannot offer complete (100 %) certainty. No known test method can offer complete certainty. Uncertainty is intrinsic to science and all progress in the field of knowledge implies that scientists push back the boundaries of scientific uncertainty. Some however equate uncertainty with anomaly and transform it into doubt [Michaels 2008; Proctor 2012].

The authors of the CHEMTrust report [2017] remind us how extremely complex the ~85 billion neurones of the brain are. A delicate and elaborate development takes place throughout our lifetimes. But the early stages of our development, from the fœtus to adolescence, are rapidly changing, and have a high sensitivity to toxic chemicals. In these early development stages, disturbance of thyroid hormones can lead to significant, adverse effects, such as reduced IQ or autism spectrum disorders. When exposure occurs after birth, the associated risks are usually decreased motor ability and concentration.

When the first exposure takes place during pregnancy, at a time when the human body is most vulnerable, when it is being shaped by the hormones, EDCs can have an irreversible effect. Then there is no cure!

Prof. Philippe Grandjean [2013] highlights the silent pandemic since industrial chemicals have begun to disrupt brain development. He confirms that we are only given one chance to develop a brain and that damage to the developing brain of a fœtus or child is very likely to have lifelong effects. Besides listing 213 industrial chemicals that are able to reach the brain and cause brain toxicity — he refers to them as the “brain drainers” — he also provides detailed examples of the effects of lead, mercury, arsenic, polychlorinated biphenyls and pesticides in his book Only one chance.

Haven’t there been enough alerts already on the dangers of EDCs? Many have raised the alarm and denounced the collusion that exists between industrial stakeholders and public health authorities when it comes to regulating pervasive chemicals in our daily lives and environment. For example, one hundred scientists appealed to Europe and the international community insisting that they act against EDCs. They blamed the industry for using doubt manufacturing strategies similar to those used in the fight against climate change  [Kortenkamp 2016]. Industry has long understood that to debate the science is mostly easier and more effective than to debate the policy. The manufacturing of doubt has resulted in significantly delayed protective actions, with adverse consequences for the health of people as well as for the environmental quality [Michaels 2008; Proctor 2012].

Professor Andreas Kortenkamp is the lead author of several detailed reports on EDCs [Kortenkamp et al. 2009; Kortenkamp et al. 2011]. He underlines the general consensus that EDCs are very unsafe and require a specific approach in terms of chemical regulation. The ultimate goal of European regulation is to reveal the dangers before exposures occur. Kortenkamp et al. strongly believe we must anticipate the danger and ensure that humans are not exposed.

On 23rd December 2011, Kortenkamp and his team published their long-awaited report State of the Art Assessment of Endocrine Disruptors. The authors concluded unambiguously  that EDCs justify the same consideration as the highly concerning carcinogenic, mutagenic and reprotoxic substances as well as the persistent, bio-accumulative and toxic products. Their toxicity is seen as extremely dangerous. They concluded that the European Commission should not only take into account the concept of potency. Instead, their report recommends a list of criteria that besides potency would include, e.g., the mode of action of the product as well as the severity and irreversibility of the effects. None of these criteria should be left out to ensure the approach is as broad and as open as possible. Considering potency alone should apply only when regulating and labelling acutely toxic chemical substances –poisonous substances that will kill you almost immediately after exposure.

Industrial stakeholders were none too happy with these conclusions. There were strong reactions and the European Commission dragged its feet.

The regulatory project was delayed following intensive lobbying by both the pesticide and chemical industries. Obviously, regulating ubiquitous chemical substances like endocrine disruptors is regarded as a sea change by the industries concerned, and a threat to their turnover.

Other striking titles that point to a highly inconvenient truth! Our intellectual climax dates back many years [Crabtree 2013 A & 2013 B; Woodley et al. [2013]. On the one hand, Woodley et al. [2013] computed the true correlation between simple reaction time and the g factor of intelligence by using a psychometric meta-analysis. The g factor — also known as general intelligence, general mental ability or general intelligence factor — is a construct developed in psychometric investigations of cognitive abilities and human intelligence [Wikipedia]. The approach of Woodley et al. [2013] yields a decline of ~1.16 IQ points per decade or ~13.35 IQ points since Victorian times. In other words, their findings demonstrate that with respect to g the Victorians were substantially smarter than modern Western populations.

On the other hand, Crabtree [2013 A & 2013 B] argues that the intelligence of human beings has been on a downward slope for quite some time. His study suggests that the human species has been stunned by involuntary changes in the human genetic code as well as by the technological developments that significantly facilitate our access to comfort.  Crabtree concludes that our intellect is fragile.

This means we need to be extremely careful not to mortgage the future and more especially, the future of younger generations. Now, more than ever, all of us need real sound science. I deliberately use the term “sound science”. Years ago Philip Morris (PM) attacked “junk science” to discredit the evidence that second-hand smoke (and other environmental toxins) causes disease. PM used public relations companies and lawyers to organise a “sound science” programme that included disseminating its own (epidemiological) information about the health effects of tobacco products and getting decision makers on side [Ong & Glantz 2001].

Polluters are keen to tout “sound science”, but what they are really promoting just “sounds like science” but isn’t [Michaels 2008].

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CHEMTrust [2017]. No Brainer – The impact of chemicals on children’s brain development: a cause for concern and a need for action, http://www.chemtrust.org.uk/

Crabtree [2013 A]. Our fragile intellect Part I, Trends in Genetics 29, 1, 1 – 3.

Crabtree [2013 B]. Our fragile intellect Part II, Trends in Genetics 29, 1, 3 – 5.

Demeneix [2014]. Losing Our Minds: How Environmental Pollution Impairs Human Intelligence and Mental Health, Oxford University Press

Fini et al. [2017]. Human amniotic fluid contaminants alter thyroid hormone signalling and early brain development in Xenopus embryos, Scientific Reports 7, Article number: 43786

Grandjean [2013]. Only one chance: how environmental pollution impairs brain development – and how to protect the brains of the next generation, Oxford University Press

Kortenkamp et al. [2009]. State of the Art Report on Mixture Toxicity, Study contract number 070307/2007/485103/ETU/D.1

Kortenkamp et al. [2011]. State of the Art Assessment of Endocrine Disrupters, Project contract number 070307/2009/550687/SER/D3

Kortenkamp [2016]. Perturbateurs endocriniens: halte à la manipulation de la science, Le Monde, November 29

Michaels [2008]. Doubt is their product – How Industry’s Assault on Science Threatens Your Health, Oxford University Press

Ong & Glantz [2001]. Constructing “Sound Science” and “Good Epidemiology”: Tobacco, Lawyers, and Publication Relations Firms, American Journal of Public Health 91, 11, 1749 – 1757

Proctor [2012]. Golden Holocaust: Origins of the Cigarette Catastrophe and the Case for Abolition, Berkeley: University of California Press

Woodley et al. [2013]. Were the Victorians cleverer than us? The decline in general intelligence estimated from a meta-analysis of the slowing of simple reaction time, Intelligence 41, 6, 843 – 850

Problems related to a one-sided menu. Corn turns hamsters into cannibals

The European hamster (Cricetus cricetus) population, still very abundant in French Alsace as late as the 1960s, has been reduced to some 450 individuals today. What is the way of life of this small rodent? Why is its habitat collapsing? What challenges are to be faced to preserve Alsatian large hamster populations?

The main reason generally put forward for the population decline remains the destruction of the hamster’s habitat by the propagation of industrial and inappropriate crops — corn in particular — and intensive (and excessive) urbanization causing fragmentation of Cricetus habitats. This sounds like a very plausible explanation for what can only be described as a very serious and extremely alarming situation. Witness this striking title in the scientific literature: Diets derived from maize monoculture cause maternal infanticides in the endangered European hamster due to vitamine B3 deficiency. A diet of corn (or maize) turns hamster mothers into deranged cannibals that devour their offspring [Tissier et al. 2017].

Worldwide changes to forests and farmlands, aquatic ecosystems, and air are driven by our need to provide food, fibre, water, and shelter to more than seven billion people. Ironically, just as our land use practices are degrading ecological conditions across the globe, humanity has become dependent on an ever increasing share of the biosphere’s resources. Global croplands, pastures, plantations, and urban areas have significantly expanded. Unfortunately, this is accompanied by large increases in energy, water, and fertilizer consumption, along with considerable losses of biodiversity [Foley et al. 2005]. Moreover, the resulting decline in biodiversity has led to a reduction in so-called ecosystem services, which are seriously affecting human safety and nutrition. Indirect land-use effects, meaning those mediated by biodiversity loss and by changes to functional composition, are found to be as strong as direct effects [Foley et al. 2005; Diaz et al. 2006; Allan et al. 2015].

Whereas it formerly found its nourishment in a variety of grains, roots and insects, the burrowing hamster now lives in a sea of industrially grown corn. Earlier investigations looked at the impact of pesticide exposures and mechanised ploughing, which can destroy the hamsters’underground caves, especially during hibernation, but the possible link with what they eat remained largely unexplored.

The findings, reported by Tissier et al. [2017], point to industrial scale monoculture as the culprit. The monotonous diet leaves the animals starving, as the French team discovered. A first set of laboratory experiments with wild specimens compared wheat and corn-based diets, with side dishes of clover or worms. Though there was virtually no difference in the number of pups born, when it came to survival rates, the difference was dramatic. About 80 % of the pups born of mothers feasting on

wheat-and-clover or wheat-and-worms were weaned. However, only ~5 % of the baby hamsters whose mothers ate corn instead of wheat made it that far. Corn lacks several micronutrients such as calcium, tryptophan, lysine, riboflavin, and especially vitamin B3. Vitamin B3 is also known as niacin and nicotinic acid.

It is one of the essential human nutrients. Pharmaceutical and supplemental niacin are primarily used to treat hypercholesterolemia (high cholesterol) and pellagra (niacin deficiency). Insufficient niacin in the diet is known to cause nausea, skin and mouth lesions, anaemia, headaches, and tiredness in humans [Wikipedia]. An unbalanced corn-based diet has been associated with high rates of homicide, suicide and cannibalism in humans [Ernandes et al. 1996; Ernandes 2002] and may cause pellagra, which decimated millions of people in North America and Europe between the mid-18th and the mid-20th century [Hegyi et al. 2004].

Even more disturbing is how the pups perished. Hamster mothers stored their living pups with their hoards of maize before eating them. Tissier et al. [2017] reported that the high propensity of corn caused abnormal maternal behaviour, infanticide and siblicide, associated with diarrhoea and skin problems in the pups. The symptoms obviously resemble those observed in humans affected by pellagra [Hegyi et al. 2004] as well as the symptoms of canine black tongue disease.

In an additional set of experiments, the hamsters were offered corn-based diets, one of them with vitamin B3 added. Sure enough, the vitamin B3-enriched diet eliminated the horrific symptoms and prevented the hamster mothers from eating their offspring. The dire consequences of the vitamin B3-deficient corn diet, the scientists concluded, stemmed not from reduced maternal hormones, but rather from a change in the nervous system that induced the same dementia-like behaviour previously diagnosed in humans.

Monoculture in agriculture is really bad for biodiversity. Given the intensification of maize monoculture across the globe ¾ inherently associated with a reduction in diversity and abundance of other plants, soil fauna and microorganisms ¾ the overabundance of corn compared with other food plants in the diet of farmland animals will be detrimental for their survival and fitness.

And what about humans who intentionally or unintentionally fail to consume well-balanced and varied diets?

 

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Allan et al. [2015], Land use intensification alters ecosystem multifunctionality via loss of biodiversity and changes to functional composition, Ecology Letters 18, 834 – 843

Diaz et al. [2006]. Biodiversity Loss Threatens Human Well-Being, PLoS Biology 4, 8, 1300 – 1305

Ernandes et al. [1996]. Maize based diets and possible neurobehavioural after-effects among some populations in the world, Human Evolution 11, 1, 67 – 77

Ernandes et al. [2002]. Aztec Cannibalism and Maize consumption: The serotonin deficiency link, The Mankind Quarterly 43, 1, 3 – 40

Foley et al. [2005]. Global Consequences of Land Use, Science 309, 570 – 574

Hegyi et al. [2004]. Pellagra: Dermatitis, dementia, and diarrhea, International journal of dermatology 43, 1, 1 – 5

Tissier et al. [2017]. Diets derived from maize monoculture cause maternal infanticides in the endangered European hamster due to vitamine B3 deficiency, Proceedings of the Royal Society B 284, 2016 – 2168

Dioxins levels in fertilizers from Belgium: Determination and Evaluation of the Potential Impact on Soil Contamination

Dioxins are harmful persistent organic pollutants (POPs) to which humans are exposed mostly via the consumption of animal products. They can enter the food chain at any stage, including crop fertilization. Fertilizers belong to several categories: synthetic chemicals providing the essential elements (mostly N, P and K) that are required by the crops but also organic fertilizers or amendments, liming materials, etc. Ninety-seven samples of fertilizers were taken in Belgium during the year 2011 and analyzed after a soft extraction procedure for polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs) and dioxin-like polychlorinated biphenyls (DL-PCBs) using GC-IDHRMS. Only small qualitative differences could be observed between the main fertilizer categories since the PCDD:PCDF:DL-PCB average ratio obtained with the results expressed in TEQ was often close to 30:30:40 (typically for sewage sludge) or 40:30:30 (typically for compost). The median dioxin levels determined were generally lower than recorded previously and were the highest for sewage sludge and compost (5.6 and 5.5 ng TEQ/kg dry weight (dw), respectively). The levels in other fertilizers were lower including manure for which the median value was only 0.2 ng TEQ/kg dw. Several fertilization scenarios relying on the use of those fertilizers were assessed taking into consideration the application conditions prevailing in Belgium. From this assessment it could be concluded that the contribution of fertilizers to the overall soil contamination will be low by comparison of other sources of contamination such as atmospheric depositions. At the field scale, intensive use of compost and sewage sludge will increase dramatically the dioxin inputs compared with other fertilization practices but this kind of emission to the soil will still be relatively low compared to the dioxin atmospheric depositions.

Bisphenol-A: review of food and non-food sources

Due to the large number of applications of bisphenol-A (BPA), the human exposure routes are multiple. We aimed to review shortly the food and non-food sources of BPA, and to evaluate their contribution to the human exposure. Food sources discussed here include epoxy resins, polycarbonate and other applications, such as paperboard and polyvinylchloride materials. Among the non-food sources, exposures through dust, thermal paper, dental materials and medical devices were summarized. Based on the available data for these exposure sources, it was concluded that the exposure to BPA from non- food sources is generally lower than that from exposure from food by at least one order of magnitude for most studied subgroups. The use of urinary concentrations from biomonitoring studies was evaluated and the backcalculation of BPA intake seems reliable for the overall exposure assessment. In general, the total exposure to BPA is several orders of magnitude lower than the current tolerable daily intake of 50 µg/kg bw/day. Finally, the paper concludes with some critical remarks and recommendations on future human exposure studies to BPA.Due to the large number of applications of bisphenol-A (BPA), the human exposure routes are multiple. We aimed to review shortly the food and non-food sources of BPA, and to evaluate their contribution to the human exposure. Food sources discussed here include epoxy resins, polycarbonate and other applications, such as paperboard and polyvinylchloride materials. Among the non-food sources, exposures through dust, thermal paper, dental materials, and medical devices were summarized. Based on the available data for these exposure sources, it was concluded that the exposure to BPA from non-food sources is generally lower than that from exposure from food by at least one order of magnitude for most studied subgroups. The use of urinary concentrations from biomonitoring studies was evaluated and the backcalculation of BPA intake seems reliable for the overall exposure assessment. In general, the total exposure to BPA is several orders of magnitude lower than the current tolerable daily intake of 50 lg/kg bw/ day. Finally, the paper concludes with some critical remarks and recommendations on future human exposure studies to BPA.

A predictive algorithm for the global migration testing of food contact moulds

For reasons of food safety, packaging and food contact materials must be submitted to migration tests. Testing of silicone moulds is often very laborious, since three replicate tests are required to decide about their compliancy. This paper presents a general modelling framework to predict the sample’s compliance or non-compliance using results of the first two migration tests. It compares the outcomes of models with multiple continuous predictors with a class of models involving latent and dummy variables. The model’s predictionability was tested using cross and external validations, i.e. model revalidation each time a new measurement set became available. At the overall migration limit of 10 mg.dm-2 relative uncertainty on a prediction was estimated to be ∼10%. Taking the default values for a and b equal to 0.05, the maximum value that can be predicted for sample compliance was therefore 7mg.dm- 2 . Beyond this limit the risk for false compliant results increases significantly, and a third migration test should be performed. The result of this latter test defines the sample’s compliance or non-compliance. Propositions for compliancy control inspired by the current dioxin control strategy are discussed. , the