27.04.2010: Nicotine dependence
Recent articles report that genetic mutations on chromosomes 8, 15 and 19 make addiction to smoke more critical, and they are more prone to lung cancer compared to persons without this mutation. Also chromosome 11 is known to intensify the addiction, but chromosome 9 contains a gene which make it less difficult to stop smoking.
The researchers say that some genes are responsible for the synthesis of enzymes which may be active in metabolising nicotine. Nicotine activates the nicotine receptors in the brain which releases the "feel good" hormones dopamine and serotonine.

Genes associated with smoking behaviour [1]
The Tobacco and Genetics Consortium together with the European Network of Genetic and Genomic Epidemiology and the Oxford-GlaxoSmithKline identified three loci associated with number of cigarettes smoked per day. These loci were the 15q25 single-nucleotide polymorphism (SNP) in the nicotinic receptor gene CHRNA3, two 10q25 SNPs, and one 9q13 SNP in EGLN2. Other genes were found which facilitate smoking initiation, and other genes which are. The good news are that one loci located on chromosome 9 was significantly associated with smoking cessation.

Smoking behaviour and genetics [2]
Thorgeirsson and colleagues report that variants in the genomic regions at 15q25, 19q13, 8p11, and rs6474412-T are related to number of cigarettes smoked per day. Two loci are genes encoding nicotine-metabolizing enzymes (CYP2A6 and CYP2B6) and nicotinic acetylcholine receptor subunits (CHRNB3 and CHRNA6), already known to be related to smoking and nicotine dependence. The genes at 8p11 and 19q13 are linked with lung cancer

Gene locus on 15q25 associated with smoking quantity [3]
Liu and colleagues 2010 confirmed an effect on smoking quantity at a locus on 15q25 that includes CHRNA5, CHRNA3 and CHRNB4, three genes encoding neuronal nicotinic acetylcholine receptor subunits.

Genetics as culprit to failure to quit smoking? [4]
Chapman and MacKenzie 2010 argue that the volume of research and effort devoted to professionally and pharmacologically mediated cessation is in inverse proportion to that examining how most ex-smokers actually quit.
The authors say that final results of nicotine replacement therapy or other drugs is dramatically overestimated. Many of these studies are funded by pharmaceutical companies.

Up to three-quarters of ex-smokers have quit without assistance, and unaided cessation is by far the most common method used by most successful ex-smokers. Recidivism is normal if efforts are not serious attempts. The increasing medicalisation of smoking cessation implies professionally mediation. The author call on health authorities emphasise the positive message that the most successful method used by most ex-smokers is unassisted cessation. Nicotine replacement therapy may help, but is not used in most cases of successful cessations.

Small hint to quit smoking: The most stringent factor needed to stop smoking is a strong will to do it. The first 4 days of cessation are difficult. You have to avoid any trouble. Take a vacation or some days off for the start. You will feel sick and nervous. Remember that after this period you will feel better each day. You will be proud of your mental strength and you will be able to handle other weaknesses much easier. Do not blame genetics. Pharmaceutical companies, like Oxford-GlaxoSmithKline, pose to much emphasis on studies related to nicotine replacement and genetics. It is your strength which you have to rely on.

[1] The Tobacco and Genetics Consortium: Genome-wide meta-analyses identify multiple loci associated with smoking behavior. Nature Genetics Published online: 25 April 2010. Doi:10.1038/ng.571

http://www.nature.com/ng/journal/vaop/ncurrent/abs/ng.571.html#/

[2] Thorgeirsson et al.: Sequence variants at CHRNB3–CHRNA6 and CYP2A6 affect smoking behavior. Nature Genetics. 25 April 2ß1ß. Doi:10.1038/ng.573
http://www.nature.com/ng/journal/vaop/ncurrent/abs/ng.573.html#/

[3] Liu et al: Meta-analysis and imputation refines the association of 15q25 with smoking quantity. Nature Genetics. 25 April 2010. Doi:10.1038/ng.572
http://www.nature.com/ng/journal/vaop/ncurrent/abs/ng.572.html#/ar

[4] Chapman, Simon; MacKenzie, Ross: The Global Research Neglect of Unassisted Smoking Cessation: Causes and Consequences. PLoS Med 7(2), February 9, 2010: e1000216. doi:10.1371/journal.pmed.1000216
http://www.plosmedicine.org/article/info:doi/10.1371/journal.pmed.1000216

27.04.2009: Guar gum thickening agent contaminated with high levels of dioxin [1]
In 2007 after high levels of the dioxin pentachlorophenol (PCP) were discovered in Indian guar gum shipments. India is leading guar gum producer, counting for 80 to 90% of the world production.

The latest inspection mission of the EU in 2009 discovered serious serious deficiencies of the Indian control measures to prevent contamination of guar gum with pentachlorophenol (PCP) and dioxins.
With availability of sodium pentachlorophenolate and its use in the guar gum industry, and with a largely self regulated industry, there are inadequate controls in place to ensure that this contamination does not occur again. [2]
To avoid further risks of dioxins in Indian guar gum the European Commission introduce a compulsory inspection system of 5% of imports. Food industry says that these inspections will increase price pressure on European food producers.

Consumer should avoid products with thickening agent guar gum E412
The call for low prices on detriment of food safety cannot be justified. The consumer can da his own safety inspection reading the ingredient list and ban those products bearing guar gum.

A call for cost reductions disastrous for pork meat in Ireland [3]
In December 2008 pig farms were blocked as meat of their livestock were found contaminated with polychlorinated biphenyls (PCBs) at levels up to 200 pg WHO-TEQ / g fat in pig meat originating in Ireland.
The use of feed containing contaminated bread crumbs produced from bakery waste was identified to be the source. The contamination was due to a cost efficient direct heating process whereby chimney stack combustion gases came in direct contact with the material to dry and whereby an inappropriate fuel was used.

The toxic responses to dioxins include dermal toxicity, immunotoxicity, carcinogenicity, reproductive and developmental toxicity. The toxicity of dioxins is related to the amount accumulated in the body during a lifetime, the so-called body burden. A tolerable weekly intake (TWI) of 14 pg WHO-TEQ/kg body weight (b.w.) has been established by the Scientific Committee on Food (SCF) in 2001.

The term “dioxins” refers to a group of chemically and structurally related halogenated aromatic hydrocarbons, including 75 polychlorinated dibenzo-p-dioxin (PCDD) and 135 polychlorinated dibenzofuran (PCDF) congeners. Dioxins are widely distributed contaminants formed as unwanted by-products in a number of anthropogenic activities, involving incomplete combustion processes, both industrial and natural. They also occur as contaminants during various industrial processes, e.g. the chemical manufacture of some chlorinated compounds and chlorine bleaching of paper pulp.

[1] Commission Regulation (EU) No 258/2010 of 25 March 2010 imposing special conditions on the imports of guar gum originating in or consigned from India due to contamination risks by pentachlorophenol and dioxins, and repealing Decision 2008/352/EC
http://eur-lex.europa.eu/LexUriServ/LexUriServ.do?uri=OJ:L:2010:080:0028:0031:EN:PDF

[2] Dioxins in guar gum from India
http://ec.europa.eu/food/food/chemicalsafety/contaminants/dioxins_en.htm

[3] Statement of EFSA on the risks for public health due to the presence of
dioxins in pork from Ireland (Question No EFSA-Q-2008-777) Issued on 10 December 20081.
http://www.efsa.europa.eu/en/efsajournal/doc/contam_ej_911_dioxins_rev2.pdf?ssbinary=true

25.04.2010: Dark chocolate reduces liver blood pressure [1]
The cocoa flavonoids, which are present in dark chocolate, are strong antioxidants. De Gottardi and colleagues 2010 found dark chocolate to exert beneficial effects on patients with liver cirrhosis reducing the damage to the blood vessels.
The researchers compared the effect of a diet containing dark chocolate with a diet containing white chocolate. Both meals caused a highly significant increase in portal blood flow which was lower in patients receiving the dark chocolate, compared with the white chocolate diet. A smaller post-prandial hepatic vein pressure gradient HVPG reduces the risk of blood vessel ruptures. The authors concluded that meals containing dark chocolate reduces post-prandial increase in portal pressure in liver patients, caused by a reduction of the oxidant stress of the hepatic endothelial cells. This results in vasorelaxation and consequent reduction of the blood pressure in the liver..

[1] De Gottardi A, Berzigotti A, Seijo S, D'Amico M, Abraldes J, Garcia-Pagán JC, Bosch J:Dark chocolate attenuates the post-prandial increase in HVPG in Patients with cirrhosis and portal hypertension. Oral Presentation at the International Liver Congress. April 15, 2010.
http://www.kenes.com/easl2010/orals/124.htm

25.04.2010: Fresh unmodified goat's milk is dangerous for infants [1]

Basnet and colleagues 20101 assessed the dangers of feeding infants exclusively with unmodified goat's milk. This practice is based on cultural beliefs as well on false informations in media. The risks are severe electrolyte abnormalities, metabolic acidosis, megaloblastic anemia, allergic reactions including life-threatening anaphylactic shock, hemolytic uremic syndrome, and infections.

In addition to these evidences, the authors reported a case of sustained intracranial infarctions in the setting of severe azotemia and hypernatremia on an infant following a raw goat's milk diet.

[1] Basnet S, Schneider M, Gazit A, Mander G, Doctor A: Fresh goat's milk for infants: myths and realities - a review. Pediatrics. 2010 Apr;125(4):e973-7. Epub 2010 Mar 15.
http://www.ncbi.nlm.nih.gov/pubmed/20231186

23.04.2010: No immediate concerns for animal or crop production regarding volcano ash [1]
DEFRA states that there continues to be no recorded impact on air quality, water quality or water supply, and no immediate concerns for animal health or crop production following the volcanic eruption in Iceland on Wednesday 14 April.

Any risks affect only people living close to the eruption [2]
According to Fernando Holguin, MD, much of the particulate matter that comes from volcanic eruptions are actually filtered in the upper atmosphere and are not as harmful as the particulate matter that comes from car exhaust. Any health risks would only affect people living relatively close to the eruption because of high concentrations of particles and large amounts of sulfur dioxide.

Much more dangerous are the fine particles emitted by motor vehicles that are smaller than 2.5 microns and are harmful to cardiovascular and respiratory health because they can get into the blood stream.

Health effects [3]
Volcanic ash isharp, has a crystalline structure which causes it to scratch and abrade surfaces when it is removed by wiping or brushing. Rainfall and wind are effective in removing the ash and grass and other plants will eventually bind it to the soil.

Medical services can expect an increase number of patients with respiratory and eye symptoms during and after ash fall. Ash is composed of particles of minerals quartz, cristobalite, or tridymite. These are free crystalline silica known to cause silicosis, a disabling and potential fatal lung disease typically found in miners and quarry workers exposed to high concentrations of siliceous dust over long periods of time. Exposure to respirable-sized free crystalline silica from most ash falls are typically of short duration (days to weeks), and data suggests that the recommended respirable exposure limit of 50 micrograms/m3 of air can be exceeded for short periods of times for the general population.

The Health Protection Agency sees no significant risk to public health because ash cloud is at high altitude [4]
The HPA will continue to monitor the plume's movement although is not expected to touch ground over the UK in the near future. Even if the plume does drop towards the ground the concentrations of particles at ground level are not likely to cause significant effects on health. Rainfall over the UK could cause a small amount of the ash to be deposited over the country but quantities are expected to be too small to cause health effects.

Volcano ash effect on agriculture and food safety [5]
The ash would not only fertilise plants but help the soil hold water and encourage bacteria.
However volcanoes can also spew out poisonous ash and government officials are keeping an eye on the situation because of the risk to UK agriculture.

Soluble fluoride on volcanic ash and scoria from the eruption on Eyjafjallajökull-Fimmvörduháls [6]
The Institute of Earth Sciences. Nordic Volcanological Center. University Iceland published results of volcanic ash: Soluble fluoride on ash surface: mg F pr. kg ash (ppm).
- Sample from the eruption site - fine glassy scoria: (pH 6.45) Fluoride 92 ppm (Leached in the laboratory. Fluoride and pH of leachate measured in the laboratory).
- Ash sample from snow on the lowland - glassy ash 0.2-1 mm: (pH 5.66) Fluoride 112 ppm (Fluoride and pH measured in meltwaer).

Comment: The leachate is slightly acidic suggesting minor condensate from volcanic gases on grain surfaces. It is pointed out that the samples are coarse ash. Therefore, is has to be assumed that fluoride values will increase away from the volcano where the ash is more fine-grained and its surface are is larger.

It may be inferred that fluoride values on the Mid-southern lowlands might reach 400-500 ppm.
These values are similar to the values found during the 1973 Heimaey eruption. Even if these values are only about one third of comparable values for Hekla ash there is reason to be careful and move grazing animals form ash-contaminated fields and melt-water.

Source: Institute of Earth Sciences. Nordic Volcanological Center. University Iceland [6]

Volcano ashes and air traffic [7]
According to the British Civil Aviation Authority (CAAA) new upper limit for air traffic is 0.002 g/cubic metre of volcano ash level in air was established. At higher levels of this limit air traffic will be halted. Data of ash levels of past days were below of this limit.

[1] Icelandic volcano update. Department for Environment Foiod and Rural Affairs (DEFRA). 19 April 2010.
http://www.defra.gov.uk/news/latest/2010/environ-0415.htm

[2] Volcanic Ash From Iceland May Have Health Consequences. MedscapeToday. April 16, 2010.
http://www.medscape.com/viewarticle/720434

[3] Volcanic ash: Effects and mitigation strategies.
http://volcanoes.usgs.gov/ash/health/index.html

[4] Health Protection Agency: Statement on health effects of Icelandic volcanic ash plume.
15 April 2010
http://www.hpa.org.uk/NewsCentre/NationalPressReleases/2010PressReleases/100415volcanicash/

[5] Volcano ash could be good for gardens. Telegraph. 20 April 2010.
http://www.telegraph.co.uk/gardening/7611038/Volcano-ash-could-be-good-for-gardens.html

[6] Institute of Earth Sciences. Nordic Volcanological Center. University Iceland: Chemical composition of ash from the eruption in Eyjafjallajökull, collected April 19, 2010.
http://www2.norvol.hi.is/page/ies_Eyjafjallajokull_eruption

[7] Acht Lehren aus dem Asche-Chaos. Teil 3: Muessen Meteorologen kuenftig besser messen? Spiegel Online 23 April 2010.
http://www.spiegel.de/wirtschaft/0,1518,690538-3,00.html

23.04.2009: Added sugars, in special fructose, may be affecting cholesterol levels  [1]
Welsh and colleagues 2010 assessed the association between consumption of added sugars and blood lipid levels in adults. Carbohydrates have been associated with dyslipidemia, a lipid profile known to increase cardiovascular disease risk.

The authors found that High Density Lipoprotein (HDL), which lower blood cholesterol, decreases with higher sugar intake. The harmful blood levels, such as Low Density Lipoprotein (LDL) and the ratios of triglycerides to HDL-Cholesterol increased with high added sugar intake

The researchers say that fructose is the main component of added sugars. It is probably responsible for the increase of liver production of fat, triglycerides and Low Density Lipoproteins (LDL). The authors call for dietary guidelines that target a reduction in consumption of added sugar,

The UK Food Standards Agency is active in promoting awareness on the necessity to cut sugar
recommending that food manufacturers reduce saturated fat in foods such as biscuits, cakes, buns, chocolates and added sugar in soft drinks. [2]

Reducing saturated fat, sugar and salt content industrial food may have a significant effect on growing obesity and coronary diseases.

[1] Welsh JA, Sharma A, Abramson JL, Vaccarino V, Gillespie C, Vos MB: Caloric sweetener consumption and dyslipidemia among US adults. JAMA. 2010 Apr 21;303(15):1490-7.
http://www.ncbi.nlm.nih.gov/pubmed/20407058

[2] Reducing saturated fat and sugar in sweet foods. EFSA 26 March 2010
http://www.food.gov.uk/news/newsarchive/2010/mar/reducesat

22.04.2010: Metals as contaminants in food
Arsenic in food [1]
The European Food Safety Agency (EFSA) reports that arsenic is a widely-occurring contaminant which occurs both naturally and as a result of human activity. Foodstuffs are the main source of exposure for the general population in Europe.
The EFSA recommended that exposure to inorganic arsenic should be reduced. The main sources of inorganic arsenic intake are cereal grains and cereal based products, food for special dietary uses (e.g. algae), bottled water, coffee and beer, rice and rice-based products, fish and vegetables.
The highest total arsenic levels were measured in the following food commodities: fish and seafood, food products or supplements based on algae, especially hijiki, and cereal and cereal products, with particularly high concentrations in rice grains and rice-based products, and bran and germ. Values for inorganic arsenic are 0.03 mg/kg in fish and 0.1 mg/kg in seafood.
The Efsa estimates that the national inorganic arsenic exposures from food and water range from 0.13 to 0.56 µg/kg body weight (b.w.) per day for average consumers, and from 0.37 to 1.22 µg/kg b.w. per day.
High consumers of rice in Europe, such as certain ethnic groups, are estimated to have a daily dietary exposure of inorganic arsenic of about 1 µg/kg b.w. per day, and high consumers of algae-based products can have dietary exposure of inorganic arsenic of about 4 µg/kg b.w. per day.

Children under three years of age are the most exposed to inorganic arsenic. Exposure estimates reported in two different studies show an inorganic arsenic intake ranging from 0.50 to 2.66 µg/kg b.w. per day.
The Panel noted that, since the provisional tolerable weekly intake (PTWI) of 15 µg/kg b.w. was established by the Joint FAO/WHO Expert Committee on Food Additives (JECFA), new data had established that inorganic arsenic causes cancer of the lung and urinary tract in addition to skin, and that a range of adverse effects had been reported at exposures lower than those reviewed by the JECFA. Therefore the CONTAM Panel concluded that the JECFA PTWI of 15 µg/kg b.w. is no longer appropriate and, in its assessment, focussed on more recent data showing effects at lower doses of inorganic arsenic than those considered by the JECFA.

The main adverse effects reported to be associated with long term ingestion of inorganic arsenic in humans are skin lesions, cancer, developmental toxicity, neurotoxicity, cardiovascular diseases, abnormal glucose metabolism, and diabetes. There is emerging evidence of negative impacts on foetal and infant development, particularly reduced birth weight.

The CONTAM Panel therefore concluded that the overall range of BMDL01 values of 0.3 to 8 μg/kg b.w. per day should be used instead of a single reference point in the risk characterisation for inorganic arsenic.

Of the organic forms of arsenic, arsenobetaine, which is the major form in fish and most seafood, is widely assumed to be of no toxicological concern. For other organoarsenic compounds no human toxicity data are available. The CONTAM Panel recommended that dietary exposure to inorganic arsenic should be reduced.

Arsenic in animal feed [2]
Regions with high geological occurrence of inorganic arsenic have been identified in particular in Asia and other non-European countries. Drinking water many contain significant amounts of inorganic arsenic and upper limits have been set in most countries. Seafood and fish have been identified as major source of arsenic in the human diet, and in animal feed materials that contain products derived from fish or other marine organisms.
In seafood and fish, arsenic is present predominantly in the organic forms of arsenobetaine and arsenocholine, which are virtually non-toxic. Data on total arsenic in feed materials do not indicate arsenic levels of concern in materials others than fish-derived products. Food derived from terrestrial animals contributes only insignificantly to human exposure.

Uranium in foodstuffs [3]
Uranium is a naturally occurring radioactive metal, which can be found in varying concentrations in the environment, water and foodstuffs.

The Panel did not identify any new data which would have called for a revision of the TDI for uranium of 0.6 µg/kg b.w. per day established by the World Health Organisation (WHO), and therefore it endorsed this TDI.

The Panel concluded that average dietary exposure to uranium for the general population and high consumers across Europe is currently below the TDI. In specific areas where uranium concentrations in drinking water are high, the exposure estimates are close, but still below the TDI. For infants fed with infant formula made up with water containing uranium, the Panel noted that exposure in relation to body weight may be up to three times higher than for adults, and concluded that such exposure should be avoided.

This opinion focuses on uranium’s chemical toxicity, while the radiological risk will be addressed by another Group of Experts of the European Atomic Energy Community (EURATOM).
Uranium (U) is a silvery-white metal occurring in a number of minerals such as uraninite, carnotite and pitchblende. Uranium is also a naturally occurring radioactive element. Uranium can be present in water, air, food and feed in varying concentrations through leaching from natural deposits such as soil or rocks, emission from nuclear industry, nuclear weapons, dissolution in fertilizers and combustion of coal and other fuels.

Tap and bottled water had mean concentrations of uranium of slightly above 2 μg/L while soft drinks had concentrations less than half of this. Concentrations in food are less representative since they are reported only from one country and there are few samples in selected categories only.

The overall lower- and upper-bound uranium exposure estimates varied between 0.05 and 0.28 μg/kg body weight (b.w.) per day. For infants, the exposure scenario included mean and high consumption of infant formula reconstituted with water containing both average and high levels of uranium. The lower- and upper-bound uranium exposure estimates varied between 0.18 and 1.42 μg/kg b.w. per day, for both bottled and tap water.

Toxicity: Toxicity of ingested uranium is related to the solubility of the uranium compound; the higher the oral uranium compound solubility is, the greater its toxicity is expected to be. The kidney is recognized as the primary target organ for uranium both in experimental animals and humans. Kidney damage results from the accumulation of uranium in the renal tubular epithelium, where it can cause cell necrosis and atrophy of the tubules, leading to a compromised tubular secretion of organic anions and reabsorption of filtered glucose and amino acids. Besides nephrotoxicity, reproductive and developmental alterations (e.g. decreased pup growth and internal/external malformations), diminished bone growth and neurotoxicity have been documented in animal models but only at higher doses.

The World Health Organization (WHO) has established a tolerable daily intake (TDI) for soluble uranium of 0.6 μg/kg b.w. per day, based on the lowest-observed-adverse-effect-level (LOAEL) for uranium nephrotoxicity of 0.06 mg/kg b.w. per day from a 91-day study in male rats. The Panel on Contaminants in the Food Chain (CONTAM Panel) noted that no new data were identified that would require a revision of this TDI and endorsed it.

The CONTAM Panel noted that for all exposure scenarios evaluated for infants fed with infant formula reconstituted with water containing uranium, the exposure may be up to 3 times higher than the uranium exposure of adults on the body weight basis. The CONTAM Panel concluded that such exposure in infants should be avoided.

Cadmium in food [4]
establishing a new Tolerable Weekly Intake level (TWI). Foodstuffs are usually the main source of cadmium intake for the non-smoking general population. The Panel reduced the TWI for cadmium to 2.5 micrograms per kilogram of body weight (µg/kg b.w.), based on analysis of new data. The current average dietary exposure to cadmium for adults is around this level and exposure for certain subgroups, such as vegetarians and smokers, may be higher. However, the risk of adverse effects even for groups that have exposure at levels above the TWI is very low because the TWI is not based on actual kidney damage, but on an early indicator of changes in kidney function suggesting possible kidney damage later in life.

Cadmium is a heavy metal which enters the environment from natural sources, such as volcanic emissions and the weathering of rocks, as well as from industry and agriculture. It is found in the air, soil and water and can subsequently accumulate in plants and animals. Cadmium is primarily toxic to the kidney, but can also cause bone demineralisation, and has been classified as carcinogenic to humans by the International Agency for Research on Cancer . Foodstuffs are the main source of cadmium exposure for the non-smoking population. Cereals and cereals products, vegetables, nuts and pulses, starchy roots and potatoes as well as meat and meat products contribute most to human exposure. High levels were also found in some other foodstuffs (e.g. seaweed, fish and seafood, food supplements, mushrooms, chocolate) but as they are consumed to a lesser extent, they were no major contributors to exposure.

The Panel concluded that the risk of adverse effects even for groups that have exposure at levels above the TWI was very low because the TWI was not based on actual kidney damage, but on an early indicator of changes in kidney function suggesting possible kidney damage later in life.

The Panel also analysed data on levels of cadmium in food from 20 different countries, alongside national dietary surveys and EU-wide consumption data collected by EFSA. This information indicated that average and high-level[3] exposure were 2.3 µg/kg bw and 3.0 µg/kg bw per week respectively.

Vegetarians - who eat relatively high amounts of foods containing cadmium, including cereals, nuts, oilseeds and pulses - were estimated to have an average weekly exposure of up to 5.4 µg/kg bw. The Panel also stated that locally-produced food in highly contaminated areas may lead to higher exposure levels. Furthermore, dietary exposure could be higher for children than adults, due to the greater amount of food consumed by children in relation to their bodyweight.

The Panel also stated that smoking can contribute to a similar internal exposure as the diet, and that house dust can be an important source of overall exposure to cadmium for children.

Cadmium in animal feed [5]
Dietary cadmium exposure affects the absorption of trace elements, particularly that of copper resulting in an apparent copper deficiency in ruminants. In turn, high copper supplementation of feeds for pigs was considered to comprise the risk of an undesirable cadmium accumulation in the liver and kidneys, whereas zinc supplementation of feed reduces cadmium bioavailability. Within the EU maximum levels have been set for trace elements in animal diets, including copper and zinc (Commission Regulation (EC) 1334/2003). If these permissible levels are not exceeded, the overall tissue burden of cadmium is unlikely to exceed the maximum levels set for foods from animal origin under the conditions of current agricultural practice. Ruminants and horses, however, may be exposed during their entire lifespan to cadmium present in pastures. In distinct regions, this may result in an undesirable cadmium accumulation particularly in kidneys. The frequent consumption of kidney tissue from older animals (cattle and horses), as well as the frequent consumption of liver and kidneys from wildlife may thus contribute significantly to the overall human exposure.

Mercury in food [6]
The EFSA reported in 2004 that methylmercury toxicity has been demonstrated at low exposure levels, and therefore exposure to this compound should be minimised. However, it also noted that fish constitutes an important part of a balanced diet.

EFSA has also provided advice on the safety and nutritional contribution of wild and farmed fish in 2005. The CONTAM Panel assessed the health risks related to human consumption of wild and farmed fish, including an overall risk assessment related to the consumption of Baltic herring. EFSA’s advice concentrated on the most relevant metals and persistent organic contaminants, namely methylmercury, dioxins and dioxin-like PCBs. It also reviewed the nutritional value and benefits from consuming fish.

Mercury is an environmental contaminant that is present in fish and seafood products largely as methylmercury. Food sources other than fish and seafood products may contain mercury, but mostly in the form of inorganic mercury. Based on the available data the contribution to methylmercury exposure from these foods is considered to be insignificant. Inorganic mercury in food is considerably less toxic than methylmercury. Methylmercury is highly toxic particularly to the nervous system, and the developing brain is thought to be the most sensitive target organ for methylmercury toxicity. The JECFA established a Provisional Tolerable Weekly Intake (PTWI) of 1.6 µg/kg body weight based on two epidemiological studies that investigated the relationship between maternal exposure to mercury and impaired neurodevelopment in their children. A previous evaluation by the (U.S.) National Research Council (NRC) established an intake limit of 0.7 µg/kg body weight per week.

Taking into account the important nutritional contribution that fish makes to the diet, EFSA recommends that women of childbearing age (in particular, those intending to become pregnant), pregnant and breastfeeding women as well as young children select fish from a wide range of species, without giving undue preference to large predatory fish such as swordfish and tuna. Due to their place in the food chain, these fish are likely to contain higher levels of methylmercury than other fish species.


Lead in food [7]
According to the EFSA lead is an environmental contaminant that occurs naturally and, to a greater extent, from anthropogenic activities such as mining and smelting and battery manufacturing. Human exposure to lead can occur via food, water, air, soil and dust. Food is the major source of exposure to lead.

Cereals, vegetables and tap water to were found to contribute most to dietary exposure to lead for most Europeans. Non-dietary exposure to lead was considered to be of minor importance to adults, although house dust and soil can be important sources of exposure for children.

The Panel identified reduced intelligence quotient (IQ) levels in young children, and high blood pressure in adults, as the key health effects on which to base its assessment. Following a review of the available data, the Panel considered that the PTWI (provisional tolerable weekly intake)was no longer appropriate. A new guidance level could not be established, as there was no clear threshold below which the Panel was confident that adverse effects would not occur. The Panel therefore compared current exposure estimates for different groups of the population to levels above which adverse effects may occur. As a result, the Panel concludes that in particular there is a potential concern for neurodevelopmental effects in foetuses, infants and children.

Lead limits
Lead dietary exposure for average adult consumers in 19 European countries ranged from 0.36 to 1.24 µg/kg body weight (b.w.) per day (lower bound for country with lowest average exposure – upper bound for country with highest average exposure) and from 0.73 to 2.43 µg/kg b.w. per day for high consumers, respectively. Overall, cereals, vegetables and tap water were the most important contributors to lead exposure in the general European population. More specifically, the following food groups were identified as the major contributors to lead exposure: cereal products, followed by potatoes, cereal grains (except rice), cereal-based mixed dishes and leafy vegetables and tap water.

Lead levels in breast milk are highly variable but exposure of infants is estimated to be 0.21 µg/kg b.w. per day on average or 0.32 µg/kg b.w. per day for high consumers. For infants fed with ready-to-consume infant formula, the average exposure estimates range from 0.27 to 0.63 µg/kg b.w. per day, based on lower bound and upper bound assumptions, respectively; for high consumers, lead exposure estimates range from 0.40 to 0.94 µg/kg b.w. per day. For children aged 1-3 years mean lead dietary exposure estimates range from 1.10 to 3.10 µg/kg b.w. per day based on lower bound and upper bound assumptions, respectively; for high consumers, lead exposure estimates range from 1.71 to 5.51 µg/kg b.w. per day. For children aged 4-7 years mean lead dietary exposure estimates range from 0.80 to 2.61 µg/kg b.w. per day based on lower bound and upper bound assumptions, respectively; for high consumers, lead exposure estimates range from 1.30 to 4.83 µg/kg b.w. per day.

Breast-fed 3-month old infants are predicted to have a lead exposure that is below the BMDL01 intake value of 0.50 µg/kg b.w. per day for neurodevelopmental effects. Estimated exposure in children up to age seven exceeds the BMDL01 intake level of 0.50 µg/kg b.w. per day for neurodevelopmental effects.

Lead in foods, conclusions
Compared to dietary exposure, non-dietary exposure to lead is likely to be of minor importance for the general population in the European Union (EU). House dust and soil can be an important source of exposure to lead for children.

In humans, the central nervous system is the main target organ for lead toxicity. In adults, lead-associated neurotoxicity was found to affect central information processing. There is considerable evidence demonstrating that the developing brain is more vulnerable to the neurotoxicity of lead than the mature brain. In children, an elevated blood lead level is inversely associated with a reduced Intelligence Quotient (IQ) score and reduced cognitive functions up to at least seven years of age.

The CONTAM Panel concluded that the provisional tolerable weekly intake (PTWI) of 25 μg/kg b.w. set by the Joint FAO/WHO Expert Committee on Food Additives is no longer appropriate.

The CONTAM Panel does consider it appropriate to calculate margins of exposure to support the risk characterisation. Estimates of dietary exposure to lead based on lower bound assumptions and upper bound assumptions for the level of reporting for average adult consumers in Europe are lower than the limit of the benchmark dose BMDL intake value for effects on systolic blood pressure (SBP) (1.50 µg/kg b.w. per day), but vary from above to below the BMDL intake value for effects on the prevalence of chronic kidney disease (0.63 µg/kg b.w. per day). The respective margins of exposure (MOEs) range from 1.2 to 4.2 and from 0.51 to 1.81, respectively. Hence, if exposure were closer to the upper bound estimates, the possibility of an effect on some consumers cannot be excluded.

The Panel concluded that current levels of exposure to lead pose a low to negligible health risk for most adults but there is potential concern over possible neurodevelopmental effects in foetuses, infants and children.


[1]Scientific Opinion on Arsenic in Food. Question number: EFSA-Q-2008-425. Question number: EFSA-Q-2008-425. 12 October 2009.
http://www.efsa.europa.eu/en/scdocs/scdoc/1351.htm

[2] Opinion of the Scientific Panel on contaminants in the food chain [CONTAM] related to Arsenic as undesirable substance in animal feed. Question number: EFSA-Q-2003-031. 31.January 2005
http://www.efsa.europa.eu/en/scdocs/doc/180.pdf

[3] Uranium in foodstuffs, in particular mineral water .Question number: EFSA-Q-2007-135
25 March 2009.
http://www.efsa.europa.eu/en/scdocs/scdoc/1018.htm

[4] EFSA sets lower tolerable intake level for cadmium in food. EFSA Press Release 20 March 2009.
http://www.efsa.europa.eu/en/press/news/contam090320.htm

[5] Opinion of the Scientific Panel on contaminants in the food chain [CONTAM] related to cadmium as undesirable substance in animal feed. Question number: EFSA-Q-2003-033. 2 June 2004
http://www.efsa.europa.eu/en/scdocs/scdoc/72.htm

[6] Opinion of the Scientific Panel on contaminants in the food chain [CONTAM] related to mercury and methylmercury in food. Question number: EFSA-Q-2003-030. 24 February 2004
http://www.efsa.europa.eu/en/scdocs/scdoc/34.htm

[7] EFSA assesses health implications of lead in food. 18.03.2010
http://www.efsa.europa.eu/en/scdocs/scdoc/1570.htm

19.04.2010: Unsafe bleaching agent in flour [1]
China daily reports that some flour bleaching agents contain as much as 30 percent pulverized lime, a substance linked to gradual damage to the lungs and eventually the entire respiratory system. Pulverized lime was added to the bleaching agent to achieve low selling prices by the Yuzhong Food Additive Company in Rugao in East China's Jiangsu province.
The bleaching agent used in flour production is usually a blend of benzoyl peroxide (BPO) and corn flour. Experts say the use of lime is forbidden in flour production, because there are no regulations which allows its use, but no clear regulations exist. Benzoyl peroxide is one of the most important organic peroxides to improve flour.

A social problem
Chen Junshi,of the national food safety and risk assessment committee, points out that the use of unregulated additives in food production is unavoidable in the current peasant population.


Allowed flour bleaching agents [2]
Bread improvers and other bakery ingredients are used to make the bread white, soft and get the the dough optimized for industrial production lines.

Flour bleaching agent is a food additive added to flour in order to make it appear whiter (freshly milled flour is yellowish) and to oxidize the surfaces of the flour grains and help with developing of gluten.
Usual bleaching agents are: Organic peroxides, namely benzoyl peroxide, calcium peroxide, nitrogen dioxide, chlorine, chlorine dioxide (which is reported to produce diabetes-causing contaminant alloxan when reacting with the proteins contained in flour), Azodicarbonamide

Use of chlorine, bromates, and peroxides is not allowed in the European Union.
Flours treated with bleaches and improving agents generally show higher loaf volume and finer grain.

The oxygen from air bleaches flour while it ages during storage. Chemical bleaching, however reduces the transit time and reduces costs.

Flour treatment agents: (also called improving agents) are food additives added to flour in order to improve its properties.
Flour bleaching agents are added to flour in order to make it appear whiter (freshly milled flour is yellowish) and to oxidize the surfaces of the flour grains and help with developing of gluten.

Maturing agents: are added to flour in order to help with gluten development. They may or may not also act as bleaching agents. Common maturing agents are:
Flour bleaching agents, azodicarbonamide (E927), carbamide (E927b), potassium bromate (E924), (acts as a bleaching agent in USA), ascorbic acid (helps form gluten), phosphates, malted barley.

Processing agents: help with various aspects of handling the dough during baking. L-cysteine (E920, E921 (quantities in the tens of ppm range help soften the dough and thus reduce processing time)

The bromate, after reacting with the yellow compounds in the flour, is converted into harmless bromide. Chlorine dioxide is a gas that dissipates, so there is none of that left in the flour either. Any excess of benzoyl peroxide would (theoretically) decompose as soon as the flour is heated.

Dough conditioners [3]
Dough conditioners contain emulsifiers, such as DATEM (Diacetyl tartaric acids)Ester of Monoglyceride) and calcium stearoyl-2-lactylate, to increasing water absorption and gluten strength. Other dough conditioners are:

Calcium carbonate or monocalcium phosphate adjust water hardness and pH. Calcium carbonate increases both water hardness and pH; monocalcium phosphate increases water hardness and decreases pH.

Potassium bromate, ascorbic acid, potassium iodate, and azodicarbonamide (ADA), are maturing agents which improve gluten strength

Ammonium salts improve yeast fermentation.
Amylase and other enzymes are used to improve yeast fermentation and browning,
and to delay staling.

Dough conditioners are used to get dough better handled in automated equipment. Dough conditioners are added to frozen doughs to avoid damage of the gluten structure. Dough conditioners also reduce mixing and fermentation time.

Not allowed in the EU: Potassium bromate, azodicarbonamide, calcium peroxide, benzoyl peroxide.

Natural bleaching agents [4]
Roozen and colleagues 1993 looked for natural bleaching agents. Teey report that native soya flour contains at least 3 lipoxygenase isoenzymes, which improve dough characteristics by peroxidizing unsaturated fatty acids followed by oxidation of proteins and carotenoids, improving rheology and bleaching of the dough. Their data suggest that bread improvers containing enzyme active soya flour were more resistant to storage in form of powder compared with a paste type.

[1] Unsafe ingredient in some flours. China Daily. 08.04.210
http://www.chinadaily.com.cn/china/2010-04/08/content_9699679.htm

[2] Wikipedia: Benzoyl peroxide
http://en.wikipedia.org/wiki/Benzoyl_peroxide

[3] Figoni: Chapter 5 Wheat Flour
http://media.wiley.com/product_data/excerpt/69/04712685/0471268569.pdf

[4] Roozen J P, Lining PA, van Ruth SM: Use of Enzyme-Active Soya Flour in Making White Bread. Chapter 15, pp 192–199. ACS Symposium Series, Vol. 528. Doi:10.1021/bk-1993-0528.ch015
http://pubs.acs.org/doi/abs/10.1021/bk-1993-0528.ch015

18.04.2010: Contagious period of swine influenza H1N1 [1]
De Serres and colleagues 2010 report that, according to their data, persons infected with pandemic (H1N1) 2009 virus, a minimum of 8% of outpatients shed replicating virus on day 8. The authors conclude that self-isolation only until fever abates appears insufficient to limit transmission. They call for a self-isolation at the household, for a week and caution that some patients may shed infectious virus for a longer period.

Some studies with seasonal influenza state that virus shedding after day 7 is rare, but clinical studies have shown that shedding may persist beyond that period in some populations, such as elderly persons, immunocompromised patients, and children.

Contagiousness: According to the authors, contagiousness depends on viral load and depends on the spread of droplets (such as coughing, rhinorrea, or sneezing), the number and proximity of contacts between a case-patient and a susceptible person.

CDC recommend outpatients to extend the reclusion 1 day after end of fever : CDC recommends that people with influenza-like illness remain at home until at least 24 hours after they are free of fever (37.8°C). [2]

Duration of isolation precautions for hospitalized patients: CDC says that the recommended duration of isolation precautions for hospitalized patients is longer than that recommended for other populations because duration of virus shedding is likely to be longer than for outpatients with milder illness. De Serres, however, calls to extend the precautionary measures of hospitalized patients also to outpatients.

Isolation precautions for patients who have influenza symptoms should be continued for the 7 days after illness onset or until 24 hours after the resolution of fever and respiratory symptoms, whichever is longer, while a patient is in a healthcare facility.

Because some patients with influenza may not have fever but may be shedding influenza virus, patients with any respiratory symptoms should follow hand and respiratory hygiene recommendations. [3]

With pandemic (H1N1) 2009, fever generally persists 1–4 days and may be absent in 6%–11% of patients. In our study, of the 32 pH1N1 PCR–positive household members who had been symptomatic for <7 days, 78% had fever at any time since onset of their illness, but only 34% were still febrile on the day they tested positive. Nonetheless, 97% of specimens obtained from these patients were positive by cell culture

Before policy implications can directly follow from these findings, the association of self-isolation with substantial social impact needs to be carefully weighed against the possible benefits of reducing community transmission. In the general population, a 1-week self-isolation period seems more likely to prevent transmission than does isolation until fever has resolved. However, given that 8%–13% of patients may still shed infectious virus on day 8, longer periods of self-isolation for persons expected to come into contact with vulnerable persons (e.g., pregnant women, newborns, or immunocompromised persons) also may be prudent.

Infectious viral shedding
Ling and colleagues 2010 write that virus shedding in pandemic (H1N1) 2009-infected patients in Singapore, treated with oseltamivir, were still PCR positive by 37% of the patients on day 7 of their illness and 9% on day 10. The authors also note that oseltamivir, prescribed during the first 3 days of illness, shortened the duration of viral shedding. [4]

According to Li and colleagues 2010, oral oseltamivir medication initiated 2 day or earlier, suppresses infectious viral load of nasopharyngeal aspirate of pandemic 2009 influenza A(H1N1) more effectively compared with patients with an onset of medication after 2 days, and was significantly lower, compared with nontreated. No viral load was determined at day 6 of medication. [5]

Highest viral load in respiratory samples, stool and urine occurred on the day of onset of symptoms. Eight days after onset of symptoms the RT-PCR 8 and after 5 days the were negative with only one exception. Younger age was associated with prolonged respiratory tract and stool shedding was observed in younger people. [6]

Quick test for H1N1 [7]
Louie and colleagues 2010 say that diagnose influenza at the point of care, using commercial rapid enzyme immunoassay, are unable to differentiate between influenza A virus subtypes and the sensitivity varies between 40% and less, up to 90 %, compared with PCR and culture methods.
The authors compared the QuickVue Influenza test (Quidel Corp., San Diego, CA, USA) with PCR and culture methods, and found that the test had suboptimal sensitivity and specificity for the detection of pandemic (H1N1) 2009. Their results should be confirmed with PCR. The authors call for the development of more accurate point-of-care rapid tests.

[1] De Serres, G; Rouleau, I; Hamelin,M-E; Quach, C; Skowronski, D; Flamand, L; Boulianne, N; Li, Y; Carbonneau, J; Bourgault, A-M; Couillard, M; Charest, H; Boivin, G: Contagious Period for Pandemic (H1N1) 2009. EID Journal. Volume 16, Number 5–May 2010
http://www.cdc.gov/eid/content/16/5/783.htm

[2] Centers for Disease Control and Prevention. Recommendations for amount of time persons with influenza-like illness should be away from others. October 23, 2009
http://www.cdc.gov/h1n1flu/guidance/exclusion.htm

[3] Centers for Disease Control and Prevention. Interim Guidance on Infection Control Measures for 2009 H1N1 Influenza in Healthcare Settings, Including Protection of Healthcare Personnel. March 10, 2010.
http://www.cdc.gov/h1n1flu/guidelines_infection_control.htm

[4] Ling LM, Chow AL, Lye AC, Tan AS, Krishnan P, Cui L, et al.: Effects of early oseltamivir therapy on viral shedding in 2009 pandemic influenza A (H1N1) virus infection. Clin Infect Dis. 2010;50:963–9.
http://www.ncbi.nlm.nih.gov/pubmed/20180701

[5] Li IW, Hung IF, To KK, Chan KH, Wong SS, Chan JF, Cheng VC, Tsang OT, Lai ST, Lau YL, Yuen KY: The natural viral load profile of patients with pandemic 2009 influenza A(H1N1) and the effect of oseltamivir treatment. Chest. 2010 Apr;137(4):759-68. Epub 2010 Jan 8.
http://www.ncbi.nlm.nih.gov/pubmed/20061398

[6] To KK, Chan KH, Li IW, Tsang TY, Tse H, Chan JF, Hung IF, Lai ST, Leung CW, Kwan YW, Lau YL, Ng TK, Cheng VC, Peiris JS, Yuen KY: Viral load in patients infected with pandemic H1N1 2009 influenza A virus. J Med Virol. 2010 Jan;82(1):1-7.
http://www.ncbi.nlm.nih.gov/pubmed/19950247

[7] Louie, J K; Guevara, H; Boston, E; Dahlke, M; Nevarez, M; Kong, T; Schechter, R; Glaser, CA, Schnurr, DP: Rapid Influenza Antigen Test for Diagnosis of Pandemic (H1N1) 2009. EID Journal. Volume 16, Number 5–May 2010.
http://www.cdc.gov/eid/content/16/5/824.htm

16.04.20101: The genome sequence of the agent of trypanosomiasis [1]
Trypanosomiasis, also called "sleeping sickness", is common in Western and Central Africa. The symptoms include changes in personality, alteration of the biological clock, confusion, slurred speech, seizures, and difficulty walking and talking. The disease is caused by Trypanosoma parasites and is transmitted by the female tsetse fly. It affects the human central nervous system. Berriman and colleagues 2010 describe the genome sequence for the strain of Trypanosoma brucei gambiense which is the most common causer of the sleeping sickness.

The authors compared this genome with that of Trypanosoma brucei brucei (T. b. brucei 927), a non-human infecting parasite from bovine infections. The sequence of genes were identical in 98.2 per cent in both genomes, varying only on one locus. However, ability to infect humans cannot be explained simply by the addition or removal of a few genes. The authors postulate that single letter changes in the genome, differences in the number of copies of genes; changes in how the activity of genes is regulated may be the cause of the virulence of Trypanosoma brucei gambienses. The genome sequences may help to find new drugs to fight the disease.

The authors also described a group of VSG proteins which gather at the surface of the Trypanosoma, protecting the parasite from the immune system of the host. A catalogue of VSGs might also provide valuable informations for further immunologic studies.

[1] Jackson AP, Sanders M, Berry A, McQuillan J, Aslett MA, et al. (2010) The Genome Sequence of Trypanosoma brucei gambiense, Causative Agent of Chronic Human African Trypanosomiasis. PLoS Negl Trop Dis 4(4): e658. doi:10.1371/journal.pntd.0000658
http://www.plosntds.org/article/info%3Adoi%2F10.1371%2Fjournal.pntd.0000658