Poisons and Policy: Arsenic and Aflatoxins
Sep20

Poisons and Policy: Arsenic and Aflatoxins

In the past 24 hours, do you recall hearing anything about arsenic in rice? If you're in the United States, the answer is very likely, "yes!" A great many pixels were spilled yesterday when Consumer Reports and the US Food and Drug Administration released -- almost simultaneously -- analytical data on inorganic arsenic concentrations in 200 samples of commercial rice products, particularly those grown in the southern US. You can't do any better in understanding this story than reading, "Arsenic and Rice. Yes, again," on Deborah Blum's Elemental blog at Wired Science Blogs. Professor Blum has been discussing arsenic in the diet for a few years, an interest she developed while composing her superb book, The Poisoner's Handbook: Murder and the Birth of Forensic Science in Jazz Age New York. Deborah's post puts in perspective the risks of inorganic (and organic) arsenic concentrations in food products such as rice relative to drinking water. Arsenic occurs in nature but exists in higher concentrations in water from areas where arsenical pesticides have been used in cotton farming or poultry deworming (the latter discussed in 2006 at NYTimes). While she closes in being critical of the FDA for lack of clear consumer guidance, let it suffice to say that no character in Blum's book was killed by poisoning with rice from Louisiana. Pick your poison What caught my attention yesterday was a completely different report from the US FDA -- actually a FDA ruling released by the Iowa Department of Agriculture and Land Stewardship. Corn containing one of the most potent natural toxins and carcinogens -- a class of compounds called aflatoxins -- can be legally blended with other corn for use in animal feed.  A standing rule of the FDA, when invoked, allows farmers to blend corn containing up to 20 parts per billion of aflatoxins with corn containing lower concentrations (or none) of the toxin family. Here's where 20 parts per billion falls in the FDA's guidelines according to the Iowa Dept of Agriculture statement: The FDA has established guidelines for acceptable aflatoxin levels in corn based on its intended use.  Corn containing aflatoxin in concentrations of greater than 20 ppb cannot be used for human consumption and cannot be used for feed for dairy animals or for immature livestock of others species. Corn containing aflatoxin at 100 ppb or less can be used in breeding cattle and swine and mature poultry.  Corn with 200 ppb or less can be used with finishing swine greater than 100 lbs. in weight and corn with 300 ppb or less can be used in finishing beef cattle. Where is this aflatoxin coming from...

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Bummer SNP doesn’t mix with beer for gastric cancer risk
Apr04

Bummer SNP doesn’t mix with beer for gastric cancer risk

A study from led by investigators at the Catalan Institute of Oncology (ICO) in Barcelona has revealed that high consumption of beer combined with a single nucleotide polymorphism (SNP) in the alcohol dehydrogenase gene is associated with a nearly nine-fold increased risk of gastric cancer. Thanks to the lovely folks in the American Association for Cancer Research (AACR) press office who recognize science bloggers as press, I was able to sit in on a press conference this morning at the AACR annual meeting in Orlando where several studies were discussed on genetic and environmental factors in cancer risk. Lead author of this particular study, cancer epidemiologist Eric Duell, Ph.D., presented a study of Europeans on alcohol consumption and risk of gastric cancer due to SNPs in the alcohol dehydrogenase gene, ADH1. Recall from biochemistry that ADH1 and other ADH forms catalyze the rate-limiting step in the ethyl alcohol oxidation to acetaldehyde, a known carcinogen. Acetaldehyde, in turn, is oxidized to acetate by aldehyde dehydrogenases (ALDHs). This is an impressive retrospective analysis. The study data was culled the European Prospective Investigation into Cancer and Nutrition (EPIC), a study of 521,000 individuals aged 35 to 50 who completed diet and alcohol use questionnaires at 23 centers across 10 European countries between 1992 and 1998. A subset, or nested-study, called EurGast examined environmental factors and genetic susceptibility to gastric cancer in 364 cases relative to 1272 controls. When examined as a pool only one SNP was associated with a modest, 30% increased risk for gastric cancer.  Combining this SNP with alcohol consumption data revealed that 60 g EtOH/day increased risk by 75%. (Sixty grams of ethanol per day is the amount present in approximately four 12 oz beers at 5% alcohol by volume, four 5 oz glasses of wine at 12% ABV, or four 1oz shots of 100 proof liquor.) However, the subanalysis of that SNP stratified for alcohol consumption and type of alcohol revealed the big surprise. Consumption as beer, but not wine or liquor, combined with this SNP at both alleles was associated with increased gastric cancer risk of 8.72-fold in this high consumption group (just one allele increased risk by only 33%). This SNP in the ADH1 gene, rs1230025, is an intergenic T→A polymorphism, neither in the promoter or the coding region of the gene. The influence of this SNP has only been evaluated in one study where it was shown to be associated with a lower breath alcohol concentration - and presumably higher acetaldehyde concentration, although not explicitly measured - at late timepoints when normal volunteers are given a challenge of 0.75 g/kg of ethanol. But why is...

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