Is “Made in the U.S.A.” safe?  Or, is this a trade war?

When I was a kid in the early 1960s, I recall that “Made in Japan” meant cheap, but also sub-par in quality.  Interesting how that has changed (compare Japanese made cars to those made in the U.S. for quality and sales).

More recently, in my world we continue to hear people voice a fear of food made “overseas”–in China or Mexico–that is somehow supposed to be unsafe, or less safe than food produced in the U.S.  Yes, there have been instances of foreign food products sickening Americans (melamine in dog and cat food from China, Salmonella in cantaloupes from Honduras, hepatitis A in green onions from Mexico), but in 17 years of being involved in litigation resulting from nearly every foodborne illness outbreak in the U.S., in my experience most of the food products that sicken us are home-grown and mass-produced.  As I have said more that a few times, “U.S. corporations do a marvelous job of poisoning us.”

It seems that other countries are now paying attention to what we sell (or try to sell) them.  Perhaps, like me in the 1960s, they think “Made in the USA” means something far different that what the producers and manufacturers would wish.  

Look at the recent dust-up over chicken in Russia.  Russia may stop importing poultry by 2015, Prime Minister Vladimir Putin said recently, backing a ban imposed on U.S. chicken imports at the beginning of the year.   “We haven’t seen any readiness to meet Russian standards on the part of some of our partners, mainly the companies from the United States,” he said.

“If our foreign suppliers are unable or reluctant to meet our security requirements, we will use other sources.”

Perhaps Putin is playing to the Russian poultry industry (goodness, we never see U.S. politicians doing the same here), or, perhaps he read the study released by Consumer Reports that found two-thirds of fresh broiler chicken purchased harbored Salmonella and/or Campylobacter.  The study also found that most of the bacteria sampled from the raw chicken was resistant to at least one antibiotic.

And, what about Asia?  In the latest controversy over “Made in the U.S.A.,” in late December, Taiwan’s ruling and opposition parties reached an agreement to amend the island nation’s Food Sanitation Act to bar the import of bone-in and certain other beef products from the U.S. for fear of Mad Cow disease.

True or not, can you blame them for being a bit worried over U.S. beef after reading about the use of ammonia-treated meat, a substance compared to “pink slime”, in hamburgers served at fast food restaurants and through the United States Department of Agriculture’s (USDA’s) National School Lunch Program?

Carl Custer, a former USDA microbiologist, told the New York Times that he and other scientists were concerned about the potential safety risks associated with the consumption of ammonia-treated beef without independent validation of the meat’s safety.  “I do not consider the stuff to be ground beef, and I consider allowing it in ground beef to be a form of fraudulent labeling,” he told the Times.

Trade war? Perhaps.  Or not. However, you must admit that the meat industry and our own government are handing the stick to allow foreign politicians to beat the meat industry in the head.  

Seriously, we have Salmonella and Campylobacter found in a large percentage of chicken in our stores, and a “pink slime” being served to our school children in ground beef–“ground beef” that a former USDA employee did not even consider to be ground beef–“ground beef” that contains “pink slime” but is not labeled as containing ammonia or ammonia-treated beef as an ingredient, which caused the same former government employee to consider omission of ammonia on food labels as “fraudulent.”

“Made in USA” used to mean something different.

  • You wrote; Taiwan’s ruling and opposition parties reached an agreement to amend the island nation’s Food Sanitation Act to bar the import of bone-in and certain other beef products from the U.S. for fear of Mad Cow disease (BSE)….
    However, BSE can be a naturally occurring disease, so not an infectious disease. WHY? Because, about the BSE disease; this was never justified scientifically! It was pure, math-model-driven science fiction. But it was pushed very vigorously by the British science establishment, which has never confessed to its errors, and is therefore likely to make the same ones again.
    See recently; the swine flu outbreak was a ‘false pandemic’; said Wolfgang Wodarg, head of health at the Council of Europe (January 8, 2010). He has branded the H1N1 outbreak as ‘one of the greatest medical scandals of the century’!
    However, the pandemic has started on May 1, 2009 when Roy Anderson was interviewed on the BBC´s Today programme about the 2009 swine flu outbreak. He was a member of a group set up to give scientific advice to the British government over health issues relating to swine flu. However, swine flu is not the first time we have suffered this nonsense. See predictions about BSE/ vCJD by Roy M. Anderson. He has mathematically modelled the spread of new variant Creutzfeld- Jakob disease (v CJD), published in Nature (406, 583-584; 10 August 2000).
    There his team showed that the current mortality data are consistent with between 63 and 136,000 cases among the population known to have a susceptible genotype (about 40% of the total population), with on average less than two cases of vCJD arising from the consumption of one infected bovine. However, far fewer people are carrying the human form of mad cow disease than previously feared. There have been (to date) 168 definite or probable cases of vCJD since 1995, suggesting that the risk had been „overestimated“.
    This led to an obscene £5 billion campaign of British cattle destruction and compensation. And about the USA ? The International Trade Commission released a report estimating that trade restrictions resulting from BSE cost the cattle industry $11 billion from 2004 to 2007
    (www.beefusa.org/NEWSTradeRestrictionsCostCattlemen11BillioninLostSales36991.aspx). This could be “more greatest medical scandal”!
    See other relationships, according to my recent presentation at 29th World Veterinary Congress in Vancouver; Neurodegenerative Diseases and Schizophrenia as a Hyper or Hypofunction of the NMDA Receptors (www.bse-expert.cz/pdf/Veter_kongres.pdf).
    Sincerely
    Josef Hlasny, DVM, PhD., veterinary surgeon in Bludov, Czech Republic

  • Continued…In Britain, much of the alarmism about Mad Cow disease was never justified scientifically. It was pure, math-model-driven science fiction… There are some; „eight BSE/ vCJD mathematical examples“, mostly headed by R.G.WILL (National Creutzfeldt-Jakob Disease Surveillance Unit in Edinburgh):
    1. Dev Biol Stand. 1998;93:79-84.
    New variant Creutzfeldt-Jakob disease.
    Will RG.
    National Creutzfeldt-Jakob Disease Surveillance Unit, Western General Hospital, Edinburgh, UK.
    New variant Creutzfeldt-Jakob disease is a novel human spongiform encephalopathy with a consistent clinico-pathological phenotype. Epidemiological evidence indicates that this disease is occurring almost exclusively in the UK, where there has been an epidemic of spongiform encephalopathy in the cattle population. Current evidence strongly supports the hypothesis that there is a causal link between bovine spongiform encephalopathy and new variant Creutzfeldt-Jakob disease.
    2. Nature 406, 583-584 (10 August 2000) | doi:10.1038/35020688
    Predicted vCJD mortality in Great Britain
    Azra C. Ghani1, Neil M. Ferguson1, Christl A. Donnelly1 & Roy M. Anderson1
    Top of page
    Abstract
    Modelling the latest data puts a ceiling on the likely number of vCJD cases.
    Top of page
    Abstract
    There is continued speculation about the likely number of cases of variant Creutzfeldt–Jakob disease (vCJD) that will occur in Great Britain in the wake of the BSE epidemic in cattle and in light of a recent cluster of vCJD cases in Leicestershire, England. We show here that the current mortality data are consistent with between 63 and 136,000 cases among the population known to have a susceptible genotype (about 40% of the total population), with on average less than two cases of vCJD arising from the consumption of one infected bovine.
    3. Lancet. 2000 Aug 5;356(9228):481-2.
    Incidence of variant Creutzfeldt-Jakob disease in the UK.
    Andrews NJ, Farrington CP, Cousens SN, Smith PG, Ward H, Knight RS, Ironside JW, Will RG.
    The number of deaths from variant CJD (vCJD) in the UK increased in the last quarter of 1998, although numbers were lower in subsequent quarters. We analysed the numbers of definite and probable (living and dead) vCJD cases since 1994 to assess trends in incidence. We estimated that the number of onsets increased by 23% per year for 1994-2000 (p=0.004), and that deaths increased by 33% for 1995-2000 (p=0.005). The absolute number of cases in the UK is still low, but such an increase should be a matter of concern.
    4. Science. 2001 Nov 23;294(5547):1729-31. Epub 2001 Oct 25.
    Predictability of the UK variant Creutzfeldt-Jakob disease epidemic.
    d’Aignaux JN, Cousens SN, Smith RG.
    London School of Hygiene and Tropical Medicine, Infectious Disease Epidemiology Unit, Keppel Street, London WC1E 7HT, UK. jerome.huillard@lshtm.ac.uk
    Comment in: Science. 2001 Nov 23;294(5547):1663-4.
    Back-calculation analysis of the variant Creutzfeldt-Jakob disease epidemic in the United Kingdom is used to estimate the number of infected individuals and future disease incidence. The model assumes a hazard of infection proportional to the incidence of bovine spongiform encephalopathy in the United Kingdom and accounts for precautionary control measures and very wide ranges of incubation periods. The model indicates that current case data are compatible with numbers of infections ranging from a few hundred to several millions. In the latter case, the model suggests that the mean incubation period must be well beyond the human life-span, resulting in
    5. Lancet. 2003 Mar 1;361(9359):751-2.
    Deaths from variant Creutzfeldt-Jakob disease in the UK.
    Andrews NJ, Farrington CP, Ward HJ, Cousens SN, Smith PG, Molesworth AM, Knight RS, Ironside JW, Will RG.
    Public Health Laboratory Service, Communicable Disease Surveillance Centre, London, UK.
    In 2002, 17 people died from variant CJD (vCJD) in the UK, compared with 20 in 2001 and 28 in 2000. We analysed data for deaths from vCJD since 1995 and estimated the underlying trend in mortality. The trend had a quadratic component (p=0.005), suggesting that the increase was not exponential, and that the previously increasing trend is slowing down. The death rate peaked in 2000. These findings are encouraging, but mortality might increase again in the future.
    6. Stat Methods Med Res. 2003 Jun;12(3):203-20.
    The predictability of the epidemic of variant Creutzfeldt-Jakob disease by back-calculation methods.
    Huillard d’Aignaux JN, Cousens SN, Smith R,G.
    Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London, UK.
    We present a back-calculation analysis of the variant Creutzfeldt-Jakob (vCJD) epidemic in the UK to estimate the number of infected individuals and to explore the likely future incidence of the disease. The main features of the model are that the hazard of infection was assumed proportional to the incidence of BSE in the UK with allowance for precautionary control measures taken in 1988 and in 1996, and that the incubation period distribution of vCJD follows an offset generalized F distribution. Our results indicate that current the numbers of cases with onset up to 31 December 2000 data are broadly compatible with numbers of primary infections ranging from a few hundred to several million. However, if a very large number of persons were infected, the model suggests that the mean incubation period is likely to be well beyond the human lifespan, resulting in a disease epidemic of much smaller size (maximum several thousand). A sensitivity analysis indicates that our results are sensitive to the underreporting of vCJD cases before 1996. Finally, we show that, in the absence of a reliable test for asymptomatic infection, uncertainty in estimates of the total number of infections is likely to remain for at least several years, even if the number of clinical cases remains low.
    7. Curr Top Microbiol Immunol.
    2004;284:161-91.
    The epidemiology of variant Creutzfeldt-Jakob disease.
    Smith PG, Cousens SN, d’ Huillard Aignaux JN, Ward HJ, Will RG.
    Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, Keppel Street, London WC1E 7HT, UK. p.smith@lshtm.ac.uk
    Variant Creutzfeldt-Jakob disease (vCJD) was identified as a new disease in 1996. It was linked to infection with the bovine spongiform encephalopathy (BSE) agent although the epidemiological evidence for this was not strong, but later strain typing studies confirmed the association. The disease has affected predominantly young adults whose dietary and other characteristics are unexceptional compared to control groups, other than that all patients to date have been methoinine homozygous at codon 129 of the prion protein gene and the incidence has been about two times higher in the North of the UK. The number of cases in the 7 years after first identification of the disease has been considerably lower than initially feared, given the likely widespread exposure of the UK population to the BSE agent through contaminated beef products. Predictions of the possible future course of the epidemic have many associated uncertainties, but current mathematical models suggest that more than a few thousand cases is unlikely. Such modelling is limited by the absence of a test for infection with the vCJD agent. The development of a test that could be used on easily accessible tissue to detect infection early in the incubation period would not only advance understanding of the epidemiology of infection with the agent but would also aid the implementation of control measures to prevent potential iatrogenic spread.
    sease epidemics of at most several thousand cases.
    8. 2006 Jan;59(1):111-20.
    Risk factors for variant Creutzfeldt-Jakob disease: a case-control study.
    Rizikové faktory pro nemoc vCJD: případ-kontrolní studie.
    Ward HJ, Everington D, Cousens SN, Smith-Bathgate B, Leitch M, Cooper S, Heath C, Knight RS, Smith PG, Will RG.
    National Creutzfeldt-Jakob Disease Surveillance Unit, University of Edinburgh, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, UK. h.ward@ed.ac.uk
    OBJECTIVE: To investigate the potential risk factors for variant Creutzfeldt-Jakob disease (VCJD) in the United Kingdom. METHODS: Definite and probable vCJD cases (n = 136) were residing in Great Britain at disease onset, and were referred between May 1995 and November 2003. Control subjects (n = 922) were recruited between 2002 and 2003, from 100 randomly selected geographical clusters sampled to represent the geographical distribution of vCJD.
    RESULTS: Reported frequent consumption of beef and beef products thought likely to contain mechanically recovered or head meat, or both, including burgers and meat pies, was associated with increased risk for vCJD, as was reported frequent chicken consumption. Surgical operations were generally similarly reported for cases and control subjects, with the exception of a small group of minor operations, possibly attributable to underreporting in control subjects. Cases and control subjects had similar reported occupational histories and exposure to animals. INTERPRETATION: These findings are consistent with dietary exposure to contaminated beef products being the main route of infection of vCJD, but recall bias cannot be excluded. There was no convincing evidence of increased risk through medical, surgical, or occupational exposure or exposure to animals.
    Sincerely
    Josef Hlasny, DVM,PhD., veterinary surgeon, Czech Republic