UK refuses to test cattle for BSE
London Times calls mainstream sheep scientist a 'terrorist'
The 41st case of mad cow in France; 5th case in Belgium
Sept. 28 public meeting on risk analysis for BSE in the United States
Four cases in Utah
Britain hopes beef ban can be lifted by year-end
Is the US still importing meat and edible meat offals from BSE countries?
Welsh correspondent 12 Sept 98"Professor Anderson, the epidemiology modeller, at the recent conference in Cardiff, disclosed that 2, 200 sheep had been tested in the UK. These had died of suspicious causes, ie, were 'downer' sheep. Nine were found to have a spongiform encephalopathy [0.4%, extrapolates to 180,000 of the 44 million UK sheep, ignoring selection effects -- webmaster]. Prof. Lacey immediately asked why, if they had decided to test sheep for scrapie, did they not test cattle for BSE (as the level of under-reporting in the UK of BSE has not been measured). (Lacey's new book is out, 'Poison on a plate, the making of a modern plague' It basically reviews the history of his involvement in BSE and food safety. Available from Metro Ltd, 19 Gerard St, London. 0171 734 1411. Three part serialisation in the Daily Mail 14-16.9.98 --the most comic thing in the first article is about how an attempt was made in the House of Commons to have Lacey committed for insanity!)
Anderson replied that the cost would be vast, which was immediately denied by Prof. Collinge. There followed a heated argument in which Anderson claimed testing cows was not necessary and Lacey implied Anderson was in the pocket of industry. (There was a report at the August 98 Iceland about under-reporting that Anderson had not considered.)
Anderson said that mean nvCJD incubation period was 9 years. This seemed odd to scientists in attendance -- from other TSEs such as kuru, one might expect it to be over 25 years. The political advantage of a low figure like 9 years is that it results in the total number of cases of nvCJD pencilling out much lower. "
Comment (webmaster): The case group of 27 is surely unrepresentative of the UK population of 18 million people who share their prion protein genotype because the group had low to moderate exposure; other factors, such as over-producing control regions, must be present.
The cost of immunological testing cows amounts to tuppence relative to the 5.5 billion dollars spent on the epidemic so far -- or the cost of treating one more case of nvCJD. Anderson was evidently speaking to resumption of UK exports, not to public health. He wants to model the nominal BSE epidemic (cows officially recorded as having clinical BSE). This is far smaller than the total clinical BSE caseload because of on-farm burial, off-farm carcass dumping, non-reporting at the slaughterhouse, smuggled exports, etc. In turn, this is far smaller than the total BSE epidemic, which must include preclinical animals (infectious, but slaughtered before developing behavioral disorders) and subclinical animals (infectious, but never going clinical during their lifespan). The scrapie epidemic has persisted in sheep for 250 years despite a lack of offal feeding -- why should BSE be any different? Clinical BSE is surely just the tip of the infectivity iceberg.
Gross behavioral symptoms are not a reliable proxy for infectivity levels. Animals can be highly infectious in bioassays without displaying the slightest overt symptoms. The issue is specific infectivity: how many infection-causing doses per thousand cows (or femtomoles of rogue prion per gram of meat). Before beef exports can be safely begin, the UK needs to be BSE-free. As a practical matter, this means demonstrating, using the most sensitive available immunological tests on a large random sample, that only background levels of prion disease still occur. (Sporadic and familial TSE are believed by molecular biologists to occur in roughly one per million individuals of any species of mammal, so the EU cannot ask for zero).
15 Sept 98 press releaseFSIS and the Animal and Plant Health Inspection Service (APHIS) will hold a September 28 public meeting to assess USDA measures to prevent Bovine Spongiform Encephalopathy (BSE) from entering the United States.
On April 24, 1998, USDA entered into a cooperative agreement with Harvard University's School of Public Health to conduct a risk analysis to assess the potential pathways for entry into U.S. cattle and the U.S. food supply, to evaluate existing regulations and policies, and to identify any additional measures that could be taken to protect human and animal health. This meeting will provide an opportunity for public input and a chance to comment on the scope of the BSE risk analysis project.
A Federal Register notice with additional information is expected to be published soon. The meeting will be held September 28, from 9:00 a.m. to 4:00 p.m. at the:
National Rural Electric Cooperative Association 4301 Wilson Boulevard Arlington, VA 22203-1850 (703) 907-5500For more information or to register for the meeting, contact: Jennifer Callahan, FSIS Planning staff at (202) 501-7251. For technical information, contact: Dr. Ruth Etzel, Director, Epidemiology and Risk Assessment Division, FSIS Office of Public Health and Science, at (202) 501-7472.
In other words, if a UK citizen can't donate blood for plasma at home, should they be allowed to donate in the US. American servicemen and women who served in the UK in the 1980s and 1990s for extended periods of time are questionable as blood blood in the US.
To register a protest, the address is:
Linda Smallwood, Executive Secretary Blood Products Advisory Committee Office of Blood Research and Review Center for Biologics Evaluation and Research FDA 1401 Rockville Pike Suite 200N Rockville, MD. 20852-1448
London Times 9 Sept 98 "Scientific Terrorism" Simon JenkinsComment by J Ralph Blanchfield:
"Jenkins's article contains numerous incorrect and misleading assumptions, including that the 27 cases of nvCJD is the ultimate sum total, when at present, for reasons that have been repeated aired here and which even a Times journalist should understand, nobody can yet say what the future holds.
In contrasting Jeff Almond's words with 'Seac had told the Government's Chief Medical Officer that there were "no grounds" for taking action on sheep', Jenkins is both paraphrasing inaccurately (a Times journalist, no less!) and being dishonestly selective. The bit that he quotes is a paraphrase from the public report by SEAC on 30 July 1998, and comes at the end of a section which says
"SEAC had previously noted that BSE could be transmitted experimentally by mouth to sheep and, in July 1996 and May 1997, had provided advice to Government on precautions which should be taken to protect public health. (Copy of previous advice attached.) The Committee considered the theoretical possibility that BSE could exist in the UK sheep flock noting that no evidence of BSE in sheep in commercial UK flocks had so far been found.
The Committee noted that, on the basis of the limited experimental evidence available, the clinical disease caused by inoculating sheep with BSE appeared to be very similar to the natural disease of sheep called scrapie. As in scrapie, infectivity was found in the spleen of sheep experimentally infected with BSE, although no infectivity has been found in the spleen of BSE infected cattle.
To distinguish the BSE strain from scrapie strains requires lengthy and expensive post mortem testing of sheep tissue. Such work must continue because, as previously explained (July 1996), finding the BSE strain in the national flock might have important implications for public health. The Committee noted that valuable preliminary information was emerging from the studies which they had previously recommended. They concluded that additional work was required to determine the extent of scrapie in UK sheep and the strains involved and decided to set up a sub-group to develop further recommendations on this. The Committee agreed that, at present, there was no need to recommend further action to protect public or animal health. "
Jeff Almond, as chairman of the sub-group referred to and that has now been set up, is saying no more than SEAC said.
The paper by Foster J D et al (1996) "Detection of BSE infectivity in brain and spleen of experimentally infected sheep", Veterinary Record, 1 June , 546-548, reported that inoculation of 0.5 ml of a 10 per cent homogenate from a pool of four brains of BSE-confirmed cows resulted in five out of six sheep succumbing with incubation periods of between 440 days and 2553 days, dependent on their PrP genotypes. Oral challenge of six sheep with 50 ml of 1 percent of the same homogenate (equivalent to 0.5 g of brain per sheep) resulted in one sheep succumbing, with an incubation period of 734 days. Brain and spleen were recovered from the latter case and from one of the inoculation cases (both sheep being of the same PrP genotype, alanine/alanine 136 and glutamine/glutamine 171), and subjected separately to strain-typing experiments. All four samples resulted in the characteristic "BSE signature" totally different from that of scrapie."
Yves Le Pape INRA Grenoble FRANCE 13 sept 98The 41 th case of mad cow in Francee and the 10 th of 1998 appeared last week in a Manche'farm. The dairy Holstein was born in 1989 in the northwestern province of Manche, part of Lower Normandy.. The whole herd of 134 cows was destroyed.
L'animal atteint est une vache laitiere de race Prim' Holstein nee en 1989 dans un elevage de la Manche. Il a ╚t╚ proced╚, hier, ř l'elimination et ř la destruction totale de ce troupeau de 134 bovins.
Reuters News Service September 11, 1998A fifth case of mad cow disease in Belgium was confirmed Thursday at a dairy farm in east Flanders, the Belgian Agricultural Ministry said on Friday. It is the fifth case of mad cow disease, or bovine spongiform encephalopathy (BSE), discovered in Belgium. The last case was discovered in April.
The diseased 4-year-old cow was slaughtered on Thursday. The farm's 38 other cows were slaughtered on Friday, the Agricultural Ministry said in a statement.
The outbreak of BSE in Europe has been concentrated in Britain, where the fatal brain-wasting disease has been linked to the use of high-protein cattle feed. The discovery that humans could develop a form of the fatal brain-wasting disease from eating BSE-infected beef sparked an international scare in 1996.
Sunday, September 13, 1998 BY NORMA WAGNER The Salt Lake TribuneTaylorsville payroll clerk Ellie Steiger. Ogden apartment manager Donald Doerr. West Valley City Councilman Leland DeLange.
Each died suddenly and horribly this year, their brains eaten away by a rare disease even the world's most accomplished researchers do not fully understand.
Cruetzfeldt-Jakob disease (CJD) has claimed the lives of at least four Utahns this year, including a Layton mother of four who did not die suddenly, but atypically lived with the disease for a year. At 44, Layton dental assistant Jill Fordham Cunliffe also was younger than most CJD patients.
The deaths have aroused interest because a variant strain of CJD has been associated with mad-cow disease in Great Britain. However, doctors and epidemiologists say there is no link between the Utah cases and contaminated beef products.
Steiger, 57, Doerr, 68, and DeLange, 64, left behind devastated spouses, siblings, offspring and friends who had mere weeks to prepare emotionally for their impending deaths. ``It's how it degenerates a person, the shakes, the jerks they go into, how they get this blank stare, how their mouth droops open,'' said Mel Steiger, Ellie's husband of nearly 40 years. ``They don't know anybody and they can't communicate with you. And it comes and it goes. By the end, they can't eat and they can't drink and you think they're going to starve to death. ``But one of the worst things is the inability to communicate. It really tore the oldest grandson up when he got on the bed and my wife said, `Who are you?' He said, `You mean Grandma didn't even know who I was?' That's pretty tough for a 10-year-old.''
The cause of CJD is unknown. It is incurable. Researchers don't know how it is transmitted, but there are several theories. The most accepted is that CJD is caused by abnormal proteins -- called prions -- in brain cells. If there is a mutation in the prion gene, abnormally shaped prions are produced. The rogue prions then convert normal prions, accelerating the disease. That theory was developed by California biochemistry professor Stanley B. Prusiner, who won the Nobel Prize last year for his research.
CJD comes in three forms, said J. Richard Baringer, chairman of the neurology department at the University of Utah.
-- The ``sporadic'' form is most common, and develops for no apparent reason. -- An inherited form which occurs in about 10 percent of cases. -- And a few cases that result from contamination.``An overwhelming majority of cases in America and in the Western world seem to be sporadic,'' said University Hospital neurologist Gregory Call, who diagnosed two CJD victims this year. ``There's really not a clue as to why a person gets the disease.''
CJD has been transmitted through transplantation of corneas or other tissues from infected donors, instruments contaminated during brain surgery, and growth hormones (which now are synthetically produced) from the pituitary glands of infected cadavers. Variant CJD, associated with mad-cow disease, is different from the classic strain. British researchers believe variant CJD has been transmitted to humans through diseased cow brains and spinal cords that were ground up and fed as protein supplements to cattle. The cattle contracted mad-cow disease and were either slaughtered and fed to other cows or packaged for human consumption. However, American epidemiologists and neurologists believe classic CJD is what causes the deaths of about 240 Americans annually.
The insidious disease lies dormant in its victims for as long as 30 years before it manifests and kills its hosts quickly. Doctors can only treat symptoms. While incidence of CJD throughout the world is estimated at one case per 1 million population on average per year, but many experts believe the actual number is higher. Though Utah has had four cases this year, some years -- 1990 through 1993 -- there were none. In 1989 there were six and two in 1996, according to the Utah Department of Health. In all,
16 Utahns have been known to die of CJD over the past nine years. During the same time, Utah's population has eclipsed the 2 million mark, putting the state close to the one-in-one-million estimate. The disease progresses from a lack of coordination to involuntary movements. Those symptoms are followed by problems with speech and thought processes, impaired vision or blindness, severe dementia and immobility. The patient soon becomes comatose and dies. ``This can actually happen right before your eyes,'' neurologist Call said. ``There aren't many diseases that do that.''
Steiger and Doerr underwent drastic personality changes at first. Steiger, who died in March, became angry and aggressive, said her husband. Doerr, who died in July, changed from suffering depressive episodes to near manic happiness, said his daughter Diane Bosgieter.
DeLange's symptoms started when he could not remember how to tie his necktie. After that he deteriorated rapidly, said his wife JoAnne. He was not diagnosed with CJD until he was semi-comatose. DeLange died Aug. 29.
Call, who cared for Steiger and Doerr, said he usually treats one CJD case per year. But he added that more may exist since not every doctor recognizes its symptoms, which mimic dementia. ``There are probably some slower instances where it's not so obvious, where a person has neurological problems, including thinking problems, over many months and we don't recognize it [as CJD] because it appears more like dementia, such as Alzheimer's disease.''
Cunliffe, the Layton dental assistant, died Aug. 5 after slowly suffering from the disease for almost one year. She was not diagnosed with CJD until after her death, said her husband, Robert.
Experience in dealing with cases and escalating research on CJD is giving physicians the tools to recognize it more quickly. Cases can initially be diagnosed through electroencephalogram (EEG) tests, which often show specific characteristics, or changes, in a patient's brain waves from one to three months after the onset of symptoms. A firm diagnosis can be made through a brain biopsy after death.
Even though there have been four CJD deaths in Utah this year, Call does not believe the number of cases is on the rise. ``A lot of things that are uncommon occasionally occur in clusters and don't seem to have much meaning,'' he said. ``I would like to reassure people that this really is a sporadic disease and that if it is communicable, it is minimally so, very difficult to get.''
CJD is among a family of progressive neurological diseases called transmissable spongiform encephalopathies, or TSEs. (Spongiform refers to deteriorated areas of the brain that look like sponges). Other TSE forms affect animals and include bovine spongiform encephalopathy (BSE), which results in mad-cow disease, scrapie in sheep and chronic wasting disease in elk and mule deer, which has been spreading in Wyoming and Colorado. Some researchers suspect that TSE diseases may cross species and change forms when ground-up organs and body parts of infected animals are fed to their own or other species, such as scrapie in sheep becoming bovine spongiform encephalopathy in cows and onto variant Creutzfeldt-Jacob disease in humans.
Less than 10 years after mad-cow disease began devastating Britain's cattle industry in 1986, doctors began diagnosing the first of 26 patients in the United Kingdom (and one in France) with the variant strain of CJD. While the traditional CJD strain usually afflicts victims in their late 50s, the new strain attacks people in their 20s and 30s. Symptoms include psychiatric problems and pain in their extremities. Variant CJD also lasts much longer, 14 months as opposed to one to six months in classic CJD. As a result, the younger patients suffer a slower, more agonizing death. Because of those atypical cases, British researchers now suspect that mad-cow disease has led to the creation of a new human pathogen. ``[Variant] CJD can now be regarded as human BSE [bovine spongiform encephalopathy],'' said Sir John Pattison, of the Medical School of University College of London.
Because America traditionally had shared the practice of feeding rendered animal protein supplements to cattle, some wonder if a variant strain of CJD could crop up here. In 1988, Britain imposed bans on using cattle brains, spinal cords and other animal parts that had been found to contain infectious material for use in animal feed. Top American agencies -- including the Food and Drug Administration and the U.S. Department of Agriculture -- assured Americans mad-cow disease does not exist here.
``We are monitoring the cattle industry in the United States for mad-cow disease,'' said state veterinarian Mike Marshall. ``We really want to make sure that people understand that any animal at a packing plant that shows any type of nervous system problem is killed and we take that brain and examine it. ``We have examined thousands of animals in the past three years and we have found nothing in this country [on mad-cow disease]. Additionally, there's been a ban on live cattle imports into this country for several years and we have not accepted anything from Britain since 1990.''
While the FDA later banned the use of animal brains and spinal tissue and meat-and-bone meal in rendered animal supplements fed to cows, such supplements continue to be fed to pigs and horses. Additionally, American cows continue to feed on cow's blood meal because federal officials contend TSE diseases have not been shown to be transmitted through animal blood to humans.
Reuters World Report Mon, Sep 14, 1998BRUSSELS - Britain's new Agriculture Minister Nick Brown said on Monday he hoped the worldwide ban on mainland beef exports imposed over mad cow disease would be lifted before the end of the year. Visiting Brussels for talks with European Commissioners Franz Fischler and Emma Bonino, Brown said the easing of export restrictions was his "number one priority." "We want to get this dealt with before Christmas...we have done everything we have been asked to do, and more. I want this ban lifted because it is not fair," Brown told a press briefing.
The European Commission in June proposed lifting the crippling trade embargo, more than two years after it was imposed over the BSE (bovine spongiform encephalopathy) crisis. In March 1996, the British government admitted a possible link between BSE and the human condition Creutzfeldt-Jakob Disease. But the proposal still has to be approved by a majority of member states, and some including Germany remain sceptical.
The plan, known as the Date-Based Export Scheme, would allow a resumption in British exports of beef from animals born after August 1996 -- the date when a ban on feeding cattle meat and bone meal became fully effective. EU veterinary experts last week examined what EU officials have described as a favourable Commission report on Britain's new meat controls but have yet to hold a substantial discussion on it. Another vets' meeting is scheduled for next week. Further discussions at the veterinary committee stage mean EU farm ministers are unlikely to debate the issue before October, with a decision seen as possible in November.
Member states have already agreed a separate scheme, under which beef shipments were allowed to restart from Northern Ireland, where a computerised database system for cattle has been in operation for years.
Brown, who replaced Jack Cunningham as agriculture minister this summer, also said Britain would soon present new proposals on phasing out the EU's system of milk quotas after 2006 under reforms to the Common Agriculture Policy. He said Britain remained broadly supportive of the Commission's plans to reform the CAP, discussions on which are expected to restart in earnest after the German elections.
July 8/98 Reuters[The web address of the DoH CJD New Releases has now changed ; it can also be reached via "Statistics" -- "CJD statistics" links on the MAFF BSE page]
LONDON -- The U.K. National Audit Office was cited as saying today that the cost of clearing up Britain's mad-cow crisis is set to top $5.5 billion, and that it could take until 2003 to incinerate huge stocks of meat, bone meal and tallow from cattle slaughtered because they were judged at risk from the disease. Since March 1996, over 1.35 million cattle have been put to death under one cull scheme, affecting those over 30 months old.
The report said total spending on tackling the disease, compensating farmers and paying slaughterhouses, renderers and other professionals was almost 1.5 billion pounds ($2.5 billion) in 1996-7, of which 800 million pounds would come from the European Union. It forecast additional spending between 1997 and 2000 at 1.9 billion pounds, taking the total to 3.4 billion pounds ($5.5 billion).
PA News Fri, Sep 11, 1998 By Nick Drainey, PA NewsHundreds of farmers protested outside a court today as a restaurant manager faced charges of selling beef on the bone. Christopher Bowman, who is a chef and the manager of the Drovers Inn, Bishop Thornton, near Harrogate, North Yorkshire, was remanded on bail until October 24 by the town's magistrates.
He was charged with selling T-bone steak to a trading standards officer, failing to give information about the sale, allowing Byjade Trading Ltd - the company which the pub trades under - to sell the steak and being the manager of Byjade Trading Ltd who sold the steak.
Mr Bowman left court to the cheers of local farmers who were cooking T-bone steaks on barbecues. More than 100 tractors and Landrovers also drove around Harrogate slowing traffic and protesting against the ban on beef on the bone and the handling of the BSE crisis. Farmer Ben Atkinson, spokesman for the demonstrators, said the protest had been peaceful.
He added: "They are not a law breaking lot in the farming community but the support stems from the inability to choose. "If you like a chop you have it on the bone and if somebody does not want a piece of meat on the bone they buy a piece of fillet steak." Mr Atkinson added that farmers still needed a voice as they had lost up to 30% on the price of beef in the last 12 months alone.
Correspondent opinion: Terry S. Singeltary Sr Letter submitted to Atlantic Monthly 15 Sept 98"I hope these governtment websites help you for 1996 and 1997 imports -- see under ' meat and edible meat offals' section."
Marva Thompson Foreign Trade Reference Room 202/482-2185"The U.S. is apparently still importing beef, pork, sheep, and lamb from countries in which BSE is found [this is probably completely legal under regulations applicable at time of import-- webmaster]:
Bovine anmls bnlss ex prcssd frozen/U.S. Imports for Consumption 1997 year to date (custom value, in thousands of dollars) (units of quantity: kilograms) United Kingdom 37,122 kilograms, 43 thousand dollars Netherlands 56,260 kilograms, 413 thousand dollars Canada 18,141,481 kilograms, 23,914 million dollars Livers of bovine animals, edible, frozen. U.S. Imports for consumption Netherlands 19,230 kilograms, 25 thousand dollars Canada 160,632 kilograms, 147 thousand dollars Tongues of bovine animals, edible, frozen u.S. Imports for consumption Netherlands 1,047 kilograms, 4 thousand dollars Canada 767,859 kilograms, 2,028 million Hi-qulty beef cuts w/bone in prcssd f/c u.S. Imports for consumption Canada 25,332 kilograms, 37 thousand dollars Beef cuts w/bone in excpt prcdssd fr/ch u.S. Imports for consumption Netherlands 5,276 kilograms, 30 thousand dollars Canada 117,142 kilograms, 353 thousand dollars Meat bovine anmls cuts w/bone ex prrocssd fr us imports for consumption Netherlands 51,836 kilograms, 444 thousand dollars Canada 120,955,010 kilograms, 253,199 million Cattle hides, whole, fresh or wet-salt u.S. Imports for consumption Belgium 1,270 pieces, 112 thousand dollars United kingdom 36 pieces, 3 thousand dollars Ireland 12,797 pieces, 839 thousand dollars Italy 50 pieces, 10 thousand dollars Fr germany 2,500 pieces, 36 thousand dollars Canada 1,405,430 pieces, 67,320 million dollars Hides/skins bovine anmls nesoi whole frh/wet-saltd u.S. Imports for consumption United kingdom 13 pieces, 1 thousand dollars Italy 4 pieces, 4 thousand dollars Germany 9,455 pieces, 139 thousand dollars Canada 567,816 pieces, 17,196 million dollars Cattle hides, whole, fresh or wet-salted u.S. Imports for consumption 1998 year to date Italy 7 pieces, 2 thousand dollars Ireland 1,408 pieces, 85 thousand dollars France 25 pieces 2 thousand dollars Canada 965,355 pieces, 37,244 million dollars Hides and skins of bovine animals, whole, nesoi, fresh or wet-salted U.S. Imports for consumption United kingdom 18 pieces, 3 thousand dollars Sweden 1 pieces, 1 thousand dollars Italy 2 pieces, 2 thousand dollars Germany 5,565 pieces, 72 thousand dollars Canada 84,327 pieces, 2,257 million dollars Sheep, lamb skins, no wool, nesoi, pickled not split, u.S. Imports for Consumption United kingdom 9,504 pieces, 88 thousand dollars Sheep, lamb skins, no wool, nesoi, pickled, split u.S. Imports for Consumption United Kingdom 149,580 pieces, 1,212 million dollars Netherlands 50,400 pieces, 267 thousand dollars Italy 4,175 pieces, 64 thousand dollars France 13,644 pieces, 57 thousand dollars Canada 131,642 pieces, 241 thousand dollars Carcasses and half-carcasses of swine, frozen u.S. Imports for consumption United kingdom 85,003 kilograms, 201 thousand dollars Netherlands 24,000 kilograms, 33 thousand dollars Ireland 24,567 kilograms, 39 thousand dollars Fr germany 23,032 kilograms, 32 thousand dollars Denmark 112,345 kilograms, 168 thousand dollars Canada 17,889 kilograms, 41 thousand dollars Hams and cuts therof, bone in processed frsh/chld u.S. Imports for Consumption Belgium 9,406 kilograms, 34 thousand dollars Canada 95,515 kilograms, 172 thousand dollars Italy 6,459 kilograms, 86 thousand dollars
9-11-98 Knight Rider Tribune NewsThe government's current system to check food imports for possible health dangers is dangerously flawed, experts in the food business told a Senate subcommittee Thursday. U.S. inspectors check only 2 percent of all foreign shipments and consistently issue low penalties to importers who break the rules, experts said. Unscrupulous importers typically import large amounts of products that will not pass (Food and Drug Administration) inspection, said a former West Coast customs broker.
He said importers easily bypass inspections by docking at high-volume ports, such as Los Angeles-Long Beach and New York, where the inspection force is stretched thin. Inspections are so low there they virtually pass right through.
I hope all of you at THE ATLANTIC MONTHLY find some interest in this. ..."