Safe Food: The Politics of Food Safety (9 page)

If the extent of foodborne illness is uncertain, so must be estimates of its cost to society. Here are some examples of the wide range of figures reported from 1989 to 1998: $4.8 to $23 billion in 1989, $23 million to $6 billion in 1994, $5.6 to $9.4 billion in 1995, $12.9 billion (from illness caused by just six types of bacteria) in 1996, and $37.1 billion in 1998. Agricultural economists estimate that the costs of foodborne illness in children alone came to $2.3 billion in 2000.
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Whatever the correct figure might be, it surely underestimates the costs to the victims in pain and inconvenience; to taxpayers in medical treatment for the indigent, higher health insurance premiums, public health surveillance systems, and investigations of outbreaks (estimated at $200,000 each); and to the food industry in plant closings, cleanup, and recalls as well as in legal fees, claim settlements, and higher insurance premiums.
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Regardless of the accuracy of cost and case estimates, one trend is clear: an increasingly broad range of foods is contaminated with harmful bacteria. Back in the 1970s, outbreaks of foodborne illness were most often traced to improperly stored turkey stuffing and deviled eggs prepared by home cooks.
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Before examining how the food sources of contamination have expanded, we need to deal with one further complication: the distinction between cases and outbreaks.
Cases
refers to the number of individuals who become ill—whether or not they report the disease. In contrast,
outbreaks
always are reported; authorities discover them when more than one person gets sick from the same food source and doctors report the illnesses to health officials. It is easier to identify cases—and, therefore, report them—when an illness occurs right after the food is eaten. Cases that occur with a delay in onset are more difficult to attribute to specific foods and are much more likely to go unreported, even when they affect much larger numbers of people.

With these distinctions in mind, the tracking information indicates a change in the food sources of
outbreaks:
seafood ranks first, followed by eggs, fruits and vegetables (sprouts, lettuce, berries, cantaloupe), beef, poultry, and foods such as salads and sandwiches made with multiple ingredients.
In part because so many more meals are consumed outside the home, foods other than those prepared by home cooks now account for 80% of the
outbreaks
(although not necessarily 80% of the
cases
of food-borne illness).
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The outbreaks have changed in one additional respect: they are getting nastier. Most used to be due to relatively benign species of
Salmonella
,
Staphylococcus
,
Clostridium
,
Shigella
, and
Vibrio
, but the more pathogenic strains observed since the 1990s are quite unforgiving. Among outbreaks of illness caused by
Listeria monocytogenes
, a particularly virulent species of bacteria, the death rate is 20% (
table 3
). For example, some years ago a carefully investigated
Listeria
outbreak among 142 people who had eaten a commercially produced unpasteurized soft cheese caused 48 deaths (of which 30 were fetuses or newborn children) and 13 cases of meningitis.
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Salmonella
infections can cause arthritis, and
Campylobacter
is a precipitating factor for up to one-fourth of reported cases of Guillain-Barré syndrome, a leading cause of paralytic disease.

Twenty years ago, three of today’s worst bacterial pathogens—C
ampylobacter, Listeria
, and
E. coli
O157:H7 (described below)—were not recognized as hazards. Also new are bacteria capable of flourishing under refrigeration (
Yersinia
and
Listeria
) or acidic or dry conditions (
E. coli
O157:H7). The alarming survival features of such bacteria undoubtedly evolved in response to changes in methods of food production and distribution that select for the hardiest bacteria and encourage their wide dispersal. Whereas undercooked hamburger and ground beef products used to be the only known source of
E. coli
O157:H7, other foods cross-contaminated by exposure to infected cattle or meat are now involved: apple cider, sprouts, and any number of vegetables. Outbreaks of the especially virulent
Salmonella enteritidis
used to be restricted to eggs; now they have been traced to carriers as unlikely as tomatoes, melons, and orange juice. As we examine the societal and commercial forces that foster these unwelcome trends, we need to understand a bit more about one of the three newly emergent pathogens,
E. coli
O157:H7.

E. coli
O157:H7 merits special attention not only because of its exceptional virulence but also because it illustrates so well how changes in the food system and in society provide new opportunities for spreading microbial disease through food. When I first encountered the more common form of
E. coli
in a college biology class, instructors presented it as
a harmless inhabitant of the digestive tracts of animals and humans, spread by accidental transfer of excreted material. It was known best as an indicator of fecal contamination of water supplies; if water supplies contained
E. coli
, they were likely to contain more dangerous bacteria. We now know much more about the biology of this organism. Like many bacteria,
E. coli
is able to accept genes from related bacterial species to form “stable variants” that can pass the borrowed genes along to other bacteria as they divide and multiply (see appendix). The
E. coli
variant known as O157:H7 is especially dangerous; at some point, it picked up a
Shigella
gene for a toxin that destroys red blood cells and induces a syndrome of bloody diarrhea, kidney failure, and death. This toxin is particularly damaging to young children.
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Other features of the O157:H7 variant are also noteworthy. Unlike common
E. coli
, this type resists heat; it grows at temperatures up to 44°C (111°F). It also resists drying, can survive short exposures to strong acid (pH 2.5), and sometimes resists radiation and antibiotics. For these reasons, controlling it is not easy. Worse,
E. coli
O157:H7 is infectious at very low doses. The normal digestive tract contains hundreds of billions of bacteria that compete for space and nutrients. In this environment, it takes thousands of
Salmonella
to induce symptoms, but the lowest infectious dose of
E. coli
O157:H7 appears to be less than 50—a minuscule number in bacterial terms. Control measures, therefore, must do more than just prevent growth; they must eliminate the very presence of these bacteria. Foods containing
E. coli
O157:H7 must be cooked at temperatures high enough to kill
all
of them.
Table 4
presents recommendations for food-handling techniques to prevent problems with this microbe.

E. coli
O157:H7 infections originate with farm animals, and such animals increasingly harbor this variant. Although earlier studies suggested that perhaps 10% of adult ruminant (cud-chewing) animals—mainly cows and cattle—were infected with
E. coli
O157:H7, the proportion now is as high as 28%, and may exceed 40% in slaughtered animals not yet processed. Young infected animals exhibit mild diarrhea, but most do not appear sick and go untreated. Deer, sheep, goats, dogs, birds, and flies also harbor the variant, almost certainly because they have come in contact with cattle feces. People pick up
E. coli
O157:H7 infections from direct contact with feces, from foods and water that have come in contact with feces, or from infected people who shed it in their feces and pass it along from unwashed hands—which is why hand washing is so important as a control measure. Uncooked foods derived from cattle (raw hamburger, for example) are the origin of most
E. coli
O157:H7 outbreaks.
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As we will see, fruits and vegetables that have come into contact with cattle feces or with contaminated raw meat also have become common sources.

TABLE 4
. Recommendations for reducing the risk of infection from
E. coli
O157:H7

SOURCE
: Buchanan RL, Doyle MP.
Food Technology
1997;51(10):69–76.

*
Bringing a food to 155°F is sufficient to kill these bacteria; recommended cooking temperatures provide a 5°F margin of safety. Pasteurization brings liquids to scalding temperatures (about 140°F) for short times; this process destroys most bacteria and delays the growth of those that survive.

E. coli
O157:H7 is considered newly emergent because its recognition is so recent. The earliest case seems to have occurred in 1975, but the first reported outbreak occurred in 1982. Infections have now been observed in 30 countries on six continents. Outbreaks are increasing in frequency; there were 6 in 1997 but 17 in 1998. The infections are exceptionally serious; 82% of people infected with
E. coli
O157:H7 see a physician, 18% require hospitalization, and the mortality rate is 3–5%.
¹⁸
How
E. coli
O157:H7 emerged and spread throughout the food supply is a subject of considerable speculation. The most reasonable explanation involves the profound changes in society and food production that have taken place in recent years, matters to which we now turn.

Most of us imagine that the rapid advances in science and medicine of the last century would make microbial diseases a thing of the past, and we would hardly think agriculture to be a cause of medical problems. But alterations in the ways we produce food, choose diets, and live our lives have created conditions that favor the spread of pathogens into more foods consumed by more people. These changes foster the emergence of microbial pathogens that resist heat, cold, acid, and other preservation methods. They also encourage pathogens to develop resistance to treatment with antibiotic drugs. Refer back to
figure 2
in the introductory chapter to see how the food system has changed from one based primarily on locally raised meat, fruits, and vegetables to one in which commodities like StarLink corn travel great distances—across many states and between different countries—before reaching supermarkets.
Table 5
summarizes some of the developments in food production, consumer preferences, and demographics that favor foodborne illness. Because such developments involve consumers as well as food companies, they illustrate why food safety has to be a shared responsibility but also why it is difficult to determine accountability when outbreaks occur.

TABLE 5
. Modern developments in food production practices, dietary preferences, and demographics that favor the emergence and spread of foodborne illness

The most important trends favoring the growth and dispersion of microbial pathogens relate to methods of production, particularly the production of food animals. As a consequence of advances in technology,
the globalization of food marketing, and economic imperatives, small farms raising multiple species of animals and crops have been replaced by incomprehensibly large “factory” systems. In the early 1970s, for example, many thousands of small farmers raised chickens; these were supplied by numerous feed mills and processed in thousands of local plants throughout the country. Today, just a few gigantic corporations control every aspect of chicken production, from egg to grocery store.

One measure of industry concentration is the proportion of an industry controlled by its four leading firms. The proportion of chickens slaughtered by the top four chicken-processing corporations increased from 18% in 1972 to 49% in 1998. Similarly, the top four hog-slaughtering firms controlled 32% of all hogs processed in 1972, but 43% in 1992, and the top four cattle-slaughtering firms increased their share from 30% in 1972 to 79% by 1998. Equivalent trends are seen in the dairy industry.
¹⁹
As a further example of such consolidation, Tyson Foods, “the world’s largest fully integrated producer, processor and marketer of chicken and chicken-based convenience foods,” merged with IBP, “the world’s largest supplier of premium fresh beef and pork products,” to create the world’s largest provider of animal protein. This 2001 merger resulted in a company that controls about 28% of the world’s beef, 25% of the chicken, and 18% of the pork.
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