A Trace of Arsenic
The cans of baby formula invaded Brian Jackson’s Dartmouth College lab late in 2010. His team picked up an armful of popular brands at the food co-op in Hanover, N.H. Then another armload. Eventually Jackson had a cabinet full of the brightly labeled canisters. Today, he still keeps a few in his office. Not as clutter — that’s not his style. He just likes to keep his toxicology evidence close at hand.
A 47-year-old analytical chemist with sandy-gray hair and blue eyes, Jackson has a chemist’s passion for the picky details of analysis, the skill his colleagues tapped when they asked him to investigate a disturbing possibility: that baby foods and formulas made with rice might contain arsenic, a known carcinogen. Ingested even at the trace levels the scientists suspected, devastating health outcomes could result.
In a first round of tests, arsenic levels in all the products Jackson’s group studied fell within the 10 parts per billion safety limit the EPA sets for water. (There is no limit for arsenic for most foods.) But a short time later, while shopping at the co-op, Jackson noticed two brands of toddler formula, both high-end organic products, that his team had missed on the first sweep.
This time, to the team’s surprise, the arsenic readings flew off the chart.
“My first thought,” Jackson says, “was that I’d better reanalyze these samples in case I’d screwed up.”
His second thought, after confirming the readings, was to wonder: What made the arsenic levels spike in those two cans? In answering that question, Jackson traced not just the story of the metal-loving rice plant, but also the tangled and troubling path of a notorious poison through our past and present.
A naturally occurring metallic element, arsenic permeates the Earth’s crust. Glinting silver-gray in rocks and soils, it mixes with other minerals as it seeps into water supplies, drifts on the dusty plumes of volcanic eruptions and travels on the wind. It also spreads through industrial use, from mining to agriculture.
Arsenic coils like a dark smoke through our history. The word derives from the ancient Greek arsenikon, meaning “potent.” It was used to describe the compound arsenic trioxide, which can be lethal at 100 milligrams, about one-fiftieth of a teaspoon. Arsenic trioxide is famously tasteless and odorless, which helped make it one of the most frequently used homicidal poisons in history.
But in recent years, studies have revealed that exposure to far smaller doses poses a more subtle — but also insidious — threat. The pure element arsenic mixes into many compounds, either organic (in chemical lingo, meaning that it contains carbon) or inorganic (without carbon).
And even at concentrations of parts per billion (ppb), closer to a drop in a swimming pool than a drop in a teacup, long-term exposure to inorganic arsenic — generally considered the most toxic form — has been linked to an increased risk of cancer and other life-threatening illnesses. Although arsenic hasn’t been studied in as much detail as other toxins found in industrial materials, such as mercury or PCBs, scientists say it underscores the finding that minute exposures to such substances can do great harm.
At low doses, arsenic doesn’t overwhelm body systems immediately or even cause death over the course of months. Rather, explains Dartmouth molecular toxicologist Joshua Hamilton, chronic exposure to trace arsenic inflicts damage at a cellular level, increasing the body’s vulnerability to a wide array of sicknesses, including cancer, cardiovascular disease and diabetes. While trace arsenic won’t kill on its own, he says, it “seems to make everything worse.”
For decades, officials have focused on trace arsenic in drinking water as the chemical’s primary public health threat; in 2001, the EPA dropped the limit for arsenic in water from 50 ppb to 10 ppb. But in the past few years, regulators have also begun to worry about exposure from foods and beverages. This summer, concerned about arsenic in pesticide residues found in imported juices, the FDA announced it will limit the amount of arsenic allowed in apple juice to 10 ppb, the same amount permitted in water.
The FDA has also investigated arsenic’s presence in other foods. Chicken, for example, has come under scrutiny because of the longtime use of an arsenic additive in poultry feed. But the top-priority food on the list is rice, which became a focus when researchers realized that it takes up inorganic arsenic from soil far more efficiently than other grains. A July study revealed the first evidence directly linking consumption of rice containing arsenic to genetic damage in humans.
Such findings are especially alarming because rice is a major part of the diet in certain communities, such as those with an Asian heritage, and because rice is a staple for infants and young children, whose developing bodies and brains are especially vulnerable to harm.
It’s that last concern that sparked the formula studies in Jackson’s Dartmouth lab.
Evidence of Harm
The realization that trace amounts of arsenic might pose a health threat began with mysterious outbreaks of disease in Southeast Asia. In the 1960s, scientists in Taiwan traced an outbreak of blackfoot disease, caused when dying blood cells lead to gangrene, to arsenic-contaminated well water. In many wells, arsenic levels exceeded 800 ppb (80 times as high as today’s EPA standards); some wells registered as high as 1 part per million.
Still, researchers didn’t pay serious attention to the problem for decades, after a massive public health crisis came to light in Bangladesh. In the 1970s, villages began drilling wells to prevent the deadly infectious diseases that flourished in warm, sewage-tainted surface waters. As predicted, infectious disease rates dropped.
What was not predicted was the insidious growth of other diseases: lung and bladder cancers, cardiovascular problems, diabetes and severe skin lesions. As part of a search for the cause, geologic tests revealed large deposits of arsenic-rich minerals steadily leaching into groundwater, causing levels in many wells to top 500 ppb.
After investigating the arsenic situation in Bangladesh at the request of the World Health Organization in the late 1990s, Allan Smith, an epidemiologist at the University of California in Berkeley, recommended that officials declare a public health emergency for what he considered “the largest mass poisoning of a population in history.”
Smith had also investigated evidence of similar poisoning in Antofagasta, a Chilean port city that in 1958 had switched from well water to a cheaper supply sluicing down from the Andes. In 1970, city administrators realized arsenic from mountain mineral deposits was contaminating the city’s water supply, with exposures of 500 to 800 ppb for the public at large.
Antofagasta quickly returned to using well water, but those dozen years provided a unique window into the long-term health effects of drinking water containing trace amounts of arsenic. Smith’s analysis showed that Antofagasta residents exposed to the city’s water between 1958 and 1970 had experienced markedly higher rates of bladder and lung cancer.
By his estimates, arsenic accounted for about 7 percent of deaths among Antofagastans age 30 and older. “I believe arsenic poses the highest cancer and mortality risks we know of compared to any other environmental exposure,” Smith says. “The only exposure we can compare it to is active smoking.”
But researchers are also compiling evidence that arsenic poses a health threat at far lower doses than in such highly contaminated water supplies. New York University epidemiologist Yu Chen has followed up on both the Taiwan and Bangladesh findings by looking at water contaminated by arsenic levels of 50 ppb and below.
At this trace exposure, she’s found evidence of troubling changes in blood cells. And in tracking human disease patterns, she’s established a clear link between such low-dose chronic exposure and increases in high blood pressure and heart disease. In one study, she estimated that among Bangladeshis whose drinking water contained as little as 50 ppb of arsenic, exposure accounted for some 29 percent of heart disease deaths.
Animal studies strengthen the case. In one study, Dartmouth’s Hamilton found that arsenic exposure at 10 ppb compromised the immune systems of mice so much that they could not fend off an ordinary influenza infection. In another study, his team found that mice given chow containing trace amounts of arsenic, then exposed to a standard daily dose of ultraviolet light, had higher rates of skin cancers than mice given untainted chow.
“This is a very, very subtle poison at low doses,” Hamilton says. “Each passing year, we’ve discovered health effects at lower and lower doses. There isn’t any other toxicant that we know of that even comes close to arsenic in terms of the number of health effects at the doses we’re seeing and the numbers of people worldwide who are potentially exposed.” The Rice Connection
As evidence of harm from low-dose arsenic in water mounted, scientists began to wonder about the food grown in that water and distributed to dinner tables worldwide.
The first person to tackle the issue was biogeochemist Andrew Meharg. In 1999, Meharg, then at the University of Aberdeen, Scotland, was studying the environmental effects of arsenic in Bangladesh when a student noted that rice was being irrigated with vast quantities of arsenic-contaminated water.
Could that raise the risk? The question was urgent because rice is a dietary staple — not only in the typical vegetarian Bangladeshi diet, but everywhere: in whole form and also in rice flour, malt, bran, pasta, noodles, breakfast cereals, cereal bars, crackers, rice cakes and more.
“While a range of other foods may show arsenic elevation, we do not eat them two or three times a day, in a multitude of forms,” says Meharg, now at Queen’s University in Ireland. “In terms of importance: rice, rice and rice again. Nothing matches it.”
Testing the rice paddies in Bangladesh, Meharg found his fears realized. Rice plants took up inorganic arsenic from water and soil with dismaying efficiency: at 10 times the rate of other grains. And the flooded fields — which turned out to foster the release of inorganic arsenic — only made things worse.
Later, comparing samples of multiple species of rice grown in numerous regions around the world, he found arsenic levels almost universally elevated, including in the U.S. Notably, much of the U.S. rice crop is grown in regions of the South where the soil is contaminated by old arsenic-based pesticides, once used by farmers to protect cotton crops from boll weevils. In a 2007 study, Meharg found that rice grown in some South-central states contained nearly twice as much arsenic (an average of 30 ppb) as rice grown in California (an average of 17 ppb).
Health Food Surprise
The leap to early childhood exposure was straightforward. In 2008, Meharg reported that arsenic in baby rice cereal sold in the U.K. exceeded safety levels set for drinking water by both the U.S. and the European Union.
That finding caught the attention of scientists at Dartmouth’s Toxic Metals Superfund Research Program, which tracks high-profile metallic elements, mainly arsenic and mercury, for the federal government. One Dartmouth scientist, epidemiologist Margaret Karagas, had already found that babies whose mothers relied on water from wells drilled in New Hampshire’s arsenic-rich bedrock — with contamination measured at levels as high as 1 ppm (1,000 ppb) — were disproportionately likely to have low birth weight and might also be more vulnerable to childhood infections. But now the Dartmouth researchers decided to investigate food as well.
Baby foods were the starting point.
The Dartmouth researchers realized that all kinds of baby formulas and foods contained rice; many were thickened with rice starch. It was that awareness that prompted Jackson’s investigation of formulas.
Although the team’s initial tests found barely a trace of arsenic in baby formula and pureed baby food, later tests showed that two organic toddler formulas contained up to 60 ppb of arsenic (adjusted for dilution) — six times the EPA safety limit for water.
Labels on the formula canisters told why: They were sweetened with organic brown rice syrup, considered a healthy alternative to corn syrup. And while brown rice syrup is rare in baby foods, it is common in crackers, cereals, snack bars, energy bars and many products marketed as health foods. “We didn’t choose the syrup as a study subject,” Jackson says. “The syrup chose us.”
The Dartmouth team expanded their tests, analyzing 29 cereal bars and energy bars as well as three varieties of pure brown rice syrup. Rice-free bars, they found, had the lowest arsenic levels, as little as 8 ppb. Arsenic concentrations in the rice bars ranged from 23 to 128 ppb; those sweetened with brown rice syrup were at the high end. Organic brown rice syrups registered as high as 400 ppb of arsenic — mostly the more dangerous inorganic form.
It made sense that syrup, which concentrates sugars, would also concentrate other chemicals, including arsenic. But the Dartmouth team did not expect it to concentrate arsenic so intensely. So another member of the group, plant geneticist Mary Lou Guerinot, decided to take a closer look. Using a technique that creates high-resolution, three-dimensional images, Guerinot and her colleague Tracy Punshon, an expert at imaging metals moving through living systems, found arsenic concentrated in the grain’s nutrient-rich outer layers, which are polished off in the processing of white rice but remain in brown rice.
As the data emerged in detail, Punshon stopped buying rice-based cereal bars and started making her own rice-free bars. Another researcher, a runner, had been a devotee of energy bars sweetened with rice syrup — until analyses showed she was taking in some five times the EPA drinking-water standard for arsenic.
She stopped eating them.
Still, when the Dartmouth team published their results in the journal Environmental Health Perspectives in February 2012, they were unprepared for the public outcry. Parents called, frightened they had been poisoning their children. Media outlets clamored for quotes. Some producers of rice-based foods publicly criticized the group’s methods.
“It was a bit of a bother,” says Jackson, characteristically understated. He doesn’t gravitate to being onstage. “I don’t want to get into a fight. I published what I published, I’ve gone through the whole peer review process. That was really enough for me.” And in the end, even his industry critics accepted his point. The organic formula maker Nature’s One, whose products were implicated in the research, announced a new zero-tolerance policy for the element.
Yet Jackson points out that a central problem remains: No one really knows how much rice is safe to eat. But recent research provides further evidence that a diet high in rice that contains arsenic is worth avoiding.
In July, researchers in the U.K. and India reported that people who ate arsenic-tainted rice on a daily basis showed troubling signs of chromosomal damage — and that such damage increased with greater amounts of arsenic in the rice.
As such connections are made, Jackson and his colleagues argue that what’s really needed isn’t a patchwork of voluntary responses but an official safety standard for arsenic in all foods. That stance is affirmed by other public safety advocates as well, including scientists working with Consumer Reports who have recently reported elevated arsenic levels in both juice and rice.
The FDA’s 10 ppb limit for apple juice, announced this summer, is widely regarded as a response to such concerns. The agency is now considering a limit for rice as well. Although FDA officials have not commented publicly on what a rice standard might look like, scientists working with the agency say one focus is on the most visible risk groups — infants, children and high-rice-consumption populations such as those on gluten-free diets and people of Asian and Hispanic descent, who often eat rice and rice products several times a day.
Whatever the regulatory future holds for arsenic, it is only one piece of a bigger issue of trace contamination, says Hamilton, who considers the arsenic story a cautionary tale. As we consider the health threat that low-dose arsenic can pose, he says, we must also consider other toxicants that have not yet been carefully examined but that might be equally or more dangerous.
The Risks of Imported Food
Like our cars and our kids’ toys and of course those designer bags, the food we eat often comes from overseas. Almost 15 percent of foods consumed in the U.S. come from outside the country. That includes about half our fruit, 20 percent of our vegetables and 80 percent of our seafood. Fully 90 percent of the shrimp that hits American tables hails from abroad, primarily from Southeast Asia, Ecuador and Mexico.
Thousands of ingredients used in countless food products are imported from foreign lands; penetration from overseas is so vast and complex that a single product might contain ingredients from multiple countries, a fact you would never discern from labeling on the food itself.
The situation might sound exotic, but it puts us at risk. Technically, the U.S. asks foreign food producers to hew to the same standards as American counterparts. But in reality, no government-mandated system ensures that occurs. Some shrimp grown in Southeast Asian factory ponds, for instance, are doused with toxic antibiotics outlawed here, according to Michael Doyle, director of the University of Georgia’s Center for Food Safety.
When it comes to food grown at home, the FDA and the U.S. Department of Agriculture (USDA) have greater reach to find problems and the teeth to clamp down. Every food factory in the U.S. is supposed to undergo rigorous inspection. On the local level, when a restaurant fails to meet standards for food safety and cleanliness, local inspectors can shut it down.
But when food comes from abroad, it is only as safe as the laws of the producer-nation can guarantee. And many of the countries our food comes from are far less vigilant or consumer-oriented than the U.S. Once imported foods reach our shores, they enter the distribution chain with little fanfare and scrutiny; some argue they are barely vetted at all. Instead, by and large, problems come to light when Americans get sick.
Part of the problem is the lack of resources we ourselves direct to food from abroad: The FDA has a minuscule team of some 1,500 inspectors devoted to food imports, a workforce too small to screen more than a tiny fraction of the food that arrives at U.S. ports each year for microbial pathogens or other disease-causing contaminants.
“We have been a domestic agency operating in a globalized world,” says Charlotte Christin, a senior policy adviser at the FDA. But things are set to change.
The change-agent, optimists say, is the Food Safety Modernization Act of 2011. Regarded as the biggest update to the FDA since the agency’s founding, the act is intended to turn the agency from what it has traditionally been — a watchdog with exclusively domestic fangs — into what the public expects it to be: a proactive international tiger that vets all foods (as well as medicines) entering the U.S.
But it may not be good enough. A lack of funding and resources can still render the FDA somewhat helpless to work across borders to implement food safety plans as stringent as the ones we apply to domestic food products. “Ultimately, we’re going to have to collaborate with other countries to help them change their food safety culture,” says the University of Georgia’s Doyle, especially where food is produced under less than satisfactory sanitary practices.
Underwater Robots Patrol the Red Tide of Harmful Algal Blooms
Concentrations of algae in our oceans and lakes have long bloomed naturally, but climate change and fertilizer runoff from farms have exacerbated the situation in recent years. The outcome: algal blooms so massive that ecosystems turn into dead zones, resource-poor realms inhospitable to other life. The most dangerous of the blooms, called harmful algal blooms, or HABs, are often reddish in color, leading observers to call them red tides.
The dangers are as ominous as the name. Some of the algae, or phytoplankton, manufacture saxitoxin, a poison so devastating it is the underlying cause of paralytic shellfish poisoning, an often-lethal reaction to shellfish that are storing toxic algal cells. This January, two people in Malaysia died after eating cockles tainted with the stuff. Other phytoplankton produce domoic acid, a neurotoxin that kills people, birds and marine mammals snacking on contaminated fish and shellfish.
To head off the danger, the National Oceanic and Atmospheric Administration (NOAA) has recently begun monitoring the toxins with an underwater robot fleet. The bots, named BreveBusters, patrol off the Gulf Coast of Florida, where researchers have linked the fumes of Karenia brevis, a toxic phytoplankton, to respiratory problems in beachgoers. The bots use optical technology to monitor when Karenia species start to move in.
At the Georgia Institute of Technology, meanwhile, researchers are using special diatoms, another type of phytoplankton, to metabolize the toxins produced by Karenia brevis and reduce the toxicity of HABs. The fight against red tides may be taking place one algal and shellfish species at a time. Elsewhere in the Gulf of Mexico, researchers are testing ways to protect clams from contamination by treating them with the amino acid cysteine, which blocks toxins from binding to clam tissue.
Foodborne UTIs: Direct From the Birds
Antibiotics have been a powerful force since the discovery of penicillin in the late 1920s. But with massive overuse, bacteria have evolved to resist numerous antibiotics. When those treatment-resistant microbes infect humans, we are left with the specter of incurable disease.
One trend shows the problem in microcosm: a worrisome surge of antibiotic-resistant urinary tract infections, or UTIs. Considered common bacterial infections, UTIs are traditionally isolated events treated with amoxicillin, ampicillin and other antimicrobial drugs. But new resistant strains of E. coli have now been linked to outbreaks of foodborne UTIs, or FUTIs.
Added in low doses to chicken and turkey feed, antibiotics promote growth in poultry by helping them to maintain healthier digestive systems, or so the theory goes. But overuse has promoted the growth of stronger E. coli as well. By some estimates, more than 75 percent of poultry is contaminated with E. coli, much of it resistant to antibiotic drugs. Handling the bacteria-ridden food could spread E. coli to the urinary tract.
This could be the harbinger of a “perfect storm,” says Lance Price, director of the Translational Genomics Research Institute’s Center for Food Microbiology and Environmental Health, a nonprofit based in Arizona. He is working on a study to see whether E. coli strains found in grocery stores in a given area genetically match E. coli causing local UTIs. Confirmation would prove that UTIs are coming from the birds. “We see compelling evidence that some UTIs have foodborne origins,” he says.
The Trouble With Plastics
Sometimes you can’t win: Just when you stop littering the environment with throwaway water bottles and switch to reusable containers comes an uproar over bisphenol A (BPA), a chemical found in some can linings and hard plastics. A known endocrine disruptor, BPA has been linked to anxiety, obesity and prostate and breast cancers.
The panic over BPA follows prior assessment from the Swiss Official Food Control Authority, which held that food contamination from packaging could be a hundred times as high as contamination from chemicals found in pesticides or environmental pollutants.
To see whether BPA was guilty as charged, researchers from the Silent Spring Institute in Newton, Mass., studied 20 people who switched from canned and plastic-stored foods to fresh items for three days.
According to the study’s results, published in 2011 in Environmental Health Perspectives, the subjects’ BPA levels dropped by 66 percent. Several physiological indicators of another plastics ingredient, phthalates, dropped by more than 50 percent. When the test subjects went back to their normal diets, BPA levels shot back up. “It was a very clean demonstration that a majority of BPA exposure is from food packaging,” says lead author Ruthann Rudel.
Now that BPA has come under scrutiny, Rudel and others wonder what surprises other plastics and packaging may hold.
Honey's Sticky Mess
Bee-assisted pollination helps produce about 30 percent of our food, but bees have fallen on hard times, posing a serious threat to food security. According to the USDA, we’ve lost 3.5 million colonies to parasites, disease, genetics, poor nutrition and pesticide exposure since the late 1940s, when bee colonies were 5 million to 6 million strong.
A widespread and poorly understood cause of die-off is called colony collapse disorder (CCD), marked by unusually high bee losses (up to 90 percent per hive) in which worker bees vanish.
A single explanation for CCD has yet to emerge. Recent research indicates a link between CCD and the use of pesticides derived from nicotine that target insects’ nervous systems and could impair their homing instincts. In May, the European Union approved a two-year restriction on nicotine-derived pesticides; U.S. officials have yet to take similar action.
Regardless of what’s causing the collapse, bee products themselves have seen better days. Bacteria and trace amounts of heavy metals and PCBs, once used to manufacture electrical equipment, have also been found in honey. The same is true of antibiotics, which beekeepers use to protect hives against infections that are also suspected as a cause of the bees’ demise.
It’s no surprise that honey can pose health risks. One rare but natural danger is “mad honey poisoning,” caused by grayanotoxin, a poison found in the nectar of Rhododendron species most common in northeastern Turkey. Another risk comes from honey containing Clostridium botulinum spores, associated with paralytic disease.
While many of these trace pollutants and toxins are found at extremely low levels, researchers at the National Institutes of Health recommend paying close attention to the latest honey findings and the source of your sweetener.
Big Data for Outbreak Sleuths
When a Salmonella Montevideo outbreak swept across 44 states several years ago, sickening hundreds, investigators hit a wall. They ran patients through some 300 questions about their eating habits, asking them to recall all the food consumed over the course of weeks. Sleuths suspected salami but had no idea what brand to begin testing, much less recall.
The big break came only after investigators realized that many of the afflicted had shopped at a national warehouse grocery store chain. With the victims’ permission and the store’s cooperation, they quickly identified a particular brand of salami — more specifically, the red and black pepper coating it — as the common source. A recall was quickly instated.
Shopper cards proved their mettle in that crisis, recalls Ian Williams, chief of outbreak response and prevention at the CDC’s National Center for Emerging and Zoonotic Infectious Diseases. The cards helped again after a five-state Salmonella outbreak in 2011, when shopper data indicated many victims had purchased Turkish pine nuts — pointing food detectives to the infectious source. Without those data, “this stuff would have been on the shelves for weeks, or months, possibly even years,” Williams says.
Outbreak sleuths also tap big data through DNA analysis. Indeed, the current backbone of CDC foodborne-illness investigations is its PulseNet laboratory network, which stores the DNA fingerprints of half a million bacterial samples from food, humans and the environment. By comparing microbial fingerprints, investigators can track outbreaks. The network’s international arm collects data from almost 80 countries.
The newest strategy uses whole genome sequencing to identify not just bacterial species but the individual strain causing the disease; Listeria outbreaks have been among the first traced with this powerful technique. “More detailed information may make it possible to better understand where the bacteria came from — from what sort of animal, or from what part of the world,” explains Robert Tauxe, deputy director of foodborne, waterborne and environmental diseases at the CDC.
Consuming Fear: Add a Grain of Salt
We’ve come a long way since Upton Sinclair described making sausage from rancid meat in his 1906 novel The Jungle. Organic, factory farmed, genetically modified, high-fat, non-fat, refined, raw, vegetarian, gluten-free, local, imported — these are the food choices many of us now have the luxury of making every day. Less under our control is the legacy of environmental pollution and the unforeseen consequences of industry, including rice products containing trace levels of arsenic, antibiotic-resistant bacteria, mercury-laced fish and plastic containers leaching poorly understood toxins.
Increasingly sophisticated detection methods provide new insight into food risks and a better means of targeting contamination. But especially when it comes to low-dose exposure, it is often difficult to make a direct connection between evidence of harm from animal studies (the source of most data) and the implications for human health, says Ann Yaktine, a researcher at the Institute of Medicine who has authored several papers on trade-offs between nutrition and contamination. The result: an unsettling uncertainty.
Chemical and biological dangers in food are nothing new. And risky or not, we all still need to eat. The most cautious among us might eschew fish, avoid imports and cook food so relentlessly that no bacteria remain. But does doing so mean sacrificing important nutrients, flavor and culinary adventure?
In the absence of clear answers, the best solution may be an old-fashioned one: eat balanced, low-fat meals and avoid obvious pitfalls like unwashed produce and uncooked meat. Eating lean meats, in addition to being heart-healthy, lessens exposure to organic pollutants, which tend to accumulate in fatty tissues. A varied diet also reduces exposure to any single contaminant.
The CDC’s Robert Tauxe suggests keeping your refrigerator below 40 degrees, to prevent the growth of harmful bacteria, and avoiding cross-contamination when handling raw meat. A bit of perspective is important here. “Ninety-nine-point-nine percent of our meals are not a problem,” says Tauxe of pathogens. “The risk is not everywhere all of the time, but it is an important one.”
Harvard University risk analyst James Hewitt compares the food quandary to the climate change debate: When do we know enough to alter the way we act? “Some people will say we shouldn’t regulate until we are more certain,” he says. Others feel the “consequences of what we do now will persist into the future,” and want to act.
[This article originally appeared in print as "Food at Risk."]