Owls are all the rage: they’re making a comeback on greeting cards, jewelry, and chatchkes galore. California vintners and other growers put up owl boxes, realizing that the big birds bring big pest control benefits—bye-bye gophers. The city of Berkeley even named the barn owl as city bird recently, to honor its ghostly denizens. If you are an owl-ophile, Hans Peeters’ new book will only fuel your obsession.

Fortunately for Westerners, all of the nineteen North American owl species can be found in the West, and every county in California has at least two or three species of owls. Peeters starts with the basics of owl phylogeny (a few surprises here: owls are more closely related to nighthawks than to raptors), and moves through owl anatomy, senses, and vocalizations: owls not only hoot, they “scream, screech, moan, purr, chuckle, bleat, yowl, cackle, hiss, and tick like a grandfather clock.” Chapters on predators of owls contain more surprises: snakes, foxes, raccoons, coyotes, other owls and raptors, bobcats, and (sadly) the occasional human.

A chapter is devoted to human attitudes toward owls, both past and present. Despite the lasting “wise old owl” stereotype, humans have often been ambiguous or negative about these creatures of the night. The Greeks thought of owls as both evil omens and portents of victory while many Native Americans had elaborate superstitions and rituals involving owls. Owls are no longer persecuted as they once were; however, in some Mediterranean countries, they continue to be shot from the sky, as are raptors, and in China, owl soup is a delicacy.

Peeters is not only an engaging and captivating writer; he also is an artist, and the book includes color plates of each species, including a rather comical page of chubby owl nestlings. The book also has many gorgeous and unusual photos of owls perched, nesting, and flying, and of their habitats.

Importantly, Peeters includes a chapter on threats to owls—primarily human destruction of habitat and other human-caused problems like car strikes, secondary poisoning from rodenticides, fence entanglements, or (in the case of burrowing owls) nests being plowed under for parking lots. Even birders—who play owl call recordings to lure owls into range so they can see them—can cause great damage by harassing the owls, sometimes to the point where they fail to breed. Peeters describes the conservation status of each species of owl: six of the nineteen included in the book are endangered, threatened, or species of concern. Species accounts are given for each, detailing their ranges, distribution, and habitat and their daily activities and feeding patterns, along with tips on identification. In some urban areas, barn owls in particular are making a comeback, and when given even a tiny piece of open field, burrowing owls will try to make do (although it’s often not enough). But as Peeters describes, owls need all kinds of habitats, from forests to grasslands to oak woodlands. In a modest strip of oak riparian woodland along a tiny seasonal stream, he found eight barn owls, a pair of great horned owls, and a pair of western screech owls. If we want to keep hearing their nighttime hoots (or bloodcurdling screams), we need to leave them some space.

—Lisa Owens Viani

Every day, the media bombards us with news about health, food safety, emerging diseases, and cures in the offing. Since Merck’s Vioxx scandal in 2004, a clutch of drug safety problems has come to light; most recently, GlaxoSmithKline’s Aventis, for patients with Type II diabetes, has been found to increase risk of heart failure. Elsewhere we hear that alcohol, obesity, or even under-wire bras increase the risk of breast cancer, and we are asked to vote on euthanasia and genetically modified crops.

Should you go out of your way to feed your child genetically unmodified food? How can we predict the long-term effects of new technologies on the environment, and who is responsible for those predictions? For those who want to develop an educated opinion and a context in which to understand the increasing role of biochemistry in our lives, Greif and Merz’s book offers an excellent overview.

A collection of loosely related essays explores many topics, including boundaries of research, intellectual property, reproductive technologies, the role of the FDA in drug safety, forensic testing and the legal system, cosmetic surgery, the public health response to anthrax, media coverage of science, scientific misconduct, public misunderstandings, environmental toxins, organ transplants, and the right to die. The scare over silicone breast implants is discussed, the debate over genetically modified organisms is critiqued, and Terri Schiavo’s story is retold.

Although the book overlaps a class I took a class at UC Berkeley a few years ago, I learned something new in every chapter, such as legal precedents, historical background, and details I hadn’t gleaned from the news. Each section gives legal and biological background in easily accessible, functional language and includes references. If your interest is truly piqued by a debate, Greif and Merz provide an annotated list of reading suggestions.

—Vivian Choi

This hefty tome ought to become a new bible for aspiring landscape designers, botanists, and obsessive amateurs compelled to learn the identity of every tree they see in California whether native or introduced. Author Charles R. Hatch does an exuberantly thorough job of identification; he employs over a thousand of his own excellent photographs. Each tree listing includes a photograph of a medium- sized specimen (the size most likely to be encountered), close-ups of the tree’s bark and its foliage (flowers and fruit included when noticeable), and for deciduous trees, a photo of the bare tree. Descriptions are precise and technical. Hatch’s taxonomy chapter is the best explication of plant identification and terminology I’ve encountered, with one page of text and over thirty pages of illustrations (mostly leaf photographs).

A detailed chapter on trees in urban landscape design positions the book as a must-have textbook in the field, while the overview of California topography, geology, climate, and plant communities will make it useful for students of California ecosystems. Identification keys can be used by any reader strong enough to carry the book around outdoors (or smart enough to photocopy the relevant pages).

—Gina Covina

Conducting biodefense and nuclear weapons research in a crowded suburban setting has embroiled the lab in decades of controversies, with the same question at the bottom: What are the health risks to Bay Area residents and to the environment? After all, the lab investigates dangerous pathogens and detonates toxic substances, and now it’s being considered to research even deadlier pathogens in a Biosafety Level 4 lab. Moreover, it’s applied for a permit to increase its open-air explosives testing by a factor of eight.

The Centers for Disease Control (CDC) defines four Biosafety Levels based on the lethality of the pathogen, its infectious potential, and what types of experiments are performed upon it. The CDC has developed a protocol for each level, from wearing protective equipment at BSL1 to complete isolation of the facility from its surroundings at BSL4. BSL3 precautions are taken for work done on potentially lethal organisms that can be transmitted through the air. Included are anthrax and the bacteria that cause tuberculosis.

Though construction of a BSL3 facility at LLNL was completed in December 2005, the facility has never been used. Livermore-based activist group Tri-Valley CAREs (Communities Against a Radioactive Environment) began contesting the facility in 2002, when the Department of Energy proposed siting it at LLNL. In 2005, the group sought an injunction to prevent the facility from opening, and it has been caught up in litigation ever since. Despite this, LLNL is on the short list for a BSL4 facility funded by the Department of Homeland Security.

Tri-Valley CAREs staff attorney Loulena Miles has concerns about the level 3 facility beyond its possible health risk to Bay Area residents. She worries that conducting advanced biodefense research at a site that also engages in classified nuclear weapons research invites suspicion, since bioweapons research and biodefense research look very similar. “LLNL is not a neutral agency,” she says. “It looks bad because the US is putting an advanced biodefense lab together with a super secret nuclear research lab.”

Moreover, the Bush administration refused to sign the international Verification Protocol in 2001. The protocol would give an international oversight group the authority to enforce the Biological Weapons Convention. LLNL itself lacks a transparent oversight committee that would ensure that biodefense research doesn’t cross the line into bioweapons development. Miles believes the research planned for the BSL3 facility is more appropriate for a civilian lab, and that much of the research LLNL scientists want to pursue could be conducted at a BSL2 level, such as the work that went into developing BioWatch.

The lab’s BioWatch system is used in 30 cities across the nation to provide authorities with early warnings of a bioterrorist attack. The system, which uses air filters, tests for the presence of pathogens; each pathogen contains stretches of unique DNA sequences that can be used to identify them. Other research deals with quickly differentiating between different strains of a pathogen, such as anthrax; determining the ability of certain microorganisms to survive under a variety of environmental conditions; and developing a detection system similar to BioWatch that would alert people to the presence of mosquito-borne diseases.

Miles says there are a number of ways that pathogens could be accidentally released. To prevent contamination from the lab into the environment, High Efficiency Particulate Air filters, more commonly called HEPA filters, are used. Miles explains, “HEPA filters are prone to fail if they’re damaged by heat, smoke, explosions, or fire. LLNL seems to think that the HEPA filters will just work.” Lab workers can make human errors. A scientist exposed to a pathogen could carry it into his community, and the lab has a spotty history of minor incidents involving mislabeled or inappropriately stored materials. Then there’s the earthquake danger: LLNL is close to the Las Positas and Greenville fault lines. And it seems a tempting target for a terrorist attack.

Lab officials respond that BSL3 labs have operated safely with HEPA filters for decades—and in crowded areas. A BSL4 lab is located in Atlanta. Thankfully, there have been no major incidents or epidemics of lab-acquired infections spreading to a surrounding community. LLNL acknowledges that it has a history of accidents but says that none have had a significant impact on the community or the environment.

And lab officials point out that researchers at LLNL have been using strains of plague and anthrax since 2000. According to CDC guidelines, anthrax in clinical materials or in diagnostic quantities can be used at BSL2 labs. Guidelines for plague are similar. LLNL officials believe the new facility is earthquake-secure and that the risk of a terrorist attack is not significant. Plus, if there were an explosion due to a terrorist attack or a lab accident, the heat generated would kill most of the microorganisms around, says LLNL.

While the events leading to a breach in the BSL3 facility’s containment seem unlikely, a release could expose millions of people to dangerous microorganisms. The Environmental Impact Assessment defines a 50-mile radius around LLNL as the affected zone, and about seven million people live in that area. Nuclear physicist Matthew McKinzie developed computer simulations that show anthrax spores released into the air from LLNL spreading to San Francisco or further depending on weather conditions. Anthrax is one of the organisms that would be used in the facility, and its spores survive very well under extreme conditions.

Miles points out that research at the facility would be concerned mostly with pathogens that are “the most pernicious, the ones historically associated with weapons.” For obvious reasons, these tend to be hardier and more infectious than your run-of-the-mill germs. If an accident did take place, the results could be catastrophic.

Hold Your Breath

LLNL is a top contender for the Department of Homeland Security’s National Bio and Agro-defense Laboratory, a BSL4 facility, which would be housed at the lab’s Site 300, an explosives testing area near Tracy. According to the CDC, BSL4 precautions are used to work with “dangerous and exotic agents that pose a high individual risk of life-threatening disease, which may be transmitted through the aerosol route and for which there is no available vaccine or therapy.” In other words, if you breathe them in, you’re in deep trouble. The primary purpose of the facility would be to conduct research on diseases that affect agriculture and livestock, such as foot-and-mouth disease. However, it could also handle the most dangerous pathogens, including Ebola.

A number of groups involved in California agriculture, such as the Farm Bureau, the California Veterinary Association, and the Poultry Federation and Cattlemen’s Association, as well as Governor Arnold Schwarzenegger, welcome the lab. Siting the lab in the Bay Area gives researchers access to scientists and prestigious research institutes such as UC Berkeley, Stanford, UC Davis, Lawrence Berkeley Lab, and others that would foster a rich environment for scientific inquiry. Proponents argue that since California’s agricultural products feed much of the nation, plant and animal diseases here are a national food security risk and that the lab would provide a valuable resource to the state’s agriculture.

But others, including Tracy city councilmembers and Tri-Valley CAREs, oppose the lab. The planned BSL4 facility is much bigger than the lab’s BSL3 facility—according to Miles, “five Wal-Marts could fit inside it”—in order to provide space to house and experiment on large animals and birds. If these animals (mostly livestock) were to escape, they could carry diseases to animals and humans in surrounding areas. Since Tracy stands at the gateway to the Central Valley, the goal of protecting California’s agriculture could instead wreak havoc. Critics argue that siting the BSL4 lab in a place where there is a geographic barrier to agriculture makes more sense. Tri-Valley CAREs is considering bringing another lawsuit to prevent construction if the Department of Homeland Security chooses to house the Bio and Agro-defense Lab at Site 300.

Says UCSF assistant researcher Dr. Judith Flanagan, “In my experience of 20 years spent as a researcher, I am keenly aware that no matter what safety procedures are enforced accidents will happen.” Flanagan points to incidents discovered by investigative journalists, such as those involving a lab worker testing positive for anthrax and a package containing West Nile exploding in the Columbus, Ohio airport. She points out that accidents that occur under a culture of secrecy are likely not to be reported or admitted.

“Even when mistakes are not made,” she says, “unforeseen consequences of genetic modification of pathogenic organisms can produce devastating new super-bugs. For example, Australian researchers recently engineered a mouse disease to make the animals sterile. They inserted a new gene into the mouse pox virus as part of the genetic engineering process to create the bug that would make the mice sterile. But the extra gene did more than that; it transformed the mouse pox into a super strain that killed almost every mouse it came across. Now that’s a frightening bio-weapon if you’re a mouse—but mouse pox is very close to its human equivalent, smallpox.”

Bigger Booms

But the majority of LLNL’s research continues to be nuclear, some of which requires explosives testing. Currently, most of this testing is done in an enclosed facility at Site 300. Now LLNL is applying for a permit to increase the amount of open-air detonation of depleted uranium (DU) at Site 300 by a factor of eight, from 1,000 to 8,000 pounds per year.

DU is the uranium remaining after enriched uranium is formed from natural uranium. It can also come from reprocessing spent reactor fuel. Since most of the radioactive uranium has been removed, it is only weakly radioactive, which means it can be stored as low-level nuclear waste. Because it’s more expensive to store than to use, scientists have developed uses for DU. The military uses it for ammunition and in armor plating because of its high density. Non-military uses include counterweights in aircraft, dental porcelain, and as shields during medical imaging.

It becomes much more dangerous when detonated. When temperatures reach 3000 ¡ F, uranium catches fire, burns, and aerosolizes. Early studies assumed that DU particles would quickly settle out of the air so that people more than a few kilometers away would be unaffected. But nine days after the US began its 2003 “shock and awe” campaign in Iraq, DU particles were found in an air filter in England.

DU damages the reproductive system, causes birth defects, mutates DNA, and acts as a neurotoxin. Some suspect it of causing Gulf War Syndrome—immune system disorders, chronic fatigue, headaches, memory problems, loss of balance, and muscle and joint pain—as well as some cancers, though only circumstantial evidence exists. The US used DU in ammunition during the first Gulf War. Data from the Basra hospital and university show a 426 percent increase in cancers and a 600 percent increase in birth defects after the war, but other pollutants, such as those released from burning oil wells, could cause this spike as well.

It is unclear whether Livermore and Tracy residents are exposed to levels of DU sufficient to cause health problems, and it would be difficult to prove a causal relationship between DU exposure and health problems. Miles says she’s talked to a lot of residents who feel they have health problems because of the (DU) testing. Data showing high levels of uranium present in a child’s hair was presented at a Tracy city council meeting; the parents believe that uranium exposure is responsible for their child’s autism.

How much and how necessary is the risk? Very few of the seven million or more who might be at risk have participated in debate or even know about it. As with the DU drift, conventional wisdom and assurances can turn out to be best-case scenarios or unrealistic assessments. The political question is a matter of public policy, as lab sitings should be. A more thorough public process and transparent oversight of biodefense research would go a long way towards calming people’s fears. But ultimately we must decide what kind of research our tax dollars should fund.

Wrong. If you think that you’re not eating MSG, take a closer look. According to former food process engineer and food scientist Carol Hoerlein and her colleagues, MSG or free glutamate, MSG’s active component, is found in an astonishing array of today’s processed and restaurant food—and even on produce.

Hoerlein’s group has compiled independent research on its nonprofit web site, MSGTruth.org. A partial list of affected foods includes some McDonald’s products, most KFC products, Hamburger Helper Microwave Singles, Doritos, Pringles, Boar’s Head cold cuts, Progresso Soups, Lipton Noodles and Sauce, Lipton instant soup mix, almost all Kraft products, all Knorr products, Cup-a-Soup, Cup-o-Noodles, soy sauce, and Worcestershire sauce (for more, see www.msgtruth.org). In addition, the EPA has approved the use of Auxigro, which contains free glutamate, as a fertilizer, so produce sprayed with Auxigro also may contain the chemical. On average, a person in an industrialized country consumes 0.3-1.0 grams of synthetic MSG a day.

The FDA classified MSG into the GRAS category (generally recognized as safe) in 1958 and has reaffirmed that position in subsequent evaluations. MSG need only be listed on the product label when synthetic MSG is added. When other ingredients containing up to 20 percent MSG are added to a product, the FDA does not require MSG to be listed. Such ingredients that may contain MSG include natural flavors, protein hydrolates, and soy protein isolate. Also, MSG produced as a result of the processing of ingredients does not need to be listed. Adding to the confusion, these products often claim to have “No MSG” or “No added MSG.”

Says Hoerlein: “I think it should be labeled properly. [The FDA] finally labeled transfats so you know what you’re eating. What the food companies are doing now is hiding it. It’s in the best interest of the food industry to say what they’re using, because a lot of people are avoiding things they don’t need to.”

Though synthetic MSG has been in use for almost a century, the question of whether it has toxic effects remains a topic of heavy debate. The glutamate lobby (www.msgfacts.com/index.html) cites studies showing MSG is completely safe, while its opponents charge that MSG (and other substances such as aspartame) are linked to the worldwide spread of obesity, exacerbation of asthma, and brain damage.

First, what is MSG? The simplest answer is that MSG is a salt composed of a sodium atom and a molecule of glutamate, a nonessential amino acid. In solid form, it is a white crystalline powder, but once it has dissolved into a liquid, its two components separate. Free glutamate is the agent that gives MSG its flavoring properties as well as its possible toxic effects.

There are many sources of free glutamate; it is released when protein is digested and occurs naturally in some foods, including breast milk, parmesan cheese, and tomatoes. Free glutamate entering the body through the gastrointestinal tract is identical and is processed identically. Glutamate is the most common amino acid in animal proteins and is a precursor for the production of other amino acids and glutathione, a compound that protects cells in the gastrointestinal tract from damage due to dietary toxins. Also, glutamate serves as an energy source for some types of muscle, including cardiac muscle.

The largest and most rigorous toxicity study involved researchers at Harvard University, Northwestern University, and UCLA. They took 130 subjects who believed that they were MSG-sensitive and exposed them to up to 5 grams of MSG a day with or without food. Twenty-four people did not complete the study, but of those who did, only two people had reactions. The symptoms these two experienced were not present when MSG was given with food. Researchers concluded that there were no reproducible responses to MSG, and that there was no evidence indicating that MSG has a toxic effect when used at levels reasonable for a food additive. In another study, human adults, infants, and premature babies were given up to 150 mg MSG per kg of body weight. Only a slight rise in plasma glutamate concentrations was produced, indicating that people of all ages can metabolize MSG efficiently.

Additional studies have shown that glutamate does not readily pass the placental barrier between mother and fetus. Pregnant rhesus monkeys were fed enough MSG to cause a ten-fold rise of glutamate in their blood levels, but little or no increase in glutamate concentration was observed in fetal blood level. Mice fed with diets containing four percent free glutamate for up to two years and including a reproductive phase did not suffer any ill effects. A two-year study in dogs fed with ten percent glutamate did not find any change in weight gain, organ weights, or general behavior.

However, large doses of MSG in newborns reproducibly cause neuronal damage in the hypothalamus of the brain. The hypothalamus is more susceptible to toxins because the blood-brain barrier surrounding it is not effective, particularly in the young. Appetite, thirst, a number of endocrine pathways, and muscle contraction are all regulated by the hypothalamus. The dose required to produce this damage is, fortunately, quite high. In very young mice, the most sensitive species, 500 mg MSG per kg body weight by average is necessary to produce neuronal damage. By contrast, the largest palatable dose for people is about 60 mg per kg body weight. Higher doses cause nausea.

These studies portray MSG as a relatively harmless flavor enhancer, but some nutritionists insist that even minute amounts of MSG can cause severe toxic reactions and cite studies conflicting with the Harvard research. A group called Truth in Labeling claims that pro-MSG studies are funded by industry advocates and that while naturally derived free glutamate has no toxic effects, synthetically produced glutamate contains toxic impurities. More alarmingly, some connect MSG, the spread of obesity, and the increase in incidence of neurological disorders.

Clinical nutritionist Carol Simontacchi writes that MSG has subtle neurological effects, including dyslexia or frequent bursts of uncontrollable anger and that, “There is evidence that MSG may be concentrated on the fetal side of the placenta so that the child receives a higher dose,” which can cause abnormal brain development. In one study, mice injected with MSG have lower free glutathione levels. Glutathione protects against mercury poisoning, a suspected cause of autism. Also, glutamate blockers are used to treat manic depression, depression, and seizures. While most evidence against MSG remains circumstantial, it is still thought-provoking.

Additional studies link glutamate to obesity and type II diabetes. According to MSGTruth.org, higher levels of glutamate in the blood can cause an increase in insulin levels that triggers hunger, and continued exposure to high insulin levels leads to insulin resistance and type II diabetes. Injection of MSG into lab animals is used to cause obesity, and these animals become resistant to leptin, a hormone secreted by fat tissue to suppress hunger. More evidence linking obesity and MSG comes from a recent study done in Germany. Young rats fed five grams of MSG a day had increased appetite, body fat percentage, and insulin resistance. However, experimental groups were small, consisting of only six to nine rats each, and the doses of MSG used were very high given that a rat weighs less than a kilogram.

Given MSG’s prevalence in our food and the conflicting studies, how does one decide what to eat or to feed children? In the end, it’s an individual choice, but that choice would be aided by proper labeling. “If you just listed on the label how much MSG is in the final product then that would help, because people are really getting fat,” says Hoerlein. “Processed foods haven’t been a blessing for humanity. We should go back to whole foods, the way we used to eat.”

In 2004, California’s Public Energy Commission linked with institutions such as Scripps, UC Berkeley, UC Davis, and Lawrence Berkeley Laboratory, to form the state Climate Change Center, charged with investigating what will happen as the temperature rises over the next century. In a new report, “Our Changing Climate: Assessing the Risks to California,” scientists speculate on the impacts of three different emissions scenarios. In a best-case low emissions scenario, we would shift immediately to more efficient technologies to lower our use of fossil fuels. But even in this version, atmospheric concentration of carbon dioxide doubles by 2100. Climate models predict a 3-5.5¡F temperature increase as a result. In the medium emissions scenario, emissions grow over the next century but as other energies come online, the rate slows. In this version, atmospheric carbon dioxide triples by 2100, with a predicted 5.5 to 8¡F increase in temperature. If we persist in denial and continue with “business as usual,” carbon dioxide in the atmosphere more than triples, resulting in temperatures 8-10¡F higher.

The results were less conclusive about rainfall, but the models suggest that while the amount might remain the same, the location and form of precipitation could change. Sea level will rise due to melting ice and thermal expansion of water. Between 1900 and 2003, sea level at the Golden Gate Bridge rose 8.15 inches, and that level is predicted to increase 22 to 35 more inches over the next hundred years. And yes, expect more severe weather, including droughts, heat waves, and massive storms. Big surprise—the forecasted rise in state population from 37 million to 55 million won’t help our plight.

Dr. Michael Hanemann, head of the California Climate Change Center at UC Berkeley, says that in terms of the state’s water resources, “the crucial thing is timing and location.” Hanemann explains that 80 percent of precipitation falls between October and March, but 75 percent of that is used between April and September, primarily for agricultural irrigation. The state’s snow pack helps cope with the timing difference by acting as a natural reservoir.

The current system relies heavily on the Sierra Nevada snow pack to supply water during spring and summer months. Significant snow packs also form in the Cascades north of the Central Valley. Snow packs form a third of California’s water storage, and melt accounts for more than a third of the state’s usable surface water supply. But the snow pack could diminish by as much as 70 to 90 percent by the end of the century due to changes in precipitation and temperature. Precipitation will fall as rain rather than snow when temperatures increase, and what snow there is could melt earlier. Unless another form of storage is developed, less water will be available during the summer.

More water can be stored in existing reservoirs, but current policy is to leave reservoirs partially empty to provide space for snow melt and protect against winter and spring flooding. More reservoirs could be built but at prohibitively high economic and environmental costs.

Meanwhile, rising sea levels threaten California’s drinking water quality. Higher sea levels increase the chances of sea water intrusion into coastal groundwater basins. In an average year, 30 percent of urban and agricultural water needs are met with groundwater. In drought years, this figure increases to 40 percent. And as more people move to the state, the demands on groundwater will grow.

Freshwater injections into coastal aquifers to prevent ocean water moving farther inland can act as hydraulic barriers, and California Department of Water Resources officials can develop policies that restrict well construction and other activities that use groundwater. Seawalls could protect the coast from rising sea levels. These measures also come at a cost and are often unpopular, so they’re less likely to be championed by politicians and policymakers.

Another threat to California’s water is the likelihood of flooding in the Sacramento-San Joaquin Valley. The State Water Project relies heavily on water from the Delta to supply two-thirds of California’s population and 600,000 acres of farmland. Most of the Delta is at or below sea level, and the bottoms of all Delta waterways are below sea level. The Delta is protected from breaching by 1,100 miles of levees, some already on the verge of collapse. As the sea level rises, levees are likely to fail. Many Californians get their drinking water from the Delta, which will also be subject to seawater intrusion if levees fail. Salinity could increase to unacceptable levels, taking weeks or even months to return to normal.

Not only does sea level rise threaten water quality, all coastal areas will face higher risks of flooding. Rising sea levels puts more pressure on levees and seawalls while more severe storms will damage them further. Areas most at risk include Santa Cruz and the Delta. The Climate Change Center predicts that billions of dollars will be spent for flood control and to repair damage.

Along with rising seas and changing rainfall patterns, our state is likely to get hotter. Assuming that all else remains constant, the temperature increase of 5.5 to 8¡F predicted by the medium emissions scenario will lead to a 3-6 percent increase in energy consumption: hot people turn on air conditioners. California spent about $26 billion on electricity in 2003. If the cost remains constant, expenditures on electricity could increase by $780 million to $1.56 billion. However, because 15 percent of state-generated electricity comes from hydropower generated from the snowmelt, electricity will probably become more expensive. Increased development in California’s interior will also increase energy use, so these estimates are extremely conservative.

A hotter climate will also affect the state’s agricultural bonanza. California produces over half the fruits, nuts, and vegetables in the nation. As of this June, 374,600 people were employed as farm workers. When you count people processing and selling food, the number of Californians employed in agriculture is considerably higher. In 2003, the value of the crops produced totaled almost $30 billion. Most of this production occurs in the Central Valley, where hotter weather will make already bad working conditions less tolerable.

Warming increases the length of the growing season. A longer growing season can increase the quantity of some produce, such as wine grapes. But warmer temperatures will decrease quality. For example, if temperatures rise by 6¡F, grapes will have higher sugar content and less acidity, making them unsuitable for winemaking. Warmer temperatures during the growing season will also increase fruit development rates. Fruit will ripen at a smaller size.

And change in timing of the growing season affects plant pollination. An early spring could throw off the timing between plants flowering and the emergence of their pollinators, decreasing the chances that flowers will become fruit. Pollen itself is extremely sensitive to warm temperatures, so earlier, warmer springs will result in lower pollen viability. As if all this isn’t enough, consider pests. Higher temperatures and growth seasons mean that pests and weeds multiply faster—and they can expand their range. For example, pink bollworms are a problem for cotton farmers in the south, but winter frosts in the north kill them off. An increase of 3 to 4.5¡F in winter temperatures would allow the pink bollworm’s range to expand northward.

Warmer temperatures during the winter will also affect fruit yield. Fruit trees need from 200 to 1,200 hours of winter chill during which temperatures are below 45¡F in order to flower, but climate models predict that there will not be sufficient winter chill by 2100 for many fruits.

Finally, warmer temperatures promote the release of volatile hydrocarbons from plants. These compounds react with nitrous oxides in the atmosphere to produce ozone that is toxic to plants.

Agriculture will also make increasing demands of California’s water resources. Higher temperatures mean that plants need more water to sustain themselves, but farmers have less storage than urban users so agriculture will be more heavily affected by shortages. The predicted increase in intensity and frequency of severe weather events adds even more complexity to the situation. In an average year, agriculture will be able to cope with global warming, but Hanemann says that in the worst cases, which could be a third of the time, there may not be enough water to go around. The number of dry years is expected to double.

Models predict not only an increase in average temperature, but an increased duration and frequency of heat waves, which will in turn increase air pollution. California already has the poorest air quality in the nation—and it will probably worsen because high temperatures promote the formation of air pollutants. If temperatures rise from 5.5 to 80 F, the number of days with weather conducive to ozone formation in the San Joaquin Valley will increase by 75 percent. Also, scientists predict that large wildfires, which release fine particulates and increase air pollution, could be up to 55 percent more frequent due to increased temperature. Air pollution exacerbates a wide variety of health problems, including asthma and other acute respiratory and cardiovascular diseases.

In addition to worsening preexisting health conditions, high temperatures increase the risk of death from dehydration, heat stroke, heart attack, stroke, and respiratory distress. By 2050, heat-related mortality in urban centers, such as Sacramento, could double or triple. Most affected will be the elderly, young, ill, and poor.

With these scary scenarios lurking just around the corner, the next few years will make a critical difference in just how dire things will be. Hanemann says California has the resources to cope with global warming, but we need to act now. We need to start preparing because some consequences are now inevitable. “There will be effects early in the century that require action now,” Hanemann says. “We need to start actively planning for adaptation to water supply problems and increased heat waves. We need to plan because we’ll experience these things in the next decade or so.”

Hanemann believes the state needs to participate in the international efforts to reduce heat-trapping emissions. The point of the impact studies performed by the California Climate Change Center is to illustrate that reducing emissions is both significant and doable. “Comparing impacts associated with business-as-usual and preventing a more than doubling of carbon dioxide in the atmosphere sheds light on why it’s important to moderate growth and emissions,” he says.

Consider that California is the fourth largest economy in the world and the twelfth highest emitter of greenhouse gases. We have the power to change global emissions standards and affect not only our own future but also that of those Greenlanders and penguins—in fact, the future of the earth.

Conventional wisdom blames the docs for decades of prescribing antibiotics too often and too quickly. But it turns out that excessive reliance on the prescription pad may not be not the only culprit behind the rise in antibiotic resistance. Some scientists believe that resistant bacteria arise when livestock are treated with antibiotics and that this resistance can be transferred to bacteria that cause human illness.

How can this happen? Consider the following chain of events: an E. coli bacteria is living in the gut of a cow. This cow is regularly given antibiotics, and so to survive, the E. coli contains a gene to help it resist the antibiotic. When this cow is slaughtered, the E. coli, perhaps through sloppy handling, makes its way from the gut to ground meat that is sold in a supermarket. Mrs. Smith buys this meat and makes a hamburger. Smith gets a phone call midway through meal prep and doesn’t wash her hands thoroughly, and the E. coli manages to stay on her skin. Eventually it meets a staph bacteria and transfers its antibiotic resistance. Smith now has antibiotic-resistant staph bacteria. Staph are capable of causing toxic shock syndrome and various types of skin infection, and treatment usually includes antibiotics.

The Union of Concerned Scientists estimates that every year 24.6 million pounds of antibiotics are used for non-therapeutic purposes in pigs, poultry, and cattle. When humans ingest the flesh of these animals, they may also be exposing themselves to the genes of antibiotic-resistant bacteria. Only 3 million pounds of antibiotics are used in human medicine each year. Put another way, over 70 percent of antibiotics produced each year are used for animal husbandry.

Antibiotic use in livestock falls into three categories: therapy, prevention, and growth promotion. If an animal exhibits symptoms of an infection, it is given antibiotics as therapy, but it also may be dosed preventatively to ward off infection from exposure to sick animals or unhealthy housing conditions. Low, sub-therapeutic levels of antibiotics are also administered to promote growth. Why antibiotics promote growth is unclear, but some speculate that it suppresses disease, so the animal does not expend as much energy on maintaining its immune system. Low doses may also increase the efficiency of digestion and metabolism through manipulation of the microbial life found in the animal’s gut.

Resistance develops through a process of selection. Ideally, a dose kills off all target bacteria. But if the dose is not sufficiently high, some of the bacterial population remains. These survivors are more resistant to antibiotics—and it’s possible that resistance developed to one class of antibiotics may increase resistance to others. Six classes of antibiotics used in livestock are also used to treat people. Since most livestock receive sub-therapeutic doses of antibiotics as growth promoters and preventives over extended periods of time, antibiotic-resistant bacteria can easily develop in livestock—bacteria resistant to the same drugs used to control infection and disease in people.

Livestock excrete bacteria as well as antibiotics in their waste, which is stored in large lagoons. From these lagoons, antibiotics and resistant bacteria can make their way into the environment. Antibiotic-resistant bacteria have been isolated from groundwater and soil near animal waste lagoons. Often waste is used as fertilizer on crops, spreading resistance farther. Bacteria in the soil can pick up resistance from any resistant bacteria in the waste, and the presence of antibiotics in the soil continues the process of killing off less resistant bacteria while favoring the more resistant strains. In short, use of antibiotics in livestock has led to the formation of reservoirs of resistance both in the livestock themselves and in the surrounding environment.

Resistance can pass not only from mother to daughter cells but also between cells. Genes for antibiotic resistance usually reside on plasmids, small circular pieces of DNA separate from the genome, or on transposons, small DNA elements that can cut themselves out of the genome and paste themselves back in at a different location. Some transposons are also able to copy themselves to insert elsewhere in the genome. Resistance genes can be swapped between different bacteria, meaning resistance genes may eventually find their way from the reservoir in livestock to human bacteria. These may be beneficial bacteria that are part of the normal ecosystem in the gut, but they can become their own reservoir of resistance genes in people.

Eventually, a resistance gene may link up with pathogenic bacteria. Initial treatment of the sick individual is likely to be less effective because the doctor is unaware of the resistance. Higher, perhaps more toxic, dosages of antibiotics must be prescribed, with fewer antibiotics to choose from. Bacteria with resistance genes may also be more virulent.

The solution is simple—stop using antibiotics. Resistant bacteria have more genes and must spend more time and energy copying and repairing DNA before dividing. In the absence of antibiotics, the resistance gene is no longer needed, and the extra energy used to maintain the DNA that codes for resistance outweighs the benefit. Bacteria with such genes reproduce more slowly, so the number of antibiotic-resistant bacteria will eventually decline.

Simple in theory does not mean simple in practice: consider Denmark. By 1999, through a combination of voluntary and regulatory measures, Denmark’s broiler chicken and swine industries had stopped using antibiotics as growth promoters. To compensate, many Danish livestock producers improved sanitation and offered roomier housing. They also used alternative feed additives such as amino acids to mimic the growth-promoting effect of antibiotics. Despite these measures, more feed and time were required to raise animals to slaughter weight. Farmers also increased their use of therapeutic antibiotics. The number of antibiotic-resistant bacteria in the environment surrounding the farms has decreased significantly although there has been no clear impact on human health. Granted, Denmark did not have many problems with antibiotic resistance in human illnesses to begin with. Controversy continues over whether the growth promoter ban is beneficial.

How frequently does this chain of events occur? Is it worth it to discontinue use of antibiotics in livestock?

Compelling evidence suggests that antibiotic resistance in people originated from livestock. The impacts of antibiotic-resistant Salmonella and Campylobacter are well documented. Salmonella and Campylobacter are food-borne pathogens with extremely low rates of person-to-person transmission, so resistance found in human infections can be attributed to the reservoir of resistance genes originating from livestock. For Salmonella, there are many cases dating back to 1984 linking resistant bacteria in human infections to farms, and there has been an increasing frequency of such reports. In addition, studies have linked antibiotic resistance to greater virulence. Infection with antibiotic-resistant Campylobacter is associated with increased length of illness and greater risk of death. A Danish study reports that antibiotic-resistant Salmonella is associated with a tripling of the risk of death. While this is worrying, Salmonella and Campylobacter are for the most part foodborne, and illness can be prevented through thorough cooking and adherence to sanitary measures.

In most cases, the effects of resistant bacteria are not so obvious. Much of the evidence for other bacteria is circumstantial. Studies have found that an increase in levels of antibiotic-resistant bacteria in livestock and people follows introduction of that antibiotic into livestock. For example, a class of antibiotics called fluoroquinolones was approved for human use in the US in 1986 and for animal use in 1995. There were no reports of fluoroquinolone-resistance in foodborne Campylobacter until 1995. As another example, only countries that use avoparcin in livestock have cases of a urinary tract infection in humans that is difficult to treat with vancomycin, an antibiotic very similar to avoparcin. Vancomycin resistance is especially disturbing because it is a drug of last resort. After the EU banned the use of avoparcin, levels of vancomycin-resistant bacteria in meat products, livestock, and people decreased.

In a 1976 study conducted by Dr. Stuart Levy, author of The Antibiotic Paradox, chickens on a farm were divided into two groups, one of which received an antibiotic in their feed. After two weeks, 90 percent of the antibiotic-receiving chickens excreted resistant bacteria. Moreover, after twelve weeks, multidrug resistance developed. Resistance transferred to the farmers. After six months, more than 30 percent of people on the farm excreted bacteria, 80 percent of which were resistant, compared to 6.8 percent resistance for people who lived in the surrounding area. Researchers speculated that farmers developed resistance through handling the feed and because the genes were in the environment. People who ate eggs from the chickens did not develop resistant bacteria.

Other studies compare DNA sequences of resistance genes from different bacteria. Results from these experiments show that often the bacteria infecting people are the same as those in livestock. For example, in 1982 a streptotricin antibiotic was introduced as a growth promoter for pigs. Streptotricin has never been used in people. Within one year of its introduction, resistant bacteria were detected in pigs. Within two years, bacteria with the same gene were also found in pig farmers, their families, urban residents, and E. coli from urinary tract infections. A few years later, the resistance gene was found in pathogenic bacteria. Strikingly, it not only found its way into bacteria that can infect both animals and humans but also to Shigella, bacteria that resides only in people. While not all people who are infected by Shigella exhibit symptoms, Shigella infection can lead to stomach cramping, diarrhea, and fever. A more recent study used two variants of a vancomycin resistance gene. These two variants differ only by one DNA base. In poultry, the resistance gene has a G where in pigs there is a T. In humans, there is an even mix of G and T variants except in Muslim countries (which don’t raise or consume pigs) where people contain only the G variant.

Based on such evidence, the EU, which follows the precautionary principle, has banned the use of antibiotic growth promoters that can select for resistance to human antibiotics. US policy is based on proof of principle, and there is not enough evidence to justify eliminating the positive effects of antibiotic growth promoters. If antibiotics were discontinued, the cost of meat would increase by $5 to $40 per person per year, and an additional 2 million acres of cropland would be needed because animals would grow more slowly and produce more waste in the bargain. Dr. Ian Phillips, from the University of London, writes, “The banning of any antibiotic usage in animals based on the ‘precautionary principle’ in the absence of a full quantitative risk assessment is likely to be wasted at best and even harmful, both to animal and to human health.”

And skeptics remain. These scientists believe that only in the cases of Salmonella and Campylobacter is there sufficient evidence to show negative impact on human health, and even then they believe it is minimal. They point out that in almost every case, interpretation of data is complicated by use of antibiotics in humans as well as animals. Antibiotic resistance could have arisen first in people and then spread to animals. It is safe to say that these theories represent a minority in the scientific community.

Says Dr. Lee Riley, professor of epidemiology and infectious disease at UC Berkeley, “To be blunt, the likelihood of anything changing in the industry is very low. This has been going for more than fifty to sixty years, and there’s really lots of good evidence that a lot of the antibiotic resistance in humans is traceable to animal feed. The industry has not reacted to the overwhelming evidence for many good reasons, both legal and economic.”

Riley believes the solution is to look at European practices and appreciate their results. “Decreasing the use of antibiotics doesn’t contribute to any bad effect on the food industry. And ultimately we have to consider the negative impact of what we’re doing. Europe and Asia might stop imports of American food products. We need to weigh the risks and benefits. But they’ll only do it if they see that it’s to their benefit to sell antibiotic-free products. They need to get pressure from American consumers.”

Government interference never works, Riley says: “The most powerful weapon is the consumer.”