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Executive summary:

The Global Burden of Disease Study 2010 (GBD 2010) is the largest ever systematic effort to describe the global distribution and causes of a wide array of major diseases, injuries, and health risk factors. The results show that infectious diseases, maternal and child illness, and malnutrition now cause fewer deaths and less illness than they did twenty years ago. As a result, fewer children are dying every year, but more young and middle-aged adults are dying and suffering from disease and injury, as non-communicable diseases, such as cancer and heart disease, become the dominant causes of death and disability worldwide. Since 1970, men and women worldwide have gained slightly more than ten years of life expectancy overall, but they spend more years living with injury and illness.GBD 2010 consists of seven Articles, each containing a wealth of data on different aspects of the study (including data for different countries and world regions, men and women, and different age groups), while accompanying Comments include reactions to the study’s publication from WHO Director-General Margaret Chan and World Bank President Jim Yong Kim. The study is described by Lancet Editor-in-Chief Dr Richard Horton as “a critical contribution to our understanding of present and future health priorities for countries and the global community.”

Link to the study here.

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From: The New York Times:

The tiny black particles released into the atmosphere by burning fuels are far more powerful agents of global warming than had previously been estimated, some of the world’s most prominent atmospheric scientists reported in a study issued on Tuesday.

These particles, which are known as black carbon and are the major component of soot, are the second most important contributor to global warming, behind only carbon dioxide, wrote the 31 authors of the study, published online by The Journal of Geophysical Research-Atmospheres.

The new estimate of black carbon’s heat-trapping power is about double the one made in the last major report by the United Nations’ Intergovernmental Panel on Climate Change, in 2007. And the researchers said that if indirect warming effects of the particles are factored in, they may be trapping heat at almost three times the previously estimated rate.

The new calculation adds urgency to efforts to curb the production of black carbon, which is released primarily by diesel engines in the industrialized world and by primitive cook stoves and kerosene lamps in poorer nations. Natural phenomena like forest fires also produce it.

Read entire article here.

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“Phthalates: Are They Safe?” 60 Minutes on CBS …, posted with vodpod

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The Disappearing Male – CBC Documentary, posted with vodpod

From Science News (quoting Upstream Contributor, Dr. Ana Soto):

An ingredient in plastics and food-can linings coaxes cells from the pancreas to inappropriately secrete the hormone insulin, a finding that bolsters earlier links between type 2 diabetes and low-dose exposure to the chemical.

Bisphenol-A, or BPA, can mimic the effects of estrogen, a hormone that is involved in regulating insulin production in the body. Although controversy persists over BPA’s potency as an estrogen mimic, the new study, published online February 8 in PLoS ONE, finds that the pollutant is every bit as potent as the body’s natural estrogen in terms of triggering insulin release.

“I don’t think that anyone can say now that low-dose effects don’t occur,” says endocrinologist Ana Soto of the Tufts University School of Medicine in Boston, who was not involved in the new work. “It shows that changes happen in human cells — and at concentrations comparable to current levels of human exposure.”

The new work shows that BPA stimulates insulin release through a hormone-activating protein called estrogen receptor beta, or ER-beta, says Angel Nadal of Miguel Hernández University in Elche, Spain, who led the new study. Tiny concentrations of either estrogen or BPA boost the release of insulin. When his group tested mice engineered to produce no ER-beta, the effect went away, demonstrating that the protein is integral to BPA’s perturbation of insulin secretion.

For people with diabetes, oversecretion of insulin might be viewed as a positive development, he says. But in healthy individuals, it could eventually desensitize tissues to the hormone, creating insulin resistance — a hallmark of type 2 diabetes.

“If this happens in people with a genetic predisposition to diabetes, it will accelerate the induction of that disease,” Nadal says. His team has shown that exposure to BPA elevates an animal’s risk of developing insulin resistance. And people with type 2 diabetes — the type caused by the body’s diminished sensitivity to insulin — tend to have elevated concentrations of BPA in urine, a 2008 study showed.

“I don’t think BPA alone will cause type 2 diabetes,” says Franck Mauvais-Jarvis of Northwestern University’s Feinberg School of Medicine in Chicago. Dozens of environmental chemicals can mimic hormones, he says, “and I suspect it’s a cocktail of these nasties that predisposes individuals to developing metabolic disease, whether its type 2 diabetes or obesity.”

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From American Scientist:

When research suggests that a single chemical may cause harm, public concern rises, as it has for the plastic additive bisphenol A (BPA) in recent years. But many more of the 83,000 or so humanmade chemicals used in the United States receive little attention. The possible effects of chemicals in combination get still less scrutiny, even though the potential that some chemicals will interact is high, given their numbers.

This may be due in part to the staggering amount of work required to discern those effects. It would be a very difficult task to keep up with research on all of these substances, much less evaluate their relative risk as new results appear. The U.S. Environmental Protection Agency (EPA) has put considerable effort into this under the Toxic Substances Control Act, but the Act has not been updated since its passage in 1976 and excludes many substances from the agency’s purview.

Substances that have the potential to disrupt development in an organism are of special concern. The results of exposure to such chemicals can range from birth defects to developmental irregularities that don’t appear until later in life. Determining whether a substance is an endocrine disruptor, how strongly it acts and at what concentrations, not to mention deciphering hormone pathways themselves, takes a great deal of time and resources. Studies in the lab can’t be directly extrapolated to real-life situations, but they can offer clues about new routes to explore, along with help in evaluating the risk posed by various chemicals.

Heather Patisaul, a biologist at North Carolina State University, studies the effects of BPA and other compounds suspected to disrupt hormonal processes, using female rats as models. “The biggest unknown,” she says, “is if human harm is indeed resulting from exposure to these chemicals at low doses. If it is, it requires a major paradigm shift in how we approach toxicology, because the current strategies are ill equipped to deal with endocrine disruptors.”

A new study adds several more pieces to the puzzle. In a September 2011 study in the Proceedings of the National Academy of Sciences of the U.S.A., Eunah Chung, Maria C. Genco, Laura Megrelis and Joan V. Ruderman chose a less known, but widely used, substance to investigate: triclocarban (3,4,4’-trichlorocarbanilide, or TCC).

TCC has been used as an antimicrobial in consumer products since the 1950s. A 2001 study found that it was present in 84 percent of antimicrobial bar soaps sold in the United States. It’s often mentioned in the same breath with triclosan: Both are halogenated carbons used in soaps and other products, but their chemical identities are unique. The EPA reports that between 1 and 10 million pounds of TCC were used in the United States in 2002. People who shower with soap containing TCC absorb it through their skin. It is metabolized quickly by humans but persists in surface waters and in sewage sludge that is spread on agricultural fields.

Ruderman and her coauthors looked at the gene aromatase-B (AroB) in the brains of developing zebrafish embryos. AroB is regulated by estrogen, among other compounds, and is expressed in subregions of the brain including the hypothalamus and preoptic areas. To determine what concentration of TCC to use, they tested a range, then chose one that did not show signs of developmental delay or toxicity. The 0.25 micromolar experimental concentration was about 1600 times higher than a high-end estimate of levels in surface waters in an industry report to the EPA, and about 12 times higher than a high-end estimate from a university-based study in Environmental Health Perspectives.

The team found that TCC had little effect on AroB when introduced without estrogen, but that it strongly enhanced the effects of introduced estrogen on the gene, with a twofold greater increase than that induced by estrogen alone. They also tested the effects of BPA and found that it induced the gene’s expression even without estrogen present.

Then the researchers exposed embryos to TCC and BPA together. Rather than amplifying the effect of the estrogen-mimicking BPA, TCC suppressed it: Its presence along with BPA resulted in about a twofold decrease in transcription of aromatase-B compared to embryos exposed to BPA alone.

“The experiments we did with BPA plus TCC were an example where each one has a positive effect on an estrogenlike process,” Ruderman says. “But you put them together and they are not additive—in fact in some ways they suppress each other.” It’s surprising that TCC would amplify estrogen’s effect but reduce the effect of an estrogen mimic—a reminder that chemicals in combination can act unpredictably.

In a 2008 study in Environmental Health Perspectives, Bruce Hammock, an entomologist at the University of California, Davis, and colleagues found that TCC enhanced estrogen- and testosterone-dependent gene expression by 2.5 times in human cells. “The major significance” of Ruderman’s study, he says, “is an elegant demonstration that there is the potential for two known environmental chemicals to synergize for an enhanced biological effect.” He thinks it’s unlikely that environmental exposure to both chemicals will be high enough to create such effects, but he notes, “This is a cautionary tale in terms of mixtures in general. As a society we are using thousands of high-volume chemicals with little regard to environmental or human health effects.”

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From Environmental Health News:

Maybe a ho-hum is in order about some of the reminders from the Institute of Medicine’s environment and breast cancer report released last week: Exercise is good, while exposure to unnecessary medical radiation, being overweight, consuming alcohol and using estrogen-progestin hormone treatments for menopause can increase risk.

But most of the news media missed the significance of the assessment on environmental chemicals. The real news is that the report is an authoritative statement that a cascade of scientific evidence plausibly links consumer product chemicals and pollutants with biological activity suggesting breast cancer risk.

Instead of saying what is in the report, glass-empty stories said that the IOM “failed” to “definitely” link any chemicals to breast cancer or find “clear” environmental links. Some incorrectly said the report tells women to stop worrying about consumer product risks. These stories ignore the report’s important explanation that definitive evidence is not attainable and lack of human evidence of harm doesn’t mean something is safe.

Breast cancer develops over many years, with influences beginning even before birth, and we are all exposed to myriad suspect chemicals, so clear human evidence of links to particular chemicals or mixtures is likely to remain elusive. That’s why the IOM committee also looks to experimental evidence, including animal studies, to evaluate chemicals that damage DNA or affect hormones. Their recommendation for better chemicals safety testing based on breast cancer biology is a major departure from prevailing medical skepticism and past messages that tagged concerns about chemicals as myths.

The IOM is partly to blame for the confusion. The slim “Questions and Answers” says, “we don’t know enough” about environmental chemicals. Sure, we need to know more, but the report gives a very different impression with its recommendation to “limit or eliminate workplace, consumer, and environmental exposures to chemicals that are plausible contributors to breast cancer risk while considering risks of substitutes.” That recommendation was ignored by most media.

The report calls out three chemicals in particular – ethylene oxide, benzene, and 1,3-butadiene – as “probably human breast carcinogens.” As far as we know, this is the first statement by an authoritative medical group linking any specific environmental chemical to breast cancer. The primary exposures to benzene and 1,3-butadiene are from vehicle exhaust. Ethylene oxide is a sterilant used, for example, in medical settings and food sanitation. My own list of chemicals with both human and animal evidence would be longer, including polychlorinated biphenyls (PCBs), found in certain fish and in air in older buildings; polycyclic aromatic hydrocarbons (PAHs), from combustion-related air pollution, tobacco smoke, and grilled food; and organic solvents, used in glues and cleaners.

The IOM highlights chemicals with hormonal activity, including perfluorinated compounds, bisphenol A and the pesticide atrazine, as priorities for research because the evidence of plausible biological links to breast cancer is “provocative” but difficult to interpret so far. The committee calls for better consumer information about product ingredients, so shoppers can make choices while science and regulatory assessments unfold.

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From IWatch:

For the past three decades, Jeani Thomson has been pleading with New York state officials to protect her and her neighbors from air pollution that regularly spreads into her yard from an industrial plant a mile away. Many mornings, a foul-smelling, thick fog settles around her modest house in Tonawanda, a working class town of 16,000 just outside Buffalo. The “toxic blue haze,” as Thomson calls it, smells like ammonia, sulfur and “an oily exhaust.”

She believes it has made her sick. Ailments have transformed her, she said, from a fit mail carrier who walked a 13-mile route into a survivor of multiple illnesses who takes 22 medications and now moves with difficulty on stiff legs. Though only 57 years old, she has only one lung, and half a stomach. Her doctors have diagnosed her with a rare skin rash, as well as asthma and arthritis. Though she claims never to have had a cigarette, her voice has the raspy sound of a smoker. On bad days, she says, she inhales oxygen.

“It’s not anything that I ate. It’s not anything that I drank,” said Thomson. “It’s from living here and breathing the air.”

Whether her illnesses, or anyone else’s, came from the plant’s pollution can be difficult to prove. Still, concerns about toxic emissions rallied Thompson and a small group of other local people — most of them sick, later joined by dozens of other citizens complaining of similar ailments — to force complacent regulators to clean up their air.

Residents started in 2004 by using buckets and hand-held vacuums to test the air. They found shockingly high levels of benzene. With a hint from a state regulator, they figured out the main source was a plant called Tonawanda Coke Corp., a relic of the industrial age that since 1917 has been producing material needed for smelting iron.

They enlisted the help of a plant insider to help them expose practices at the plant. They recruited residents who lived closest to the plant to report to the state and the media when plumes of soot and the odors became intolerable. And they wouldn’t give up.

It took five years of prodding before state regulators formally blamed Tonawanda Coke for the high levels of benzene and moved aggressively to enforce the Clean Air Act. Finally in 2009 the state, together with the U.S. Environmental Protection Agency, swooped down on the plant for a week-long surprise inspection. Inspectors found it in such a state of disrepair that huge amounts of benzene and other dangerous chemicals were seeping from cracks in worn-out equipment and leaky pipes.

In a cascade of civil and criminal enforcement actions since then, the EPA has accused the plant of vastly underestimating its toxic emissions, operating illegal equipment that pumped untreated toxic gas into the air and failing to use pollution controls required by its permit that would have prevented releases of hazardous particles.

The case highlights not just possible corporate wrongdoing but the risks posed to communities around the country by an environmental regulatory system that largely entrusts companies to disclose how much toxic pollution they emit, and can take years to act once violations are discovered.

State and federal records in the Tonawanda Coke case illustrate the failure of that honor system. For many years, regulators apparently had no idea the company was discharging into the air benzene, formaldehyde and other chemicals — known to be harmful to health — in quantities many times greater than the company estimated to regulators.

Even after regulators forced the firm to fix blatant sources of benzene, sophisticated measuring equipment found the solvent seeping out of the plant at a rate of 91 tons per year, according to an EPA analysis. That was almost 30 times higher than the 6,754 pounds the firm had reported to the EPA in 2009 as part of the Toxics Release Inventory. Benzene has been associated with blood disorders, infertility, and cancer, especially leukemia.

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CSB Safety Video detailing three accidents at the Dupont facility in Belle, West Virginia.

From Huffington Post:

Mike Burke was enjoying a round of golf with fellow firefighters when two hijacked planes struck the twin towers ten years ago.

“We immediately left to go to the Trade Center,” said Burke, then with Engine 201 of Sunset Park, Brooklyn. He spent the rest of that day — and much of the night — laboring in the cloud of dust and debris at ground zero. He returned to the smoldering site again every day for the next two weeks, and then three days a week until February 2002.

Like so many others who worked at or lived near ground zero, Burke, 39, is now dealing with a lengthening list of health problems, the most troubling of which is kidney cancer. Officials originally told him the disease could not be tied to his time at ground zero.

“They said that there are no studies out there that can support it. I said, ‘No shit, there are no studies out there.’ We are the guinea pigs being studied.”

Years of rancorous political debate on Capitol Hill over which illnesses could be attributed to time spent at ground zero — and whether to provide health coverage for those illnesses — finally yielded the James Zadroga 9/11 Health and Compensation Act, which was signed into law in January. The bill, named for a police officer considered by many to be the first to die from an illness tied to ambient pollutants at ground zero, provides $1.8 billion for medical costs relating to specific 9/11-related illnesses, as well as $2.7 billion to compensate victims for other associated losses.

Cancer, however, is not covered — although new research from the Fire Department of New York suggests that it should be, and that a new round of debate over the issue is in the offing.

Researchers estimate that somewhere between 10 and 30 percent of the more than 50,000 people who were exposed to the foul air and other environmental hazards at the site of the collapsed towers continue to suffer from a variety of ailments — from asthma and other respiratory illnesses to digestive problems and mental health disorders.

And while no one will ever know the full inventory of pollutants people were exposed to at ground zero — air monitors were not in place until days later — analyses of the dust that rose and lingered and then settled at the site have revealed a long list of potentially cancer-causing ingredients, from benzene and diesel exhaust to pulverized glass, hydrochloric acid, black soot, polychlorinated biphenyls (PCBs), organochlorine, lead, dioxins and hundreds of tons of asbestos.

“It was an unprecedented mix of proven human carcinogens and other toxic chemicals,” said Philip Landrigan, dean for global health at the Mount Sinai School of Medicine in New York.

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From

[Upstream Contributor] Dr. Frederica Perera touches on how the environment around us can make a big impact very early in life and stick with us for a long time. This short take was shot during a break at Keystone Symposia’s meeting on Environmental Epigenomics and Disease Susceptibility held in March 2011 in Asheville, North Carolina.

 

From California Watch:

California’s former top pesticide regulatory official dismissed safety guidelines suggested by her own staff scientists on the grounds that they were “excessive” and too onerous for the pesticide manufacturer, recently released internal documents show.

In response, the scientists lodged a formal protest, calling the official’s actions “not scientifically credible,” according to the documents released by court order last week.

The documents amount to a “smoking gun,” says Paul Blanc, a professor of occupational and environmental medicine at UC San Francisco. Last year, Blanc helped advise the staff scientists on their evaluation of the pesticide, methyl iodide.

“The decision by the regulatory superiors was not science-based,” Blanc said.

In one of the documents, Mary-Ann Warmerdam, who led the state’s Department of Pesticide Regulation until this year, weighs a recommendation from her staff that farm workers be exposed to no more than a trace amount of methyl iodide per day. The recommendation – intended to protect farm workers from cancer and miscarriage – is “excessive and difficult to enforce,” Warmerdam wrote in April 2010, about two weeks before the department made its recommendation that California approve methyl iodide. If the restrictions on methyl iodide were approved, she wrote, the pesticide manufacturer might find the recommendations “unacceptable, due to economic viability.”

“(Warmerdam’s) method was to consult with the pesticide manufacturer and determine what was acceptable to them, and then decide on what an acceptable level of exposure was,” said Susan Kegley, a consulting scientist for the Pesticide Action Network, a group suing the state.

Department spokeswoman Lea Brooks declined to comment on the documents, citing the pending litigation. “It is inappropriate to try this case in the media,” Brooks said.

Warmerdam resigned from the department in January. Gov. Jerry Brown has yet to appoint a successor.

Methyl iodide was approved in December 2010, at the tail end of the Schwarzenegger administration. It’s a chemical fumigant used primarily by strawberry growers. A coalition of environmental and farm-worker groups has sued the state to try to ban the chemical.

As part of the suit, the groups asked the Department of Pesticide Regulation to release documents explaining how the agency decided to approve the chemical. The plaintiffs wanted to know how the agency had settled on exposure levels more than 100 times higher than what scientists within the agency believed were safe.

When pressed for documents that might reveal the agency’s rationale, Warmerdam declined to release them, citing the “deliberative process” exemption, which allows government agencies to keep the thought process behind a decision private. A public records act request filed by California Watch and KQED QUEST elicited the same response.

Earlier this month, a judge disagreed, ordering the department to release the documents, which plaintiffs shared with reporters on Thursday.

“DPR has an obligation to explain to the public the basis for its decision,” said Earthjustice attorney Greg Loarie, who is representing the plaintiffs. “The public has every right to know that DPR approved methyl iodide over the objections of its own staff scientists.”

That rift between scientists and regulators first became public last year, in an e-mail exchange unearthed by KQED QUEST and California Watch’s Public Records Act request. In the e-mails, two staff toxicologists – Lori Lim and Ruby Reed – said they had not been part of the decision to approve methyl iodide, and they stood by their original work.

“We had to read between the lines to figure out how the target levels were calculated,” they wrote. Both Lim and Reed have since resigned from the department.

The new documents show staff scientists sending their complaints up the department’s chain of command.

“I am puzzled by the numbers,” staff scientist Jay Schreider wrote in a memo to the state’s top toxicologist, Gary Patterson. Approving methyl iodide was “management’s prerogative,” Schreider wrote. But he said managers should not imply that the scientists’ findings “are the basis for that decision, or that the apparent ‘mix and match’ approach provides a scientifically credible basis for the decision.”

In his order, Judge Frank Roesch of the Alameda County Superior Court found that the “great majority” of the department’s documents should never have been withheld in the first place. As for the rest, Roesch found “the interest in public disclosure clearly outweighs agency interest in non-disclosure.”

The documents reveal a rare point of agreement between the department’s scientists and its managers: that methyl iodide may cause brain damage in developing fetuses.

When California first began evaluating methyl iodide, it took the unusual step of bringing in an outside group of scientists, hired to work alongside department scientists, as an independent peer-review group. The scientists, including UCSF’s Blanc, worried that methyl iodide could drift up from strawberry fields and be inhaled by pregnant farm workers or children playing nearby, causing subtle effects such as IQ loss, which might never be detected or traced back to the chemical.

“Methyl iodide concentrates in the fetal brain to levels well above those in the mother,” they wrote in their assessment. “There is a high likelihood that methyl iodide is a developmental neurotoxin.”

The new documents show department managers also contending with the lack of data about methyl iodide’s potential effects on developing brains. In animal tests, they wrote, “several measures of neurological deficiency were measured. … Overall, there is a need for a more thorough investigation into developmental neurotoxicity in pre- and post-natal exposures to methyl iodide, because the existing data do not address these exposures.”

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(Image Creative Commons by Donnaphoto.)

From Melbourne Florida Today:

Nearly 1,600 children age 5 and younger live close enough to an airport in Brevard County to be at risk from leaded gasoline used by small piston planes and helicopters.

With the release of a new study from Duke University and other research identifying 1 kilometer, about 0.6 miles, as a significant threshold for health risks from lead, FLORIDA TODAY examined local data to gauge the potential lead threat to Space Coast residents. The threat is especially dangerous for young children, who suffer most from exposure to lead.

The newspaper analysis of U.S. Environmental Protection Agency, Census and Brevard County housing numbers found:

  • About 13,480 homes and 25 schools, including eight elementary schools and seven day care centers are within the at-risk zone of an airport, heliport or private airstrip. Given Brevard’s average of 2.4 residents per household, an estimated 32,350 people live within that threshold distance.
  • Brevard’s 20 aviation facilities emitted 1.3 tons of lead in 2008, the most recent data available. Forty percent, or 1,043 pounds, came from Melbourne International, ranking it 52nd highest for lead emissions among the nation’s 20,000 aviation facilities.
  • 3,500 homes, or about 8,400 people, are within that threshold of Melbourne International Airport.”I’m concerned about it,” said Andrea Cattaneo, a mother of two whose home on Bridle Path in Hacienda Estates is less than a half-mile from Melbourne International. “You get that black dust. I’m constantly washing off my back porch.”

To protect her sons, Nicholas, 6, and Jack, 9, she makes sure to change out her air-conditioning filter regularly to capture any air pollutants from planes. But she still worries how lead and other air pollution might affect her family, especially as the airport expands.

“It’s really in those early years that lead can make an impact on children’s intelligence levels,” said Rebecca Anthopolos, a statistical analyst at Duke who co-authored the study on lead exposure from leaded aviation gasoline published in the journal Environmental Health Perspectives. The researchers found lead-blood levels increase significantly in children who live near an airport.

No level of lead exposure is accepted as safe, according to the EPA, and the agency has found serious health effects at much lower levels in blood than previously thought. The agency is considering a phase-out of lead from general aviation gasoline, called avgas, but has set no timeline.

In May, Friends of the Earth, a California-based environmental group, notified the EPA it plans to sue the agency to force a timeline.

But industry officials say there is no viable substitute for lead as an octane booster. Forcing more expensive alternative fuels too soon could batter a $150 billion industry already in a tailspin from the recession, they say, as well as create safety concerns.

“Engines could literally disintegrate on you,” said Glenn Vera, director of Florida Institute of Technology aviation, which has 54 planes at Melbourne International Airport.

Conservation groups counter that industry and the EPA have delayed for decades and must commit to deadlines for a phaseout. They list Melbourne International among 32 airports nationwide — 13 of them in Florida — that are the worst lead offenders because of high general aviation traffic and proximity to homes, schools and low-income areas.

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Image by Boltron.

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From KUOW News:

Washington state might seem immune to the hot temperatures that are affecting the rest of the country, but that’s not the case. Some people may reject the idea of climate change, but scientists say summer temperatures have been climbing over the years, and it will continue to get hotter over time. It’s these kinds of heat conditions that put many people at risk. Some researchers estimate that in 2004 alone the cost of hospitalizing people due to extreme heat was nearly a billion dollars. In the first part of our report on heat and health, KUOW’s Ruby de Luna reports on the health impacts of climate change.

TRANSCRIPT

Remember the heat wave of 2009?

News Clip: “Seattle tied an all–time record high Tuesday, and it’s getting hotter… “

That heat event in the Pacific Northwest lasted a week.

News Clip: “Today, Seattle is supposed to reach triple–digit temps for the first time ever.”

Seattle peaked at 103 degrees, a record high for the area. Well, scientists say we can expect hotter days ahead.

Richard Fenske is professor of environmental occupational health sciences at the University of Washington.

Fenske: “When we look across a period of 20 to 40 years, we are confident that temperatures are increasing, and this will result in severe heat events and probably longer heat events, but not necessarily every year.”

In 2009, Fenske and his colleagues in the School of Public Health were awarded a federal grant to study how climate change will affect people’s health. In a nutshell, the study concluded that heat events will likely lead to what they call excess deaths. How do researchers know that?

Michael Yost: “We counted the dead bodies, and we continue to count them.”

That’s Michael Yost, also a UW professor in the same department. He and Fenske are part of the research team that’s analyzing the data for the study.

Here’s what they did: They tracked Washington’s previous weather records between May and September for the last 26 years. They noted a rise in overall temperatures during that time. The team also looked at death records for the same time period. They found that whenever there was a heat event, there were more deaths, mostly elderly people.

The thinking goes that if temperatures continue to rise in the next few decades, so will the number of excess deaths. But it’s hard to predict just exactly how much warmer it’s going to be, or how many hot days we’re going to have. So, Fenske and Yost came up with a range of scenarios. On the low end, the region may have only 16 extreme heat days in a given year; or, on the high end, as many as 30 days.

Yost: “What we’re trying to do is to not simply say this is one possible outcome in the future, but to simulate many possible outcomes, and so what we end up with is a range of possible values for how many heat events might occur in, say, 2025.”

The study’s goal is to help local public health agencies and emergency responders prepare for heat events. Richard Fenske says this will prevent deaths and unnecessary hospitalizations.

Fenske: “We can develop a warning systems, education, transportation systems to get elderly people to cool environments, like a public library, during a heat event. There are ways to prevent these deaths if we choose to do so, but we have to know where and when they might occur.”

And since extreme heat days are uncommon in the Puget Sound region, most homes don’t have cooling systems. And when it does get hot, especially for an extended period of time, most people don’t know how to deal with the heat or lose the ability to take precaution.

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