Homeowners try to assess formaldehyde risks in floors

Laminate wood flooring may look nice, but some brands
release formaldehyde fumes into the air, experts say.

Installing a new wood floor is usually about aesthetics: brown or black? Glossy or matte?

Now, some Americans and businesses are grappling with another feature: formaldehyde.

Uneasy consumers have flooded state and federal safety agencies with inquiries about Lumber Liquidators, the discount flooring retailer accused in a “60 Minutes” episode of selling laminate wood with high levels of formaldehyde, a known carcinogen.

Should they rip it out? Leave it in? And what are the dangers to adults, children or even pets?

Attorney General Eric T. Schneiderman of New York has opened an inquiry into whether the company violated safety standards. Safety officials in California are also likely to investigate.

But federal regulators, armed with murky rules or none at all, have scrambled to respond, leaving consumers largely responsible for assessing the risk.

Formaldehyde exposure can cause immediate health problems like respiratory and sinus effects, but the effects of long-term exposure remain unclear.

Regulators, at least for now, are advocating a tempered approach.

“We are not encouraging people to rip out their flooring right now,” said Lynn Baker, an air pollution specialist with the California Air Resources Board, which enforces the state formaldehyde rules that Lumber Liquidators is accused of breaking.

Commercial customers could also be affected, although Lumber Liquidators estimates that commercial sales make up less than 10 percent of the market for laminate flooring, a cheaper alternative to hardwood. Homeowners account for the bulk of its sales.

Lumber Liquidators disputes the “60 Minutes” report and says its flooring is safe. The company also said it was considering offering air testing services to reassure concerned consumers.

Installers, too, find themselves on the front lines after the report.

No federal rules for airborne chemicals in the home

While federal rules exist for workers, no federal rules protect consumers from formaldehyde or most other airborne chemicals in their homes.

And while research exists on formaldehyde’s health effects, experts have difficulty correlating levels of exposure with cancer risk since so many factors can affect the development of the disease.

“Any exposure to a carcinogen can increase your risk of cancer,” said Marilyn Howarth, a toxicologist at the University of Pennsylvania’s Perelman School of Medicine.

Mr. Baker, with the California agency, said consumers should ask two questions: How long has the flooring been installed, and have they been feeling sick?

“If the flooring has been installed more than a couple of years ago, most of it has probably already off-gassed,” he said, meaning that the chemical would probably have been released.

“If it was just installed last week, that’s a different story — you definitely want to ventilate the home.”

The floorboard controversy bears a resemblance to the cases of Chinese-made drywall that released sulfur gases into thousands of homes built after the 2005 hurricane season, which resulted in metal corrosion and health complaints.

But while the drywall gases were expected to be released for decades, formaldehyde emissions in flooring may not last as long.

Most new floors emit small levels of formaldehyde. But it also seeps out of adhesives used to bind furniture and other household items, affecting the quality of the air residents breathe.

To combat its harmful effects, governments around the world have limited the use of formaldehyde in household products, particularly those made of wood.

In Europe, chemical emissions from composite wood products are tightly regulated, and Japanese regulators put the onus on home builders to limit formaldehyde levels over all within houses they construct.

The United States, however, trails when it comes to such regulations. California enacted rules to cap emissions from composite wood products sold in the state.

As far back as 2009, the Environmental Protection Agency said it was considering adopting California’s limits nationwide, and it issued a proposed rule in 2013.

But after many delays at the request of the wood products industry, the E.P.A. has yet to complete its rule. The E.P.A. said it had no plan to investigate Lumber Liquidators, citing the lack of a finished rule.

Agency proposes ventilation and air testing

The agency says it is trying to give consumers “actionable guidance” when it comes to formaldehyde from composite woods, according to Bob Axelrad, a policy adviser in the office of air and radiation.

That includes proper ventilation, when possible, and using reliable air testing methods.

David Krause, an environmental consultant at the consulting firm Geosyntec and the former state toxicologist of Florida, said ventilation helped but was not always a solution: Humidity, for example, can intensify the problem.

Testing indoor air quality is also not a simple proposition — mainly because federal standards are geared toward workplaces, not homes. There are no definitive testing levels, and people react in different ways to the chemical.

“We really don’t have anything that is enforceable,” Dr. Krause said.

Still, based on current knowledge of the Lumber Liquidators’ product, he added: “This is not a ‘Your hair’s on fire’ emergency.”

The Consumer Product Safety Commission may take a lead role in investigating Lumber Liquidators. The commission can push for a recall if it can prove direct harm to human health.

But that would involve a long regulatory inquiry. Several consumers have begun pursuing a different path: suing the company.

Source: New York Times; This article has been edited for length.

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Children's exposure to secondhand smoke tied to clogged arteries

Exposure to tobacco smoke can have long-term
effects in cardiovascular health: Researchers

(Reuters Health) – In a Finnish study spanning 26 years, kids exposed to parental smoking were more likely to develop plaque in their carotid arteries as young adults than kids who were not exposed to secondhand smoke.

These findings and others suggest the health effects of passive smoking on children are not limited to respiratory or developmental health, but can have a long-term impact on cardiovascular health, said senior author Costan G. Magnussen of Menzies Research Institute Tasmania in Hobart, Australia.

Researchers used frozen blood samples from more than 1,000 kids ages three to 18 collected in 1980, along with parental reports of smoking status in 1980 and 1983 from a larger group of kids. They also had ultrasounds of the adult children in 2001 and 2007.

They tested the blood samples for levels of cotinine, a byproduct of cigarette smoke exposure, and looked for a buildup of plaque in the carotid arteries, two large blood vessels of the neck, on the adult ultrasounds.

Carotid plaque can cause narrowing of the arteries, increasing blood clot and stroke risk, according to the National Institutes of Health.

About two percent of the grown-up kids had a carotid plaque uncovered by ultrasound at an average age of 36.

More than 84 percent of kids of nonsmokers had no cotinine in their blood, compared to 62 percent of those with one smoking parent and 43 percent when both parents smoked.

The authors assumed that kids with a parent who admitted to smoking who did not have cotinine in their blood had been exposed to less secondhand smoke, possibly because parents had been careful to keep their smoking away from the child.

Compared to kids of nonsmokers, these kids were about one and a half times as likely to have carotid artery plaque as adults. But kids of smokers with poorer “smoking hygiene” that exposed them to more smoke (and resulted in cotinine in their blood) were four times as likely to have carotid artery plaque as those with nonsmoking parents.

“What we were able to do that others have not, is show that parents who are unable or unwilling to quit smoking can still limit the impact of their smoking on their child’s future cardiovascular health by changing their smoking behavior to limit the amount of smoke their child is exposed to,” Magnussen told Reuters Health by email.

Early smoke exposure is dangerous in
many ways, health experts suggest.

Many smoking parents did not smoke inside the home or car, or smoked well away from their children, to the point where there was no evidence for passive smoke exposure in their child’s blood, Magnussen said.

Plaque buildup, or “atherosclerosis,” can begin in childhood so the results are not surprising, according to Karin B. Michels, an epidemiologist and associate professor at Harvard Medical School in Boston.

But only 64 out of more than 2,000 grown subjects did develop plaque, which is a very small number, Michels told Reuters Health by phone.

“I would be a little cautious but overall I think it’s an important study and lends more support to the risk of passive smoking for children,” she said. “I don’t doubt that there is a risk and it could be affecting other things like blood pressure.”

Atherosclerotic plaque is particularly dangerous when it develops at an early age, she said.

This group of kids grew up in a time when smoking was much more ubiquitous, and they would have been exposed to more secondhand and thirdhand smoke, said Melbourne Hovell of San Diego State University, who was not part of the new study.

“Thirdhand smoke” is that which lingers on surfaces or in environments and may combine with other chemicals to create toxic substances over time, Hovell told Reuters Health by phone.

Early smoke exposure may have several deleterious effects other than just plaque buildup in the arteries, including an increased risk of later breast cancer and a predisposition to nicotine addiction, Hovell said.

Plus, children of smokers are more likely to become smokers themselves, triggering a cascade of other health risks.

“It’s pretty much a perfect storm,” Hovel said.

“The other message for the lay public is to not allow any smoking in your home or car,” as it will contaminate the environment indefinitely, he said. “Parents with young children probably should avoid buying a used car that has been smoked in.”

Source: Reuters

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Video: Indoor air concerns in baby rooms and nurseries

The arrival of a new baby prompts periods of extreme happiness - and stress. Keeping babies safe and healthy is paramount, but the advice new parents get is often conflicting.

One thing is for sure: Newborns and babies are among the most vulnerable when it comes to polluted air and exposure to airborne contaminants.

Watch this video courtesy of Cochrane & Associates for more information:



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Why you need an air purifier in your home or office

Poor indoor air quality can lead to short-term and long-term
health effects, especially in children and the elderly.

As air purifier manufacturers, we get a lot of calls from people who are starting to notice the effects of poor indoor air quality.

This comes as no surprise. After all, people spend up to 90% of their time indoors (think about yourself – where do you spend most of your time? At home, at the office, in school, in other indoor spaces?)

Fact is, we spend most of our time indoors and many buildings are not equipped to provide the best quality air.

Common indoor air contaminants include:

• Airborne chemicals coming from various sources such as building materials, cleaning products, cosmetics, scents (air “fresheners”), paint, furniture, cooking
• Stale air
• Mold
• Radon
• Dust
• Tobacco smoke
• Pollen
• Mold

We have no choice in breathing. But if we keep breathing contaminated air, we run the risk of developing health concerns, either short-term, or long-term.

The American College of Allergists says that 50% of all illnesses are either caused by, or aggravated by, polluted indoor air. Pregnant women, fetuses, infants, children and the elderly are most vulnerable to indoor air pollution.

And while short-term health effects sound merely bothersome, including irritation of the eyes, nose and throat, headaches and fatigue, the long-term health effects are rather scary: These can include respiratory diseases, heart disease and cancer (EPA). 

According to the latest research, cancer has become the second leading cause of death worldwide. Toxic exposures in the environment are responsible for a substantial percentage of all cancers, between 7 and 19%, according to Environmental Health Perspectives.

How to protect yourself from poor IAQ

Even though we have no choice in breathing, we can control the quality of the air we are exposed to the most. This can be done through source control, improved ventilation and humidity control,

Open windows regularly. Even when it is cold outside, it is important to avoid a buildup of stale and contaminated air indoors.

Avoid using products that can release harmful chemicals or fumes.

Replace your HVAC filters regularly.

Use an indoor air purifier. A complete indoor air purifier needs to have activated carbon, HEPA and UV filters as well as prefilters. They can be free-standing, or attached to the HVAC system and they can run continuously to help remove airborne chemicals, fumes, odors, particles, allergens, asthmagens, mold, bacteria and viruses.

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Air pollution affects children's memory, IQ: Study

Exposure to air pollution  can damage the brain,
a new study shows.

City smog lowers children's IQ.

This is among findings from a recent University of Montana study that found children living in cities with significant air pollution are at an increased risk for detrimental impacts to the brain, including short-term memory loss and lower IQ.

Findings by UM Professor Dr. Lilian Calderón-Garcidueñas, MA, MD, Ph.D., and her team of researchers reveal that children with lifetime exposures to concentrations of air pollutants above the current U.S. standards, including fine particulate matter, are at an increased risk for brain inflammation and neurodegenerative changes, including Alzheimer's and Parkinson's diseases.

Calderón-Garcidueñas' findings are detailed in a paper titled "Decreases in Short-Term Memory, IQ and Altered Brain Metabolic Rations in Urban Apolipoprotein ε4 Children Exposed to Air Pollution," which can be found online here.

The study found that clinically healthy children who live in a polluted environment and who also carry a gene - the apolipoprotein ε4 allele, already known to increase a person's risk of developing Alzheimer's disease - demonstrated compromised cognitive responses when compared with children carrying a gene with apolipoprotein ε3 allele.

Urban growth leads to environmental pollution

Metropolitan Mexico City is an example of extreme urban growth and serious environmental pollution, where 8 million children are involuntarily exposed to harmful concentrations of fine particulate matter in the air every day beginning at conception.

The study matched two groups of children living in Mexico City by multiple variables, including age, gender, socioeconomic status and education, among others.

They then compared children carrying the ε4 allele to children carrying the ε3 allele and found that those with the ε4 allele had three significant alterations.

They had short-term memory shortfalls, an IQ that while within the normal limits measured 10 points less, and changes in key metabolites in the brain that mirror those of people with Alzheimer's disease.

"The results add to growing data suggesting ε4 carriers could have a higher risk of developing early Alzheimer's disease if they reside in a polluted urban environment," Calderón-Garcidueñas said.

She said the study also raises concerns about important educational issues. Since Mexico City children mostly attend underprovided public schools, children do not build cognitive reserves that serve as a defense to pollution impacts.

"A IQ difference of 10 points will likely have a negative impact on academic and social issues, including bullying and teen delinquency," she said.

A serious public health issue

The authors argue that sustained exposures to urban air pollution result in cognitive underperformance and metabolic brain changes that could lead to an acceleration of neurodegenerative changes.

Air pollution is a serious public health issue, and exposures to concentrations of air pollutants at or above the current standards have been linked to neuroinflammation and neuropathology.

In the U.S. alone, 200 million people live in areas where pollutants such as ozone and fine particulate matter exceed the standards.

There are significant associations between exposures to particulate matter and increased mortality due to stroke, cardiovascular disease and respiratory events. The problem in children living in megacities like Mexico City is much worse.

"There is an urgent need to have a broader focus on APOE ε4 and air pollution interactions impacting children's brains, and their responses could provide new avenues toward the unprecedented opportunity for Alzheimer's disease prevention," Calderón-Garcidueñas said.

"We have a 50-year window of opportunity between the time urban children experience the detrimental effects we are describing here and when they will present with mild cognitive impairment and dementia. We need support for studying the current pediatric clinical and imaging evidence in highly exposed urban children. Our efforts should be aimed to identify and mitigate environmental factors influencing Alzheimer's disease."

Source: Press release via EurekAlert

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Build a cleaner fire this winter season

Woodsmoke contains fine particles
that may affect your health.

It's not just during the holiday season - all winter long, families and friends will gather around fires in woodstoves or fireplaces.

But how you build that fire – and what you burn – can have a significant impact on air quality and health, both inside your home and out.

Whether you’re using a woodstove, pellet stove, or your fireplace, seeing smoke from your chimney means your fire isn’t burning efficiently or cleanly as it could.

Woodsmoke contains fine particles – also called fine particle pollution or PM2.5  -- which can harm the lungs, blood vessels and heart. People with heart, vascular or lung disease, and older adults and children are more at risk.

Here are some simple tips for building cleaner-burning fires this holiday season:

• Burn only dry, seasoned wood. Wet, or green logs, create excessive smoke – and waste fuel. How do you tell if wood has been seasoned? Listen for a hollow sound when you strike two logs together.
  
• Wood burns best when the moisture content is less than 20 percent. You can purchase a wood moisture meter to test the moisture content of your wood before you burn it. You can purchase these meters for as little as $20 at most home improvement retailers.
  
• Start a small fire with dry kindling, then add a few pieces of wood. Be sure there’s space between the pieces of wood – and give the fire plenty of air until it’s roaring.
  
• A smoldering fire, “dirty” glass doors on a wood stove, or smoke from the chimney are all signs that your fire needs more air – or the wood is too moist.
  
• Never burn household garbage, cardboard, painted or treated wood, or any wood that contains glue, such as plywood or particle board. These items release toxic chemicals when burned -- and if you’re using a woodstove, they can damage it.
  
• Check your air quality forecast on airnow.gov before you burn. Some local areas limit woodstove and fireplace use under certain air quality conditions.

If you heat your home with wood, using an EPA-certified wood stove can help you save wood while putting less smoke into the air.

In January 2014, the agency proposed updates to its requirements for newly manufactured wood heaters that will make new woodstoves, outdoor wood boilers and other wood heaters cleaner in the future. EPA anticipates issuing final requirements by Feb. 3, 2015.

Source: EPA

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Smokers' homes may be as polluted as worst cities: Study

Polluted air due to smoking has been
linked to heart disease, strokes and cancer.

Living with a smoker can be like breathing the air in the world’s most polluted cities, according to a new study from Scotland.

“The message is pretty simple really - smoking in your home leads to really poor air quality and results in concentrations of fine particles, that you can’t see, that would cause real concern to us if they were found outside,” said lead author Sean Semple, of the Scottish Center for Indoor Air at the University of Aberdeen.

Tiny particles 2.5 microns in diameter or smaller, known as PM2.5, can penetrate deep into the lungs and even enter the blood. They’ve been linked to heart disease, strokes and cancer.

“Making your home smoke-free is key to reducing your exposure to PM2.5; for non-smokers who live with a smoker the impact of implementing smoke-free house rules would reduce their daily intake of PM2.5 by 70 percent or more,” Semple told Reuters Health in an email.

Such tiny particles typically result from combustion. Outdoors, the primary sources are vehicle exhaust, power plants and wildfires. Indoors, wood-burning or coal-burning stoves, gas cooking and heating fires and tobacco smoke are the most common sources of PM2.5 in the air.

For outdoor air, the World Health Organization says the safe exposure limit for PM2.5 particles is an average of 25 micrograms, or 25 millionths of a gram, per cubic meter of air over a 24-hour period, or average annual levels of 10 micrograms per cubic meter.

The U.S. Environmental Protection Agency sets the 24-hour limit at an average of 12 micrograms.

Semple and his colleagues wanted to bring together two scientific communities: those involved in tobacco control work and those interested in outdoor air pollution and health.

“We think there is a lot that each can learn from the other,” he said.

Many studies have examined outdoor air pollution or indoor air quality in workplaces. But home is where most people spend the majority of their time, particularly small children and homebound elderly people, the researchers write.

By comparing indoor air pollution in the homes of smokers and non-smokers, then comparing that to the most polluted cities, they hoped to illustrate the perils of indoor tobacco smoke over a lifetime.

The study team looked at data from four separate studies that measured PM2.5 levels in 93 Scottish homes where people smoked and 17 homes that were smoke free.

On average, PM2.5 levels in smokers' homes were around 31 micrograms per cubic meter – 10 times greater than the average of 3 micrograms in non-smoking homes.

There was a wide range of smoke concentrations in the smokers’ homes, however, and in one quarter of them, the 24-hour averages were 111 micrograms.

Semple pointed out, “A considerable proportion of smokers’ homes had air pollution levels that were the same or higher than the annual average PM2.5 concentration measured in Beijing,” a heavily polluted city.

The study team estimates that over a lifetime, a non-smoker living with a smoker will inhale about 6 grams more particulate matter than a non-smoker living in a smoke-free home.

Semple said that isn’t much, but this amount is likely to "have a substantial effect on the risk of developing diseases of the cardiovascular and respiratory systems.”

Semple said smokers often express the view that outdoor traffic pollution is a bigger problem than second-hand smoke pollution in the home.

“What this work shows is that, for most people living outside of major heavily polluted mega-cities like Beijing or Delhi, outdoor air pollution is much, much lower than what is measured inside homes where someone smokes,” he said.

“We have a lot of data and it’s an established fact how bad secondhand smoke is,” said Lucy Popova, from the Center for Tobacco Control Research and Education at the University of California, San Francisco. “There’s no safe level of exposure to it.”

“Smoke-free rules help not only by reducing the particulate matters for non-smokers but it actually helps smokers to quit too,” said Popova, who was not involved in the Scottish study.

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“Research shows when you have smoke-free rules in your home, that motivates smokers to make more cessation attempts and decrease the number of cigarettes that they smoke.”

Source: Fox News

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Study sheds light on asthma and respiratory viruses

Researchers try to find out why people with asthma have
more difficulty when contracting a respiratory virus.

People with asthma often have a hard time dealing with respiratory viruses such as the flu or the common cold, and researchers have struggled to explain why.

In a new study that compared people with and without asthma, the answer is becoming clearer. The researchers found no difference in the key immune response to viruses in the lungs and breathing passages.

The work, at Washington University School of Medicine in St. Louis, suggests that a fundamental antiviral defense mechanism is intact in asthma.

This means that another aspect of the immune system must explain the difficulty people with asthma have when they encounter respiratory viruses.

Among researchers who study asthma, there is debate over why patients with this common breathing disorder might have more trouble dealing with airway viruses than people without asthma.

The debate has centered on the role of proteins called interferons, which are released by cells lining the airways and are so named because they "interfere" with an invading virus.

"One school of thought says there is a defect in interferon production — that patients with asthma don't produce enough interferon," said senior author Michael J. Holtzman, MD, the Selma and Herman Seldin Professor of Medicine. "But we couldn't find any significant differences between the two groups. In fact, we were struck by how similar they were."

Holtzman and his colleagues looked at two common airway viruses — influenza A and respiratory syncytial virus (RSV) — and the interferon response they triggered in airway cells sampled from 11 patients with mild to severe asthma and seven control participants without asthma.

Though the study's sample size was small, the researchers performed an elaborate analysis that took into consideration the downstream events triggered by interferon release.

"Even though we showed both groups made similar amounts of interferon, we recognized that there might be a difference in effectiveness, a difference in how well it triggered downstream events necessary to fighting the virus," Holtzman said.

To find out whether the same amount of interferon might be less effective in patients with asthma, the investigators compared the genes activated by interferon in both groups of patients.

"The products of these genes are very effective in their antiviral action," Holtzman said. "But on the other side, the virus has a lot of ways of getting around them. So it's a battlefield. Who will win out? The interferon-stimulated genes or the viral genes?"

Holtzman and his colleagues showed that even in this downstream activation of genes, asthma patients and those without the condition were remarkably similar.

They also measured similar amounts of virus living in the cells at various points of time during the study, indicating that the battles against the viruses progressed similarly in both groups.

"Whatever is causing asthmatics and non-asthmatics to experience differences in how well they recover from these respiratory infections — why patients with asthma are more likely to end up in the hospital, for example — this interferon mechanism is not the deciding factor based on what we've seen so far," Holtzman said.

Given the complexity of the immune system, there are many other possible culprits to investigate. Holtzman and his colleagues are continuing to research these possibilities in similar studies with larger sample sizes and in studies looking at different aspects of the immune system.

One likely possibility that the group has proposed is that viruses have a special means to induce inflammatory airway disease, and the susceptibility to this process may be an essential feature of asthma and related lung diseases such as chronic obstructive pulmonary disease.

_________________________________________________________________________

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Greenest neighbourhoods produce bigger babies

Expecting mothers with access to trees and
grass delivered heavier babies: Study

Mothers who live in Metro Vancouver’s greenest neighbourhoods tend to deliver bigger babies and are more likely carry a baby to term than those who live in less green parts of the city, according to a new study published in the journal Environmental Health Perspectives.

Using data from more than 64,000 births and analysis of satellite imagery, researchers found that babies from the greenest residential spaces ­­— those with access to trees and grass within 100 metres — were up to 45 grams heavier, had a reduced likelihood of preterm birth and were less likely to be small for gestational age, according to the lead researcher Michael Brauer, a professor in the School of Population and Public Health at the University of British Columbia.

The positive effects of greenness persist even when the researchers control for other factors known to influence gestation and birth weight, including air pollution, noise, income, access to parks, opportunities for physical activity and the walkability of the immediate neighbourhood.

“We know from other studies that birth outcomes are influenced by pollution and noise in a negative way, so we went looking for something (in the urban environment) that is healthy,” said Brauer.

Cities in most of the developed world are designed to accommodate the automobile, which usually results in relatively barren, noisy and polluted environments. Brauer’s study seeks to quantify the benefits of a different approach to urban planning.

“If we didn’t design for automobiles and instead designed for people, the hope is that we would be healthier,” he said. “With the high cost of health care, modifying urban design features such as increasing green space may turn out to be an extremely cost-effective strategy to prevent disease.”

While 45 grams isn’t a lot of extra weight for one healthy infant, the effect of increased birth weight across the entire distribution of births moves thousands of babies from birth weights that are dangerously low into a healthier range.

“From a medical standpoint, those are small changes in birth weight, but across a large population, those are substantial differences that would have a significant impact on the health of infants in a community,” said co-author Perry Hystad, assistant professor in the College of Public Health and Human Sciences at Oregon State University.

Even in an urban area as rich in green space as Metro Vancouver the benefits conferred by the very greenest neighbourhoods compared with the least green neighbourhoods were substantial, including a 20-per-cent reduction in severely premature births and 13 per cent fewer moderately pre-term births.

The mechanism by which greenness translates into healthier babies is not exactly clear, but greener environments are known to facilitate social connectedness and reduce blood pressure, heart rate and stress-related hormones, according to the study, the third in a series of similar inquiries on the health impacts of urban spaces.

“Even when we eliminate the noise and the pollution and (a measure) of physical activity, we still see this benefit of green space,” he said. “What we don’t know is whether it is enough to see a tree out your window or do you have to have a park across the street where you chat with your neighbours.”

Source: Vancouver Sun

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Air pollution actually beat first explorers to the South Pole

Roald Amundsen/ public domain

Norwegian explorer Roald Amundsen became the first man to reach the South Pole in December 1911, but scientists say industrial air pollution beat him to it.

"Our new record shows the dramatic impact of industrial activities such as smelting, mining and fossil fuel burning on even the most remote parts of the world," said Joe McConnell of the Desert Research Institute (DRI) in Reno, Nevada.

Using data from 16 ice cores collected from widely spaced locations around the Antarctic continent, including the South Pole, a group led by McConnell, created the most accurate and precise reconstruction to date of lead pollution over Earth’s southernmost continent.

"It is very clear that industrial lead contamination was pervasive throughout Antarctica by the late 19th century, more than two decades before the first explorers made it to the South Pole," he added. "The idea that Amundsen and Scott were traveling over snow that clearly was contaminated by lead from smelting and mining in Australia, and that lead pollution at that time was nearly as high as any time ever since, is surprising to say the least."
This study included ice cores collected as part of projects funded by the National Science Foundation. Additional ice cores were contributed to the study by international collaborators including the British Antarctic Survey, the Australian Antarctic Division and the Alfred Wegener Institute in Germany.

"The ice cores obtained through international collaborations were critical to the success of this study in that they allowed us to develop records from parts of Antarctica not often visited by U.S.-based scientists," said co-author Tom Neumann of NASA’s Goddard Space Flight Center in Greenbelt, Maryland, who participated in a Norway-U.S. traverse that collected several of the cores used in this study. "This included the Law Dome region of East Antarctica and a big section of East Antarctica visited by the Norwegian-United States Scientific Traverse of East Antarctica."

"Lead is a toxic heavy metal with strong potential to harm ecosystems," said co-author Paul Vallelonga of the University of Copenhagen. "While concentrations measured in Antarctic ice cores are very low, the records show that atmospheric concentrations and deposition rates increased approximately six-fold in the late 1880s, coincident with the start of mining at Broken Hill in southern Australia and smelting at nearby Port Pirie."

Data from the new ice core array illustrates that Antarctic lead concentrations reached a peak in 1900 and remained high until the late 1920s, with brief declines during the Great Depression and the end of World War II. Concentrations then increased rapidly until 1975 and remained elevated until the 1990s.
 "Our measurements indicate that approximately 660 tonnes [1.5 million pounds] of industrial lead have been deposited on the snow-covered surface of Antarctic during the past 130 years," McConnell said. "While recent contamination levels are lower, clearly detectable industrial contamination of the Antarctic continent persists today, so we still have a ways to go."

The report is published in the online edition of the Nature Publishing Group’s journal Scientific Reports.

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Common chemical in mothers may negatively affect the IQ of their unborn children

In some women abnormally high levels of a common and pervasive chemical may lead to adverse effects in their offspring. The study, published recently in the Journal of Clinical Endocrinology and Metabolism, is the first of its kind to shed light on the possible harmful side effects of perchlorate in mothers and their children.

"The reason people really care about perchlorate is because it is ubiquitous. It's everywhere," said Elizabeth Pearce, MD, MSc, associate professor of medicine at the Boston University School of Medicine (BUSM). "Prior studies have already shown perchlorate, at low levels, can be found in each and every one of us."

Using data from the Controlled Antenatal Thyroid Study (CATS), researchers at Boston University School of Medicine (BUSM) and Cardiff University studied the effect of perchlorate, an environmental contaminant found in many foods and in some drinking water supplies, and its effects on children born to mothers with above average levels of this substance in their system. They studied 487 mother-child pairs from women with underactive thyroid glands and in the 50 women with the highest levels of perchlorate in their body, their offspring had below average IQ levels when compared to other children.

Perchlorate is a compound known to affect the thyroid gland, an organ needed to help regulate hormone levels in humans. According to Pearce, previous studies have attempted to implicate this anti-thyroid activity in pregnant mothers as a possible cause of hypothyroidism, or an underactive thyroid gland. Hypothyroidism in newborns and children can lead to an array of unwelcome side effects, including below average intelligence.

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Air pollution and climate change will curb world food supplies

Howden/freedigitalphotos

Researchers at MIT say that the double-whammy of air pollution and rising world temperatures could affect our most important food sources.

The study looked in detail at global production of four leading food crops — rice, wheat, corn, and soy — that account for more than half the calories humans consume worldwide. It predicts that effects will vary considerably from region to region, and that some of the crops are much more strongly affected by one or the other of the factors: For example, wheat is very sensitive to ozone exposure from air pollution, while corn is much more adversely affected by heat.

The research was carried out by Colette Heald, an associate professor of civil and environmental engineering (CEE) at MIT, former CEE postdoc Amos Tai, and Maria van Martin at Colorado State University. Their work is described this week in the journal Nature Climate Change.

Heald explains that while it's known that both higher temperatures and ozone pollution can damage plants and reduce crop yields, "nobody has looked at these together." And while rising temperatures are widely discussed, the impact of air quality on crops is less recognized.

In the United States, tougher air-quality regulations are expected to lead to a sharp decline in ozone pollution, mitigating its impact on crops. But in other regions, the outcome "will depend on domestic air-pollution policies," Heald says. "An air-quality cleanup would improve crop yields."

Overall, with all other factors being equal, warming may reduce crop yields globally by about 10 percent by 2050, the study found. But the effects of ozone pollution are more complex — some crops are more strongly affected by it than others — which suggests that pollution-control measures could play a major role in determining outcomes.

Ozone pollution can also be tricky to identify, Heald says, because its damage can resemble other plant illnesses, producing flecks on leaves and discoloration.

Potential reductions in crop yields are worrisome: The world is expected to need about 50 percent more food by 2050, the authors say, due to population growth and changing dietary trends in the developing world.

While heat and ozone can each damage plants independently, the factors also interact. For example, warmer temperatures significantly increase production of ozone from the reactions, in sunlight, of volatile organic compounds and nitrogen oxides. Because of these interactions, the team found that 46 percent of damage to soybean crops that had previously been attributed to heat is actually caused by increased ozone.

Under some scenarios, the researchers found that pollution-control measures could make a major dent in the expected crop reductions following climate change. For example, while global food production was projected to fall by 15 percent under one scenario, larger emissions decreases projected in an alternate scenario reduce that drop to 9 percent.

Air pollution is even more decisive in shaping undernourishment in the developing world, the researchers found: Under the more pessimistic air-quality scenario, rates of malnourishment might increase from 18 to 27 percent by 2050 — about a 50 percent jump; under the more optimistic scenario, the rate would still increase, but that increase would almost be cut in half, they found.

Agricultural production is "very sensitive to ozone pollution," Heald says, adding that these findings "show how important it is to think about the agricultural implications of air-quality regulations. Ozone is something that we understand the causes of, and the steps that need to be taken to improve air quality."

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Asthma drugs suppress children's growth say researchers

Corticosteroid drugs that are given by inhalers to children with asthma may suppress their growth, evidence suggests.

Two new systematic reviews published in The Cochrane Library focus on the effects of inhaled corticosteroid drugs (ICS) on growth rates.

The authors found children’s growth slowed in the first year of treatment, although the effects were minimized by using lower doses.

Inhaled corticosteroids are prescribed as first-line treatments for adults and children with persistent asthma.

They are the most effective drugs for controlling asthma and clearly reduce asthma deaths, hospital visits and the number and severity of exacerbations, and improve quality of life.

Yet, their potential effect on the growth of children is a source of worry for parents and doctors.

Worldwide, seven ICS drugs are currently available: beclomethasone, budesonide, ciclesonide, flunisolide, fluticasone, mometasone and triamcinolone.

Ciclesonide, fluticasone and mometasone are newer and supposedly safer drugs.

The first systematic review focused on 25 trials involving 8,471 children up to 18 years old with mild to moderate persistent asthma.

These trials tested all available inhaled corticosteroids except triamcinolone and showed that, as a group, they suppressed growth rates when compared to placebos or non-steroidal drugs. 14 of the trials, involving 5,717 children, reported growth over a year.

The average growth rate, which was around 6-9 cm per year in control groups, was reduced by about 0.5 cm in treatment groups.

The researchers found that growth suppression varied across studies, and so they looked at the relationship between a variety of factors and their effects on growth. Some of the variation could be explained by the drugs used, although since this was an indirect comparison the authors say more evidence is needed.

“Conclusions about the superiority of one drug over another should be confirmed by further trials that directly compare the drugs,” said Zhang.

More long-term trials and trials comparing different doses are also needed, particularly in children with more severe asthma requiring higher doses of inhaled corticosteroids, the researchers conclude.

“Only 14% of the trials we looked at monitored growth in a systematic way for over a year. This is a matter of major concern given the importance of this topic,” said Francine Ducharme, one of the authors of both reviews and senior author of the second review, based at the Department of Paediatrics at the University of Montreal in Montreal, Canada.

“We recommend that the minimal effective dose be used in children with asthma until further data on doses becomes available. Growth should be carefully documented in all children treated with inhaled corticosteroids, as well in all future trials testing inhaled corticosteroids in children.”

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Air Quality Alert: High health risk for Canada's Northern Territories

Environment Canada has issued a high health risk warning for Yellowknife and surrounding area because of heavy smoke in the region due to forest fires. Currently 160 wildfires are burning across the region. 
 
This satellite image was collected by the Moderate Resolution Imaging Spectroradiometer (MODIS) aboard the Aqua satellite on July 20, 2014. Actively burning areas, detected by MODIS’s thermal bands, are outlined in red.

Fire danger in this area remains very high to extreme, with no discernible change in that forecast in the near future.

Source:: NASA/Goddard, Lynn Jenner with information from Canada's National Wildland Fire Situation site.

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What's third-hand smoke? Researchers say it's far more dangerous than we ever realized.

"The results indicate potentially severe, long-term consequences, particularly to children."

Have you ever walked out of a building and smelled smoke even after the smoker has moved on? Or maybe caught a whiff on someone's clothes long after their cigarette has been extinguished? That's what scientists have termed - third hand smoke, and its effects may have been greatly underestimated.

Research led by the University of York has highlighted the potential cancer risk in non-smokers – particularly young children – of tobacco smoke gases and particles deposited to surfaces and in household dust.

Until now, the risks of this kind of exposure have not been well studied or considered in public policy.

However, a new study published in the journal Environment International, has estimated for the first time the potential cancer risk by age group through non-dietary ingestion and skin exposure to third hand smoke. The results indicate potentially severe, long-term consequences, particularly to children.

The research was carried out by York’s Wolfson Atmospheric Chemistry Laboratories, the National Centre for Atmospheric Science, and the Chromatography and Environmental Applications research group at the Universitat Rovira i Virgili, Spain.

The study demonstrates for the first time the widespread presence of tobacco related carcinogens in house dust, even in ‘smoke-free’ environments.

Scientists collected dust samples from private homes occupied by both smokers and non-smokers. Using observations of house dust composition, they estimated the cancer risk by applying the most recent official toxicology information.

They found that for children aged one to six years old, the cancer risks exceeded the limit recommended by the US Environmental Protection Agency (EPA) in three quarters of smokers’ homes and two thirds of non-smokers’ homes. The maximum risk predicted from the third hand smoke levels in a smoker occupied home equated to one extra cancer case per one thousand population exposed.

Lead investigator, Dr Jacqueline Hamilton, from York’s Wolfson Atmospheric Chemistry Laboratories, said: “The risks of tobacco exposure do not end when a cigarette is extinguished. Non-smokers, especially children, are also at risk through contact with surfaces and dust contaminated with residual smoke gases and particles, the so-called third hand smoke. This risk should not be overlooked and its impact should be included in future educational programs and tobacco-related public health policies.”

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Gene discovered that could stop the spread of a common type of lung cancer

Scientists at the Salk Institute have identified a gene responsible for stopping the movement of cancer from the lungs to other parts of the body, indicating a new way to fight one of the world’s deadliest cancers.

By identifying the cause of this metastasis—which often happens quickly in lung cancer and results in a bleak survival rate—scientists are able to explain why some tumors are more prone to spreading than others. The newly discovered pathway, detailed in Molecular Cell, may also help researchers understand and treat the spread of melanoma and cervical cancers.

“Lung cancer, even when it’s discovered early, is often able to metastasize almost immediately and take hold throughout the body,” says Reuben J. Shaw, professor of molecular and cell biology and a Howard Hughes Medical Institute. “The reason behind why some tumors do that and others don’t has not been very well understood. Now, through this work, we are beginning to understand why some subsets of lung cancer are so invasive.”

Lung cancer, which also affects nonsmokers, is the leading cause of cancer-related deaths in the country (estimated to be nearly 160,000 this year). The United States spends more than $12 billion on lung cancer treatments, according to the National Cancer Institute. Nevertheless, the survival rate for lung cancer is dismal: 80 percent of patients die within five years of diagnosis largely due to the disease’s aggressive tendency to spread throughout the body.

Deviously, cancer can switch on and off their "molecular anchors" protruding from the cell membrane , preparing the cell for migration. This allows cancer cells to begin the processes to move through the bloodstream and take up residence in new organs.

In addition to different cancers being able to manipulate these anchors, it was also known that about a fifth of lung cancer cases are missing an anti-cancer gene called LKB1 (also known as STK11). Cancers missing LKB1 are often aggressive, rapidly spreading through the body. However, no one knew how LKB1 and focal adhesions were connected.

Now, the Salk team has found the connection and a new target for therapy: a little-known gene called DIXDC1. The researchers discovered that DIXDC1 receives instructions from LKB1 to go to focal adhesions and change their size and number.

When DIXDC1 is “turned on,” half a dozen or so focal adhesions grow large and sticky, anchoring cells to their spot. When DIXDC1 is blocked or inactivated, focal adhesions become small and numerous, resulting in hundreds of small “hands” that pull the cell forward in response to extracellular cues. That increased tendency to be mobile aids in the escape from, for example, the lungs and allows tumor cells to survive travel through the bloodstream and dock at organs throughout the body.

“The communication between LKB1 and DIXDC1 is responsible for a ‘stay-put’ signal in cells,” says first author and Ph.D. graduate student Jonathan Goodwin. “DIXDC1, which no one knew much about, turns out to be inhibited in cancer and metastasis.”

Tumors, Shaw and collaborators found in the new research, have two ways to turn off this “stay-put” signal. One is by inhibiting DIXDC1 directly. The other way is by deleting LKB1, which then never sends the signal to DIXDC1 to move to the focal adhesions to anchor the cell. Given this, the scientists wondered if reactivating DIXDC1 could halt a cancer’s metastasis. The team took metastatic cells, which had low levels of DIXDC1, and overexpressed the gene. The addition of DIXDC1 did indeed blunt the ability of these cells to be metastatic in vitro and in vivo.

“It was very, very surprising that this gene would be so powerful,” says Goodwin. “At the start of this study, we had no idea DIXDC1 would be involved in metastasis. There are dozens of proteins that LKB1 affects; for a single one to control so much of this phenotype was not expected.”

Right now, there is no specific treatment for cancers harboring LKB1 or DIXDC1 alterations, but those with a deletion of either gene would likely see results from cancer drugs that target the focal adhesions, says Shaw.

“The good news is that this finding predicts that patients missing either gene should be sensitive to new therapies targeting focal adhesion enzymes, which are currently being tested in early-stage clinical trials,” says Shaw, who is also a member of the Moores Cancer Center and an adjunct professor at the University of California, San Diego.

“By identifying this unexpected connection between DIXDC1 and LKB1 in certain tumors, we have expanded the potential patient population that may be good candidates for these therapies,” adds Goodwin.

Source: Press Release

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