Scientists at
Washington University School of Medicine in St. Louis have discovered a molecule involved in asthma and allergies that seems to make mice resistant to skin cancer.
The molecule, called TSLP (thymic stromal lymphopoietin), is produced
by damaged skin and activates the immune system. Chronic low levels of
TSLP are suspected in making the immune system oversensitive to what
should be a harmless environment, leading to the skin rashes and
overproduction of mucus common in allergies and asthma.
“But at extremely high levels, TSLP appears to train the immune
system to recognize skin cancer cells, and target those cells for
elimination,” says Raphael Kopan, PhD, the Alan A. and Edith L. Wolff
Professor of Developmental Biology. “These experiments demonstrate that
there is a way for a natural molecule to help immune cells recognize and
reject tumors, at least in the skin.”
The study appears online Oct 15 in Cancer Cell.
These findings are surprising because most current evidence suggests
that the allergic inflammation and release of TSLP increases — not
decreases — the risk of tumor development.
The disparity may be explained by the amount of TSLP that is
produced. The mice that were resistant to skin tumor growth had blood
levels of TSLP that were 1,000-fold higher than normal. And levels in
the skin — where it is made — may be even higher.
“This is an example of where hyper-vigilance of the immune system may
end up paying dividends,” Kopan says. “Not only does it respond
aggressively to an innocuous allergen, but it begins to monitor, survey
and destroy cells that are mutant.”
The results are supported by another study in the same issue of Cancer Cell also showing TSLP prevents skin cancer in mice.
Helping you breathe easier. Learn about air quality & air purification, chemical exposure and the pollutants that aggravate asthma, allergy and COPD.
Tuesday, October 16, 2012
Monday, October 15, 2012
Genetic error linked to rare disease that causes chronic respiratory infections
Scanning the DNA of two people with a rare disease has led scientists to
identify the precise genetic error responsible for their disorder, primary
ciliary dyskinesia.
The condition affects the tiny hair-like structures, called cilia, that extend from various cells in the body, and causes a range of symptoms: persistent lung, sinus and ear infections, male infertility, and sometimes a reversed orientation of major organs in the body.
The new discovery, by a team at Washington University School of Medicine in St. Louis, is reported online in the American Journal of Human Genetics.
The research highlights the potential for using DNA sequencing technology to quickly identify genes responsible for rare diseases, an approach that likely will improve diagnosis.
“Primary ciliary dyskinesia is difficult to diagnose,” says senior author Thomas Ferkol, MD, director of the division of allergy, immunology and pulmonary medicine and a pediatric specialist at St. Louis Children’s Hospital. “Because it is inherited, we should be able to diagnose the disease using genetic tests, so we can identify and treat affected children earlier and hopefully avoid the most severe chronic infections.”
The researchers found the error in a gene, HEATR2, which had never been linked to primary ciliary dyskinesia or to cilia. It brings the number of genes associated with the disorder to 15, but they are still thought to account for fewer than half of all cases of the disorder.
Ferkol, along with first author Amjad Horani, MD, a fellow in pediatric pulmonology, identified the mutation by sequencing the genes from two people with primary ciliary dyskinesia and, as a comparison, the genes from both sets of their parents, who did not have the disease. The family members came from two related Amish families that now live in Missouri, Arkansas and Wisconsin. Nine of them have the disorder, and the researchers can now attribute their cases to the HEATR2 mutation.
About 1 in every 20,000 babies is born with primary ciliary dyskinesia. Because the disease is rare and symptoms like chronic respiratory and sinus infections don’t always raise a red flag, making a diagnosis can be difficult.
Typically, newborns with the disorder have respiratory distress shortly after birth and may need the help of a ventilator to breathe. As they grow, the children develop persistent cough. Runny or stuffy noses and respiratory infections are common year round.
The wide-ranging symptoms can be traced to defects in cilia that sit atop cells lining the respiratory tract, from the nose to the airsacs of the lungs. Cilia normally beat rapidly – roughly 10 times a second – to clear inhaled pollutants and bacteria from the lungs, nose and middle ear.
Early in development, cilia also move fluid across the embryo’s surface and detect signals that indicate where the heart, lungs, spleen and other internal organs should be placed. Sperm sport similar structures, called flagella, that propels their movement.
But in patients with primary ciliary dyskinesia, the cilia don’t beat effectively if at all. In many patients, the cilia clearly look defective under an electron microscope. However, cilia can appear normal in some patients. The newly identified mutation in HEATR2 changes the structure of cilia and affects the microscopic motors that power them to beat.
“In these patients, the cilia motors are not assembled properly, and they just sputter,” Ferkol says. “Without the motor, cilia don’t beat.”
In the lab, the researchers confirmed their discovery by silencing the HEATR2 gene in normal, healthy cells that line the respiratory tract and in a simple model system, a single-celled green algae called Chlamydomonas. This caused the same defect in the motors that the scientists observed in the family members with primary ciliary dyskinesia.
While the new discovery will help scientists unravel the disparate genetic origins of primary ciliary dyskinesia, it also could help them identify biological similarities between this rare disease and more common ailments.
“Many young children without primary ciliary dyskinesia experience chronic or repeated sinus or ear infections,” Ferkol explains. “It is possible that a more subtle error in one or more genes linked to this rare disorder may be at the root of these common conditions.”
The research is an unusual collaboration that brought together Washington University physicians and scientists in diverse fields. Ferkol and Horani, both pediatric pulmonologists, teamed with Steven Brody, MD, a specialist in pulmonary medicine, Susan Dutcher, PhD, a geneticist who studies green algae, and Philip Bayly, PhD, an engineer who investigates the mechanics of beating cilia. Funding for the project came from the National Institutes of Health (NIH) and the Children’s Discovery Institute, a partnership between St. Louis Children’s Hospital and Washington University School of Medicine.
“Ultimately, we want to identify all the mutations responsible for primary ciliary dyskinesia,” Ferkol says. “In our dreams, we hope that one day we can correct ciliary defects that lead to respiratory disease. But in the short term, a more complete understanding of the genetics of primary ciliary dyskinesia will be a huge step forward toward improving diagnosis and allow us to better connect particular mutations with specific symptoms.”
The condition affects the tiny hair-like structures, called cilia, that extend from various cells in the body, and causes a range of symptoms: persistent lung, sinus and ear infections, male infertility, and sometimes a reversed orientation of major organs in the body.
The new discovery, by a team at Washington University School of Medicine in St. Louis, is reported online in the American Journal of Human Genetics.
The research highlights the potential for using DNA sequencing technology to quickly identify genes responsible for rare diseases, an approach that likely will improve diagnosis.
“Primary ciliary dyskinesia is difficult to diagnose,” says senior author Thomas Ferkol, MD, director of the division of allergy, immunology and pulmonary medicine and a pediatric specialist at St. Louis Children’s Hospital. “Because it is inherited, we should be able to diagnose the disease using genetic tests, so we can identify and treat affected children earlier and hopefully avoid the most severe chronic infections.”
The researchers found the error in a gene, HEATR2, which had never been linked to primary ciliary dyskinesia or to cilia. It brings the number of genes associated with the disorder to 15, but they are still thought to account for fewer than half of all cases of the disorder.
Ferkol, along with first author Amjad Horani, MD, a fellow in pediatric pulmonology, identified the mutation by sequencing the genes from two people with primary ciliary dyskinesia and, as a comparison, the genes from both sets of their parents, who did not have the disease. The family members came from two related Amish families that now live in Missouri, Arkansas and Wisconsin. Nine of them have the disorder, and the researchers can now attribute their cases to the HEATR2 mutation.
About 1 in every 20,000 babies is born with primary ciliary dyskinesia. Because the disease is rare and symptoms like chronic respiratory and sinus infections don’t always raise a red flag, making a diagnosis can be difficult.
Typically, newborns with the disorder have respiratory distress shortly after birth and may need the help of a ventilator to breathe. As they grow, the children develop persistent cough. Runny or stuffy noses and respiratory infections are common year round.
The wide-ranging symptoms can be traced to defects in cilia that sit atop cells lining the respiratory tract, from the nose to the airsacs of the lungs. Cilia normally beat rapidly – roughly 10 times a second – to clear inhaled pollutants and bacteria from the lungs, nose and middle ear.
Early in development, cilia also move fluid across the embryo’s surface and detect signals that indicate where the heart, lungs, spleen and other internal organs should be placed. Sperm sport similar structures, called flagella, that propels their movement.
But in patients with primary ciliary dyskinesia, the cilia don’t beat effectively if at all. In many patients, the cilia clearly look defective under an electron microscope. However, cilia can appear normal in some patients. The newly identified mutation in HEATR2 changes the structure of cilia and affects the microscopic motors that power them to beat.
“In these patients, the cilia motors are not assembled properly, and they just sputter,” Ferkol says. “Without the motor, cilia don’t beat.”
In the lab, the researchers confirmed their discovery by silencing the HEATR2 gene in normal, healthy cells that line the respiratory tract and in a simple model system, a single-celled green algae called Chlamydomonas. This caused the same defect in the motors that the scientists observed in the family members with primary ciliary dyskinesia.
While the new discovery will help scientists unravel the disparate genetic origins of primary ciliary dyskinesia, it also could help them identify biological similarities between this rare disease and more common ailments.
“Many young children without primary ciliary dyskinesia experience chronic or repeated sinus or ear infections,” Ferkol explains. “It is possible that a more subtle error in one or more genes linked to this rare disorder may be at the root of these common conditions.”
The research is an unusual collaboration that brought together Washington University physicians and scientists in diverse fields. Ferkol and Horani, both pediatric pulmonologists, teamed with Steven Brody, MD, a specialist in pulmonary medicine, Susan Dutcher, PhD, a geneticist who studies green algae, and Philip Bayly, PhD, an engineer who investigates the mechanics of beating cilia. Funding for the project came from the National Institutes of Health (NIH) and the Children’s Discovery Institute, a partnership between St. Louis Children’s Hospital and Washington University School of Medicine.
“Ultimately, we want to identify all the mutations responsible for primary ciliary dyskinesia,” Ferkol says. “In our dreams, we hope that one day we can correct ciliary defects that lead to respiratory disease. But in the short term, a more complete understanding of the genetics of primary ciliary dyskinesia will be a huge step forward toward improving diagnosis and allow us to better connect particular mutations with specific symptoms.”
Friday, October 12, 2012
Can your taste buds determine your ability to fight off chronic sinusitis and other upper respiratory ailments?
A new study has revealed that a person’s ability to taste certain bitter flavors is directly related
to their ability to fight off upper respiratory tract infections,
specifically chronic sinus infections.
Most humans experience five types of tastes: sweet, salty, sour, bitter, and savory. The sense of taste is mediated by taste receptor cells which are bundled in our taste buds. “Sour” and “bitter” taste sensations alert the body to harmful foods that have spoiled or are toxic. But based on genetics, up to 25 percent of the population cannot detect certain bitter flavors (non-tasters), 25 percent can detect exceedingly small quantities (super-tasters), and the rest of us fall somewhere between these two extremes.
Recent investigations have shown that these taste receptors (T2Rs) are also found in both upper and lower human respiratory tissue, likely signaling a connection between activation of bitter tastes and the need to launch an immune response in these areas when they are exposed to potentially harmful bacteria and viruses.
“With this information in mind, we wanted to better understand the exact role that bitter taste receptors play in the upper airway, especially between these super and non-tasters,” says Noam Cohen, MD, PhD, assistant professor of Otorhinolaryngology: Head and Neck Surgery, staff physician at the Philadelphia VAMC, and senior author of the new study.
Cohen and his colleagues formulated the following hypotheses around the connection: (1) bitter taste receptors are functional in the nose (upper respiratory tract), and each receptor detects a specific type of bacteria; (2) upon activation by a specific bacterial product, the bitter taste receptor initiates a local defensive response to combat the attacking bacteria; and (3) genetic variability of the bitter taste receptors alters the vigorousness of the response, thus leaving certain individuals with very strong defenses and others with weak defenses against a specific bacteria.
To test these hypotheses, the team grew cell cultures from sinus and nasal tissue samples collected during sinus surgical procedures. These cultures develop cilia, produce mucus, and reflect many of the defensive workings found inside the nose and sinuses.
They found that one of the bitter taste receptors that functions in upper airway cells, known as T2R38, acts as a type of “security guard” for the upper airway by detecting molecules that a certain class of bacteria secretes. “These molecules instruct other bacteria to form a biofilm, which helps harbor the bacteria. From previous work, we know that these biofilms spur the immune system to mount an over-exuberant inflammatory response that can lead to sinusitis symptoms. When the T2R38 receptor detects these molecules, it activates local defensive maneuvers to increase mucus clearance and kill the invading bacteria. It’s really like modern warfare – intercept the enemies’ early communications to thwart their plans and win the battle,” Cohen said, who is also the director of the Rhinology Research Lab at Penn.
Through the cultures, the research team demonstrated that super-tasters detect very small concentrations of the offending molecules, while non-tasters and the middle-ground individuals require 100 times more of the molecule for detection. The research team also examined the patients that the original sinus tissue samples were collected from. They found that none of the super tasters were infected with the specific type of bacteria that are detected by the T2R38 receptor, known as a gram-negative bacteria.
“Based on these findings, we believe that other bitter taste receptors in the airway perform the same “guard duty” function for early detection of attack by different types of bacteria, and we hope to translate these findings into personalized diagnostics for patients with chronic rhinosinusitis,” Cohen says.
The research team is also using the results of the current study to develop a simple “taste-test” protocol to be conducted during clinic visits. “We’re optimistic that a test of this nature will help us predict who is at risk to develop biofilms based on their ability to taste various bitter compounds. Additionally, we are looking at therapeutic outcomes, both surgical and medical, based on the taster/non-taster genetic status to determine whether knowing this status will stratify patients to either surgical or medical interventions.”
The new research is published in the latest edition of the Journal of Clinical Investigation.
Most humans experience five types of tastes: sweet, salty, sour, bitter, and savory. The sense of taste is mediated by taste receptor cells which are bundled in our taste buds. “Sour” and “bitter” taste sensations alert the body to harmful foods that have spoiled or are toxic. But based on genetics, up to 25 percent of the population cannot detect certain bitter flavors (non-tasters), 25 percent can detect exceedingly small quantities (super-tasters), and the rest of us fall somewhere between these two extremes.
Recent investigations have shown that these taste receptors (T2Rs) are also found in both upper and lower human respiratory tissue, likely signaling a connection between activation of bitter tastes and the need to launch an immune response in these areas when they are exposed to potentially harmful bacteria and viruses.
“With this information in mind, we wanted to better understand the exact role that bitter taste receptors play in the upper airway, especially between these super and non-tasters,” says Noam Cohen, MD, PhD, assistant professor of Otorhinolaryngology: Head and Neck Surgery, staff physician at the Philadelphia VAMC, and senior author of the new study.
Cohen and his colleagues formulated the following hypotheses around the connection: (1) bitter taste receptors are functional in the nose (upper respiratory tract), and each receptor detects a specific type of bacteria; (2) upon activation by a specific bacterial product, the bitter taste receptor initiates a local defensive response to combat the attacking bacteria; and (3) genetic variability of the bitter taste receptors alters the vigorousness of the response, thus leaving certain individuals with very strong defenses and others with weak defenses against a specific bacteria.
To test these hypotheses, the team grew cell cultures from sinus and nasal tissue samples collected during sinus surgical procedures. These cultures develop cilia, produce mucus, and reflect many of the defensive workings found inside the nose and sinuses.
They found that one of the bitter taste receptors that functions in upper airway cells, known as T2R38, acts as a type of “security guard” for the upper airway by detecting molecules that a certain class of bacteria secretes. “These molecules instruct other bacteria to form a biofilm, which helps harbor the bacteria. From previous work, we know that these biofilms spur the immune system to mount an over-exuberant inflammatory response that can lead to sinusitis symptoms. When the T2R38 receptor detects these molecules, it activates local defensive maneuvers to increase mucus clearance and kill the invading bacteria. It’s really like modern warfare – intercept the enemies’ early communications to thwart their plans and win the battle,” Cohen said, who is also the director of the Rhinology Research Lab at Penn.
Through the cultures, the research team demonstrated that super-tasters detect very small concentrations of the offending molecules, while non-tasters and the middle-ground individuals require 100 times more of the molecule for detection. The research team also examined the patients that the original sinus tissue samples were collected from. They found that none of the super tasters were infected with the specific type of bacteria that are detected by the T2R38 receptor, known as a gram-negative bacteria.
“Based on these findings, we believe that other bitter taste receptors in the airway perform the same “guard duty” function for early detection of attack by different types of bacteria, and we hope to translate these findings into personalized diagnostics for patients with chronic rhinosinusitis,” Cohen says.
The research team is also using the results of the current study to develop a simple “taste-test” protocol to be conducted during clinic visits. “We’re optimistic that a test of this nature will help us predict who is at risk to develop biofilms based on their ability to taste various bitter compounds. Additionally, we are looking at therapeutic outcomes, both surgical and medical, based on the taster/non-taster genetic status to determine whether knowing this status will stratify patients to either surgical or medical interventions.”
The new research is published in the latest edition of the Journal of Clinical Investigation.
Thursday, October 11, 2012
Pesticides a key contributor to childhood diseases and disorders
Learning disabilities, childhood cancer and asthma are on the rise in the United States. And a new report points to pesticides – with over 1 billion pounds applied on farms and homes annually – as a critical contributor to these health harms in children.
"Protecting our children from harm is the fundamental duty of parenthood, but how can we do this when developmental toxicants are allowed to freely circulate in our economy?" says Sandra Steingraber, ecologist and acclaimed author. "PAN's report shines a light on a completely preventable tragedy - that an entire generation of children will not reach its full potential. As such, it describes a violation of human rights and a crisis of family life both. For the healthy development of children to become a national priority, we parents must walk ourselves into the political arena and, waving this good report, speak truth to power."
In particular, the report points to the fact that children are sicker today than a generation ago, confronting serious health challenges from pesticides and other chemical exposures that their parents and grandparents were unlikely to face.
Health professionals, mothers and rural leaders across the country released the new report, which draws from academic and government research, to chronicle the emerging threat of pesticides to children’s health. Compiled by researchers and scientists at Pesticide Action Network, A Generation in Jeopardy: How pesticides are undermining our children’s health and intelligence focuses on studies published within the past five years – a growing body of evidence that convincingly demonstrates a link between pesticide exposure and childhood health harms.
“Pesticides can have unique and profound impacts on the developing child, even in very small amounts. The research shows that prenatal exposure to pesticides, in combination with other environmental and genetic factors, can contribute to increased risk of adverse health consequences, such as effects on the developing brain” said Dr. Tracey Woodruff, Director, Program on Reproductive Health and the Environment, University of California San Francisco, “We must take swift action to reduce exposure to harmful environmental chemicals to ensure healthier generations”
The report shines a light on the growing links between exposure to pesticides where children, live, learn and play and an array of impacts on the mind and body – including diminished IQ, ADHD & autism, childhood cancers and asthma. In particular, the report points to the following trends across studies:
“Enough scientific evidence is in – we can’t fail our children. While individual household choices can help, protecting kids from the health harms of pesticides requires real and swift policy change,” said Emily Marquez, PhD, report co-author and staff scientist at Pesticide Action Network. “Dramatically reducing pesticide use, starting with those most hazardous to children, is the best way to protect current and future generations.”
The report points to the need for the following reforms to reduce pesticide use:
The report was released today in ten cities across the country, including Bakersfield, Des Moines, Fresno, Los Angeles, Minneapolis, Sacramento, Salinas, San Francisco, Stockton, and Ventura.
"Protecting our children from harm is the fundamental duty of parenthood, but how can we do this when developmental toxicants are allowed to freely circulate in our economy?" says Sandra Steingraber, ecologist and acclaimed author. "PAN's report shines a light on a completely preventable tragedy - that an entire generation of children will not reach its full potential. As such, it describes a violation of human rights and a crisis of family life both. For the healthy development of children to become a national priority, we parents must walk ourselves into the political arena and, waving this good report, speak truth to power."
In particular, the report points to the fact that children are sicker today than a generation ago, confronting serious health challenges from pesticides and other chemical exposures that their parents and grandparents were unlikely to face.
Health professionals, mothers and rural leaders across the country released the new report, which draws from academic and government research, to chronicle the emerging threat of pesticides to children’s health. Compiled by researchers and scientists at Pesticide Action Network, A Generation in Jeopardy: How pesticides are undermining our children’s health and intelligence focuses on studies published within the past five years – a growing body of evidence that convincingly demonstrates a link between pesticide exposure and childhood health harms.
“Pesticides can have unique and profound impacts on the developing child, even in very small amounts. The research shows that prenatal exposure to pesticides, in combination with other environmental and genetic factors, can contribute to increased risk of adverse health consequences, such as effects on the developing brain” said Dr. Tracey Woodruff, Director, Program on Reproductive Health and the Environment, University of California San Francisco, “We must take swift action to reduce exposure to harmful environmental chemicals to ensure healthier generations”
The report shines a light on the growing links between exposure to pesticides where children, live, learn and play and an array of impacts on the mind and body – including diminished IQ, ADHD & autism, childhood cancers and asthma. In particular, the report points to the following trends across studies:
- The brains and nervous systems of boys are significantly more affected than girls.
- Timing of exposure is critically important. If a child is exposed to even very small amounts of a harmful pesticide during a particular moment of development, the impacts can be severe – and often irreversible.
- Studies link exposure to pesticides during pregnancy to increased risk of childhood leukemia and brain cancer. And children who live in intensively agricultural areas are more likely to have childhood cancer.
“Enough scientific evidence is in – we can’t fail our children. While individual household choices can help, protecting kids from the health harms of pesticides requires real and swift policy change,” said Emily Marquez, PhD, report co-author and staff scientist at Pesticide Action Network. “Dramatically reducing pesticide use, starting with those most hazardous to children, is the best way to protect current and future generations.”
The report points to the need for the following reforms to reduce pesticide use:
- Create stronger policy tools so enforcement agencies can take swift action to pull existing pesticides off the market and block new pesticides when independent studies suggest they are harmful to children.
- Increase investment and support for innovative farmers as they transition away from pesticide use.
- Set and track national pesticide use reduction goals, focusing first on those pesticides that studies show are harmful to children.
- Withdraw harmful pesticide products from use in homes, daycare centers and schools.
- Establish pesticide-free zones around schools, daycare centers and neighborhoods in agricultural areas to protect children from harmful exposures, especially pesticide drift.
The report was released today in ten cities across the country, including Bakersfield, Des Moines, Fresno, Los Angeles, Minneapolis, Sacramento, Salinas, San Francisco, Stockton, and Ventura.
Wednesday, October 10, 2012
Allergy News: The fall sneezing capitals of the U.S. : Louisville, Wichita, Knoxville, Jackson, McAkllen...
Fall
is a time to enjoy beautiful colors and autumn weather outdoors. But for 40
million Americans with seasonal allergies, this time of year brings an unwelcome
harvest: trillions of pollen particles traveling through the air right into
your eyes, nose and mouth. Allergic rhinitis – also called nasal allergies,
seasonal allergies or hay fever – is among the most common chronic diseases for
children and adults, affecting more than 12 percent of the U.S.
population.
The
primary fall allergy trigger – ragweed pollen – causes itchy runny nose, nasal
congestion, repeated sneezing, watery eyes, inflamed sinuses and, in severe
cases, difficulty breathing. It can be more problematic if you also have
asthma.
The
Asthma and Allergy Foundation of America (AAFA) recently announced its 2012 Fall
Allergy Capitals™ ranking, and Louisville, Kentucky, tops the list as “the most
challenging place to live with fall allergies.” The annual report names 100 U.S.
cities based on an analysis of three factors including pollen, allergy
medications usage and the number of allergists per patient. See the full
list at www.AllergyCapitals.com.
The Top 5
Fall Allergy Capitals this year are:
1. Louisville,
KY
2. Wichita, KS
3. Knoxville, TN
4. Jackson, MS
5. McAllen, TX
2. Wichita, KS
3. Knoxville, TN
4. Jackson, MS
5. McAllen, TX
“Everyone
seems to be feeling allergies these days and fall is the most common allergy
season after spring,” says Dr. Beth Corn, a Board Certified Allergist in New
York City and a member of the American College of Allergy, Asthma and Immunology
(ACAAI). “No matter if it’s men, women or children, in the city, suburbs or the
country, allergies don’t discriminate,” says Corn.
Tuesday, October 09, 2012
Could installing a satellite dish expose you to asbestos?
When a technician comes to install a new satellite dish the last thing most of us think to ask is whether he's trained to recognize asbestos.
In Australia, thousands of home owners are now awaiting the results of a study launched by the government after it was revealed inadequately trained contractors had dislodged asbestos in more than 20 government-owned houses. They also reviewed 1,733 private homes where the satellite dishes had been installed.
Asbestos was frequently used in home construction in some areas until the 1990's. It has been been deemed a carcinogenic substance by most major health agencies. If the fibrous material is disturbed, tiny particles can become airborne and can be inhaled.
Asbestos exposure has been linked to lung cancer, and other respiratory illnesses.
Source: :The Australian
Photo: freedigitalphotos.net
In Australia, thousands of home owners are now awaiting the results of a study launched by the government after it was revealed inadequately trained contractors had dislodged asbestos in more than 20 government-owned houses. They also reviewed 1,733 private homes where the satellite dishes had been installed.
Asbestos was frequently used in home construction in some areas until the 1990's. It has been been deemed a carcinogenic substance by most major health agencies. If the fibrous material is disturbed, tiny particles can become airborne and can be inhaled.
Asbestos exposure has been linked to lung cancer, and other respiratory illnesses.
Source: :The Australian
Photo: freedigitalphotos.net
Monday, October 08, 2012
Fast food and excessive hygene blamed for allergy increase in Europe
Paediatricians at Vienna's Medical University have raised the alarm about an increase of a third in the number of child allergy sufferers - blaming fast food and excessive hygiene.
The experts say that the allergies are a growing problem for children and even food allergies are on the increase, as well as the more common allergies such as asthma, eczema and hay fever.
They estimate that one in every five children in Europe now suffers from an allergy and it's getting worse.
Professor Dr Zsolt Szepfalusi says one possible cause is that people are deciding far too early on to have a clean and hygienic life.
"The so-called hygiene hypothesis is that a certain amount of dirt is healthy and tends to protect one from allergies."
But the medics also say that current diet may also be to blame.
"We have much more pasteurised and cooked food stuffs. This fast food industry didn't exist 20 years ago on such a scale and that has certainly had a strong influence on our digestive process - and in particular in the development of allergies."
He added that parents who believe that children have an allergy should get medical advice as soon as possible because early treatment means a better chance of an effective treatment.
Source: The Australian Independent
Friday, October 05, 2012
Indoor Air Quality FAQ’s: Volatile Organic Compounds (VOCs)
Among the most serious concerns in indoor air quality are Volatile Organic Compounds. VOCs are emitted as vapours from thousands of household products. According to studies by U.S. Environmental Protection Agency, VOC levels are much higher in indoor air than outdoor air regardless of whether homes are located in rural, urban or industrial areas. An air purifier for VOCs uses an adsorbent to clean the air and is very different from a standard HEPA air purifier.
What products emit VOCs?
Organic chemicals are used widely in household products and release vapours while they are being used, and also while being stored. Cleaning supplies, air fresheners, paints and varnishes contain organic chemicals, as do many other products like building materials, furniture, office equipment and even dry-cleaned clothing. Due to the constant release of VOC’s in indoor air, an air purifier designed to remove chemicals and odors should be left on continuously on low speed. Turning off the air purifier could lead to a build-up of pollutants.
What are the health effects?
Many organic compounds have been directly linked to cancer in animal studies and are known or suspected human carcinogens. While individual VOCs have been tested, very little is known about the combined effects of the numerous products we use every day. Immediate short-term health effects include eye irritation, breathing problems, headaches, dizziness, nausea and problems with concentration and memory.
How does an air purifier for VOC’s work?
A good quality air purifier designed for chemicals and odors is a specialized product that is usually sold through a dealer and is rarely found in your local “mart” or hardware store. It uses a completely different filtration system than a cheaper air purifier for dust. That’s because standard HEPA air purifier filters can’t trap chemical vapours. The most effective filtration method for chemicals is deep-bed activated carbon. This heavy air purifier filter (usually 18 lbs. and over) is packed with highly porous granules that attract and trap chemicals, gases and odors. An activated carbon air purifier is considered so effective that they are widely used by the military and heavy industry for some of the world’s most toxic chemicals and odors. Some types of carbon air purifier filters are better suited for different chemicals. An expert air purifier manufacturer like AllerAir can recommend one of 40 blends to best deal with the chemicals in your indoor air.
Other Steps to Reduce Exposure
Along with an air purifier for chemicals and odors, there are some
other simple steps to reduce VOC exposure:
·
When using chemical products, try to open
windows to increase ventilation
·
Buy products in very small qualities that can
be used-up quickly
·
Purchase new products that contain low or no
VOCs
·
Avoid storing cleaners, paint cans, and
varnishes in areas attached to the home
Learn More
For more information on VOCs, indoor air and which air purifier is
right for you call an AllerAir Air Quality Expert at 1-888-852-8247 or chat
live at www.allerair.com.
Thursday, October 04, 2012
Air Purifier Deals: Buyer Beware
Air purifier deals are much harder to come by than most home
appliances. Unlike products such as stoves, fridges and televisions, air
purifier manufacturers don’t usually release new models annually or make
significant changes to their design or technologies. That means they really
don’t need to liquidate units. In general, if you find a deeply discounted air
purifier online you may want to check into why the price is so low. Here are a
few things to consider before falling for an air purifier deal that may be too
good to be true.
The Air Purifier
Industry is Not Regulated
There are no official industry standards in air
purification. Although you may see something called CADR (clean air delivery
rate) when researching air purifier deals, these standards are not applicable
to some technologies including more advanced air cleaners that use large carbon filters for chemicals, gases and odors. So, if you find a really hot air
purifier deal, first examine the type of technology used. Are you getting an
overpriced fan or something that will truly clean the air? Most air purifiers that
really work will not come cheap. To remove airborne dust, chemicals and odors
look for an air purifier with a HEPA filter and a deep-bed activated carbon filter.
Size Matters
Another point to consider if you come across a cheap air
purifier is size. A low priced, small air cleaner that can sit on a desk may
seem like a good deal initially, but it won’t have the capability to clean more
than a few feet around the unit. Some smaller units also use controversial
ionizing or ozone technologies that may produce dangerous ozone gas.
Is it Refurbished?
Imagine buying a used mop. Sure it may be a dirt cheap deal,
but you’d be bringing someone else’s dust and germs into your home. The same
may be true for a used or refurbished air purifier. The moment it’s shipped to
someone’s home and turned on even for a few minutes, the filters have already
removed dust, skin particles, hair, chemicals, odors and germs from the air.
That’s why most quality air purifier companies will charge a restocking fee for
returned products – because the filters must be thrown out and they lose money
on the return. Trust-worthy manufacturers will never turnaround and resell a
returned air purifier as is.
Who is the Seller?
Probably the most important aspect to examine when
double-checking an air cleaner deal is the seller or dealer. Be sure the vendor
is “authorized”. This guarantees that the seller or dealer has an official
relationship with the manufacturer. This will also protect the integrity of the
unit’s warranty.
The Real Deal
Sometimes getting what you paid for is really the best deal
of all. Choosing a quality product over a rock bottom price will likely result
in a better buying experience and cleaner air. For more advice on affordable
air cleaners chat live with an air quality expert at www.allerair.com.
Photo: Freedigitalphotos.net
Photo: Freedigitalphotos.net
Wednesday, October 03, 2012
Study finds 36 cell phones, including iPhone 5, have toxic chemicals
Source: Detroit Free Press
Thirty-six different cell phones, including the iPhone 5 and Samsung Galaxy S III, were found to contain toxic chemicals, according to the results of a study released today.
The study, from the Ann Arbor-based Ecology Center and www.ifixit.com did not look at whether users are exposed to the chemicals, but instead highlights the ways in which chemicals used in cell phones can pollute throughout their life cycle.
“We’re not making any claim that there’s any in-use exposure hazards from these mobile phones,” said Ecology Center Research Director Jeff Gearhart, who noted that the hazardous chemicals are primarily found in the “guts” of the phones.
Gearhart said the study was an attempt to inform consumers that cell phones are chemical-intensive products and their manufacture and disposal or recycling can pollute.
“These chemicals, which are linked to birth defects, impaired learning and other serious health problems, have been found in soils at levels 10 to 100 times higher than background levels at e-waste recycling sites in China. We need better federal regulation of these chemicals, and we need to create incentives for the design of greener consumer electronics,” Gearhart said in a news release.
The phones all “contained at least one of (the) following hazardous chemicals: lead, bromine, chlorine, mercury and cadmium,” according to the news release.
Samsung had the best overall rating, and Apple’s phones — the iPhone 5 ranked fifth best — were among the most improved, the study found. The Motorola Citrus was the least toxic phone, and the iPhone 2G was the most toxic, according to the study. Gearhart noted that cell phone companies have been making positive strides in their use of toxic chemicals and that continued consumer interest in this area would likely push the industry to do better.
A call seeking comment was left with a spokesman for CTIA-The Wireless Association, an industry group.
Photo: freedigitalphotos.net
Thirty-six different cell phones, including the iPhone 5 and Samsung Galaxy S III, were found to contain toxic chemicals, according to the results of a study released today.
The study, from the Ann Arbor-based Ecology Center and www.ifixit.com did not look at whether users are exposed to the chemicals, but instead highlights the ways in which chemicals used in cell phones can pollute throughout their life cycle.
“We’re not making any claim that there’s any in-use exposure hazards from these mobile phones,” said Ecology Center Research Director Jeff Gearhart, who noted that the hazardous chemicals are primarily found in the “guts” of the phones.
Gearhart said the study was an attempt to inform consumers that cell phones are chemical-intensive products and their manufacture and disposal or recycling can pollute.
“These chemicals, which are linked to birth defects, impaired learning and other serious health problems, have been found in soils at levels 10 to 100 times higher than background levels at e-waste recycling sites in China. We need better federal regulation of these chemicals, and we need to create incentives for the design of greener consumer electronics,” Gearhart said in a news release.
The phones all “contained at least one of (the) following hazardous chemicals: lead, bromine, chlorine, mercury and cadmium,” according to the news release.
Samsung had the best overall rating, and Apple’s phones — the iPhone 5 ranked fifth best — were among the most improved, the study found. The Motorola Citrus was the least toxic phone, and the iPhone 2G was the most toxic, according to the study. Gearhart noted that cell phone companies have been making positive strides in their use of toxic chemicals and that continued consumer interest in this area would likely push the industry to do better.
A call seeking comment was left with a spokesman for CTIA-The Wireless Association, an industry group.
Photo: freedigitalphotos.net
Inner city kids may be more prone to asthma as a result of respiratory illnesses in infancy
Children living in low-income urban areas appear especially prone to developing asthma, possibly related to infections they acquire early in life. In a new study in The Journal of Infectious Diseases, available online, researchers from the University of Wisconsin in Madison investigated viral respiratory illnesses and their possible role in the development of asthma in urban versus suburban babies. The differences in viral illness patterns they found provide insights that could help guide the development of new asthma treatments in children.
To document patterns of respiratory viruses in infants living in urban and suburban locations, James E. Gern, MD, and his team of investigators collected nasal secretions from 500 infants from four inner-city areas in the U.S. (Boston, Baltimore, New York City, and St. Louis) and 285 infants from suburban Madison, Wis. Nasal secretions were sampled during periods when the babies had respiratory illnesses and when they were healthy.
The inner-city infants had lower rates of viral detection overall. This may suggest that other factors, such as bacteria or allergic reactions to air pollutions or toxic exposures, contribute significantly to respiratory illness. Sick urban infants had lower rates of two kinds of viruses, HRV and RSV, and higher rates of adenovirus infections, compared to suburban infants. In the urban babies, 4.8 percent of nasal washes tested positive for only adenovirus, while just 0.7 percent of samples from suburban babies were positive for only adenovirus. “Adenovirus infections, either as a single pathogen or when detected in concert with other viruses, were significantly more common in the urban population, and this held true for each of the four urban locations where our study was conducted,” the authors wrote.
This is of particular interest, the researchers noted, because adenovirus can cause persistent infections. The study authors believe this may suggest that development of the lungs or airways could be altered by adenovirus infections in early life.
In an accompanying editorial, Peter W. Heymann, MD, and Thomas A.E. Platts-Mills, MD, PhD, of the University of Virginia in Charlottesville, noted that the findings are of interest given the pervasiveness and the morbidity and mortality of asthma in poor urban areas. “The results clearly show differences in the detection of viral infections during the first year of life,” they wrote, “and this approach is likely to provide novel insights that will serve to guide the development of treatment interventions to decrease the prevalence and severity of asthma during childhood.”
In an effort to better understand the origins of non-viral respiratory illnesses, Dr. Gern and colleagues are planning experiments to evaluate other pathogens and microbes in the airways. They also plan to follow the urban children in this study for at least 10 years to “test the hypothesis that infections with adenoviruses might be associated later on in childhood with an increased rate of asthma and perhaps lower levels of lung function.”
Photo: David Castillo Dominic, freedigitalphotos.net
To document patterns of respiratory viruses in infants living in urban and suburban locations, James E. Gern, MD, and his team of investigators collected nasal secretions from 500 infants from four inner-city areas in the U.S. (Boston, Baltimore, New York City, and St. Louis) and 285 infants from suburban Madison, Wis. Nasal secretions were sampled during periods when the babies had respiratory illnesses and when they were healthy.
The inner-city infants had lower rates of viral detection overall. This may suggest that other factors, such as bacteria or allergic reactions to air pollutions or toxic exposures, contribute significantly to respiratory illness. Sick urban infants had lower rates of two kinds of viruses, HRV and RSV, and higher rates of adenovirus infections, compared to suburban infants. In the urban babies, 4.8 percent of nasal washes tested positive for only adenovirus, while just 0.7 percent of samples from suburban babies were positive for only adenovirus. “Adenovirus infections, either as a single pathogen or when detected in concert with other viruses, were significantly more common in the urban population, and this held true for each of the four urban locations where our study was conducted,” the authors wrote.
This is of particular interest, the researchers noted, because adenovirus can cause persistent infections. The study authors believe this may suggest that development of the lungs or airways could be altered by adenovirus infections in early life.
In an accompanying editorial, Peter W. Heymann, MD, and Thomas A.E. Platts-Mills, MD, PhD, of the University of Virginia in Charlottesville, noted that the findings are of interest given the pervasiveness and the morbidity and mortality of asthma in poor urban areas. “The results clearly show differences in the detection of viral infections during the first year of life,” they wrote, “and this approach is likely to provide novel insights that will serve to guide the development of treatment interventions to decrease the prevalence and severity of asthma during childhood.”
In an effort to better understand the origins of non-viral respiratory illnesses, Dr. Gern and colleagues are planning experiments to evaluate other pathogens and microbes in the airways. They also plan to follow the urban children in this study for at least 10 years to “test the hypothesis that infections with adenoviruses might be associated later on in childhood with an increased rate of asthma and perhaps lower levels of lung function.”
Photo: David Castillo Dominic, freedigitalphotos.net
Tuesday, October 02, 2012
Tenn. meningitis outbreak tied to Aspergillus mold
From NBC News:
A dozen people have been sickened and two have died after an outbreak of fungal meningitis tied to injections given at outpatient surgical centers in Tennessee and North Carolina, health officials said.
At least 737 people who received lumbar epidural steroid injections between July 30 and Sept. 20 have been notified of the cluster of rare aspergillus meningitis infections, which attack the central nervous system, said Curtis Allen, a spokesman for the Centers for Disease Control and Prevention.
Aspergillus is a mold present in the environment, and the meningitis is not related to the more common bacterial or viral types of meningitis.
“The main thing is that it’s not transmissible person-to-person,” said Allen.
Federal, state and local health officials are investigating the source of the outbreak. Eleven of the victims received injections at the Saint Thomas Outpatient Neurosurgery Center in Nashville. Another patient received an injection at an unidentified clinic in North Carolina. The Tennessee clinic was closed Sept. 20 and has been shuttered until further notice, officials said.
The patients were older people, between the ages of 40 and 80, who were receiving the steroid injections as treatment for musculoskeletal disorders, said Woody McMillin, spokesman for the Tennessee Department of Health.
Neither federal nor state health officials would identify the brand of epidural steroids given to the patients nor the manufacturer of the drugs. Asked whether the drugs themselves could have been contaminated, McMillin said that’s one possibility.
“Right now, we’re not taking anything off the table,” he said.
Erica Jefferson, a spokeswoman for the federal Food and Drug Administration, said that it’s too soon to speculate about that because the investigation is still “evolving.”
Meningitis caused by aspergillus is very rare, according to the Journal of Microbiology. Symptoms often include a fever and headache that might be present for weeks before a diagnosis is made.
Tennessee officials have set up a hotline to answer questions about meningitis: 1-800-222-1222.
A dozen people have been sickened and two have died after an outbreak of fungal meningitis tied to injections given at outpatient surgical centers in Tennessee and North Carolina, health officials said.
At least 737 people who received lumbar epidural steroid injections between July 30 and Sept. 20 have been notified of the cluster of rare aspergillus meningitis infections, which attack the central nervous system, said Curtis Allen, a spokesman for the Centers for Disease Control and Prevention.
Aspergillus is a mold present in the environment, and the meningitis is not related to the more common bacterial or viral types of meningitis.
“The main thing is that it’s not transmissible person-to-person,” said Allen.
Federal, state and local health officials are investigating the source of the outbreak. Eleven of the victims received injections at the Saint Thomas Outpatient Neurosurgery Center in Nashville. Another patient received an injection at an unidentified clinic in North Carolina. The Tennessee clinic was closed Sept. 20 and has been shuttered until further notice, officials said.
The patients were older people, between the ages of 40 and 80, who were receiving the steroid injections as treatment for musculoskeletal disorders, said Woody McMillin, spokesman for the Tennessee Department of Health.
Neither federal nor state health officials would identify the brand of epidural steroids given to the patients nor the manufacturer of the drugs. Asked whether the drugs themselves could have been contaminated, McMillin said that’s one possibility.
“Right now, we’re not taking anything off the table,” he said.
Erica Jefferson, a spokeswoman for the federal Food and Drug Administration, said that it’s too soon to speculate about that because the investigation is still “evolving.”
Meningitis caused by aspergillus is very rare, according to the Journal of Microbiology. Symptoms often include a fever and headache that might be present for weeks before a diagnosis is made.
Tennessee officials have set up a hotline to answer questions about meningitis: 1-800-222-1222.
Monday, October 01, 2012
Chemical widely used in antibacterial hand soaps may impair muscle function
Triclosan, an antibacterial chemical widely used in hand soaps and other personal-care products, hinders muscle contractions at a cellular level, slows swimming in fish and reduces muscular strength in mice, according to researchers at the University of California, Davis, and the University of Colorado. The findings appear online in the Proceedings of the National Academy of Sciences of the United States of America.
“Triclosan is found in virtually everyone’s home and is pervasive in the environment,” said Isaac Pessah, professor and chair of the Department of Molecular Biosciences in the UC Davis School of Veterinary Medicine and principal investigator of the study. “These findings provide strong evidence that the chemical is of concern to both human and environmental health.”
Triclosan is commonly found in antibacterial personal-care products such as hand soaps as well as deodorants, mouthwashes, toothpaste, bedding, clothes, carpets, toys and trash bags. The U.S. Environmental Protection Agency in 1998 estimated that more than 1 million pounds of triclosan are produced annually in the United States, and that the chemical is detectable in waterways and aquatic organisms ranging from algae to fish to dolphins, as well as in human urine, blood and breast milk.
The investigators performed several experiments to evaluate the effects of triclosan on muscle activity, using doses similar to those that people and animals may be exposed to during everyday life.
In “test tube” experiments, triclosan impaired the ability of isolated heart muscle cells and skeletal muscle fibers to contract. Specifically, the team evaluated the effects of triclosan on molecular channels in muscle cells that control the flow of calcium ions, creating muscle contractions. Normally, electrical stimulation (“excitation”) of isolated muscle fibers under experimental conditions evokes a muscle contraction, a phenomenon known as “excitation-contraction coupling,” the fundamental basis of any muscle movement, including heartbeats. But in the presence of triclosan, the normal communication between two proteins that function as calcium channels was impaired, causing skeletal and cardiac muscle failure.
The team also found that triclosan impairs heart and skeletal muscle contractility in living animals. Anesthetized mice had up to a 25-percent reduction in heart function measures within 20 minutes of exposure to the chemical.
“The effects of triclosan on cardiac function were really dramatic,” said Nipavan Chiamvimonvat, professor of cardiovascular medicine at UC Davis and a study co-author. “Although triclosan is not regulated as a drug, this compound acts like a potent cardiac depressant in our models.”
In addition, the mice had an 18-percent reduction in grip strength for up to 60 minutes after being given a single dose of triclosan. Grip strength is a widely used measure of mouse limb strength, employed to investigate the effects of drugs and neuromuscular disorders.
Finally, the investigators looked at the effects of triclosan exposure on fathead minnows, a small fish commonly used as a model organism for studying the potential impacts of aquatic pollutants. Those exposed to triclosan in the water for seven days had significantly reduced swimming activity compared to controls during both normal swimming and swim tests designed to imitate fish being threatened by a predator.
“We were surprised by the large degree to which muscle activity was impaired in very different organisms and in both cardiac and skeletal muscle,” said Bruce Hammock, a study co-author and professor in the UC Davis Department of Entomology. “You can imagine in animals that depend so totally on muscle activity that even a 10-percent reduction in ability can make a real difference in their survival.”
The UC Davis research team has previously linked triclosan to other potentially harmful health effects, including disruption of reproductive hormone activity and of cell signaling in the brain.
Chiamvimonvat cautioned that translating results from animal models to humans is a large step and would require further study. However, the fact that the effects were so striking in several animal models under different experimental conditions provides strong evidence that triclosan could have effects on animal and human health at current levels of exposure.
“In patients with underlying heart failure, triclosan could have significant effects because it is so widely used,” Chiamvimonvat said. “However, without additional studies, it would be difficult for a physician to distinguish between natural disease progression and an environmental factor such as triclosan.”
Pessah questioned arguments that triclosan — introduced more than 40 years ago — is safe partly because it binds to blood proteins, making it not biologically available. Although triclosan may bind to proteins in the blood, that may not necessarily make the chemical inactive, he said, and actually may facilitate its transport to critical organs. In addition, some of the current experiments were carried out in the presence of blood proteins, and disrupted muscle activity still occurred.
Although triclosan was first developed to prevent bacterial infections in hospitals, its use has become widespread in antibacterial products used in the home. However, according to the U.S. Food and Drug Administration, other than its use in some toothpastes to prevent gingivitis, there is no evidence that triclosan provides other health benefits or that antibacterial soaps and body washes are more effective than regular soap and water. Experts also express concern about the possibility of resistant bacterial strains developing with the overuse of antibacterial products.
Because the chemical structure of triclosan resembles other toxic chemicals that persist in the environment, the FDA and the U.S. Environmental Protection Agency are conducting new risk assessments of the chemical. Based on their study outcomes, the researchers argue that the potential health risks call for greater restrictions.
“We have shown that triclosan potently impairs muscle functions by interfering with signaling between two proteins that are of fundamental importance to life,” said Pessah. “Regulatory agencies should definitely be reconsidering whether it should be allowed in consumer products.”
Said Hammock: “Triclosan can be useful in some instances, however it has become a ubiquitous ‘value added’ marketing factor that actually could be more harmful than helpful. At the very least, our findings call for a dramatic reduction in its use.”
Photo: freedigitalphotos.net
“Triclosan is found in virtually everyone’s home and is pervasive in the environment,” said Isaac Pessah, professor and chair of the Department of Molecular Biosciences in the UC Davis School of Veterinary Medicine and principal investigator of the study. “These findings provide strong evidence that the chemical is of concern to both human and environmental health.”
Triclosan is commonly found in antibacterial personal-care products such as hand soaps as well as deodorants, mouthwashes, toothpaste, bedding, clothes, carpets, toys and trash bags. The U.S. Environmental Protection Agency in 1998 estimated that more than 1 million pounds of triclosan are produced annually in the United States, and that the chemical is detectable in waterways and aquatic organisms ranging from algae to fish to dolphins, as well as in human urine, blood and breast milk.
The investigators performed several experiments to evaluate the effects of triclosan on muscle activity, using doses similar to those that people and animals may be exposed to during everyday life.
In “test tube” experiments, triclosan impaired the ability of isolated heart muscle cells and skeletal muscle fibers to contract. Specifically, the team evaluated the effects of triclosan on molecular channels in muscle cells that control the flow of calcium ions, creating muscle contractions. Normally, electrical stimulation (“excitation”) of isolated muscle fibers under experimental conditions evokes a muscle contraction, a phenomenon known as “excitation-contraction coupling,” the fundamental basis of any muscle movement, including heartbeats. But in the presence of triclosan, the normal communication between two proteins that function as calcium channels was impaired, causing skeletal and cardiac muscle failure.
The team also found that triclosan impairs heart and skeletal muscle contractility in living animals. Anesthetized mice had up to a 25-percent reduction in heart function measures within 20 minutes of exposure to the chemical.
“The effects of triclosan on cardiac function were really dramatic,” said Nipavan Chiamvimonvat, professor of cardiovascular medicine at UC Davis and a study co-author. “Although triclosan is not regulated as a drug, this compound acts like a potent cardiac depressant in our models.”
In addition, the mice had an 18-percent reduction in grip strength for up to 60 minutes after being given a single dose of triclosan. Grip strength is a widely used measure of mouse limb strength, employed to investigate the effects of drugs and neuromuscular disorders.
Finally, the investigators looked at the effects of triclosan exposure on fathead minnows, a small fish commonly used as a model organism for studying the potential impacts of aquatic pollutants. Those exposed to triclosan in the water for seven days had significantly reduced swimming activity compared to controls during both normal swimming and swim tests designed to imitate fish being threatened by a predator.
“We were surprised by the large degree to which muscle activity was impaired in very different organisms and in both cardiac and skeletal muscle,” said Bruce Hammock, a study co-author and professor in the UC Davis Department of Entomology. “You can imagine in animals that depend so totally on muscle activity that even a 10-percent reduction in ability can make a real difference in their survival.”
The UC Davis research team has previously linked triclosan to other potentially harmful health effects, including disruption of reproductive hormone activity and of cell signaling in the brain.
Chiamvimonvat cautioned that translating results from animal models to humans is a large step and would require further study. However, the fact that the effects were so striking in several animal models under different experimental conditions provides strong evidence that triclosan could have effects on animal and human health at current levels of exposure.
“In patients with underlying heart failure, triclosan could have significant effects because it is so widely used,” Chiamvimonvat said. “However, without additional studies, it would be difficult for a physician to distinguish between natural disease progression and an environmental factor such as triclosan.”
Pessah questioned arguments that triclosan — introduced more than 40 years ago — is safe partly because it binds to blood proteins, making it not biologically available. Although triclosan may bind to proteins in the blood, that may not necessarily make the chemical inactive, he said, and actually may facilitate its transport to critical organs. In addition, some of the current experiments were carried out in the presence of blood proteins, and disrupted muscle activity still occurred.
Although triclosan was first developed to prevent bacterial infections in hospitals, its use has become widespread in antibacterial products used in the home. However, according to the U.S. Food and Drug Administration, other than its use in some toothpastes to prevent gingivitis, there is no evidence that triclosan provides other health benefits or that antibacterial soaps and body washes are more effective than regular soap and water. Experts also express concern about the possibility of resistant bacterial strains developing with the overuse of antibacterial products.
Because the chemical structure of triclosan resembles other toxic chemicals that persist in the environment, the FDA and the U.S. Environmental Protection Agency are conducting new risk assessments of the chemical. Based on their study outcomes, the researchers argue that the potential health risks call for greater restrictions.
“We have shown that triclosan potently impairs muscle functions by interfering with signaling between two proteins that are of fundamental importance to life,” said Pessah. “Regulatory agencies should definitely be reconsidering whether it should be allowed in consumer products.”
Said Hammock: “Triclosan can be useful in some instances, however it has become a ubiquitous ‘value added’ marketing factor that actually could be more harmful than helpful. At the very least, our findings call for a dramatic reduction in its use.”
Photo: freedigitalphotos.net
Friday, September 28, 2012
What a difference a freeway makes; highway closure improves air quality by 83%
In study findings announced today UCLA researchers report that air quality near the closed section of highway 405 last year improved within minutes, reaching levels 83 percent better than on comparable weekends.
Because traffic dipped all over Southern California that weekend, air quality also improved 75 percent in parts of West Los Angeles and Santa Monica and an average of 25 percent regionally — from Ventura to Yucaipa, and Long Beach to Santa Clarita.
The study was led by two professors at UCLA's Institute of the Environment and Sustainability: Yifang Zhu, who is also an associate professor of environmental health sciences at the UCLA Fielding School of Public Health, and Suzanne Paulson, who is also a professor of atmospheric and oceanic sciences.
While the researchers expected cleaner air, they didn't expect the improvement to be so dramatic.
"The air was amazingly clean that weekend," Paulson said. "Our measurements in Santa Monica were almost below what our instruments could detect, and the regional effect was significant. It was a really eye-opening glimpse of what the future could be like if we can move away from combustion engines."
The research gives a peek at what the air would look like in a healthier Los Angeles with a vast majority of hybrid and electric vehicles and shows how quickly less driving can improve key measures of air quality.
Taking measurements
The researchers measured ultrafine particles (less than 0.1 microns in diameter), which are key indicators of real-time traffic levels, and also fine particulate matter known as "PM2.5" (less than 2.5 microns in diameter), which includes tailpipe emissions and new particles created when the emissions interact with the atmosphere. PM2.5 can spread farther from the freeway and last longer than ultrafine particles, but both are pollutants with health risks. Exposure to near-roadway pollutants has been linked to increases in asthma, heart attacks, strokes, diabetes, low birth weight, pre-term births and other ailments, the researchers noted.
Zhu and Paulson found that when traffic dropped more than 90 percent on the closed 405, with only construction vehicles still on the move, ultrafine particles dropped by 83 percent. PM2.5 concentrations dropped 36 percent.
More broadly, ultrafine particles and PM2.5 levels dropped 75 percent across a swath of West Los Angeles near the I-405/I-10 interchange stretching from Santa Monica to Westwood. Elsewhere, they measured PM2.5 and found the air 31 percent cleaner in Ventura, 19 percent cleaner in Yucaipa, 30 percent cleaner in Long Beach, 23.2 percent cleaner in Santa Clarita and 19.9 percent cleaner in Northridge.
"There is no safe level of PM2.5 concentrations, where you would no longer observe health impacts, so any reduction is an improvement," Zhu said. "This study shows that with such dramatic traffic reductions, there are specific air-quality improvements. It gives policymakers and the public incentives to put more effort into reducing traffic emissions."
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