~dGossip
~tAcrolein and Neuro Disorders
~w2011-02-02
In the United States, neurologic disorders are among the leading
causes of death and illness. At present, the causes of these
disorders is poorly understood, but one of the emerging suspected
culprits is the substance acrolein, which tends to be significantly
elevated in the brains or spinal cords of people who have Alzheimer
disease, Parkinson disease, amyotrophic lateral sclerosis (ALS), and
other neurologic disorders. Now, a new study adds multiple sclerosis
(MS) to the list of disorders potentially affected by this substance.
Acrolein is produced naturally in the body as a by-product of
membrane lipid peroxidation. In addition, it occurs in combustion byproducts such as vehicle exhaust, industrial emissions, oil- and
coal-fired power plant emissions, cooking fumes, and the smoke from
burning cigarettes, wood, and plastics. It’s used as a biocide and to
manufacture other chemicals and products such as chemical weapons.
The U.S. Environmental Protection Agency (EPA) has determined the
ubiquitous pollutant is a major source of respiratory damage.
However, there is very little information available on the neurologic
effects of environmental acrolein. In the new study, Riyi Shi of
Purdue University and colleagues injected mice with substances known
to induce experimental autoimmune encephalomyelitis, an animal model
for MS. Within 2 weeks acrolein–lysine adduct levels in the spinal
cord began to rise, peaking at 65% higher than in controls at about
day 20. At the same time, the mice began to display significant
muscle control problems. Treatment with the acrolein-scavenging
substance hydralazine reduced those effects to a great although not
significant degree. Furthermore, the researchers detected significant
mitigation of damage to the myelin sheath by hydralazine. Shi and
colleagues say their study provides the first evidence that
endogenous acrolein plays a key role in MS. Shi says it’s plausible
that environmental acrolein can act in the same general way: “There’s
no reason not to believe that the same type of damage could occur.”
Richard LoPachin, a neurochemist and director of research at
Montefiore Medical Centre in New York, partially agrees. “Because
acrolein is highly reactive with proteins at the site of exposure, it
has limited distribution in the body and, therefore, limited access
to the brain,” he says. But acrolein is just one of many type-2
alkenes, a large family of environmental and food contaminants that
includes acrylamide, methyl vinyl ketone, methyl acrylate, and 4hydroxynonenal. LoPachin says type-2 alkenes share a common mechanism
of action at nerve terminals in the brain, and he thinks the combined
effects of these substances could contribute to some neurologic
disorders. Robert Kavlock, director of the EPA National Centre for
Computational Toxicology, says acrolein’s physical properties make it
difficult to assess the compound using the agency’s ToxCast™ highthroughput chemical screening program using currently available
technology. But pinning down the causes of these neurologic disorders
could help millions of people. In the United States alone, about 5.3
million people have Alzheimer disease, about 1.5 million have
Parkinson disease, about 400,000 have MS, and about 30,000 have ALS.
Environmental Health Perspectives, 1 February 2011
<a href="http://ehponline.org">http://ehponline.org</a>
~dGossip
~tEpstein Calls for FDA, EPA to Ban Uses of Fluoride
~w2011-02-02
Cancer Prevention Coalition Chair Samuel S. Epstein, M.D., recently
said that "A ban by the FDA on fluoridated toothpaste is well
overdue, as is a ban by the EPA on the fluoridation of drinking
water." Epstein said a ban would protect people against the risks of
bone cancer from the use of fluoride in most toothpaste and from the
fluoridation of drinking water. In 1977, the National Academy of
Sciences expressed concerns on the strong relation between the
fluoridation of drinking water and risks of bone cancer to young
boys, Epstein pointed out. A decade later, the International Agency
for Research on Cancer reported that fluorides in drinking water
induced bone cancer in rats. This finding was confirmed by the
National Toxicology Program in its 1989, 1990, and 1991 reports.
"Not surprisingly, Procter & Gamble, the leading manufacturer of
fluoridated toothpastes, denied that these results were statistically
significant," Epstein said. "Surprisingly, the Food and Drug
Administration (FDA) supported this claim." Evidence for the bone
cancer link comes from studies and reports from the National Cancer
Institute (NCI), the New Jersey Department of Health, and Harvard
University. In 1990, the NCI reported that, based on an analysis of
1973 to 1987 data, the incidence of a bone cancer, known as
osteosarcoma, was increased in males under the age of 20 living in
areas where the drinking water was fluoridated. In 1992, the New
Jersey Department of Health published a study confirming higher rates
of bone cancer in young boys living in fluoridated versus nonfluoridated areas of the state. Then in 1993, an independent analysis
of the 1990 NCI data confirmed excess risks and deaths from bone
cancer in young boys exposed to fluoride. These findings were
confirmed in a 2001 report by the Harvard School of Dental Medicine.
In 2006, a Harvard University team of scientists published a study
reporting a five-fold increased risk of bone cancer in teenage boys
who had drunk fluoridated water between the ages of 6 and 8. Apart
from exposure to fluoride in drinking water, these finding also
incriminated fluoride commonly added to toothpaste. "Concerns on
fluoride as a major avoidable cause of bone cancer are further and
urgently validated by its unrecognized 20 percent increased incidence
in children under the age of 15 over the last three decades," Epstein
said, "as documented in the 1975-2007 National Cancer Institute
Surveillance Epidemiology and End Results report." On 7 January 2011,
the U.S. Department of Health and Human Services (HHS) and the U.S.
Environmental Protection Agency (EPA) announced steps to ensure that
standards and guidelines on fluoride in drinking water continue to
provide the maximum protection to support good dental health,
especially in children. HHS is proposing that the recommended level
of fluoride in drinking water can be set at the lowest end of the
current optimal range to prevent tooth decay, and EPA is initiating
review of the maximum amount of fluoride allowed in drinking water.
Epstein is professor emeritus of Environmental and Occupational
Medicine at the University of Illinois at Chicago School of Public
Health.
Environmental Protection News, 25 January 2011
<a href="http://www.eponline.com">http://www.eponline.com</a>
~dGossip
~tCholera toxin nanoparticle detector
~w2011-02-02
A complex sugar may become one of the most effective weapons to stop
the spread of cholera, a disease that has claimed thousands of lives
in Haiti since last year’s devastating earthquake. A technique
developed by researchers at the University of Central Florida would
allow relief workers to test water sources for contamination with the
cholera toxin. The new test involved the sugar dextran being coated
onto iron oxide nanoparticles and then added to a sample of the
water. If the cholera toxin is present, the toxin will bind to the
nanoparticles' dextran, because dextran looks similar to the cholera
toxin receptor (GM1) found on the surface of cells in the victim's
gut. The technique would likely be less expensive than those
currently available. In addition, it would provide results more
quickly, enabling workers to restrict access to contaminated sources
and limit the spread of the disease. 'It's really quite amazing',
said UCF assistant professor J. Manuel Perez, the lead researcher on
the project. 'It means we have a quicker diagnostic tool using a
simple and relatively cheap sugar-nanoparticle combination.’ Early
studies also show that the technique could someday be used to treat
someone infected with cholera, which is caused by poor sanitation and
dirty water, and potentially other diseases. More studies are
required to prove the adaptability of the technique, but its impact
could be huge. In countries with poor sanitation, outbreaks caused by
drinking contaminated water often prove fatal. Deadly toxins can also
result from bioterrorism or food contamination. The World Health
Organisation estimates that there are 3-5 million cholera cases and
100,000-120,000 deaths worldwide every year. A cholera outbreak has
killed more than 3,000 people in Haiti since the earthquake, and WHO
warned earlier this month that the outbreak has not yet reached its
peak. Details of the research, funded by the National Institute of
General Medical Sciences at the National Institutes of Health, are
published in the journal Bioconjugate Chemistry. The findings may
provide the Federal Drug Administration, Centres for Disease Control
and Prevention and several other agencies additional screening tools
to combat toxins. The UCF-developed technique is faster than current
detection methods and could be less expensive because these
nanoparticles are cheap to make in large quantities. The detection
instruments are compact (in some cases the size of a desktop computer
and a handheld calculator) and they could be turned into mobile
devices that relief workers or food screeners could use in the field.
'As we have seen in the 2010 outbreak in Haiti, cholera remains a
serious threat', said Janna Wehrle of the National Institutes of
Health, who oversees Perez' and other grants that focus on protein
structures and interactions. 'By developing a fast and sensitive test
for cholera toxin that does not require sophisticated equipment or
refrigeration, Drs Perez and Teter have provided health care workers
with a potentially valuable tool for use in areas struck by natural
disasters or with inadequate infrastructure. The possibility that the
novel chemistry discovered by these investigators might also be
useful for treating cholera is especially exciting.'
Environmental Expert, 27 January 2011
<a href="http://www.environmentalexpert.com">http://www.environmental-expert.com</a>
~dGossip
~tExtra calcium, vitamin D no bone booster for men
~w2011-02-02
According to the findings of a new study by Australian researchers,
taking extra vitamin D and calcium doesn't seem to prevent bonethinning in older men. However, exercise did boost bone mineral
density, a proxy for bone strength, their report shows. Despite the
findings, people still need to get enough calcium and vitamin D to
reduce the risk of osteoporosis, or bone thinning, said Dr. Mone
Zaidi, an osteoporosis researcher at the Mount Sinai School of
Medicine in New York, who was not involved in the study. "It's like
the four legs of the stool: vitamin D and calcium, exercise,
medications if a person is losing bone, and the fourth leg is telling
people how to prevent fractures," Zaidi said. In the United States,
more than 40 million people are affected by osteoporosis. It's most
common in older women, but about seven percent of white men and five
percent of black men are affected, according to the American College
of Physicians. During the new study, published in the Journal of
Clinical Endocrinology and Metabolism, Robin M. Daly from the
University of Melbourne, and colleagues randomly assigned men aged 59
to 70 to an exercise program, drinking milk fortified with calcium
and vitamin D, doing both, or doing nothing. They measured the men's
bone density before and after the study, which took place over 18
months, but they didn't look at fractures. At the end of the study,
men who exercised had higher bone density than those who had
supplemented their diet with 1000 milligrams of calcium and 800
international units (IU) of vitamin D per day. Adding the supplements
to the exercise program provided no extra benefit, hinting that the
men already had enough vitamin D and calcium in their diets to be
able to boost their bone strength through exercise alone. The
recommended daily intake of vitamin D is 600 IU in adults up to age
70, and 800 IU for older people, according to the National Institutes
of Health (NIH). As for calcium, the NIH advises 1,000 mg per day for
men ages 19-70, and then 1,200 mg per day for men older than 70. To
build bone density, weight-bearing exercise is needed, such as
running or weight-lifting, according to the NIH. Previous animal
studies have found that a lack of vitamin D is associated to several
diseases, such as multiple sclerosis and some types of cancer.
However, there isn't enough data to say if vitamin D can help treat
or prevent these diseases, Zaidi said. To reduce the risk of bone
weakening, the NIH recommends not smoking, drinking less alcohol and
exercising more. Zaidi said that both vitamin D and calcium are
extremely important for human health, so people should follow the
previous vitamin D and calcium recommendations. "You've got to have
it to build a wall," he said. "Adding more might not strengthen the
wall, but you have to take enough to keep the wall strong. Otherwise
it might fall apart."
Reuters Health, 27 January 2011
<a
href="http://www.reuters.com/news/health">http://www.reuters.com/news
/health</a>
~dGossip
~tBreast implants may be linked to rare cancer: FDA
~w2011-02-03
U.S regulators recently said that women with silicone or saline
breast implants may face a small increase in risk for a rare immunesystem cancer near their implants. Officials need more data to
determine if the implants caused the cancer and are asking doctors to
report confirmed cases, the Food and Drug Administration said in a
statement. Overall the agency still considers implants safe and said
women without symptoms should not change their routine monitoring.
The cancer warning could hit sales of implants sold by Allergan Inc
and Johnson & Johnson's Mentor unit. Safety concerns have dogged
breast implants for years. Silicone implants were banned for most
U.S. women in 1992 after some complained the devices leaked and made
them chronically ill. Widespread sales resumed in 2006 with FDA
approval over vocal protests from consumer advocates. "This is
exactly the kind of problem we were concerned about when we said we
don't know enough about these products and whether they are safe,"
said Amy Allina, policy director at the National Women's Health
Network. An estimated 5 million to 10 million women around the world
have breast implants. The FDA said its review found about 60 cases
since 1997 of anaplastic large cell lymphoma (ALCL), a type of
immune-system cancer. The number is tough to verify and some reports
could be duplicates, the agency said. The FDA said "women with breast
implants may have a very small but increased risk of developing this
disease in the scar capsule adjacent to the implant." "We need more
data" to better understand the issue, said Dr. William Maisel, chief
scientist in the FDA's device unit. ALCL is rare in women without
implants. In the United States, the disease is found in breast tissue
in about three out of every 100 million nationwide without implants.
Mentor and Allergan said they supported the FDA action and agreed the
number of cases was small. ALCL is "extremely rare and not to be
mistaken for breast cancer," Allergan spokeswoman Caroline Van Hove
said. "A woman is more likely to be struck by lightning than get this
condition," she said. Symptoms, including persistent swelling or pain
near the implant, appeared between one year and 23 years after the
devices were inserted, the FDA's Maisel said. He advised women to
contact a doctor if they have symptoms. Data on treatments is limited
but they may include removal of the implants, chemotherapy or
radiation. Officials do not know if women face a higher risk if they
get implants for reconstruction after cancer surgery or for cosmetic
reasons, Maisel said. The agency is setting up a registry to track
implants and working to add information to implant labels. "We fully
support FDA's efforts to gather additional data and study ALCL in
patients with breast implants," Mentor spokesman Christopher Allman
said. The agency plans to release interim findings from ongoing
studies of silicone implants soon. As a condition of approval, each
maker was required to study risks in 40,000 women for 10 years.
Reuters Health, 26 January 2011
<a
href="http://www.reuters.com/news/health">http://www.reuters.com/news
/health</a>
~dGossip
~tSalmon farms contaminate wild fish
~w2011-02-03
A new study has discovered that salmon farms may be contaminating
local wild fish, but how much depends on the species. The findings
from the new study raise concerns about the environmental impacts of
salmon farming. Wild fish living off the coast of Norway near salmon
farms are getting a free lunch – and more. The fish are eating food
pellets meant for their penned neighbours – pellets that can be
contaminated with chemicals known to end up in farmed fish. Now, the
wild fish harbour these chemicals, too, according to recent study
that compared contaminant levels in wild fish living near the pens
with those that live farther away and do not eat the fish food
pellets. The new study reported that the wild fish living in areas
adjacent to Norwegian salmon farms had twice the levels of certain
pollutants than fish not living near the farms. Important differences
were seen between the two fish species – salmon and saithe – studied.
The results suggest that eating wild fish that live near salmon farms
may also be a concern for human exposure to these contaminants. Farmraised salmon are fed fish pellets that have higher concentrations of
contaminants than wild salmon would have in their natural diets.
Previous research has demonstrated that this is true. These findings
have caused concerns surrounding the safety of eating farmed fish
because of human exposure to these pollutants. There are many health
benefits associated with eating fish – especially salmon – due to
their high levels of omega-3-fatty acids. These 'good' fats are
purported to protect against some heart and blood pressure health
risks. In addition, fish carry such pollutants as mercury and
persistent organic pollutants that have their own set of health
effects. To reduce exposures – especially for pregnant women and
children – experts suggest limiting the number of fish meals and
choosing to eat species with lower levels.
During the new study, the researchers collected two species of fish –
Atlantic cod and saithe – next to the penned fish at three salmon
farms and from control sites miles away from the salmon. They
analysed stomach contents and measured liver tissue for a number of
chemicals, including organochlorines, flame retardants PBDE and HBCD,
and the surfactant chemical known as PFOS. The results from the wild
fish neighbours were then compared with the distant wild fish. The
results showed that almost half of the cod and the saithe living near
the salmon farms had fish food pellets in their stomachs, indicating
that these wild fish ate residual pellets that escaped the salmon
pens. Pellets were not found in any of the control fish. The cod
living near the salmon farms had significantly higher concentrations
of pesticides, such as DDT and chlordanes, the industrial
contaminants PCBs, and the flame retardants PBDEs and
hexabromocyclododecane (HBCD), than the control fish. The saithe had
less than half the amounts of chemicals than the cod, yet they are
known to eat higher amounts of the pellets. These differences are
likely due to fish lifestyles and physiology. Furthermore, the
researchers observed that the fish living near the salmon farms had
higher amounts of lipids in their liver compared to fish from the
control sites. This is important because most of the contaminants
that were studied accumulate in lipid-rich tissues. The findings from
this study suggest that the salmon feed is escaping from the salmon
pens and is either directly ingested by wild fish living in these
areas, or settling into the underlying sediment where it may be
ingested by animals living there. These factors most likely
contribute to contamination of wild fish in the areas close to the
farms. Further studies are required in order to determine if wild
birds and marine mammals (such as seals and otters) are also at risk
for higher chemical exposures from residing near salmon farms.
Environmental Health News, 10 January 2011
<ahref="http://www.environmentalhealthnews.org/">http://www.environme
ntalhealthnews.org/</a>
~dGossip
~tAcross the world, parents pass on heart risks
~w2011-02-03
Based on the results from a new study, having a parent with a history
of heart disease almost doubles a person's risk of also getting heart
disease, no matter the person's ethnicity or home country. Every
year, heart disease kills more than 7 million people worldwide. While
previous studies have confirmed the relationship between a family
history of heart disease and a person's own heart risk in certain
populations, the new research suggests that the effect of family
history is about the same in cultures across the world. In addition,
the findings from the study suggest that if your parents had a heart
attack, changing your behaviour to a more-healthy pattern, while
helpful, isn't guaranteed to protect you completely. That's because
people whose parents had a heart attack were still more at risk
themselves after many known factors associated with heart disease
were accounted for, including diet and lifestyle choices, as well as
some genes known to be involved in heart disease. "This study
reinforces the important role of family history as one of the very
important risk factors, in addition to other known modifiable risk
factors," Dr. Christopher O'Donnell, who studies heart disease at the
National Institutes of Health and was not involved in the current
study, said. It "reinforces the need to integrate the family history
into the day-to-day practice of prevention and therapy for heart
disease." The new findings are the latest from the INTERHEART study,
which was led by Dr. Salim Yusuf of McMaster University in Ontario,
Canada and involved patients in 52 countries on every continent
except Antarctica. Altogether it included about 12,000 patients who
were being treated for their first heart attack in 1999-2003, and
about 15,000 people of the same age and sex with no history of heart
disease who were used for comparison. Approximately 18 percent of
study patients who had suffered a heart attack also had a parent with
a history of heart attack, compared to 12 percent of participants
without heart disease, according to the findings, which are published
in the Journal of the American College of Cardiology. When the
researchers factored in the patient's age, sex, and region of
residence, those who had at least one parent with a history of heart
disease were still 1.8 times more likely to get heart disease
themselves - a number that was consistent across different
ethnicities and world regions. The risk was the same whether it was
an individual's mother or father who had the heart attack, but higher
if both parents were affected or if either or both parents had a
heart attack before the age of 50.
Accounting for known heart disease risk factors including smoking and
alcohol consumption, fruit and vegetable consumption, and obesity
didn't explain the increased risk that comes with having a parent
with heart disease. And when the authors tested some of the
participants for eight genes that have been implicated in heart
disease, genetic differences still did not explain that risk. That
could be because there are so many small but important factors in
behaviour, diet, and lifestyle that play a part in explaining why
people whose parents had heart disease are more likely to get heart
disease themselves -- including many factors that haven't been
discovered yet. Furthermore, there could be hundreds or even
thousands of genes that play some role in determining a person's risk
of heart disease when they are passed from parent to child, doctors
say. "We know that family history represents many things," said Dr.
Themistocles Assimes from the Stanford University School of Medicine,
the author of an editorial accompanying the study. "A lot of those
things are genetic. Some are almost certainly environmental (factors)
that we don't know about that we can't measure," he said. But,
Assimes added, this study showed that "the excess risk associated
with family history is about the same everywhere. Whatever those
things are that are unknown, they average out to be about the same in
terms of increasing risk." Despite the many questions that still
exist about how heart disease risks are shared between generations,
just knowing that those risks are there can help doctors in different
parts of the world prevent heart disease in their patients. "A family
history is a very cheap, simple thing to (find out about)," Dr. Erin
Michos, a cardiologist at the Johns Hopkins School of Medicine who
was not involved in the study, said. "You don't have to measure
anything, there's no lab tests." When you put that together with the
fact that doctors, both in the developing and developed world, are
getting better at being able to determine who has suffered even a
small heart attack, linking parents and children to predict who is
likely to get heart disease is only going to get more accurate,
Assimes said.
Reuters Health, 26 January 2011
<a
href="http://www.reuters.com/news/health">http://www.reuters.com/news
/health</a>
~dGossip
~tBanned, contemporary chemicals widespread in U.S. pregnant women
~w2011-02-03
U.S. pregnant women are exposed to many and varied chemicals – some
have long been banned, others currently used – that may harm the
foetus during sensitive periods of development. For the fist time, a
new study has discovered that the bodies of virtually all U.S.
pregnant women – and possibly their unborn children – carry multiple
chemicals, including some banned since the 1970s and others used in
common products such as non-stick cookware, processed foods and
personal care products. While the Centres for Disease Control (CDC)
has published previous reports on chemical levels in the general
population, this is the first study to examine a broad range of
chemicals specifically in pregnant women. During the new study, the
researchers analysed the data for 163 chemicals and detected about
three-quarters of them at varying levels in some or all of the women.
They found almost all – 99 to 100 percent – of the pregnant women
carried polychlorinated biphenyls (PCBs), organochlorine pesticides,
perfluorinated compounds (PFCs), phenols, polybrominated diphenyl
ethers (PBDEs), phthalates, polycyclic aromatic hydrocarbons (PAHs)
and perchlorate. Other chemicals detected in the study group were
PBDEs – compounds used as flame retardants and now banned in many
states, including California – and DDT – an organochlorine pesticide
banned in the United States in 1972. DDT was found at lower levels
and in fewer women than its breakdown product DDE. The health risks
for mother and child associated with exposure to this many chemicals
at detectable – and sometimes high – levels is unknown. Low-level
exposures to some of these chemicals during the prenatal period – a
time of rapid growth – can lead to a host of long-term health
effects, including birth defects, reproductive problems, and cancer.
Surprisingly, DDE – a breakdown product of the long-banned DDT
pesticide – was found in every woman and at some of the highest
levels measured for any of the chemicals.
Other chemicals found at high levels include perfluoroctane sulfonic
acid (PFOS), which is found in waterproof clothing and stain
repellent treated carpets; triclosan, found in antibacterial soap and
products; and mono-ethyl phthalate (MEP), found in cosmetics and
fragrances. Animal or human studies show all of these chemicals can
interfere with the endocrine system. What these results imply for the
women's health – or the health of the developing foetus – is not
clear. Although the chemicals found are similar to those identified
previously in nonpregnant women, pregnant women are more vulnerable
than the general population. Many of the pollutants measured in the
study can pass through the placenta from the mother to the developing
foetus. They have been measured in cord blood, foetal blood and
amniotic fluid. Many of the chemicals found in the women, though, are
known to contribute to similar health problems. Broadly, these can
include effects on the heart, immune system and reproduction. A more
specific example is how low exposures to lead or mercury alone may
only slightly increase the risk of adverse neurological effects while
exposures to both of them at the same time can produce a higher risk.
The cumulative health risk from exposure to such a broad range of
compounds is just beginning to be studied. The researchers from the
University of California, San Francisco, used data from the National
Health and Nutritional Examination Survey (NHANES) to determine if
the 163 chemicals were in the blood or urine of 268 U.S. pregnant
women sampled between 2003 and 2004. The CDC conducts NHANES every
two years. The authors recommend that future work should focus on
understanding sources of exposure and the health impacts from
exposures to multiple chemicals.
Environmental Health News, 14 January 2011
<ahref="http://www.environmentalhealthnews.org/">http://www.environme
ntalhealthnews.org/</a>
~dGossip
~tDoes the Smoke Ever Really Clear? Thirdhand Smoke Exposure Raises
New Concerns
~w2011-02-03
While you may have never heard of thirdhand smoke, or THS, chances
are you have smelled it. THS is, in the words of The New York Times,
“the invisible yet toxic brew of gases and particles clinging to
smokers’ hair and clothing, not to mention cushions and carpeting,
that lingers long after secondhand smoke [SHS] has cleared from a
room.” In a recent study investigating the potential dangers of THS
has received a flurry of coverage in the international media and the
scientific press. In the United States, court cases are beginning to
appear in which plaintiffs are citing these alleged dangers, despite
a lack of human health studies on the long-term health effects of THS
exposure. So how dangerous might THS really be? The answer, still to
be pronounced, will depend on many factors. THS was a topic of
interest long before it received its present name. The seed of the
idea that cigarette smoke toxicants might linger on room and car
surfaces long after the smoke itself was gone was planted in 1953,
when it was reported that smoke condensate painted onto mice caused
cancer. Thirdhand smoke consists of residual tobacco smoke pollutants
that 1) remain on surfaces and in dust after tobacco has been smoked,
2) are re-emitted back into the gas phase, or 3) react with oxidants
and other compounds in the environment to yield secondary pollutants.
In 1991 the house dust of smokers’ homes was first found to be
contaminated with nicotine. Later, in 2004, nicotine was quantified
in the dust of nonsmokers’ homes and homes in which mothers smoked in
the house over the preceding 3 months. In homes with the highest SHS
exposure, in which the mothers smoked in areas where their children
were present, nicotine in dust averaged 64.0 µg/m2 in living rooms
and 15.8 µg/m2 in infants’ bedrooms. Surfaces in living rooms and
infants’ bedrooms averaged nicotine coatings of 73.05 µg/m2 and 56.26
µg/m2, respectively. The same study showed the dust and surfaces of
homes in which smokers had tried to limit their children’s exposure
(for instance, by sometimes smoking outdoors) were also contaminated,
although to a lesser degree. However, no nicotine was found in the
dust or on the surfaces of homes never exposed to tobacco smoke. In
2008 similar findings were reported for cars. Nicotine was detected
in significantly greater quantities in the dust (mean 19.51 µg/g) and
on the dashboards (mean 8.61 µg/m2) of 78 vehicles belonging to
people who smoked in their vehicles than in the dust (mean 3.37 µg/g)
and on the dashboards (mean 0.06 µg/m2) of 20 vehicles of
nonsmokers.
Eight smokers had imposed a smoking ban in their vehicles for at
least 12 months. Their vehicles nevertheless were contaminated with
nicotine (mean 11.61 µg/g in dust and 5.09 µg/m2 on the dashboard).
However, the authors note that the cars may have been contaminated by
smoke that entered the car from outside and that smoking bans may not
have been complied with 100% of the time. In a study conducted in
2010, research found that THS also remains after smokers move out of
their homes, even after being vacant for two months and being
prepared for new residents, sometimes with new carpeting and paint.
Meanwhile, other lines of research have confirmed some smoke
compounds adsorb onto surfaces and then desorb back into the air over
time, providing a source of tobacco toxicants that lingers long after
people finish smoking. The term thirdhand smoke may have first
appeared in print in 2006, but it became more widely known in 2009
when it was used by Jonathan Winickoff, an associate professor of
paediatrics at Harvard Medical School, and colleagues in a paper
published in Pediatrics. In that study, the researchers reported that
65.2% of nonsmokers and 43.3% of smokers believed THS could harm
children and that such beliefs were independently associated with the
imposition of home smoking bans. In addition, the authors wrote that
emphasising the potential dangers of THS to children’s health might
be important in encouraging parents not to smoke around their
children. A new development emerged when Mohamad Sleiman, a chemist
with the Indoor Environment Department of the Lawrence Berkeley
National Laboratory (LBNL) Environmental Energy Technologies
Division, and colleagues reported that nicotine adsorbed onto
surfaces reacted with nitrous acid—an air pollutant found in vehicle
exhaust and produced by improperly vented gas stoves and burning
tobacco—to form tobacco-specific nitrosamines (TSNAs) including 1-(Nmethyl-N-nitrosamino)-1-(3-pyridinyl)-4-butanal (NNA), 4-(Nnitrosomethylamino)-1-(3-pyridinyl)-1-butanone (NNK), and Nnitrosonornicotine (NNN). There is some evidence NNA is mutagenic.
NNK and NNN are classified by the International Agency for Research
on Cancer as human carcinogens and by the National Toxicology Program
as reasonably anticipated to be human carcinogens.
Environmental Health Perspectives, 1 February 2011
<a href="http://ehponline.org">http://ehponline.org</a>
~dGossip
~tNovel, sugar-based surfactants more stable and sustainable
~w2011-02-03
Researchers from the University of Yale have developed a new family
of surfactants based on simple sugars and natural oils, which hold
promise for cleaning without a long list of environmental side
effects. Surfactants – the active ingredients in many household
products, including cleaners and personal care products – are
produced on the scale of millions of tons per year. In nearly every
application, after a few minutes of use, they are rinsed with water
either down the drain or directly into the environment.
Unsurprisingly, there have been harmful effects from such large-scale
releases. When surfactants are slow to break down in the environment,
problems range from unsightly foaming to toxic effects on aquatic
organisms. Some of these chemicals – for example, the widely used
nonylphenol ethoxylates – have been implicated in endocrine
disruption. The term is used to describe substances that can alter
hormone activity in the body. In recent years, there has been a push
toward sugar-based surfactants because of improved biodegradability
and lower toxicity. In addition, they are derived from natural and
renewable sources, adding another "green chemistry" benefit. Sugarbased surfactants have been commercially available for more than a
decade. Formulations of the alkyl polyglycosides (APGs) are used in a
variety of consumer products for laundry, hair and skin care. On an
ingredient label they are usually identified as a variety of
"glucosides," for example decyl glucoside or lauryl glucoside. The
use of APGs is growing at a faster rate than petroleum-based
surfactants. However, chemists are trying to improve APGs. Many of
the sugar-derived chemicals can fall apart when exposed to acids in
water because the link between the water-loving and oil-loving ends
of the APG molecules is vulnerable. Furthermore, depending on the
variety of the APG produced, the manufacturing process relies on high
temperature and pressure and energy-consuming purification steps. In
the new study, the researchers investigated a new process to make a
stronger chemical bond in one particularly weak spot of sugar-based
surfactant molecules.
The researchers transformed a precursor chemical by treating it with
a chemical mix that included alkyl aldehydes. Several sugar
derivatives with straight or cyclic tails were produced, depending on
the conditions that were used to convert the intermediary chemical.
The new chemicals were tested for surface tension and foaming and the
results were compared to current APG surfactant performance. The
researchers showed that the new surfactants could be prepared in a
two-step reaction under mild conditions, using only a minimum of
solvent. It was not necessary to purify the products by column
chromatography, a procedure that would consume large volumes of
potentially hazardous solvents. This improves the prospects for
producing the chemicals on a large scale. The researchers
demonstrated that the technical performance of the new surfactants is
as good as existing APG technology. This was determined by measuring
surface activity – how efficient the chemicals are at reducing the
surface tension of water. It is important for surface tension to drop
quickly with just a small amount of added chemical, for surfactant
applications. The best chemical tested in the study worked at just 40
milligrams (the weight of a few grains of rice) per litre. In
addition, the researchers explored the foaming properties of the new
chemicals. Foaming is desirable for some personal care products like
shampoos, but would be a disadvantage in laundry applications and
some industrial cleaners. The Yale chemicals were low foamers
compared to a conventional surfactant, sodium dodecyl sulphate (SDS).
But when mixed with SDS, the resulting foam lasted longer. Thus they
could be useful in either low- or high-foam formulations. The
biodegradability of the new chemicals was not measured, but U.S.
Environmental Protection Agency software suggests that the changes
made to improve acid stability will not affect how microbes
disassemble the chemicals. The glucose end of the molecule contains
many carbon-oxygen bonds that are common places for microbial attack.
If the surfactants are made from long, straight-chain aldehydes, that
should also provide bacteria with a familiar food source.
The new sugar-based surfactants may offer more stable and sustainable
varieties to use in consumer products. The novel chemicals are more
stable under harsh conditions and work just as well in laboratory
tests as the sugar-based surfactants currently used. In addition,
their chemical production is a significant improvement over current
methods in that it uses fewer resources and produces a wider array of
chemicals with surfactant properties. This new family of sugar-based
surfactants complements APGs that are already on the market. A wider
variety of molecular structures means that manufacturers of green
consumer products are more likely to come up with formulations that
meet all the goals of function, performance, economy and low
environmental footprint. Replacing the weak spot in APGs with a
sturdier alternative allows the sugar-based chemicals to be used in
more applications. The two parts of the new molecule are linked with
a bond between two carbon atoms instead of a bond between an oxygen
and a carbon atom. The stronger carbon-carbon bond is unaffected by
strong acid. That robustness could help in industrial applications
and heavy-duty household formulations, for example acidic tile
cleaners. The new surfactants are made from glucose, which is widely
found in nature. It is one of the components of table sugar and is
the repeating chain unit in cellulose, which gives plants their
supporting structure. Glucose acts as the water-loving part of the
surfactant. The oil-loving part of the surfactant is made from
aldehydes. Aldehydes are a diverse set of chemicals; some occur in
nature and others are produced from petrochemicals. In this study,
the aldehydes could be obtained by treating plant oils. The
researchers say their next step will be to explore algae as a
possible source for all of the surfactants' starting materials. The
carbohydrate portion of algal biomass could provide the sugar, and
algal oils could give the right kinds of aldehydes. Algae oils are
particularly rich in carbon-carbon double bonds that can react with
ozone to produce aldehydes. If that approach is successful,
surfactant production could supplement algae-to-fuel technology.
Environmental Health News, 12 January 2011
<ahref="http://www.environmentalhealthnews.org/">http://www.environme
ntalhealthnews.org/</a>
~dGossip
~tMercury in San Francisco Bay Fish a Legacy of California Mining
~w2011-02-03
Mercury contamination, a worldwide environmental problem, has been
called "public enemy No. 1" in California's San Francisco Bay.
Mercury mining and gold recovery in the mid-1800s to late 1900s,
combined with its use in present-day oil refineries, chemical
manufacturing plants and wastewater treatment plants have contributed
enough mercury to threaten wildlife and prompt a fish-consumption
advisory in the Bay Area. With so many possible sources of
contamination, environmental scientists and regulatory agencies would
like to know which specific sources contribute most to harmful levels
of mercury in the aquatic food web. In the past, obtaining this sort
of information would not have been possible. However, with the use of
a mercury "fingerprinting" technique, researchers from the University
of Michigan, the University of California, Davis, and the San
Francisco Estuary Institute have identified the main sources of
mercury in bay floor sediments and shown that small fish near the
base of the food web acquire their mercury from those sediments.
Without a clear answer to what was responsible for mercury in fish in
San Francisco Bay, we needed a way to trace its origins," said Joel
Blum, a professor of ecology at University of Michigan. "This is the
first study to track mercury directly from source to sediment to food
web." While this study draws conclusions for only San Francisco Bay,
the fingerprinting technique can be broadly applied, said graduate
student Gretchen Gehrke, the paper's lead author. "Mercury
contamination is a problem in areas all over the world, and most of
those places have multiple possible mercury sources. There's a lot of
interest in figuring out which sources are contributing the mercury
that most readily gets into the food web and creates environmental
and health risks."
The findings from the new study appear in two companion papers, one
in the 1 February issue of the journal Geochemica et Cosmochimica
Acta and the other published online 21 January in Environmental
Science & Technology. Mercury is a naturally occurring element, but
some 2,000 tons of it enter the global environment each year from
human-generated sources. Deposited onto land or into water, mercury
is picked up by some types of microorganisms, which convert a small
portion of it to methylmercury, a highly toxic form that builds up in
fish and the animals—and people—that eat them. The primary way people
in the United States are exposed to methylmercury is by eating fish
and shellfish. Health effects include damage to the central nervous
system, heart and immune system. The developing brains of young and
unborn children are especially vulnerable. In San Francisco Bay,
Gehrke, Blum and colleagues suspected small fish such as silverside
and topsmelt were acquiring mercury from sediments on the bay floor
and then passing it along to larger fish and other fish-eating
animals, but it also was possible that mercury from the atmosphere or
localized industrial sources was ending up in the fish. In order to
resolve the question, the research team compared chemical
"fingerprints" of mercury in sediments and in fish, much as a
detective compares a suspect's fingerprints to those found at a crime
scene. The fingerprints result from a natural phenomenon called
isotopic fractionation, in which different isotopes of mercury react
to form new compounds at slightly different rates. In one type of
isotopic fractionation, mass-dependent fractionation (MDF), the
different rates depend on the masses of the isotopes. In massindependent fractionation (MIF), the behavior of the isotopes depends
not on their absolute masses but on whether their masses are odd or
even.
The team sampled sediment at 20 sites in the bay and fish at 26
sites. "We used young fish, less than four months old, that have a
very small home habitat," said Gehrke. "Because they're restricted to
one location, rather than migrating around the bay, any mercury they
have is most likely present in that location." Looking at MDF
fingerprints in sediments, the researchers saw that the values were
distributed along a gradient from north to south. MDF fingerprints in
the fish from different locations mirrored the pattern found in the
sediments, suggesting the fish were acquiring mercury directly from
the sediments. Where did the mercury in the sediments come from? "Our
analysis of the sediments showed that it's most likely coming from
either two or three dominant sources," Gehrke said. "There's one
distinct fingerprint coming from historic mercury mines to the south
and a different fingerprint coming from historic gold mines to the
north. We see intermediate values in sediments in the middle of the
bay, which could represent either mixing of the two or possibly a
separate third source, so we can't say for sure whether it's two or
three sources. But the fact that we see at least two separate
fingerprints and a strong spatial gradient instead of a hodgepodge of
many different fingerprints tells us that the mercury is coming from
a small number of large sources rather than a lot of localised
sources like a power plant here, a refinery there." The researchers
hope the results will help local agencies decide where to focus their
efforts to protect wildlife from exposure to mercury.
Environmental Protection News, 2 February 2011
<a href="http://www.eponline.com">http://www.eponline.com</a>
~dGossip
~tMemory problems? Sleep on it
~w2011-02-03
According to the researchers of a new study, the best way not to
forget a newly learned poem, card trick or algebra equation may be to
take a quick nap. The researchers were surprised by their own
findings. Researchers in Germany have found the brain is better
during sleep than during wakefulness at resisting attempts to
scramble or corrupt a recent memory. During their recent study,
published in Nature Neuroscience, the researchers were able to
provide new insights into the hugely complex process by which we
store and retrieve learned information. Previous studies have
demonstrated fresh memories, stored temporarily in a region of the
brain called the hippocampus, did not gel immediately. In addition,
it was known that reactivation of those memories soon after learning
played a crucial role in their transfer to more permanent storage in
the brain's "hard drive", the neocortex. However, during wakefulness,
this period of reactivation renders the memories more fragile.
Learning a second poem at this juncture, for example, will likely
make it harder to commit the first one to deep memory.
The Australian, 25 January 2011
<a
href="http://www.theaustralian.com.au">http://www.theaustralian.com.a
u</a>
~dGossip
~tBeastly Beauty Products: Exposure to Inorganic Mercury in SkinLightening Creams
~w2011-02-03
The most common exposure to mercury is from organic methylmercury
found in fish. People with no workplace exposure to mercury typically
have low levels of exposure to inorganic or elemental mercury,
although nonoccupational exposure can occur from dental amalgams,
some herbal medicine products, and cosmetics that contain mercury.
When a New York City (NYC) biomonitoring study revealed that
thousands of women in that city may have been exposed to dangerous
levels of inorganic mercury from imported skin-lightening creams,
city health officials enlisted the help of U.S. and international
health agencies in getting the creams off local store shelves. In
2004 the NYC Department of Health and Mental Hygiene (DOHMH)
conducted the nation’s first local Health and Nutrition Examination
Survey. Analysis of urine specimens from 1,840 adult New Yorkers
collected during the survey yielded a geometric mean mercury
concentration of 0.73 µg/L, slightly higher than the national average
of 0.5 µg/L. The authors took note when 13 women were found to have
urine mercury concentrations exceeding the state’s reportable level
of 20 µg/L; 4 women had levels exceeding 50 µg/L. All 13 highly
exposed women were Hispanic or black, and 10 had been born in the
Dominican Republic. Each of the 9 women interviewed on followup had
used mercury-containing skin-lightening cream. One such product
sampled by DOHMH workers contained 6,190 ppm mercury. The U.S. Food
and Drug Administration (FDA) limit for mercury in skin-care products
is 1 ppm.
Extrapolating from the population sampled, the authors estimate
nearly 27,000 New Yorkers may have urine mercury levels exceeding 20
µg/L. Although the researchers did not assess potential health
effects among the highly exposed women, occupational studies indicate
kidney and neurologic toxicity may occur when urine mercury levels
exceed 20 µg/L.City health officials responded to the survey results
by seizing 12 brands of illegally imported cosmetics from store
shelves. All the products listed mercury as an active ingredient.
Press releases issued by the DOHMH urged residents to report mercurytainted cosmetics and the shops selling them, and New Jersey
investigators were enlisted to plug the pipeline to importers in that
state. The Pan American Health Organisation called on the Dominican
Republic to stop manufacturing the dangerous products. The Dominican
Secretary of Health reportedly has notified all laboratories to stop
manufacturing mercury-containing skin-care products. The authors
realise some tainted products may still cross the border, as they
have for years despite FDA prohibitions. But they believe their
efforts, coupled with evidence of mercury’s toxicity and continued
vigilance, will substantially reduce the availability and use of
these products.
Environmental Health Perspectives, 1 February 2011
<a href="http://ehponline.org">http://ehponline.org</a>