1. Culprit hidden in plain sight in Alzheimer disease development

    June 21, 2017 by Ashley

    From the IOS Press press release:

    A new study by researchers at the University of Montana, Universidad del Valle de México, Instituto Nacional de Pediatría, Boise State, and Universidad Nacional Autónoma de México, heightens concerns over the detrimental short- and long-term impact of airborne iron-rich strongly magnetic combustion-derived nanoparticles (CDNPs) present in young urbanites’ brains. Using transmission electron microscopy, the researchers documented by abundant combustion nanoparticles in neurons, glial cells, choroid plexus, and neurovascular units of Mexico City children, teens and young adults chronically exposed to concentrations above the US-EPA standards for fine particulate matter. Residents in Mexico City are exposed from conception to harmful neurotoxic air pollutants. These findings are published in the Journal of Alzheimer’s Disease.

    The detrimental impact of these tiny particles getting into the brain through the nasal and olfactory epithelium, the lungs and the gastrointestinal system is quickly recognized by extensive alterations in critical neuronal organelles including mitochondria, as well as axons and dendrites. Since these nanoparticles are in close contact with neurofilaments, glial fibers and chromatin, the researchers are very concerned about their potential for altering microtubule dynamics, accumulation and aggregation of unfolded proteins, mitochondrial dysfunction, altered calcium homeostasis and insulin signaling, and epigenetic changes.

    Mexico City children, teens and young adults have shown key markers of Alzheimer’s disease (AD): hyperphosphorylated tau and amyloid plaques along with significant brain and intrathecal neuroinflammation, dysregulated immune responses, breakdown of epithelial and endothelial barriers, extensive damage to the neurovascular unit, and brain accumulation of metals associated with combustion. Moreover, these seemingly healthy young people have olfaction deficits, dysregulation of feeding hormones, deficiencies in attention and short-term memory, and below-average scores in Verbal and Full Scale IQ compared to age, gender, and socioeconomic status-matched low air pollution residents. The cognitive problem is particularly serious for overweight female teens carrying an allele of the apolipoprotein E (APOE) ?4, the most prevalent genetic risk factor for AD.

    “In the context of serious continuous exposures to high concentrations of fine particulate matter (PM 2.5) and ozone, our current electron microscopy findings and the extensive literature associating air pollutants with brain damage, the issue of who is at risk of neurodegeneration at an early age should be an urgent public health concern,” said Dr. Lilian Calderon-Garcidue?as. “The effects of poverty, urban violence and urban stress on impaired cognitive skills are also very important for the developing brain and can’t be ignored. We know gender, BMI, and APOE influence children’s cognitive responses to air pollution.”

    According to the researchers, the problem of having combustion-derived nanoparticles in children’s brains — developing brains — is very serious. These particles are ubiquitous and present in high concentrations in children as young as 3 years old. The particles contain transition neurotoxic metals and they are certainly causing extensive brain damage in key organelles. “The predominant combustion particles in young brains have properties that enable them to cause oxidative damage because these nanoparticles are capable of crossing all barriers. No barrier is spared,” Dr. Calderón-Garcidue?as emphasized.

    Angélica González-Maciel added, “People with children and teens struggling in school and facing a significant increase of violence in school, streets, parks, and public transportation are deeply concerned about the impact these particles have on children’s behavioral patterns and academic performance and parents question what they can do to protect their families.”

    All involved researchers agreed that in spite of the driving restrictions policies [that are clearly ineffective (Davis LW. Sci Rep 7: 41652, 2017)], millions of Mexico City residents continue to be exposed to very unhealthy concentrations of both PM 2.5 and ozone, both known risk factors for AD.

    “Our results,” said Dr. Calderón-Garcidue?as, “highlight the urgent need for significantly decreasing the concentrations of fine particulate matter and ozone in Mexico City and the adjacent polluted states. Multidisciplinary intervention strategies could provide paths for prevention or amelioration of air pollution targeted cognitive deficits and possible long-term AD progression.”

    The combined effects of combustion-derived nanoparticles, residency in a highly-polluted city, poor nutrition, obesity, metabolic syndrome, urban stress, lower brain and cognitive reserves, and APOE ?4 could lead to an acceleration of neurodegenerative changes among precarious young brains.

    The authors concluded: highly oxidative, combustion nanoparticles entering young developing brains — the culprit hidden in plain sight in Alzheimer’s disease development — constitute a very serious public health issue, with grave social and economic consequences.

    Efforts should also be aimed to identify and neuroprotect high risk young populations. Unfortunately, to date that is not happening.


  2. Exposure to specific toxins and nutrients during late pregnancy and early life correlate with autism risk

    June 15, 2017 by Ashley

    From the The Mount Sinai Hospital / Mount Sinai School of Medicine press release:

    Using evidence found in baby teeth, researchers from The Senator Frank R. Lautenberg Environmental Health Sciences Laboratory and The Seaver Autism Center for Research and Treatment at Mount Sinai found that differences in the uptake of multiple toxic and essential elements over the second and third trimesters and early postnatal periods are associated with the risk of developing autism spectrum disorders (ASD), according to a study published June 1 in the journal Nature Communications.

    The critical developmental windows for the observed discrepancies varied for each element, suggesting that systemic dysregulation of environmental pollutants and dietary elements may serve an important role in ASD. In addition to identifying specific environmental factors that influence risk, the study also pinpointed developmental time periods when elemental dysregulation poses the biggest risk for autism later in life.

    According to the U.S. Centers for Disease Control and Prevention, ASD occurs in 1 of every 68 children in the United States. The exact causes are unknown, but previous research indicates that both environmental and genetic causes are likely involved. While the genetic component has been intensively studied, specific environmental factors and the stages of life when such exposures may have the biggest impact on the risk of developing autism are poorly understood. Previous research indicates that fetal and early childhood exposure to toxic metals and deficiencies of nutritional elements are linked with several adverse developmental outcomes, including intellectual disability and language, attentional, and behavioral problems.

    “We found significant divergences in metal uptake between ASD-affected children and their healthy siblings, but only during discrete developmental periods,” said Manish Arora, PhD, BDS, MPH, Director of Exposure Biology at the Senator Frank Lautenberg Environmental Health Sciences Laboratory at Mount Sinai and Vice Chair and Associate Professor in the Department of Environmental Medicine and Public Health at the Icahn School of Medicine at Mount Sinai. “Specifically, the siblings with ASD had higher uptake of the neurotoxin lead, and reduced uptake of the essential elements manganese and zinc, during late pregnancy and the first few months after birth, as evidenced through analysis of their baby teeth. Furthermore, metal levels at three months after birth were shown to be predictive of the severity of ASD eight to ten years later in life.”

    To determine the effects that the timing, amount, and subsequent absorption of toxins and nutrients have on ASD, Mount Sinai researchers used validated tooth-matrix biomarkers to analyze baby teeth collected from pairs of identical and non-identical twins, of which at least one had a diagnosis of ASD. They also analyzed teeth from pairs of normally developing twins that served as the study control group. During fetal and childhood development, a new tooth layer is formed every week or so, leaving an “imprint” of the micro chemical composition from each unique layer, which provides a chronological record of exposure. The team at the Lautenberg Laboratory used lasers to reconstruct these past exposures along incremental markings, similar to using growth rings on a tree to determine the tree’s growth history.

    “Our data shows a potential pathway for interplay between genes and the environment,” says Abraham Reichenberg, PhD, Professor of Psychiatry and Environmental Medicine and Public Health at the Icahn School of Medicine at Mount Sinai. “Our findings underscore the importance of a collaborative effort between geneticists and environmental researchers for future investigations into the relationship between metal exposure and ASD to help us uncover the root causes of autism, and support the development of effective interventions and therapies.”

    Additional studies are needed to determine whether the discrepancies in the amount of certain metals and nutrients are due to differences in how much a fetus or child is exposed to them or because of a genetic difference in how a child takes in, processes, and breaks down these metals and nutrients.


  3. Study links flower pesticides to neurobehavioral effects in children

    May 21, 2017 by Ashley

    From the University of California – San Diego press release:

    Ecuador is the third largest producer of cut flowers in the world, primarily roses, many of which are destined to be sold for Mother’s Day. The industry employs more than 103,000 people, and relies heavily on agricultural pesticides.

    In a paper published in the May 2017 issue of the journal NeuroToxicology, researchers at the University of California San Diego School of Medicine, with colleagues in Ecuador and Minnesota, have found altered short-term neurological behaviors in children associated with a peak pesticide spraying season linked to the Mother’s Day flower harvest. This study examined children who did not work in agriculture but who lived in agricultural communities in Ecuador.

    “Our findings are among the first in non-worker children to suggest that a peak pesticide use period (the Mother’s Day flower production) may transiently affect neurobehavioral performance,” said first author Jose R. Suarez-Lopez, MD, PhD, assistant professor in the Department of Family Medicine and Public Health at UC San Diego School of Medicine.

    “Children examined sooner after the flower harvest displayed lower performance on most measures, such as attention, self-control, visuospatial processing (the ability to perceive and interact with our visual world) and sensorimotor (eye-hand coordination) compared to children examined later in a time of lower flower production and pesticide use.”

    “This discovery is novel because it shows that pesticide spray seasons can produce short-term alterations in neurobehavioral performance in addition to the long-term alterations that have been previously described. This is troublesome because the altered mental functions observed are essential for children’s learning, and in May-July, students typically take their end-of-year exams. If their learning and performance abilities are affected in this period, they may graduate from high school with lower scores which may hinder their ability to access higher education or obtain a job.”

    Early exposure to commonly applied agricultural pesticides is associated with neurobehavioral delays in children, such as attention deficit hyperactivity disorder. Pesticide exposure has been linked to altered development of reflexes and psychomotor and mental function in newborns. Boys appear more susceptible than girls.

    Suarez-Lopez, who is principal investigator of the ESPINA study, an on-going, long-term study of environmental pollutants and child development in Ecuador, said past animal research had suggested that fluctuating levels of pesticide exposure might also produce corresponding, short-term neurobehavioral effects.

    He and colleagues tested 308 children, ages four to nine, living in floricultural communities in Ecuador (but who did not actually work in agriculture themselves) prior to peak Mother’s Day flower production and within 100 days after harvest. Behavior and blood tests were conducted.

    Organophosphate-based insecticides, commonly used to treat flowers for pests before export, inhibit an enzyme called acetylcholinesterase (AChE) that regulates acetylcholine, a neurotransmitter vital to promoting communications between nerve cells in the brain and body. The insecticides are also directly toxic to neurons and supporting cells called glia. In previous research, Suarez-Lopez and colleagues had shown that lower AChE activity is associated with lower attention, inhibitory control and memory scores, again affecting boys more than girls.

    The authors note that the study was cross-sectional, collecting and analyzing observational data on a representative population for a specific point in time. “Our findings need to be replicated in studies of children with assessments conducted before, during and after peak exposure periods,” said Suarez-Lopez. “But given the evidence thus far, and the potential for pesticide exposure to alter both short- and long-term learning abilities, cognition, social interactions and overall well-being, taking additional precautions to shield children from exposure is certainly advised.”

    Co-authors include: Harvey Checkoway, Wael K. Al-Delaimy, Sheila Gahagan, UC San Diego; and David R. Jacobs, Jr., University of Minnesota.


  4. Social challenges amplify negative effects of childhood lead exposure

    May 10, 2017 by Ashley

    From the American Academy of Pediatrics press release:

    Scientists already know early lead exposure can slow a child’s cognitive and language development. Findings of an abstract being presented at the 2017 Pediatric Academic Societies Meeting show lead’s impact is especially strong for children in families also facing socioeconomic challenges.

    Researchers will present the abstract, “Interrelationships Between Social Determinants of Health and Early Lead Exposure: A Longitudinal Analysis of Impacts on Child Development,” on Monday, May 8, beginning at 10:30 a.m. in the Moscone West Convention Center.

    Abstract author Bridget Wieczkowski, MD, said the goal of the study was to determine whether the impact of lead, a biotoxin, was greater for children who also faced the “toxic stress” of poverty such as exposure to violence, homelessness, food insecurity and low parent literacy.

    Many studies have documented impacts of low level lead exposure on child development, she said. However, there has been limited research examining these impacts in the context of Centers for Disease Control and Prevention (CDC) guidelines updated in 2012 that recognize blood lead levels of less than half the amount previously considered safe are linked with delayed cognitive skills, inattention, impulsivity, aggression and hyperactivity.

    Dr. Wieczkowski worked with a team of researchers to analyze data that had been collected as part of the Bellevue Early Language and Education (BELLE) Project, a large, National Institutes of Childhood Health and Human Development-funded study that followed 450 newborns and their families from birth.

    They found that levels above 5 micrograms per deciliter of lead in a child’s blood, which is the current threshold set by the CDC as cause for concern, was associated with reduced cognition and vocabulary at age 3 that continued when tested again a year and a half later. Further analysis showed larger impacts on development at age 54 months for families with psychosocial risks and low literacy.

    “These findings underscore the importance of monitoring children during infancy and the toddler years, which are critical periods for both brain development and lead exposure,” Dr. Wieczkowski said. Young children, with their rapidly developing brains, also are more likely to ingest lead in their environment because they put more objects in their mouths and spend more time on the floor.

    “This is true for all children, but especially for those most vulnerable to lead’s harmful effects because of poverty,” she said.

    “Our health care system needs to be funded so that it can help all children reach their potential as adults,” she said, noting that programs like Medicaid are critically important to achieve this goal.


  5. Flame retardant chemicals may affect social behavior in young children

    March 12, 2017 by Ashley

    From the Oregon State University press release:

    Some chemicals added to furniture, electronics and numerous other goods to prevent fires may have unintended developmental consequences for young children, according to a pilot study released today.

    Researchers from Oregon State University found a significant relationship between social behaviors among children and their exposure to widely used flame retardants, said Molly Kile, an environmental epidemiologist and associate professor in the College of Public Health and Human Sciences at OSU.

    “When we analyzed behavior assessments and exposure levels, we observed that the children who had more exposure to certain types of the flame retardant were more likely to exhibit externalizing behaviors such as aggression, defiance, hyperactivity, inattention and bullying,” said Kile, the corresponding author of the study, which was published today in the journal Environmental Health.

    “This is an intriguing finding because no one had previously studied the behavioral effects of organophosphate classes of flame retardants, which have been added to consumer products more recently.”

    Flame retardants are found throughout the built environment in furniture, mattresses, carpeting, electronics, vehicles and more. The chemicals are added to the products and are not bound in the material, which causes them to be released into indoor environments.

    Manufacturers began adding flame retardants in 1975, in response to new legislation in California designed to reduce flammability in common household items. The state updated its flammability standards in 2014, and now allows furniture manufacturers to meet the standards without adding flame retardant chemicals to their products, but the chemicals are still widely used and they linger in the indoor environment.

    There are growing concerns that some flame retardants may have unintended impacts on health and development in children, and this study contributes to that body of research.

    The most common types of flame retardants found in the built environment are brominated diphenyl ethers (BDEs) and organophosphate-based flame retardants (OPFRs). OPFRs emerged as an alternative to BDEs in an effort to address some of the environmental health concerns posed by BDEs, which tend to remain in the environment for long periods.

    Past research has shown that both BDEs and OPFRs are linked to poorer cognitive function in children. But less is known about the relationship between the flame retardants and children’s social and emotional health, particularly during early childhood, a key developmental period for learning.

    “The social skills children learn during preschool set the foundation for their success in school, and also for their social and emotional health and well-being later in life,” said Shannon Lipscomb, an associate professor and lead of the human development and family sciences program at OSU-Cascades and a co-author of the study.

    For this study, the OSU research team recruited 92 Oregon children between ages 3-5 to wear a silicone wristband for seven days to measure exposure to flame retardants.

    The team included Kile, Lipscomb; Megan McClelland and Megan MacDonald of the OSU College of Public Health and Human Sciences; Kim Anderson of the OSU College of Agricultural Sciences; and Andres Cardenas of the Harvard T.H. Chan School of Public Health and an OSU doctoral graduate. The research was supported by OSU’s Hallie E. Ford Center for Healthy Children and Families and the Environmental Health Science Center at OSU.

    The wristbands, developed by Anderson at OSU, have a porous surface that mimics a cell, absorbing chemicals that people are exposed to through their environment. When the wristbands are returned, Anderson can screen for up to 1,200 chemicals that may accumulate. The wristband is an easy and non-invasive way to sample children’s chemical exposure.

    The researchers had parents or primary caregivers complete questionnaires about socio-demographics and the home environment, and preschool teachers completed behavior assessments for each participating child. In all, researchers had complete data and wristband results for 69 children.

    Their analysis showed that all of the children were exposed to some level of flame retardant. Children who had higher exposure rates of OFPRs showed less responsible behavior and more aggression, defiance, hyperactivity, inattention and bullying behaviors. Children with higher exposure to BDEs were seen as less assertive by their teachers. All of these social skills play an important role in a child’s ability to succeed academically and socially.

    “We detected these links between flame retardant and children’s social behaviors while controlling for differences in family demographics, home learning environments and adversity,” Lipscomb said. “This suggests that flame retardants may have a unique effect on development apart from the effects of children’s early social experiences.”

    Further study is needed to better understand the links between flame retardants and children’s social skill development, the researchers said. They plan to pursue funding for a new study that continues for a longer period of time and considers how other aspects of children’s lives might affect the impact of flame retardants on their development.

    “The results of this research to date have shown potential impacts for child health and warrant a more thorough investigation,” Kile said.”If scientists find strong evidence that exposure to flame retardants affects children’s behaviors, we can develop strategies that prevent these exposures and help improve children’s lives. This type of public health science is needed to figure out how to address the root causes of behavioral concerns that can affect children’s school readiness and overall well-being.”


  6. Rat study reveals long-term effects of adolescent amphetamine abuse on the brain

    April 5, 2016 by Ashley

    From the University of Illinois at Urbana-Champaign media release:

    addiction pillsA study of rats given regular, high doses of amphetamine finds that those exposed to the drug at an age corresponding to human adolescence experience long-term changes in brain function that persist into adulthood.

    The study, reported in the journal Neuroscience, found that amphetamine leads to changes in dopamine signaling. Dopamine is a neurotransmitter that plays a role in memory, attention, learning and feelings of pleasure.

    “The dopamine system, which continues to develop throughout adolescence and young adulthood, is a primary target of psychostimulant drugs like amphetamine,” said University of Illinois psychology professor Joshua Gulley, who led the new research. “Changes in dopamine function in response to repeated drug exposure are likely to contribute to the behavioral consequences — addiction and relapse, for example — that abusers experience.”

    Parallels between rat and human development make rats a worthy model for the study of human drug addiction, which often begins in adolescence, Gulley said.

    Rats exhibit many of the characteristics that human adolescents do. They tend to be more impulsive than adult rats; they tend to make more risky decisions,” he said. They also can engage in “addiction-like behaviors,” he said.

    They show increased drug use in response to stress,” Gulley said. “And, just as in humans, there is evidence that animals that start using drugs in adolescence are more likely to relapse than animals that start in adulthood.”

    A limitation of the new study was that, unlike humans, who generally choose whether or not to partake in drug use, “the rats had no say in whether they got amphetamine,” Gulley said.

    A previous study from Gulley and his colleagues looked at the effects of amphetamine abuse on working memory — the ability to retain information just long enough to use it — in young and adult rats.

    “In that study, we found that animals that were exposed to the drug during adolescence had much more significant deficits in working memory than those exposed during adulthood,” Gulley said.

    The researchers hypothesized that drug exposure during adolescence, a time of vast changes in the brain, “somehow influences the normal developmental trajectory,” Gulley said. “But how?”

    To get at this question, the team focused on the prefrontal cortex, a brain region behind the forehead that is among the last to fully develop during adolescence. The researchers found that repeated exposure to amphetamine — beginning in adulthood or in adolescence — reduced the ability of key cells in the rats’ prefrontal cortex to respond to dopamine. In this part of the brain, dopamine influences “inhibitory tone,” telling cells to stop responding to a stimulus, Gulley said.

    “Inhibition in the nervous system is just as important as activation,” he said. “You need cells that are firing and communicating with one another, but you also need cells to stop communicating with one another at certain times and become quiet.

    “Our research suggests that a subtype of dopamine receptor, the D1 receptor, is altered following amphetamine exposure,” Gulley said. “It’s either not responding to dopamine or there are not as many of these receptors after exposure as there used to be.”

    This change in dopamine signaling persisted for 14 weeks after exposure to amphetamine in the adolescent-exposed rats, he said.

    “That’s akin to a change in humans that persists from adolescence until sometime in their 30s, long after drug use stopped,” he said.

    “Along with other studies, this shows pretty clear evidence that drug use during adolescence, a time when the brain is still developing, has extremely long-lasting consequences that go far beyond the last drug exposure,” Gulley said.


  7. Compound in magnolia may combat head and neck cancers

    August 17, 2015 by Ashley

    From the Veterans Affairs Research Communications media release:

    lab_testingMagnolias are prized for their large, colorful, fragrant flowers. Does the attractive, showy tree also harbor a potent cancer fighter?

    Yes, according to a growing number of studies, including one from VA and the University of Alabama at Birmingham that is now online in the journal Oncotarget.

    The study focused on squamous cell head and neck cancers, a scourge among those who use tobacco and alcohol. According to the National Cancer Institute, at least 3 in 4 head and neck cancers are caused by the use of tobacco and alcohol. The cancers have only a 50 percent survival rate, killing some 20,000 Americans each year.

    Enter honokiol — chemical formula C18H18O2. As one of the major active compounds in magnolia extract, the phytochemical has been used for centuries in traditional Chinese medicine and traditional Japanese medicine to treat anxiety and other conditions. More recently, scientists have been discovering that the compound, found in magnolia bark, is a wily and versatile adversary of cancer. It seems to exploit many biochemical pathways to shrink tumors of various types, or to keep them from growing in the first place.

    The Alabama scientists have now shown how it works against head and neck cancers: It blocks a protein called epidermal growth factor receptor, or EGFR. Prior research has found that almost all head and neck cancer cells display an over-abundance of the protein, and it had been suggested in the literature as a potential target.

    The VA-UAB team says, based on its lab studies, that honokiol binds more strongly with EGFR than does the drug gefitinib (sold as Iressa), which is commonly used to treat head and neck cancers.

    The researchers tested honokiol on cell lines derived from human cancers of the oral cavity, larynx, tongue, and pharynx. In all cases, the botanical shut down the aberrant cells. The team also tested it against tumors implanted into mice, with similar results.

    Senior author Dr. Santosh K. Katiyar and his colleagues wrote, “Conclusively, honokiol appears to be an attractive bioactive small molecule phytochemical for the management of head and neck cancer which can be used either alone or in combination with other available therapeutic drugs.”

    Katiyar has published extensively in the past on other natural substances that work against tumors, especially skin cancer. Some of his recent work has focused on compounds in green tea, for example, and grape seed proanthocyanidins.

     


  8. Disputed theory on Parkinson’s origin strengthened

    October 22, 2014 by Ashley

    From the Lund University media release:

    walker parkinsonsParkinson’s disease is strongly linked to the degeneration of the brain’s movement center.

    In the last decade, the question of where the disease begins has led researchers to a different part of the human anatomy. In 2003, the German neuropathologist Heiko Braak presented a theory suggesting that the disease begins in the gut and spreads to the brain. The idea has since, despite vocal critics, gained a lot of ground. Researchers at Lund University in Sweden now present the first direct evidence that the disease can actually migrate from the gut to the brain.

    The so-called Braak’s hypothesis proposes that the disease process begins in the digestive tract and in the brain’s center of smell. The theory is supported by the fact that symptoms associated with digestion and smell occur very early on in the disease.

    Researchers at Lund University have previously mapped the spread of Parkinson’s in the brain. The disease progression is believed to be driven by a misfolded protein that clumps together and “infects” neighboring cells. Professor Jia-Yi Li’s research team has now been able to track this process further, from the gut to the brain in rat models. The experiment shows how the toxic protein, alpha-synuclein, is transported from one cell to another before ultimately reaching the brain’s movement center, giving rise to the characteristic movement disorders in Parkinson’s disease.

    “We have now been able to prove that the disease process actually can travel from the peripheral nervous system to the central nervous system, in this case from the wall of the gut to the brain. In the longer term, this may give us new therapeutic targets to try to slow or stop the disease at an earlier stage”, says Professor Jia-Yi Li, research group leader for Neural Plasticity and Repair at Lund University.

    The research team will now carry out further studies in which the mechanisms behind the transport of the harmful protein will be examined in detail. The current study suggests that the protein is transferred during nerve cell communication. It is at this point of interaction that the researchers want to intervene in order to put a stop to the further spread of the disease.


  9. Flame retardant exposure linked to lower IQs — study

    June 5, 2014 by Ashley

    From the Simon Fraser University media release:

    pregnancy coupleA new study involving Simon Fraser University researchers has found that prenatal exposure to flame retardants can be significantly linked to lower IQs and greater hyperactivity in five-year old children. The findings are published online today in the journal Environmental Health Perspectives.

    The researchers found that a 10-fold increase in PBDE concentrations in early pregnancy, when the fetal brain is developing, was associated with a 4.5 IQ decrement, which is comparable with the impact of environmental lead exposure.

    SFU health sciences professor Bruce Lanphear is part of the research team that measured the levels of flame retardants, or polybrominated diphenyl ethers, (PBDEs) in 309 U.S. women at 16 weeks of pregnancy, and followed their children to the age of five.

    Researchers say their results confirm earlier studies that found PBDEs, which are routinely found in pregnant women and children, may be developmental neurotoxicants.

    PBDEs have been widely used as flame retardants in furniture, carpet padding, car seats and other consumer products over the past three decades. While most items containing PBDEs were removed voluntarily from the market a decade ago, some are still in commerce and others persist in the environment and human bodies. Nearly all homes and offices still contain some PBDEs.

    “The results from this and other observational human studies support efforts to reduce Penta-BDE exposures, especially for pregnant women and young children,” says Lanphear. “Unfortunately, brominated flame retardants are persistent and North Americans are likely exposed to higher PBDE levels than people from other parts of the world. Because of this it is likely to take decades for the PBDE levels in our population to be reduced to current European or Asian levels.”

    The United Nations Environment Program (UNEP) added two of three existing commercial PBDE formulas to the list of banned Persistent Organic Pollutants (PIPs) due to concerns over toxicity in wildlife and mammals in 2009. While PBDEs were voluntarily withdrawn from the U.S. market in 2004, products manufactured before then may still contain PBDEs, which can continue to be released into the environment and accumulate via indoor dust.

    The latest research highlights the need to reduce inadvertent exposure to PBDEs in the home and office environment (e.g., via dust), and in diet (e.g., via fish or meat products), to avert potential developmental neurotoxicity in pregnant women and young children.

    Lanphear says additional research is needed to highlight the impact of PBDE exposure on the developing brain. He also notes that it is important to investigate related chemicals and other flame retardants used to replace PBDEs.

    The study was carried out by researchers from SFU, the University of Cincinnati, the Cincinnati Children’s Hospital Medical Centre, the B.C. Children’s and Women’s Hospital, and the Centre for Disease Control and Prevention in Atlanta, Georgia. The National Institute of Environmental Health Sciences funded the research.


  10. Improving air quality in NYC would boost future earnings for children

    May 8, 2014 by Ashley

    From the Columbia University’s media release:

    city aerial viewReducing air pollution in New York City would result in substantial economic gains for children as a result of increasing their IQs.

    The study is the first to estimate the costs of IQ loss associated with exposure to air pollution, and is based on prior research on prenatal exposure to air pollutants among low-income children by Frederica Perera, PhD, lead author of the current study, and colleagues at the Columbia Center for Children’s Environmental Health at the Mailman School of Public Health.

    The researchers made their calculation using a hypothesized modest reduction of .25 nanograms per cubic meter air (ng/m3) of ambient concentrations of polycyclic aromatic hydrocarbon (PAH), a family of chemicals created by burning fossil fuels that is ubiquitous in urban air. By way of comparison, the current estimated annual mean PAH concentration is approximately 1 ng/ m3.

    The analysis focused on the 63,462 New York City children born in 2002 to women on Medicaid, a group sharing the same socio-demographic characteristics as the cohort studied by Dr. Perera and colleagues linking IQ and PAH, and used methods employed in published studies estimating earnings potential related to exposures to lead and mercury. Gains in IQ related to the hypothetical 25% reduction in PAH translated to increased lifetime earnings of $215 million.

    The researchers previously reported that children born to nonsmoking mothers exposed to higher levels of airborne PAH during pregnancy had IQs three points lower at age 5 than children whose mothers had lower PAH exposures. The IQ reduction was modest but in the range of that seen with low-level lead.

    The researchers say they have likely underestimated the total economic benefit associated with reduction in prenatal PAH exposure because it does not include estimates of economic gains due to broader neurotoxic, respiratory, and carcinogenic effects, all also linked with PAH. While based on children born to mothers on Medicaid in New York City, the authors say, the results likely apply to children more broadly. IQ affects academic performance and earnings.

    According to Dr. Perera, “Our analysis suggests that a modest reduction in urban air pollution would provide substantial economic benefits and help children realize their full potential.”

    Support for the study was provided by the National Institute of Environmental Health Sciences grants (5P01ES09600, 5R01ES08977), US Environmental Protection Agency grants (R827027, RD832141, RD83450901), the John and Wendy Neu Family Foundation, the Blanchette Hooker Rockefeller Fund, and the New York Community Trust.

    Katherine Weiland, Matthew Neidell, and Shuang Wang are co-authors of the report. None of the authors have financial relationships with a commercial entity that has an interest in the subject of this manuscript.