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By Lisa Friedman and Coral Davenport WASHINGTON — The Trump administration on Thursday finalized a decision not to impose any limits on perchlorate, a toxic chemical compound found in rocket fuel that contaminates water and has been linked to fetal and infant brain damage. The move by the Environmental Protection Agency was widely expected, after The New York Times reported last month that Andrew Wheeler, the E.P.A. administrator, had decided to effectively defy a court order that required the agency to establish a safe drinking-water standard for the chemical by the end of June. In addition to not regulating, the E.P.A. overturned the underlying scientific finding that declared perchlorate a serious health risk for five million to 16 million people in the United States. The E.P.A. said California and Massachusetts and other states had already taken regulatory steps to reduce the contamination. “Today’s decision is built on science and local success stories and fulfills President Trump’s promise to pare back burdensome ‘one-size-fits-all’ overregulation for the American people,” Mr. Wheeler said in a statement. “State and local water systems are effectively and efficiently managing levels of perchlorate. Our state partners deserve credit for their leadership on protecting public health in their communities, not unnecessary federal intervention.” Environmentalists said both moves showed a disregard for science, the law and public health, and they criticized the agency for claiming credit for state regulations done in the face of federal inaction. “Today’s decision is illegal, unscientific and unconscionable,” said Erik D. Olson, the senior strategic director for health at the Natural Resources Defense Council, an advocacy group. “The Environmental Protection Agency is threatening the health of pregnant moms and young children with toxic chemicals in their drinking water at levels that literally can cause loss of I.Q. points. Is this what the Environmental Protection Agency has come to?” © 2020 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27308 - Posted: 06.19.2020

By Joshua Sokol The city of Minamata, Japan, is dotted with monuments commemorating victims of an industrial mass poisoning decades ago. High in the hills, a small stone memorial honors other deaths—of cats sacrificed in secret to science. Now, after restudying the remains of one of those cats, a team of scientists is arguing, controversially, that the long-standing explanation for the tragedy is wrong. No one questions the root cause of the disaster, which at minimum poisoned more than 2000 people: mercury in a chemical factory’s wastewater that was dumped into Minamata Bay and taken up by seafood eaten by fishermen and their families. At first, the chemical form of the mercury, which ultimately killed many of its victims and left many babies with severe neurological disorders, was unknown. But in 1968, the Japanese government blamed methylmercury, a common byproduct of mercury pollution. Many studies supported that conclusion, finding methylmercury spikes in shellfish, bay sludge, and even hundreds of umbilical cords from babies delivered during the time. But methylmercury is not the culprit, says Ingrid Pickering, an x-ray spectroscopist at the University of Saskatchewan. “Our work is indicating that it’s something else”: an unusual mercury compound that may say little about the broader threat of mercury pollution. Minamata has long been a vivid case study of mercury’s dangers. The metal is toxic on its own, but it becomes far more dangerous when bacteria in natural environments convert it into methylmercury, an organic compound, readily absorbed by living tissues, that can be concentrated and passed up food chains. Since the 1990s, scientists have argued that the Chisso chemical factory in Minamata produced methylmercury and dumped it directly into the bay. © 2020 American Association for the Advancement of Science.

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27140 - Posted: 03.25.2020

Davide Castelvecchi The group of nerve agents known as Novichoks are to be added to the Chemical Weapons Convention’s list of controlled substances, in one of the first major changes to the treaty since it was agreed in the 1990s. The compounds, developed by the Soviet Union during the cold war, came to prominence after they were used in a high-profile assassination attempt on a former Russian military officer, Sergei Skripal, in Salisbury, UK, in March last year. The Organisation for the Prohibition of Chemical Weapons (OPCW), which is tasked with enforcing the treaty, announced the decision to explicitly ban Novichoks on 27 November as representatives from the 193 member states met in The Hague this week for a periodic review of the convention. The member states agreed unanimously to classify Novichoks as chemical weapons, the OPCW said. The update to the treaty, which will come into effect in 180 days, was initially proposed by the United States, Canada and the Netherlands. “There is a recognition that we all win with this agreement,” says Alastair Hay, an environmental toxicologist at the University of Leeds, UK, who was at the meeting. “The decision means that OPCW can now keep tabs on these chemicals.” The OPCW has the power to send inspectors to any signatory country to search for evidence of production of banned chemicals. It also can send experts to help countries to investigate crime scenes where chemical agents may have been used. © 2019 Springer Nature Limited

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26863 - Posted: 12.02.2019

By Nicholas Bakalar Long-term exposure to air pollution is associated with lower scores on tests of mental acuity, researchers have found. And one reason may be that air pollution causes changes in brain structure that resemble those of Alzheimer’s disease. The scientists studied 998 women ages 73 to 87 and free of dementia, periodically giving them tests of learning and memory. They used magnetic resonance imaging to detect brain atrophy, or wasting, and then scored the deterioration on its degree of similarity to the brain atrophy characteristic of Alzheimer’s disease. They matched Environmental Protection Agency data on air pollution to the women’s residential addresses. Over 11 years of follow-up, they found that the greater the women’s exposure to PM 2.5, the tiny particulate matter that easily penetrates the lungs and bloodstream, the lower their scores on the cognitive tests. After excluding cases of dementia and stroke, they also found a possible reason for the declining scores: The M.R.I. results showed that increased exposure to PM 2.5 was associated with increased brain atrophy, even before clinical symptoms of dementia had appeared. The study is in the journal Brain. “PM 2.5 alters brain structure, which then accelerates memory decline,” said the lead author, Diana Younan, a postdoctoral researcher at the University of California. “I just want people to be aware that air pollution can affect their health, and possibly their brains.” © 2019 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 26849 - Posted: 11.26.2019

Catherine Offord When Lilian Calderón-Garcidueñas discovered abundant hallmarks of Alzheimer’s disease in a batch of human brain samples a few years ago, she initially wasn’t sure what to make of it. The University of Montana neuropathologist had been studying the brains as part of her research on environmental effects on neural development, and this particular set of samples came from autopsy examinations carried out on people who had died suddenly in Mexico City, where she used to work as a researcher and physician. Although Calderón-Garcidueñas had collected much of the tissue herself while attending the autopsies in Mexico, the light-microscope slides she was analyzing had been prepared by her colleagues, so she was in the dark about what patient each sample came from. By the end of the project, she’d identified accumulations of the Alzheimer’s disease–associated proteins amyloid-ß and hyperphosphorylated tau in almost all of the 203 brains she studied. “When I started opening envelopes to see who [each sample] belonged to . . . I was devastated,” she says. The people whose brains she’d been studying were not only adults, but teens and even children. The youngest was 11 months old. “My first thought was, ‘What am I going to do with this? What am I going to tell people?’” she says. “I was not expecting such a devastating, extreme pathology.” Despite her shock, Calderón-Garcidueñas had a reason to be on the lookout for signs of a disease usually associated with the elderly in these samples. For the last three decades, she’d been studying the health effects of Mexico City’s notoriously polluted air—a blight that earned the capital the dubious distinction of most polluted megacity on the planet from the United Nations in 1992. During that time, she’s discovered many links between exposure to air pollution and signs of neural damage in animals and humans. Although her findings are observational, and the pathology of proteins such as amyloid-ß is not fully understood, Calderón-Garcidueñas argues that air pollution is the most likely culprit behind the development of the abnormalities she saw in her postmortem samples—plus many other detrimental changes to the brains of Mexico City’s residents. © 1986–2019 The Scientist

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory, Learning, and Development
Link ID: 26665 - Posted: 10.02.2019

The mysterious ailments experienced by some 40 Canadian and U.S. diplomats and their families while stationed in Cuba may have had nothing to do with sonic "attacks" identified in earlier studies. According to a new Canadian study, obtained exclusively by Radio-Canada's investigative TV program Enquête, the cause could instead be neurotoxic agents used in pesticide fumigation. A number of Canadians and Americans living in Havana fell victim to an unexplained illness starting in late 2016, complaining of concussion-like symptoms, including headaches, dizziness, nausea and difficulty concentrating. Some described hearing a buzzing or high-pitched sounds before falling sick. In the wake of the health problems experienced over the past three years, Global Affairs Canada commissioned a clinical study by a team of multidisciplinary researchers in Halifax, affiliated with the Brain Repair Centre, Dalhousie University and the Nova Scotia Health Authority. "The working hypothesis actually came only after we had most of the results," Dr. Alon Friedman, the study's lead author, said in an interview. The researchers identified a damaged region of the brain that is responsible for memory, concentration and sleep-and-wake cycle, among other things, and then looked at how this region could come to be injured. "There are very specific types of toxins that affect these kinds of nervous systems ... and these are insecticides, pesticides, organophosphates — specific neurotoxins," said Friedman. "So that's why we generated the hypothesis that we then went to test in other ways." Twenty-six individuals participated in the study, including a control group of people who never lived in Havana. ©2019 CBC/Radio-Canada

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 14: Attention and Consciousness
Link ID: 26627 - Posted: 09.20.2019

By Maanvi Singh The world’s most widely used insecticides may delay the migrations of songbirds and hurt their chances of mating. In the first experiment to track the effects of a neonicotinoid on birds in the wild, scientists captured 24 white-crowned sparrows as they migrated north from Mexico and the southern United States to Canada and Alaska. The team fed half of those birds with a low dose of the commonly used agricultural insecticide imidacloprid and the other half with a slightly higher dose. An additional 12 birds were captured and dosed with sunflower oil, but no pesticide. Within hours, the dosed birds began to lose weight and ate less food, researchers report in the Sept. 13 Science. Birds given the higher amount of imidacloprid (3.9 milligrams per kilogram of body mass) lost 6 percent of their body mass within six hours. That’s about 1.6 grams for an average bird weighing 27 grams. Tracking the birds (Zonotrichia leucophrys) revealed that the pesticide-treated sparrows also lagged behind the others when continuing their migration to their summer mating grounds. The findings suggest that neonicotinoid insecticides, already implicated in dropping bee populations, could also have a hand in the decline of songbird populations across North America. From 1966 to 2013, the populations of nearly three-quarters of farmland bird species across the continent have precipitously dropped. The researchers dosed the birds in the lab with carefully measured amounts of pesticide mixed with sunflower oil. In the wild, birds might feed on seeds coated with imidacloprid. The highest dose that “we gave each bird is the equivalent of if they ate one-tenth of [a single] pesticide-coated corn seed,” says Christy Morrissey, a biologist at the University of Saskatchewan in Saskatoon, Canada. “Frankly, these were minuscule doses we gave the birds.” © Society for Science & the Public 2000–2019.

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 26608 - Posted: 09.13.2019

Tina Hesman Saey ORLANDO — Being exposed to a chemical early in life can be a bit like a choose-your-own-adventure book: Some things that happen early on may hurt you later, but only if you make certain choices, an unpublished study in mice suggests. Mouse pups were exposed to the chemical bisphenol A (BPA) for only five days after birth, a crucial time during which mice’s livers develop. BPA, once common in plastics, has been linked to a host of health problems in people, from diabetes to heart disease (SN: 10/11/08, p. 14). But depending on diet as adults, the mice either grew up to be healthy or to have enlarged livers and high cholesterol. As long as the BPA-exposed mice ate mouse chow for the rest of their lives, the rodents remained healthy, molecular biologist Cheryl Walker of Baylor College of Medicine in Houston reported April 7 at the 2019 Experimental Biology meeting. But researchers switched some BPA-exposed mice to a high-fat diet as adults. Those mice had larger livers, higher cholesterol and more metabolic problems than mice who ate a high-fat diet but were not exposed to BPA as pups, Walker said. BPA exposure immediately altered epigenetic marks at more than 5,400 genes, including 3,000 involved in aging. Epigenetic marks are chemical tags on DNA or on histones — protein around which DNA winds in a cell — that don’t change information in genes themselves, but affect gene activity. |© Society for Science & the Public 2000 - 2019

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26134 - Posted: 04.13.2019

By Jennifer Couzin-Frankel For the millions of people treated for cancer, “chemo brain” can be an unnerving and disabling side effect. It causes memory lapses, trouble concentrating, and an all-around mental fog, which appear linked to the treatment and not the disease. Although the cognitive effects often fade after chemotherapy ends, for some people the fog persists for years, even decades. And doctors and researchers have long wondered why. Now, a new study suggests an answer in the case of one chemotherapy drug: Brain cells called microglia may orchestrate chemo brain by disrupting other cells that help maintain the brain’s communication system. “I can’t tell you how many patients I see who look at me when I explain [chemo brain] and say, ‘I’ve been living with this for 10 years and thought I was crazy,’” says Michelle Monje, a pediatric neuro-oncologist and neuroscientist at Stanford University in Palo Alto, California. It’s still mostly a mystery how common long-term cognitive impairment is after chemo. In one recent study by clinical neuropsychologist Sanne Schagen at the Netherlands Cancer Institute in Amsterdam, it affected 16% of breast cancer survivors 6 months after treatment. Monje began to probe the cognitive effects of cancer treatment in the early 2000s, starting with radiation, a therapy that can be far more debilitating than chemotherapy. A Science paper she and her colleagues published in 2003 suggested radiation affected a type of brain cell called microglia, which protect the brain against inflammation. Just like immune cells in the blood, microglia—which make up at least 10% of all brain cells—become activated during injury or infection. © 2018 American Association for the Advancement of Science

Related chapters from BN8e: Chapter 17: Learning and Memory; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 25759 - Posted: 12.07.2018

By Donald G. McNeil Jr. The first treatment for sleeping sickness that relies on pills alone was approved on Friday by Europe’s drug regulatory agency, paving the way for use in Africa, the last bastion of the horrific disease. With treatment radically simplified, sleeping sickness could become a candidate for elimination, experts said, because there are usually fewer than 2,000 cases in the world each year. The disease, also called human African trypanosomiasis, is transmitted by tsetse flies. The protozoan parasites, injected as the flies suck blood, burrow into the brain. Before they kill, drive their victims mad in ways that resemble the last stages of rabies. The personalities of the infected change. They have terrifying hallucinations and fly into rages; they have been known to beat their children and even attack family members with machetes. They may become ravenous and scream with pain if water touches their skin. Only in the end, do they lapse into a long coma and die. The new drug, fexinidazole, cures all stages of the disease within 10 days. Previously, everyone with the parasites found in a blood test also had to undergo a spinal tap to see if the parasites had reached their brains. If so, patients had to suffer through a complex and sometimes dangerous intravenous regimen requiring hospitalization. An oral treatment that can safely be taken at home “is a completely new paradigm — it could let us bring treatment down to the village level,” said Dr. Bernard Pecoul, founder and executive director of the Drugs for Neglected Diseases Initiative, which was started in 2005 by the medical charity Doctors Without Borders to find new cures for tropical diseases. © 2018 The New York Times Company

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 25695 - Posted: 11.17.2018

By Eric Schlosser In April 1906, a Republican president of the United States met privately with a notorious socialist at the White House. The president was Theodore Roosevelt; the socialist was Upton Sinclair; and the two set aside their political differences to discuss an issue of great mutual concern: food safety. A few months earlier, Sinclair’s novel “The Jungle” had created public outrage about the sanitary conditions at America’s slaughterhouses. Roosevelt had distrusted the meatpacking industry for years, angered by the putrid meat sold to the Army and served to his troops during the Spanish-American War. In 1906 the United States was the only major industrialized nation without strict laws forbidding the sale of contaminated and adulterated food. In their absence, the free market made it profitable to supply a wide range of unappetizing fare. Ground-up insects were sold as brown sugar. Children’s candy was routinely colored with lead and other heavy metals. Beef hearts and other organ meats were processed, canned and labeled as chicken. Perhaps one-third of the butter for sale wasn’t really butter but rather all sorts of other things — beef tallow, pork fat, the ground-up stomachs of cows and sheep — transformed into a yellowish substance that looked like butter. Historians have long credited the unlikely alliance of Roosevelt and Sinclair for passage of the Meat Inspection Act and the Pure Food and Drug Act of 1906. In “The Poison Squad,” Deborah Blum makes a convincing case that a now forgotten chemist at the Department of Agriculture, Harvey Washington Wiley, played a more important role — not only in ensuring the passage of those bills but also in changing popular attitudes toward government intervention on behalf of consumers. The origins of today’s food safety laws, drug safety laws, labeling requirements and environmental regulations can be found in the arguments of the Progressive movement at the turn of the last century. As the Trump administration proudly weakens or eliminates those measures, the life work of a 19th-century U.S.D.A. chemist has an unfortunate significance. © 2018 The New York Times Company

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 25582 - Posted: 10.17.2018

By Mike Ives HONG KONG — A large study in China suggests a link between air pollution and negative effects on people’s language and math skills. The link between pollution and respiratory diseases is well known, and most experts now believe that small particulates may also raise the risk for strokes and heart attacks. Whether this form of air pollution impairs cognition is not yet certain, but several studies have hinted at a connection. The latest study, by researchers based in China and the United States, analyzed how long-term exposure to air pollution affected performance on nationwide math and word-recognition tests by more than 25,000 people across 162 Chinese counties. It was published on Monday in Proceedings of the National Academy of Sciences. The authors based their findings on models they built that combined weather and pollution data from specific locations in China where people had taken nationwide tests in 2010 and 2014, as well as the test scores themselves. Their analysis tried to document how short- and long-term pollution exposure might have affected the scores — and, by extension, the test-takers’ brains. The authors found that the cognitive impact of cumulative exposure among the test takers was especially pronounced among older men, and that the results were troubling in part because cognitive decline and impairment are risk factors for Alzheimer’s disease and other forms of dementia. The study “further amplifies the need to tackle air pollution now to protect the health of particularly the young and elderly populations,” Heather Adair-Rohani, a technical officer for public health and environment at the World Health Organization in Geneva, which was not involved in the study, said in an email. © 2018 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 25393 - Posted: 08.29.2018

By Melissa Healy At some point in their treatment for cancer, somewhere between 17% and 75% of patients with malignancies that don’t affect the central nervous system report the sensation that a mental fog has set in. For months or years after their hair has grown back, the exhaustion has lifted and the medical appointments taper off, the “new normal” for these patients includes problems with concentration, word-finding, short-term memory and multitasking. Their doctors nod their heads knowingly: It’s “chemobrain,” they report. Among the nation’s roughly 15.5 million cancer survivors, the ranks of those who’ve experienced mental fog after cancer treatment are probably increasing as detection and therapies improve, survival rates rise and lives are extended. But when it comes to cancer’s cognitive aftermath, the medical profession’s expertise ends. Why chemobrain happens, how long it will linger, and what deficits it actually causes — and especially whether it could be treated, or even prevented — are questions for which oncologists have no answers. But they want them. And three specialists from the National Cancer Institute have issued an appeal to neuroscientists for help. “We need an infusion of new ideas," said Todd S. Horowitz, a cognitive psychologist and program director in the institute’s Division of Cancer Control and Population Sciences. “Cognitive neuroscience would help us characterize the deficits people have and allow us to connect them to particular brain systems." Writing this week in the journal Trends in Neurosciences, Horowitz and two fellow researchers at the institute drafted a road map toward a better understanding of the condition officially known as cancer-related cognitive impairment, which was first described by breast cancer survivors.

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 14: Attention and Consciousness
Link ID: 25089 - Posted: 06.14.2018

Geoff Brumfiel Sergei Skripal and his daughter, Yulia, were found slumped on a bench in the city of Salisbury on March 4. Experts quickly assessed that Skripal — a former Russian intelligence official accused of spying for the British — had been poisoned with a nerve agent. On Monday, British Prime Minister Theresa May named the agent in a speech before Parliament. "It is now clear that Mr. Skripal and his daughter were poisoned with a military-grade nerve agent of a type developed by Russia," she said. "This is part of a group of nerve agents known as Novichok." Novichok agents are extremely rare. "As far as I know, I don't know anybody who knows how to make it except these guys in Russia," says Dan Kaszeta, a chemical weapons expert with Strongpoint Security in London. "They've been a deep, dark secret." Novichok means "newcomer" in Russian. Kaszeta says that Novichok agents were developed in the 1980s as a new weapon in the waning days of the Cold War. Novichok chemicals were designed to evade equipment carried by NATO troops. "They wanted to develop nerve agents that the West couldn't detect," he says. According to a defector's report published by the Stimson Center in 1995, they were developed at the State Scientific Research Institute of Organic Chemistry and Technology in Moscow. As the U.S. and Russia were laying the groundwork to dismantle their chemical weapons stockpiles, researchers at the institute were working in secret to develop the new Novichok chemicals. © 2018 npr

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 24747 - Posted: 03.13.2018

By Richard Stone Even 3 decades later, Seyed Naser Emadi's first encounter with nerve agents haunts him. In 1987, as a soldier fighting for Iran in its war with Iraq, he came across a hillside strewn with comrades killed by an Iraqi nerve agent, perhaps tabun or sarin. Unable to breathe, the victims had clawed at their necks to try to open a hole in their throats, recalls Emadi, now a dermatologist in Tehran. In fact, their windpipes were clear; the nerve agent had shut down control of breathing in the central nervous system. They "had no choice except death," he says. The long-term effects of nerve agents remain uncertain, but with the right antidotes, these poisons need not be an immediate death sentence. A few years after Emadi's experience, U.S. soldiers in 1991's Gulf War carried autoinjectors filled with drugs that—in principle—would keep them breathing and protect them from seizures if Iraqi forces again unleashed nerve agents. They never did, most historians agree, but the threat remains real today, as chemical attacks in Syria's ongoing civil war make clear. It is spurring urgent efforts to find better countermeasures, with several promising compounds in the pipeline. First synthesized by German chemists on the eve of World War II, nerve agents kill by binding to acetylcholinesterase (AChE), an enzyme that dismantles the neurotransmitter acetylcholine when it is released into synapses. One of the most efficient enzymes known, a single AChE molecule can hydrolyze 600,000 acetylcholine molecules per minute, says Palmer Taylor, a pharmacologist at the University of California, San Diego. © 2018 American Association for the Advancement of Science

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 24492 - Posted: 01.05.2018

By Nicholas Kristof The colored parts of the image above, prepared by Columbia University scientists, indicate where a child’s brain is physically altered after exposure to this pesticide. This chemical, chlorpyrifos, is hard to pronounce, so let’s just call it Dow Chemical Company’s Nerve Gas Pesticide. Even if you haven’t heard of it, it may be inside you: One 2012 study found that it was in the umbilical cord blood of 87 percent of newborn babies tested. And now the Trump administration is embracing it, overturning a planned ban that had been in the works for many years. The Environmental Protection Agency actually banned Dow’s Nerve Gas Pesticide for most indoor residential use 17 years ago — so it’s no longer found in the Raid you spray at cockroaches (it’s very effective, which is why it’s so widely used; then again, don’t suggest this to Dow, but sarin nerve gas might be even more effective!). The E.P.A. was preparing to ban it for agricultural and outdoor use this spring, but then the Trump administration rejected the ban. That was a triumph for Dow, but the decision stirred outrage among public health experts. They noted that Dow had donated $1 million for President Trump’s inauguration. So Dow’s Nerve Gas Pesticide will still be used on golf courses, road medians and crops that end up on our plate. Kids are told to eat fruits and vegetables, but E.P.A. scientists found levels of this pesticide on such foods at up to 140 times the limits deemed safe. © 2017 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 24264 - Posted: 10.30.2017

Christie Wilcox Many tadpoles ward off predators with potent poisons — but those toxins also seem to help win battles with their own kind, a new study finds. Tadpoles of common toads (Bufo bufo) are more poisonous when raised in crowded conditions, which may give them a competitive edge, according to the work published on 23 September in Functional Ecology1. Many noxious plant species are known to modulate their defences to fend off different threats2, but it is less clear whether animals possess similar toxin-tuning abilities. Although predation pressure is known to induce tadpole chemical defences3, the new findings are the first unequivocal evidence of toxin synthesis spurred by competition in vertebrate animals. Being poisonous can make a species essentially inedible to predators, but making potent toxins comes at a metabolic cost — so it’s best to make that investment count. “It would be very profitable for such animals to kill two birds with one stone by using their anti-predatory toxins as chemical weapons against their competitors, too,” says the study’s lead author, Veronika Bókony, an ecologist with the Hungarian Academy of Sciences in Budapest. Common toads are equipped with bufadienolides, potent toxins that cause harm by accelerating and disrupting the heart’s rhythms4. Field studies have found that common toad toxicity varies geographically, with the intensity of competition being the most reliable predictor5. But it has been unclear whether such patterns occur because populations are genetically isolated from one another in different ponds, or whether they reflect defences induced by environmental factors. © 2017 Macmillan Publishers Limited,

Related chapters from BN8e: Chapter 6: Evolution of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress
Link ID: 24124 - Posted: 09.30.2017

By BENEDICT CAREY Dr. Herbert Needleman, whose studies of children exposed to low levels of lead prompted regulations that limited or banned the metal in a range of common products, like gasoline and paint, and set a standard for the modern study of environmental toxins, died on July 18 in Pittsburgh. He was 89. His son, Dr. Joshua Needleman, said the cause was lung failure resulting from edema, an excess of fluid. Dr. Needleman was working at a community psychiatric clinic in North Philadelphia after medical school when he met a young man who would become a touchstone for a crusading career. The boy approached Dr. Needleman and explained his ambitions, which were large, even as the boy struggled with words. He was bright and open; nonetheless he had deficits that struck Dr. Needleman as similar to those found in children with lead poisoning. “I thought, how many of these kids who are coming to the clinic are in fact a missed case of lead poisoning?” he said in a later interview. His clinic office overlooked a school playground; the view gave him an idea. Doctors had long known that exposure to high doses of lead caused mental lapses, even permanent brain damage and death. But what about the low-level exposure that many children, like the ones playing in the yard, absorbed every day — merely by living in older urban neighborhoods thick with lead paint and industrial contamination? No one knew. No one could study the effects carefully, because the available tests for lead exposure were of hair, blood, or fingernails — each flawed in its own way. Bone is the most accurate long-term repository: Once absorbed into the body, lead circulates in the blood and accumulates in the skeleton. But taking bone samples — biopsies — is painful and hardly justifiable for the sake of a hypothesis, especially in young children. Yet Dr. Needleman had seen an earlier study of lead poisoning, a small one, which measured accumulated lead exposure in teeth. Teeth are a part of the human skeleton. And young children shed them. “That was the insight that changed everything,” said Dr. Bernard Goldstein, former dean of the University of Pittsburgh’s graduate school of public health. “Herb became the Tooth Fairy.” © 2017 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23887 - Posted: 07.28.2017

Geoff Brumfiel When the half-brother of North Korean leader Kim Jong Un collapsed at a Malaysian airport last week, poisoning was instantly suspected. But on Friday, Malaysian authorities revealed that an autopsy had turned up not just any poison, but a rare nerve agent known as VX. VX is among the deadliest chemical weapons ever devised. A colorless, odorless liquid, similar in consistency to motor oil, it kills in tiny quantities that can be absorbed through the skin. A relative of the nerve agent Sarin, VX disrupts communications between nerves and muscles. Victims of VX initially experience nausea and dizziness. Without an antidote, the chemical eventually paralyzes the diaphragm, causing suffocation. That may have been the fate of Kim Jong Nam, the estranged half-brother of North Korea's leader. Security footage showed that Kim was approached by two women who appeared to cover his face with a cloth. Moments later, he fell ill and sought help. He died before reaching a hospital. If the Malaysian analysis is correct and VX was the culprit, that would seem to suggest that the North Korean state itself is behind the killing. "Hardly anybody has it," says Dan Kaszeta, a chemical weapons expert and consultant based in London. The U.S. has destroyed nearly all of its stocks of VX in recent years. North Korea is among the few states in the world that have an active chemical weapons program. It is not a signatory to the Chemical Weapons Convention, which bans the use of such weapons. © 2017 npr

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23282 - Posted: 02.25.2017

By SHARON LERNER IN the fall, I began to research an article that I gave the working title “The Last Days of Chlorpyrifos.” A widely used pesticide, chlorpyrifos affects humans as well as the bugs it kills. Back in the halcyon days before the election, the optimism of the title seemed warranted. After years of study, the Environmental Protection Agency had announced in October 2015 that it could no longer vouch for the safety of chlorpyrifos on food. The agency had acknowledged for decades that chlorpyrifos can cause acute poisoning and in the early 2000s it had prohibited its use in most home products and reduced the amounts that could be used on some crops. But the 2015 announcement stemmed from the agency’s recognition of mounting evidence that prenatal exposure to chlorpyrifos could have lasting effects on children’s brains. Though the process of re-evaluating the safety of the pesticide had stretched on for years, at long last, chlorpyrifos seemed to be going down. Another report was expected to provide all the ammunition necessary to stop its use on fruits and vegetables, and I was eager to document its demise. For a reporter who covers the environment, this was going to be the rare happy story. The election of President Trump has thrown that outcome — indeed, the fate of many of the E.P.A.’s public health protections — into question. On Monday, Mr. Trump signed an executive order requiring federal agencies to scrap two regulations for every one they institute on small businesses. In its first week, his administration suspended 30 environmental regulations issued under President Barack Obama. And Myron Ebell, who oversaw the agency’s transition team, suggested recently that the E.P.A.’s staff may soon be reduced by as much as two-thirds. How will the agency’s mission “to protect human health and the environment” fare under this assault? What happens with chlorpyrifos may be our best indication. “I think it’ll be a very early test of their commitment to environmental protection,” Jim Jones, who oversaw the evaluation of chlorpyrifos as the E.P.A.’s assistant administrator for chemical safety and pollution prevention, told me, not long after he stepped down on Inauguration Day. © 2017 The New York Times Company

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory, Learning, and Development
Link ID: 23190 - Posted: 02.06.2017