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What Is Pollution Doing to Our Brains? 'Exposomics' Reveals Links to Many Diseases

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Friday, April 12, 2024

B1992, burgeoning population, choking traffic, and explosive industrial growth in Mexico City had caused the United Nations to label it the most polluted urban area in the world. The problem was intensified because the high-altitude metropolis sat in a valley trapping that atmospheric filth in a perpetual toxic haze. Over the next few years, the impact could be seen not just in the blanket of smog overhead but in the city’s dogs, who had become so disoriented that some of them could no longer recognize their human families. In a series of elegant studies, the neuropathologist Lilian Calderón-Garcidueñas compared the brains of canines and children from “Makesicko City,” as the capital had been dubbed, to those from less polluted areas. What she found was terrifying: Exposure to air pollution in childhood decreases brain volume and heightens risk of several dreaded brain diseases, including Parkinson’s and Alzheimer’s, as an adult.Calderón-Garcidueñas, today head of the Environmental Neuroprevention Laboratory at the University of Montana, points out that the damaged brains she documented through neuroimaging in young dogs and humans aren’t just significant in later years; they play out in impaired memory and lower intelligence scores throughout life. Other studies have found that air pollution exposure later in childhood alters neural circuitry throughout the brain, potentially affecting executive function, including abilities like decision-making and focus, and raising the risk of psychiatric disorders.The stakes for all of us are enormous. In places like China, India, and the rest of the global south, air pollution, both indoor and outdoor, has steadily soared over the course of decades. According to the United Nations Foundation, “nearly half of the world’s population breathes toxic air each day, including more than 90 percent of children.” Some 2.3 billion people worldwide rely on solid fuels and open fires for cooking, the Foundation adds, making the problem far worse. The World Health Organization calculates about 3 million premature deaths, mostly in women and children, result from air pollution created by such cooking each year.On supporting science journalismIf you're enjoying this article, consider supporting our award-winning journalism by subscribing. By purchasing a subscription you are helping to ensure the future of impactful stories about the discoveries and ideas shaping our world today.In the United States, meanwhile, average air pollution levels have decreased significantly since the passage of the Clean Air Act in 1970. But the key word is average. Millions of Americans are still breathing outdoor air loaded with inflammation-triggering ozone and fine particulate matter. These particles, known as PM2.5 (particles less than 2.5 micrometers in diameter), can affect the lungs and heart and are strongly associated with brain damage. Wildfires—like the ones that raged across Canada this past summer—are a major contributor of PM2.5. A recent study showed that pesticides, paints, cleaners, and other personal care products are another major—and under-recognized—source of PM2.5 and can raise the risk for numerous health problems, including brain-damaging strokes.Untangling the relationship between air pollution and the brain is complex. In the modern industrial world, we are all exposed to literally thousands of contaminants. And not every person exposed to a given pollutant will develop the same set of symptoms, impairments, or diseases—in part because of their genes, and in part because each exposure may occur at a different point in development or impact a different area of the body or brain. What’s more, social disparities are at play: Poorer populations almost always live closer to factories, toxins, and pollutants.The effort to figure it out and intervene has sparked a new field of study: exposomics, the science of environmental exposures and their effects on health, disease, and development. Exposomics draws on enormous datasets about the distribution of environmental toxins, genetic and cellular responses, and human behavioral patterns. There is a huge amount of information to parse, so researchers in the field are turning to another emerging science, artificial intelligence, to make sense of it all.“Anything from our external environment—the air we breathe, food we eat, the water we drink, the emotional stress that we face every day—all of that gets translated into our biology,” says Rosalind Wright, professor of pediatrics and co-director of the Institute for Exposomic Research at the Icahn School of Medicine at Mount Sinai in New York. “All these things plus genes themselves explain the patterns of risk we see.” When an exposure is constant and cumulative, or when it overwhelms our ability to adapt, or “when you’re a fetus in utero, when you’re an infant or in early childhood or in a critical period of growth,” it can have a particularly powerful effect on lifelong cognitive clarity and brain health.Neuroscientist Megan Herting at the University of Southern California (USC) has been studying the impact of air pollution on the developing brain. “Over the past few years, we have found that higher levels of PM2.5 exposure are linked to a number of differences in the shape, neural architecture, and functional organization of the developing brain, including altered patterns of cortical thickness and differences in the microstructure of gray and white matter,” she says. On the basis of neuroimaging of exposed youngsters, Herting and fellow researchers suspect the widespread differences in brain structure and function linked with air pollution may be early biomarkers for cognitive and emotional problems emerging later in life.That suspicion gains support from an international meta-analysis (a study of other studies) published in 2023 that correlated exposure to air pollution during critical periods of brain development in childhood and adolescence to risk of depression and suicidal behavior. The imaging parts of the studies showed changes in brain structure, including neurocircuitry potentially involved in movement disorders like Parkinson’s, and white matter of the prefrontal lobes, responsible for executive decision-making, attention, and self-control.In a 2023 study, Herting and colleagues tracked children transitioning into adolescence, when brains are in a sensitive period of development and thus especially vulnerable to long-term damage from toxins. Among brain regions developing during this period is the prefrontal cortex, which helps with cognitive control, self-regulation, decision-making, attention, and problem-solving, Herting says. “Your emotional reward systems are also still being refined,” she adds.Looking at scan data from more than 9,000 youngsters exposed to air pollution between ages 9 and 10 and following them over the next couple of years, the researchers found changes in connectivity between brain regions, with some regions having fewer connections and others having more connections than normal. Herting explains that these structural and functional connections allow us to function in our daily lives, but how or even whether the changes in circuitry have an impact, researchers do not yet know.The specific pollutants involved in the atypical brain circuits appear to be nitrogen dioxide, ozone, and PM2.5—the small particles that worry many researchers the most. Herting explains: Limits set on fine particulate matter are stricter in the United States than in most other countries but still inadequate. The U.S. Environmental Protection Agency currently limits annual average levels of the pollutant to 12 micrograms per cubic meter and permits daily spikes of up to 35 micrograms per cubic meter. Health organizations, on the other hand, have called for the agency to lower levels to 8 micrograms and 25 micrograms per cubic meter, respectively. Thus, even though it may be “safe” by EPA standards, “air quality across America is contributing to changes in brain networks during critical periods of childhood,” Herting says. And that may augur “increased risk for cognitive and emotional problems later in life.” She plans to follow her group of young people into adulthood, when advances in science and the passage of time should reveal more about the effect of air pollution exposure during adolescence.Other research shows that air pollution increases risk of psychiatric disorder as years go by. In work based on large datasets in the United States and Denmark, University of Chicago computational biologist Andrey Rzhetsky and colleagues found that bad air quality was associated with increased rates of bipolar disorder and depression in both countries, especially when exposure occurs early in life. Rzhetsky and his team used two major sources: in Denmark, the National Health Registry, which contains health data on every citizen from cradle to grave; and in the United States, insurance claims with medical history plus details such as county of residence, age, sex, and importantly, linkages to family—specifics that helped reveal genetic predisposition to develop a psychiatric condition during the first 10 years of life.“It's possible that the same environment will cause disease in one person but not in another because of predisposing genetic variants that are different in different people,” Rzhetsky says. “The different genetic predisposition, that’s one part of the puzzle. Another part is varying environment.”Indeed, these complex diseases are spreading much faster than genetics alone seems to explain. “We definitely don’t know for sure which pollutant is causal. We can’t really pinpoint a smoking gun,” Rzhetsky says. But one pesky culprit continues to prove statistically significant: “It looks like PM2.5 is one of those strong signals.” To figure it out specifically, we’ll need much more data, and exposomics will play a vital role."This is a wake-up call,” Frances Jensen told her fellow physicians at the American Neurological Society’s symposium on Neurologic Dark Matter in October 2022. The meeting was an exploration of the exposome –the sum of external factors that a person is exposed to during a lifetime— driving neurodegenerative disease. It was focused in no small part on air pollution. Jensen, a University of Pennsylvania neurologist and president of the American Neurological Association, argued that researchers need to pay more attention to contaminants because the sharp rise in the number of Parkinson’s diagnoses cannot be explained by the aging population alone. “Environmental exposures are lurking in the background, and they’re rising,” she said.Parkinson’s disease is already the second-most common neurodegenerative disease after Alzheimer’s. Symptoms, which can include uncontrolled movements, difficulty with balance, and memory problems, generally develop in people age 60 and older, but they can occur, though rarely, in people as young as 20. Could something in the air explain the increasing worldwide prevalence of Parkinson’s? Researchers have not identified one specific cause, but they know Parkinson’s symptoms result from degeneration of nerve cells in the substantia nigra, the part of the brain that produces dopamine and other signal-transmitting chemicals necessary for movement and coordination.A host of air pollution suspects are now thought to play a role in the loss of dopamine-producing cells, according to Emory University environmental health scientist W. Michael Caudle, who uses mass spectrometry to identify chemicals in our bodies. One suspect he’s looking at are lipopolysaccharides, compounds often found in air pollution and bacterial toxins. Although lipopolysaccharides cannot directly enter the brain, they inflame the liver. The liver then releases inflammatory molecules into the bloodstream, which interact with blood vessels in the blood-barrier. “Then the inflammatory response in the brain leads to loss of dopamine neurons, like that seen in Parkinson’s disease,” Caudle says.More evidence comes from neuroepidemiologist Brittany Krzyzanowski, based at the Barrow Neurological Institute in Phoenix. Krzyzanowski had an “aha!” moment when she saw a map highlighting the high risk of Parkinson’s disease in the Mississippi–Ohio River Valley, including areas of Tennessee and Kentucky. At first she wondered whether the Parkinson’s hotspot was due to pesticide use in the region. But then it hit her: The area also had a network of high-density roads, suggesting that air pollution could be involved. “The pollution in these areas may contain more combustion particles from traffic and heavy metals from manufacturing, which have been linked to cell death in the part of the brain involved in Parkinson’s disease,” she said.In a study published in Neurology in October 2023, Krzyzanowski and colleagues, using sophisticated geospatial analytic techniques, went on to show that those with median levels of air pollution have a 56 percent greater risk of developing Parkinson’s disease compared to those living in regions with the lowest level of air pollution. Along with the Mississippi-Ohio River Valley, other hotspots included central North Dakota, parts of Texas, Kansas, eastern Michigan, and the tip of Florida. People living in the western half of the U.S. are at a reduced risk of developing Parkinson’s disease compared with the rest of the nation.As to the hotspot in the Mississippi-Ohio River Valley, Parkinson’s there is 25% higher than in areas with the lowest air particulate matter. Aside from that, Krzyzanowski and her research team noted something especially odd: Frequency of the disease rose with the level of pollution, but then it plateaued even as air pollution continued to soar. One reason could be that other air pollution-linked diseases, including Alzheimer’s, are masking the emergence of Parkinson’s; another reason could be an unusual form of PM2.5. “Regional differences in Parkinson’s disease might reflect regional differences in the composition of the particulate matter, and some areas may have particulate matter containing more toxic components compared to other areas,” Krzyzanowsk says. Tapping the tenets of exposomics, she expects to explore these issues in the months and years ahead.The hunt is on for the connections between environmental factors and Alzheimer’s as well. USC neurogerontologist Caleb Finch has spent years studying dementia, especially Alzheimer’s disease, which affects more than six million Americans. As with Parkinson’s, Alzheimer’s numbers are rising in the United State and much of the world. Degenerative changes in neurons become increasingly frequent after the age of 60, yet half of the people who make it to 100 will not get dementia. Many factors could explain those discrepancies. Air pollution may be an important one, Finch says.Researchers like Finch and his USC colleague Jiu-Chiuan Chen are joining forces to explore the connections between environmental neurotoxins and decline in brain health. It’s a challenging project, since air pollution levels and specific pollutants vary on fine scales and can change from hour to hour in many areas of the globe. On the basis of brain scans of hundreds of people over a range of geographic areas, this much we know: “People living in areas of high levels of air pollution and who have been studied on three continents showed accelerated arterial disease, heart attacks, and strokes, and faster cognitive decline,” Finch says.Not everyone reacts the same way when exposed to pollutants, of course. Greatest risk for Alzheimer’s seems to hit people who have a genetic variant known as apolipoprotein E (APOE4), which is involved in making proteins that help carry cholesterol and other types of fat in the bloodstream. About 25 percent of people have one copy of that gene, and 2 to 3 percent carry two copies. But inheriting the gene alone doesn’t determine a person’s Alzheimer’s risk. Environmental exposures count too.A recent study by Chen, Finch, and colleagues published in the Journal of Alzheimer’s Disease looked at associations between air pollution exposure and early signs of Alzheimer’s in 1,100 men, all around age 56 when the study began. By age 68, test subjects with high PM2.5 exposures had the worst scores in verbal fluency. People exposed to high levels of nitrogen dioxide (NO2) air pollution were also linked to worsened episodic memory. The men who had APOE4 genes had the worst scores in executive function. The evidence indicates that the process by which air pollution interacts with genetic risk to cause Alzheimer’s in later life may begin in the middle years, at least for men.A separate USC study of more than 2,000 women found that when air quality improved, cognitive decline in older women slowed. When exposure to pollutants like PM2.5 and NO2 dropped by a few micrograms per cubic foot a year over the course of six years, the women in the study tested as being a year or so younger than their real age. This suggests that when exposure air pollution is lowered, dementia risk can go down.In parallel, an international study by the Lancet Commission concluded that the risk of dementia, including Alzheimer’s, can be lowered by modifying or avoiding 12 risk factors: hypertension, hearing impairment, smoking, obesity, depression, low social contact, low level of education, physical inactivity, diabetes, excessive alcohol consumption, traumatic brain injury—and air pollution. Together, the 12 modifiable risk factors account for around 40 percent of worldwide dementias, which theoretically could be prevented or delayed.In light of all this, Finch and Duke University social scientist Alexander Kulminski have proposed the “Alzheimer’s disease exposome” to assess environmental factors that interact with genes to cause dementia. Where medicines have failed, exposomics just might help. Studies of Swedish twins show that half of individual differences in Alzheimer’s risk may be environmental, and thus modifiable; and while vast sums of research funding have been poured into the genetic roots of the disease, it could be that altering the exposome would provide a better preventive than all the ongoing drug trials to date. Environmental toxins broadly disrupt cell repair and protective mechanisms in the brain, the researchers point out. And factors like obesity and stress contribute to chronic inflammation, which likely damages neurons’ ability to function and communicate. The research framework of the Alzheimer's disease exposome offers a comprehensive, systematic approach to the environmental underpinnings of Alzheimer's risk over individuals’ lifespans—from the time they are pre-fertilized gametes to life as a fetus in the womb to childhood and beyond.For three decades, Rosalind Wright at Mount Sinai has wanted to trace critical problems in neurodevelopment and neurodegeneration to pollutants—from highway emissions to heavy metals to specific household chemicals and a host of other factors—but the mass of data has been overwhelming. With the advent of artificial intelligence (AI) and sophisticated neuroimaging technology, high-precision research using vast genomic databanks is finally possible. “I knew we needed to ask these kinds of questions, but I didn't have the tools to do it. Now we do and it’s very exciting,” Wright says.Using machine learning—an AI approach to data analysis—Wright looks at giant datasets that include the precise location of an individual’s residence as well as the myriad of pollutants he or she encounters. “It's no different fundamentally from other statistical models we use,” she says. “It’s just that this one has been developed to be able to take in bigger and bigger data, more and more types of exposures.” The resulting data breakdown should tell us which factors drive which types of risk for which people. That information will help people know where they should target their efforts to reduce exposures to risky pollutants, and ultimately how to lower risk of impairment and disease, brain or otherwise.The tools used by Wright and her colleagues are being trained on diseases like Alzheimer’s. If you put genes and the environment together, “you start to see who might be at higher risk and also what underlying mechanisms might be driving it in different ways in different populations,” Wright says. The exposome could also explains more subtle cognitive effects of pollution that may emerge over long periods, such as harms to attention, intelligence, and performance.To address environmental brain risks, it’s important to know which pollutants are present—another target of exposomic research. In the United States, the EPA has placed stationary environmental monitors all over our major cities, conducting daily measurements of small particulates from traffic and industry, along with secondary chemicals that emerge as a result. There are also thousands of satellites all over the globe calibrating heat waves that can alter how the pollutants react with each other.Pioneers like Wright are just starting to chart the terrain of environmental exposures that affect the brain. “As we measure more and more of the exposome, we may be able to tailor prevention and intervention strategies. New weapons include a silicone bracelet that we have in the laboratory. You wear it and it will tell us what pollutants you are exposed to,” Wright says. She also is exploring more ways to collect data on the toxins people have already encountered: “With a single strand of hair, we can tell you what you’ve been exposed to. Hair grows about a centimeter a month, so if we get a hair from a pregnant woman and she has nine centimeters of hair, we can go back a full nine months, over the entire life of the fetus. Or we can create a life-long exposome history when a child loses a tooth at age six.”“We're designed to be pretty resilient,” Wright adds. The problem comes when the exposures are chronic and accumulative and overwhelm our ability to adapt. We’re not going to fix everything, “but if I know more about myself than before, that empowers me to think, ‘I’m optimizing the balance, and I’m intervening as best I can.’ ”Additional reporting and editing was done by Margaret Hetherman.This story is part of a series of OpenMind essays, podcasts, and videos supported by a generous grant from the Pulitzer Center's Truth Decay initiative.This story originally appeared on OpenMind, a digital magazine tackling science controversies and deceptions.

The new science of "exposomics" shows how air pollution contributes to Alzheimer’s, Parkinson’s, bipolar disorder and other brain diseases

B1992, burgeoning population, choking traffic, and explosive industrial growth in Mexico City had caused the United Nations to label it the most polluted urban area in the world. The problem was intensified because the high-altitude metropolis sat in a valley trapping that atmospheric filth in a perpetual toxic haze. Over the next few years, the impact could be seen not just in the blanket of smog overhead but in the city’s dogs, who had become so disoriented that some of them could no longer recognize their human families. In a series of elegant studies, the neuropathologist Lilian Calderón-Garcidueñas compared the brains of canines and children from “Makesicko City,” as the capital had been dubbed, to those from less polluted areas. What she found was terrifying: Exposure to air pollution in childhood decreases brain volume and heightens risk of several dreaded brain diseases, including Parkinson’s and Alzheimer’s, as an adult.

Calderón-Garcidueñas, today head of the Environmental Neuroprevention Laboratory at the University of Montana, points out that the damaged brains she documented through neuroimaging in young dogs and humans aren’t just significant in later years; they play out in impaired memory and lower intelligence scores throughout life. Other studies have found that air pollution exposure later in childhood alters neural circuitry throughout the brain, potentially affecting executive function, including abilities like decision-making and focus, and raising the risk of psychiatric disorders.

The stakes for all of us are enormous. In places like China, India, and the rest of the global south, air pollution, both indoor and outdoor, has steadily soared over the course of decades. According to the United Nations Foundation, “nearly half of the world’s population breathes toxic air each day, including more than 90 percent of children.” Some 2.3 billion people worldwide rely on solid fuels and open fires for cooking, the Foundation adds, making the problem far worse. The World Health Organization calculates about 3 million premature deaths, mostly in women and children, result from air pollution created by such cooking each year.


On supporting science journalism

If you're enjoying this article, consider supporting our award-winning journalism by subscribing. By purchasing a subscription you are helping to ensure the future of impactful stories about the discoveries and ideas shaping our world today.


In the United States, meanwhile, average air pollution levels have decreased significantly since the passage of the Clean Air Act in 1970. But the key word is average. Millions of Americans are still breathing outdoor air loaded with inflammation-triggering ozone and fine particulate matter. These particles, known as PM2.5 (particles less than 2.5 micrometers in diameter), can affect the lungs and heart and are strongly associated with brain damage. Wildfires—like the ones that raged across Canada this past summer—are a major contributor of PM2.5. A recent study showed that pesticides, paints, cleaners, and other personal care products are another major—and under-recognized—source of PM2.5 and can raise the risk for numerous health problems, including brain-damaging strokes.

Untangling the relationship between air pollution and the brain is complex. In the modern industrial world, we are all exposed to literally thousands of contaminants. And not every person exposed to a given pollutant will develop the same set of symptoms, impairments, or diseases—in part because of their genes, and in part because each exposure may occur at a different point in development or impact a different area of the body or brain. What’s more, social disparities are at play: Poorer populations almost always live closer to factories, toxins, and pollutants.

The effort to figure it out and intervene has sparked a new field of study: exposomics, the science of environmental exposures and their effects on health, disease, and development. Exposomics draws on enormous datasets about the distribution of environmental toxins, genetic and cellular responses, and human behavioral patterns. There is a huge amount of information to parse, so researchers in the field are turning to another emerging science, artificial intelligence, to make sense of it all.

“Anything from our external environment—the air we breathe, food we eat, the water we drink, the emotional stress that we face every day—all of that gets translated into our biology,” says Rosalind Wright, professor of pediatrics and co-director of the Institute for Exposomic Research at the Icahn School of Medicine at Mount Sinai in New York. “All these things plus genes themselves explain the patterns of risk we see.” When an exposure is constant and cumulative, or when it overwhelms our ability to adapt, or “when you’re a fetus in utero, when you’re an infant or in early childhood or in a critical period of growth,” it can have a particularly powerful effect on lifelong cognitive clarity and brain health.

Neuroscientist Megan Herting at the University of Southern California (USC) has been studying the impact of air pollution on the developing brain. “Over the past few years, we have found that higher levels of PM2.5 exposure are linked to a number of differences in the shape, neural architecture, and functional organization of the developing brain, including altered patterns of cortical thickness and differences in the microstructure of gray and white matter,” she says. On the basis of neuroimaging of exposed youngsters, Herting and fellow researchers suspect the widespread differences in brain structure and function linked with air pollution may be early biomarkers for cognitive and emotional problems emerging later in life.

That suspicion gains support from an international meta-analysis (a study of other studies) published in 2023 that correlated exposure to air pollution during critical periods of brain development in childhood and adolescence to risk of depression and suicidal behavior. The imaging parts of the studies showed changes in brain structure, including neurocircuitry potentially involved in movement disorders like Parkinson’s, and white matter of the prefrontal lobes, responsible for executive decision-making, attention, and self-control.

In a 2023 study, Herting and colleagues tracked children transitioning into adolescence, when brains are in a sensitive period of development and thus especially vulnerable to long-term damage from toxins. Among brain regions developing during this period is the prefrontal cortex, which helps with cognitive control, self-regulation, decision-making, attention, and problem-solving, Herting says. “Your emotional reward systems are also still being refined,” she adds.

Looking at scan data from more than 9,000 youngsters exposed to air pollution between ages 9 and 10 and following them over the next couple of years, the researchers found changes in connectivity between brain regions, with some regions having fewer connections and others having more connections than normal. Herting explains that these structural and functional connections allow us to function in our daily lives, but how or even whether the changes in circuitry have an impact, researchers do not yet know.

The specific pollutants involved in the atypical brain circuits appear to be nitrogen dioxide, ozone, and PM2.5—the small particles that worry many researchers the most. Herting explains: Limits set on fine particulate matter are stricter in the United States than in most other countries but still inadequate. The U.S. Environmental Protection Agency currently limits annual average levels of the pollutant to 12 micrograms per cubic meter and permits daily spikes of up to 35 micrograms per cubic meter. Health organizations, on the other hand, have called for the agency to lower levels to 8 micrograms and 25 micrograms per cubic meter, respectively. Thus, even though it may be “safe” by EPA standards, “air quality across America is contributing to changes in brain networks during critical periods of childhood,” Herting says. And that may augur “increased risk for cognitive and emotional problems later in life.” She plans to follow her group of young people into adulthood, when advances in science and the passage of time should reveal more about the effect of air pollution exposure during adolescence.

Other research shows that air pollution increases risk of psychiatric disorder as years go by. In work based on large datasets in the United States and Denmark, University of Chicago computational biologist Andrey Rzhetsky and colleagues found that bad air quality was associated with increased rates of bipolar disorder and depression in both countries, especially when exposure occurs early in life. Rzhetsky and his team used two major sources: in Denmark, the National Health Registry, which contains health data on every citizen from cradle to grave; and in the United States, insurance claims with medical history plus details such as county of residence, age, sex, and importantly, linkages to family—specifics that helped reveal genetic predisposition to develop a psychiatric condition during the first 10 years of life.

“It's possible that the same environment will cause disease in one person but not in another because of predisposing genetic variants that are different in different people,” Rzhetsky says. “The different genetic predisposition, that’s one part of the puzzle. Another part is varying environment.”

Indeed, these complex diseases are spreading much faster than genetics alone seems to explain. “We definitely don’t know for sure which pollutant is causal. We can’t really pinpoint a smoking gun,” Rzhetsky says. But one pesky culprit continues to prove statistically significant: “It looks like PM2.5 is one of those strong signals.” To figure it out specifically, we’ll need much more data, and exposomics will play a vital role.

"This is a wake-up call,” Frances Jensen told her fellow physicians at the American Neurological Society’s symposium on Neurologic Dark Matter in October 2022. The meeting was an exploration of the exposome –the sum of external factors that a person is exposed to during a lifetime— driving neurodegenerative disease. It was focused in no small part on air pollution. Jensen, a University of Pennsylvania neurologist and president of the American Neurological Association, argued that researchers need to pay more attention to contaminants because the sharp rise in the number of Parkinson’s diagnoses cannot be explained by the aging population alone. “Environmental exposures are lurking in the background, and they’re rising,” she said.

Parkinson’s disease is already the second-most common neurodegenerative disease after Alzheimer’s. Symptoms, which can include uncontrolled movements, difficulty with balance, and memory problems, generally develop in people age 60 and older, but they can occur, though rarely, in people as young as 20. Could something in the air explain the increasing worldwide prevalence of Parkinson’s? Researchers have not identified one specific cause, but they know Parkinson’s symptoms result from degeneration of nerve cells in the substantia nigra, the part of the brain that produces dopamine and other signal-transmitting chemicals necessary for movement and coordination.

A host of air pollution suspects are now thought to play a role in the loss of dopamine-producing cells, according to Emory University environmental health scientist W. Michael Caudle, who uses mass spectrometry to identify chemicals in our bodies. One suspect he’s looking at are lipopolysaccharides, compounds often found in air pollution and bacterial toxins. Although lipopolysaccharides cannot directly enter the brain, they inflame the liver. The liver then releases inflammatory molecules into the bloodstream, which interact with blood vessels in the blood-barrier. “Then the inflammatory response in the brain leads to loss of dopamine neurons, like that seen in Parkinson’s disease,” Caudle says.

More evidence comes from neuroepidemiologist Brittany Krzyzanowski, based at the Barrow Neurological Institute in Phoenix. Krzyzanowski had an “aha!” moment when she saw a map highlighting the high risk of Parkinson’s disease in the Mississippi–Ohio River Valley, including areas of Tennessee and Kentucky. At first she wondered whether the Parkinson’s hotspot was due to pesticide use in the region. But then it hit her: The area also had a network of high-density roads, suggesting that air pollution could be involved. “The pollution in these areas may contain more combustion particles from traffic and heavy metals from manufacturing, which have been linked to cell death in the part of the brain involved in Parkinson’s disease,” she said.

In a study published in Neurology in October 2023, Krzyzanowski and colleagues, using sophisticated geospatial analytic techniques, went on to show that those with median levels of air pollution have a 56 percent greater risk of developing Parkinson’s disease compared to those living in regions with the lowest level of air pollution. Along with the Mississippi-Ohio River Valley, other hotspots included central North Dakota, parts of Texas, Kansas, eastern Michigan, and the tip of Florida. People living in the western half of the U.S. are at a reduced risk of developing Parkinson’s disease compared with the rest of the nation.

As to the hotspot in the Mississippi-Ohio River Valley, Parkinson’s there is 25% higher than in areas with the lowest air particulate matter. Aside from that, Krzyzanowski and her research team noted something especially odd: Frequency of the disease rose with the level of pollution, but then it plateaued even as air pollution continued to soar. One reason could be that other air pollution-linked diseases, including Alzheimer’s, are masking the emergence of Parkinson’s; another reason could be an unusual form of PM2.5. “Regional differences in Parkinson’s disease might reflect regional differences in the composition of the particulate matter, and some areas may have particulate matter containing more toxic components compared to other areas,” Krzyzanowsk says. Tapping the tenets of exposomics, she expects to explore these issues in the months and years ahead.

The hunt is on for the connections between environmental factors and Alzheimer’s as well. USC neurogerontologist Caleb Finch has spent years studying dementia, especially Alzheimer’s disease, which affects more than six million Americans. As with Parkinson’s, Alzheimer’s numbers are rising in the United State and much of the world. Degenerative changes in neurons become increasingly frequent after the age of 60, yet half of the people who make it to 100 will not get dementia. Many factors could explain those discrepancies. Air pollution may be an important one, Finch says.

Researchers like Finch and his USC colleague Jiu-Chiuan Chen are joining forces to explore the connections between environmental neurotoxins and decline in brain health. It’s a challenging project, since air pollution levels and specific pollutants vary on fine scales and can change from hour to hour in many areas of the globe. On the basis of brain scans of hundreds of people over a range of geographic areas, this much we know: “People living in areas of high levels of air pollution and who have been studied on three continents showed accelerated arterial disease, heart attacks, and strokes, and faster cognitive decline,” Finch says.

Not everyone reacts the same way when exposed to pollutants, of course. Greatest risk for Alzheimer’s seems to hit people who have a genetic variant known as apolipoprotein E (APOE4), which is involved in making proteins that help carry cholesterol and other types of fat in the bloodstream. About 25 percent of people have one copy of that gene, and 2 to 3 percent carry two copies. But inheriting the gene alone doesn’t determine a person’s Alzheimer’s risk. Environmental exposures count too.

A recent study by Chen, Finch, and colleagues published in the Journal of Alzheimer’s Disease looked at associations between air pollution exposure and early signs of Alzheimer’s in 1,100 men, all around age 56 when the study began. By age 68, test subjects with high PM2.5 exposures had the worst scores in verbal fluency. People exposed to high levels of nitrogen dioxide (NO2) air pollution were also linked to worsened episodic memory. The men who had APOE4 genes had the worst scores in executive function. The evidence indicates that the process by which air pollution interacts with genetic risk to cause Alzheimer’s in later life may begin in the middle years, at least for men.

A separate USC study of more than 2,000 women found that when air quality improved, cognitive decline in older women slowed. When exposure to pollutants like PM2.5 and NO2 dropped by a few micrograms per cubic foot a year over the course of six years, the women in the study tested as being a year or so younger than their real age. This suggests that when exposure air pollution is lowered, dementia risk can go down.

In parallel, an international study by the Lancet Commission concluded that the risk of dementia, including Alzheimer’s, can be lowered by modifying or avoiding 12 risk factors: hypertension, hearing impairment, smoking, obesity, depression, low social contact, low level of education, physical inactivity, diabetes, excessive alcohol consumption, traumatic brain injury—and air pollution. Together, the 12 modifiable risk factors account for around 40 percent of worldwide dementias, which theoretically could be prevented or delayed.

In light of all this, Finch and Duke University social scientist Alexander Kulminski have proposed the “Alzheimer’s disease exposome” to assess environmental factors that interact with genes to cause dementia. Where medicines have failed, exposomics just might help. Studies of Swedish twins show that half of individual differences in Alzheimer’s risk may be environmental, and thus modifiable; and while vast sums of research funding have been poured into the genetic roots of the disease, it could be that altering the exposome would provide a better preventive than all the ongoing drug trials to date. Environmental toxins broadly disrupt cell repair and protective mechanisms in the brain, the researchers point out. And factors like obesity and stress contribute to chronic inflammation, which likely damages neurons’ ability to function and communicate. The research framework of the Alzheimer's disease exposome offers a comprehensive, systematic approach to the environmental underpinnings of Alzheimer's risk over individuals’ lifespans—from the time they are pre-fertilized gametes to life as a fetus in the womb to childhood and beyond.

For three decades, Rosalind Wright at Mount Sinai has wanted to trace critical problems in neurodevelopment and neurodegeneration to pollutants—from highway emissions to heavy metals to specific household chemicals and a host of other factors—but the mass of data has been overwhelming. With the advent of artificial intelligence (AI) and sophisticated neuroimaging technology, high-precision research using vast genomic databanks is finally possible. “I knew we needed to ask these kinds of questions, but I didn't have the tools to do it. Now we do and it’s very exciting,” Wright says.

Using machine learning—an AI approach to data analysis—Wright looks at giant datasets that include the precise location of an individual’s residence as well as the myriad of pollutants he or she encounters. “It's no different fundamentally from other statistical models we use,” she says. “It’s just that this one has been developed to be able to take in bigger and bigger data, more and more types of exposures.” The resulting data breakdown should tell us which factors drive which types of risk for which people. That information will help people know where they should target their efforts to reduce exposures to risky pollutants, and ultimately how to lower risk of impairment and disease, brain or otherwise.

The tools used by Wright and her colleagues are being trained on diseases like Alzheimer’s. If you put genes and the environment together, “you start to see who might be at higher risk and also what underlying mechanisms might be driving it in different ways in different populations,” Wright says. The exposome could also explains more subtle cognitive effects of pollution that may emerge over long periods, such as harms to attention, intelligence, and performance.

To address environmental brain risks, it’s important to know which pollutants are present—another target of exposomic research. In the United States, the EPA has placed stationary environmental monitors all over our major cities, conducting daily measurements of small particulates from traffic and industry, along with secondary chemicals that emerge as a result. There are also thousands of satellites all over the globe calibrating heat waves that can alter how the pollutants react with each other.

Pioneers like Wright are just starting to chart the terrain of environmental exposures that affect the brain. “As we measure more and more of the exposome, we may be able to tailor prevention and intervention strategies. New weapons include a silicone bracelet that we have in the laboratory. You wear it and it will tell us what pollutants you are exposed to,” Wright says. She also is exploring more ways to collect data on the toxins people have already encountered: “With a single strand of hair, we can tell you what you’ve been exposed to. Hair grows about a centimeter a month, so if we get a hair from a pregnant woman and she has nine centimeters of hair, we can go back a full nine months, over the entire life of the fetus. Or we can create a life-long exposome history when a child loses a tooth at age six.”

“We're designed to be pretty resilient,” Wright adds. The problem comes when the exposures are chronic and accumulative and overwhelm our ability to adapt. We’re not going to fix everything, “but if I know more about myself than before, that empowers me to think, ‘I’m optimizing the balance, and I’m intervening as best I can.’ ”

Additional reporting and editing was done by Margaret Hetherman.

This story is part of a series of OpenMind essays, podcasts, and videos supported by a generous grant from the Pulitzer Center's Truth Decay initiative.

This story originally appeared on OpenMind, a digital magazine tackling science controversies and deceptions.

Read the full story here.
Photos courtesy of

The bid to make Illinois a leader on electric trucking

A coalition of environmental justice advocates is pushing Illinois to become the first Midwest state to adopt California’s Advanced Clean Trucks standards designed to spur a transition to zero-emission heavy-duty vehicles over the next decade. “Air pollution is an equity issue,” Griselda Chavez, an environmental…

A coalition of environmental justice advocates is pushing Illinois to become the first Midwest state to adopt California’s Advanced Clean Trucks standards designed to spur a transition to zero-emission heavy-duty vehicles over the next decade. “Air pollution is an equity issue,” Griselda Chavez, an environmental justice organizer with Warehouse Workers for Justice, said at a recent press conference. The group represents workers and residents in communities heavily impacted by warehouses, including the Chicago-area town of Joliet, a major logistics hub. “Black, brown, and low-income communities in and around Joliet are disproportionately affected by diesel pollution, large amounts of truck traffic, and increasing growth of the warehouse industry,” Chavez said. ​“Those workers also go home to their families and go to schools that are surrounded by large amounts of truck traffic and poor air quality.” The Illinois Pollution Control Board is considering adopting not only California’s clean truck standards but also the Golden State’s Advanced Clean Cars II program, which would phase out the sale of most non-electric passenger vehicles by 2035, and its stricter nitrogen oxide limits on heavy-duty vehicles. The deliberations are happening as the Trump administration seeks to block California’s unique authority to set vehicle emission standards that exceed federal rules. Illinois advocates have focused mostly on the clean trucks program because of the health and environmental justice implications of diesel-powered trucks throughout the state. They are especially concerned about places like Joliet and Chicago’s Little Village neighborhood, a largely immigrant community where warehouses have also proliferated. In 2023, the Little Village Environmental Justice Organization worked with the Center for Neighborhood Technology on a truck-counting study that showed on one June day, an average of 1.5 heavy-duty trucks per minute drove along a residential street in the heart of the community. Sally Burgess, downstate lead organizing representative for Sierra Club’s Illinois chapter, told the Pollution Control Board during a March 10 hearing that she counted more than 300 diesel-burning semi-trucks during the 65-mile drive between her home in central Illinois and the state’s capitol. “All along our route, on both sides of the highway, farm fields, rustic barns, cows and other farm animals, some homes,” said Burgess. ​“Some would refer to it as a bucolic rural setting — clogged with diesel trucks.” Stimulating Illinois’ EV markets The Advanced Clean Trucks program would require manufacturers selling in Illinois to ensure that between 40% and 75% of their heavy-duty vehicle sales are zero-emissions by 2035, with the percentage depending on type of vehicle. They would have to sell higher percentages of electric medium-sized non-tractor trucks than pickup trucks and vans as well as larger tractor-trailers. Manufacturers could also comply by purchasing credits from other companies that go beyond those targets, or by shifting credits from types of vehicles where they exceed the mandates. “If, for example, a truck-maker sells a lot of zero-emission delivery vans but doesn’t offer a zero-emission version of their box trucks, they can convert their extra [pickup and van] credits into [midsize truck] credits and still maintain compliance,” said Trisha DelloIacono, head of policy for Calstart, a national nonprofit focused on clean transportation policy and market development, by email. DelloIacono said demand for zero-emissions heavy-duty vehicles is so high that manufacturers should not have trouble meeting the sales targets if they make the inventory available. After a certain number of years, those that don’t comply either through electric vehicle sales or credit purchases could be fined. Advocates say that the state mandates benefit people nationwide since they motivate manufacturers to increase their EV offerings.

Could electric drones you can sit in take off?

Skyfly's aircraft promises the flexibility of a helicopter without the cost, noise or emissions.

Could electric drones you can sit in take off?Katharine Da CostaReporting fromOxfordshireBBCThe Skyfly Axe can take off vertically like a helicopter or land on a runwayImagine an electric drone mixed with a fixed wing plane - that is the concept behind a new two-seater aircraft being developed by start-up company, Skyfly.The Axe promises the flexibility of a helicopter but without the cost, noise pollution or carbon emissions.It is a vertically capable aircraft, or Electric Vertical Take-off and Landing (eVTOL) aircraft, which means it can take off like a helicopter.It also has two fixed wings that allows it to take off and land from a runway.The company claims the Axe has a top speed of 100mph, it can carry up to 172kg - approximately the weight of two 13.5st adults - and has a range of 100 miles, about the distance from Oxford to the Isle of Wight.Michael Thompson, CEO of Skyfly, is optimistic the new model will be delivered to customers early next yearThe team, based near Banbury in Oxfordshire, has taken five years to fine tune the design."Compared to a conventional aircraft it's got eight motors which is very strange," says Dr Bill Brooks, Skyfly's chief technical engineer."And it's a tail-first layout called a canard so it's got the tail at the front. The all up weight is 750kg but 240kg of that are batteries so all the structure is carbon fibre to keep it as light as possible," Dr Brooks says.Safety is an important part of the design too. 'Environmental benefits'The large wings help it to glide in the event of power failure and there are two motors at the end of each wing so that if one fails the other can compensate.It is also equipped with an emergency ballistic parachute to bring the aircraft and passengers down safely.As well as being safer and cleaner than conventional aircraft, Michael Thompson, Skyfly's chief executive, says electric models are significantly quieter too."When you're taking off, you're no longer annoying everyone around you from a noise perspective, so I do think electric propulsion brings not only environmental benefits but from a noise pollution point of view, it's a huge benefit as well," he says.Dr Bill Brooks is the chief engineer and test pilot at SkyflyWho is it marketed at?Other eVTOLs under development include those looking to provide an electric flying-taxi service like Bristol-based Vertical Aerospace (VA) . VA, as well as Archer and Joby in the US, are designing electric powered aircraft to carry up to four passengers.Skyfly's Axe, by comparison, is more compact and aimed at the private market.The do-it-youself kit-plane comes with a price tag of £250,000.It is aimed at existing pilots who want to transition away from diesel piston engines.Jason Pritchard, executive editor of eVTOL Insights, says it is also likely to appeal to flying clubs in order to train new members:"The eVTOL aircraft industry is still in its infancy with initial operations a few years away, but it also needs to train large numbers of pilots in the coming years," he says."Additionally, the Axe's design can also train pilots with the skills and controls necessary to land an aircraft without power, which is a necessary tool."SkyflyThe two-seater light aircraft has a range of around 100 milesWhat about charging infrastructure?While the Axe can be charged up overnight with a conventional three-pin plug, just like EV cars, electric aircraft will need the charging infrastructure to be scaled up. Aerovolt, based in West Sussex, has installed rapid chargers at seven UK airports with 40 more in the pipeline.Its founder, Philip Kingsley-Dobson, says demand is growing. "A lot of piston aircraft can't use leaded fuel in the future so they're looking for alternatives and ways we can decarbonise the lower end of aviation," he says.'Cutting edge'There are no eVTOL aircraft currently permitted to fly in the UK.Skyfly's Axe has successfully completed manned test flights in both hover and forward flight modes but still needs to be certified by the Civil Aviation Authority (CAA).With 40 pre-orders from buyers all over the world, the company hopes to deliver the new model to customers early next year.A CAA spokesperson said: "We are working with innovators to test and fly brand new forms of aviation that keeps the UK at the cutting edge of flight technology and supports the sector to grow."New technology comes with new challenges and safety remains our priority in all this work."

Record number of illegal sewage spills in Windermere last year

Campaigners identified 140 illegal spill days into the beauty spot in 2024

Record number of illegal sewage spills in Windermere last yearJonah FisherBBC environment correspondentReutersSewage spilled illegally into Britain's largest lake on a record number of days last year, an analysis of water company data by campaigners suggests.The analysis, which the BBC had exclusive access to, used United Utilities operational data to establish when the company was discharging sewage into Windermere when it should by law have been treating some of it.The campaigners from Windrush Against Sewage Pollution (WASP) and Save Windermere identified 140 illegal spill days in 2024, more than in any of the three previous years. United Utilities told BBC News that the campaigners' findings were "inaccurate" and some of the data "erroneous". The company declined to put in writing, despite repeated requests, any specific examples of mistakes or omissions. Regulators Ofwat and the Environment Agency are both currently investigating United Utilities operations. PAWindermere is one of Britain's most loved beauty spotsLast week the Environment Agency said United Utilities had spilled 77,817 times in 2024, the highest figure of all England's water companies. Many of the spills will have been legal. All water companies are legally allowed to discharge raw sewage to stop the network getting overwhelmed and this now happens regularly during periods of heavy rain.But almost all pumping stations and treatment plants operate under an environmental permit which specify that they must process or "pass forward" a certain amount of sewage and rainwater before spilling starts.The campaigners cross-referenced United Utilities datasets showing when an asset was spilling against how much sewage it was treating at the time. The campaigners' analysis – which has been shared with and scrutinised by the BBC - found days when illegal spills appear to have occurred at each of six sewage facilities around the lake, which combined to 140 days in 2024. That's more than in any of the previous three years, as the chart below shows.The longest illegal spill the analysis identified was for 10 days from Hawkshead pumping station, which flows into Windermere via Cunsey Beck."This is an indication that their works have not been maintained properly or they're not being watched over properly," says Prof Peter Hammond, a mathematican and retired academic from campaign group Windrush Against Sewage Pollution. Prof Hammond's analysis of water company data has been cited by regulators and he has been praised in Parliament by water company executives for bringing problems to light they were previously unaware of. The latest analysis covers four years of data from six sites that discharge sewage into the Lake Windermere catchment.Comparisons over a longer time period are impossible as United Utilities has only had made full data sets available since 2021.Prof Hammond's analysis of water company data has been praised in ParliamentThe regulators Ofwat and the Environment Agency have since 2021 been investigating whether the water companies have been treating enough sewage before they start to spill. The EA call it a "major criminal investigation" while Ofwat call it "the largest and most complex Ofwat has ever undertaken". Last week Yorkshire Water agreed to a £40m "enforcement action" after Ofwat uncovered "serious failures" in how it operated its treatment plant and network. Ofwat declined to comment on the campaigner's findings as their investigation into United Utilities is ongoing. In response to concerns about United Utilities the Environment Agency last year reviewed all of its environmental permits in the Windermere catchment and says this led directly to the water company tripling its investment plans for the area to £200m."We are currently carrying out investigations into suspected pollution incidents on the Windermere catchment and are unable to comment on these in detail until they have reached a conclusion," an EA spokesperson said when the campaigners' analysis was shared with them."Where we find breaches of environmental permits, we will take the appropriate enforcement action up to and including a criminal prosecution."Save WindermereSewage has been blamed for turning parts of the lake green – so called "algal blooming"United Utilities, which provides services to more than seven million people across north-west England, is more than £9bn in debt. Its chief executive Louise Beardmore confirmed to parliament in February that she was last year paid £1.4m including a bonus of £420,000."The methodology used by the campaigners is different to that used by the Environment Agency for its compliance assessments," the water company said in a statement."On top of that, erroneous data has been used, tags and naming conventions in data sets appear to have been misunderstood, and assumptions seem to have been made on whether different types of flow meters have been installed.""The methodology fails to use other corroborating information from the sites which would prove that spills did not occur. As a result, the numbers quoted are inaccurate."BBC News presented United Utilities with five examples of illegal spills the campaigners' analysis had identified using the company's data and asked for any evidence or explanation as to why they were not illegal. United Utilities repeatedly declined to do so in writing or on camera."What we're seeing is the failure of privatisation. We're seeing a prioritisation of dividend returns over the long-term environmental protection of places like Windermere" says Matt Staniek from Save Windermere."The bill payer has paid for a service that has never fully been provided, and the illegality demonstrates that for all to see."Over the next five years bills in the United Utilities area will go up by 32% above the rate of inflation. On average that will mean a rise of £86 for the year that starts in April. Louise Beardmore said the rises will fund the "largest investment in water and wastewater infrastructure in over 100 years". For Windermere that's set to mean nine wastewater treatment works, including two that were included in the campaigners' analysis being upgraded and a reduction in the number of overflows discharging into the lake.

Cadia goldmine operators fined $350,000 for breaches of NSW clean-air laws

Testing had previously revealed the mine was emitting more than 11 times the legal limit of dust containing heavy metalsElection 2025 live updates: Australia federal election campaignGet our breaking news email, free app or daily news podcastThe operators of Cadia goldmine have been ordered to pay $350,000 in fines and convicted of three offences after a prosecution by the New South Wales Environmental Protection Authority.Cadia Holdings Limited, trading as Cadia Valley Operations, pleaded guilty to three offences under the environmental protection act relating to breaches of clean air regulations at the mine in central west NSW.Sign up for Guardian Australia’s breaking news email Continue reading...

The operators of Cadia goldmine have been ordered to pay $350,000 in fines and convicted of three offences after a prosecution by the New South Wales Environmental Protection Authority.Cadia Holdings Limited, trading as Cadia Valley Operations, pleaded guilty to three offences under the environmental protection act relating to breaches of clean air regulations at the mine in central west NSW.Justice Sarah Pritchard handed down her judgment in the land and environment court on Monday.The mine operator was fined $150,000 for offences in November 2021 and March 2022, and $200,000 for an offence in May 2023, but given a reduction in its penalty because of its guilty plea and other mitigating factors.It must also pay the EPA’s legal costs, and cover the cost of installing a new “dust tracking system” in Mudgee.Pritchard ordered that Newmont Australia, the owner of the mine, also had to publicise the ruling in a print advertisement in three newspapers, and on its Facebook and X accounts.Newmont acquired the previous owner, Newcrest, in November 2023.The EPA began investigating the central-west mine in 2023 after a community-driven water testing program that found elevated levels of heavy metals in the rainwater tanks of some nearby residences.It subsequently found that these levels were caused by dust emissions. The mine operator was exceeding the standard concentration for solid particles being emitted from mine surface exhaust fans at its main vent, known as Ventilation Rise 8 (VR8).In June 2023, the head of the NSW EPA criticised the operators of Australia’s largest goldmine for “completely unacceptable” levels of air pollution after testing revealed it was emitting more than 11 times the legal limit of dust containing heavy metals.skip past newsletter promotionSign up to Breaking News AustraliaGet the most important news as it breaksPrivacy Notice: Newsletters may contain info about charities, online ads, and content funded by outside parties. For more information see our Privacy Policy. We use Google reCaptcha to protect our website and the Google Privacy Policy and Terms of Service apply.after newsletter promotionThe EPA ordered the operators to take immediate action to reduce air pollution after they had provided preliminary air pollution test results to the EPA.That report found that VR8, also known as the “crusher vent” because it extracts contaminated air from where the ore is crushed deep underground, was expelling between 200 and 570 milligrams per cubic metre of dust – more than 11 times the regulatory limit for air pollution.This was despite a new ventilation system that included installing a bag house, which catches 1 tonne of dust an hour.The EPA chief executive officer, Tony Chappel, said at the time that the level of pollution recorded in those test results was “completely unacceptable” and that the mine had fallen well short of its legal obligations to meet clean air standards.“The clean air regulation states that for any point source of pollution, which that vent is, the maximum allowable standard of dust is 50 milligrams per cubic metre,” he said. “That’s the standard we’re talking about when we say they have to immediately comply.”

Mysterious foam on South Australian beaches caused by bloom of tiny but toxic algae

Algae blooms can be a problem for marine life and people but it’s not yet clear if warmer oceans and nutrient runoff are causing more of themConfronting images of dead seadragons, fish and octopuses washed up on South Australian beaches – and disturbing reports of “more than 100” surfers and beachgoers experiencing flu-like symptoms after swimming or merely breathing in sea spray – attracted international concern last week.Speculation about the likely cause ranged from pollution and algae to unusual bacterial infections or viruses. We can reveal the culprit was a tiny – but harmful – type of planktonic algae called Karenia mikimotoi. Continue reading...

Confronting images of dead seadragons, fish and octopuses washed up on South Australian beaches – and disturbing reports of “more than 100” surfers and beachgoers experiencing flu-like symptoms after swimming or merely breathing in sea spray – attracted international concern last week.Speculation about the likely cause ranged from pollution and algae to unusual bacterial infections or viruses. We can reveal the culprit was a tiny – but harmful – type of planktonic algae called Karenia mikimotoi.The South Australian government sent us water samples from Waitpinga beach, Petrel Cove beach, Encounter Bay boat ramp and Parsons Headland on Tuesday. We studied the water under the microscope and extracted DNA for genetic analysis.Our results revealed high numbers of the tiny harmful algal species – each just 20 microns in diameter (where one micron is one thousandth of a millimetre). While relatively common in Australian coastal waters, blooms of K. mikimotoi occur only sporadically. But similar harmful algal blooms and fish kills due to K. mikimotoi have happened in the past, such as the 2014 bloom in Coffin Bay, South Australia. And this latest one won’t be the last.Harmful algal bloomsSingle-celled, microbial algae occur naturally in seawater all over the world.They are also called phytoplankton because they float in the water column and photosynthesise like plants. “Phyto” comes from the Greek word for plant and “plankton” comes from the Greek word for wanderer, which relates to their floating movement with ocean currents and tides.Like plants on land, the microalgae or phytoplankton in the ocean capture sunlight and produce up to half the oxygen in our atmosphere. There are more than 100,000 different species of microalgae. Every litre of seawater will normally contain a mixed group of these different microalgae species.But under certain conditions, just a single species of microalgae can accumulate in one area and dominate over the others. If we are unlucky, the dominant species may be one that produces a toxin or has a harmful effect.This so-called “harmful algal bloom” can cause problems for people and for marine life such as fish, invertebrates such as crabs, and even marine mammals such as whales and seals.K. mikimotoi causes harmful deadly algal blooms in Asia, Europe, South Africa and South America, as well as Australia and New Zealand. Photograph: Anthony RowlandThere are hundreds of different species of harmful algae. Each produces its own type of toxin with a particular toxic effect.Most of these toxic chemical compounds produced by harmful algae are quite well known, including neurotoxins that affect the brain. But others are more complicated, and the mechanisms of toxicity are poorly understood. This can make it more difficult to understand the factors leading to the deaths of fish and other marine life. Unfortunately, the toxins from K. mikimotoi fall into this latter category.Introducing Karenia mikimotoiThe species responsible for recent events in South Australia, K. mikimotoi, causes harmful algal blooms in Asia, Europe, South Africa and South America, as well as Australia and New Zealand. These blooms all caused fish deaths, and some also caused breathing difficulties for some beachgoers.The most drastic of these K. mikimotoi blooms have occurred in China over the past two decades. In 2012, more than 300 sq km of abalone farms were affected, causing about A$525m in lost production.Explaining the toxic effectsMicroalgae can damage the gills of fish and shellfish, preventing them from breathing. This is the main cause of death. But some studies have also found damage to the gastrointestinal tracts and livers of fish.Tests using fish gill cells clearly show the dramatic toxic effect of K. mikimotoi. When the fish gill cells were exposed to intact K. mikimotoi cells, after 3.5 hours more than 80% of the fish cells had died.Leafy seadragons were among the dead sea creatures that washed up on South Australian beaches. Photograph: Anthony RowlandFortunately, the toxin does not persist in the environment after the K. mikimotoi cells are dead. So once the bloom is over, the marine environment can recover relatively quickly.Its toxicity is partly due to the algae’s production of “reactive oxygen species”, reactive forms of oxygen molecules which can cause the deaths of cells in high doses. K. mikimotoi cells may also produce lipid (fat) molecules that cause some toxic effects.Finally, a very dense bloom of microalgae can sometimes reduce the amount of dissolved oxygen in the water column, which means there is less oxygen for other marine life.The human health effects are not very well known but probably relate to the reactive oxygen species being an irritant.K. mikimotoi cells can also produce “mucilage”, a type of thick, gluey substance made of complex sugars, which can accumulate bacteria inside it. This can cause “sea foam”, which was evident on beaches last week.Unanswered questions remainA question for many people is whether increasing water temperatures make blooms of K. mikimotoi more likely.Another concern is whether nutrient runoff from farms, cities and aquaculture could cause more harmful algal blooms.Unfortunately, for Australia at least, the answer to these questions is we don’t know yet. While we know some harmful algal blooms do increase when nutrient runoff is higher, others actually prefer fewer nutrients or colder temperatures.We do know warmer water species seem to be moving farther south along the Australian coastline, changing phytoplankton species abundance and distribution.While some microalgal blooms can cause bioluminescence that is beautiful to watch, others such as K. mikimotoi can cause skin and respiratory irritations.If you notice discoloured water, fish deaths or excessive sea foam along the coast or in an estuary, avoid fishing or swimming in the area and notify local primary industry or environmental authorities in your state.

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