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The air you breathe may be hazardous to your brain.
Health risks associated with air pollution are well-documented, but for the most part, effects on the brain have been regarded as limited and conjectural. Recent research provides stronger evidence for—and expands the list of—potential harms, and suggests underlying pathways and mechanisms.
“We started out looking at the lungs,” says epidemiologist Michael Brauer, professor in the University of British Columbia School of Population and Public Health. “Then the statistics started showing clear cardiac effects.” Based primarily on these, the World Health Organization attributes one in eight deaths to air pollution.
“Now a lot of people are looking at things like mental health, and cognitive development in children and decline in adults,” says Brauer. “This is the next wave of research.”
An editorial by Brauer in a recent issue of The BMJ (formerly the British Medical Journal) commented on two new studies of bad air’s effects on the brain.
Anoop Shah and colleagues at the University of Edinburgh conducted what Brauer calls “the largest systematic review and meta-analysis” yet undertaken of the connection between air pollution and stroke. Earlier research was inconsistent, and largely addressed the association with long-term exposures. The Shah paper focused on short-term risk: the possibility that airborne toxins may trigger strokes.
The analysis, which included data from 94 studies involving 6.2 million cases of stroke in 28 countries, found a significant association between air pollution during the prior seven days and hospitalization for and mortality from stroke. The association was strongest for exposure on the day of the stroke, and held for such components as sulfur dioxide, nitrogen dioxide, and solid particles.
While the evolving process leading up to stroke may have more fundamental public health importance, Shah’s findings are “quite strong” and could have practical implications, Brauer says. “With such solid evidence, clinicians might give direct advice to those at risk—to stay indoors on horrible air pollution days, for example, or to use an air cleaner.”
Cause for alarm
Another paper in the same issue of The BMJ considered a health problem rarely associated with environmental neurotoxicity: anxiety.
“There’s been a lot more work on traditional neurodegenerative disorders, particularly Parkinson’s disease,” says Melinda C. Power of Johns Hopkins Bloomberg School of Public Health. While some earlier research suggests associations with depression and suicide, “[Power’s] is the first study of this scope connecting air pollution and anxiety,” says Brauer. “And it’s a very well-done study.”
In her paper, Power and colleagues at Brigham and Women’s Hospital and Harvard School of Public Health, Boston, analyzed data on more than 71,000 women whose anxiety symptoms were assessed as part of the Nurses’ Health Study. Using meteorological and geographical data and air monitoring as well as distance from major roadways, the researchers estimated pollution exposure for periods ranging from one month to 15 years prior to assessment.
What they tracked, specifically, was fine particulate matter—airborne particles under 2.5 microns (PM2.5), about one-thirtieth the diameter of fine beach sand. (Such particles carry diverse compounds, principally products of combustion.) They found that high anxiety symptoms were significantly more common among women exposed to higher concentrations of PM2.5.
“While it’s difficult to say for certain, our results indicate a [relatively] immediate effect,” says Power. “Air pollution exposure in the last month is most relevant to anxiety level, as opposed to long-term exposure.”
Fine particulates have been identified as “the most health-relevant measure of air pollution,” says Brauer: they are associated with a wide range of diseases. One possibility, Power says, is that the rise in anxiety is a consequence of medical illness related to PM2.5 exposure. But her analysis found no association with comorbid conditions.
A more promising hypothesis is that PM2.5 does its mental dirty work by promoting inflammatory processes and increasing oxidative stress. There is increasing evidence, Brauer points out, that systemic inflammation is a principal pathway from fine particulates, deposited deep in the lung, to cardiovascular and other medical ills. Complementary research links inflammatory processes with psychiatric disturbances—including anxiety.
An animal study in Molecular Psychiatry, in fact, indicated a direct link. Mice exposed to ten months of PM2.5-laden air displayed more depressive-like behaviors than those exposed to filtered air, along with increased expression of inflammatory cytokines in their hippocampi, and changes in neuron structure suggesting inflammation.
Which specific components of fine particles affect mental state, and how do they get at the brain (some may reach it directly, via olfactory nerves)? “We’ll have to do additional research to get at that,” says Power. But first, she stressed, “this is just one paper; it needs to be replicated.” And even if the role of air pollution is confirmed, “the effects are modest. It’s not The Cause of anxiety, although it may contribute significantly at a population level.”
More broadly, Power sees “an incredibly encouraging interest in how environmental risk factors, including air pollution, impact brain health. I think it’s something that had been overlooked.” Besides ongoing work on neurodegenerative diseases, particularly Parkinson’s, and research like hers on psychiatric conditions, “there’s a growing literature on air pollution and cognition,” she says.
Most of these studies were done in the past five years. A 2011 paper by Power and colleagues reporting cognitive function in a group of 680 men, mean age 71, found significantly worse performance, equivalent to nearly two years of aging, among those with a history of long-term exposure to traffic-related air pollution.
More recently, a 2014 analysis of data on 14,000 older adults across the US, published in American Journal of Epidemiology, found cognitive function to be significantly poorer among those living in areas with higher PM2.5 concentration—a difference that corresponded to 1.7 to 2.8 years of brain aging. The deficit was most marked in regard to episodic memory–an early sign of dementias such as Alzheimer’s disease (AD).
Most of this research has taken advantage of studies originally designed to explore other health outcomes, observes epidemiologist Jennifer Weuve, of Rush University Institute on Healthy Aging, Chicago. They’ve provided valuable data, “but we need more studies of cognitive decline, measuring cognition repeatedly and evaluating the trajectory over time, in people at different levels of exposure.”
And while studies of cognitive function may suggest that air pollution negatively impacts the brain, “we need to see studies of dementia itself,” she says. If evidence emerges that supports air pollution as a risk factor for AD, “people will really pay attention.”
Some researchers are probing beneath statistics to actual changes in brain structure. “There’s pretty robust evidence associating air pollution with stroke and with cognitive impairment, but not much known about what’s going on mechanistically,” says Elissa H. Wilker of Beth Israel Deaconess Medical Center and Harvard School of Public Health , Boston.
In a study reported in a recent issue of Stroke, Wilker and colleagues analyzed MRI and air pollution data for nearly 1000 people age 60 and up. They found that those with higher PM2.5 exposure were 1.5 times more likely to have evidence of covert brain infarcts (CBIs)—so-called “silent strokes” reflecting ischemic damage deep inside the brain without apparent symptoms—compared to those with low exposure.
The presence of CBI increases the risk of overt strokes—the kind that cause lasting damage—neurological deficits like difficulty in walking, and depression.
Pollution was also linked to brain atrophy. In fact, reduced brain volume for individuals at the 75th percentile of PM2.5 exposure corresponded to an additional year of aging, compared to those at the 25th percentile, Wilker says.
This difference in exposure was not enormous: “It was the range you might observe across a city like Boston. We’re not comparing downtown LA to a rural area,” she pointed out.
“We think we’re seeing subclinical evidence that something important is going on,” Wilker says. And the culprit may be familiar. “We can’t say for certain what’s happening; it may be multifactorial, but there’s good evidence that inflammation is involved.”
“This is a really important study,” says Weuve. “What Wilker and her colleagues found definitely supports some sort of cerebrovascular mechanism [behind cognitive impairment] and suggests other possibilities as well.
“It’s an important piece of evidence and complement [to epidemiological data],” she says. “Hopefully we will see more such imaging studies.”