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
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
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
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
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
Most of this research has taken advantage of
studies originally designed to explore other health outcomes, observes epidemiologist
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."