February
22, 2016
This story was originally published by Mother Jones and is
reproduced here as part of the Climate Desk collaboration.
“We
should get out of here,” says air pollution chemist Eben Cross. At 7 a.m. on
this cold November day the wind blows steadily through the Massachusetts
Institute of Technology’s Cambridge campus, cutting through our thin jackets.
But Cross isn’t afraid of the cold. He worries about the air we’re breathing —
especially considering the six fire trucks directly ahead, idling in the dim
morning light.
“We’re
getting hammered right now,” Cross says, shouting over the hum of the engines.
He’s taken his gloves off to manipulate the display panel on his pollution
monitor. The acrid smell of diesel is unmistakable. “Anytime you can smell it,
you are in a regime that is very polluted,” he says. “In many ways your nose is
a bettermass spectrometer than any device on the market.”
Cross’
monitor measures the presence of microscopic particles suspended in the air.
Earlier, in his home, the device reported average concentrations of between
10,000 and 100,000 airborne particles per cubic centimeter of air (the latter
after he burned some toast). Now it detects millions. The massive size of the
fire trucks’ engines, combined with their inefficient combustion in cold
weather, means that the air reaching us is replete with fine and ultrafine
particles — specks of waste at least 36 times finer than a grain of sand, often
riddled with toxic combinations of sulfate, nitrate and ammonium ions,
hydrocarbons, and heavy metals. Though we have long known that these tiny
particles cause and exacerbate respiratory problems — like asthma and
infections and cancers of the lungs — they are also suspected to
contribute to a diverse range of disorders, from heart disease toobesity.
And now cutting-edge research suggests that these particles play a role in some
of humanity’s most terrifying and mysterious illnesses: degenerative brain
diseases.
While
coarse pollution particles seldom make it past our upper lungs, fine and
ultrafine particles can travel from our nostrils along neural pathways directly
into our brains. Once there, they can wreak a special havoc that appears to
kick off or accelerate the downward spiral of degenerative diseases like
Alzheimer’s and Parkinson’s. While much of the research is still preliminary,
the findings so far are compelling. Autopsies of the brains of people who lived
in highly contaminated areas have turned up traces of pollution and
corresponding brain trauma. And among those still living, epidemiologists have
recorded elevated rates of brain disease and accelerated mental decline.
All of
this is especially scary when you consider how many people are at risk.
Alzheimer’s and Parkinson’s already afflict 50 million people worldwide and
about 6 million in the United States. In 2015, nearly 1-in-5 Medicare
dollars will be spent on Alzheimer’s; this disease and other types of dementia
will cost the United States $226 billion. By 2050, experts predict, that cost
will rise to $1.1 trillion — the baby boomers are only now entering the phase
of life when degenerative diseases usually emerge. Because boomers were born
before the improvements of the Clean Air Act, passed in 1970, they likely have
had a greater lifetime exposure to air pollution than any other generation
before or after them.
But
although American air today is the cleanest it has been in four decades,
pollution is still a major public health problem. According to estimates from
the American Lung Association, more than 46 million Americans — about 15
percent of the U.S. population — are chronically exposed to levels of particle
pollution that exceed Environmental Protection Agency (EPA) standards, with a
further 44.1 million plagued by periodic unhealthy exposures on bad air days
or, as in parts of California, seasonal air pollution spikes. Meanwhile, in
some Chinese and Indian cities, air pollution levels are routinely three to six
times higher than World Health Organization standards. A recent study in the
peer-reviewed journal Environmental Health and Technology estimated that we
could avoid 2 million deaths globally by cleaning up the world’s air.
Researchers
have struggled for decades to pinpoint the risk factors that, in addition to
genetics, can contribute to a person’s likelihood of developing Alzheimer’s and
Parkinson’s diseases; theories have ranged from viral infection to aluminum
exposure to high-fat diets, but none of these has withstood scientific
scrutiny. The research implicating air pollution is in its early stages, and
many questions remain unanswered — for example, it’s unclear whether particle
pollution initiates degenerative disease or merely accelerates it. Still, the
evidence so far suggests that pollution could be the most pervasive potential
cause of brain disease that scientists have ever discovered. We’re not “beyond
a doubt,” says Michelle Block, a neurobiologist at the Indiana University
School of Medicine, but “everything we do says this is probably happening.”
In a
small room on the third floor of a lab at the University of Southern
California’s gerontology department, graduate student Nick Woodward shows me
one front line in the global effort to understand the link between air
pollution and brain disease: nine black mice in clear plastic cages. They are
breathing highway exhaust, piped in by Woodward, that was gathered from the
busy 110 freeway. Because of the heavy truck traffic on that road, the exhaust
is especially rich in ultrafine particles laced with metals and hydrocarbons,
in hundreds of combinations. To simulate life in a nearby neighborhood,
Woodward explains, the mice will be exposed to exhaust for five hours a day,
three days a week, until they are finally sacrificed and their organs examined
for the presence of particles and disease.
This
study and similar ones have their roots in Mexican research from the 1990s,
when the United Nations had just deemed Mexico City one of the most polluted
metropolitan areas on the planet. Even modern Beijing sees relatively clear
skies20 percent of the year — but in 1992, Mexico City air quality
monitors recorded only eight smog-free days. By the early 2000s, researchers in
Mexico City studying the effects of urban pollution on dogs, which live longer
than mice and can be raised outdoors to approximate human exposures, began to
discover unusual symptoms.
Lilian
Calderón-Garcidueñas, lead investigator of the studies, noted that some dogs
exposed to Mexico City air began to exhibit “decrements of attention and
activity.” Caretakers of other dogs “were aware of alterations of sleep
patterns and barking,” she wrote. Some “reported transient episodes during
which the dogs failed to recognize [them].” Inside their brains,
Calderón-Garcidueñas founddramatic tissue damage — the cells in the dogs’
olfactory-processing center were dying, with the scars of disease traceable out
to the nose itself — that was strangely reminiscent of the damage that
sometimes appears in an entirely different study population: Alzheimer’s and
Parkinson’s patients.
Domesticated
dogs have an exquisite sense of smell; they possess as many as 220 million
olfactory neurons, while humans are thought to have between 5 million and 12
million. Dogs are also one of only a handful of animal species known to
naturally develop Alzheimer’s-type dementia. What Calderón-Garcidueñas
discovered more than a decade ago may prove to be the missing element in a
long-standing theory of neurodegenerative disease origin. For reasons poorly
understood, degenerative diseases like Alzheimer’s and Parkinson’s often reveal
themselves in humans through early breakdowns in the olfactory system.
Degenerative disease sufferers lose some of their sense of smell so
predictably, and so long before more overt symptoms manifest, that doctors
sometimes use smell tests as a diagnostic tool. As a result, many neurologists
have long suspected that these disorders might be caused by foreign substances
that we inhale through our noses. The most recent studies have looked at the
most common of these substances: particle pollution.
In
order to understand how exactly a particle travels from the nose to the brain,
you’ll need a quick lesson in human respiratory anatomy. When you breathe in
polluted air, particles enter your body through both your nose and your mouth.
Large, coarse particles, like bits of windblown dust, are caught there and in
your upper lungs and are eventually removed by coughing, sneezing, and nose
running. Smaller particles can bypass these natural defense lines to reach your
body’s more sensitive tissue. In the lungs, scientists have long known, they
can embed and foster infection and cancer or pass directly into the
bloodstream, where they create a host of dangerous byproducts that can
circulate with the blood and cause damage to organs and bodily systems.
But
particles that make it past your nose may be even more damaging. The lining of
the human nasal cavity contains millions of specialized nerve cells that wave
tens of millions of tiny hairs in a gel of mucus. These hairs detect inhaled
chemicals and transmit information about them to the smell center of your
brain, called the olfactory bulb. This is the process that allows you to tell,
say, whether a carton of milk is spoiled. Your nasal nerve, whose hairs are
exposed to the outside air in your nose, reaches all the way into your brain.
This direct line allows your nose to communicate very quickly with your mind,
an advantage in hunting, gathering, and predator avoidance. But it also makes
us susceptible to pollution — particles entering your nose can actually travel
along the olfactory neuron pathways from the nasal hairs right into the brain.
In other words, as with cocaine, what you inhale through your nose can go
straight to your brain.
Once
in the brain, pollutant particles can directly kill or damage neurons if toxic
metals or compounds are attached to them. But scientists now know that they can
also cause more widespread damage by disrupting microglia, the brain’s unique
army of immune cells. Microglia are the sentinels, bodyguards, and trash
collectors of the brain. Among other things, they identify threats to brain
health, from dead neurons to pathogens, and work collectively to neutralize and
remove the offenders. When microglia encounter a pollution particle, they
mistake it for a germ — with disastrous results.
Microglia
in the presence of a particle produce a variety of chemical compounds meant to
kill the interloper. The chemicals then accumulate and begin to damage or even
kill surrounding cells. And the toxins attached to particles can corrupt the
microglia, leaving them permanently in attack mode or otherwise unable to
perform other important functions, like removing waste from the brain.
Researchers
believe that chronic inflammation — the long-term overactivation of the body’s
immune response — is harmful, even at very low levels. Studies have connected
it to a broad range of illnesses; in the skeletal system, for example, it can
cause the pain associated with arthritis, while in the gut it can lead to
metabolic disorders such as diabetes. In the brain, chronic inflammation has
been consistently implicated in neurological degeneration. This is, relatively
speaking,old and established science. In scans and autopsies of patients with
Alzheimer’s and Parkinson’s, highly active microglia are found in the regions
of the brain that have lost the most neurons. And, in mice, scientists have
actually observed the microglia killing neurons.
With
air pollution, “there is indication that we are creating inflammatory responses
that are in the direction of Alzheimer’s disease,” says Caleb Finch, a
gerontologist who runs the lab that is studying pollution and mice at USC. If
that assessment sounds overly cautious, it’s meant to: Researchers in the
Alzheimer’s field are extremely wary of overstating the evidence. Still fresh
are the memories of an aluminum scare in the mid-1980s, when preliminary
studies linking aluminum in the brain to Alzheimer’s disease fed provocative
news headlines and initiated needless hand-wringing over antiperspirants and
cooking pans. Also, scientists now increasingly believe that it’s likely that
no one environmental factor or trigger causes the disease; rather, “it’s
probably a multiple hit,” says Indiana University’s Block. “It’s an assault
across your entire lifetime that’s going to culminate with disease in age.”
Even
so, of all the potential environmental drivers of degenerative disease, air
pollution has by far the most promising scientific evidence behind it. “The
longer I’ve been doing this research, the more I’m convinced that, most likely,
urban air pollution is the most readily available source of microglial
activation,” Block says.Jennifer Ailshire, a social demographer at USC, also
sees growing evidence along these lines. It “just hardly ever happens,” she
says, that human studies and animal models are in such strong agreement.
In
epidemiology, one of the best ways to figure out what leads to a disease is the
prospective study, in which scientists track patients over decades, monitoring
their diet, lifestyle, exposures to toxins, and health outcomes. Several
prospective studies on pollution’s effect on neurodegenerative diseases are
underway, but we won’t know their results for decades. What we do have so far
are retrospective epidemiological studies, which are kind of the opposite:
Scientists study groups of older people with and without a given disease,
comparing their life experiences, genetic factors, and environmental exposures.
The problem with retrospective studies is that they rely heavily on subjects’
self-reporting, which is notoriously fallible; subjects probably wouldn’t be
able to accurately recall, for example, how much time they’ve spent near an
idling school bus. Another problem is inconsistent data. For example:
Fine-particle levels in the United States have been regularly recorded for only
the last 15 years, so epidemiologists often use proxy measures to estimate
exposures from the distant past.
Still,
evidence from retrospective studies is sobering. Controlling for things like
ethnicity, gender, income, education, and other possible environmental
exposures (including cigarette smoke), elderly individuals living in areas with
polluted air appear to lose their mental abilities faster, show more
predementia symptoms (also known as mild cognitive impairment), and develop
Alzheimer’s disease at greater rates. Six years ago, researchers in Germany
assessed the cognitive abilities of 399 elderly women who lived in the same
place for more than 20 years. Regardless of her socioeconomic status, the
closer a woman lived to a busy road, the authors reported, the greater the
chance that she would have mild cognitive impairment.
Four
years ago, researchers from Harvard linked estimates of higher daily exposure
to black carbon, a solid type of fine particulate matter, to lower cognitive
ability in older men in Boston. In a larger, national study tracking the mental
status of more than 19,000 retired nurses over several years, researchers
connected the rate of mental decline in women 70 and older to their exposure to
coarse- and fine-particle pollution and found that those exposed to more
particles lost their mental abilities at a faster rate. In a group of 95,690
elderly Taiwanese, researchers this year found that a slight increase in
fine-particle exposure over 10 years led to a 138 percent increased risk of
developing Alzheimer’s disease. A smaller, more recent study published in
the Annals of Neurology followed 1,403 elderly women without dementia.
Scientists found that exposure to air pollution over time to led to a major
decrease in the subjects’ white matter, a part of the brain essential for
cognition.
So how
much pollution might the brain be able to withstand? Unfortunately, that’s not
yet clear. In the study from Taiwan, an increase in annual pollution exposure
of four micrograms of particles per cubic meter of air — the additional amount
you might experience within a block or two from a busy road — was sufficient to
dramatically alter Alzheimer’s risk. But that was in addition to already high
levels of pollution exposure, which were greater than anything you would
routinely experience in America. In the nationwide study of retired U.S.
nurses, exposure to an additional 10 micrograms of fine particles per cubic
meter of air per year over several years seemed to speed up damage to mental
abilities “as if your brain were aged an extra two years,” says Rush
University’s Jennifer Weuve, the study’s lead author. That’s about the
same increase in pollution you would experience if you moved from Beverly Hills
to South Central Los Angeles.
And
there is growing evidence that particle pollution’s assault on the mind is not
limited to elderly brains. Researchers in Mexico City, which still has some of
the worst urban air on the planet, have found signs of advanced brain damage in
children as young as 6 and 7 years old: overactive immune cells,
degraded white matter, and damaged vasculature typically seen only in older
brains. In one autopsy study comparing children raised in Mexico City with
their counterparts in less polluted parts of the country, half the Mexico City
children had notable aggregations of a protein called amyloid beta — which
is strongly associated with Alzheimer’s — grouped in clumps across their brains.
In the children from less polluted areas, there were none.
In
America, as in most of the world, the burden of pollution does not fall
evenly. Fine particles can travel thousands of miles through the air, but
ultrafine particles drop out much sooner, typically after only a few thousand
feet. This means that unless you live within a few miles of a coal-fired power
plant or metal smelter, most of the ultrafine particles you breathe are
probably from vehicles, particularly old diesel engines.
In our
pass through Cambridge and then Boston, which has average air pollution levels
for an American city, Cross detects numerous and dramatic ultrafine-particle
pollution hot spots: bike lanes near highways where diesel clouds plague
commuters for miles; schoolyards full of emissions from idling buses;
apartments downwind of trucking routes. The worst places tend to be near busy
roads; one EPA study found the concentration of ultrafine particles in Los
Angeles to be 25 times greater near freeways than in the rest of the city.
Because
pollution falls hardest near road traffic and crowded urban areas, people who
are more likely to live there — the poor, the elderly, people of color — are
disproportionately exposed to airborne neurotoxins. In 2014, researchers from
the University of Minnesota found that minorities in the United States are
exposed on average to 38 percent higher levels of air pollution than white
people. (Though they looked at nitrogen dioxide, a nonparticle pollutant, their
findings are indicative of traffic-related exposures.) In 2012, researchers
from Yale matched census tracts to particle pollution data for areas around the
continental United States. They found that “non-Hispanic blacks, the least
educated, the unemployed, and those in poverty” suffered the highest pollution
burden.
The
good news is that air pollution is one of the United States’ greatest
environmental success stories. Particle emissions have been dropping steadily
since the 1970s, along with other pollutants governed by laws like the Clean
Air Act. The EPA regulates levels of coarse- and fine-particle pollution, and
two years ago it strengthened the national standards for fine particles. But
there is still no regulation for ultrafine-particle pollution, here or in any
other country. While the EPA did consider the new science implicating ultrafine
particles in brain disease during its last review, an agency representative
told me by email that there was “insufficient evidence to draw conclusions.”
The agency has said that it will consider the new science on ultrafine
particles in its current review, which is ongoing.
The
quickest way to rid our cities of particle pollution would be by cleaning up
diesel engines. That may be in the works; the Obama administration
recently proposed much tougher emissions standards for trucks. Since 2007,
the EPA has required new diesel buses and trucks to utilize cleaner-burning
engines, but because diesel engines last 20 or 30 years, millions of the older
ones are still on the roads. Beginning around 2000, California started
requiring owners of old diesel vehicles — from Greyhounds to big rigs and
school buses — to begin replacing their engines. But a significant number of
old, dirty engines are still on the road — and in many parts of the United
States, engine upgrades are not yet mandatory.
Another
option to reduce exposure is to move away from hot spots. But as Columbia
University epidemiologist Shakira Suglia points out, because the risk tends to
be highest in poorer neighborhoods, the people with the worst exposures “simply
don’t have the resources to move. The less you have, the harder it is to
control what it is you are being exposed to.” Some public health advocates’
suggestions for people who can’t move — like telling them to stay indoors on
the worst pollution days — can seem impractical, even cruel. Broader
efforts, like limiting vehicle traffic through neighborhoods and building
schools and nursing homes far from busy roads, could offer a measure of relief,
as could the installation of expensive air filters. (A California law requires
new schools to be built away from freeways or equipped with filters, but there
are major loopholes. Meaningful improvement may be decades away even in places
like Los Angeles — not to mention developing megacities like Beijing and New
Delhi.)
Meanwhile,
it’s worth noting that those who study brain disease and air pollution are
taking matters into their own hands. Every time she moves to a new place, Weuve
says she aims to live “at least 50 meters away from an interstate expressway,
state highway, or truck route.” When USC’s Finch moved to Los Angeles, he
“chose to live at as high an altitude as possible” in order to escape the
pollution that clusters around the city’s low-lying highways. Last year, before
their daughter was born, MIT’s Cross and his wife began looking for a new home
for their young family. “Minimizing her exposure to roadside emissions is
something that played into our decisions,” Cross says. For any potential home,
proximity to a busy road “was a deal-breaker.”
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