A Canadian study is getting volunteers to breathe the kind of dirty air we find in many of our cities – to see what the toxins may be doing to our genes.

Spending two hours breathing diesel exhaust in the basement of a hospital doesn't sound like the most pleasant way to while away a morning.

But it's what Julia, subject COPA-03, is doing in an airtight glass box four-by-six-feet wide and seven feet tall as she sits watching Netflix on her iPad. Every now and then she gets on an exercise bike to modify her breathing, and the amount of diesel exhaust she inhales is roughly equivalent to air pollution levels in Mexico City or Beijing. Her task is not much of a tourism endorsement for these polluted big cities. Instead, her boxed-in inhalations are helping to advance what we know about the effects of air pollution, hinting at the ongoing need to clean up the air we breathe, and focus on the breathing difficulties of those most vulnerable.

Air pollution has been a major concern recently; in late 2014, German carmaker VW was embroiled in a major scandal after it emerged that it had fitted ‘defeat devices’ to its diesel cars to make them appear cleaner than they were during emissions tests.

By 2030, Chronic Obstructive Pulmonary Disease (COPD) is predicted by the World Health Organisation to be the third leading worldwide cause of premature death. It’s a condition usually associated with smoking (but not always) and research suggests that in non-smoker cases, air pollution including diesel exhaust may be to blame. In London alone, bad air quality is thought to kill nearly 10,000 people a year – though during extreme periods such as the Great Smog of 1952, death rates used to be far higher.

Diesel exhaust is a ubiquitous pollutant in developing nations, says the University of British Columbia’s Dr Jeremy Hirota, where it’s common to “see clouds of black plumes coming out of the trucks.” That black soot is diesel particulates.

Which brings us back to Julia, who is breathing exhaust piped in from a whirring diesel-powered generator located in a blind alley outside Vancouver General Hospital. Exhaust is piped in to her chamber, and diluted en route with clean, filtered air. After two hours of controlled inhalation, Julia is whisked by taxi to St Paul's Hospital, where she gets on and off another exercise bike. There, inside an even smaller, telephone-box sized glass room with her nose sealed shut, a technician coaches Julia to inhale and exhale forcefully into a tube.

Her lung function is visualised as a series of wiggly graphs, and she is tested for changes to her blood, urine, and lung function. This is no job for a faint-hearted volunteer. Later, respiratory specialist  Dr Chris Carlsten will stick a tube down her anaesthetised throat, squirt saline into the top of her lungs, and suck back fragments of lung tissue loosened with a prickly brush.

We know that our bodies respond to inhaled air pollution in multiple troubling ways

Air pollution is often studied by looking for disease patterns against a long list of contaminants. But city air is such a soup of gases and small particles that this pattern-seeking (epidemiological) quest for links between cause and effect has seemed like a tall task.

That’s why this experimental approach is valuable. Exposing each volunteer to a controlled mixture of clean or polluted diesel air, in random order, means that each subject doesn’t know whether the air he or she is breathing is dirty or clean, thus acting as their own control.

Using this set-up, Carlsten and Hirota, professors of medicine at the University of British Columbia’s Centre for Occupational and Environmental Respiratory Disease, are examining how pollution particles affect us in real-time. Carlsten’s previous work suggests that even two hours of air pollution exposure affects our genes. These are not changes to our DNA sequence – the ‘recipe’ that makes us unique. Instead, air pollution appears to add a chemical onto our gene sequence.

Reversible effects?

It’s something known as epigenetic change, explains Dr David Diaz-Sanchez, chief of the clinical research branch of the National Health and Environmental Effects Research Laboratory at the US Environmental Protection Agency. As Diaz-Sanchez explains, environmental factors like pollution, diet, and stress “can turn genes on or off, or affect how a cell looks at the genes.” Until recently, there’s been very little evidence that pollution can affect this chemical cross-talk. But that is beginning to change.

Are the epigenetic changes due to air pollution reversible? We don’t yet know. Air pollution-induced epigenetic changes are not suspected to be long-lasting, but only time, and more research, will tell.

Whether or not the changes are reversible, we know that our bodies respond to inhaled air pollution in multiple troubling ways, explains Dr Neil Alexis, at the University of North Carolina Department of Pediatrics and Center for Environmental Medicine, Asthma and Lung Biology. One way our lungs respond is via inflammation, the body’s positive response to an insult. Nevertheless, “it’s the same old story – too much of a good thing can likely turn bad, so the inflammation ultimately has to be quieted or resolved,” he says. That’s one of the jobs of the body’s overall host-defence system. During exposure to dirty air, lung function is also compromised, impeding our ability to breathe.

The most effective way to avoid population-wide health impacts of air pollution is to avoid producing it in the first place

People with pre-existing airway diseases like COPD and asthma have host defence response systems that are altered, with the end result that they are either under or overachieving. In the context of polluted air, says Alexis, “either scenario likely isn’t good”.

Carlsten estimates that at least 15% of the worldwide cases of COPD are related to air pollution. That’s important;  compared to asthma, COPD comes with a bigger social and economic burden. Whereas asthma is an airway obstruction that can be quickly reversed with drugs, in COPD, the spider-web like network of lung tissue becomes riddled with irreversibly severed connections. “There is still some framework to the spider web, but there are these big holes that no longer can exchange gas, and you can’t get any air,” explains Hirota.

If you look at the research on air pollution, “it’s mostly been epidemiology and basic science,” so the third pillar, says Carlsten, is these controlled, experimental human exposures. “Historically, when policy decisions have been made about air pollution, the controlled human exposures have always been a very important piece of the puzzle,” he says. That, argues Carlsten, is because the controlled nature of the studies make the data difficult for polluters to dispute.

Of course, as Diaz-Sanchez points out, the most effective way to avoid population-wide health impacts of air pollution is to avoid producing it in the first place. “There is no alternative than to clear up the air,” he says. But in many situations that continues to be difficult. So by identifying those most at risk from air pollution, it opens up the possibility for targeted therapeutics to be developed to treat those who are most vulnerable.

“This is an area which is burgeoning,” says Diaz-Sanchez. “Even five years ago there was very little research in this area, and it’s only going to increase in relevance over time.”

That’s why Julia’s claustrophobic inhalations, added to the data discerned from dozens of volunteers before and after her, could generate a new initiative to clear the air.

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