What happens on the molecular level when smog gets into the lungs?
Coughing. A sore throat. Maybe a pain in your chest as
you take a deep breath.
These are all
common symptoms for many city-living people when smog levels are high. And
while it is well understood that smog can cause such problems, new research has
for the first time given us a glimpse as to what might be happening at the
molecular level.
The University of
Melbourne's Professor Richard O'Hair, from the School of Chemistry's Bio21
Institute, in collaboration with Professor Stephen Blanksby (from the
Queensland University of Technology and formerly the University of Wollongong)
co-authored a study examining how ozone reacts with models of lung proteins.
Smog is made up of
ozone -- an invisible gas and a well-known air pollutant made up of three
oxygen atoms. Ozone is also the pollutant that leaves a distinctive smell in
the air after using a photocopier.
Using a mass
spectrometer, the research team was able to introduce the amino acid cysteine
-- a component of lung proteins -- with ozone molecules in a highly-controlled,
near-vacuum environment.
The effect was
instant, or in scientific terms, close to the "collision rate."
"We observed
that the cysteine became 'radicalised' in the presence of ozone," said
Professor O'Hair.
"No one had
really noticed that you can form free radicals in the reaction of proteins with
ozone, and since these are highly reactive species, you don't want them around.
"Free
radicals can unleash fury and cause many chemical transformations.
"If they get
out of control, they can just chew through a system and destroy it. For
example, free radical damage is thought to play a key role in heart disease and
some cancers.
"So when free
radicals are formed in the body, such as the lining of the lung, damage occurs,
that may ultimately result in inflammation and breathing difficulties."
The research
pushes forward the understanding of the molecular effect of ozone on proteins.
But because the tests were conducted in an artificial environment, more work
needs to be done to confirm the creation of protein free radicals in lungs and
link their effects on human lung physiology.
Professor O'Hair
hopes the research inspires fellow scientists to build on the findings.
Associated
research will be of the most benefit to those with asthma, other respiratory
illnesses or the young and the elderly who are most susceptible to smog.
"If there is
free radical damage to lung proteins, it's unlikely to be reversible, so you
won't be able to design a magic-bullet drug to undo the damage," Professor
O'Hair said.
"Ozone is the
result of pollution. So the message has to go out that we need to be proactive
on reducing smog levels and pollution."