Lung damage lingers even after quitting fags
COPD is projected to be the third-leading cause of death worldwide by 2020.
Melbourne: Smokers, beware! Lung damage
due to puffing can last long even after you kick the butt, a
new study has claimed.
Researchers at University of Sydney have found that
smoking fundamentally alters airway tissue in people with
chronic obstructive pulmonary disease (COPD), and even while
other aspects of health improve, the lung damage lasts long
after a smoker quits.
COPD is projected to be the third-leading cause of
death worldwide by 2020, and is characterised by thickening of
the airway wall. The primary cause is chronic exposure to air
pollution, most often cigarette smoke.
In their study, the researchers found that smoking
lays the groundwork for airway thickening and precipitates
precancerous changes in cell proliferation that may be
self-perpetuating long after cigarette smoke exposure ends.
"We have demonstrated for the first time that the
extracellular matrix (ECM) produced by fibroblasts following
stimulation with cigarette smoke extract is functionally
different than non-exposed ECM, and that the cigarette smoke
itself may prime the airways in such a way to create an
environment whereby airway remodeling is encouraged," lead
researcher David Krimmer said.
The researchers examined the response of human lung
tissue from donors with and without COPD to cigarette smoke
extract (CSE). They found CSE exposure led to changes in the
tissue of donors with COPD over the tissue of individuals
Similarly, they found CSE increased levels of perlecan - a protein associated with tumor growth and angiogenesis in COPD lung tissue. These findings demonstrate cigarette smoke has the capacity to directly change the make-up of airways.
"This will change the way researchers think about the
development of fibrosis in COPD. We have known for a long time
that development of fibrosis is irreversible in people with
COPD. Our findings suggest that cigarette smoking alters the
lung composition in such a way that fibrosis becomes self-
perpetuating," Krimmer said.
The findings have been published in the latest edition
of the `American Journal of Respiratory Cell and Molecular