COPD Causes and Risk Factors Everyday Health
COPD Causes and Risk Factors Everyday Health
COPD Causes and Risk Factors Everyday Health
Everyday Health
EVERYDAY GUIDE TO
COPD 6 of 7
In general, all forms of chronic obstructive pulmonary disease (COPD), including and emphysema
and chronic bronchitis, stem from airborne irritants that are inhaled.
The Centers for Disease Control and Prevention (CDC) notes that smoking accounts for up to 90
percent of all deaths related to COPD.
Cigarette smoke contains thousands of chemical components. When you breathe in cigarette
smoke, the chemicals irritate and activate certain white blood cells (macrophages) and cells that
make up the lining of the airways (epithelial cells).
This causes the cells to release multiple types of cytokines, which are small signaling proteins that
cause the airway lining to thicken and airways to become inflamed.
The persistent airway inflammation caused by cigarette smoke can cause a cycle of injury and
repair that changes the structure of the airways and makes them narrower.
Cigarette smoke also induces a cascading effect that results in certain cells producing more mucus
than normal.
What's more, the irritants decrease the number and length of cilia — hair-like appendages that beat
rapidly to move particles, fluid, and mucus through your airways.
With the cilia unable to do their jobs, mucus blankets the lining of the airways, providing a home for
bacteria, which release toxins that promote mucus production and further damage cilia.
Some research suggests that certain inflammatory cells release enzymes that break down the
proteins responsible for alveolar elasticity. Cigarette smoke may also somehow induce
programmed cell death (apoptosis) in alveolar cells.
There is even some evidence that cigarette smoke causes an autoimmune response in which the
immune system attacks alveoli tissue, according to a report in the journal Physiological Reviews.
Quitting Smoking
Airway inflammation might continue after you quit smoking, even after one year of abstinence,
according to a 2009 report in the International Journal of Environmental Research and Public
Health.
Despite this, it's important to stop smoking if you have COPD because this can prevent the
continued loss of lung function.
Telephone counseling
Support groups and cessation classes
Self-help materials
Indoor air pollution, particularly from the burning of wood and other biomass in fireplaces
and stoves
Asthma
Frequent respiratory infections during childhood
In rare cases, emphysema can also be caused by an inherited disorder called alpha-1 antitrypsin
(A1AT) deficiency, in which a normally beneficial enzyme called neutrophil elastase damages
alveoli tissue.
Risk Factors for COPD
The majority of people who develop COPD are current or former smokers who are at least 40 years
old, according to the CDC.
Additionally, the CDC notes that the people who are most likely to report being diagnosed with
COPD are those who:
Abnormal lung development in the womb and HIV infection may also be risk factors for COPD.
You can develop the disorder if you have a certain type of mutation to the SERPINA1 gene, which is
responsible for encoding the A1AT protein.
However, other genes may also make you more or less likely to get COPD.
For instance, while smoking is the biggest cause of COPD, only about 20 percent of smokers
develop COPD, suggesting that genetic factors may make some people more susceptible to the
chemicals of cigarette smoke (and possibly other inhaled irritants), according to a 2014 report in
the journal PLoS ONE.
The study found that, compared with non-smokers, certain airway cells in smokers abnormally
express a number of genes, including four genes (NFKBIB, LTBP4, EGLN2, and TGFB1) that have
been previously linked to COPD.
Numerous other genes may also be involved in the development of COPD, such as MMP12,
according to a 2012 report in the journal EMBO Molecular Medicine.
Sources
Smoking and COPD; CDC.
Rafael Laniado-Laborín (2009). "Smoking and chronic obstructive pulmonary disease (COPD). Parallel
epidemics of the 21st century." International Journal of Environmental Research and Public Health.
Yoshida and Tuder (2007). "Pathobiology of cigarette smoke-induced chronic obstructive pulmonary
disease." Physiological Reviews.
Ryan et al. (2014). "Smoking dysregulates the human airway basal cell transcriptome at COPD risk locus
19q13.2." PLoS ONE.
Peter Barnes (2008). "The cytokine network in asthma and chronic obstructive pulmonary disease." The
Journal of Clinical Investigation.
Sharafkhaneh et al. (2008). "Pathogenesis of emphysema." American Thoracic Society.
Tuder and Petrache (2012). "Pathogenesis of chronic obstructive pulmonary disease." Journal of Clinical
Investigation.
Ford et al. (2013). “COPD surveillance—United States, 1999-2011.” CHEST Journal.
Chronic obstructive pulmonary disease; University of Maryland Medical Center/A.D.A.M.
What Is Alpha-1?; Alpha-1 Foundation.
SERPINA1; Genetics Home Reference.
Marciniuk et al. (2012). "Alpha-1 antitrypsin deficiency targeted testing and augmentation therapy: A
Canadian Thoracic Society clinical practice guideline." Canadian Respiratory Journal.
Berndt et al. (2012). "Emerging genetics of COPD." EMBO Molecular Medicine.
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