Mini-Med at McGill: Question and Answer Corner

Mini-Med Study Corner

Respirology: Take a Breath: Take a Deep Breath
Dr. David Eidelman

Written Question and Answer Section:

1. Does second hand smoke cause COPD?

There have been a number of studies addressing this important question. While there is no question that second hand smoke is dangerous for one's health, the data linking second hand smoke to COPD is mixed. Most studies have failed to find an association, although there are some studies, particularly in China, that show as much as a 50% increase in the rate of COPD among individuals exposed to second hand smoke either at home or at work. Please keep in mind that in order for “COPD” to be diagnosed there must be measurable changes in breathing tests (lung function). Although this has not been shown in most studies outside China, there is a definite effect of second hand smoke on respiratory symptoms due to irritation of the bronchial tubes.

There is excellent, non-controversial evidence to indicate that second hand smoke leads to increased rates of heart disease (about 30% higher) and lung cancer (also about 30% higher). It may also cause some other cancers such as cancer of the nasal sinuses. In children, it is associated with increased risk of sudden infant death, ear infections, colds, pneumonia, bronchitis and contributes to worsening childhood asthma. For additional information, check out the following fact sheets on the web:

National Cancer Institute of the US NIH
(http://www.cancer.gov/cancertopics/factsheet/Tobacco/ETS)

Centers for Disease Control and Prevention (Atlanta)
(http://www.cdc.gov/tobacco/data_statistics/fact_sheets/secondhand_smoke/health_effects/index.htm)

2. Does lung function change with age, in the absence of disease?

The lung changes continually throughout life. Healthy children are born with incompletely formed lungs. Although a baby has a complete set of airways (trachea and bronchial tubes), the alveoli develop mainly after birth, up to about age 8. After that age the lung continues to grow, reaching a maximum in size and efficiency in early adulthood (around age 20). Although it remains almost constant until age 30, there is an inexorable decline in lung function with age.

The most common and best validated measurement of lung function is the FEV1 (forced expiratory volume in 1 sec), which measures how much air can be exhaled in one second during a maximal manoeuvre. In middle age the FEV1 will decrease by almost 25 cc per year and in those over 75, this may reach as much as 50 cc per year. The major cause of decreased lung function with age is degenerative changes in the tissues of the lung. As with other body tissues, ageing is associated with a slow but steady decline in tissue elasticity. In the case of the lungs, this has the effect of reducing the efficiency of maximal forced exhalation. Note that the rate of decline among active smokers is double that of the general population.

Although as with other aspects of ageing, this is not “good news”, for most healthy non-smokers, there is enough reserve so that this decline in function is not a practical problem until advanced old age, if ever.

3. Since not all smokers get symptomatic COPD, is there a genetic predisposition to this disease?

COPD is an example of a “complex trait” disease. It involves abnormalities in multiple systems and is likely to be caused by a variety of environmental and genetic factors. In the case of the environment, there is very strong evidence of an association with cigarette smoke exposure. There is also a suggestion that exposure to other environmental agents such as cooking fires and certain mineral dusts can contribute to or cause COPD.

There is a form of emphysema (part of COPD), which is clearly genetic. Individuals who are deficient in the enzyme alpha-1 antitrypsin (sometimes called alpha-1 antiprotease) are at very high risk of developing lung disease (especially emphysema but also bronchiectasis) if they smoke. They also develop a form of liver disease and other problems. Alpha-1 antitrypsin deficiency is not thought to account for more than 1% of COPD. In addition, there are a number of very rare genetic diseases, mainly involving the connective tissues of the body, that are associated with COPD but these account for a tiny fraction of cases.

As to the more common form of COPD, there are hints that some genetic factors are at work but no definitive evidence. For example, there are major variations in COPD rates around the world and some data suggests that people of African origin are at increased risks. There is also data convincingly demonstrating that women are at higher risk, although this may have to do with the relatively higher exposure to cigarette smoke that women receive because their lungs are smaller.

A number of studies have tried to investigate COPD genetics using current population based techniques. Although some associations between variables of lung function have been associated with particular locations on different chromosomes, no clear, unequivocal genetic causes for ordinary COPD have been identified.

The COPD Gene website is dedicated to the topic of the genetics of COPD. They are running a large scale study of the question out of the National Jewish Hospital in Denver and the Brigham and Women's Hospital in Boston. The study is funded by the US National Heart, Lung and Blood Institute of the NIH.

http://www.copdgene.org/genetics

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