Dr. Schiffman received his B.S. degree with High Honors in biology from Hobart College in 1976. He then moved to Chicago where he studied biochemistry at the University of Illinois, Chicago Circle. He attended Rush Medical College where he received his M.D. degree in 1982 and was elected to the Alpha Omega Alpha Medical Honor Society. He completed his Internal Medicine internship and residency at the University of California, Irvine.
Dr. Charles "Pat" Davis, MD, PhD, is a board certified Emergency Medicine doctor who currently practices as a consultant and staff member for hospitals. He has a PhD in Microbiology (UT at Austin), and the MD (Univ. Texas Medical Branch, Galveston). He is a Clinical Professor (retired) in the Division of Emergency Medicine, UT Health Science Center at San Antonio, and has been the Chief of Emergency Medicine at UT Medical Branch and at UTHSCSA with over 250 publications.
Cigarette smoking is
by far the most dangerous behavior that causes people to develop emphysema, and it is also
the most preventable cause. Other risk factors include a deficiency of an enzyme
called alpha-1-antitrypsin, air pollution, airway reactivity, heredity, male sex, and age.
The importance of cigarette smoking as a risk factor for
developing emphysema cannot be overemphasized. Cigarette smoke contributes to
this disease process in two ways. It destroys lung tissue, which results in
the obstruction of air flow, and it causes inflammation and irritation of airways that can
add to air flow obstruction.
Destruction of lung tissue occurs in several ways.
First, cigarette smoke directly affects the cells in the airway responsible
for clearing mucus and other secretions. Occasional smoking temporarily
disrupts the sweeping action of tiny hairs called cilia that line the
airways. Continued smoking leads to longer dysfunction of the cilia.
Long-term exposure to cigarette smoke causes the cilia to disappear from the
cells lining the air passages. Without the constant sweeping motion of the
cilia, mucous secretions cannot be cleared from the lower respiratory tract.
Furthermore, smoke causes mucous secretion to be increased at the same time
that the ability to clear the secretions is decreased. The resulting mucous
buildup can provide bacteria and other organisms with a rich source of food and lead to
The immune cells in the lung, whose job it is to
prevent and fight infection, are also affected by cigarette smoke. They
cannot fight bacteria as effectively or clear the lungs of the many
particles (such as tar) that cigarette smoke contains. In these ways
cigarette smoke sets the stage for frequent lung infections. Although these infections may not even be serious enough to require medical care, the inflammation caused by the immune system constantly attacking bacteria or tar leads to the release of destructive enzymes from the immune cells.
Over time, enzymes released during this persistent
inflammation lead to the loss of proteins responsible for keeping the lungs
elastic. In addition, the tissue separating the air cells (alveoli) from one
another also is destroyed. Over years of chronic exposure to cigarette smoke, the decreased elasticity and destruction of alveoli leads to the slow destruction of lung function.
Alpha-1-antitrypsin (also known as alpha-1-antiprotease) is a substance that fights a destructive enzyme in the lungs called trypsin (or protease). Trypsin is a digestive enzyme, most often found in the digestive tract, where it is used to help the body digest food. It is also released by immune cells in their attempt to destroy bacteria and other material. People with alpha-1-antitrypsin deficiency cannot fight the destructive effects of trypsin once it is released in the lung. The destruction of tissue by trypsin produces similar effects to those seen with cigarette smoking. The lung tissue is slowly destroyed, thus decreasing the ability of the lungs to perform appropriately. The imbalance that develops between trypsin and antitrypsin results in an “innocent bystander” effect. Foreign objects (e.g. bacteria) are trying to be destroyed but this enzyme destroys normal tissue since the second enzyme (antiprotease) responsible for controlling the first enzyme (protease) is not available or is poorly functioning. This is referred to as the “Dutch” hypothesis of emphysema formation.
Air pollution acts in a similar manner to cigarette smoke. The pollutants cause inflammation in the airways, leading to lung tissue destruction.
Close relatives of people with emphysema are more likely to develop the disease themselves. This is probably because the
tissue sensitivity or response to smoke and other irritants may be inherited. The role of genetics in the development of emphysema, however, remains unclear.
Abnormal airway reactivity, such as bronchial asthma, has been shown to be a risk factor for the development of emphysema.
Men are more likely to develop emphysema than women. The exact reason for this is unknown, but differences between male and female hormones are suspected.
Older age is a risk factor for emphysema. Lung function normally declines with age. Therefore, it stands to reason that the older the person, the more likely they will have enough lung tissue destruction to produce emphysema.
It is important to emphasize that COPD is often not purely emphysema or
bronchitis, but varying combinations of both.