What Causes Asthma?

According to recent estimates, asthma affects
300 million people in the world and more than
22 million in the United States. Although people
of all ages suffer from the disease, it most often
starts in childhood, currently affecting 6 million
children in the US. Asthma kills about 255,000
people worldwide every year.
Children at Risk
Asthma is the most common chronic disease
among children - especially children who have
low birth weight, are exposed to tobacco smoke,
are black, and are raised in a low-income
environment. Most children first present
symptoms around 5 years of age, generally
beginning as frequent episodes of wheezing with
respiratory infections. Additional risk factors for
children include having allergies, the allergic skin
condition eczema, or parents with asthma.
Young boys are more likely to develop asthma
than young girls, but this trend reverses during
adulthood. Researchers hypothesize that this is
due to the smaller size of a young male's airway
compared to a young female's airway, leading
to a higher risk of wheezing after a viral
infection.
Allergies
Almost all asthma sufferers have allergies. In
fact, over 25% of people who have hay fever
(allergic rhinitis) also develop asthma. Allergic
reactions triggered by antibodies in the blood
often lead to the airway inflammation that is
associated with asthma.
Common sources of indoor allergens include
animal proteins (mostly cat and dog allergens),
dust mites, cockroaches, and fungi. It is possible
that the push towards energy-efficient homes
has increased exposure to these causes of
asthma.
Tobacco Smoke
Tobacco smoke has been linked to a higher risk
of asthma as well as a higher risk of death due
to asthma, wheezing, and respiratory infections.
In addition, children of mothers who smoke -
and other people exposed to second-hand
smoke - have a higher risk of asthma
prevalence. Adolescent smoking has also been
associated with increases in asthma risk.
Environmental Factors
Allergic reactions and asthma symptoms are
often the result of indoor air pollution from mold
or noxious fumes from household cleaners and
paints. Other indoor environmental factors
associated with asthma include nitrogen oxide
from gas stoves. In fact, people who cook with
gas are more likely to have symptoms such as
wheezing, breathlessness, asthma attacks, and
hay fever.
Pollution, sulfur dioxide, nitrogen oxide, ozone,
cold temperatures, and high humidity have all
been shown to trigger asthma in some
individuals.
During periods of heavy air pollution, there tend
to be increases in asthma symptoms and
hospital admissions. Smoggy conditions release
the destructive ingredient known as ozone,
causing coughing, shortness of breath, and even
chest pain. These same conditions emit sulfur
dioxide, which also results in asthma attacks by
constricting airways.
Weather changes have also been known to
stimulate asthma attacks. Cold air can lead to
airway congestion, bronchoconstriction (airways
constriction), secretions, and decreased
mucociliary clearance (another type of airway
inefficiency). In some populations, humidity
causes breathing difficulties as well.
Obesity
Overweight adults - those with a body mass
index (BMI) between 25 and 30 - are 38% more
likely to have asthma compared to adults who
are not overweight. Obese adults - those with a
BMI of 30 or greater - have twice the risk of
asthma. According to some researchers, the risk
may be greater for nonallergic asthma than
allergic asthma.
Pregnancy
The way you enter the world seems to impact
your susceptibility to asthma. Babies born by
Caesarean sections have a 20% increase in
asthma prevalence compared to babies born by
vaginal birth. It is possible that immune system-
modifying infections from bacterial exposure
during Cesarean sections are responsible for this
difference.
When mothers smoke during pregnancy, their
children have lower pulmonary function. This
may pose additional asthma risks. Research has
also shown that premature birth is a risk factor
for developing asthma.
Stress
People who undergo stress have higher asthma
rates. Part of this may be explained by
increases in asthma-related behaviors such as
smoking that are encouraged by stress.
However, recent research has suggested that the
immune system is modified by stress as well.
Genes
It is possible that some 100 genes are linked to
asthma - 25 of which have been associated with
separate populations as of 2005.
Genes linked to asthma also play roles in
managing the immune system and
inflammation. There have not, however, been
consistent results from genetic studies across
populations - so further investigations are
required to figure out the complex interactions
that cause asthma.
Mom and Dad may be partially to blame for
asthma, since three-fifths of all asthma cases
are hereditary. The Centers for Disease Control
(USA) say that having a parent with asthma
increases a person's risk by three to six times.
Genetics may also be interacting with
environmental factors. For example, exposure to
the bacterial product endotoxin and having the
genetic trait CD14 (single nucleotide
polymorphism (SNP) C-159T) have remained a
well-replicated example of a gene-environment
interaction that is associated with asthma.
Airway Hyperreactivity
Researchers are not sure why airway
hyperreactivity is another risk factor for asthma,
but allergens or cold air may trigger
hyperreactive airways to become inflamed.
Some people do not develop asthma from
airway hyperreactivity, but hyperreactivity still
appears to increase the risk of asthma.
Atopy
Atopy - such as eczema (atopic dermatitis),
allergic rhinitis (hay fever), allergic conjunctivitis
(an eye condition) - is a general class of allergic
hypersensitivity that affects different parts of
the body that do not come in contact with
allergens. Atopy is a risk factor for developing
asthma.
Some 40% to 50% of children with atopic
dermatitis also develop asthma, and it is
probable that children with atopic dermatitis
have more severe and persistent asthma as
adults.
This asthma information section was written
by Peter Crosta. It was first published in
September 2007 and last updated on 5 March
2013.