
Asthma is a disease that develops due to genetic and
environmental factors. Studies of
have shown a dramatic increase in the prevalence of asthma over the past few
decades (Crain). The rates have
been growing highest in urban settings (Etzel). However, these observations cannot be accounted for by
changes on the genetic level.
Therefore, many researchers have concluded that the bulk of the increase
in asthma prevalence must be due to changes in environmental exposures. Many studies that have attempted to
describe asthma risk factors in urban areas have focused on outdoor air
pollution, mainly due to increased traffic. In fact, researchers have shown a correlation between
increases in outdoor air pollution and increases in asthma (DÕAmato). This is controversial, however, as many
studies show no association between development of asthma and outdoor
pollution. Rather, these studies
suggest that indoor pollution is responsible for the development of asthma in
children and that outdoor pollution is only a trigger (Kunzil, Etzel,
Hirsch). In either scenario,
asthma morbidity is on the rise and pollution appears to be the culprit.
Air pollution is also associated with a variety of other
ailments. These include colds,
influenza, bronchitis, days of reduced activity and cardiovascular disease
(Kunzil).
At Risk Populations: Those individuals that are at risk of
air pollution related asthma include the elderly, young children, chronic
disease sufferers, and those predisposed to asthma.
Distribution:
Increased rates of asthma
associated with air pollution tend to be high in Westernized/urbanized
countries. Countries with a high
prevalence include Australia, New Zealand, United Kingdom and many countries of
Eastern Europe (http://www.asthma.co.uk.org).
Mechanism: A proposed mechanism by which air pollution
initiates an asthma attack is through the creation of highly reactive oxidative
molecules. These oxidants
aggravate the epithelium of the respiratory system and initiate an immune
response. The surrounding tissue
becomes inflamed and the individuals experiences asthma symptoms (Lee).
Interaction:
Research has shown that air
pollution can interact with allergens (ragweed, animal dander) to intensify
asthma symptoms. It is believed
that air pollutants act as a ÒprimerÓ that irritates the respiratory
epithelium. This allows for easier
access by allergens to the epithelium and results in increased asthma symptoms
(DÕAmato).
Potential Causes:
Air pollution in urban areas can be
created from a variety of sources.
These include power plants, industry, and even the home. However, the main source of outdoor air
pollution in cities is from traffic emissions. The chemicals that are associated with Òtraffic emissionsÓ
include:
A study of Korean children under 14 years old demonstrated
that that each of these chemicals significantly increased the risk of
hospitalization due to asthma attacks.
Each chemical, individually, was associated with a 10-15% increased risk
of hospitalization. One key item
to note is that the concentration levels of each of these chemicals were
monitored during the entire study.
These levels did not exceed the current maximum allowable levels in
Korea (Lee).
Smog: Smog formation due to increased traffic
has become a problem for many cities.
In response to this, smog alert systems have been developed in order to
inform communities about potential smog hazards. These alerts are typically targeted to those considered high
risk.
Other Potential Asthma Triggering Chemicals (Delfino):
[O2] [CO] [Diesel Exhaust Particulates (DEP)]
[Acetaldehyde] [Acetone] [Formaldehyde] [Benzene] [1,3-Butadiene]
[Chloromethane] [p-Dichlorobenzene] [Ethylbenzene] [Methylene chloride]
[Styrene] [Tetrachloroethylene] [Toluene] [m,p-Xylene] [o-Xylene]
Prevention: The best method to avoid asthma attacks due to
pollution is for:
During the collapse of the World Trade Center Towers on
September 11, 2001, a large cloud of particulate matter was created. One individual reported that the air
was Òdarker than a sealed vault and thicker than pea soup.Ó This dust cloud which spread over
Manhattan and surrounding boroughs deposited:
All of these building components can cause eye irritation,
rashes and upper respiratory distress.
It is also believed that long-term exposure to such items may cause lung
cancer (1 case per 10,000 exposed) and other respiratory diseases. Short-term exposure, as seen on
September 11, may trigger severe asthma attacks (http://www.cdc.gov/mmrw).
WTC Cough: In the months that followed, 332 firefighters who
were exposed to the dust cloud after the collapse developed World Trade Center
cough. This was defined as a
persistent and severe cough in which the firefighter had to take at least four
weeks of medical leave. In
addition, these firefighters coughed up a dark sputum that was infiltrated with
pebbles and particles. Such
instances have only been seen in occupational settings after decades of
exposure, not after an exposure of a few hours. Furthermore, 0 of the 202 firefighters not present at the
collapse developed WTC cough (Prezant).
Airway Hyperreactivity: In a study of September 11 rescue
workers, it was observed that those who had the highest exposure levels to the
particulate cloud were approximately 7 times (OR=6.8; 95%CI:1.8-25.2, p=0.004)
more likely to have asthma like symptoms 6 months after the collapse. This trend continued for an additional
3 months.
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Kattan M., Malindzak G.,
Enright P., Evans III R., Morgan W., Stout J. Home and allergic characteristics of
children with asthma in seven U.S. urban communities and design of an
environmental
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Delfino R., Gong Jr. H., Linn W., Pellizzari E., Hu Y. Asthma
symptoms in Hispanic children and daily ambient exposures to toxic and criteria
air pollutants. Environmental
Health Perspectives, April 2003; 111 i4 p647(10).
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Exacerbation of
Asthma.
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N., Kaiser R., Medina S.,
Studnicka M., Chanel O., Filliger P., Herry M., Horvak Jr. F.,
Puybonnieux-Texier V., Quenel P., Schneider J., Seethaler R., Vergnaud J.,
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Prezant
D., Weiden M., Banauch G., McGuinness G., Rom W., Aldrich T., Kelly K. Cough and Bronchial Responsiveness
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