THUNDERSTORM-ASSOCIATED BRONCHIAL ASTHMA: A FORGOTTEN BUT VERY PRESENT EPIDEMIC
This article has been cited by other articles in PMC.
Abstract
Acute
episodes of bronchial asthma are associated with specific etiological
factors such as air pollutants and meteorological conditions including
thunderstorms. Evidence suggests that thunderstorm-associated asthma
(TAA) may be a distinct subset of asthmatics, and, epidemics have been
reported, but none from Saudi Arabia.
The trigger for
this review was the TAA epidemic in November 2002, Eastern Saudi Arabia.
The bulk of patients were seen in the King Fahd Hospital of the
University, Al-Khobar. The steady influx of acute cases were managed
effectively and involved all neighboring hospitals, without evoking any
“Major Incident Plan”.
Three groups of factors are
implicated as causes of TAA: pollutants (aerobiologic or chemical) and
meteorological conditions. Aerobiological pollutants include air-borne
allergens: pollen and spores of molds. Their asthma-inducing effect is
augmented during thunderstorms.
Chemical pollutants
include greenhouse gases, heavy metals, ozone, nitrogen dioxide, sulfur
dioxide, fumes from engines and particulate matter. Their relation to
rain-associated asthma is mediated by sulfuric and nitric acid.
Outbreaks
of non-epidemic asthma are associated with high rainfall, drop in
maximum air temperature and pressure, lightning strikes and increased
humidity. Thunderstorm can cause all of these and it seems to be related
to the onset of asthma epidemic.
Patients in epidemics
of TAA are usually young atopic adults not on prophylaxis steroid
inhalers. The epidemic is usually their first known attack. These
features are consistent with the hypothesis that TAA is related to both
aero-allergens and weather effects. Subjects allergic to pollen who are
in the path of thunderstorm can inhale air loaded with pollen allergen
and so have acute asthmatic response. TAA runs a benign course
Doctors
should be aware of this phenomenon and the potential outbreak of asthma
during heavy rains. A & E departments and ICU should be alert for
possible rush of asthmatic admissions and reinforce ventilators and
requirements of cardio-pulmonary resuscitation. Scientific approach
should be adopted to investigate such outbreaks in the future and must
include meteorological, bio-aerosole pollutants and chemical pollutant
assessment. Regional team work is mandatory.
Keywords: Thunderstorm-associated asthma, epidemic
The
prevalence of bronchial asthma is increasing and its etiology remains
obscure, but acute episodes have been associated with specific etiologic
factors. These include air pollutants such as ozone, nitrogen dioxide,
sulfur dioxide and other chemicals, as well as particulate matter of
respirable diameter (e.g. fog, organic dust, and aero-biological
products). It is difficult to standardize “measures of exposure”.
Accordingly, researchers employ ecological designs to seek associations
between, on one hand, “exposure” measured in terms of the environmental
factors and, on the other hand, “outcome” measured as individuals’
asthma attacks or their utilization of health care facilities. In spite
of the volume of research done, the assertion that air pollution causes
asthma remains controversial.1.
Some
reports suggest a “point source” of environmental causative agents. An
example is the Barcelona asthma epidemic which was linked to soya bean
dust.2
Other reports of asthma epidemics have implicated meteorological
conditions such as thunderstorms and sudden changes in atmospheric
temperature or pressure.3–5
Factors associated with non-epidemic asthma differ from those
associated with the epidemic form. This suggests that patients attending
Accidents and Emergencies (A & E) departments with reversible
airway obstruction related to rain (“Thunderstorm-associated asthma”),
may be a distinct sub-set of asthmatics who are more sensitive to
environmental stimuli.6
Indeed, epidemics of thunderstorm-associated asthma have been
documented in the literature, but no Saudi experience has been reported.
Throughout
Saturday, 2 November 2002, an epidemic of acute episodes of asthma
after a heavy downpour of rain was observed by the A & E Department,
King Fahd Hospital of the University (KFHU), Al-Khobar, Eastern
Province. It has been observed that the number of asthmatics requiring
emergency room services increases during and following rains or
thunderstorms. The KFHU epidemic, however, was striking for two reasons:
the number of patients affected was large, and, the geographic area
involved was wide. Thus, on that day, other hospitals in the Eastern
Province reported a similar pattern of cases.
None of
the treating hospitals in the region evoked their “Major Incident Plan”
although the number of additional patients in some of these hospitals
was big enough to trigger a mass casualty response. The “Major Incident
Plan” is also termed Mass Casualty Plan or Disaster Plan. This may be
explained by at least two possibilities. First, there may have been a
delay in appreciating and accepting that extraordinary measures were
necessary because the influx of patients had resulted from a “medical
incident” rather than a major accident. Secondly, most patients were not
severely affected. The majority were treated and discharged home; only a
few required admissions, and less than 1% needed to be in the Intensive
Care Unit (ICU).
However, if a higher
proportion of those admitted had needed to be in the ICU, there would
have been serious logistical problems. This is because in major
incidents, the hospital's capacity to handle patients requiring
resuscitation and artificial ventilation is a limiting factor. Once a
designated hospital becomes saturated, patients are diverted to
supporting hospitals in the same region. Thus, should all hospitals in
an area be affected simultaneously in asthma epidemics, even greater
logistical and management problems would ensue.
POSSIBLE AETIOLOGY OF THUNDER-STORM-ASSOCIATED ASTHMA (TAA)
Three
groups of factors have been suggested as causes of TAA, but it is not
yet known which ones play the major role. The groups are (1)
Aero-biological pollutants, (2) Chemical pollutants and (3)
Meteorological conditions.
1. Aero-biological pollutants
A
sudden rise in bio-aerosol concentrations has been observed during
thunderstorms. Recent studies of the kinetics of the release of
aero-allergens (air-born allergens) and their effects on patients have
confirmed the presence of high concentrations of pollen grains and mold
spores in the surrounding atmosphere.
Pollen is a fine
powdery substance produced by flowers. Insect and natural agents such as
air, rain and storm transfer pollen from one plant to another for
pollination. Pollen is responsible for most asthmatic attacks in
flowering seasons. Produced in large quantities, pollen is of respirable
size2–10
and, therefore, enters the airways. It is readily carried long
distances by winds and therefore affects individuals miles away from
source. The maximal concentration in the atmosphere occurs before
sunrise and after sunset.
Molds are plant species which
grow in damp areas with high humidity. They are microscopic, reproduced
by the release of millions of spores into the air which then settle on
organic matter and grow. Inhaled air-borne spores can cause asthmatic
attacks.
Raised concentrations of
bio-aerosol during thunderstorm is attributed to sudden onset of high
winds which trigger the sudden release of spores and pollen into the
atmosphere. This is probably responsible for asthma epidemics. Winds
associated with thunderstorms may have re-suspended residual pollen
locally. It is conceivable that aero-allergens are carried, firstly, up
in the rapid up-lift of air associated with connective storms,7
and secondly, horizontally with the storm. They are then re-deposited
by a cold downdraft ahead of the rainstorm. Lastly, rainfall itself
causes rapid changes of humidity or temperature or both. This may lead
to a rapid rise in respirable allergens. Exposure to allergen can
increase non-specific bronchial reactivity; the magnitude and duration
are proportional to the last asthmatic response.8,9
If recent exposure to allergens increased bronchial responsiveness,
acute airway narrowing might then be triggered by a variety of
precipitants.
2. Chemical Pollutants
Air
pollution, a side effect of global industrialization and urbanization,
has become a fact in today's world. The earth is a closed system;
nothing gets out. Today's greenhouse gases, heavy metals and other
compounds, accumulate as they are produced in greater quantities than
nature can absorb. It is like smoking in a closed room. Today's world
harbors millions of people and machines. Gas, diesel engines and
industrial pollutants result in a haze of smog hanging over most major
cities around the world.
Ozone, nitrogen dioxide,
sulfur dioxide and particulate matter are the main forms of air
pollution of the out-doors. These oxidizing gases are formed as
by-products of combustion and can cause airway inflammation in humans
whether or not they have asthma. Since the level of ozone and pollutants
increases and temperatures also increase, the phenomenon of global
warming threatens to make this a continuing problem.
An
average human consumes 12 kg of air per day to form carbon dioxide. It
is about twelve times higher than the food we take. Hence, even small
concentrations of pollutants in the air become more significant in
comparison to similar levels present in food. Nearly 15 kg of air is
consumed to burn one liter of fuel in automobiles. Carbon monoxide, lead
and hydrocarbons are emitted in high quantities in petrol combustion.
These can cause the loss of visual accuracy and mental alertness. Diesel
combustion emits considerably higher amounts of nitrogen dioxide,
particulate matter and sulfur dioxide. Pollutants of diesel combustion
are important trigger factors which aggravate asthma. A consensus on
research studies indicate that air pollutants cannot induce asthma in a
person who is not predisposed to it (except ozone effect), but they can
trigger an acute attack in asthmatic patients, and can cause other lung
diseases such as chronic bronchitis in healthy, non-asthmatic persons.
The relation of Chemical Pollutants to Rain-associated Asthma
Air
pollution is a major cause of acidic deposition or acid rain as it is
commonly known. It occurs when emissions of sulfur dioxide (SO2)
and nitrogen dioxide mix in the atmosphere with water, oxygen and
oxidants to form mild solutions of sulfuric and nitric acid. Sunlight
increases the rate of these reactions. These compounds then fall to the
earth in the wet forms of rain, snow, fog or in dry forms as gas and
particles. About half of the acidity in the atmosphere falls back to
earth through these dry depositions which the wind blows into buildings,
cars and homes. Prevailing winds transport these compounds, hundreds of
miles across countries and national borders, resulting in a significant
negative impact on health.
3. Meteorological Conditions
Climate
variation has only marginal effect on normal persons. However, for
asthmatic patients who are prone to dust, humidity, high temperature and
changes in atmospheric pressure, bivariate and multivariate analyses
have shown significant association between lightning strikes and asthma
presentations. Celenze et al, using multivariate analysis of
environmental factors, showed that between one and nine lightning
strikes a day was associated with increased asthma presentations by a
factor of 2.21 compared with when there was no lightning (P<0.05).
Bivariate
and multivariate analyses of other meteorological variables suggest
that there are significant associations of increased cases of
non-epidemic asthma with the following four variables: high rainfall,
drop in maximum air temperature, fall in air pressure and increased
humidity. A sudden thunderstorm causes the greatest sudden fall in
temperature and air pressure as well as the most pronounced increase in
humidity, rainfall, and lightning strikes. Hence, it seems to be related
to the onset of asthma epidemic.
WHO IS AT RISK OF TAA?
During
the epidemic of thunderstorm-associated asthma (TAA),
characteristically, the patients were young atopic adults. A high
prevalence of atopy was also a feature of similar outbreaks.10
In a significant number of the patients, the episode was the first
known attack of asthma. Most gave a history of asthma, but were probably
not on prophylaxis with steroid inhalers. A history of hay fever and
allergy to rey grass were found to be strong predictors for asthma
exacerbation during thunderstorms.11
These are consistent with the hypothesis that TAA is related to
aero-allergens as well as the effect of weather. Subjects allergic to
pollen who are in the path of thunderstorm are likely to inhale air
which is heavily loaded with pollen allergen and consequently experience
an acute airway asthmatic response.
TAA
seems to have had a benign course in most patients in the epidemic
alluded to, as they did not require hospital admission. However, there
should be no complacency in the treatment of many patients presenting to
A &E departments with acute asthma.
No comments:
Post a Comment