Ozone (O₃) is a reactive gas composed of three oxygen atoms that is
"good" in the upper atmosphere (stratosphere) and "bad" at ground level
(troposphere). The naturally occurring stratospheric ozone layer protects
Earth from harmful ultraviolet (UV) radiation. In contrast, ground-level
ozone is a major component of smog and a dangerous air pollutant that forms
from pollutants like nitrogen oxides (NOx) and volatile organic compounds
(VOCs) reacting with sunlight. This ground-level ozone is harmful to human
health, causing respiratory problems and aggravating existing conditions
like asthma.
The Good Ozone: The Ozone Layer is Found in the stratosphere, roughly 6 to
31 miles above the Earth's surface. Naturally forms a protective "ozone
layer" that absorbs most of the sun's damaging UV-B radiation. Shields
plant and animal life from harm.
The Bad Ozone: Ground-Level Ozone is Found in the troposphere, from the
Earth's surface up to the stratosphere. Created by chemical reactions
between precursor pollutants, primarily NOx and VOCs, in the presence of
intense sunlight. NOx: Emitted from burning fossil fuels in power plants
and vehicle tailpipes. VOCs: Released from evaporating consumer products
like paints and solvents. Acts as a powerful air pollutant and greenhouse
gas, contributing to smog and causing irritation and damage to lung tissue.
Exposure to ground-level ozone can trigger coughing, throat irritation, and
aggravate asthma and emphysema. It also harms ecosystems and is a major
component of smog. While the ozone layer itself has been depleted by
human-made chemicals, it is on a path to recovery thanks to global efforts
under the Montreal Protocol.
What effects does ozone have at the cellular level?
As a result of short-term exposure, ozone and/or its reactive intermediates
cause injury to airway epithelial cells followed by a cascade of other
effects. These effects can be measured by a technique known as
bronchoalveolar lavage (BAL), in which samples of epithelial lining fluid
(ELF) are collected during bronchoscopy on volunteers experimentally
exposed to ozone. Cells and biochemical markers in the lavage fluid and in
the blood can be analyzed to provide insight into the effects of exposure.
Evidence for airway inflammation following ozone exposure includes
visible redness of the airway seen during bronchoscopy as well as an
increase in the numbers of neutrophils in the lavage fluid. Cellular
injury is suggested by an increase in the concentration of lactate
dehydrogenase (LDH), an enzyme released from the cytoplasm of injured
epithelial cells, in the ELF. Mediators (e.g., cytokines, prostaglandins,
leukotrienes) that are released by injured cells include a number that
attract inflammatory cells resulting in a neutrophilic inflammatory
response in the airway. In addition, ozone reaction products as well as
some mediators produced in the lung can be detected in the blood providing
a possible mechanism for extrapulmonary effects of ozone exposure.
Other documented ozone-induced effects that may be related to the
underlying injury and inflammatory response are:
An increase in small airway obstruction
A decrease in the integrity of the airway epithelium
An increase in nonspecific airway reactivity
A decrease in phagocytic activity of alveolar macrophages
The decrease in epithelial integrity can be measured by an increase in the
concentration of plasma proteins appearing in the ELF following exposure
and by more rapid clearance of inhaled radio-labeled markers from the lung
to the blood. This has the potential for allowing increased movement of
inhaled substances (e.g. allergens or particulate air pollution) from the
airway to the interstitium or the blood and could modify the known effects
of inhaled allergen on asthma and particulate matter on mortality.
Although the significance of increased nonspecific airway reactivity to
substances such as methacholine or histamine is not understood in healthy
individuals, it is clearly of concern for people with asthma, as increased
airway reactivity is a predictor for asthma exacerbations. (See bulleted
section, How does ozone affect people with asthma?).
A decrease in macrophage function has the potential to interfere with
host defense. Over a period of several days following a single short-term
exposure, inflammation, small airway obstruction, and increased epithelial
permeability resolve; damaged ciliated airway epithelial cells are replaced
by underlying cells; and damaged type I alveolar epithelial cells are
replaced by more ozone-resistant type II cells. Over a period of weeks,
the type II cells differentiate into type I cells, and following this
single exposure, the airway appears to return to the pre-exposure state.
How does response vary among individuals?
One striking characteristic of the acute responses to short-term ozone
exposure is the large amount of variability that exists among individuals.
For example, for a 2-hour exposure to 400 ppb ozone (note: 400 ppb is equal
to .4 ppm) that includes 1 hour of heavy exercise, the least responsive
individual may experience no symptom or lung function changes while the
most responsive individual may experience a 50% decrement in FEV1 and have
severe coughing, shortness of breath, or pain on deep inspiration. A
similar range of response is evident for a 6.6-hour exposure to 80 ppb with
5 hours of moderate activity. Other individual responses fall into what
appears to be a unimodal distribution between these two extremes. Those
with large responses following exposure on one day also tend to have large
responses upon re-exposure. Similarly, those with small responses
following exposure on one day tend to have small responses upon
re-exposure. A small fraction of the observed variability in lung function
and symptom responsiveness can be explained by differences in age and in
body mass index (BMI) with young adults (teens to thirties) and those with
high BMI being much more responsive than older adults (fifties to eighties)
and those with low BMI. Results similar to those in Figure 8 are also seen
with longer duration exposures to concentrations more relevant to ambient
levels (e.g. over a range of 60 to 120 ppb).
Individual differences in the intensity of the inflammatory response
also exist, and it appears that these differences in response are also
stable over time. The magnitude of the neurally-mediated lung function
response, however, is not related to the degree of cell injury and
inflammation for a given individual suggesting that these two effects are
the result of different mechanisms of action. Further evidence for
multiple mechanisms of action is provided by drug intervention studies.
There is some evidence that Vitamin C and E supplements may slightly reduce
the lung function effects of ozone but not the inflammatory or symptom
responses. Pre-treatment with non-steroidal anti-inflammatory drugs
(NSAID) reduces lung function and symptom responses but not the
inflammatory responses in non-asthmatics. In asthmatic volunteers NSAID
pretreatment did not block the restrictive lung function changes seen in
nonasthmatics, but did blunt some of the changes due to airway
obstruction. Pre-treatment with high doses of inhaled steroids has been
shown to reduce the neutrophil influx following ozone exposure in people
with asthma, but not in those without asthma.
True differences in individual responsiveness to ozone can be the
result of either environmental or genetic factors. Research has
demonstrated that genetic differences among strains of mice can explain the
large range of inflammatory responses seen. Some preliminary evidence
suggests that genetic polymorphisms for antioxidant enzymes and for genes
regulating the inflammatory response may modulate the effect of ozone
exposure on pulmonary function and airway inflammation.
What are the effects of ozone on mortality?
Studies show:
Ozone is associated with increased mortality
The absolute effect of ozone on mortality is considerably higher in older
adults
The ozone-mortality relationship is most prominent during the warm season
Recent epidemiologic research has clearly demonstrated that both short-term
and longer-term exposures to low concentrations of particle pollution, a
common air pollutant, are associated with increased mortality.
Re-examination of the data upon which those findings are based as well as
new studies indicate that short-term exposure to ozone is also associated
with increased daily mortality.
The study most representative of the U.S. population (Bell et al 2004)
evaluated the relationships between daily mortality counts and ambient
ozone concentration for 95 large U.S. communities over the period of
1987-2000. Although there was considerable heterogeneity in the magnitude
of effect among the various communities, a 0.5 % overall excess risk in
non-accidental daily mortality was observed for each 20 ppb increase in the
24-hour average ozone concentration (approximately equal to a 30 ppb
increase in the 8-hour average) on the same day. There was evidence that
the effect was greatest on the day of exposure with smaller residual
effects being evident for several days. A cumulative 1.04% excess risk was
observed for each 20 ppb increase in the 24-hour average concentration
during the previous week. The ozone-mortality relationship was robust even
after controlling for possible effects of particulate matter and other air
pollutants.
Although ozone mortality risk estimates tend to be only slightly
higher for the older population compared to the younger population (based
predominantly on Medicare studies of people 65 and older), the absolute
effect of ozone on mortality is considerably higher in older adults due to
their higher baseline death rates. Even for older adults, however, the
risk of dying on any given day as a result of ozone exposure is quite
small. However, because of the large number of individuals at risk across
the country, an effect of this magnitude has meaningful public health
implications.
A preponderance of other time series studies supports the existence of
an ozone-mortality relationship although with a wider range of effect
estimates primarily due to the smaller sizes of the studies. An
independent review of this literature by the National Research Council
concludes that short-term ozone is likely to be associated with premature
mortality.
Other observations made in these studies include the finding that the
ozone-mortality relationship is most prominent during the warm season, with
few or smaller effects in the winter. It also appears that the
ozone-mortality association persists when deaths are limited to those
caused by either cardiac or pulmonary disease or to those caused by
cardiovascular disease alone. Risk estimates for other causes of death are
generally inconsistent across studies probably reflecting the lower
statistical power associated with smaller daily death rates. In the Bell
study of 95 cities, the observed city-specific effect rates varied widely.
The degree to which this variability reflects different ozone-mortality
relationships in the different cities is not clear, but it does raise the
question as to whether a single average 0.5% increase in daily mortality
rates should be applied to all cities. Other unanswered questions pertain
to the lowest concentrations at which these effects occur and the possible
mechanisms of action responsible for increased mortality among many who
spend much of their time indoors where ozone levels are generally quite
low. Bell et al. divided days into those with a 24-hour average ozone
concentration above and below 60 ppb and found that the relationship was
similar for both subsets suggesting that the relationship is present at
even very low levels of ozone. Biological mechanisms responsible for the
ozone-mortality relationship are largely unknown although effects of ozone
on the autonomic control of the cardiovascular system, on coagulation
mechanisms, and on vasoactive substances in the blood are being actively
investigated.
What are the other potential effects of short-term ozone exposure?
Other potential effects of short-term ozone exposure include:
hospital admissions and emergency room visits for respiratory causes
school absences
There is consistent epidemiologic evidence that ambient ozone levels
are associated with other markers of respiratory morbidity, particularly
during the warm season. In general, studies have reported positive
relationships between short-term ozone concentrations and hospital
admissions and emergency room visits for respiratory causes. Although not
all studies have found significant effects, risk estimates for the majority
of studies are positive. It is likely that those most at risk of serious
respiratory morbidity are those with underlying respiratory disease. The
evidence indicates that some of the increase in hospital visits for
respiratory morbidity is due to exacerbations of asthma and possibly
chronic obstructive pulmonary disease (COPD). Because of the small numbers
of daily hospital admissions, the effects of ozone on other subcategories
of respiratory disease are not clear.
A relationship has also been observed between ozone and school absences
in two studies. However, in one case the absences were related to a
measure of longer-term exposure, and in the other case absences were not
limited to those due to illness. Although these latter results are
consistent with increased infections secondary to impaired host defense,
more research needs to be done before reaching any conclusion regarding any
effect of ozone exposure on respiratory infection.
emergency or urgent daily respiratory admissions
Respiratory admission rates to 168 hospitals in Ontario, Canada during the
period 1983 through 1988 are plotted against the distribution (deciles) of
the daily 1-hour maximum ozone concentration, lagged by 1 day. Admission
rates were adjusted for seasonal patterns, day-of-week effects, and
hospital effects. Ozone displayed a positive and statistically significant
association with respiratory admissions for 91% of the hospitals during the
Spring through Fall seasons, but not during the Winter months of December
to March when ozone levels were low. Source: Burnett et al., 1994; U.S.
EPA, 1996
Ozone has been associated with daily hospitalizations for
cardiovascular disease in some studies but it is not a consistent finding.
A number of studies have explored the relationships between ozone and
various other aspects of cardiovascular pathophysiology including heart
rate variability, acute myocardial infarction, and tachyarrhythmias in
those with implanted cardiac devices. Although some data are suggestive of
a relationship, the results at this time do not fully substantiate a
relationship between ozone exposure and adverse cardiovascular events.
At what exposure levels are effects observed?
The concentration of ozone at which effects are first observed depends upon
the level of sensitivity of the individual as well as the dose delivered to
the respiratory tract. The dose, in turn, is a function of the ambient
concentration, the minute ventilation, and the duration of exposure. This
can be expressed as a rough formula:
Dose = Ambient concentration X Level of exertion (minute ventilation) X
Duration of exposure.
Thus individuals performing strenuous activity (higher minute ventilation)
for several hours are likely to respond to lower concentrations than when
exposed at rest (lower minute ventilation) for a shorter time. The
following examples illustrate this point:
An average young adult playing an active sport such as soccer or full court
basketball outdoors for 2 hours would be expected to experience small to
moderate lung function and symptom effects as well as lung injury and
inflammation following exposure to 120 ppb ozone.
If the same average young adult is at rest outdoors for the two hours, such
effects would not be expected until exposures reach 300-400 ppb.
An average outdoor laborer doing intermittent work might experience similar
small to moderate lung function and symptom effects as well as lung injury
and inflammation following an 8-hour exposure to 60 to 70 ppb ozone.
More sensitive individuals will experience such effects at lower
concentrations while less sensitive individuals will experience these
effects only at higher concentrations.
Children without asthma experience lung function decrements similar to
those of young adults. But children often do not report respiratory
symptoms at the lowest ozone concentrations. It is not clear whether this
is the result of reduced sensitivity with regard to symptoms or whether
children are less likely to recognize and report symptoms.
There are chamber studies and field studies that look at the ozone exposure
level at which effects are first observed. It is not surprising that field
studies show effects at much lower levels than chamber studies. This is
because field studies can look at sensitive populations (including
children), include exposure to all oxidant species of pollution, and may
include longer exposure times. For example, field studies of agricultural
workers and hikers suggest that lung function changes may be associated
with prolonged ozone exposures at lower levels than those observed in
chamber studies. Below are findings from key field and observational
studies.
Although the results vary somewhat, several field studies suggest that the
lung function of highly active asthmatic and ozone sensitive children and
the exercise performance of endurance athletes may be affected on days when
the 8-hour maximum ozone concentration is less than 80 ppb ozone.
Emergency room data from one study indicate that asthma attacks in the most
sensitive population (e.g., children with asthma or reactive airway
disease) increase following days on which the 1-hour maximum ozone
concentrations exceeded 110 ppb (approximately equivalent to an 8-hour
average of 82 ppb). (White et al., 1994) Another study observed increased
emergency room visits for asthma on days following those when 7-hour
averages exceeded 60 ppb compared to those with lower ozone concentrations.
(Weisel et. al., 1995).
For effects measured in some other types of observational studies, the
lowest levels at which effects are expected to occur are more difficult to
identify for a number of reasons. Effects of ozone on daily mortality have
been detected even when study days are restricted to those with a 24-hour
average ozone concentration below 60 ppb (approximately equivalent to an
8-hour average below 90 ppb). In one study, hospital admissions for
respiratory causes appear to follow a linear relationship down to
background levels. Limited exposure-response modeling suggests that if a
population threshold for these ozone effects exists, it is likely near the
lower limit of ambient ozone concentrations in the United States.
What are the effects of recurrent or long-term exposure to ozone?
One of the major unanswered questions about the health effects of ozone is
whether repeated episodes of damage, inflammation, and repair induced by
years of recurrent short-term ozone exposures result in adverse health
effects beyond the acute effects themselves.
Daily ozone exposure for a period of 4 days results in an attenuation of
some of the acute, neurally-mediated effects (e.g., lung function changes
and symptoms) for subsequent exposures occurring within 1 to 2 weeks. Some
health experts have, therefore, suggested that individuals living in high
ozone areas may be protected from any harmful effects of long-term ozone
exposure. Others suggest, however, that the attenuation of the
ozone-induced tendency to take rapid and shallow breaths may blunt a
protective mechanism, resulting in greater delivery and deposition of ozone
deeper in the respiratory tract and other airway responses described below.
Studies including bronchoalveolar lavage and bronchial mucosal biopsies
indicate that, unlike the neurally-mediated lung function changes, the
processes of airway injury, inflammation, and repair continue to occur
during repeated exposure. After either 4 or 5 days of exposure, markers of
cell injury and increased epithelial permeability remain elevated, and an
increase in airway mucosal PMN, which was not present following a single
exposure, has been noted. Also, unlike the neurally-mediated effects,
small airway function has been observed to remain depressed over the course
of exposures and is thought to be related to the ongoing inflammation.
Studies of laboratory animals have consistently demonstrated that long-term
exposure to ozone concentrations above ambient levels results in persistent
morphological changes that could be a marker of chronic respiratory
disease. Exposed animals experience mucous cell metaplasia and epithelial
cell hyperplasia in the upper airway as well as structural changes in the
lower airway including an increase in fibrous tissue in the basement
membrane area and a remodeling of the distal conducting airways. In
addition to airway remodeling and basement membrane changes, concurrent
long-term exposure of very young primates to ozone and house dust mite
allergen has been observed to result in changes in the innervation of the
airways as well as an accumulation of eosinophils in the distal airways
suggesting induction of an allergic phenotype. Other studies indicate that
sensitization of animals to antigen occurs more easily during ongoing ozone
exposures. Based on traditional measures, there is little evidence that
long-term exposure in animals results in substantial changes in airway
function. However, these morphological findings suggest that long-term
ozone exposure might play a role in the development or progression of
chronic lung disease and/or asthma.
The epidemiologic evidence is inconclusive with regard to whether long-term
exposure of humans is related to chronic respiratory health effects in
humans. Several cross-sectional studies have found that young adults who
spent their childhoods in locales with high ozone concentrations had lower
measures of lung function than those from locales with lower ozone.
Similar results have not been observed, however, in a recent well-conducted
longitudinal study of lung function in children or in other cross-sectional
studies. Two longitudinal studies have observed associations between
development of asthma and long-term ozone concentrations in subgroups of
the population. These findings have not been confirmed in other
longitudinal or cross-sectional studies, but they are consistent with the
animal toxicological literature. Part of the difficulty in evaluating such
associations has been the small number of longitudinal epidemiologic
studies specifically designed to evaluate respiratory health in samples
with differing ozone exposures. The mobility of the population as well as
the inability to precisely estimate exposure to ozone and other potential
confounders over a period of many years degrades the power of, and leads to
bias in, both longitudinal and cross-sectional studies.
In spite of the inconclusive nature of the epidemiologic literature, the
repeated cycles of damage, inflammation, and repair in humans and the
morphological findings from the animal toxicological studies suggest that
it would be prudent to avoid repeated short-term exposures, particularly in
young children, until more is known about the effects of long-term ozone
exposure.
K RAJARAM IRS 16925 today ozone day
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