Health Effects of Criteria Air Pollutants from Power Plants 2002
Author: Jefferson H. Dickey MD
Health Effects/New Data: 1996-2000
New Data / Pulmonary Function / Chamber
A new model has been published which seems to better predict the mean
decrease in FEV1 as a function of ozone concentration, minute ventilation,
duration of exposure, and age. We currently know that the magnitude of
the FEV1 decline increases with ozone concentration, minute ventilation,
and duration of exposure, and decreases with age. McDonnell, et al19
combined the results of a series of chamber - spirometry studies performed
at the US EPA Clinical Research Facility over a 13 year period on 485
non-smoking healthy subjects. Ozone concentrations ranged from 0 to 400
ppb; ventilation rates varied from about 5 L/min/m2BSA (body surface area)
at rest to about 40 L/min/m2BSA. The latter represents a moderately heavy
workload. Spirometry was performed at zero, 1 and 2 hours after exposure
began.
This model is quite useful within its constraints. Exposures are limited
to 2 hours. Exposure to persons working or exercising outdoors in the
community are commonly 6 or 8 hours. The subjects were healthy young men.
Sensitive subgroups, especially those with asthma, may be more vulnerable.
Nonetheless, this model is probably the most useful data set for predicting
FEV1 decline as a result of relatively short duration of ozone exposures.
A recent study confirmed previous observations that ozone induced declines
in FEV1 do not correlate with development of bronchial hyperreactivity.
In chamber exposures to 400 ppb for 3 hours per day on 5 consecutive days
at moderate exercise (about 32 L/min), asthmatic subjects demonstrated
attenuated FEV1 decline after several days of exposure. However, the ozone
caused bronchial hyper responsiveness which did not attenuate.20
Another study of elderly subjects with COPD were much more susceptible
to ozone induced declines in FEV1 and increased airway resistance than
subjects without COPD. The COPD subgroup decline in FEV1 after 4 hours
exposure to 240 ppb ozone with intermittent light exercise was 19% compared
with 2% in the healthy controls. About half of this effect was due to
ozone and half to the effect of exercise in COPD.21
One study of ozone effects on cardiac parameters found that 300 ppb ozone
for 3 hours with intermittent exercise resulted in an increase in cardiac
rate and heart rate * blood pressure product, but otherwise no major effects
on right heart catheterization cardiac parameters.22
One study exposed 41 subjects aged 9-12 years, both with and without
asthma, to a combination of 100 ppb ozone, 0.10 ppm SO2, and 100 mcg/m3
H2SO4 for 4 hours with intermittent exercise. The subjects responded with
changes in spirometry, symptoms, and overall discomfort level, but the
results were not statistically significant.23
Overall, the chamber spirometry studies continue to find decrements in
pulmonary function as a result of ozone exposure. The magnitude of the
decrements are relatively small or are observed after prolonged exposure.
The clinical implications for pulmonary function declines, hence, continue
to be limited to sensitive subpopulations - those with underlying lung
disease and those with prolonged outdoor exposures with elevated ventilation
rates (children playing outdoors and adults working or exercising outdoors).
New Data: 1996-2000 / BAL / Ozone Chamber Studies
A handful of studies address the effects of air pollution on bronchoalveolar
lavage measures of inflammation and its consequences. Some of the more
interesting ones are summarized here.
In an attempt to better understand interindividual variability, a chamber
study of healthy subjects exposed to 220 ppb of ozone for 4 hours with
exercise was performed. The expected declines in FEV1 occurred with interindividual
variability - some persons experienced a greater than 15% decline in FEV1
(designated responders) and some experienced a less than 5% decline (non-responders).
Increases in BAL polymorphonuclear leukocytes, and interleukins 6 and
8 appeared early, and lymphocytes, mast cells, and eosinophils increased
later in all groups, regardless of smoker or FEV1 responder status.24
A similar result occurred in a study which exposed asthmatic and healthy
individuals to 125 and 250 ppb ozone over 3 hours of intermittent exercise.
The magnitude of the inflammatory response measured on BAL was consistent
within individuals, and the decrement in FEV1 was highly reproducible,
but the BAL inflammation was not highly correlated with the decrement
in FEV1.25
These studies help clarify the poor correlation between lung inflammation
and declines in lung function.
Previous work has shown that the decline in FEV1 attenuates after several
days of exposure to ozone, although the bronchial hyperreactivity tends
to persist. A newer study finds that when subjects are repeatedly exposed
to ozone (200 ppb over 4 hours over 4 days), significant decreases in
the number of PMNs, fibronectin, and IL-6 were found after 4-d exposure
versus single-day exposure.26
One study of dust mite allergic asthmatics found ozone exposure (160
ppb) to be associated with significant increases of eosinophils in the
BAL fluid.27 Another study compared BAL of asthmatic subjects
with that of normal subjects after exposure to ozone (200 ppb over 4 hours).
The asthmatic subjects showed significantly greater O3-induced increases
in several inflammatory endpoints (percent neutrophils and total protein
concentration) in BAL as compared with normal subjects.28
Substance P (a neurotransmitter with many functions, including nocioception)
has been shown to be observed in greater amounts in BAL fluid in larger
amounts after ozone exposure.29
In sum, although the exposures above are generally higher than commonly
encountered in the community, data continue to accrue that ozone induces
bronchioalveolar inflammation, that asthmatics may have a heightened response,
and that ozone induced inflammation observed on BAL does not correlate
well with declines in FEV1.
New Data: 1996-2000 / BAL / Community Air Pollution
One of the more interesting BAL studies examined the effects of community
air pollution on recreational joggers in New York City.30 15
subjects were examined during summer (high ozone period) and retested
during winter (low ozone period). Release of reactive oxygen species was
lower in the summer than the winter. In contrast, LDH, IL-8, and PGE2
levels were all roughly two fold higher in summer. These results suggest
a possible ongoing inflammatory response in the lungs of recreational
joggers exposed to ozone and associated co-pollutants during the summer
months, and that the inflammatory response observed during controlled
chamber exposures seems to be occurring during community exposures.
New Data: 1996-2000 / Chamber Studies / Allergen - Pollutant Interaction
One of the most interesting areas of current research concerns the potential
for ozone to exacerbate asthmatic allergen induced bronchoconstriction.
Previous work had discovered that ozone at higher doses increased asthmatic
allergen sensitivity, but it was controversial whether lower ozone doses
had the same effect. The current data suggest that 1 hour exposure of
mild asthmatics at rest to 120 ppb, or with intermittent moderate exercise
to 100 ppb ozone, does not enhance allergen sensitivity, but 3 hours exposure
to 200 ppb with intermittent moderate exercise does. Unanswered at this
time is whether asthmatics with more severe disease, or exposed to lower
levels for longer periods or with higher activity levels (minute ventilation
rates), would demonstrate ozone induced allergen hypersensitivity.31-33
Unusually high exposures to NO2 (with our without SO2) appear to increase
asthmatic sensitivity to allergen as well.32, 34-36
Although this data suggests that air pollutants at levels uncommonly
encountered in most areas of the USA will enhance asthmatic allergen sensitivity,
at lower levels which are commonly encountered, the pollutants do not
consistently enhance asthmatic allergen sensitivity.
New Data: 1996-2000 / PEFR - Time Series Diary
I identified 24 studies which examined the relationship between air pollutants
and asthma exacerbations and declines in peak flow rates. All studies
except one demonstrated significant associations between air pollution
levels and one of the health effects. Generally, studies which failed
to find associations with drops in peak flow rates found increases in
asthma medication use.37-60
New Data: 1996-2000 / PEFR - Time Series Diary / Combined Analysis
I found 2 studies which performed combined analysis of time series peak
flow studies in children. One61 looked at 5 previously performed
studies of peak flow decrements as a function of PM10 particulate air
pollution levels. They found a particulate to be associated with lower
average peak flow rates and a higher prevalence of significant drops in
peak flow rates.
The other study62 re-analyzed six studies which examined the
effect of ozone air pollution on children playing outside at summer camps
in New Jersey, New York, Ontario, and southern California. All of the
studies found ozone to be associated with drops in FEV1. Combining the
data, the authors estimate a decline of 0.5 ml of FEV1 per ppb O3. This
is a surprisingly large, clinically important result, and suggests that
chamber exposure studies are underestimating the effect of exposure in
the community.
New Data: 1996-2000 / Pulmonary Function / Cross Sectional
I identified 7 studies which examined the association between air pollution
and cross sectional measures of lung function. All found significant associations
between air pollution levels and lower lung function. This type of study
is generally much less likely to differentiate between the effects of
different types of pollutants unless very large numbers of cities are
examined.
Abbey et al63 examined a group of 1,391 non-smokers and found
that PM10, ozone, and SO2 all had significant associations with lower
lung function. Interestingly, persons with a family history of lung disease
(asthma, bronchitis, emphysema, or hay fever) may be much more vulnerable
to the air pollution effects.
Peters et al64 studied 3,293 school children from 12 southern
California communities with different air pollution levels. Significant
associations were found between measures of lung function (FEV1 and FVC)
and PM10, PM2.5, NO2, and O3 in girls, and O3 in boys. Both effects were
stronger when stratified according to the amount of time the child spent
outdoors. This study is forming the basis of a prospective cohort, and
follow up data will be available in a few years.
In the largest study of its kind, Raizenne et al65 examined
10,251 children from 24 US and Canadian cities and found that acid aerosols
were associated with about a 3% lower lung function (FEV1 and FVC).
Two studies examined the association between bronchial hyperreactivity
and air pollution. Both found bronchial hyperreactivity to be associated
with air pollution.66, 67
Other studies found significant associations between air pollution and
cross sectional lung fucntion decrements.68, 69
New Data: 1996-2000 / Pulmonary Function / Prospective Cohort
I found one study70 which examined the relationship between
chronic air pollution and lung growth in children. This study followed
1,150 children prospectively for 3 years, performing spirometry at the
beginning and end of each summer. Air pollution in the various communities
was evaluated for PM10, SO2, NO2, and O3. Adjusting for a child's sex,
atopy, passive smoking, baseline lung function, and increase in height,
the researchers found that summertime ozone was associated with a lesser
summertime children’s lung growth as reflected by a lower than expected
increase in FEV(1) and FVC. PM10, SO2, and NO2 did not show this association.
One study should never be considered to have proven anything, and this
is no exception. Alternative explanations are not excluded; however, this
study suggests that ozone air pollution may impair normal lung growth
in children.
New Data: 1996-2000 / Morbidity / Prospective Cohort
Data continue to be generated by one of the most important ongoing prospective
cohort projects - the Seventh Day Adventists study. This study is following
a large cohort of a non-smoking population and associating local air pollution
levels with health outcomes. In this analysis, 3,091 non-smoking subjects
were followed for 15 years and about 3.5% of them reported a new diagnosis
of asthma.71 The authors report that, regardless of adjusting
for other air pollutants, the asthma rates were roughly doubled in the
men exposed to the higher mean ozone levels. This effect was not observed
in women. The analysis was not adjusted for the percentage of time working
outdoors. While this analysis cannot be considered to have proven that
ozone causes asthma, because the results are consistent with expectations
generated from pathophysiologic studies, it raises important questions
about whether ozone causes asthma. Unfortunately, this study is going
to be difficult to replicate because of the unique population, large group
size, and long duration required.
New Data: 1996-2000 / Cardiac Monitor / Time Series / Particulate
Many of the epidemiologic studies examining the cause of death in persons
dying on high particulate air pollution days
I found 2 studies72, 73 which examined cardiac rate (24 hour
holter monitor) in association with particulate air pollution levels.
Both studies found elevated cardiac rates on days with elevated particulate
levels. One of these studies additionally examined heart rate variability
and found particulate to be associated with decreased overall heart rate
variability.
NEW DATA: 1996-2000 / EMERGENCY ROOM VISITS / TIME SERIES STUDIES
I identified 14 studies in the recent medical literature which examined
the association between air pollution and acute physician consultations
or emergency room visits. Eight of these specifically examined asthma
or acute wheezy episodes; 3 additional studies examined respiratory complaints
generally; 1 each reviewed doctors house calls in Paris, France and childrens’
ER visits in Santiago, Chile. One study looked at ER visits during a series
of bush fires in Sidney, Australia. I could not obtain the results of
one study.74
Only the study of Australian bush fires75, and another in
Switzerland76 (which admitted to potentially poor exposure
assessment) failed to find significant associations.
One important study examined ER visits in one summer for respiratory
disease in Montreal. Ozone, PM10, PM2.5 and sulfate were all associated
with emergency room use for persons over the age of 65. A 36% increase
in ozone levels was associated with a 21% increase in ER visits for respiratory
complaints. In examining the effects of particulate and acid aerosols,
the relative mass effects were PM2.5 > PM10 > SO4.77
The association between asthma ER visits and particulate was observed
even when air pollution levels were below the new NAAQS for PM2.5. In
this study, a moderate increase in air pollution (11 microg/m3 in fine
PM) was associated with a 15% increase in the rate of ER visits.78
All the other studies also found consistent associations between air
pollution levels and emergency room visits and respiratory disease.79-87
In all, 11 of the 13 studies for which results were available found significant
associations between air pollution and emergency room use or acute physician
consultations.
NEW DATA: 1996-2000 / EMERGENCY ROOM VISITS / PROSPECTIVE COHORT
Two recent prospective cohort studies of asthmatics examined the relationship
between air pollution levels and emergency room visits (a relatively new
epidemiologic technique). One88 found a significant association
between acid aerosol fog (a complex mixture of pollutants) and ER visits
for asthma; the other89 found significant air pollution associations,
with air pollution (NOx, SO2, and ozone) plus weather accounting for 69%
of the variance.
NEW DATA: 1996-2000 / HOSPITALIZATIONS / TIME SERIES STUDIES
I identified 19 studies which examined the association between air pollution
and daily hospital admissions. Ozone and particulate air pollution were
robustly associated with hospital admissions. One additional study examined
the relationship between characteristic of air masses and asthma hospital
admissions. It found that during the spring and summer, air masses with
high air pollution levels were more likely to be associated with increased
asthma admissions.
Nineteen90-108 new studies examined the association between
particulates and hospitalization rates. Only one98 of these
studies failed to find an association between combustion derived air pollution
and increased hospitalization rates. Two97, 104 of the studies
found the association with SO2 instead, and one found the association
with particulate only when NOx was also in the model. Hence, in 18 of
19 studies, the association with particulate air pollution or its chemical
antecedents was observed.
Fifteen new studies examined the association between ozone air pollution
and hospitalization rates. Twelve90-94, 96, 97, 99, 102, 103, 107,
108 studies found a significant association, and one104 study found
the association with NO2 instead. Two95, 98 studies failed
to find the association. In all, 13 of 15 studies found the association
with ozone or its chemical antecedents.
Outcomes which were commonly associated with air pollution included asthma,
COPD (chronic obstructive pulmonary disease = chronic bronchitis and emphysema),
and heart disease.
In summary, ozone and particulate air pollution were robustly associated
with hospital admission rates. Common outcomes were asthma, COPD, and
heart disease.
NEW DATA: 1996-2000 / MORTALITY / TIME SERIES STUDIES
In late 1995 and early 1996 most of the major review articles emerged
examining the relationship between air pollution and adverse health effects.
These reviews found consistent and coherent associations between particulate
air pollution and daily mortality levels. In addition, data was beginning
to emerge suggesting that ozone air pollution was associated with daily
mortality. While some authors considered the association between particulate
air pollution and daily mortality to be causal, others were more circumspect.
Hence, I examined the subsequent data in search of validation or refutation
of these concerns.
I was able to identify 21 time series studies published since 1996 examining
the association between daily air pollutant levels and daily mortality.
These studies generally are quite well designed, adjusting for weather
variables and other considerations.
Eighteen14, 105, 106, 109-123 new studies examined the association
between particulate air pollution and excess mortality. One120
of these, a study of asthma mortality, failed to find the association.
Twelve new studies examined the association between ozone air pollution
and excess mortality. Ten92, 110, 111, 113, 115, 118, 120-122, 124
found the association and one114 found the association with
NO2 instead. One study109 found ozone to be marginally associated.
No study completely failed to find an association with ozone or its chemical
antecedent, NO2.
One120 study specifically examined the relationship between
asthma mortality and air pollution. Only NO2 and ozone air pollution were
found to be associated with asthma mortality.
I identified 1 study which attempted to differentiate the fine fraction
(PM2.5) of particulate air pollution from the coarse fraction (PM2.5 -
PM10).14 This study found the fine fraction to be implicated
in elevated mortality rates. One106 studies examined acid sulfate
aerosol, a common constituent of particulate fine fraction. Those studies
found sulfate aerosol to be strongly associated with mortality. (Note
is made that previous studies have shown that sulfate aerosol is sufficient,
but not necessary, to be associated with mortality).12
Time series studies have continued to flood the medical journal market
in the last few years, and continue to overwhelmingly find that particulate
air pollution is associated with mortality. Data increasingly suggest
that the fine fraction, which generally arises from combustion sources,
is consistently implicated. In addition, a remarkably robust data set
is emerging associating high ozone exposure with daily mortality. Although
some studies find associations between SO2 and NO2 and daily mortality,
these association are less consistent.
NEW DATA: 1996-2000 / MORTALITY / TIME SERIES META-ANALYSIS
Several meta-analyses of the association between particulate air pollution
and daily mortality have appeared previously in the literature. All have
found significant associations between particulate air pollution and daily
mortality. I have found one meta-analysis published in the recent literature.
This meta-analysis125 examined the effect of between study
variability on the effect estimate of the association between particulate
and daily mortality. More precisely, they examined the possible effects
of air pollution patterns and characteristics of the exposed population.
There was some evidence that PM effects were influenced by climate, housing
characteristics, demographics, and the presence of sulfur dioxide and
ozone. However, the effect of particulate on mortality was robust, not
changing with inclusion of potential confounders and effect modifiers.
The increase in daily mortality rate of 0.7% per 10 mcg/m3 increase in
PM10 is similar to previous meta-analysis estimates (1% per 10 mcg/m3
increase in PM10), and was found to be higher in locations which had a
higher proportion of PM10 attributed to the fine fraction (PM10). In other
words, the effect estimate of this meta-analysis was quite consistent
with previous meta-analyses, was able to adjust for the presence of many
potential confounders and effect modifiers, and supported evidence from
other studies which implicates the fine fraction of particulate in excess
mortality.
NEW DATA: 1996-2000 / MORTALITY / PROSPECTIVE COHORTS
Three large prospective cohort studies examining the relationship between
particulate air pollution and premature mortality were conducted in the
last decade.13, 16, 126 Prospective cohort studies are considered
the most reliable study possible in air pollution epidemiology because
individual subjects are identified and individual risk factors for mortality
(such as smoking) are considered and adjusted for. All three prospective
cohort studies found significant associations between particulate air
pollution levels and premature mortality. Interestingly, all three studies
also found associations between air pollution and lung cancer.
The most recent prospective cohort was published in 1999.126
This is a cohort of 6,338 nonsmoking Seventh-day Adventists. PM10 was
strongly associated with non-malignant respiratory mortality adjusting
for a wide range of potentially confounding factors, including occupational
and indoor sources of air pollutants. The mortality rate was 18% higher
for persons exposed to 43 days per year with PM10 levels higher than 100
mcg/m3. Both ozone and PM10 were associated with lung cancer in males,
and sulfur dioxide showed strong associations with lung cancer in both
sexes. Other pollutants showed weak or no associations with mortality.
NEW DATA: 1996-2000 / CAUSALITY
The new data on health effects or air pollution has been reviewed above.
One substantial new review of particulate air pollution has recently been
published by the National Institutes of Health127 in their
academic journal, Environmental Health Perspectives. This new review concludes
that the case for adverse health effects from particulate air pollution
has been made, and that the effect should be considered causal.
"The question of when it would be appropriate to conclude that the associations
between particulate pollution and various outcomes (including mortality)
should be judged as causal in nature has been difficult and controversial.
Although such a judgment must be subject to revision, the volume of new
information and new experimental findings has been so great that such
a reevaluation is required at frequent intervals. The useful summary by
Gamble [PM2.5 and Mortality in Long-Term Prospective Cohort Studies: Cause-Effect
or Statistical Associations? Environ Health Perspect 106:535-554 (1998)]
of the reasons why a causal inference was, in his opinion, not justified
provides a basis for reevaluation in the light of new data. Such a reexamination
indicates that the associative evidence is now stronger and that the biologic
basis for a number of adverse effects has now been demonstrated. All of
the useful guideline criteria customarily applied to such questions seem
to have been met, although there is still much to be learned about interactive
effects and the possibility of statistical thresholds."
NEW DATA: 1996-2000 / COSTS
A recent review has examined the health based financial benefit of reducing
particulate air pollution in the USA.128
"Most Americans are exposed daily to airborne particulate matter (PM),
a pollutant regulated by the U.S. Environmental Protection Agency. Current
national standards are set for PM10 (particles less than 10 microns in
diameter) and new standards have been promulgated for PM2.5 (particles
less than 2.5 microns in diameter). Both particle sizes have been associated
with mortality and morbidity in studies in the United States and elsewhere
and an unambiguously safe level of ambient PM has been difficult to identify.
PM10 concentrations have been reduced significantly in U.S. cities over
the past two decades and relatively few locations continue to exceed national
PM10 standards. However, the new PM2.5 standards will require further
reductions in PM concentrations and additional expenditures for emission
controls. Information about the health and economic benefits of achieving
lower PM concentrations is important because: (1) expected costs of further
PM reductions rise after the least-cost options are exhausted, and (2)
there is uncertainty about the existence of a threshold safe level for
PM. This paper develops and applies a methodology for quantifying the
health benefits of potential reductions in ambient PM. Although uncertainties
exist about several components of the methodology, the results indicate
that the annual nationwide health benefits of achieving the new standards
for PM2.5 relative to 1994-1996 ambient concentrations are likely to be
between $14 billion and $55 billion annually, with a mean estimate of
$32 billion."
NEW DATA: 1996-2000 / ENERGY POLICY
Finally, lest one doubt that the public health community is behind curtailing
air pollution as a needed public health measure, a journal of the American
Public Health Association has published a recent review.129
"The connection between energy policy and increased levels of respiratory
and cardiopulmonary disease has become clearer in the past few years.
People living in cities with high levels of pollution have a higher risk
of mortality than those living in less polluted cities. The pollutants
most directly linked to increased morbidity and mortality include ozone,
particulates, carbon monoxide, sulfur dioxide, volatile organic compounds,
and oxides of nitrogen. Energy-related emissions generate the vast majority
of these polluting chemicals. Technologies to prevent pollution in the
transportation, manufacturing, building, and utility sectors can significantly
reduce these emissions while reducing the energy bills of consumers and
businesses. In short, clean energy technologies represent a very cost-effective
investment in public health."
More . . . Summary
and Conclusions
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