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Health Effects of Criteria Air Pollutants from Power Plants 2002
Author: Jefferson H. Dickey MD
Health Effects: American Thoracic Society (ATS) Summary
ATS Summary / Introduction
The summary of pre-1996 data above essentially reflects the thinking
in the medical literature prior to 1996, which is about when most of the
major academic reviews were published in anticipation of the EPA revision
of the NAAQS for ozone and particulate. The pre-1996 data is perhaps best
summarized by the review published by the Committee of the Environmental
and Occupational Health Assembly of the American Thoracic Society in January
1996.3 This provides a convenient and expert point of departure
for a review of the more recent research. I have excerpted the relevant
conclusions from this 50 page review tome.
ATS Summary / Ozone
"Ambient air O3 is generated in the troposphere from precursors (hydrocarbons
and NOx) in complex reactions catalyzed by light energy. ... During acute
O3 exposure, many children and young adults progressively develop substernal
pain on deep inspiration, irritative cough, and a reduced vital capacity
and FEV1. These changes recede initially fairly rapidly and then somewhat
more slowly over a period of several hours after exposure cessation, though
some FEV1 decrement and symptoms may persist for as long as 24 hours.
"There is evidence from animal and human studies that certain alveolar
macrophage antimicrobial defense functions are impaired after exposure
to O3. In mice, O3-impaired macrophage function contributes to increased
mortality after challenge with aerosolized inhaled bacteria, although
in humans O3 exposure has not been shown to be directly associated with
increased morbidity from respiratory infections.
"Acute exposure to O3 also provokes an upper and lower airway inflammatory
response that includes mucosal hyperemia, increased permeability to serum
proteins and to water soluble probe molecules placed on the airway surface,
and infiltration of the mucosa with neutrophils. O3 exopsure also results
in a large increase in inflammatory mediators and factors present in bronchial
and alveolar lining fluids. Many of these mediators are likely released
by epithelial cells in the lung. In view of the potent irritant like effects
of O3 on the airways and of O3 induced bronchial hyperreactivity and airway
inflammation, one might expect individuals with chronic airways disease
to exhibit enhanced acute susceptibility to this pollutant. Indeed, studies
of panels of asthmatics in the Los Angeles and Houston areas relating
symptoms and medication use to air pollution levels, and associations
between fluctuations in summertime O3 levels and hospital admissions from
asthma, lend some support to this hypothesis. However, the reality is
that O3 and other pollutants such as sulfates and acid aerosols commonly
rise together, and, for this reason, it is difficult to attribute increased
acute respiratory admissions to a single pollutant.
"Long term exposures of animals to O3 do not result in diffuse parenchymal
lesions such as emphysema or diffuse fibrosis nor are pressure-volume
curves usually displaced. However, there appears to be an emerging consensus
that the principal effect of chronic O3 exposure in animals is a centri-acinar
lesion in the terminal or respiratory bronchioles in which metaplastic
airways epithelium extends into the proximal acinar regions accompanied
by peribronchiolar mononuclear infiltrates, localized deposition of collagen,
and remodeled peribronchiolar airspace. More severe degrees of injury
are accompanied by restrictive impairments in airflow. These findings
indicate the importance of and support the need for additional longitudinal
and cross sectional population studies to look for evidence of excessive
obstructive airways impairment among residents of perennially O3 polluted
areas in the Los Angeles basin or elsewhere."
ATS Summary / Particulates
"Particles, SOx, and acid aerosols are a complex group of distinct pollutants
that have common sources and usually covary in concentration. During the
past two decades, the chemical characteristics and the geographic distribution
of sulfur oxide and particulate pollution have been altered by control
strategies, specifically taller stacks for power plants, put in place
in response to air pollution regulations adopted in the early 1970s. While
the increasing stack heights have lowered local ambient levels, the residence
time of SOx and particles in the air have been increased, thereby promoting
transformation to various particulate sulfate compounds, including acidic
sulfates. These sulfate particles constitute a large fraction of the total
mass of smaller particles (< 3 microns in aerodynamic diameter). Epidemiologic
studies have consistently provided evidence of adverse health effects
of these air pollutants. Particulate and SO2 pollution were strongly implicated
in the acute morbidity and mortality associated with the severe pollution
episodes in Donora (Pennsylvania), London, and New York in the 1940s,
1950s, and 1960s. There is new evidence that even current ambient levels
of PM10 (30 to 150 micrograms/m3) are associated with increases in daily
cardiorespiratory mortality and in total mortality, excluding accidental
and suicide deaths. These associations have been shown in many different
communities, as widely different in particle composition and climate as
Philadelphia, St. Louis, Utah Valley, and Santa Clara County, California.
It has recently been shown in a long-term prospective study of adults
in the United States that chronic levels of higher PM10 pollution are
associated with increased mortality after adjusting for several individual
risk factors. Daily fluctuations in PM10 levels have also been shown to
be related to acute respiratory hospital admissions in children, to school
and kindergarten absences, to decrements in peak flow rates in normal
children, and to increased medication use in children and adults with
asthma. Although some epidemiologic studies suggest that acid aerosols
are an important toxic component of PM10, other studies do not support
this hypothesis. Dockery and Pope (408) recently reviewed the epidemiologic
literature for adverse effects, assuming that reported associations can
be attributed to acute particle mass exposures. Combined effects were
estimated as percent increase in comparable measures of mortality and
morbidity, associated with each 10 micrograms/m3 increase in daily mean
PM10 exposure (Table 7). While total mortality increased by 1% for each
10 micrograms/m3 increase in PM10, respiratory mortality increased by
3.4% and cardiovascular mortality increased by 1.4%. Hospital admissions
and emergency department visits increased approximately 1% for all respiratory
complaints, and 2% to 3% for asthma. Exacerbation of asthma increased
by about 3%, as did lower respiratory symptoms. Small decreases in lung
function, approximately 0.1%, have also been observed. This review suggests
that the epidemiologic studies of adverse morbidity measures are coherent
with the mortality studies showing quantitatively similar adverse effects
of acute exposures to particulate pollution."
More . . . Health Effects/New
Data: 1996-2000
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