Beruflich Dokumente
Kultur Dokumente
1 INTRODUCTION
The mere mention of air pollution conjures up visions of huge urban smokestacks
billowing voluminous clouds of brown, black, or gray and large city skyscrapers whose
spires disappear into the hazy clouds of smog that blanket large cities. However, air
pollution is a combination of both anthropogenic and natural origins. Air pollution has
been around for as long as we have had the forces of nature. Whether it be from dust or
sandstorms suspending particulate matter into the atmosphere, lightning strikes
causing fires which contribute combustion particles and gases, volcanic eruptions
spewing toxic particles and gases for miles, or meteorological inversions which trap
pollutants near the ground, preventing their dilution and dispersion into the atmosphere, nature plays a part in pollution. Nevertheless, the anthropogenic contributions
to air pollution have been significant and relentless. We have fouled the air to such an
extent that we can no longer see through it. What once were beautifully clear vistas,
enabling one to see many miles in any direction, have been reduced to a hazy few miles
in visibility. Our clean air has been replaced with an odorous substitute. One that not
only is aesthetically displeasing but also actually unhealthy to breathe for some
individuals.
It was during the height of the industrial revolution that the health effects of air
pollution in the cities became apparent. Many individuals became sick while others
Pattys Industrial Hygiene, Sixth Edition, Edited by Vernon E. Rose and Barbara Cohrssen
Copyright 2011 John Wiley & Sons, Inc.
2549
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AIR POLLUTION
died during very bad days of pollution. During the Great London Smog of 1952,
pollution levels in the city grew to such levels over several days that nearly 4,000
excess deaths were reported. As a result, the Clean Air Act of 1956 was enacted in the
United Kingdom.
In the United States, large cities took it upon themselves to institute air pollution
control measures. The first federal legislation involving air pollution was the Air
Pollution Control Act of 1955 and provided funds for federal research on air pollution.
This was followed by the Clean Air Act of 1963 that established a program within the
U.S. Public Health Service for research on air pollution monitoring and control
techniques. Later, the Air Quality Act of 1967 expanded the federal governments role
involving air pollution by enacting enforcement procedures concerning interstate
transport of pollutants. The Clean Air Act of 1970 brought about a number of
significant changes including the establishment of the National Ambient Air
Quality Standards (NAAQS) for air pollutants and the requirement for State
Implementation Plans to achieve these new standards. In addition, it authorized
the establishment of the National Emission Standards for Hazardous Air Pollutants
and required control of motor vehicle emissions. In 1971, the Environmental
Protection Agency was created to implement the requirements of the Clean Air
Act of 1970 and currently lists six air pollutants as criteria pollutants for which
NAAQS have been established. Criteria pollutants are air pollutants having numerous
or diverse sources that in the judgment of the U.S. EPA Administrator, cause or
contribute to air pollution, which may reasonably be anticipated to endanger public
health or welfare. The current criteria pollutants consist of carbon monoxide, lead,
ozone, nitrogen dioxide, sulfur dioxide, and particulate matter. Historically, the Clean
Air Act of 1970 has undergone two amendments (1977 and 1990), which have
further defined the federal governments efforts in air pollution monitoring and
control. As a result of these legislative acts, the air quality in the United States has
significantly improved.
2 CARBON MONOXIDE
2.1 Nature and Sources
Carbon monoxide (CO) is a colorless, odorless, and tasteless gas. It has a relative
density of 0.97 and therefore distributes within an enclosed space similarly to air.
Chemically, CO can bind to iron-containing moieties found in hemoglobin, myoglobin, and other cytochromes. The binding of CO to the iron-containing heme in
hemoglobin results in oxidation of the iron atom from Fe2 to Fe3 . This prevents the
binding of oxygen (O2) to the heme iron. The affinity of the heme iron for CO is
approximately 200 times greater than for O2. This preferential binding means that
small concentrations of CO can have profound effects on O2 binding and the formation
of carboxyhemoglobin versus oxyhemoglobin.
Sources of carbon monoxide encompass natural as well as man-made sources.
Natural sources include volcanic gases, forest and brush fires, generation during
electrical storms, endogenous production by animals and plants, and microbial release
CARBON MONOXIDE
2551
from soils. Anthropogenic sources include incomplete fuel combustion from transport
vehicles (cars, trucks, planes, trains, and ships), heating sources (furnaces, hot water
heaters, and kerosene heaters), cooking appliances (stoves, grills), industrial plant
exhausts, explosive detonations, and smoking.
250,000
Highway vehicles
200,000
Off-highway
150,000
100,000
Miscellaneous
50,000
Total
19
19 7 0
1975
1980
1985
1990
1991
1992
1993
1994
19 9 5
1996
1997
1998
2099
2000
2001
2002
2003
2004
200 5
06
0
Year
FIGURE 52.1 Major sources of estimated CO emissions. Figure was generated using data
from EPAs National Emissions Inventory (NEI) database. EPA maintains a national database
of air emissions information with input from numerous state and local air agencies, tribes, and
from industry. This database contains information on stationary and mobile sources that emit
criteria air pollutants and their precursors, as well as hazardous air pollutants. The database
includes estimates of annual emissions, by source, of air pollutants in each area of the country,
on an annual basis. The NEI includes emission estimates for all 50 States, the District of
Columbia, Puerto Rico, and the Virgin Islands. Source:http://www.epa.gov/ttn/chief/trends.
2552
AIR POLLUTION
8,000
7,000
6,000
5,000
Metals processing
4,000
Petroleum & related
industries
3,000
Other industrial
processes
Solvent utilization
2,000
1,000
Waste disposal &
recycling
19
70
19
75
19
80
19
85
19
90
19
91
19
92
19
93
19
94
19
95
19
96
19
97
19
98
19
99
20
00
20
01
20
02
20
03
20
04
20
05
20
06
0
Year
FIGURE 52.2 Minor sources of estimated CO emissions. Figure was generated using
data from EPAs NEI database. Source:http://www.epa.gov/ttn/chief/trends.
0.53%
23.80%
1.09%
13.22%
0.31%
0.02%
0.14%
Metals processing
Petroleum & related industries
1.66%
9.17%
3.25%
0.67%
1.22%
53.81%
FIGURE 52.3 CO sources for 2006 (estimated). Figure was generated using data from EPAs
NEI database. Results are expressed as a percentage of the estimated total CO emissions for
2006. Source:http://www.epa.gov/ttn/chief/trends.
2553
CARBON MONOXIDE
3000
200
2500
150
2000
1500
100
1000
50
500
250
3500
0
1970 1975 1980 1985 1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006
Year
Annual vehicle miles
CO emissions
FIGURE 52.4 Comparison of annual vehicle miles traveled and CO emissions. Based on the
U.S. Department of Transportation, Federal Highway Administration estimations of annual
miles traveled and the NEI database estimations. Sources:http://www.epa.gov/ttn/chief/trends
and http://www.fhwa.dot.gov/environment/vmttext.htm.
National trend based on 144 sites
16
Concentration (ppm)
14
12
10
National standard
8
6
4
2
0
1
9
8
0
1
9
8
1
1
9
8
2
1
9
8
3
1
9
8
4
1
9
8
5
1
9
8
6
1
9
8
7
1
9
8
8
1
9
8
9
1
9
9
0
1
9
9
1
1
9
9
2
1
9
9
3
1
9
9
4
1
9
9
5
1
9
9
6
1
9
9
7
1
9
9
8
1
9
9
9
2
0
0
0
2
0
0
1
2
0
0
2
2
0
0
3
2
0
0
4
2
0
0
5
2
0
0
6
Year
19802006: 75% decrease in national average
FIGURE 52.5 CO air quality 19802006. Figure represents the second highest annual CO
concentration (based on an 8 h average) in parts per million. The blue band shows
the distribution of air pollution levels among the trend sites, displaying the middle 80%.
The white line represents the average among all the trend sites. Ninety percent of sites have
concentrations below the top line, while 10% of sites have concentrations below the bottom line.
The dashed line is the national ambient air quality standard for CO at the time of
writing. Source:http://www.epa.gov/air/airtrends/carbon.html.
2554
AIR POLLUTION
LEAD
2555
blood flow via vasodilation. A number of behavioral changes have been documented
with CO exposure but these effects have not been consistent and occur only at higher
COHb levels (generally >20%). These effects include alterations in vigilance, hand
eye coordination, and other forms of continuous performance.
2.3.5 Developmental Toxicity Another area of concern is developmental toxicity
from CO exposure. It is well documented that mothers who smoke during pregnancy
have an increased risk of developmental disorders including low birth weight. In
animal studies, maternal exposure to CO leading to 1525% COHb levels resulted in
low birth weight, cardiomegaly, delays in behavioral development, and disruption of
cognitive function (13, 6872). While these levels of CO are much greater than what
could be encountered in the ambient air, additional sources of CO such as smoking or
occupational exposure could produce a cumulative effect when combined.
3 LEAD
3.1 Nature and Sources
Lead (Pb) has been used for thousands of years in diverse applications such as paint,
ceramic glazes, water transport, and electrical components. It has useful chemical and
physical properties, including a low melting point (327.5 C), malleability, ease of
casting, and corrosion resistance. Lead is alloyed with a number of other elements
including calcium, tin, copper, silver, sulfur, bismuth, and cadmium and then used in
solder, ammunition, cables, and batteries. Other important properties of Pb are its
weight, number of electrons, and spatially diffuse valence orbitals, which determine its
behavior and toxicity in biological systems. Lead has been shown to form stable bonds
with sulfur and sulfur-containing compounds, but somewhat less so with carboxylic
acids (O-based ligands) and imidazoles (N-based ligands) (73). This allows Pb to
compete effectively with native or homeostatic metal ions (such as calcium) for
binding with the sulfhydryl, carboxyl, and imidazole side-chains comprising enzyme
active sites. This competition leads to inhibition of enzyme activity, as well as the
replacement of calcium in bone and, ultimately, to a substantial array of adverse human
health effects.
Lead is a multimedia pollutant, meaning that Pb emissions to the air contribute to Pb
concentrations in water, soil, and dusts, and further, that the Pb in soil and dust
contribute to Pb concentrations in ambient air (Fig. 52.6). Ingestion through food,
beverages, and dust is estimated to be 210 mg/day currently, compared to 50 mg/day
in 1990.
Automotive sources are no longer the major direct contributor of Pb emissions to
the atmosphere due to the phaseout of Pb from most domestic fuels. Mobile sourcerelated emissions, including brake wear, resuspension of road dust, and emissions
from piston-engine aircraft and racecars, still occur. However, the resuspension of
soil-bound Pb particles and contaminated road dust remains a significant source of
airborne Pb. The industrial sector is the major stationary source of Pb into the
environment. These industries include iron and steel foundries, coal and fuel oil
2556
AIR POLLUTION
Auto
emissions
Industrial
emissions
Crustal
weathering
Ambient
air
Surface and
ground water
Soil
Plants
Animals
Dusts
Food
Paint
Inhaled
air
Drinking
water
Man
combustion, wood combustion, waste incineration, primary and secondary Pb smelters, copper and nickel smelters, Pb-acid battery plants, and Pb mining/processing.
Only one primary smelter remains operating in the United States, in Herculaneum, MI.
The most recent data for annual Pb production and use in the United States are shown in
Figure 52.7. Natural sources of Pb, such as volcanoes, sea-salt spray, biogenic sources,
forest fires, contribute about 19,000 metric tons of Pb to the air annually (74).
1,600,000
1,400,000
Other
Bearing metals
Metric tons
1,200,000
1,000,000
800,000
Cable coverings
Solder
Ammunition
Pigments and paints
600,000
400,000
Gasoline additives
Batteries
200,000
0
1968 1972 1976 1980 1984 1989 1993 1997 2001 2003
Year
FIGURE 52.7 Annual lead production and use in the United States (19682003). Sources:
U.S. Bureau of Mines (19681995) and USGS (19962003).
LEAD
FIGURE 52.8
2557
Lead emissions in the United States from 1982 to 2002 (from Ref. 118).
2558
AIR POLLUTION
Measure B1
30
25
90th percentile
(10% of children have
this blood lead level or greater)
20
15
10*
5
0
Median value
(50% of
children have this
blood lead level
or greater)
1976
1980
1988
1991
1992
1994
1999 2001
2000 2002
* 10 g of blood lead has been identified by CDC as elevated, which indicates need for intervention. There
is no demonstrated safe concentration of lead in blood. Adverse effects may occur at lower concentrations.
FIGURE 52.9 Concentrations of lead in blood of children ages 5 and under. Source: U.S.
EPA. Americas Children and the Environment (www.epa.gov/envirohealth/children). Data
from Centers for Disease Control and Prevention, National Center for Health Statistics,
National Health and Nutrition Examination Survey.
neonatal, and later postnatal Pb exposures have been consistently observed, even after
adjusting for potential confounding by care giving, parental intelligence, and socioeconomic status (SES). Neurocognitive decrements have been associated in young
children with PbB levels of 510 mg/dL, with some evidence of effects at lower
concentrations (7679). Effects on intellectual attainment of preschool and school age
children were observed at population mean concurrent PbB of 28 mg/dL (8082). A
large international pooled analysis of seven well-conducted prospective studies
showed a decline of 6.2 points in full scale IQ for an increase in concurrent PbB
levels from 1 to 10 mg/dL (83) (Fig. 52.10). Alterations in behavior, social conduct, and
attention are also associated with Pb exposures at low levels (84, 85).
There is inconclusive evidence for the effects of environmental Pb exposure on
adults. Associations were observed between bone Pb levels and neurobehavior, but not
between PbB and neurobehavior, suggesting that cumulative Pb exposure may be
more important in adults (86, 87).
The epidemiological findings of neurocognitive deficits in children are supported
by parallel findings in animal toxicological studies in which both rodents and
monkeys, exposed developmentally to Pb, resulting in steady-state PbB levels of
10 mg/dL, demonstrated behavioral impairments that persisted into adulthood (88,
89). Mechanisms associated with these deficits include response perseveration;
insensitivity to changes in reinforcement density or contingencies; deficits in
attention; reduced ability to inhibit inappropriate responding; impulsivity; and
distractibility. No evident threshold has yet been found for the neurocognitive effects
of Pb on the nervous system and the Pb-induced deficits, for the most part, have been
found to persist into adulthood. In both rodents and nonhuman primates, reactivity to
LEAD
2559
the environment and social behavior are affected at blood Pb levels of 1540 mg/
dL (90, 91). Visual function is impaired at PbB of 19 mg/dL (92) and auditory function
is impaired at PbB of 33 mg/dL (90, 91, 93).
Two genetic polymorphisms have been identified that possibly increase the
susceptibility to the neurodevelopmental consequences of Pb exposure in children.
Variants of the aminolevulinic acid dehydratase (ALAD) gene appear to influence the
absorption, retention, and toxicokinetics of Pb in humans (94) and variants of the
vitamin D receptor gene modify Pb concentrations in bone and the rate of resorption
and excretion of Pb over time (95).
Neurotoxicological studies in animals clearly demonstrated that Pb mimics calcium and affects neurotransmission and synaptic plasticity as shown in Figure 52.11.
3.3.2 Effects of Pb on the Immune System Recent epidemiological data demonstrate that Pb exposure may be associated with effects on cellular and humoral
immunity. Associations have been found between increasing PbB concentration and
increasing serum immunoglobins at PbB of <10 mg/dL in children (96) and at
somewhat higher levels in adults (>30 mg/dL). Associations have also been observed
between increasing PbB levels and decreases in T-cell abundance, with corresponding
increases in B-cell abundance. These effects have been observed in children whose
PbB concentrations ranged from 10 to 45 mg/dL (97). Toxicological studies have
shown that Pb targets immune cells, causing suppression of delayed type hypersensitivity response, elevation of IgE, and modulation of macrophages into a hyperinflammatory phenotype. These types of changes can cause increased risk of atopy,
asthma, and some forms of autoimmunity and reduced resistance to some infectious
diseases (98). Lead exposure of embryos resulting in PbB levels <10 mg/dL can
produce persistent later-life immunotoxicity (99). Figure 52.12 shows Pb-induced
2560
AIR POLLUTION
LEAD
2561
Inflammatory tissue
T cells
Membrane
arachidonic
acid
B cells
Host proteins
T0
Activation
Reduced response
to CSF-1
Th2
IL-4
IL-5
TNF-
Th1
Cell Surface
INF-
Class II
Auto-antibodies and
possible tissue
damage
Reduced cellmediated
immunity
IL-6
NO
ROI2
IL-12
PGE2
FIGURE 52.12
3.3.4 Effects of Pb on Other Organ Systems Lead has long been known to disrupt
heme synthesis in children at 15 mg/dL (105) and in adults at 30 mg/dL (106). Studies in
animals have shown that Pb decreases red blood cell (RBC) survival and alters RBC
mobility (107). As mentioned above, Pb mimics calcium and thus, is readily taken up
and stored in bones and teeth (108). This disrupts mineralization of bone and can result
in growth suppression (109) and decreased bone density (110). During periods of bone
remodeling (e.g., pregnancy, lactation, aging), Pb can be mobilized and then transferred to the blood and other organs (111, 112). Lead exposure has been associated with
adverse dental outcomes including dental caries at PbB levels of <10 mg/dL (113).
Lead has been shown to produce both temporary and persisting effects on male and
female reproductive function and development and Pb disrupts endocrine function at
multiple points along the hypothalamicpituitarygonadal axis (114), elevating
corticosterone levels, and altering stress responsivity (115). This may be a potential
mechanism contributing to Pb-induced hypertension, with further possible roles in the
etiology of diabetes, obesity, and other disorders. Lead has been classified as a
probable carcinogen, according to the National Toxicology Program (116) and
International Agency for Research on Cancer (117). Associations between Pb exposure and DNA damage and micronuclei formation have been found, though associations with chromosomal aberrations, the more established indicator of cancer risk, are
inconsistent (118).
2562
AIR POLLUTION
4 OZONE
4.1 Nature and Sources
Ground-level ozone (O3) is a secondary pollutant formed by photochemical reactions
involving volatile organic compounds (VOCs), nitrogen oxides (NOx), and carbon
monoxide. Motor vehicles, chemical plants, refineries, factories, consumer and
commercial products, and other industries are all sources of these ambient precursors,
which react in the presence of heat and sunlight to form O3. Other sources of groundlevel O3 include intrusions of stratospheric O3 and transport by nocturnal low-level
jets. Figure 52.13 presents a diagram showing the major processes involved in O3
cycling in the atmosphere.
Stratosphere
Nonpolar
regions
H,
Cl,
Y
(X,
UV
Ozone
hole
O2
(in air)
OH
H2O
urf
ac
ew
at
e
H,
H
O3 + UV
HO2
RO2
ds
Ozone
NO
etat
io
Peroxides
NO2
to soi
l, veg
Volatile organic
compounds
NO
O+
n, a
n
O3
Y+
X or + YO
XO
+O
Depositi
on
2O 2
Polar
regions
Oxygen
Oxygen
Br)
=N
O,
+O
X
XO + O
+ O3
(X
Oxygen
+ O2
XO + O 2
X
h,
UV
XO r,)
X + or Y
Y+ O+
O O
O2 +
NO2 OH, RO
UV
Emissions
of NOx and
VDCs
Other organic
products
Troposphere
NO
2 +O
H
(m
a
Rainout
deposition
HNO3
Aerosol
uptake
FIGURE 52.13 Schematic overview of O3 photochemistry in the stratosphere and troposphere (from Ref. 119).
OZONE
2563
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AIR POLLUTION
supplements was found to diminish the O3 effect on lung function in both outdoor
workers and asthmatics (124, 125).
Controlled human exposure studies of healthy adults exposed to 0.08 ppm O3 for
6.6 h with moderate exercise had a group mean decrement in FEV1 of 6% (126).
National trend based on 275 sites
Concentration (ppm)
0.15
0.10
National standard
0.05
0.00
1
9
8
0
1
9
8
1
1
9
8
2
1
9
8
3
1
9
8
4
1
9
8
5
1
9
8
6
1
9
8
8
1
9
9
9
1
9
8
0
1
9
9
1
1
9
9
2
1
9
9
3
1
9
9
4
1
9
9
5
1
9
9
6
1
9
9
7
1
9
9
8
1
9
9
9
2
0
0
0
2
0
0
1
2
0
0
2
2
0
0
3
2
0
0
4
2
0
0
5
2
0
0
6
Year
19802006: 21% decrease in national average
(a)
0.20
Concentration (ppm)
1
9
8
7
0.15
National standard
0.10
0.05
0.00
1
9
8
0
(b)
1
9
8
1
1
9
8
2
1
9
8
3
1
9
8
4
1
9
8
5
1
9
8
6
1
9
8
7
1
9
8
8
1
9
8
9
1
9
9
0
1
9
9
1
1
9
9
2
1
9
9
3
1
9
9
4
1
9
9
5
1
9
9
6
1
9
9
7
1
9
9
8
1
9
9
9
2
0
0
0
2
0
0
1
2
0
0
2
2
0
0
3
2
0
0
4
2
0
0
5
2
0
0
6
Year
19802006: 29% decrease in national average
FIGURE 52.14 (a) Ozone air quality trends from 1980 to 2006 based on annual fourth
maximum 8 h average. The blue band shows the distribution of air pollution levels among the
trend sites, displaying the middle 80%. The white line represents the average among all the trend
sites. Source:http://www.epa.gov/oar/airtrends/ozone.html. (b) Ozone air quality trends from
1980 to 2006 based on annual second maximum 1 h average. The blue band shows the
distribution of air pollution levels among the trend sites, displaying the middle 80%. The white
line represents the average among all the trend sites. The dashed line is the national ambient air
quality standard for ozone at the time of writing. This applies to each graph a-c.Source:http://
www.epa.gov/oar/airtrends/ozone.html. (c) Ozone air quality trends from 1990 to 2006 based
on annual fourth maximum 8 h average. The blue band shows the distribution of air pollution
levels among the trend sites, displaying the middle 80%. The white line represents the average
among all the trend sites. Source:http://www.epa.gov/oar/airtrends/ozone.html.
OZONE
National trend based on 588 sites
0.15
Concentration (ppm)
2565
0.10
National standard
0.05
0.00
1990
(c)
1991 1992 1993 1994 1995 1996 1997 1998 1999 2000
Year
19902006: 9% decrease in national average
FIGURE 52.14
(continued)
Ozone exposures of 0.5 ppm are the lowest at which statistically significant reductions
in FVC and FEV1 have been demonstrated in sedentary subjects. On average, young
adults exposed at rest for 2 h to 0.5 ppm O3 had O3-induced decrements of 4% in
forced vital capacity (FVC) and 7% in FEV1 (127, 128). Controlled human exposure
studies (129) using repeated acute (16 h) O3 exposures at 0.120.45 ppm over several
days showed that FEV1 response to O3 is enhanced on the second of several days of
exposure, but spirometric responses become attenuated on subsequent days with these
repeated exposures. This tolerance is lost after about a week without exposure.
Biological plausibility for these effects is provided by animal toxicological studies
(at levels of 0.250.4 ppm O3 for several hours) showing O3-induced rapid shallow
breathing (i.e., increased frequency and decreased tidal volume) that attenuates after
several days of exposure.
Respiratory symptoms associated with O3 exposure include cough, wheeze,
shortness of breath, production of phlegm, and increased medication use. Many
studies have found associations between acute exposure to O3 and increased respiratory symptoms and as-needed medication use in asthmatic children (130, 131). In a
pooled analysis from eight U.S. cities (132), the odds ratio for the incidence of
symptoms (cough, chest tightness, and wheeze) was 1.35 (95% CI: 1.04, 1.69) per
30 ppb increase in 8-h average O3 concentration. Human clinical studies using acute
exposures of 12 h at concentrations 0.12 ppm O3 reported symptoms of cough, pain
on deep inspiration, rapid, shallow breathing patterns during exercise, throat irritation,
and wheezing. Clinical studies of young, healthy adults using exposures of 68 h at
0.08 ppm during moderate exercise demonstrated symptoms of cough and pain with
deep inspiration. As with pulmonary effects, symptoms become attenuated following
repeated O3 exposures over several days, but this tolerance is lost after about a week.
Additionally, O3-induced respiratory symptoms gradually decrease in adults with
increasing age (119).
2566
AIR POLLUTION
OZONE
2567
FIGURE 52.15 Mechanisms of ozone toxicity. The inflammatory cascade starts by interactions of O3 with lipids in the epithelial lining fluid and in cell membranes. Lipid ozonation
reaction products include aldehydes, hydroxyhydroperoxides, and H2O2. These initiate lipase
activation in epithelial cells resulting in the downstream production of phospholipases,
arachidonic acid, leukotrienes, and prostanoids. Leukotrienes and prostanoids alter
lung function. Phospholipases initiate the production of NO, inflammatory cytokines, and
PAF. NO, IL-6, and IL-8 then participate in the recruitment and activation of inflammatory
cells (AMs, PMNs, blood monocytes, and mast cells), which, in turn, can start a second
cycle of inflammatory responses. PAF increases epithelial permeability and may have thrombolytic effects. Release of substance P by neurons causes altered lung function and
increases vascular permeability. Production of NOS-1 by these neurons induces airway
hyperreactivity.
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AIR POLLUTION
4.3.2 Airway Responsiveness Evidence from human clinical and animal toxicological studies demonstrates that acute exposure to O3 can induce airway hyperresponsiveness (AHR). Asthmatic subjects, who typically have increased airway
responsiveness at baseline, have further increases in responsiveness with O3 exposure (149). Asthmatics also demonstrate an increase in specific (i.e., allergen-induced)
airway reactivity in response to O3 exposure (150). These changes in airway
responsiveness after O3 exposure resolve more slowly than changes in pulmonary
function or symptoms (129). Attenuation of AHR is less likely with consecutive O3
exposures than attenuation of FEV1 (151). Furthermore, increases in AHR are not
strongly linked to the above-mentioned O3-induced decrements in lung function or
increases in symptoms. Mechanisms responsible for O3-induced AHR are not
completely understood, but are thought to involve inflammatory cytokines, prostanoids, or neuropeptides (see Fig. 52.15). A number of cell types also become activated
with O3 exposure, including mast cells, macrophages, and eosinophils. Reflex
bronchoconstriction is thought to be due to O3-induced epithelial damage that
increases direct access of mediators to the smooth muscle or receptors in the airways.
Ozone-induced AHR occurs in human asthmatics at ambient levels and in a number
of laboratory species at O3 concentrations as low as 0.51.0 ppm. Animal studies have
shown that O3 preexposure can augment ovalbumin-induced AHR (147, 152).
Importantly, there is a temporal relationship between inflammatory cell influx and
O3-induced AHR, however, inflammation is not a prerequisite for AHR (153).
Repeated O3 exposures enhance AHR, possibly by modulating rapidly adapting
airway receptors or by altering the structure of conducting airways (154). The rapid,
shallow breathing pattern elicited by O3 causes a more evenly distributed injury
pattern rather than protection from injury (155). Some of the newer animal studies of
O3-induced AHR suggest that exercise-induced bronchoconstriction may be mediated
by changes in tonicity of the bronchial smooth muscles (156). Vagally mediated
mechanisms may affect tracheal epithelial function and increase central airway
reactivity (157). Ozone may induce direct vascular constriction and may destroy
neural endopeptidases in airway epithelial cells, thus preventing the inactivation of
SP (158). Repeated O3 exposures may diminish neutrophilic inflammation, depress
cell proliferation, and cause cumulative distal airway lesions (159). The findings of
O3-induced decrements in lung function, respiratory symptoms, inflammation, and
AHR provide support for the epidemiological associations between O3 exposure and
respiratory-related hospitalizations and asthma ED visits during the warm season (160163). The evidence generally supports the findings of significant and robust
effects of O3 on various respiratory disease hospitalization outcomes. Large multicity
studies (164), as well as many studies from individual cities (165, 166) have reported
positive O3 associations with total respiratory hospitalizations, asthma, and COPD,
particularly in studies analyzing the O3 effect during the summer or warm season.
4.3.3 Cardiovascular Effects of Short-Term O3 Exposures A limited body of
epidemiological evidence suggests that O3 directly and/or indirectly contributes to
cardiovascular-related morbidity. Some population studies of cardiovascular hospital
admissions reported positive O3 associations during the warm season between ambient
OZONE
2569
2570
AIR POLLUTION
NITROGEN OXIDES
ACP2
oxidative stress
(Wattiez et al., 2003)
2571
6 h AHR
24 h inflammation
(Savov et al., 2004)
Tol-like receptor-4
(Kleeberger et al., 2000)
Mouse chromosomes
4
6 h inflammation
6 h protein
(Savov et al., 2004)
7
11
PMN influx
(Kleeberger et al., 1997)
15
24 h AHR
(Savov et al., 1997)
17
Tnfa
(Kleeberger et al., 1997)
19
CC16
oxidant stress
(Mango et al., 1998)
epithelial permeability
(Broeckaert et al., 2003)
FIGURE 52.16
ozone.
outcomes such as decrements in lung function and respiratory symptoms (202, 208).
Studies that examined associations between O3 exposure in older adults (> 65 years of
age), mortality and hospitalizations, have reported excess risks of mortality and
hospitalizations with elevated O3 concentrations (209, 210). Human clinical studies
show that older adults (211) have decreased respiratory symptoms with O3 exposure,
which may allow this population to receive increased O3 doses causing greater injury.
Genetic susceptibility to O3 has been shown in epidemiological, human clinical,
and toxicological studies. Genetic polymorphisms for both inflammatory mediators
(TNF-a) and antioxidant enzymes (GSTM1 and NQO1) have been identified in
humans (212, 213) that may modulate the effects of O3 exposure on pulmonary
function and airway inflammation. Animal toxicological studies provide corroborative evidence of innate genetic susceptibility to O3. Various strains of mice and rats
have been identified as sensitive or resistant to the effects of O3 for a number of
different endpoints (214, 215) as shown in Figure 52.16, which shows genes or gene
loci that have been characterized in mice.
5 NITROGEN OXIDES
5.1 Nature and Sources
Nitrogen oxides (NOx) are a group of compounds composed of varying amounts of
nitrogen and oxygen. The term NOx refers to the sum of nitrogen dioxide (NO2) and
2572
AIR POLLUTION
nitric oxide (NO). Historically, the compound of concern for air pollution is NO2.
Nitrogen dioxide exists as a reddish brown gas at room temperature and has a pungent
odor. It has a vapor pressure at 20 C of 720 mmHg and a vapor density of 1.58. It is
highly reactive and decomposes in water to nitric acid and NO.
Nitrogen oxides exist as products of natural as well as man-made processes. There
are a number of natural sources for NOx. One is the burning of biomass, which utilizes
the fixed nitrogen in the fuel source for the production of NOx. The higher the fixed
nitrogen content of the biomass, the greater the production of NOx (i.e., burning
grasslands and agricultural vegetation > forest fires > wood for fireplaces and woodstoves). Another natural source of NOx is from lightning. Electrical discharges
generate NOx by thermal dissociation of nitrogen molecules in the surrounding
air. It is estimated that the annual generation of NOx by lightning is 1 million metric
tons in North America and 13 million metric tons globally (216). Lastly, soil can
release NOx through nitrification and denitrification processes. It is estimated that the
NOx contribution from the soil is 2 million metric tons in North America and 36
million metric tons worldwide (216).
The majority of nitrogen oxides in the air are the result of combustion of fossil fuels.
Based on the National Emissions Inventory calculations, the extrapolated production
of NOx for 2006 is over 16,000 metric tons. Of that, 58% of the NOx emissions will be
from highway and off-highway vehicles/equipment. Besides vehicle emissions, fuel
combustion by electric utilities and other industries produce the remainder of the NOx
emissions (Fig. 52.17).
22.06%
0.60%
0.09%
36.22%
1.00%
0.03%
4.09%
1.52%
2.38%
0.42%
0.42%
19.67%
3.97%
11.62%
Metals processing
Solvent utilization
Highway vehicles
Off-highway
Miscellaneous
FIGURE 52.17 NOx sources for 2006 (estimated). Figure was generated using data from
EPAs NEI database. Results are expressed as a percentage of the estimated total CO emissions
for 2006. Source:http://www.epa.gov/ttn/chief/trends.
NITROGEN OXIDES
2573
30,000
25,000
Fuel comb. elec. util.
20,000
Highway vehicles
15,000
Off-highway
10,000
Total
5,000
19
7
19 0
7
19 5
80
19
8
19 5
9
19 0
9
19 1
9
19 2
9
19 3
9
19 4
9
19 5
96
19
9
19 7
98
19
9
20 9
00
20
0
20 1
02
20
0
20 3
04
20
0
20 5
06
Year
FIGURE 52.18 Major sources of estimated NOx emissions. Figure was generated using data
from EPAs NEI database. EPA maintains a national database of air emissions information with
input from numerous state and local air agencies, tribes, and from industry. This database
contains information on stationary and mobile sources that emit criteria air pollutants and their
precursors, as well as hazardous air pollutants. The database includes estimates of annual
emissions, by source, of air pollutants in each area of the country, on an annual basis. The NEI
includes emission estimates for all 50 States, the District of Columbia, Puerto Rico, and the
Virgin Islands. Source:http://www.epa.gov/ttn/chief/trends.
2574
AIR POLLUTION
1,600
Fuel comb. other
1400
1200
Metals processing
1000
800
Solvent utilization
600
Storage & transport
400
Waste disposal &
recycling
200
Miscellaneous
19
7
19 0
75
19
8
19 0
8
19 5
9
19 0
9
19 1
9
19 2
93
19
9
19 4
9
19 5
9
19 6
9
19 7
9
19 8
9
20 9
00
20
0
20 1
0
20 2
0
20 3
0
20 4
0
20 5
06
Year
FIGURE 52.19 Minor sources of estimated NOx emissions. Figure was generated using data
from EPAs NEI database. Source:http://www.epa.gov/ttn/chief/trends.
0.06
Concentration (ppm)
National standard
0.05
0.04
0.03
0.02
0.01
0.00
1
9
8
0
1
9
8
1
1
9
8
2
1
9
8
3
1
9
8
4
1
9
8
5
1
9
8
6
1
9
8
7
1
9
8
8
1
9
8
9
1
9
9
0
1
9
9
1
1
9
9
2
1
9
9
3
1
9
9
4
1
9
9
5
1
9
9
6
1
9
9
7
1
9
9
8
1
9
9
9
2
0
0
0
2
0
0
1
2
0
0
2
2
0
0
3
2
0
0
4
2
0
0
5
2
0
0
6
Year
19802006: 41% decrease in national average
FIGURE 52.20 NO2 air quality 19802006. Figure represents the annual arithmetic average
in parts per million. The blue band shows the distribution of air pollution levels among the trend
sites, displaying the middle 80%. The white line represents the average among all the trend sites.
Ninety percent of sites have concentrations below the top line, while 10% of sites have
concentrations below the bottom line. The dashed line is the national ambient air quality
standard for NO2 at the time of writing. Source:http://www.epa.gov/air/airtrends/nitrogen.
html.
NITROGEN OXIDES
2575
National standard
Concentration (ppm)
0.05
0.04
0.03
0.02
0.01
0.00
1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006
Year
19902006: 30% decrease in national average
FIGURE 52.21 NO2 air quality 19902006. Figure represents the annual arithmetic average
in parts per million. The blue band shows the distribution of air pollution levels among the trend
sites, displaying the middle 80%. The white line represents the average among all the trend sites.
Ninety percent of sites have concentrations below the top line, while 10% of sites have
concentrations below the bottom line. Source:http://www.epa.gov/air/airtrends/nitrogen.html.
literature on NOx identifies the lung as the primary target organ. Typically, the effects
seen are subtle cellular or biochemical alterations. These include changes in lipids,
proteins, amino acids, and enzymes resulting in altered cell membranes and antioxidant homeostasis. A variety of toxicological effects are seen in both controlled human
and animal exposures and are discussed below.
5.3.2 Alterations in Host Defense Mechanisms Some of the more sensitive
endpoints in NOx exposure relate to its ability to affect the bodys defense mechanisms. Numerous studies have reported effects at concentrations below 1 ppm of NO2.
One such effect is the impairment of mucociliary clearance. The airway responds to
irritation by increasing mucus production. In laboratory animals, exposure to low
levels of NO2 results in either an increase in mucociliary clearance or has no
effect (217). However, at higher concentrations ciliary action was decreased in a
concentration dependent manner (218).
In addition to ciliary and mucosal alterations, clearance is also determined by
phagocytosis from resident lung cells such as alveolar macrophages as well as
recruited cells such as polymorphonuclear leukocytes. Exposures to supraambient
concentrations of NO2 result in structural, biochemical, and functional changes in
alveolar macrophages. Structural changes that have been reported include membrane
blebbing, the appearance of fenestrae, and loss of surface projections (219). While
these structural changes would be expected to effect cellular chemotaxis and/or
phagocytosis, their actual biological ramifications have yet to be determined. A
2576
AIR POLLUTION
SULFUR DIOXIDE
2577
While a number of studies have described effects from NO2 exposure on airway
responses (242256), the data for increased airway reactivity to specific allergen
challenges following NO2 exposure is more persuasive. Responses include increases
in eosinophil priming (as evidenced by an increase in eosinophil cationic protein),
inflammatory cells and immunoglobins, and enhanced airway responses to inhaled
allergens.
Both epidemiological and clinical studies have reported highly variable findings on
the effect of NO2 on lung function and airway reactivity. Based on this information, it is
possible that under the right conditions, certain individuals may be particularly
sensitive to NO2 exposures.
5.4 Potential Mechanisms of NO2-Induced Toxicity
A number of mechanisms have been proposed for NOx toxicity. One potential
mechanism is lipid peroxidation of unsaturated fatty acids in cell membranes (257).
Lipid peroxidation by reactive oxidant gases is an important mechanism of cellular
injury. NO2-induced lipid peroxidation has been demonstrated in studies measuring
exhaled ethane, as thiobarbituric acid reactive substances in tissues (258) and by
conjugated dienes in tissue homogenates. Increased ethane exhalation was reported in
rats exposed to 0.04 ppm NO2 for 9 or 18 months (259) while shorter durations
(1 week) increased exhaled ethane in rats exposed to 1.2 ppm (260).
Another proposed mechanism is the oxidation of critical proteins such as enzymes
leading to toxicological effects (261). Lastly, cellular injury may occur via interactions
with reactive metabolites of NOx. Clearly, much remains to be learned about the
complex chemistry of NOx and the resultant toxicological effects.
6 SULFUR DIOXIDE
6.1 Nature and Sources
Sulfur is prevalent in all raw materials, including crude oil, coal, and ore that contains
common metals such as aluminum, copper, zinc, lead, and iron. Sulfur oxide (SOx)
gases are formed when fuel containing sulfur is burned, gasoline is extracted from oil,
or metals are extracted from ore. The only forms of monomeric SOx of interest in
tropospheric chemistry are sulfur dioxide (SO2) and sulfur trioxide (SO3). SO3 can be
emitted from the stacks of power plants and factories; however, it reacts extremely
rapidly with H2O in the stacks or immediately after release into the atmosphere to form
sulfuric acid (H2SO4), which then partitions into the aqueous phase of particles. Thus,
only SO2 is present in the tropospheric boundary layer at concentrations significant for
atmospheric chemistry and human exposures.
SO2 is oxidized either in the gas phase or in the aqueous phase in cloud drops due to
its high water solubility. A comparison of the relative rates of oxidation by gas and
aqueous phase reactions indicates that only about 20% of SO2 is oxidized by gas phase
reactions; thus, SO2 is oxidized mainly by aqueous phase reactions (262). The rate of
2578
AIR POLLUTION
oxidation of SO2 to sulfate (SO42) ranges from 0.5% to 2% h1 as measured in
power plant plumes (263), resulting in an atmospheric lifetime ranging from about 2
days to about a week, with respect to this process. SO2 is removed from the atmosphere
by dry deposition to moist surfaces, resulting in an atmospheric lifetime with respect to
deposition on the order of 1 week, depending on humidity. These two processes,
oxidation and deposition, lead to an overall lifetime of SO2 in the atmosphere of a few
days.
Anthropogenic emissions of SO2 are mainly from combustion of fossil fuels by
electrical utilities (66%) and industry (29%), with transportation-related sources
making only a minor contribution (5%) in 2002 (264). Thus, most SO2 emissions
originate from point sources. However, these estimates are nationwide averages and
may not accurately reflect the contribution of specific local sources determining a
persons exposure to SO2 at any given location and time. For example, shipping and
associated in-port activities may be a significant source of SO2 in some coastal
cities (265).
The largest natural sources of SO2 are volcanoes and biomass burning. Even so, SO2
constitutes a relatively minor fraction (0.005% by volume) of total volcanic emissions (266). Volcanic sources of SO2 in the United States are limited to the Pacific
Northwest, Alaska, and Hawaii. Emissions of SO2 from burning vegetation are
generally in the range of 12% of the biomass burned (267). Sulfur is bound in
amino acids in vegetation and is released during combustion. Gaseous sulfur emissions
from this source are mainly in the form of SO2.
In addition to its role as an emitted primary pollutant, SO2 is also produced by the
photochemical oxidation of reduced sulfur compounds, for example, dimethyl sulfide,
hydrogen sulfide, and carbonyl sulfide. Emissions of reduced sulfur species are
associated typically with marine organisms living either in pelagic or coastal zones
and with anaerobic bacteria in marshes and estuaries. Except for carbonyl sulfide,
which is lost mainly by photolysis (atmospheric lifetime of 6 months), all the other
species are relatively short-lived, having lifetimes of the order of a few hours to a few
days. Emissions of sulfur from natural sources are small compared to anthropogenic
emissions within the United States. However, important exceptions occur locally as
the result of volcanic activity, wildfires and in certain coastal zones.
6.2 Trends in Sulfur Dioxide Levels
SO2 data collected from the State and Local Air Monitoring Stations and National Air
Monitoring Stations networks show that the decline in SO2 emissions from electric
generating utilities has improved air quality. These reductions are due, in large part, to
controls implemented under the U.S. EPA Acid Rain Program. U.S. EPAs trends data
(www.epa.gov/airtrends) reveal that the national composite average SO2 annual mean
ambient concentration decreased by 53% from 1990 to 2006, with the largest singleyear reduction coming in 19941995, the U.S. EPA Acid Rain Programs first
operating year (Fig. 52.22). For the years 20032005, the mean 24 h average and
annual average SO2 concentrations in the United States were 4 ppb, with maximum
values of >120 ppb for the 24 h average and 1415 ppb for the annual average. For
SULFUR DIOXIDE
2579
Concentration (ppm)
0.03
0.02
0.01
0.00
1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006
Year
FIGURE 52.22 SO2 air quality trends from 1990 to 2006 (based on annual arithmetic
average). Source:http://www.epa.gov/oar/airtrends/sulfur.html (from Ref. 316).
the monitors reporting a 1 h maximum in these years, the mean concentration was
13 ppb, with a maximum value of >600 ppb.
6.3 Health Effects
Controlled human exposure studies and epidemiological studies have observed
associations of short-term exposures to SO2, both peak 515 min exposures and
24 h average exposures, with effects on the respiratory system, ranging from increases
in respiratory symptoms and lung function decrements, and increasing in severity to
emergency department (ED) visits and hospitalizations for respiratory causes. These
effects were observed particularly in individuals with preexisting respiratory diseases,
children, and older adults (65 years). Epidemiological evidence is suggestive of
associations between SO2 and nonaccidental all-cause and cardiopulmonary-related
mortality, but additional research is needed to more fully establish underlying
mechanisms by which such effects occur. Health effects of long-term exposure to
SO2 have not yet been clearly established.
6.3.1 Morbidity Effects from Short-Term Exposure to SO2 Due to its high
solubility, SO2 is readily removed in the moist surfaces of the nose and other
respiratory passages. With quiescent nasal breathing, almost all inhaled SO2 is
removed in the extrathoracic (head) region. This limits the potential for direct effects
on the more sensitive thoracic regions of the respiratory tract. Factors that can increase
penetration of SO2 to these regions include oral and oronasal breathing, increased
ventilation rates and the presence of particles or fog droplets that may act as carriers for
SO2. In exercising humans, the pattern of SO2 absorption is expected to shift from the
upper airways to the tracheobronchial airways in conjunction with a shift from nasal to
oronasal breathing and associated increased ventilatory rates.
The predominant health response following peak exposure (515 min) to SO2 is
bronchoconstriction in asthmatics, which is associated with symptoms of wheezing,
2580
AIR POLLUTION
chest tightness, and shortness of breath. Studies of controlled SO2 exposures have
reported increased respiratory symptoms with SO2 concentrations of as low as 0.4
0.6 ppm in exercising asthmatic subjects (268270). One study with SO2-sensitive
asthmatics reported that respiratory symptoms (i.e., shortness of breath, wheeze, and
chest tightness) increased with increasing SO2 concentrations (0, 0.5, and 1.0 ppm
SO2) following exposures of 10 min with varying levels of exercise (269). It was also
observed that exposure to 0.5 ppm SO2 during light exercise evoked a more severe
symptomatic response than heavy exercise in clean air.
Studies have also consistently demonstrated decreases in lung function (e.g.,
decreased forced expiratory volume in 1 s (FEV1) and increased specific airways
resistance (sRaw)) following peak exposures to SO2. These effects have clearly and
consistently been shown to be exacerbated among individuals with asthma, with
asthmatics exhibiting significant decrements in lung function following 515 min
exposures to SO2 concentrations of as low as 0.40.6 ppm while performing moderate
levels of exercise (269, 271273). Increasing SO2 levels from 0 to 0.5 ppm has been
shown to have a greater effect on sRaw and FEV1 than increasing the level of
exercise (269). Studies have further observed significant decrements in lung function
in some sensitive asthmatics following 515 min exposures to SO2 concentrations of
as low as 0.25 ppm while performing moderate levels of exercise (271, 273).
Moderate-to-severe asthmatics have greater exercise-induced sRaw increases and
FEV1 decrements compared to mild asthmatics; however, respiratory response with
increasing SO2 concentration has not been shown to differ significantly between mild
and moderate/severe asthmatics (272).
Consistent associations have been observed between ambient SO2 concentrations
(generally 24 h average) and various respiratory health outcomes in recent epidemiological studies. Two important new multicity studies (132, 274) and several other
studies (208, 275) have shown an association between short-term ambient SO2
concentrations and respiratory symptoms in children. Several new studies (276
278) found no association between SO2 levels and respiratory symptoms in adults.
These findings suggest supportive evidence for an association between short-term
exposure to ambient SO2 exposure and respiratory symptoms in children, particularly
those with asthma, but not in adults. While controlled human exposure studies reported
decrements in lung function following peak 515 min exposures to SO2 at near
ambient levels 90.5 in exercising asthmatic adults, epidemiological studies did not
provide strong evidence of an association between short-term, 24 h average ambient
SO2 exposures and changes in lung function in either children (132) or adults (279).
Bronchoconstriction following SO2 is mediated by chemosensitive receptors in the
tracheobronchial tree. Rapidly adapting receptors (RARs) and sensory C-fiber receptors found at all levels of the respiratory tract are sensitive to irritant gases such as
SO2 (280, 281). Activation of these vagal afferents cause central nervous system
reflexes resulting in bronchoconstriction, mucus secretion, mucosal vasodilation,
cough, apnea followed by rapid shallow breathing and effects on the cardiovascular
system such as bradycardia and hypotension or hypertension (280283).
Early experiments demonstrated that SO2-induced reflexes were mediated by
cholinergic parasympathetic pathways involving the vagus nerve and inhibited by
SULFUR DIOXIDE
2581
2582
AIR POLLUTION
studies using a 10 ppm SO2 exposure regimen in mice found no effect on bactericidal
activity toward Staphylococcus aureus following acute (4 h) exposure (312, 313).
However, increased mortality rate and decreased survival time were observed in mice
that were exposed to the same dose for 1 day or 1, 2, or 3 weeks and then challenged
with an aerosol of Klebsiella pneumoniae (314).
6.3.2 Mortality Associated with Short-Term Exposure to SO2 Epidemiological
evidence is suggestive of associations between SO2 and nonaccidental all-cause
and cardiopulmonary-related mortality, but additional research is needed to more
fully establish underlying mechanisms by which such effects occur. Earlier studies,
including those using historical data from London and New York City air pollution
episodes, observed associations between SO2 and mortality; however, high levels
of SO2 were frequently accompanied by high levels of particulate matter, making it
difficult to resolve the relative roles of these two pollutants. The clearest mortality
associations were seen when both pollutants were at high levels (24 h average
values of both black smoke and SO2 exceeding 1000 mg/m3 (400 ppb for SO2)).
Recent epidemiological studies have reported associations between mortality and
SO2, often at mean 24 h average levels below 10 ppb. However, in the large
multicity time-series studies, the SO2 risk estimates were generally reduced
when copollutants, either particulate matter indices and/or NO2, were added in
the regression model. Thus, some extent of confounding among these pollutants is
suggested.
An intervention study from Hong Kong (315) supports the notion that a reduction in
SO2 levels results in a reduction in deaths, but this does not preclude the possibility that
the causal agent is not SO2 but rather something else that is emitted along with SO2,
such as the trace metals vanadium and nickel.
7 PARTICULATE MATTER
7.1 Nature and Sources
Particulate matter (PM) is a complex mixture of solid particles and liquid droplets that
range in shape and size. Particles are comprised of a number of components, including
acids, nitrates and sulfates, organic chemicals, metals, carbon, and biological material.
Some particles, known as primary particles are emitted directly from a source, such as
construction sites, unpaved roads, vehicles, smokestacks or fires. Others form via
complicated atmospheric reactions involving gases such as sulfur oxides and nitrogen
oxides that are emitted from power plants, industries, and automobiles. These
particles, known as secondary particles, are generally smaller in diameter than
mechanically derived particles.
As illustrated in Figure 52.23, particles typically measured in ambient air in the
United States are found to be in four general size modes, with overlapping tails of
distribution. The greatest mass of particles is in the two largest size modes, fine and
coarse particles, with an intermodal range between 1 and 3 mm. The distribution of
PARTICULATE MATTER
2583
8
Vapor
V/log Dp (m3/cm3)
Mechanically
generated
Condensation
6
Nucleation
5
4
ion
ion
lat
u
ag
lat
u
ag
Co
Co
1
0
0.001
0.01
0.1
1
Particle diameter, Dp (m)
Nucleation mode
10
100
Accumulation mode
Aitken mode
Coarse mode
Fine particles
Ultrafine particles
Coarse particles
FIGURE 52.23 An idealized size distribution showing fine and coarse particles and the
nucleation, Aitken and accumulation modes comprise fine particles. Also shown the major
formation and growth mechanisms of atmospheric particles.
particles that are above this range make up the coarse mode and the distribution of
particles that are below this range are fine particles. Fine particles can be subcategorized into three smaller size denominations: nucleation mode, Aitken mode, and
accumulation mode. Nucleation- and Aitken-mode particles comprise the ultrafine
PM size fraction. Ultrafine particles have the highest number distribution and the
greatest surface area compared to the larger particle size modes. Nucleation- and
Aitken-mode particles have relatively low mass and grow rapidly into accumulationmode particles, so they are not commonly observed or reported as separate modes in
volume or mass distributions.
Regulatory standards for fine particles often focus on particles with mass
median aerodynamic diameters (MMAD) less than 2.5 mm, or PM2.5. Numerous
agencies also monitor and regulate PM10, which refers to particles with MMAD less
than or equal to 10 mm; these particles are more likely to be inhaled past the
upper portions of the respiratory tract. The subset of coarse particles that are inhalable
(i.e., those able to penetrate the upper regions of the human respiratory system) is
thoracic coarse particles (PM102.5) and includes particles with MMAD between 2.5
and 10 mm.
2584
AIR POLLUTION
PARTICULATE MATTER
160
2585
National standard
Concentration (g/m3)
140
120
100
80
60
40
20
0
1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006
(a)
Year
30
Concentration (g/m3)
25
20
National standard
15
10
0
1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006
(b)
Year
FIGURE 52.24 (a) PM10 air quality from 1990 to 2006 based on annual second maximum
24 h average. The blue band represents the middle 80%, with the upper limit representing 90%
of sites with concentrations below that line, and 10% of sites having concentrations below the
bottom line. The white line represents the average among all sites. (b) PM2.5 air quality from
1999 to 2006 based on seasonally weighted annual average. The blue band represents the
middle 80%, with the upper limit representing 90% of sites with concentrations below that line,
and 10% of sites having concentrations below the bottom line. The white line represents the
average among all sites. The dashed line represents the national ambient air quality standard for
PM as of this writing.
2586
AIR POLLUTION
ET.
Extrathoracic
region Pharynx
Posterior
Nasal passage
Nasal part
Oral part
Larynx
Trachea
Main bronchi
Tracheobronchial
region
BB
Bronchi
Bronchioles
Bronchiolar region
Ai
Alveolar interstitial
Bronchioles
Terminal bronchioles
bb
Alveolar
region
tb
Ai
Respiratory bronchioles
Alveolar duct +
Alveoli
PARTICULATE MATTER
2587
cause-specific mortality than total mortality, but the confidence intervals may also
increase due to lack of available data for the less frequent causes of death (322, 325).
Fewer studies have evaluated associations with short-term exposure to PM102.5.
These associations are generally similar in magnitude to those for PM2.5,
although frequently statistically insignificant, possibly due to increased measurement
error in estimating PM102.5 exposure (319, 325). Limited research indicates that
there may be a relationship between short-term exposure to ultrafine particles and
mortality (331, 332).
7.3.3 Long-Term Exposure to PM
7.3.3.1 Mortality Associations between long-term (i.e., over months to years)
exposure to PM and mortality have been evaluated in several prospective cohort
studies, as summarized in EPA (325) and Pope and Dockery (322). Two large cohort
studies have provided key evidence for cardiopulmonary mortality effects, as both
have undergone extensive, independent reanalysis and are based on cohorts that were
broadly representative of the U.S. population (333, 334). The effect estimates
for deaths from all causes range from 5% to 25% increased risk per 10 mg/m3
PM2.5, while effect estimates for deaths from cardiopulmonary causes are somewhat
higher, 1040% per 10 mg/m3 PM2.5.
7.3.3.2 Respiratory Morbidity Several studies have reported associations
between long-term (e.g., averaged over months to years) PM2.5 exposure with increased
incidence of respiratory symptoms and decreased lung function growth (238, 335337).
A recent epidemiological study has also reported an association between long-term
PM2.5 exposure and a measure of atherosclerosis development (338) and progression,
which is consistent with that observed in animal toxicological studies (339, 340).
7.3.3.3 Cancer A few epidemiological studies have also reported associations
between long-term exposure to PM and incidence of lung cancer (341, 342). Lung
cancer mortality is also associated with PM2.5 exposure, as evidenced by results that
demonstrate a 1015% increase per 10 mg/m3 PM2.5 for people living in more
polluted cities compared to cleaner cities (334). As discussed later, some PM
components, particularly PAHs, have mutagenic or genotoxic properties that
provides biological plausibility for the observed PM associations with cancer
incidence and mortality.
7.3.4 Fetal and Infant Development/Mortality Recent reviews of the literature
have concluded that there is some evidence linking exposure to PM and respiratory
deaths in the postneonatal period (343, 344). Exposure to several air pollutants has
been associated with increased risk of preterm births and intrauterine growth
retardation, although the evidence is insufficient to infer causality (344, 345).
Suggestive evidence for associations with low birth weight has also been reported,
although the findings were less consistent. The associations reported for adverse
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AIR POLLUTION
birth outcomes are generally rather small, and there are challenges in interpreting
this body of evidence (325). Toxicological studies employing PM to examine birth
outcomes are scarce.
7.4 Mechanisms
As discussed above, epidemiological evidence has played a key role in identifying the
effects associated with ambient PM, as well as in policy and regulatory decisions to
control PM. More recently, studies have focused on potential pathways for the
observed cardiopulmonary effects of PM. Generally these studies have employed
PM2.5 or PM10; the evidence discussed in this section is largely derived from PM2.5
studies. Recent toxicological studies have provided important insights that support the
effects observed in community health studies. Despite the progress made in this area,
specific mechanisms have yet to be elucidated.
The available evidence supports numerous hypotheses regarding induction of PM
effects. It appears unlikely that the complex particle mixture in ambient air would act
alone through any single pathway of response. Accordingly, it is plausible that several
physiological responses might occur in concert to produce reported health endpoints.
It should be recognized that, for the most part, the evidence from toxicological and
controlled human exposure studies discussed below reflects the effects of PM2.5 or
PM2.5 constituents, with substantially less data available on the potential mechanisms
of action for larger particles, such as thoracic coarse PM.
Toxicological studies have used a variety of particle types or surrogates of ambient
particles to evaluate potential mechanisms of PM toxicity. These include acid aerosols,
fly ash from coal- or oil-fired power plants (such as residual oil fly ash), diesel, and
crustal materials (e.g., Mt. St. Helens volcanic ash and road dust). More recently,
concentrated ambient particles (CAPs) have been employed, as well as ambient PM
collected on filters from monitoring stations. The CAPs exposure systems take outdoor
PM and enhance the concentration using virtual impactor or centrifugal technology;
this enables real-time exposure of human volunteers or animals to atmospheric PM and
gases (although the gases are not concentrated).
7.4.1 Effects on the Cardiovascular System Both acute and chronic PM exposures have been implicated in the observed cardiovascular morbidity and mortality
effects. These effects are linked to systemic inflammation, oxidative stress, and
mediation by the autonomic nervous system. The development and progression of
atherosclerosis is a relatively new research focus in the PM field and may partially
explain some of the epidemiological findings. Particle properties (e.g., soluble metals,
endotoxin, organic compounds, and surface composition) play a role in the physiological response, although the exact role(s) for these characteristics is yet to be fully
determined. In addition, ultrafine PM may cross the alveolarblood barrier and
translocate into the circulation, but evidence supporting this is inconclusive and quite
controversial in the PM research field. Figure 52.26 schematically illustrates hypothesized mechanisms thought to be involved in cardiovascular responses to PM
PARTICULATE MATTER
2589
CNS
Brainstem
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PM
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ut
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ou
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o
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ar
Problematic for
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cardiac arrythmias.
COPD, etc.
Blockage of
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2590
AIR POLLUTION
destabilization (346, 351, 353). As one part of this pathway, inflammatory cytokines
induce tissue factor, which may cause endothelial cells to change from an antithrombitic to a procoagulant, clot-promoting state (354). Endothelial activation results
in the upregulation of adhesion molecules, which initiates local vascular inflammation with the recruitment of circulating leukocytes and monocytes (351, 354).
Furthermore, it has been hypothesized that stimulation of the bone marrow results
in increased release of monocytes that can participate in atherogenesis (355, 356). In
this manner, cells can enter the inflamed tissue and induce plaque formation.
PM exposure could promote hypercoagulation and hemostasis, possibly through
endothelial injury that results in platelet activation and subsequent platelet aggregation (352). Plaques may become prone to rupture with continued systemic inflammation via (1) upregulation of matrix metalloproteinases that break down collagen in
fibrous caps and/or (2) increases in CRP (346). Investigators have demonstrated that
animals exposed to PM can have increased plaque size in the aorta (340, 357) and
advanced atherosclerotic lesion phenotypes in coronary arteries (357), which may
lead to plaque instability.
The endothelium is an important regulator of vascular function, including blood
flow, coagulation, fibrinolysis, and inflammation. Vascular tone is primarily controlled
by production of nitric oxide, prostaglandins, and endothelins (ET). Endotheliumdependent alterations in vasodilation and vasoconstriction have been observed
following PM exposure, which have been linked to inhibition or decreased production
of NO and elevated levels of ET-1, respectively (346, 349, 354). It appears that
pulmonary inflammation is not a prerequisite for these vasomotor changes (348, 349).
Atherosclerosis development, acute coronary syndromes, and myocardial infarction
could all be consequences of endothelial dysfunction.
Thus, potentially dangerous alterations in systemic responses due to PM exposures
could be signaled by even small PM-related (a) changes in blood coagulation cascade
indicators, for example, increased blood platelet, fibrinogen, or Factor VII, or
decreased tissue plasminogen activator levels; (b) increased CRP or circulating
cytokines involved in the acute phase response; (c) upregulation of adhesion
molecules, such as vascular cell adhesion molecule-1 (VCAM-1), intracellular
adhesion molecule-1 (ICAM-1), and E-selectin; and/or (d) impairment or enhancement of vasomotor activity.
Neurological mechanisms have also been proposed to explain PM effects on the
cardiovascular system (325, 354). It has been suggested that inhaled particles
stimulate pulmonary vagal afferents, which induce changes in autonomic control
of heart rate. Heart rate and blood pressure changes have been detected following
exposure to PM in humans and animals, but overall, the findings are inconclusive (325).
Pathophysiological changes in cardiac function can be detected by electrocardiographic recordings, with certain ECG parameters (e.g., heart rate variability or
HRV) recently gaining widening use as indicators of PM-induced cardiac effects.
When appropriately designed and carefully interpreted, studies utilizing measures of
HRV provide insight into the relationship between the perturbation of the internal or
external environment and subsequent changes in the modulation of autonomic neural
input to the heart. Generally, decreases in HRV measurements are observed following
PARTICULATE MATTER
2591
2592
AIR POLLUTION
PARTICULATE MATTER
2593
2594
AIR POLLUTION
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