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Assessing Exposure to Air Toxics Relative to Asthma Clifford P. Weisel Environmental and Occupation Health Sciences Institute, University
of Medicine and Dentistry of New Jersey--Robert Wood Johnson Medical
School, Piscataway, New Jersey, USA
Abstract Asthma is a respiratory disease whose prevalence has been increasing since the mid 1970s and that affects more than 14.6 million residents of the United States. Environmental triggers of asthma include air pollutants that are respiratory irritants. Air toxics emitted into the ambient air are listed in the 1990 Clean Air Act Amendments as hazardous air pollutants (HAPs) if they can adversely affect human health, including the respiratory tract. HAPs include particulate and gaseous-phase pollutants, individual organic compounds and metals, and mixtures. Associations between asthma exacerbation and both particles and indoor volatile organic compounds (VOCs) , often referred to as indoor air quality, have been reported. Studies conducted in the United States, Canada, and Europe over the past two decades have shown that most people living in the developed countries spend the majority of their time indoors and that the air concentrations of many air toxics or HAPs are higher indoors than in the ambient air in urban, suburban, and rural settings. Elevated indoor air concentrations result from emissions of air toxics from consumer products, household furnishings, and personal activities. The Relationship of Indoor, Outdoor and Personal Air (RIOPA) study was designed to oversample homes in close proximity to ambient sources, excluding residences where smokers lived, to determine the contribution of ambient emissions to air toxics exposure. The ratios of indoor to outdoor air concentrations of some VOCs in homes measured during RIOPA were much greater than one, and for most other VOCs that had indoor-to-outdoor ratios close to unity in the majority of homes, elevated ratios were found in the paired samples with the highest concentration. Thus, although ambient emissions contribute to exposure of some air toxics indoors as well as outdoors, this was not true for all of the air toxics and especially for the higher end of exposures to most volatile organic air toxics examined. It is therefore critical, when evaluating potential effects of air toxics on asthma or other adverse health end points, to determine where the exposure occurs and the source contributions for each air toxic and target population separately and not to rely solely on ambient air concentration measurements. Key words: ambient emissions, exposure, indoor air, particles, RIOPA study, VOC, volatile organic compounds. Environ Health Perspect 110(suppl 4) :527-537 (2002) . http://ehpnet1.niehs.nih.gov/docs/2002/suppl-4/527-537weisel/abstract.html |
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This article is part of the monograph Environmental Air
Toxics: Role in Asthma Occurrence?
Address correspondence to C.P. Weisel, EOHSI, University
of Medicine and Dentistry of New Jersey--RWJMS, 170 Frelinghuysen Rd., Piscataway,
NJ 08854 USA. Telephone: (732) 445-0154. Fax: (732) 445-0116. E-mail: weisel@eohsi.rutgers.edu
I thank the Mickey Leland National Urban Air Toxics Research
Center (contract 96-01A/P0818769) and the Health Effects Institute (contract
98-23-3) for support of the RIOPA project and the National Institute of Environmental
Health Sciences Center for Excellence (ES-05022); Drs. Turpin, Zhang, Morandi,
Stock, Colome, and Spektor for collaborative efforts; K. Mohan for VOC analyses;
S. Alimokhtari and J. Kwon for sample collection; and the residents of Elizabeth,
NJ, who participated in the New Jersey RIOPA project.
Received 30 November 2001; accepted 4 April 2002.
Introduction
Asthma is a common respiratory disease that affects children and adults but
is without a universal definition because of a poor understanding of its causes,
natural history, and pathology (1). It is characterized by chronic inflammation
with infiltration of lymphocytes, eosinophils, and mast cells and thickening
and disorganization of tissues of the airway walls, broncoconstriction, mucus
secretion, and increased airway responsiveness to stimuli. These respiratory
responses result in the narrowing of the airways, causing difficult in breathing
(1). Asthma is a chronic disease whose prevalence has been increasing
since the mid 1970s, affecting more than 14.6 million individuals within the
United States (2). The cause of the increased prevalence has not been
definitively established. Environmental agents, along with genetic considerations,
have been suggested as both causing asthma and exacerbating existing conditions.
Environmental agents include antigens from dust mites, cockroaches, and mold,
weather condition changes, and air pollutants such as the criteria pollutants
ozone, sulfur dioxide, particulate matter (PM), and nitrogen dioxide and hazardous
air pollutants (HAPs) (3). Although the evidence for a causal association
between air pollutants and asthma is weak, evidence for exacerbation of asthma
by air pollutants, particularly the criteria pollutants, has been reported for
controlled clinical trials and epidemiologic studies (3-9). Few
studies have examined the role of ambient HAPs on asthma exacerbation. Individual
HAPs are present in the ambient environment at significantly lower concentrations
than the criteria pollutants and are often present at higher concentrations
in indoor air than in outdoor air. The presence of criteria pollutants along
with HAPs in the ambient air of cities makes it difficult to distinguish the
effects of HAPs from those of the criteria pollutants or to determine if there
is an interactive effect.
The ambient concentrations of many air pollutants have declined in urban areas
of developed countries, whereas the incidence of reported asthma has increased.
This suggests that these air pollutants are not the cause, or only cause, of
asthma, although this does not preclude their role in asthma exacerbation. Many
of the compounds listed as HAPs are included because of cancer end points due
to chronic exposures, but others have noncancer end points for acute and chronic
exposure, including effects on the respiratory system (10,11). Compounds
with noncancer, acute end points include oxygenated volatile organic compounds
(VOCs; e.g., aldehydes, ethers, and oxides), reactive VOCs (e.g., acrolein,
hydrazine, and phosgene), and organic and inorganic acids (10). Additional
HAPs have reported respiratory effects for chronic exposures and at high concentrations
are respiratory irritants. HAPs can produce nonspecific respiratory responses.
Thus, the combined concentrations may need to be considered when evaluating
asthma exacerbation and not just exposure to individual compounds. It has been
known for more than a decade that exposures to the mixture of VOCs present in
indoor air, which include many HAPs such as aromatic and chlorinated organic
compounds, can irritate the mucus membrane in the respiratory tract in both
healthy and sensitive individuals (12). Whether individual HAPs penetrate
into the lungs and can potentially affect asthmatic individuals, or only affect
the upper portion of the respiratory tract because of solubility considerations,
needs to be considered in extrapolating respiratory irritation to asthma exacerbation.
Further, differences in exposures by location and cumulative exposure of multiple
HAPs that may have the same mechanism of action should be considered in the
evaluation of potential adverse effects of HAPs on asthmatic individuals.
Physical activity level is also an important consideration in determining
the dose of an air pollutant. Physical exertion increases breathing rates and
causes pollutants to penetrate deeper into the lungs. Physical activity has
been shown to cause greater symptoms in asthmatic individuals exposed to ozone
than when they are at rest (13). Physical activity occurs outdoors more
frequently than indoors. Therefore, a final evaluation of the association between
asthma exacerbation and air pollutants should consider not only differences
in concentration with location but also the activity level in each location.
This does not address the issue of how physical activity varies with location,
microenvironment, and time of year and its role in exposure and asthma. Rather,
it is a review of the magnitude of HAP exposures in different locations to help
provide guidance in understanding the potential role of ambient air concentrations
of HAPs on asthmatic individuals and to establish sources of HAP exposures.
Concepts of Exposure
Human exposure to air toxics occurs when individuals breathe air containing
these constituents. The concentrations of air toxics vary with time and location,
and as people move among locations and activities, the resultant exposure changes.
Further, the contributions by different sources to exposure to air toxics vary
with location. The amount of pollutant delivered to the lung depends on the
person's breathing rate. Thus, activity level can be an important consideration
in determining the potential exposure and dose delivered to the lung, the site
of concern for asthmatic individuals. Inhalation exposure has been defined as
the integral of the concentrations as a function of time over the time period
of interest for each individual (14):
[1]
where E is exposure, c(t) is the concentration being
encountered as a function of time, and t1 and t2 are the starting and ending time of the exposure, respectively.
When determining exposure, it is therefore important for investigators to
measure the air concentrations of air toxics reaching individuals or a population
and not just the concentration in the ambient atmosphere, if it is possible
that the two may differ. Two approaches, direct and indirect, have been taken
to measure inhalation exposure (15). With the direct measurement method
a personal monitor is worn in the breathing zone to either continually collect
for subsequent analysis or directly measure the concentration of the pollutant
for the defined exposure period. The indirect method uses measurements of the
air concentrations in all the locations or "microenvironments" encountered by
an individual or population and determines, typically with diaries, the amount
of time spent in each microenvironment. The concept of microenvironments is
also critical in developing procedures for exposure modeling and recognizes
that people are mobile and that concentrations of air toxics are not the same
in all locations. Microenvironments have typically been defined as individual
or aggregate locations or even as activities taking place within a location,
where a homogeneous concentration of the target pollutant exists. This concept
of a microenvironment is one of a perfectly mixed or idealized compartment of
classical compartmental modeling. Because microenvironments can have gradients
in air toxic concentrations, particularly when sources exist in the microenvironment,
more recent and general definitions view the microenvironment as a volume of
air that can be fully characterized by a set of either mechanistic or phenomenologic
governing equations, when properly parameterized, given appropriate initial
and boundary conditions (16).
Microenvironments used to determine air toxics exposures typically include
indoor residences, indoor work environment, other indoor locations, outdoors
near residences, other outdoor locations, and in vehicles. The in-vehicle microenvironment
is often segregated from other locations because of air toxic emissions from
mobile sources. Indoor residences, indoor work environment, and outdoors near
residences are typically separated from other indoor and outdoor locations because
of the time spent there and potential differences between the residential, work,
and public environments. The exposure in a microenvironment is calculated using
a formula analogous to Equation 1 but as the sum of the discrete product of
"representative" concentrations for the individual or activity being examined
in that microenvironment times the duration of time spent there:
[2]
where i are microenvironments from 1 to n, ci is the concentration in the ith microenvironment, and ti is the duration spent in the ith microenvironment. The daily exposure
is the sum of the exposures in all microenvironments encountered within a day.
The exposure calculated is representative of the true exposure provided that
all microenvironments that contribute significantly to the total exposure are
included and the concentration assigned to the microenvironment is appropriate
for the time period spent there. In addition to measurement of exposure, exposure
modeling is employed for both individuals and populations. Exposure modeling
is used to determine exposures to large populations because it often is not
financially practical to make a sufficient number of exposure measurements to
completely characterize the spatial and temporal range of exposures in large
populations, and to predict what changes in emissions or activities are most
effective to obtain reduced exposure. A discussion of the underlying principles
of exposure modeling is beyond the scope of this article. However, it is important
for investigators, when examining an association between exposure to air toxics
and an adverse health effect, to determine how best to reduce emissions of HAPs
to establish where exposures occur and their sources. Thus, as discussed in
this article, a complete evaluation of exposure is necessary, and not solely
a measure of ambient air concentrations and emissions.
Ambient Air Toxics and Asthma
The 1990 Clean Air Act Amendments (17) list 188 HAPs or air toxics.
These include heavy metals (predominantly particulate components, except for
mercury, which has a gaseous phase), organic compounds (which include both volatile
and particulate components), and pesticides (18). HAPs are emitted into
the ambient air from thousands of sources, including large and small stationary
sources, area sources, and mobile sources. The HAPs emitted to the ambient air
result in potential inhalation exposure in urban settings where they are emitted
or when transported through regional, national, or global air sheds, depending
on their atmospheric residence time. Although much of the focus of health concerns
on HAPs has been toward cancer end points, some of the agents can be respiratory
irritants that may exacerbate or potentially cause asthma. On a broad scale,
in 1993 3.7 million tons of HAPs were emitted, with approximately 41% from mobile
sources, 35% from area sources, and 24% from point sources (18). A comparison
of emissions by state shows that, as expected, industrial and highly populated
areas have the highest emissions. The largest sources of HAPs are mobile sources--on-road
vehicles--that emit acetaldehyde, benzene, 1,3-butadiene, formaldehyde, toluene,
xylenes, and particles.
Chemicals are classified as air toxics because of suspected associations with
adverse health outcomes, including respiratory problems. Nearly 50 million people
are estimated to live in locations where the estimated ambient concentrations
of one or more HAPs exceed levels of concern for noncancer health effects in
humans (19). Environmental agents that may provoke bronchospasm attacks
include irritant gases, inorganic particles, allergens, and infections (20).
It is less clear whether the same environmental factors also cause asthma. There
are both seasonal patterns and day-to-day variations in asthma exacerbation.
Although the seasonal variability is likely related to respiratory virus infection,
the day-to-day variations may be more closely associated with environmental
factors, including air pollution. Higher prevalence of asthma and allergic disease
and greater number of admissions to hospitals and clinics for asthma attacks
have been reported among children living close to busy roads or heavy truck
traffic (21-23). Such an association would suggest that ambient
emissions of air toxics or particulate matter (PM) may aggravate asthma. Other
studies, however, have not found an association between asthma diagnosis, treatment,
or hospital admissions and living close to traffic (24,25).
Indoor Air Toxics and Asthma
It has been proposed that asthmatic symptoms may be caused by indoor VOCs
and formaldehyde (26-28). A European Community respiratory health
survey was used to identify individuals with (n = 47) and without (n
= 41) asthma for whom an exposure assessment was done (26). Both
apartments and single-family homes with a variety of heating sources were included.
Indoor tobacco smoking was reported in 21% of the homes. Presence of dust mites
and visible signs of dampness or microbial growth were significantly related
to asthma symptoms. Nocturnal breathlessness was found to be associated with
the presence of wall-to-wall carpeting and formaldehyde concentration, which
was presumably from indoor sources. Increases in a variety of symptoms related
to asthma were significantly associated with concentrations of total VOCs, formaldehyde,
and various subclasses of VOCs (substituted aromatic compounds), n-alkanes,
terpenes, butanols, and low-boiling-point hydrocarbons). However, correlations
were also identified between the VOCs and the presence of dust mites, which
could have confounded the results. One suggested explanation for the stronger
association between indoor air quality and nocturnal breathing symptoms compared
with daytime asthma symptoms was the greater amount of time spent at home during
the night than during the day. Other explanations included higher nighttime
indoor air concentrations and greater susceptibility to symptoms at night. VOCs
emitted from newly painted surfaces have been reported to be associated with
asthmatic symptoms in painters (27) and residents (28). Associations
of VOC exposures at air concentrations of 25 mg/m3 with both inflammation
and obstructive reaction in airways have been found in controlled chamber studies
(29,30). The controlled chamber air concentration was higher than that
measured in homes where relationships between asthma and VOCs have been reported,
but the exposure time was shorter. Formaldehyde has been observed to cause abnormal
variability in peak expiratory flow (31), but there have been inconsistent
reports on its role in exacerbating or causing asthma (32-34). Environmental
tobacco smoke has also been identified as an indoor environmental trigger for
many asthma patients, although there is only limited documentation of the effects
of passive smoke on asthma (35,36). Environmental tobacco smoke contains
a large number of air toxics (37). It is suggested that the role of passive
smoking as an initiator is related more closely to transient "wheezy bronchitis"
than to "allergic asthma." Its association with symptom prevalence and asthma
severity in school age children probably reflects a role as a trigger of symptomatic
episodes. Passive smoking increases exposure to both particles and volatile
organic air toxics and is a major source of indoor air pollution. Proximity
to industrial emissions of VOCs has been linked to increased asthma (38).
These studies suggest that various HAPs (e.g., aromatic hydrocarbons, formaldehyde,
diesel particles) or combinations can exacerbate asthma.
Duration of Exposure and Asthma Exacerbation
It is unclear whether short peak exposures to lung irritants of minutes or
longer exposures of hours to days, or both, may be responsible for reported
associations between asthma symptoms and air pollution. Because of the low air
concentrations of air toxics, sampling duration is typically 12-48 hr.
Thus, short-term variations in concentrations are not well characterized. Studies
using real-time measurements of particles have demonstrated that concentrations
of particles and specific components such as polyaromatic hydrocarbons (PAHs)
have temporal and spatial variability associated with being close to ambient
sources such as diesel emissions at roadways (39,40), and with a variety
of household activities such as cooking and vacuuming, as well as being a function
of air exchange rate (41,42). A study of indoor air concentrations of
emissions associated with cigarette smoke found large gradients in air concentrations
of particles within a room as cigarettes were smoked (43). The existence
of short-term variations in air toxics occurs when individuals are in close
proximity to localized sources or within indoor settings that have active emission
sources. Thus, peak exposure excursions occur that are several times higher
than the concentration measured in integrated samples over 12-48 hr. If
brief exposures to high concentrations are important in the exacerbation or
causation of asthma, many of the existing sampling protocols and exposure studies
do not adequately define those exposures.
Population-Based Air Toxics Exposure Studies
A series of studies called the the Total Exposure Assessment Methodology (TEAM)
Study were conducted between 1979 and 1985 to determine exposure to air toxics
on a population basis and to assess the influence of ambient sources on that
exposure (44). The TEAM study goals were to develop methods to measure
total exposure of individuals via air, water, and food and the resulting body
burden from exposure and to apply those methods, within a probabilistic-based
sampling framework, to measure air toxics exposure in several U.S. cities. No
health data on asthma were collected during the TEAM study, so it is not possible
to establish from the TEAM studies whether exposure to air toxics affected asthmatic
individuals. However, the TEAM and other exposure studies can be used to establish
where air toxics exposures occur and the source of those air toxics. This information
can be used to evaluate the role of ambient air toxic emissions on exposure
and, for those air toxics documented to adversely affect asthmatic individuals,
whether ambient emissions are potentially important contributors to exacerbation
or causation of asthma.
VOC Exposures
The original scope of the TEAM study included evaluation of four groups of
chemicals that included different types of air toxics: VOCs, semivolatile organic
compounds (pesticides and polychlorinated biphenyls), metals, and PAHs. Because,
in 1979, the most comprehensive sampling and measurement methodologies existed
for the VOCs, that group of compounds was the focus of the initial TEAM study.
VOCs were measured in personal air, fixed-site air, and in breath and water
samples in New Jersey, California, North Carolina, and North Dakota. Paired
12-hr personal air and outdoor air samples, one during the day and a second
during the night, were collected. Although it has not been definitively demonstrated
that the individual VOCs measured affect asthmatic individuals, the total loading
of VOCs indoors, as discussed above, has been found to exacerbate asthma when
the indoor air quality is poor. The relative importance of ambient and indoor
exposures and sources of the VOCs and other air toxics should be considered
in any plan to reduce emissions for compounds thought to exacerbate asthma.
To illustrate how exposure to HAPs varies by microenvironment and region,
the weighted estimates or median values of the personal air concentrations are
presented in Tables 1-3. The overall pattern observed for the VOCs is similar
to that of many but not all HAPs. The median values of the personal air concentrations
exceeded those in outdoor air during all seasons for nearly all compounds in
urban centers in New Jersey and California, in a suburban community in North
Carolina, and in a rural area of North Dakota (Tables 1-3). Estimated frequency
distribution plots prepared for each compound showed that the personal air concentrations
were predicted to exceed the outdoor air concentrations during both the day
and night for all the air toxics across the majority of the population in each
study area (44-48). The observation that the personal and indoor exposures
exceeded--often greatly--the outdoor VOC air toxic concentrations was a major
finding of the TEAM study. This led to the "conclusion that indoor air in the
home and at work far outweighs outdoor air as a route of exposure to these chemicals"
(44).
A major reason for the observed differentials between personal/indoor air
concentrations and outdoor air concentrations in the TEAM and subsequent studies
is the close proximity of individuals to small emissions in different locations
and during different activities combined with the limited volume of indoor environments
compared with the dilution that occurs outdoors. Emissions within enclosed spaces
result in higher indoor and personal concentrations than in outdoor concentrations
even though the mass of emissions of the air toxics to the ambient air is much
greater. In addition to collecting air samples, the TEAM study included a questionnaire
that was completed by each participant regarding his or her activities and duration
spent in different locations. Stepwise regression analyses were conducted for
each compound to attempt to evaluate specific activities or locations that could
have contributed to the observed exposures. Specific sources of exposures identified
included smoking (aromatic compounds); use of hot chlorinated water (chloroform);
use of air fresheners, deodorizers, or moth crystals (p-dichlorobenzene);
and travel by and refueling an automobile (aromatic compounds). The TEAM studies
clearly indicated that exposures to volatile organic air toxics occur in places
other than outdoors and that sources of volatile organic air toxics other than
ambient emissions contribute significantly to exposure.
A more recent probabilistic population-based study to assess the U.S. nationwide
exposure to multiple contaminants, including air toxics, is the National Human
Exposure Assessment Survey (NHEXAS) (49). A feasibility pilot was conducted
in three location: U.S. Environmental Protection Agency (U.S. EPA) Region 5
(Midwest); Arizona; and Baltimore, Maryland. Results reported for VOCs in Arizona
were similar to those found during the TEAM study (50). The concentrations
were typically log-normally distributed, with indoor concentrations higher than
outdoor concentrations (Table 4). Besides environmental tobacco smoke, having
an attached garage, and use of spot remover and cleaning solvents were identified
as sources of volatile organic air toxics in the U.S. EPA Region 5 portion of
NHEXAS (51).
PM Exposure
Many of the air toxics listed as HAPs are attached to PM (e.g., metals, semivolatile
and nonvolatile organic compounds, VOCs, and pesticides). PM, in the form of
environmental tobacco smoke and diesel emissions, has been suggested as an environmental
trigger of asthma, although it has not been confirmed whether it is the PM or
the individual components present, such as the air toxics, that exacerbate asthma.
The mechanisms that control the production and transport of particles differ
from those of VOCs. The particle size range of the air toxics is important when
investigators consider whether a particle will penetrate into the lung when
inhaled and its lifetime within and transport through different microenvironments.
Particles less than 10 µm can be inhaled, with various cutoff size fractions
examined in different studies. Wallace (52) summarized three major U.S.
studies conducted to understand population-based exposure to PM. These are the
Harvard Six-Cities Study conducted between 1979 and 1988 that made measurements
in 1,400 homes (53), the New York State Energy Resources and Development
Authority (ERDA) study conducted in 1986 in 433 homes,(54) and the Particle
TEAM (PTEAM) study conducted in 1990 in 178 homes (55-57). Within
the Harvard Six-Cities Study, the mean mass concentration of particles below
3.5 µm was higher in the indoor air than in the outdoor air in five of
the six cities. The major source of indoor PM was cigarette smoke, contributing
more than 25 µg/m3 additional mass to the indoor air (58).
As indicated previously, environmental tobacco smoke is an environmental trigger
of asthma. The source contributions of the indoor PM were reconstructed using
principal component and linear regression analyses of the elemental data, measured
by X-ray fluorescence analysis. Soil, wood smoke, sulfur-related particles,
mobile emissions, indoor dust, industrial emissions (steel and iron), and an
unexplained component contributed to the indoor air concentration of PM. The
proportion associated with each source varied with the sample being collected
from a smoker versus nonsmoker home or outdoors versus indoors and with season.
Ambient particles penetrate indoors, but deposition of particles occurs, with
greater losses for larger particles (59). In nonsmoker homes the ratios
of indoor to outdoor air concentrations of PM mass during the summer were near
1.0, whereas in the winter they were higher (1.04-1.4) depending on the
city. Similar results were obtained from the ERDA study, with the indoor particulate
matter having a mass median aerodynamic diameter less than 2.5 µm (PM2.5),
approximately double the outdoor concentrations, and smoking increasing the
indoor concentration [Sheldon et al. (54) as reported by Wallace (52).
The ERDA study focused on different combustion sources in the home and found
that, besides smoking, only kerosene heaters elevated indoor PM levels. Wood
stove/fireplace and gas stove use did not have a significant effect on the indoor
PM air concentration.
Although total mass of particles is not classified as an air toxic, PM contains
air toxics. Transport phenomenon governing total mass will also apply to the
particulate air toxics of the same size range. A knowledge of the sources contributing
to production and the transport of PM is therefore important in understanding
exposure to air toxics. Further, particle loading and chemical irritants contained
on the surface of particles may affect asthmatic individuals differently, so
source contributions should be considered in epidemiologic studies of asthma.
Wallace (52) used the PTEAM data to calculate the fraction of outdoor
particles found indoors at equilibrium. He estimated that the fraction of outdoor
fine particles (PM2.5) in indoor air was 0.7 ± 0.2, with an
expected range from 0.3 to 0.95 and 25th, 50th, and 75th percentiles of 0.6,
0.7, and 0.8, respectively. The fraction of outdoor PM10 (particulate
matter with a mass median aerodynamic diameter less than 10 µm) entering
the home was approximately 20% less than that for the fine particles. The fraction
of particles that actually infiltrate into an individual home is a function
of their deposition rate and removal processes as the air infiltrates into the
home. In addition, air exchange rate can alter the proportion of the indoor
particle concentration associated with ambient sources because higher air exchange
rates typically increase infiltration rates and decrease the buildup of PM from
indoor sources. Lower air exchange rates and tighter homes would lower the proportion
of particles in the home from outdoor sources. Personal air concentrations of
particulate air toxics are often higher than the outdoor levels, resulting in
higher exposures than what is measured at outdoor monitoring stations. The concentration
of PM air toxics attributed to ambient derived PM would then be lower than outdoor
concentrations, particularly for air toxics on larger particles, even though
the total exposure is greater.
Speciation of PM
PM sources associated with combustion and resuspension are expected to increase
the indoor and personal air concentrations of not only PM mass but also air
toxics. Cigarette smoke and other combustion processes produce particles containing
PAHs and metals that are classified as HAPs. Resuspended dust will include a
combination of deposited ambient aerosols and particles generated by activities
that can mobilize heavy metals (e.g., lead from paint or tracked in from soil)
(60), PAHs (61), and pesticides from residential or outdoor applications
(62,63). These indoor processes contribute to particulate air toxics
exposures. For example, smoking, construction, cleaning (sweeping, vacuuming,
dusting), and use of combustion sources were factors contributing to indoor
air particulate concentrations and individual air toxic metal concentrations
(lead, arsenic, and cadmium) in the NHEXAS U.S. EPA Region 5 study (51).
A number of other recent studies have collected samples that are expected to
provide data on particulate air toxics [Air Pollution Exposure Distributions
of Adult Urban Populations in Europe (EXPOLIS) (64), The Relationship
of Indoor, Outdoor and Personal Air (RIOPA) study, and the TEACH (Toxic Exposure
Assessment, a Columbia/Harvard) study (65). These studies have included
measurements of a range of air toxics in indoor, outdoor, and personal air.
The ranges of air concentrations of the pesticides measured during NHEXAS
in Arizona were higher indoors (chlorpyrifos `3.2-3,280 ng/m3, diazinon
< 2.1-20,500 ng/m3) than outdoors (chlorpyrifos < 3.2-22.5
ng/m3, diazinon < 2.1-131 ng/m3). Pesticides in indoor
air result not only from the direct emissions during application but also from
evaporation into the air from applied surfaces or resuspension of particles
on which pesticides are deposited. Summary data presented by Gordon et al. (50)
had consistent ranges and median concentrations across different seasons in
Florida, Massachusetts, and Texas. Thus, as was found for the VOCs, air toxic
pesticide exposures are elevated because of their use indoors.
Carbonyl Exposures
Some carbonyl compounds are respiratory irritants (66), including formaldehyde
and acetaldehyde, the two most frequently measured aldehydes (67). Formaldehyde,
acetaldehyde, and acrolein ambient air concentrations were modeled in the Cumulative
Exposure Project based on ambient emissions. The Cumulative Exposure Project
was undertaken by the U.S. EPA to estimate exposure to outdoor air concentrations
for a large portion of the HAPs using emission rate data and information on
populations from individual census tracts (68). The calculated ambient
air concentrations were above levels set to protect the population from a potential
health risk (10). In addition to the outdoor emissions, formaldehyde
and acetaldehyde have multiple indoor sources from off-gassing of common materials
and glues used in construction and furnishings (69). Paired indoor and
outdoor air concentrations of nine aldehydes, including formaldehyde and acetaldehyde,
from samples taken in New Jersey homes showed that the indoor air concentrations
exceeded the outdoor levels for all compounds except propionaldehyde, indicative
of indoor sources (67). The mean ± standard deviation, 75th percentile,
and maximum indoor and outdoor air concentrations for formaldehyde were 55 ± 20, 67, and 102 ppb and 13 ± 9, 20, and 34 ppb, respectively, whereas for
acetaldehyde they were 3.0 ± 2.7, 3.3, and 16 ppb and 2.6 ± 2.3, 2.6,
and 13 ppb, respectively. The mean indoor-to-outdoor ratios for formaldehyde
and acetaldehyde were 7.2 ± 5.9 and 1.4 ± 0.9, respectively. These
ratios confirm that indoor sources exist for these compounds and that indoor
sources dominated the indoor formaldehyde air concentration. Reliable data have
not been published on indoor air concentrations of acrolein because the standard
aldehyde collection method for air samples using 2,4-dinitrophenylhydrazine-coated
sorbents is not stable for acrolein. A recent passive sampling method using
5-dimethylaminonaphthalene-1-sulfohydrazide-coated sorbents appears to
collect and stabilize acrolein adequately (70). This sampler was used
in the RIOPA study, and evaluation of indoor exposure to acrolein and other
aldehydes from that study should be available in the near future.
In-Vehicle Air Concentrations
Traveling in automobiles and on other modes of transportation, or even being
near roadways, can result in increased air toxics exposures for compounds emitted
by mobile sources (71). Mean concentrations of benzene, toluene, and
other aromatic air toxics in the cabins of automobiles and public transportation
and near roadways exceed both indoor and ambient air concentrations (72-76).
Even higher concentrations have been measured for individuals riding motorcycles
or bicycles in or near traffic (77,78). Measurements of PM and formaldehyde
are also elevated in these microenvironments compared with indoor or ambient
outdoor levels (76,79,80).
Activity Pattern Data
To comprehend the importance of examining exposure to air toxics arising from
nonambient emissions, it has to be recognized that people spend the majority
of their time indoors and only a small fraction of their time outdoors. One
caveat to using solely the time spent in different microenvironments when considering
the role of exposure to air pollutants in asthma is that physical exertion alters
the dose delivered to the lungs, and more physical activity is done outdoors.
Physical exertion may be important in asthma exacerbation. Numerous time-activity
studies have been compiled and summarized in the U.S. EPA Exposure Factors
Handbook (81). The data in the Exposure Factors Handbook have
been grouped by age and gender and across many activities and locations. More
recently, the National Human Activity Pattern Survey (NHAPS), a 2-year probability-based
telephone survey, was conducted by the U.S. EPA to provide a resource for assessing
exposure to environmental pollutants (82,83). The NHAPS data set indicates
that nationwide the breakdown of time in different locations for the entire
U.S. population is, in a residence, 68.7%; indoors in an office/factory, 5.4%;
indoors in a bar/restaurant, 1.8%; other indoor locations, 11%; in a vehicle,
5.5%; and outdoors, 7.6%. Some variations in percentages occur for different
age groups, times of the year, and regions of the country. These variations
can be important when trying to understand whether a particular exposure is
affecting a potentially sensitive subgroup.
As suggested above, physical activity can affect exposure and dose, exacerbating
asthma if environmental triggers are present in the air being breathed because
higher levels of physical activity increase the breathing rate and the potential
dose delivered to the lungs. Further, the location of physical activity may
be preferentially outside, especially for children, and may occur during specific
times of the year. Estimates of physical activity level and duration while outside,
stratified by age, season, and gender, have been compiled based on questionnaire
data (82,83). The highest level of outdoor activity occurs for yard work/maintenance
in the spring during morning to early afternoon and for sports/exercise in the
summer (3-6% of respondents) during the middle of the day from noon to
3 pm. The time period for sports/exercise in the spring (5% of respondents)
was from 3:30 to 6 pm. Outdoor activities also vary between weekends and weekdays:
weekend activity tends to be throughout the day (9 to 5 pm), whereas during
weekdays the time when physical activity occurs outdoors is shifted to later
in the day, with an initial rise at 3 pm that extends into the evening. These
differences reflect the time periods during which people have leisure time.
Klepeis et al. (82,83) also reported differences in the amount of time
that different age groups spent in various activities, with school-age children
spending more time at sports/exercise than other age groups. The numbers of
hours that healthy, asthmatic, and wheezy children spent outdoors during the
spring and summer were similar (84). However, the amount of time asthmatic
children spent being physically active outdoors was smaller than that for the
healthy or wheezy children, particularly during the summer. Girls spent less
time outdoors and were less physically active than boys. Overall, having an
estimate of the number of hours in different microenvironments and how many
of those hours were engaged in physical activity will improve inhalation exposure
estimates in epidemiologic studies of asthma and air pollution.
Long-Term Temporal Trends
NHEXAS is the first nationwide U.S. population-based exposure study designed
with a conceptual component to examine seasonal and long-term temporal exposure
trends (49). The first phase of NHEXAS evaluated the feasibility of the
approach and methodologies. Subsequent phases of NHEXAS, pending approval of
funding, will include collection of multiple years of data. If the full NHEXAS
project is undertaken, a wealth of information on spatial and temporal exposures
to air toxics will be gathered. The NHEXAS exposure database will provide the
opportunity for establishing associations between health outcome data collected
by state health agencies on asthma, and exposure to air toxics. NHEXAS should
also provide insights into which sources contribute most to that association.
Seasonal trends for 26 VOCs, which included aromatic and chlorinated air toxics,
were examined in a Canadian study that collected 24-hr average indoor air samples
in 754 residences using a passive monitoring technique (85). It employed
a probabilistic sampling design with both weekday and weekend sampling. Seasonal
differences were observed for the average VOC indoor air concentrations, with
the spring and fall having higher average concentrations than the winter and
summer. However, not all compounds followed this pattern, suggesting differences
among houses and activity patterns of the individuals affected by the air pollutant
concentrations. The authors proposed that the use indoors of different products
such as paints, fuels, and cleaners contributed to the variability in the seasonal
pattern and the maximum concentrations measured. Outdoor temperature, indoor
temperature, and indoor relative humidity were also significant variables that
contributed to the variance in the air concentrations based on factor analysis.
Air exchange rates were evaluated in a subset of homes and found to be lowest
in the winter, intermediate in the spring, and highest in the summer and fall.
The highest average concentrations were when the temperature and air exchange
rates were the lowest.
To evaluate long-term temporal trends in the outdoor contribution of air toxics
to exposure, data from ambient monitoring sites can be used. Although a national
network of HAP monitoring sites has not been established, the photochemical
assessment monitoring station (PAMS) network in 21 ozone nonattainment areas
has collected data on ozone precursors, which include some of the volatile organic
HAPs (18). The majority of the HAPs measured had statistically significant
declines in annual mean concentrations for 1994 to 1995 and 1995 to 1996 at
all sites (ethyl benzene, toluene, m,p-xylene, and o-xylene) or
at all but one site (benzene, styrene, and 2,2,4-trimethylpentane). Hexane was
the only compound that increased at two sites between 1994 and 1996 and was
unchanged at the other sites (n = 3, 1994-1995; n = 4, 1995-1995).
Several states have voluntary ambient air quality programs that include air
toxics. The station in Camden, New Jersey, has been operated since 1990. Decreases
in ambient air levels have been measured for all volatile organic HAPs (Table
5). These data suggest that exposure to volatile organic air toxics associated
with ambient emissions has decreased during the 1990s. Although it is unclear
if any of the HAPs individually, at ambient concentrations, exacerbate asthma,
the combined VOC concentration may be a respiratory irritant. Long-term trends
of PM10 have been reported because it is a criteria pollutant. Its
concentration has been decreasing with time in most locations. Long-term trends
of carbonyls and other air toxic respiratory irritants have not been reported.
Results from the RIOPA Study
The RIOPA study is a multicity, multipollutant study undertaken to evaluate
the impact of ambient sources in urban settings on exposure. Homes close to
ambient sources were oversampled during RIOPA. Only homes without smokers were
included. Smoking elevates the indoor and personal air concentrations of many
air toxics, and cigarette smoke is the dominant exposure source of many air
toxics for smokers. Only the data on the indoor and outdoor air concentrations
for VOCs in homes in Elizabeth, New Jersey, one of the cities sampled during
RIOPA, are presented in this article. As discussed above, VOCs may have a role
in exacerbation of asthma. Integrated 48-hr air samples were collected from
100 homes. Elizabeth, New Jersey, contains a mixture of mobile, commercial area,
and industrial point sources. The 48-hr VOC samples were collected using passive
monitors, a different method from that used when the two sequential 12-hr active
samples were taken during the TEAM study, which also sampled in Elizabeth, New
Jersey, for a similar suite of VOCs. However, the RIOPA project was not a probabilistic
population-based study; rather, two-thirds of the homes were selected to be
close to ambient source emissions.
Figure 1. Box plots of VOC outdoor (A), indoor
(B), and personal air (C) concentrations from the Elizabeth, New Jersey,
site in the RIOPA study. MTBE, methyl tert-butyl ether.
|
Although many of the VOCs have mean, median, and upper outlier air concentrations
in the indoor and personal samples that exceed those for outdoor air, others
had VOC air concentrations that were similar (Figure 1). Thus, as was found
during the TEAM study, indoor VOC sources and VOC sources close to people can
contribute to inhalation exposure. The exclusion of homes with smokers from
the RIOPA but not the TEAM study resulted in a smaller differential between
indoor and outdoor mean and median concentrations of aromatic VOCs. The temporal
pattern of many ambient air VOC concentrations shows spikes in the air concentrations
on individual days over the 1.5 years that the samples were collected (Figures
2, 3). The concentrations for compounds with mobile sources were higher than
those of chlorinated compounds with industrial or commercial sources. No obvious
seasonal pattern was observed for either data set, which could reflect the varying
sampling locations selected throughout the year rather than a true lack of seasonality
in the air concentrations. The temporal pattern of the three chlorinated compounds
shows two different patterns. Carbon-tetrachloride shows little variability
throughout the year among the different locations where the samples were collected
throughout the city, consistent with few ambient sources of this compound. Other
chlorinated compounds, represented by tetrachloroethene and 1,4-dichlorobenzene,
have periodic spikes in their ambient concentrations above a very low background
concentration, which was typically at the detection limits of the method. Such
spikes suggest individual releases of these compounds from ambient sources either
near the sampling location or within the urban settings, or under meteorological
conditions that enhance the buildup of concentrations from a constant release.
|
Figure 2. Temporal air concentration
of selected mobile source compounds [methyl tert-butyl ether (MTBE),
and toluene] from the Elizabeth, New Jersey, site in the RIOPA study. |
|
Figure 3. Temporal air concentration
of selected chlorinated compounds (tetrachloroethene, carbon tetrachloride,
and 1,4-dichlorobenzene) from the Elizabeth, New Jersey, site in the RIOPA
study. |
The relative importance of ambient sources on indoor air concentrations for
different compounds can be observed in the scatter plots of indoor versus outdoor
air concentrations of the New Jersey RIOPA data. Data for five example compounds,
methyl tert-butyl ether, benzene, toluene, 1,4-dichlorobenzene, and carbon
tetrachloroethane, are provided here (Figures 4-8). These compounds were
selected because they have potentially different contributions to indoor air
and exposure by ambient sources and indoor sources. Mobile emissions are the
major ambient air sources for methyl tert-butyl ether, benzene, and toluene.
Few other ambient emissions or indoor sources exist for methyl tert-butyl
ether. Although benzene is contained in cigarette smoke, which should not be
present in the vast majority of the samples collected because of the exclusion
criteria of the RIOPA study; the use of benzene in most personal and household
products has been banned and is limited in industrial and commercial settings.
Toluene is a component of cigarette smoke and used as a solvent in personal,
household, commercial, and industrial products. These differences are reflected
in the scatter plots of each compound (Figures 4-6). Each compound has
general scatter around the 1:1 line at the lower end of the concentration range.
The scatters of the benzene and toluene data pairs are biased to slightly higher
indoor air concentrations, whereas the methyl tert-butyl ether data are
more equally distributed. At the higher concentration range, the indoor benzene
concentrations are higher than the outdoor concentrations, consistent with a
subset of homes having indoor sources of benzene. Methyl tert-butyl ether
also has several homes with higher indoor than outdoor concentrations, which
was unexpected because none of the homes had attached garages, one of the few
known sources of indoor methyl tert-butyl ether. It also had paired samples
where the outdoor air concentrations exceeded the indoor concentrations. The
outdoor level could be higher if the outdoor sampler was near a localized source
of methyl tert-butyl ether such as evaporative emissions from a car parked
near the outdoor samplers, sometimes located in driveways. Toluene shows the
greatest amount of variability, consistent with the larger number of ambient
and indoor sources of toluene than of the other compounds.
|
Figure 4. Scatter plot
of the outdoor and indoor air concentrations (µg/m3)
of methyl tert-butyl ether (MTBE) from the Elizabeth, New Jersey,
site in the RIOPA study.
|
|
Figure 5. Scatter plot
of the outdoor and indoor air concentrations (µg/m3)
of benzene from the Elizabeth, New Jersey, site in the RIOPA study.
|
|
Figure 6. Scatter plot
of the outdoor and indoor air concentrations (µg/m3)
of toluene from the Elizabeth, New Jersey, site in the RIOPA study.
|
|
Figure 7. Scatter plot
of the outdoor and indoor air concentrations (µg/m3)
of carbon-tetrachloride from the Elizabeth, New Jersey, site in the
RIOPA study.
|
|
Figure 8. Scatter plot
of the outdoor and indoor air concentrations (µg/m3)
of 1,4-dichlorobenzene from the Elizabeth, New Jersey, site in the RIOPA
study.
|
The two chlorinated compounds selected show distinctly different patterns
that can be explained based on known emission sources. Carbon-tetrachloride
has few current uses and a fairly narrow range of indoor and outdoor concentrations,
with values near the global background levels of less than 1 µg/m3 (Figure 7). The data are distributed around the 1:1 line, with more points having
higher outdoor than indoor concentrations, possibly caused by sinks in homes,
such as absorption of the compound by the padding in furniture. Eleven homes
have higher indoor values, suggesting the presence of carbon-tetrachloride in
some product used in those homes. The scatter plots of 1,4-dichlorobenzene are
consistent with a compound having minimal outdoor sources and large indoor sources
(Figure 8). This compound had some of the highest indoor air concentrations
measured for any VOC during the study, consistent with its use as a room air
deodorizer and a major component of moth cakes [e.g., Wallace (86)].
If compounds present in deodorizers, such as dichlorobenzene, limonene, or pinenes,
are respiratory irritants, the elevated exposure that occurs indoors may be
a trigger for asthma, and controlling ambient sources of these compounds will
not be effective in reducing exposure to them. It is therefore evident that
although there is a major contribution to air toxics exposures from ambient
emissions because these compounds penetrate into homes where people spend the
majority of their time, other sources also contribute and exposure to each air
toxic must be determined individually.
Conclusions
Asthma is a common respiratory disease whose prevalence is increasing. Many
environmental triggers can exacerbate asthma and could include nonspecific responses
to HAPs. Inhalation exposure to air toxics occurs in multiple microenvironments,
with the major source contributions varying by the air toxic, but the majority
of the exposure occurs indoors. It may be important to consider different activity
patterns and where those occur, particularly those related to physical exercise,
because increased breathing rates increase the dose delivered to the lungs.
Ambient emissions are transported through the environment and into houses. However,
many air toxics have air concentrations higher indoors than outdoors and even
higher in personal samples collected near the breathing zone. This is because
the sources of air toxics within homes, even though they are small compared
with ambient emissions, can contribute greatly to exposure because of the proximity
of the source to the receptor, that is, people. In establishing whether an air
toxic is associated with asthma exacerbation or causation, it is necessary to
determine where the exposure occurs, the duration of exposure in each location,
and the activities the individuals are involved in and not to assume that ambient
measurements adequately define the exposure. The total concentration of multiple
HAPs, rather than the concentration of individual compounds, may be important.
These considerations, along with the source of the exposures, need to be included
in any attempt to reduce exposure to protect the health of asthmatic individuals
and any other population susceptible to air toxics exposures. |
|
|
[References Listed in PubMed] References and Notes 1. Woolcock A. Asthma, in Textbook of Respiratory Medicine
(Murray JF, Nadel JA, eds). Philadelphia:W.B. Saunders Company, 1998;1288-1330.
2. Mannino DM, Homa DM, Akinbami LJ, Moorman JE, Gwynn
C, Redd SC. Surveillance for Asthma--United States, 1980-1999. Atlanta, GA:Centers
for Disease Control and Prevention, 2002.
3. Bielory L, Denner A. Seasonal variation in the effects
of major indoor and outdoor environmental variables on asthma. J Asthma 35(1):7-48
(1998).
4. Schwela D. Air pollution and health in urban areas.
Rev Environ Health 15(1-2):13-42 (2000).
5. Peden DB. Air pollution in asthma: effect of pollutants
on airway inflammation. Ann Allergy Asthma Immunol 87(6 suppl 3):12-17
(2001).
6. Chan-Yeung M. Air pollution and health. Hong Kong Med
J 6(4):390-398 (2000).
7. Teague W, Bayer C. Outdoor air pollution. Asthma and
other concerns. Pediatr Clinics North Am 48(5):1167-1183 (2001).
8. D'Amato G, Liccardi G, D'Amato M, Cazzola M. The role
of outdoor air pollution and climatic changes on the rising trends in respiratory
allergy. Respir Med 95(7):606-611 (2001).
9. Bardana EJ. Indoor pollution and its impact on respiratory
health. Ann Allergy Asthma Immunol 87(6 suppl 3):33-40 (2001).
10. Caldwell JC, Woodruff TJ, Morello-Frosch R, Axelrad
DA. Application of health information to hazardous air pollutants modeled in
EPA's cumulative exposure project. Toxicol Ind Health 14(3):429-454 (1998).
11. Morello-Frosch RA, Woodruff RJ, Axelrad DA, Caldwell
JC. Air toxics and health risks in California: the public health implications
of outdoor concentrations. Risk Anal 20(2):273-291 (2000).
12. Kjaergaard SJ, Molhave L, Pedersen OF. Human reactions
to a mixture of indoor air volatile organic compounds. Atmos Environ 25a(8):1417-1426
(1991).
13. Koenig JQ, Covert DS, Smith MS, van Belle G, Pierson
WE. The pulmonary effects of ozone and nitrogen dioxide alone and combined in
healthy and asthmatic adolescent subjects. Toxicol Ind Health 4(4):521-532
(1988).
14. Lioy PJ. Assessing total human exposure to contaminants.
Environ Sci Technol 24(7):938-945 (1990).
15. Ott WR. Total human exposure. Environ Sci Technol
19(10):880-886 (1985).
16. Georgopoulos PG, Lioy PJ. Conceptual and theoretical
aspects of human exposure and dose assessment. J Expos Anal Environ Epidemiol
4(3):253-285 (1994).
17. Clean Air Act Amendments of 1990. CFR Title 42, Chap
85 Available: http://www.epa.gov/oar/oaq_caa.html.
Washington, DC:U.S. Environmental Protection Agency, 1990. 18. U.S. EPA. National Air Quality and Emissions Trends
Report. EPA 454/R_97_013). Research Triangle Park, NC:U.S. Environmental Protection
Agency, 1996.
19. Hasset-Sipple B, Cote I. Toxic air pollutants and
non-cancer health risks. Morb Mortal Wkly Rep 430:278-279 (1990).
20. Strachan DP. The role of environmental factors in
asthma. Br Med J 56(4):865-882 (2000).
21. Wjst M, Reitmeir P, Dold S, Wulff A, Nicolai T, von
Loeffelholz-Colberg EF, von Mutius E. Road traffic and adverse effects on respiratory
health in children. Br Med J 307:596-600 (1993).
22. Weiland S Mundt KA, Ruckmann A, Keil AU. Self-reported
wheezing and allergic rhinitis in children and traffic density on street of
residence. Ann Epidemiol 4:243-247 (1994).
23. Edwards J, Waters S, Griffiths RK. Hospital admissions
for asthma in preschool children: relationship to major roads in Birmingham,
United Kingdom. Arch Environ Health 49(4):223-227 (1994).
24. Livingstone A, Shaddick G, Grundy C, Elliott P. Do
people living near inner city main roads have more asthma needing treatment?
Case control study. Br Med J 312(7032):676-677 (1996).
25. Wilkinson P, Elliott P, Grundy C, Shaddick G, Thakrar
B, Walls P, Falconer S. Case-control study of hospital admission with asthma
in children aged 5-14 years: relation with road traffic in north west London.
Thorax 54(12):1070-1074 (1999).
26. Norbäck D, Björnsson E, Janson C, Widström
J, Boman G. Asthmatic symptoms and volatile organic compounds, formaldehyde,
and carbon dioxide in dwellings. Occup Environ Med 52:388-395 (1995).
27. Wieslander G, Norback D, Edling C. Airway symptoms
among house painters in relation to exposure to volatile organic compounds (VOCS)--a
longitudinal study. Ann Occup Hygiene 41(2):155-166 (1997).
28. Wieslander G, Norback D, Bjornsson E, Janson C, Boman
G. Asthma and the indoor environment: the significance of emission of formaldehyde
and volatile organic compounds from newly painted indoor surfaces. Int Arch
Occup Environ Health 69(2):115-124 (1997).
29. Koren HS, Graham DE, Devlin RB. Exposure of humans
to volatile organic mixtures. III: Inflammatory response. Arch Environ Health
47:39-44 (1992).
30. Harving H, Dahl R, Mölhave L. Lung function and
bronchial reactivity in asthmatics during exposure to volatile organic compounds.
Am Rev Respir Dis 143:751-754 (1991).
31. Quackenboss J, Lebowitz M, Michaud J, Bronniman D.
Formaldehyde exposure and acute health effects study. Environ Int 15:169-179
(1989).
32. Bardana EJ, Montanaro A. Formaldehyde: an analysis
of its respiratory, cutaneous, and immunologic effects. Ann Allergy 66(6):441-452
(1991).
33. Krakowiak A, Gorski P, Pazdrak K, Ruta U. Airway response
to formaldehyde inhalation in asthmatic subjects with suspected respiratory
formaldehyde sensitization. Am J Ind Med 33(2):274-281 (1998).
34. Akbar-Khanzadeh F, Mlynek J. Changes in respiratory
function after one and three hours of exposure to formaldehyde in non-smoking
subjects. Occup Environ Med 54(5):296-300 (1997).
35. Coultas DB. Passive smoking and risk of adult asthma
and COPD: an update. Thorax 53:381-387 (1998).
36. Abbey DE, Petersen F, Mills PK, Beeson WL. Long-term
ambient concentrations of total suspended particulates, ozone and sulfur dioxide
in a non-smoking population. Arch Environ Health 48:33-47 (1993).
37. Löfroth G, Burton RM, Forehand L, Hammond K,
Sella RL, Zweldinger RB, Lewtas J. Characterization of environmental tobacco
smoke. Environ Sci Technol 23(5):610-614 (1989).
38. Ware JH, Spengler JD, Neas LM, Samet JM, Wagner GR,
Coultas D, Ozkaynak H, Schwab M. Respiratory and irritant health effects of
ambient volatile organic compounds. The Kanawha County health study. Am J Epidemiol
137(12):1287-1301 (1993).
39. Buckley TJ, Ott WR. Demonstration of real-time measurements
of PAH and CO to estimate in-vehicle exposure and identify sources. In: Proceedings
from the International Specialty Conference on Measurement of Toxic and Related
Air Pollutants, 1996. Research Triangle Park, NC:Air & Waste Management
Association/U.S. Environmental Protection Agency, 1996;803-810.
40. Ramachandran G, Adgate JL, Hill N, Sexton K, Pratt
GC, Bock D. Comparison of short-term variations (15-minute averages in outdoor
and indoor PM2.5 concentrations. J Air Waste Manage Assoc 50(7):1157-1166
(2000).
41. Abt EI, Suh HH, Allen G, Koutrakis P. Characterization
of indoor particle sources: a study conducted in the metropolitan Boston area.
Environ Health Perspect 108(1):35-44 (2000).
42. Long CM, Suh HH, Catalano PJ, Koutrakis P. Using time-
and size-resolved particulate data to quanitfy indoor penetration and deposition
behavior. Environ Sci Technol 35(10):2089-2099 (2001).
43. Furtaw EJJ, Pandian MD, Nelson DR, Behar JV. Modeling
indoor air concentrations near emissions sources in imperfectly mixed rooms.
J Air Waste Manage Assoc 46(9):861-868 (1996).
44. Wallace L. The Total Exposure Assessment Methodology
(TEAM) Study: Summary and Analysis, Vol 1. Washington, DC:U.S. Environmental
Protection Agency, 1987.
45. Wallace LA, Pellizzari E, Hartwell T, Rosenzweig M,
Erickson M, Sparacino C, Zelon H. Personal exposure to volatile organic compounds.
Environ Res 35:293-319 (1984).
46. Wallace LA, Pellizzari ED, Hartwell TD, Sparacino
CM, Sheldon LS, Zelon H. Personal exposures, indoor-outdoor relationship and
breath levels of toxic air pollutants measured for 355 persons in New Jersey.
Atmos Environ 19:1651-1661 (1985).
47. Wallace LA. Personal exposure, indoor and outdoor
air concentrations, and exhaled breath concentrations of selected volatile organic
compounds measured for 600 residents of New Jersey, North Dakota, North Carolina
and California. Toxicol Environ Chem 12:215-236 (1986).
48. Wallace LA, Pellizzari ED, Hartwell TD, Sparacino
C, Whitmore R, Sheldon L, Zelo H, Perritt R. The TEAM study: personal exposures
to toxic substances in air, drinking water and breath of 400 residents of New
Jersey, North Carolina, and North Dakota. Environ Res 43:290-307 (1987).
49. Sexton K, Kleffman DE, Callahan MA. An introduction
to the National Human Exposure Assessment Survey (NHEXAS) and related Phase
I field studies. J Expos Anal Environ Epidemiol 5(3):229-232 (1995).
50. Gordon SM, Callahan PJ, Nishioka MG, Brinkman MC,
O'Rourke MK, Lebowitz MD, Moschandreas DJ. Residential environmental measurements
in the National Human Exposure Assessment Survey (NHEXAS) pilot study in Arizona:
preliminary results for pesticides and VOCs. J Expos Anal Environ Epidemiol
9(5):456-470 (1999).
51. Bonanno LJ, Freeman NCG, Greenberg M, Lioy PJ. Multivariate
analysis on levels of selected metals, particulate matter, VOC, and household
characteristics and activities from the Midwestern states NHEXAS. Appl Occup
Environ Hyg 16(9):859-874 (2001).
52. Wallace L. Indoor particles: a review. J Air Waste
Manage Assoc 46(2):98-126 (1996).
53. Spengler JD, Thurston GD. Mass and elemental composition
of fine and coarse particles in six U.S. cities. J Air Pollut Control Assoc
33:1162-1171 (1983).
54. Sheldon LS, Hartwell TD, C.B. G, Sickles JE II, Pellizzari
ED, Smith ML, Perritt RL, Jones SM. An investigation of infiltration and indoor
air quality. Albany, NY:NYS Energy Research and Development Authority, 1989.
55. Clayton CA, Perritt RL, Pellizzari ED, Thomas KW,
Whitmore RW, Ozkaynak H, Spengler JD, Wallace LA. Particle total exposure assessment
methodology (PTEAM) study: distribution of aerosol and element concentrations
in personal, indoor and outdoor air samples in a southern California community.
J Expos Anal Environ Epidemiol 3:227-250 (1993).
56. Thomas KW, Pellizzari ED, Clayton CA, Whitaker DA,
Shores RC, Spengler JD, Ozkaynak H, Wallace LA. Particle total exposure assessment
methodology (PTEAM) study: method performance and data quality for personal,
indoor and outdoor aerosol monitoring at 178 homes in Southern California. J
Expos Anal Environ Epidemiol 3:203-226 (1993).
57. Ozkaynak H, Xue J, Spengler JD, Wallace LA, Pellizzari
ED, Jenkins P. Personal exposure to airborne particles and metals: results from
the Particle Team Study in Riverside, CA. J Expos Anal Environ Epidemiol 6(1):57-78
(1996).
58. Spengler JD, Dockery DW, Turner WA, Wolfson JM, Ferris
BG Jr. Long-term measurements of respirable sulfates and particles inside and
outside homes. Atmos Environ 15:23-30 (1981).
59. Santanam S, Spengler JD, Ryan PB. Particulate matter
exposures estimated from an indoor-outdoor source apportionment study. in Indoor
Air '90: Proceedings of the 5th International Conference on Indoor Air Quality
and Climate. 29 July- 3 August 1990, Ottawa, Ontario, Canada. Vol 2:583-588
(1990).
60. Adgate JL, Rhoads GG, Lioy PJ. The use of isotope
ratios to apportion sources of lead in Jersey City, NJ, house dust wipe samples.
Sci Total Environ 221(2-3):171-180 (1998).
61. Chuang JC, Callahan PJ, Menton RG, Gordon SM, Lewis
RG, Wilson NK. Monitoring methods for polycyclic aromatic hydrocarbons and their
distribution in house dust and track-in soil. Environ Sci Technol 29(2):494-500
(1995).
62. Gurunathan S, Robson M, Freeman N, Buckley B, Roy
A, Meyer R, Bukowski J, Lioy PJ. Accumulation of chlorpyrifos on residential
surfaces and toys accessible to children. Environ Health Perspect 106(1):9-16
(1998).
63. Lu C, Fenske RA, Simcox NJ, Kalman D. Pesticide exposure
of children in an agricultural community: evidence of household proximity to
farm land and take home exposure pathways. Environ Res 84(3):290-302 (2000).
64. EXPOLIS. Air Pollution Exposure Distributions of Adult
Urban Populations in Europe. Available: http://www.ktl.fi/expolis/ [accessed 4 September 2001].
65. Kinney PL, Chillrud SN, Ramstrom S, Ross J, SpenglerJD.
Exposures to multiple air toxics in New York City. Environ Health Perspect 110(suppl
4):539-546 (2002).
66. Bardana EJ, Montanaro A. Formaldehyde: an analysis
of its respiratory, cutaneous, and immunologic effects. Ann Allergy 66(6):441-452
(1991).
67. Zhang J, He Q, Lloy PJ. Characteristics of aldehydes:
concentrations, sources, and exposures of indoor and outdoor residential microenvironments.
Environ Sci Tech 28:146-152 (1994).
68. Woodruff TJ, Axelrad DA, Caldwell J, Morello-Frosch
R, Rosenbaum A. Public health implications of 1990 air toxics concentrations
cross the United States. Environ Health Perspect 106(5):245-251 (1998).
69. Crump DR, Squire RW, Yu CWF. Sources and concentrations
of formaldehyde and other volatile organic compounds in the indoor air of four
newly build unoccupied test houses. Indoor Built Environ 6(1):45-55 (1997).
70. Zhang J, Zhang L, Fan Z, Ilacqua V. Development of
the personal aldehydes and ketones sampler based on DNSH derivatization on solid
sorbent. Environ Sci Technol 34(12):2601-2607 (2000).
71. Weisel CP. Transportation, in Indoor Air Quality Handbook
(Spengler JD, Samet JM, McCarthy JF, eds). New York:McGraw-Hill, 2000;68.1-68.20.
72. Chan C-C, Spengler JD, Ozkaynak H, Befkopoulou M.
Commuter exposures to VOCs in Boston, Massachusetts. J Air Water Manage Assoc
41:1594-1600 (1991).
73. Chan C-C, Ozkaynak H, Spengle JD, Sheldon L. Driver
exposure to volatile organic compounds, CO, ozone, and NO2 under
different driving conditions. Environ Sci Technol 25(5):964-972 (1991).
74. Lawryk NJ, Weisel CP. Concentrations of volatile organic
compounds in the passenger compartment of automobiles. Environ Sci Technol 30(3):810-816
(1996).
75. Jo W-K, Park K-H. Exposure to carbon monoxide, methyl-tertiary
butyl ether (MTBE), and benzene levels inside vehicles traveling on an urban
area in Korea. J Exposure Anal Environ Epidemiol 8(2):159-171 (1998).
76. SCAQMD. Report on In-Vehicle Characterization Study
in the South Coast Air Basin. Los Angeles:South Coast Air Quality Management
District, 1989.
77. Chan C-C, Lin S-H, Her G-R. Student's exposure to
volatile organic compounds while commuting by motorcycle and bus in Taipei City.
J Air Waste Manage Assoc 43:1231-1238 (1993).
78. van Wijnen JH, Verhoeff AP, Jans HWA, van Bruggen
M. The exposure of cyclists, car drivers and pedestrians to traffic-related
air pollutants. Int Arch Occup Environ Health 67:187-193 (1995).
79. Ptak TJ, Fallon SL. Particulate concentration in automobile
passenger compartments. Partic Sci Technol 12:313-322 (1994).
80. Fischer PH, Hoek G, van Reeuwijk H, Briggs DJ, lebret
E, van Wijnen JH, Kingham S, Elliott PE. Traffic-related differences in outdoor
and indoor concentrations of particles and volatile organic compounds in Amsterdam.
Atmos Environ 34:3713-3722 (2000).
81. U.S. EPA. Exposure Factors Handbook. Vol I: General
Factors. Vol II: Food Ingestion Factors. Vol III: Activity Factors. Washington,
DC:U.S. Environmental Protection Agency (1997).
82. Klepeis NE, Tsang AM, Behar JV. Report on: Analysis
of the National Human Activity Pattern Survey (NHAPS) Respondents from a Standpoint
of Exposure Assessment. Las Vegas, NV:U.S. Environmental Protection Agency,
1996.
83. Klepeis NE, Nelson WC, Ott WR, Robinson JP, Tsang
AM, Switzer P, Behar JV, Hern SC, Englemann WH. The National Human Activity
Pattern Survey (NHAPS): a resource for assessing exposure to environmental contaminants.
J Expos Anal Environ Epidemiol 11(3):231-252 (2001).
84. Avol EL, Navidi WC, Colome SD. Modeling ozone levels
in and around southern California homes. Environ Sci Technol 32(4):463-468
(1998).
85. Fellin P, Otson R. Assessment of the influence of
climatic factors on concentration levels of volatile organic compounds (VOCs)
in Canadian homes. Atmos Environ 28(22):3581-3586 (1994).
86. Wallace LA. Human exposure to volatile organic pollutants:
implications for indoor air studies. Annu Rev Energy Environ 26:269-301
(2001).
87. U.S. EPA. The Total Exposure Assessment Methodology
(TEAM) Study: Elizabeth and Bayonne, New Jersey, Devils Lake, North Dakota and
Greensboro, North Carolina, Vol II. Parts 1 and 2. Washington, DC:U.S. Environmental
Protection Agency 1987.
88. U.S. EPA. The Total Exposure Assessment Methodology
(TEAM) Study: Selected Communities in Northern and Southern California, Vol
III. Washington, DC:U.S. Environmental Protection Agency, 1987.
89. New Jersey Department of Environmental Protection.
NJDEP Bureau of Air Monitoring. Available: http://www.state.nj.us/dep/airmon/index.html [accessed 1 June 2001].
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