TRI Releases Discussion I have a 3 part that need to be done. One you look up the TRI data and answer. The other 2 part questions I have attached an articl

TRI Releases Discussion I have a 3 part that need to be done. One you look up the TRI data and answer. The other 2 part questions I have attached an article for each, that you would get the answer from.

Look up what TRI releases are present in a place you live or formerly lived. Use 83706, or 83705 zip code to access the data for 2016, 2017, 2018.

2. What were the top three releases & how much of each was released?

3. Are the releases per day, per month, per year?

4. Do these data take into account all of releases of these chemicals in this area? Why or why not?

Here is The link to the website: https://enviro.epa.gov/triexplorer/tri_getcounties…

From the reading attached

2. Read the article – TRI, what it means and how it is used by Christine Osbourne, DEQ Utah, 2019

– Look up the criteria for TRI reporting – what are the 3 main criteria?

– List some benefits of the TRI report

– List 5-6 issues or concerns with the report / data

3. Read the article – Pollutants and Asthma: The role of Air Toxics by D. Peden in Environmental

Health perspective.

– What is the problem with diesel exhaust?

– What does ozone induce?

– What are endotoxins?

– What is the main point of the article? Asthma Occurrence
Pollutants and Asthma: Role of Air Toxics
David B. Peden
Department of Pediatrics, Division of Allergy, Immunology and Environmental Medicine, and Center for Environmental Medicine
and Lung Biology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
Asthma is a disease characterized by intermittent bronchoconstriction due to increased airway
reactivity to both allergic and nonallergic stimuli. Most asthma exacerbations that result in hospitalization are associated with viral upper respiratory tract infections. Such infections typically
induce T-helper type 1 (TH1) responses in the airway, involving activation of nuclear factorkappaB (NF-?B). However, a more recently appreciated cause of asthma exacerbation is exposure
to pollutants, including ozone and various components of particulate matter (PM), including transition metals, diesel exhaust, and biologicals such as endotoxin. Although the role of air toxics in
asthma pathogenesis remains incompletely examined, many components of PM that are active
exacerbants of asthma are also prominent air toxics (metal ions and organic residues). These
agents have been observed to activate NF-?B. Reviewed in this article are the actions of specific air
pollutants on airway inflammation in humans and potential common response pathways for
ozone, PM, and several air toxics. Key words: air toxics, asthma, exacerbation, TH1, TH2. Environ
Health Perspect 110(suppl 4):565–568 (2002).
http://ehpnet1.niehs.nih.gov/docs/2002/suppl-4/565-568peden/abstract.html
Asthma is a disease characterized by intermittent bronchoconstriction due to increased
airway reactivity to both allergic and nonallergic stimuli. Underlying these phenomena is a
chronic, eosinophilic airway inflammation.
Perhaps the most common and significant
risk factor for development of asthma in children is induction of an immunoglobulin E
(IgE; allergic) response against indoor allergens (1,2). However, nonallergic stimuli,
which do not directly interact with IgE, are
common causes of asthma exacerbation.
Asthmatic individuals have been identified as a
population that is especially sensitive to the
effect of ambient air pollutants. Although pollutants might enhance IgE-mediated chronic
inflammation via T-helper type 2 (T H 2)
processes, they more likely induce exacerbation
of asthma. Indeed, many pollutants associated
with asthma exacerbation induce neutrophilic
inflammation in nonallergic subjects.
Viral infections and pollutants typically
induce T H 1-type responses in the airway,
involving activation of nuclear factor-kappaB
(NF-?B). Yet in asthmatic individuals, these
processes may also exacerbate eosinophilic
inflammation. This observation suggests that
chronic allergic airway inflammation may
modify the response to nonallergic stimuli,
thus magnifying the impact of such agents.
The agents more commonly examined for
asthma exacerbation are criteria air pollutants,
such as ozone and particulate matter (PM).
The role of air toxics in asthma has not been
vigorously examined, despite the frequency in
which they are encountered. However, many
of the agents identified in PM can also be
considered air toxics and demonstrate that
this important class of pollutants likely has a
significant impact on asthma. Reviewed in
Environmental Health Perspectives
this article are studies that exemplify the
impact of ozone, particulates, and toxic components of particulates on asthma.
Ozone and Asthma
Epidemiologic studies clearly demonstrate
that increases in ambient air ozone are linked
with increased occurrence of acute asthma
exacerbations. Markers for such events,
including increased hospitalizations and
emergency room visits, are usually noted
24 hr after the increase in inflammation, suggesting that inflammation may play a role in
such events (3–8). During the 1996 Summer
Olympic games, an effort to decrease automobile traffic in Atlanta, Georgia, resulted in
decreases in ambient ozone levels. Asthma
exacerbations decreased as well, again demonstrating a link between ambient ozone levels
and asthma exacerbations (9).
Exposure to ozone is known to induce
increases in airway inflammation (10–12). In
asthmatic individuals, the effect of ozone
exposure is exaggerated, resulting in either
increased neutrophilic inflammation (13–15)
or an augmentation of eosinophilic inflammation (16,17). In addition to asthmatic
individuals being more sensitive to ozone
per se, ozone appears to augment both the
immediate and late-phase response to allergens. Initially, Molfino and colleagues (18)
described increased sensitivity to inhaled
allergen after exposure to a relatively low level
of ozone (0.12 ppm for 2 hr). Although other
studies examining this dose of ozone do not
reveal such an effect (19), higher levels of
ozone clearly enhance the immediate effect of
inhaled allergen on bronchoconstriction
(20,21). Nasal challenge studies also demonstrate that ozone exposure might enhance the
• VOLUME 110 | SUPPLEMENT 4 | AUGUST 2002
late-phase response to allergen (22,23). Thus,
persons with allergic inflammation of the airway are differentially susceptible to the effect
of ozone, an agent that in nonallergic subjects
induces neutrophilic inflammation (24–26).
Toxic Components of
Particulate Matter and Asthma
Particulate matter is an important pollutant
and is associated with increased morbidity
and mortality (24,27–30). PM is also associated with increased disease severity in asthma
(31–33). Indeed, increased admissions to
hospital for asthma are linked to increased
PM exposure, as are decreased peak flow
measurements in children (31,34,35). An
interesting study in the Utah Valley, Utah,
showed a marked decrease in admissions to
hospital for asthma and respiratory tract illnesses when a local steel mill was closed, with
subsequent increase in such events when it
reopened (32,33).
Although a clear mechanism for the
action of PM in asthma exacerbation has not
been identified, studies with model pollutants, including residual oil fly ash (ROFA)
and Utah Valley dust (UVD) particles, suggest that PM enhances TH1-like, neutrophilic
inflammation. Many of the active agents in
various PM species also fall into the broad
category of air toxics. ROFA is a potent
proinflammatory agent that has oxidant activity, likely mediated by vanadium species and
nickel (36–40). UVD is another PM in
which its biological activity is associated with
metal content and oxidant character (41–44).
Diesel exhaust particles (DEPs) contain polyaromatic aromatic hydrocarbons. Each of
these PM components can be considered air
toxics. The specific impact of these agents in
humans is outlined below.
ROFA particles have been shown in vitro
to affect prostaglandin metabolism and induce
cytokine production in epithelial cells (45–48).
Animal studies have also demonstrated
that ROFA is associated with increased
This article is part of the monograph Environmental
Air Toxics: Role in Asthma Occurrence?
Address correspondence to D.B. Peden, Center for
Environmental Medicine and Lung Biology, 104
Mason Farm Rd., CB #7310, School of Medicine,
University of North Carolina at Chapel Hill, Chapel
Hill, NC 27599-7310 USA. Telephone: (919) 9620126. Fax: (919) 966-9863. E-mail: peden@
med.unc.edu
Received 20 November 2001; accepted 4 March
2002.
565
Asthma Occurrence
•
Peden
neutrophilic airway inflammation (49).
Animal studies also show that ROFA can
exacerbate allergic inflammation in mice and
that it enhances sensitization to allergens in a
rat model (50–52).
UVD has also been shown to induce
airway inflammation in animal studies and to
induce proinflammatory changes in epithelial
cells in vitro. Perhaps most intriguing is the
decreased effect of UVD particles collected
during the time that the local steel mill was
closed (44,53,54). In humans, instillation of
extracts made from UVD collected during
the years the mill was open versus those collected when it was closed was consistent with
animal and in vitro studies demonstrating
that influx of neutrophils was associated with
dust collected during active years and was
blunted in extracts made from UVD collected during a year the mill was closed (42).
Humans exposed to concentrated ambient
air particles also show subtle evidence of
increased respiratory tract inflammation
(43). Thus, it seems clear that PM can
induce inflammation, not unlike ozone. This
proinflammatory effect of PM may account
for its ability to exacerbate asthma.
Diesel exhaust and resultant DEPs are
also an interesting component of PM.
Human challenge studies with diesel exhaust
reveal increases in airway inflammation,
including increases in airway neutrophils and
mast cells (55–57). Diesel exhaust exposure
has been shown to enhance nonspecific airway reactivity in asthmatic individuals as well
(58). DEPs, in nasal instillation studies, have
been shown to induce increases in total and
antigen-specific IgE, increase cellular response
to nasally applied allergen, and enhance production of TH2 cytokines such as interleukin
(IL)-4 and IL-13 (59–64). DEPs also enhance
sensitization to a neoantigen, keyhole limpet
hemocyanin (KLH), such that antigen-specific IgE against KLH is generated (65).
In vitro studies suggest that the active agents
in DEPs that affect IgE production are polyaromatic hydrocarbons (66). Animal studies
also demonstrate that polyaromatic hydrocarbons enhance IgE production in animals via
actions on B lymphocytes (67). Taken
together, these data suggest that diesel particles and DEPs may play a significant role not
only in asthma exacerbation but also in TH2
inflammation via the actions of polyaromatic
hydrocarbons on B lymphocytes.
Endotoxin and Asthma
Endotoxin is a common component of PM
and is also encountered in domestic (68,69)
and occupational settings (70,71). A number
of studies have demonstrated increased airway
symptoms in workers who encounter high
levels of endotoxin in the workplace
(70,72–77). Endotoxin is known to stimulate
566
innate immune responses that have a TH1type character (neutrophilic inflammation,
lack of IL-4 and IL-13). Endotoxin induces
neutrophilic airway inflammation in nonallergic, nonasthmatic volunteers (78–85).
This agent also has been found to enhance
nonspecific airway reactivity in asthmatic
individuals (86–88).
Recent studies suggest that endotoxin
may be a factor in increasing asthma morbidity and wheeze (89,90). Conversely, exposure
to endotoxin at a very young age may protect
against development of allergic responses to
allergens (68). However, in persons with
ongoing allergic inflammation, the degree of
allergic inflammation, as determined by enumeration of airway eosinophils, appears to
correlate with increased response to endotoxin (91). Allergen challenge enhances
expression of CD14, an important endotoxin
receptor, in asthmatic individuals (92–94)
and enhances nasal inflammatory responses to
endotoxin, including increases in neutrophils
and eosinophils (95). Treatment of asthmatic
individuals with corticosteroids blunts
response to endotoxin and decreases CD14
expression in the airway (96). Taken together,
these observations suggest that allergic
inflammation modifies the response to endotoxin, enhancing the impact of this agent on
asthma symptoms and morbidity.
Potential Common
Mechanisms
Each of the pollutants outlined above can
induce neutrophilic inflammation. NF-?B is
a key aspect of such activation. Ozone has
been shown to activate NF-?B in epithelial
cells (97) and to induce this transcription factor in vivo in animal respiratory tissue
(98,99). This activation is blunted by treatment with corticosteroids. Metal ions and
diesel exhaust also appear to induce NF-?B
(48). Endotoxin is a classic stimulus for
NF-?B activation (100). Signal transduction
of endotoxin after it binds to the CD14 cell
surface depends on interaction with the tolllike receptor (TLR) 4. An intriguing linkage
between TLR 4, a key receptor for endotoxin,
and the action of ozone suggests that TLR4
(or other similar membrane-spanning molecules) may mediate the ultimate activation of
NF-?B by ozone as well (101,102). Future
studies on the effect of environmental stimuli
in exacerbating asthma should examine
potential common response elements such as
the TLR 4, which may mediate the effect of a
number of apparently disparate pollutants.
encountered air pollutant, in asthma has not
been aggressively studied. Its potential
importance is demonstrated by studies of
PM in which the active agents are biologically active metal ions and organic residues,
both of which can be considered air toxics.
This class of compounds may have significant effects on asthma, especially modulating
immune function, as demonstrated by the
role of polyaromatic hydrocarbons from
diesel exhaust in IgE production.
Examination of the effect of air toxics in
asthma as they exist either in gas, vapor, or
particulate form warrants further study.
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