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Historic and Modern Air Pollution Studies Conducted in Utah

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Abstract and Figures

Utah’s low-smoking population and high population density concentrated in mountain valleys, with intermittent industrial activity and frequent temperature inversions, have yielded unique opportunities to study air pollution. These studies have contributed to the understanding of the human health impacts of air pollution. The populated mountain valleys of Utah experience considerable variability in concentrations of ambient air pollution because of local emission sources that change over time and episodic atmospheric conditions that result in elevated concentrations of air pollution. Evidence from Utah studies indicates that air pollution, especially combustion-related fine particulate matter air pollution and ozone, contributes to various adverse health outcomes, including respiratory and cardiovascular morbidity and mortality and increased risk of lung cancer. The evidence suggests that air pollution may also contribute to risk of pre-term birth, pregnancy loss, school absences, and other adverse health outcomes.
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atmosphere
Review
Historic and Modern Air Pollution Studies
Conducted in Utah
Judy Ou 1, *, Cheryl S. Pirozzi 2, Benjamin D. Horne 3,4 , Heidi A. Hanson 1,5,
Anne C. Kirchho1,6, Logan E. Mitchell 7, Nathan C. Coleman 8and C. Arden Pope III 8
1Huntsman Cancer Institute, Cancer Control and Population Sciences, University of Utah,
Salt Lake City, UT 84112, USA;
heidi.hanson@hci.utah.edu (H.A.H.); Anne.Kirchho@hci.utah.edu (A.C.K.)
2Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Utah,
Salt Lake City, UT 84132, USA; Cheryl.Pirozzi@hsc.utah.edu
3Intermountain Medical Center Heart Institute, Salt Lake City, UT 84107, USA; Benjamin.Horne@imail.org
4Division of Cardiovascular Medicine, Department of Medicine, Stanford University,
Stanford, CA 94063, USA
5Department of Surgery, University of Utah School of Medicine, Salt Lake City, UT 84132, USA
6Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, UT 84132, USA
7Department of Atmospheric Sciences, University of Utah, Salt Lake City, UT 84112, USA;
logan.mitchell@utah.edu
8Department of Economics, Brigham Young University, Provo, UT 84602, USA;
1nathancoleman@gmail.com (N.C.C.); cap3@byu.edu (C.A.P.III)
*Correspondence: Judy.Ou@hci.utah.edu
Received: 31 August 2020; Accepted: 6 October 2020; Published: 13 October 2020
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Abstract:
Utah’s low-smoking population and high population density concentrated in mountain
valleys, with intermittent industrial activity and frequent temperature inversions, have yielded
unique opportunities to study air pollution. These studies have contributed to the understanding
of the human health impacts of air pollution. The populated mountain valleys of Utah experience
considerable variability in concentrations of ambient air pollution because of local emission sources
that change over time and episodic atmospheric conditions that result in elevated concentrations of
air pollution. Evidence from Utah studies indicates that air pollution, especially combustion-related
fine particulate matter air pollution and ozone, contributes to various adverse health outcomes,
including respiratory and cardiovascular morbidity and mortality and increased risk of lung cancer.
The evidence suggests that air pollution may also contribute to risk of pre-term birth, pregnancy loss,
school absences, and other adverse health outcomes.
Keywords: air pollution; mortality and morbidity; Utah; particulate matter; ozone
1. Introduction
The state of Utah has a long history of poor air quality that has provided substantial opportunities
to study the health eects of air pollution. Most of Utah’s land mass includes sparsely populated
mountains, deserts, and canyonlands with relatively clean, less polluted air. However, most Utahans
live in urban areas located in valley basins surrounded by mountains. Approximately 80% of the
population of Utah lives in a contiguous urban/suburban area called the Wasatch Front [
1
]. The Wasatch
Front is a relatively narrow landmass—approximately 80 miles (130 km) long from north to south and
5 to 18 miles (8–29 km) wide—bordered on the east by the Wasatch Mountain Range. The relatively
dense population of the Wasatch Front (compared to the rest of the state and most other areas in the
Intermountain West) and related industrial, trac, and other emission sources result in substantial
levels of air pollution that can at times be the worst in the U.S. [
2
]. Furthermore, surrounding mountain
Atmosphere 2020,11, 1094; doi:10.3390/atmos11101094 www.mdpi.com/journal/atmosphere
Atmosphere 2020,11, 1094 2 of 14
topography and interaction with meteorological conditions lead to considerable temporal variability
in air pollution.
Changes in the operation of major industrial sources of air pollution in Utah—including the
intermittent operation of a steel mill and copper smelter—have provided unique natural experiments
or quasi-experimental conditions to explore health impacts of air pollution. Utah also consistently
holds the nation’s lowest smoking rate (9% compared to the national average of 17.1%) [
3
], which helps
evaluate the health eects of air pollution with less potential for confounding from smoking.
Studies of particulate matter air pollution have been the primary focus in Utah. Monitoring of
PM
10
(particles <10
µ
m in aerodynamic diameter) began at Utah monitoring sites in the mid to late
1980s, and regular monitoring of PM
2.5
(particles <2.5
µ
m in aerodynamic diameter) began at some
Utah monitoring sites in 1999. A growing number of studies have also investigated the eects of ozone
(O
3
) and nitrogen oxide (NO
x
) pollutants. These pollutants are growing in relevance because Utah’s
four largest counties (Salt Lake, Utah, Davis, and Weber, which account for 75% of the population)
are currently not compliant with federal national ambient air quality standards (NAAQS) for ozone.
This problem is projected to worsen as emissions increase from a rapidly growing population and
climate change threatens to increase ground-level ozone production [
4
,
5
]. Since 2009, Utah’s population
grew 14 percent to a current total of
3 million persons [
6
]. The population is anticipated to grow
to 5.8 million in 2065, which represents a rate of change of 1.3 percent. This is nearly double the
0.7 percent growth seen nationally from 2016 to 2017 [
7
]. Utah has reduced air emissions by 38 percent
during the past 15 years, but the winter temperature inversions still pose a major problem for the state,
and summertime ozone emissions are emerging as a major public health concerns [6].
Early epidemiology studies of air pollution in Utah contributed to the 1971 U.S. Environmental
Protection Agency (EPA) sponsored Community Health and Environmental Surveillance System
(CHESS) studies. The CHESS studies in Utah were focused on the health eects of particulate matter
and sulfur oxides, with a specific focus on sulfur dioxide and sulfates [
8
,
9
]. There was substantial
controversy surrounding the CHESS studies, compromising the ability for the program to change
public policy and move air pollution science forward.
Air pollution research in Utah resumed in the mid to late 1980s, including a unique natural
experiment related to the intermittent operation of a major industrial source of pollution [
10
,
11
]; a series
of panel studies on the link between air pollution, pulmonary function, and respiratory illness [
12
,
13
];
and early time-series studies of daily mortality [
14
,
15
]. These Utah-based studies were included in
the Environmental Protection Agency’s 1996 Air Quality Criteria for Particulate Matter Final Report,
which laid the groundwork for fine particulate matter (PM
2.5
) standards [
16
]. Today, Utah-based
studies remain a part of a much larger and broader body of research that explores the health eects of
air pollution. This article briefly summarizes the results of existing Utah-based studies of pollution’s
eects on multiple health outcomes including mortality, respiratory disease, cardiovascular disease,
cancer survivorship, and birth outcomes (Table 1).
Atmosphere 2020,11, 1094 3 of 14
Table 1. Outline and review of air pollution and health studies from Utah.
Studies Health End Points Study Designs Result Summary of Results
Mortality, all Cause, Cardiovascular, Respiratory
Mortality associated with higher levels of air
pollution, especially combustion/industrial-source
fine particles versus windblown fine particles.
Archer 1990 [17] Respiratory and lung cancer mortality 3-county ecologic +
Pope et al., 1992,1996,1999 [14,15,18] All, cardiovascular, respiratory mortality Daily time series +
Lyon et al., 1995 [19] All, cardiovascular, respiratory mortality Daily time series 0
Styer et al., 1995 [20] All mortality Daily time series 0
Ransom et al., 1995 [21] All mortality and hospitalization Natural experiment +
Pope et al., 2007 [22] All mortality Natural experiment +
Respiratory Illness/Function
Epidemiological and toxicological evidence that
air pollution contributes to pulmonary
inflammation, respiratory illness and disease and
reduced pulmonary function.
Love et al., 1982 [9] Respiratory illness incidence and severity Panel 0
Lutz 1983 [23] Diagnosis of respiratory or cardiac illness Episode study +
Pope 1989, 1991 [10,11] Hospitalization for respiratory illness Natural experiment +
Pope et al., 1991,1992 [12,13] Respiratory symptoms/function in children Panel/time series +
Pope and Kanner 1993 [24]
Pulmonary function eects for former smokers
Panel +
Ghio et al., 2001 [25] Inflammatory lung injury in humans Human in vivo +
Dye et al., 2001 [26] Pulmonary toxicity in rats Toxicology +
Watterson et al., 2007 [27] Gene expression Toxicology +
Beard et al., 2012 [28] Emergency Department visits for asthma Case-crossover +
Pirozzi et al., 2015a, 2015b [29,30] Respiratory eects for former smokers Observational/panel +/0
Horne et al., 2018 [31] Respiratory infection Case crossover +
Pirozzi et al., 2018 [32] Pneumonia incidence Case crossover +
Wagner et al., 2018, 2020 [33,34] Aerobic, pulmonary function Human experiment 0
Cardiovascular Illness/Function
Evidence that air pollution contributes to risk of
various cardiovascular events, impairs cardiac
autonomic function, and contributes to
inflammation and endothelial injury.
Pope et al., 1999b, 1999c, 2004 [3537] Heart rate variability Panel/human experiment +/0
Pope et al., 2006, 2015 [38,39] Ischemic heart disease events Case crossover +
Pope et al., 2008 [40] Heart failure, hospitalization Case crossover +
O’Toole et al., 2010 [41] Endothelial progenitor cells Panel/human experiment +
Bunch et al., 2011 [42] Atrial fibrillation hospitalization Case crossover 0
Pope et al., 2016 [43] Endothelial injury and inflammation Panel/human experiment +
Leiser et al., 2019 [44] Cardiac hospital readmission/death Medicare cohort +
Atmosphere 2020,11, 1094 4 of 14
Table 1. Cont.
Studies Health End Points Study Designs Result Summary of Results
Cancer
Evidence that radioactive fallout is associated with
cancer mortality. Contributes to evidence that air
pollution may be associated with cancer and
cancer survival.
Lyon et al., 1981 [45] Lung cancer incidence Case–control 0
Archer 1990 [17] Lung cancer mortality 3-county ecologic +
Blindauer et al., 1993 [46] Lung cancer incidence Natural experiment 0
Ball et al., 2008 [47] Lung, kidney, non-Hodgkin’s Ecological +
Ou et al., 2019 [48] Respiratory health in cancer survivors Case crossover +
Ou et al., 2020 [49] Various types of cancer mortality Cohort +
Birth Outcomes
Contributes to evidence of an association between
air pollution and pre-term birth.
Parker et al., 2008 [50] Pre-term birth Natural experiment +
Mendola et al., 2019 [51] Pre-term birth Observational cohort +
Leiser et al., 2019 [52] Pregnancy loss Case crossover 0
Other
Evidence that air pollution is associated with an
increase in school absences and other health
outcomes. Evidence for higher exposure amongst
minority populations.
Ransom et al., 1992 [53] School absences Daily time series +
Zeft et al., 2009 [54] Juvenile idiopathic arthritis Case crossover +
Bakian et al., 2015 [55] Suicide Case crossover +
Hales et al., 2016 [56] School absences Natural experiment +
Youngquist et al., 2016 [57] Emergency Medical Service calls Case crossover 0
Mullen et al., 2019 [58] Racial/ethnic exposure disparity Exposure modeling +
Collins et al., 2019 [59] Racial/ethnic exposure disparity Cross-sectional +
+ = positive association; 0 =no association; =inverse association.
Atmosphere 2020,11, 1094 5 of 14
2. Mortality
Utah-based studies provide evidence of an association between air pollution and mortality.
Archer evaluated longitudinal dierences in mortality across three counties, contrasting death rates
during periods of intermittent operation of a steel mill that was constructed during World War II in one
of the counties (Utah County) [
17
]. This initial analysis was based on a simple ecological design that
compared mortality in Utah County to two other study areas without a similar source of industrial
pollution. It was estimated that 30 to 40% of respiratory cancer and nonmalignant respiratory disease
deaths in one of these areas were associated with community air pollution emitted from the steel
mill [
17
]. Additionally, analyses that treated the intermittent operations of a local steel mill [
21
] and
the intermittent operation copper smelter [
22
] as natural experiments further observed that mortality
was associated with fine-combustion and industrial-source particulate air pollution.
Several population-based, daily time-series studies that evaluated day-to-day changes in mortality
counts with short-term (1–5 days) changes in air pollution have been conducted using Utah’s Wasatch
Front counties (Salt Lake, Utah, Davis, and Weber). The earliest study reported a 16% increase in
mortality counts in Utah County associated with a 100
µ
g/m
3
increased in exposure to particulate
matter air pollution, measured as PM
10
over the previous 5 days, after controlling for time trends,
seasonality, temperature, and relative humidity [
14
]. Pollution was most strongly associated with
respiratory and cardiovascular deaths. Additional analyses of Utah County mortality data confirmed
the PM–mortality association but questioned if the association was causal [
19
]. An extended analysis,
however, demonstrated similar PM–mortality associations of (between 11–16% per 100
µ
g/m
3
of PM
10
)
using alternative synoptic weather modeling approaches to control for weather, suggesting that the
observed PM–mortality associations were not the results of confounding by weather variables [15].
A daily time-series analysis of mortality counts and air pollution in a neighboring Wasatch Front
county (Salt Lake County) did not find evidence of an association between mortality and PM
10
[
20
].
A more comprehensive population-based daily time-series mortality study was conducted using the
populations from all three primary metropolitan areas of the Wasatch Front including the following:
the Ogden area (Weber County), the Salt Lake City area (Salt Lake and Davis Counties), and the
Provo/Orem area (Utah County) [
18
]. The Salt Lake City area experienced many more high PM episodes
dominated by windblown dust. When the pollution data were screened to exclude windblown dust
episodes (based on clearing index screening), comparable PM
10
–mortality associations were observed
across the Wasatch Front metropolitan areas (between 0.8–1.6% change in mortality per 10
µ
g/m
3
) [
18
].
It was concluded that stagnant air pollution episodes with higher concentrations of combustion-source
and industrial-source fine particles were more strongly associated with elevated mortality (as opposed
to windblown dust episodes with higher coarse, crustal derived particles).
3. Lung Disease and Respiratory Health Outcomes
3.1. Human Health Outcomes
Multiple Utah-based studies reported that air pollution is associated with adverse respiratory
health outcomes. As noted above, population-based daily time-series mortality studies observe that
short-term increases in pollution are associated with increased respiratory mortality counts [
14
,
15
,
18
].
Short-term increases in PM
10
and PM
2.5
during winter inversions are associated with significant
increases in the risk estimates for outpatient visits, emergency department visits, and hospital
admissions for respiratory disease in multiple counties [
10
,
11
,
23
,
28
]. These studies found that there
were nearly twice as many respiratory hospital admissions for children during the period the steel mill
was operating compared to when the steel mill was not operating [
10
,
11
]. One study found that for
months when PM
10
was over 50
µ
g/m
3
, the average annual standard at the time, hospital admissions
increased by 89% for children and 47% for adults [10].
Respiratory infections are a particular concern as acute lower respiratory infections, bronchitis,
and pneumonia have significant associations with short-term increases in particulate matter
Atmosphere 2020,11, 1094 6 of 14
pollution [
31
,
32
]. Pediatric populations are particularly vulnerable to respiratory infections associated
with short-term increases in PM
2.5
. One study found that the odds ratio for acute lower respiratory
infection in young children (0–2 years of age) is 1.15 (95% CI: 1.12–1.19) per 10
µ
g/m
3
PM
2.5
, with a lag
period of up to 28 days [
31
]. The associations are somewhat larger for pneumonia, with odds ratios
ranging from 1.35–1.50 [
32
]. Pediatric populations exposed to high levels of PM
2.5
also report increased
use of asthma medication, coughing, and increases in reported symptoms of respiratory disease [
12
,
13
].
3.2. Lung Function and Performance
Utah-based studies provide evidence that air pollution is associated with reduced lung function
in susceptible populations. Studies of 16 healthy adults exposed to PM
2.5
below the federal 24 h health
standard found no negative eects on respiratory function or aerobic performance after 20 min of heavy
exercise [
33
,
34
], but multiple studies reported significant eects on lung function among children and
adults with preexisting chronic obstructive pulmonary disease (COPD) [
12
,
13
,
24
]. Among fourth and
fifth grade elementary students, 150
µ
g/m
3
increases in PM
10
were associated with a 3–6% decline in
lung function [
12
]. In a cohort of fifth and sixth graders, short-term increases in PM
10
were associated
with declines in peak expiratory flow (PEF), irrespective of exhibited symptoms [
13
]. Among adult
smokers with COPD, an increase of 100
µ
g/m
3
in PM
10
was significantly associated with a 2% decrease
in forced expiratory volume [
24
]. For adult COPD patients, respiratory symptoms significantly
increased after days with increased PM2.5 [29].
3.3. Biomarkers
Multiple laboratory and human biomarker studies support local inflammation as the primary
mechanism by which particulate matter and ozone pollution exert adverse eects on the respiratory
system. An
in vitro
study reported that human bronchial epithelial cells (BEAS-2B) exposed to PM
2.5
found in Cache Valley significantly upregulated genes activating receptors to interleukins 1 and
6 (IL-1R1 and IL-6R), IL-6 and phosphorylated STAT3 protein release, indicating activation of the
IL-6/gp130/STAT3 signaling pathway [
27
]. The study also reported slight cytotoxicity of the Cache
valley PM
2.5
[
27
]. An
in vivo
study examined the eect of PM
2.5
particulates collected during the
period of intermittent steel mill operation installed in the trachea of Sprague–Dawley rats. Rats exposed
to PM
2.5
collected during steel mill operation expressed significant pulmonary injury and neutrophilic
inflammation, which was suggested to be due to metals contained in the particulate matter [26].
A human
in vivo
study installed aqueous extracts of PM collected during intermittent steel
mill operation over a 3-year period inside the lungs of 24 nonsmoking healthy volunteers.
Subjects administered the extracts of PM from filters taken while the steel mill was in operation
had significantly high levels of neutrophil infiltration and elevated concentrations of fibronectin and
α
-1-antitrypsin, indicating inflammatory lung injury [
25
]. In a separate study, human exhaled breath
condensate was collected from former smokers with moderate to severe COPD on days with PM
2.5
that was considered “clean” and on days with higher PM
2.5
pollution during winter inversions [
29
].
High PM
2.5
levels were associated with increases in nitrite plus nitrate (NO
x
), a biomarker of oxidative
stress in COPD patients (mean of 3.16 dierence between polluted and clean days), but not former
smokers without COPD. Ozone was also examined as a potential pulmonary inflammatory agent
among individuals with COPD. High ozone was associated with increased NOx and thus oxidative
stress and pulmonary inflammation in both COPD patients (8.7 vs. 28.6 on clean versus polluted days)
and persons without COPD (7.6 vs. 28.5), with no dierence between the groups [30].
4. Cardiovascular Disease
Several Utah-based studies have found an association between air pollution and cardiovascular
health. As noted above, population-based daily time-series mortality studies have observed that short-term
increases in pollution are associated with increased cardiovascular mortality [
14
,
15
,
18
]. Case-crossover
studies of patients drawn from a large cardiac catheterization registry who lived in the Wasatch Front
Atmosphere 2020,11, 1094 7 of 14
area of Utah observed that a 10
µ
g/m
3
increase in PM
2.5
air pollution was associated with a 4.5% (95% CI:
1.1–8.0) increased risk of acute ischemic coronary events (unstable angina and myocardial infarction) [
38
].
The elevated risk was primarily observed among patients with angiographically demonstrated underlying
coronary artery disease. An additional similar case-crossover study provided further evidence that,
for patients living on Utah’s Wasatch Front, a 10
µ
g/m
3
increase in PM
2.5
exposures contribute to the
triggering of acute coronary events (OR 1.06, 95% CI: 1.02–1.11), especially ST-segment elevation myocardial
infarction (OR 1.15, 95% CI: 1.03–1.29) [
39
]. Case-crossover studies of hospitalizations further observed
that air pollution was associated with heart failure hospitalizations (13.1% increase per 10 µg/m3, 95% CI:
1.3–26.2) [
40
] but not with hospitalizations for atrial fibrillations [
42
]. A cohort study examining the risk of
hospital readmission and death after cardiovascular events found that an increase of 10
µ
g/m
3
in PM
2.5
led
to a 25–30% increased risk of readmission [44].
Utah studies have explored pathophysiological pathways that link exposure to air pollution
with cardiovascular disease. PM
2.5
air pollution in Utah has been associated with changes
in cardiac autonomic function as measured by measures of heart rate variability [
35
37
],
blood markers of inflammation [
37
,
43
], decreasing circulating levels of endothelial progenitor cells [
41
],
and vascular/endothelial injury [
43
]. A recent study conducted in Utah County analyzed blood drawn
from panels of healthy, nonsmoking young adults. The timing of multiple blood draws took advantage
of frequent persistent temperature inversion episodes, allowing for blood draws at times with varying
levels of exposure to PM
2.5
pollution [
43
]. Increased air pollution exposure was associated with elevated
immune cells, a systemic increase in inflammatory and antiangiogenic cytokines with suppression
of proangiogenic growth factors. Additionally, elevated air pollution exposure was associated with
increased circulating endothelial microparticles, indicating endothelial cell apoptosis and vascular
injury [43].
5. Cancer
Although air pollution is currently classified by the International Agency for Research on Cancer as
a known carcinogen and extensive research support its association with incident cancer (especially lung
cancer) and cancer mortality [
60
], published studies in Utah on the topic are limited and inconclusive.
A cluster investigation around point sources of pollution reported no significant increase in the
incidence of cancers among residents near a coke oven in a steel mill, but did report a slight increase
in the number of excess lung cancers near the coke ovens [
45
]. In a separate study, mortality from
respiratory cancers in a low-smoking county with a steel mill was estimated to be 38% higher than
mortality in a neighboring low-smoking county without a steel mill [
17
]. In a case–control study that
adjusted for smoking, no consistent dierence was found in the rates of lung cancer incidence between
Utah county and several other counties [
46
]. A cluster study of lung, kidney, and non-Hodgkin
lymphomas found elevations in the number of kidney (Risk Ratio (RR) range: 0.50–3.17) and lung
cancers (RR range: 1.02–1.51) around Hill Air Force Base, with the authors attributing the elevated risk
of cancers to water contamination from the Air Force base rather than potential air pollutants from the
base or other emission sources [47].
To date, most research on the topic of air pollutants and cancer focused on cancer incidence or
mortality in a general population. Researchers in Utah were the first to investigate the eect of air
pollution on the pulmonary health and mortality of cancer survivors after diagnosis. Cancer itself and
the long-term toxic eects of cancer therapies on cancer survivors may increase their susceptibility
to health events and mortality associated with air pollution. In a statewide case-crossover study of
childhood cancer survivors, PM
2.5
was associated with significant increases in the risk for respiratory
hospitalization and emergency room visits or hospitalization for respiratory infection. The risk
for respiratory events was significantly higher among childhood cancer survivors than population
comparisons without a cancer history (OR 1.84, 95% CI: 1.13–3.00 per 10
µ
g/m
3
) [
48
]. PM
2.5
exposure
from diagnosis through 5 and 10 years after diagnosis was also associated with all cause and cancer
mortality among pediatric, adolescent, and young adult survivors (AYA) with certain diagnoses [
49
].
Atmosphere 2020,11, 1094 8 of 14
Pediatric patients diagnosed at age 14 years or younger with lymphoma (1.34, 95% CI: 1.06–1.68) or
central nervous system (CNS) tumors (1.27, 95% CI: 1.05–1.52) had a significant increase in their risk for
cancer mortality associated with a 5
µ
g/m
3
increase in PM
2.5
exposure within 10 years from diagnosis.
Among AYAs diagnosed from age 15 to 39 years, PM
2.5
was associated with all cause and cancer
mortality among survivors with central nervous system tumors (1.20, 95% CI: 1.04–1.38), breast cancer
(1.16, 95% CI: 0.97–1.39), and colorectal cancer (1.23, 95% CI: 1.00–52) within 10 years of diagnosis.
6. Birth Outcomes
Human epidemiologic studies in Utah of the association between air pollutant exposure and birth
outcomes are rare. Two studies reported significant associations between increased exposure to PM
2.5
and risk of preterm births [
50
,
51
]. The sources of PM
2.5
and pollutants studies varied between the
studies. An earlier study implemented a quasi-experimental design to examine the eect of a steel
mill closure on preterm births and birth weight [
50
]. Utah mothers who were pregnant around the
time of the steel mill closure were less likely to have a preterm birth than mothers who were pregnant
before or after the closure (RR 0.95, 95% CI: 0.77–1.18). Reducing exposure during the second trimester
appeared to have the highest eects in reducing preterm births. No eects on birth weight were
observed, but the authors acknowledged the small sample size found in the study and their lack of
exact exposure estimates for each mother.
The latter study examined the association of preterm births and air pollution while accounting for
the composition of the pollution among mothers with two consecutive pregnancies [
51
]. This study
reported that high exposure to sulfur dioxides, ozone, nitrogen oxides, carbon monoxides, and particles
<10
µ
g m
3
had a positive association with second pregnancy preterm births (range of 17–43% increase
in risk). Only one Utah-based study examined the associations of PM
2.5
and nitrogen dioxide with
spontaneous pregnancy loss [
52
]. The authors reported a significant 16% increase in the odds of
spontaneous pregnancy loss associated with a 10 ppb increase in 7-day levels of nitrogen dioxide,
and positive but non-significant associations with 3- and 7-day averages of PM2.5 [52].
7. Other Outcomes
Air pollution appears has additional wide-ranging eects on society that may aect public use of
emergency services, education, and mental health. Utah-based studies report significant associations
between short-term PM
2.5
exposure and emergency services calls for diabetic symptoms, but no
significant associations with CV or respiratory symptoms [
57
]. School absences may also be associated
with PM
10
and PM
2.5
, with eects varying by the lag periods of interest and scope of the study.
A single-county study found a significant association between a 28-day moving average of PM
10
equal to 100
µ
g/m
3
with a 2% increase in the rate of school absences in one school district and an
elementary school in Utah county [
53
]. A study of school districts in multiple Utah counties recently
reported a similar finding that a 10
µ
g/m
3
increase in PM
2.5
was associated with a 1.7% increase in daily
elementary school absences. These findings were robust even after controlling for structural factors
such as seasonal trends across school years, day-of-week eects, holiday eects, and weather [56].
An emerging body of research reported significant associations between suicide completion and
increases in specific air pollutants. In Utah, interquartile-range increases in 3-day cumulative averages
of nitrogen dioxide and lag-day increases in PM
2.5
were associated with an increased suicide risk
(OR 1.20, 95% CI: 1.04–1.39 and OR 1.05, 95% CI: 1.01,1.10, respectively). Exposure to nitrogen dioxide
during the spring and fall and exposure to PM
2.5
during the spring were reported as having significant
associations with suicide [55].
Although air pollution has systemic inflammatory eects, few studies in Utah have examined
its association with arthritic disease. A single study of preschool aged children living in Utah’s
Wasatch Front reported significant associations between 14-day increases in PM
2.5
concentrations and
a significant elevation in the risk of juvenile idiopathic arthritis (JIA) (RR 1.60, 95% CI: 1.00–2.54).
The risk was higher in males than females and in patients with systemic onset JIA [54].
Atmosphere 2020,11, 1094 9 of 14
Inequities in exposure to air pollutants by racial and ethnic groups have also been observed in
Utah [
58
,
59
]. A study of air pollution exposure in Salt Lake City estimated that schools with higher
proportions of racial/ethnic minority students were consistently exposed to more PM
2.5
pollution
(Hispanics and RRs: 1.02–1.12; non-Hispanic minorities and RRs: 1.01–1.04) [
58
]. Another study of Salt
Lake City residents reported inequalities in air pollution exposure across dierences in race, ethnicity,
and religion (negative association between PM
2.5
concentration and White percentage, p
0.001) [
59
].
8. Summary and Conclusions
Utah-based air pollution studies have made important contributions to understanding the health
eects of air pollution. As would be expected, the evidence suggests that Utahans experience similar
health eects of air pollution as observed elsewhere [
61
,
62
]. Figure 1summarizes key health eects
of air pollution based on evidence from the overall scientific literature, with the eects that have
been observed in Utah-based studies highlighted [
63
,
64
]. Figure 2is a photograph of the pollution in
Utah Valley around the local steel mill, the health eects of which have been examined in multiple
studies. The majority of research in Utah has been focused on particulate matter’s eects on human
health outcomes. The particulate matter measures in past studies largely originated from industrial
emissions, wood burning, and mobile transportation sources. Although the steel mill featured in
several Utah-based studies closed in the early 2000s and Utah has seen improvements in air quality
since the 1990s, Utah has seen a regular annual increase in emissions of particulate matter pollution
from wildfires that are increasing in frequency and severity as a result of warmer and drier conditions
due to climate change [
65
]. Particulate matter from these wildfires originates from fires in Utah and
in states across the west coast. The composition of the particulate matter from these wildfires likely
diers from the prior particulate matter studied, the health eects of which have yet to be determined.
Figure 1. Health effects of air pollution (attached). Adapted from Thurston et al. 2017 [63] and The
Utah Roadmap 2020 [64].
Figure 1.
Health eects of air pollution (attached). Adapted from Thurston et al. 2017 [
63
] and The
Utah Roadmap 2020 [64].
Atmosphere 2020,11, 1094 10 of 14
Figure 1. Health effects of air pollution (attached). Adapted from Thurston et al. 2017 [63] and The
Utah Roadmap 2020 [64].
Figure 2.
Photograph of Geneva Steel, Utah Valley, 1989 (PM
10
(particles <10
µ
m in aerodynamic
diameter) approximately 150 µg m3).
Ozone and nitrogen oxides are air pollutants present in Utah, but their health eects on the Utah
population are understudied relative to the research on particulate matter pollution. In addition,
Utah is one of the nation’s largest emitters of toxic air emissions [
66
], primarily due to a large copper
mine located west of the Wasatch Front. Few studies in Utah have examined how exposures to air
toxics influence health outcomes such as cancer incidence or cancer mortality. Future directions for air
pollution studies in Utah include more human health studies that examine associations between health
and wildfire smoke, ozone, nitrogen oxides, air toxics, and the results of multi-pollutant exposures.
Furthermore, as new low-cost and mobile air quality measurements are deployed, studies could focus
on the spatial pattern of health eects at smaller spatial scales than counties.
Utah has experienced rapid population growth in recent decades largely along the already densely
populated Wasatch Front. The majority of Utahans utilize cars as their primary means of transportation.
Governmental policies that can increase the availability and use of public transportation and city zoning
laws that can reduce the number of residences located near mobile and point sources of pollution are not
uniformly implemented across the Wasatch Front. Consequently, air pollution emissions in Utah from
mobile sources and chronic exposure to mobile emissions may increase as the population continues to
grow unless public policy can accelerate the adoption of low- or zero-emission technologies [64].
Utah-based studies and many others across the world report a substantial number adverse health
eects due to air pollution exposure. Despite decades of research, the debate about air pollution and
its health implications continues. One of the primary arguments against the findings of air pollution
studies is the role of causation in human epidemiologic studies. Opponents of air pollution policies
argue that human epidemiologic studies leave too much uncertainty around whether air pollution
truly has a casual eect on the adverse health outcomes documented in the literature. Because air
pollution exposure is widespread, finding counterfactual populations to demonstrate causality in air
pollution studies can be challenging. Utah is home to the nation’s only population database, the Utah
Atmosphere 2020,11, 1094 11 of 14
Population Database (UPDB), which can create longitudinal residential histories for all Utahans from
first residence or birth in the state to death or emigration from the state by linking driver license,
vital records, voter registration, and marriage and divorce records to personal identifying information.
Data about air pollution exposure at the address level, all medical history and cancer diagnoses for Utah
residents, vital status, and family history of disease for all persons living in the state are also available
through the UPDB. Future studies on the topic of health outcomes in Utah can address questions
regarding causality in epidemiologic studies by leveraging the long-term follow up, comprehensive
capture of confounders like smoking, longitudinal residential history, and matching capabilities of the
Utah Population Database.
Utah’s contribution to the literature on the health impacts of air pollution will continue to grow.
Future topics of relevance include studies of governmental policies addressing air pollution exposure;
inequities in these exposures; health studies that incorporate air toxics and ozone and nitrogen oxides;
understanding how air pollution contributes to COVID-19; eects of wildfires exacerbated by climate
change; source apportionment studies and their associated health eects; and sub-county gradients in
air pollution. The unique pollution patterns, data resources, and scientific capacity in Utah can be
leveraged to address knowledge gaps that remain in this field.
Author Contributions:
Conceptualization: J.O., C.S.P., B.D.H., L.E.M., C.A.P.III; Methodology: J.O., C.S.P., B.D.H.,
L.E.M., N.C.C., C.A.P.III; Resources: J.O., B.D.H., C.A.P.III; Writing—original draft preparation: J.O., N.C.C.,
C.A.P.III; Writing—review and editing: J.O., C.S.P., B.D.H., H.A.H., A.C.K., L.E.M., N.C.C., C.A.P.III; Visualization:
J.O., C.S.P., B.D.H., N.C.C., C.A.P.III; Supervision: J.O., C.A.P.III; Project administration: J.O., N.C.C., C.A.P.III.
All authors have read and agreed to the published version of the manuscript.
Funding:
This research received no external funding. C.A.P.III was funded in part by the Mary Lou Fulton
Professorship, Brigham Young University.
Acknowledgments:
Claire Davis provided the original illustrations for the visual abstract (Figure 1) used in
this paper.
Conflicts of Interest: The authors declare no conflict of interest.
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... Two-thirds of Utah's population, roughly 2 million residents, live adjacent to the Wasatch Mountain range and the Great Salt Lake. Air pollutants are emitted almost entirely by local sources within Utah [3] and these topographic features exacerbate air quality events, leading this urbanizing region to regularly feature some of the worst short-term air pollution episodes in the world (e.g., [4]). ...
... With air quality a dominant health risk of the 21st century (e.g., [5,6]), the prevalence of acute air pollution events in Utah presents significant challenges to public health, quality of life, and economic vitality. The impacts from poor air quality episodes on human health (e.g., respiratory, circulatory, cancer, mortality, etc.) are well documented [4,6,7], as are cascading economic impacts (e.g., health care costs, decreased worker productivity, etc.) [8,9] As we document in this narrative review, Utah's struggles with poor air quality are not new. Recent digitization of newspaper articles and scientific reports increased the availability of historical accounts of how Utahns historically grappled with air pollution issues. ...
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Background: Air pollution is a carcinogen and causes pulmonary and cardiac complications. We examined the association of fine particulate matter pollution (PM2.5) and mortality from cancer and all causes among pediatric, adolescent, and young adult (AYA) patients with cancer in Utah, a state with considerable variation in PM2.5. Methods: We followed 2,444 pediatric (diagnosed ages 0-14) and 13,459 AYA (diagnosed ages 15-39) patients diagnosed in 1986-2015 from diagnosis to 5 and 10 years postdiagnosis, death, or emigration. We measured average monthly PM2.5 by ZIP code during follow-up. Separate pediatric and AYA multivariable Cox models estimated the association of PM2.5 and mortality. Among AYAs, we examined effect modification of PM2.5 and mortality by stage while controlling for cancer type. Results: Increases in PM2.5 per 5 μg/m3 were associated with cancer mortality in pediatric lymphomas and central nervous system (CNS) tumors at both time points, and all cause mortality in lymphoid leukemias [HR5-year = 1.32 (1.02-1.71)]. Among AYAs, PM2.5 per 5 μg/m3 was associated with cancer mortality in CNS tumors and carcinomas at both time points, and all cause mortality for all AYA cancer types [HR5-year = 1.06 (1.01-1.13)]. PM2.5 ≥12 μg/m3 was associated with cancer mortality among breast [HR5-year = 1.50 (1.29-1.74); HR10-year = 1.30 (1.13-1.50)] and colorectal cancers [HR5-year = 1.74 (1.29-2.35); HR10-year = 1.67 (1.20-2.31)] at both time points. Effect modification by stage was significant, with local tumors at highest risk. Conclusions: PM2.5 was associated with mortality in pediatric and AYA patients with specific cancers. Impact: Limiting PM2.5 exposure may be important for young cancer patients with certain cancers.
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Previous studies have cataloged social disparities in air pollution exposure in US public schools with respect to race/ethnicity and socioeconomic status. These studies rely upon chronic, averaged measures of air pollution, which fosters a static conception of exposure disparities. This paper examines PM2.5 exposure disparities in Salt Lake County (SLC), Utah public schools under three different PM2.5 scenarios—relatively clean air, a moderate winter persistent cold air pool (PCAP), and a major winter PCAP—with respect to race/ethnicity, economic deprivation, student age, and school type. We pair demographic data for SLC schools (n = 174) with modelled PM2.5 values, obtained from a distributed network of sensors placed through a community-university partnership. Results from generalized estimating equations controlling for school district clustering and other covariates reveal that patterns of social inequality vary under different PM2.5 pollution scenarios. Charter schools and schools serving economically deprived students experienced disproportionate exposure during relatively clean air and moderate PM2.5 PCAP conditions, but those inequalities attenuated under major PCAP conditions. Schools with higher proportions of racial/ethnic minority students were unequally exposed under all PM2.5 pollution scenarios, reflecting the robustness of racial/ethnic disparities in exposure. The findings speak to the need for policy changes to protect school-aged children from environmental harm in SLC and elsewhere.
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Introduction: Wintertime thermal inversions can lead to the accumulation of small particulate matter (PM2.5). Despite an association between respiratory hospital admissions and elevated PM2.5 levels, many people continue to exercise outdoors during inversions. This study compared pulmonary function and exercise performance during periods of low and high ambient PM2.5 concentrations. Methods: Forced vital capacity and forced expiratory volume in 1 s were measured outdoors before and after two 3200 m running time trials: one with low ambient PM2.5 (0.6-14.7 microgram·m-3), and the other during high PM2.5 (19.1-42.5 micrograms·m-3). A 10 cm visual analog scale (VAS) administered postexercise quantified subjective ratings of respiratory discomfort. Results: The PM2.5 differential between trials was ≥18 micrograms·m-3 for 10 healthy runners. Despite feeling more respiratory discomfort (P=0.044) during the bad air trial (VAS: 4.6±1.8 cm) compared with the good air trial (VAS: 2.9±1.8 cm), the 3200 m run time (low PM2.5: 13:54±1:34 min:s; high PM2.5: 14:07±1:44 min:s) was not different (P=0.261) between trials. Postexercise forced vital capacity was not significantly different (P=0.846) between the low (4.86±1.00 L) and high (4.84±0.95 L) PM2.5 conditions. Similarly, the difference in postexercise forced expiratory volume in 1 s was not significant (P=0.750) between trials (4.22±0.89 L vs 4.23±0.85 L). Conclusions: Neither run time nor pulmonary function of healthy adults were adversely affected by an acute bout of exercise in elevated ambient PM2.5, equivalent to yellow or orange on the air quality index.
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Objective: To investigate the relationship between acute exposure to air pollutants and spontaneous pregnancy loss. Design: Case-crossover study from 2007 to 2015. Setting: An academic emergency department in the Wasatch Front area of Utah. Patient(s): A total of 1,398 women who experienced spontaneous pregnancy loss events. Intervention(s): None. Main outcome measure(s): Odds of spontaneous pregnancy loss. Result(s): We found that a 10-ppb increase in 7-day average levels of nitrogen dioxide was associated with a 16% increase in the odds of spontaneous pregnancy loss (odds ratio [OR] = 1.16; 95% confidence interval [CI] 1.01-1.33; P=.04). A 10-μg/m3 increase in 3-day and 7-day averages of fine particulate matter were associated with increased risk of spontaneous pregnancy loss, but the associations did not reach statistical significance (OR3-day average = 1.09; 95% CI 0.99-1.20; P=.05) (OR7-day average = 1.11; 95% CI 0.99-1.24; P=.06). We found no evidence of increased risk for any other metrics of nitrogen dioxide or fine particulate matter or any metric for ozone. Conclusions: We found that short-term exposure to elevated levels of air pollutants was associated with higher risk for spontaneous pregnancy loss.
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Rationale: Nearly 60% of U.S. children live in counties with PM2.5 concentrations above air quality standards. Understanding the relationship between ambient air pollution exposure and health outcomes informs actions to reduce exposure and disease risk. Objectives: To evaluate the association between ambient PM2.5 levels and healthcare encounters for acute lower respiratory infection (ALRI). Methods: Using an observational case-crossover design, subjects (N=146,397) were studied if they had an ALRI diagnosis and resided on Utah's Wasatch Front. PM2.5 air pollution concentrations were measured using community-based air quality monitors between 1999 and 2016. Odds ratios (OR) for ALRI healthcare encounters were calculated after stratification by ages 0-2, 3-17, and 18+ years. Measurements and main results: Approximately 77% (n=112,467) of subjects were 0-2 years of age. The odds of ALRI encounter for these young children increased within 1 week of elevated PM2.5 and peaked after 3 weeks with a cumulative 28-day OR= 1.15 per +10 μg/m3 (95% CI= 1.12, 1.19). ALRI encounters with diagnosed and laboratory-confirmed RSV and influenza increased following elevated ambient PM2.5 levels. Similar elevated odds for ALRI were also observed for older children, although the number of events and precision of estimates were much lower. Conclusions: In this large sample of urban/suburban patients, short-term exposure to elevated PM2.5 air pollution was associated with greater healthcare utilization for ALRI in both young children, older children, and adults. Further exploration is needed of causal interactions between PM2.5 and ALRI.