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Article

Associations Between Emergency Room Visits for Respiratory Diseases and Exposure to Zip Code-Level Criteria Air Pollutants in New York State

by
Tamba S. Lebbie
1,2,
Laura E. Jones
2,3,
Najm Alsadat Madani
2 and
David O. Carpenter
1,2,*
1
Department of Environmental Health Sciences, College of Integrated Health Sciences, University at Albany, Albany, NY 12222, USA
2
Institute for Health and the Environment, University at Albany, Albany, NY 12222, USA
3
Center for Biostatistics, Bassett Research Institute, Cooperstown, NY 13326, USA
*
Author to whom correspondence should be addressed.
Atmosphere 2026, 17(3), 322; https://doi.org/10.3390/atmos17030322
Submission received: 17 February 2026 / Revised: 12 March 2026 / Accepted: 16 March 2026 / Published: 20 March 2026
(This article belongs to the Special Issue Composition Analysis and Health Effects of Atmospheric Particulate Matter (2nd Edition))
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Abstract

We assess associations between emergency room (ER) visits, scaled to per 105 population per year, for asthma and chronic obstructive pulmonary disease (COPD), two of the most common respiratory diseases, and zip code-level exposure to criteria air pollutants (CAPs) coming from point sources in New York State (NYS) from 2010 to 2018. Exposure data on point source CAPs were retrieved from the United States Environmental Protection Agency (USEPA) National Emission Inventory (NEI) database, and ER visits for asthma and COPD were acquired from the New York State Department of Health (NYSDOH) Statewide Planning and Research Cooperative System (SPARCS). To account for within-county variability, we used log-linear mixed effects models, adjusted for year, sex, age category, county-level poverty, smoking, PM2.5, volatile organic compounds (VOCs), and CAPs sources within the study period. Results show significant associations between ER visits for asthma and COPD and most of the pollutants in the study, even after adjusting for the effects of poverty and smoking. Although point source emissions comprise a small portion of total air pollution, our findings show that zip code-level point source CAPs, especially the gaseous pollutants, pose a modest but significant contribution to the risk of respiratory disease-related ER visits.

1. Introduction

Air pollution is a well-established risk factor for respiratory morbidity and emergency room (ER) utilization. Yet, most research has emphasized particulate matter and broader ambient measures, with fewer studies isolating the contribution of local point source emissions. In our prior New York State study, we evaluated zip code-level point source emissions of volatile organic compounds (VOCs) from the National Emissions Inventory (NEI). We found compound-specific patterns and interactions associated with ER visits for asthma, COPD, and respiratory infections [1]. The present study extends this line of work by focusing on a different pollutant class, criteria air pollutants (CAPs) from point sources, and by quantifying their associations with ER visits for asthma and COPD across New York State from 2010 to 2018. A secondary goal is to determine the relative effects of the different CAPs, especially comparing the impact of particulates to that of the gaseous CAPs.
Asthma and chronic obstructive pulmonary disease (COPD) are respiratory diseases known for affecting the quality of life of people of all ages [2,3]. They pose serious public health concerns and cause millions of deaths worldwide. Asthma is a chronic disease, but asthma attacks are reversible respiratory events that are characterized by a response to hypersensitivity of airways, while COPD, for which asthma is one of the risk factors, is characterized by chronic airway obstruction [2,4]. Asthma attacks are manifested as intermittent and reversible airway obstruction, while COPD is progressive and irreversible [5]. Both diseases are disorders that are associated with increased inflammation [6]. Also, some patients with airway diseases have features of both asthma and COPD [7], indicating that both diseases can cause airway obstruction and are associated with chronic inflammation of the airways [8]. Both asthma and COPD exacerbations are responsible for approximately 1.5 million and 2 million yearly visits to the emergency room (ER), respectively, in the United States (US) [2,9].
Ambient air pollution accounts for an estimated 8% of the disease burden for respiratory infections [10]. Asthma development and exacerbation are linked to air pollution from fossil fuel combustion in traffic, power plants, and industrial facilities [11]. The relationship between air pollution and asthma attacks has been well-established, particularly in countries with rapid urbanization and industrialization [12]. Our group has previously reported adverse respiratory effects of outdoor air pollution in Karachi, Pakistan [13], Jeddah, Saudi Arabia [14], and New York State [1].
When inhaled, ambient air pollutants induce airway inflammation and oxidative stress in bronchial epithelial cells, which often lead to the development of asthma or COPD [15]. This conclusion is supported by epidemiological and clinical investigations suggesting that exposure to outdoor air pollutants, including criteria air pollutants (CAPs), induces airway inflammation, hyper-responsiveness and oxidative stress, leading to the exacerbations of asthma and COPD [16,17,18]. Several studies conducted in different parts of the world have found that day-to-day increases in pollution levels are associated with the exacerbation of asthma.
Zheng et al. [19] undertook a meta-analysis to quantify associations between short-term exposures to ozone (O3), carbon monoxide (CO), nitrogen dioxide (NO2), sulfur dioxide (SO2), and particulates (PM10 and PM2.5) and asthma-related ER visits and hospital admissions (HAs). The study found associations between these pollutants and significant increased relative risks (RRs) in asthma ER visits and hospital admissions (HAs) with O3: RR = 1.009 (1.006, 1.011), CO: RR = 1.045 (1.029, 1.061), NO2: RR = 1.018 (1.014, 1.022), SO2: RR = 1.011 (1.007, 1.015), PM10: RR = 1.010 (1.008, 1.013), and PM2.5: RR = 1.023 (1.015, 1.031). The study concluded that short-term exposures to the criteria pollutants account for increased risks of asthma-related ER visits and HAs that constitute considerable healthcare utilization and socioeconomic burden.
Additional studies of air pollution have documented relationships between ambient air pollution and respiratory disease-related ER visits for children, the most susceptible group. Strickland et al. [20] conducted a study to investigate short-term associations between ambient air pollutant concentrations and ER visits for pediatric asthma. A total of 91,386 children aged 5 to 17 years who visited the ER were collected from 41 metropolitan Atlanta hospitals between 1993 and 2004. The study results showed association between the ambient pollutants and pediatric asthma ER visits even at relatively low ambient concentrations: O3: RR = 1.062 (1.031–1.093), NO2: RR = 1.036 (1.018–1.055), CO: RR = 1.023 (1.006–1.041), PM2.5: R = 1.020 (1.002–1.039), and PM10 [RR = 1.020 (1.003–1.038)]. The study concluded that ambient pollutants contribute to the burden of ER visits for pediatric asthma.
Byers et al. [21] also undertook a time-series study to estimate short-term associations between daily changes in SO2, PM2.5 and O3 and daily asthma-related ER visits in Indianapolis, US. The study population comprised 165,056 asthma-related ER visits from 2007 to 2011. The study results show interquartile range increases in 3-day moving averages for SO2 are significantly associated with an increased risk of 3.3% (0.2%, 6.5%), especially during the warm season for the age group 5–44.
A multi-city assessment study by Alhanti et al. [22] investigated short-term relationships between ER visits for asthma and exposure to ambient O3, CO, NO2, SO2, and fine particulate matter (PM2.5) in Atlanta (1993–2009), Dallas (2006–2009), and St. Louis (2001–2007). The study was age-stratified by using city-specific daily time-series analyses. The study results suggest that age and race are susceptibility factors for asthma exacerbations in response to air pollution. Effects were stronger for the 5–18-year-olds, and there were stronger associations with O3 and NO2, particularly among non-White individuals [RRs of 1.15 (1.11, 1.19)] per 28 ppb O3 and RRs = 1.09 (1.06, 1.11) per 12 ppb of NO2 than among White individuals [RRs =1.01 (0.96, 1.06)] per 28 ppb of O3 and RR = 1.02 (1.00, 1.05) per 12 ppb of NO2. The results also showed stronger association among males than females for CO and NO2 with associations among males (RRs =1.05 (1.03, 1.06) per 0.5 ppm of CO and RRs = 1.07 (1.05, 1.09) per 12 ppb of NO2 than among females [RRs = 1.01 (0.99, 1.03)] per 0.5 ppm of CO and RRs = 1.03 (1.01, 1.06) per 12 ppb of NO2.
Similarly, a time-stratified case-crossover study investigating associations between short-term fluctuations in ambient air pollution concentrations and asthma ER visits in Windsor, Canada, was conducted by Lavigne et al. [23]. The study observed significant associations between 1-day lagged exposure to SO2, NO2, CO, O3 and ER visits for asthma. Additionally, a significant association was also observed for 1-day lagged exposure to CO and asthma visits among children throughout the year, with OR = 1.15 (1.02–1.31). In conclusion, positive associations between ambient levels of SO2, NO2, CO, O3 and ER visits for asthma were found, particularly among children.
COPD is characterized by progressive, irreversible airflow limitation and chronic inflammation of the lungs. COPD costs the US around $29.5 billion in direct costs and $20.4 billion in indirect costs [24]. While outdoor air pollution is not the major cause of COPD, it can be an important trigger for exacerbations of symptoms, resulting in the necessity of going to the ER.
Epidemiological studies have investigated the short-term effects of outdoor air pollution on COPD-related ER visits, hospital admissions, and mortality, and most report significant positive associations for exposures to criteria pollutants. One systematic review [25] included 59 studies in which the authors evaluated associations between short-term exposure to CAPs and the risk of COPD exacerbations. The results documented a positive association between short-term exposure and increased risk for COPD exacerbations. SO2 and NO2 exposure showed the strongest significance, especially in low-/middle-income countries, SO2 [RR = 1.012 (1.001, 1.023)] and NO2 [RR = 1.019 (1.014, 1.024)].
DeVries et al. [26] conducted a case crossover analysis to assess associations between short-term exposures to SO2, NO2, and PM2.5, and COPD exacerbations among 168 patients in central Massachusetts between 2012 and 2013. They report significant associations between short-term SO2 exposure and increased COPD exacerbation risk [OR  =  2.45 (1.75–3.45)] per 1 ppb increase, and short-term exposure to NO2 showed an association, but not as strong as the one for SO2 [OR  =  1.17 (1.05–1.30)] per 1 ppb increase. PM2.5, however, did not show a positive association.
Faustini et al. [27] conducted a large 4-year study in Rome by following COPD patients (n = 145,681) aged 35+, and a comparison group of people without COPD (n = 1,710,557). COPD patients showed higher mortality rates due to PM2.5, PM10, and NO2 exposures, but the comparison group did not, and PM10 showed a five times larger effect estimate for total mortality. The observed effect of PM10 was 3–7 times higher in the COPD patients, 3.5% (−0.1% to 7.2%), than in non-COPD patients, 0.7% (−0.8% to 2.2%). Respiratory mortality among COPD subjects was significantly elevated in relation to PM2.5 [interquartile range (IQR) = 11 μg/m3) 11.6% (2.0% to 22.2%), and NO2 (IQR = 24 μg/m3), 19.6% (3.5% to 38.2%)]. The authors concluded that COPD patients are more susceptible to air pollutants such as PM2.5 and NO2.
While there is strong evidence that air pollution increases the risk of asthma and COPD, most studies consider total outdoor air pollution instead of point sources [1,28,29]. A few studies have focused on individual point sources [30,31,32]. Point source pollution is just a minor part of the total air pollution exposures. However, this study was meant to determine whether emissions from the point sources alone, even though they are only a minor component of total air pollution, can still contribute to respiratory disease exacerbation.
The goal of this study, therefore, is to assess the associations between rates of ER visits for asthma and COPD and CAPs exposure from all point sources in New York as reported in the EPA NEI dataset from 2010 to 2018 in relation to living in zip codes with point sources of CAPs, and to assess relative strength of associations between each pollutant and the outcomes. This is possible since the ER data is available at a zip code level, and we know the zip code of each point source from the NEI data.

2. Materials and Methods

The health data used is information on ER visits due to asthma and/or COPD in all New York State regulated hospitals and other health facilities with emergency rooms in all NYS counties except New York City from 2010 to 2018. Information on asthma and COPD ER visits was retrieved from the NYSDOH SPARCS system database. This data is legislatively mandated to be reported to the NYSDOH upon patient discharge from inpatient and ER facilities. SPARCS data do not include federal institutions such as the Veterans’ Affairs hospitals, Indian Health Services, or psychiatric facilities. SPARCS data used in this study include date of birth, sex, race/ethnicity, zip code of residence, and the International Classification of Diseases (ICD) code for the specific disease requiring ER admission.
Asthma and COPD cases include hospital ER visits from 2010 through 2018, where asthma and/or COPD were the primary reason for the visit. There were 643,066 ER visits for asthma and 254,549 for COPD, with primary diagnosis using the ICD, 9th and 10th revisions, Clinical Modification (CM). The study looked at asthma (ICD-9-CM code 493 and ICD-10-CM code J45) and COPD (ICD-9-CM codes 490–496 and ICD-10-CM codes J40-J47). The outcome was defined as the number of cases during the period from 2010 to 2018, aggregated by gender, race, and age groups. Age data for asthma patients were categorized into six levels (0–5, 6–19, 20–44, 45–64, 65–74, and 75+ years), and for COPD, four age levels (35–44, 45–59, 60–74, and 75+). Ages 35–44 years have been used as the median age range at which COPD is usually diagnosed. This age group was therefore used as the reference age for COPD in this study. Patients younger than 35 with COPD diagnoses were dropped. The age reference used for asthma in this study was 45–64.

2.1. Data on Pollutant Exposure

Air pollution sources are categorized as point, non-point, on-road, non-road, and event, according to the EPA NEI. This study was limited to the point source emissions of the criteria pollutants because NEI provides point source exposure data at the zip code level, but not the other emission sources listed above. However, data for the other sources, such as on-road, non-road and non-point data, are provided at the county level. Since the ER data is at the zip code level, this study is limited to exposure to point source pollution. To account for within-county variability, county-level total VOCs and CAPs were used as adjusting variables since the CAPs are present with VOC pollution at the county level and the point source pollution is superimposed on that coming from on-road, non-road, and non-point sources.
A point source emission is one produced by large and stationary sources like power plants, industries, airports, or smaller non-industrial sources. Point source pollution information for PM2.5, CO, Pb, NOx, and SO2 for the years 2011, 2014, and 2017 was retrieved at the USEPA NEI website. However, data for O3, which is also a CAP, is not available in the NEI dataset, and there was so little release of Pb that it was not considered. Pollutant site latitude and longitude locations were then associated with the zip code in which the facility was located using a scheme that minimized the absolute great circle distance between the zip code centroid and the site location. Data from the United States Census Bureau (USCB) was used to determine the land area in square miles in each zip code. For each pollutant, zip code, and year, the pollution per square mile was calculated by summing all point source contributions of the pollutant and dividing by the land area size of the zip code region. The workable data was in pollution per square mile.

2.2. Data on Poverty

Poverty rates by zip code were downloaded from the United States Census Bureau (USCB) website for the study period. The official poverty measure defines poverty by comparing pretax income to a poverty threshold that is adjusted by family composition. Since poverty information was not available from 2010 to 2011, data for the year 2012 were used for the years 2010–2012. Families are considered poor if their total income falls below a certain threshold. All families that fell below the threshold were categorized as below the mean, and those above the threshold were categorized as above the mean in this study.

2.3. Smoking Data

To adjust our associations for smoking (a risk factor for both asthma and COPD), we used county-level prevalences calculated by the Behavioral Risk Factor Surveillance System (BRFSS). The BRFSS is a continuous, state-based surveillance system that collects information about modifiable risk factors for chronic diseases and other leading causes of death, and it is the nation’s premier system of health-related telephone surveys that collect state data. The county-level data was used to cover a wider range and scope. Data by year was averaged over the study period and matched with zip codes that evenly covered the geographical research area. Smoking data were obtained at the county level since the zip code-level data were not available.

2.4. Statistical Analysis

Missing Exposure Data. The years for which the NEI reports data were 2011, 2014, and 2017. Reporting for these years had inconsistencies across zip codes. For instance, in some zip codes, emitting units did not report in all given years. This can be attributed to the fact that although reporting is mandatory both at the site and unit levels, in the state of NY, this is often not enforced. Since point sources do not move, it is reasonable to assume that units still produced emissions even though emissions were not reported. Therefore, missing data for those years were input using emitting sites and unit IDs per zip code. For each zip code and site ID, missing unit IDs were inserted, and their emissions were replaced by the mean value of emissions reported, assuming emissions were the same and for the samples provided by that unit when it did report. If the unit did not report at any time during the period sampled (2011 to 2017), it will not appear in zip code-level emission totals. The largest source of missing data is cryptic and is not reflected in this study’s data because it consists of emitting units within a site and a zip code that failed to report in any of these years. This is a limitation of this dataset.
The total number of zip codes reporting may not change much after imputation, but the pollutant totals do. Changes in zip codes during the study period were resolved by using a reference set of codes from 2011. The total number of zip codes in the state of NY is estimated at 1792, and a little less than that reported some point source pollution for at least one of the target pollutants in 2011, 2014, and 2017, which also had cases of diseases in this study. Those zip codes with disease cases but without point source data over the study period were given a point source emission rate of zero. Zip codes with zero population were assumed to be post office boxes and were not considered in the analysis. A study by Madani and others [1] did a similar analysis on different air pollutants.
Single Pollutant Models. Datasets were created by merging data across years for each pollutant (available for years 2011, 2014, and 2017). All years were analyzed together. Pollutant data from 2011 were associated with zip code disease rates for 2010, 2011, and 2012. Pollutant data from 2014 were joined with disease data from 2013, 2014, and 2015, and pollutant data from 2017 were joined with disease data from 2016, 2017, and 2018. Data from all years were then stacked to complete the file.
Log-linear mixed effects regression models with random intercepts at the county level were used in this study to analyze ER visit rates for asthma and COPD and their associations with CAPs exposure. This model was chosen because it allows for both fixed and random effects, and the data in the study have hierarchical structures that include both zip code and county-level data. A p-value of <0.05 was considered statistically significant, and the R-squared likelihood ratio test was used as a measure of goodness of fit.
Adjusted associations between the rates of ER visits, scaled to per 105 population, and pollutants at the zip code level were estimated using log-linear mixed effects models with a random effect to account for within-county variability. Models were adjusted for sex (reference level female), age category (reference level at 45–64 for asthma, 35–44 for COPD), a poverty category variable (reference below median poverty), average county-level smoking, study year (reference level 2010), and county-level VOCs and CAPs from all sources. All numeric covariates are standardized, and the outcome case rate by zip code was log-transformed to achieve normality. All data preparation and analysis were performed with the R programming language and R Studio software version 2022.07.1.

3. Results

3.1. Association Between Asthma and Point Source Emissions of Criteria Air Pollutants in the Study

Point source emissions of CAPs are only 7% of total CAPs emissions, with 38% being from on-road, 31% non-road and 24% non-point. Table 1 shows the total tons of emission of the individual CAP from point sources for the whole state except NYC.
Estimates, 95% CIs and the corresponding p-values for associations between asthma ER and CAPs exposures are shown in Table 2. All pollutants are positive and significantly associated with asthma, except for PM2.5. SO2 showed the most effect, closely followed by NOx and then CO. PM10 showed significance, but the effect size is not as strong as the gaseous pollutants. This is clearly shown in Figure 1.
Below we display the exposure-response relationship between CAPs and asthma ER visits from 2010 to 2018 by zip code, given every 0.05 standard deviation increase in exposure (Figure 1). SO2 showed the largest association with asthma ER visits, followed by NOx and CO. The effect size of PM10 is greater than that of PM2.5. The figure again indicates that the gaseous pollutants showed the largest magnitude effect sizes in association with asthma.

3.2. Association Between COPD and Criteria Air Pollutants

Table 3 displays the β estimates, 95% confidence intervals, and p-values for the CAPs in the study, and their associations with ER visits for COPD. All the pollutants showed positive and statistically significant associations with COPD. Again, the gaseous pollutants showed the most effect, with NOx leading, followed by SO2 and CO.
Figure 2 shows the effect sizes of the pollutants in the study by zip code over the study period, given every 0.02 standard deviation increase in exposure. NOx showed the most effect, followed by CO and SO2. The particulate sizes are smaller than the gaseous pollutants. And this is consistent for the other diseases in the study.

4. Discussion

4.1. Criteria Air Pollutants and Respiratory Diseases

The USEPA listed the six common air pollutants as CAPs under the Clean Air Act in the 1970s. The primary CAPs include CO, SO2, NO2, O3, PM and Pb. Short or long-term exposures to these pollutants are known to cause adverse health effects that often lead to hospitalizations or ER visits [33]. In some cases, such exposure can lead to premature death [34,35].

4.2. Carbon Monoxide and Respiratory Diseases

CO is a colorless, odorless, and tasteless gaseous pollutant primarily from traffic or industry [36], produced by incomplete combustion of fossil fuels such as motor vehicles [37] and cigarette smoke [38]. It is a ubiquitous air pollutant [39], and its toxicity is the most common type of fatal air poisoning in most countries, including the US. CO is responsible for hundreds of deaths and thousands of ER visits every year [40]. The pathophysiological mechanism of the effect of CO is tissue hypoxia, due to its ability to bind with hemoglobin to form carboxyhemoglobin [41] and prevent the delivery of oxygen to tissues. Therefore, it is not surprising that exposure to an air pollutant that reduces the delivery of oxygen would exacerbate diseases that already have reduced the delivery of oxygen to tissue.
In the US, exposure limit in the workplace has been set by the Occupational Safety and Health Administration (OSHA) at 50 ppm time-weighted-average (TWA) over 8 h, 25 ppm short-term exposure limit, and 200 ppm ceiling, while the National Institute for Occupational Safety and Health (NIOSH) sets a recommended exposure limit of 35 ppm 8 h TWA [40].
Epidemiological studies have found that ambient CO has significant adverse effects on public health worldwide [36] and has been linked to increases in ER visits for asthma, COPD and other respiratory diseases [41]. It is also responsible for approximately 15,000 ER visits for respiratory diseases and 500 related deaths annually. To examine the effects of particulates and CO concentrations on asthma exacerbation among urban children, Evans et al. [42] conducted a pilot study to explore the relationship between asthma exacerbation and ambient concentrations of particles and CO. The results showed that ultrafine particles (PM0.1) and CO increase exacerbation risk in urban children. IQR for PM0.1 = 2088 p/cm3 [OR = 1.27 (0.90–1.79)] and CO IQR = 0.17 ppm [OR = 1.63 (1.03–2.59)]. Their findings regarding CO and pediatric asthma events were consistent with previous studies showing increases in the risk of ER visits and hospitalizations for asthma in children.
Song et al. [43], with a total of 72,430 hospitalized cases in Ganzhou, Southeast China, conducted a time series study to evaluate the association and the exposure-response relationship between ambient CO exposure and the risk of hospitalization for total and specific respiratory diseases, including asthma, COPD, upper respiratory tract infection, lower respiratory tract infection, and influenza pneumonia. Results showed CO exposure was significantly associated with hospitalization risk for all the respiratory diseases and further indicated that for each 1 mg/m3 increase in CO at lag 0–2, hospitalizations for total respiratory diseases increase. Asthma increased by OR = 17.74 (1.34%, 36.8%), and COPD increased by OR = 12.45 (2.91%, 22.87%). Women were more susceptible to ambient CO exposure-associated hospitalizations for asthma. The authors concluded that they found significant positive exposure–response relationships between ambient CO exposure and exposure-associated respiratory hospitalizations.
Similarly, an ecological time series study, including 4534 COPD hospitalizations in Ahvaz, Iran, carried out by Raji et al. [44] found a positive association between ambient CO exposure and COPD hospitalizations [RR = 1.643 (1.233–2.191)].
Another time-series study conducted by Zhao et al. [45] examined the short-term association between ambient CO and ER visits for respiratory diseases in Dongguan, China, from 2013 to 2017, with a total of 89,484 outpatient visits for respiratory diseases, including asthma, COPD, pneumonia and bronchiectasis cases. Results showed every IQR increase in CO at lag 0–3 corresponded to 5.62% (3.24%, 8.05%) for all respiratory diseases, 8.86% (4.89%, 12.98%) for asthma, 6.67% (0.87%, 12.81%) for bronchiectasis and 7.20% (2.35%, 12.29%) for pneumonia. The study concluded that short-term exposure to ambient CO was associated with increased risk of outpatient visits for respiratory diseases.

4.3. Lead Exposure and Respiratory Diseases

Lead (Pb) is an environmental toxin that is associated with numerous adverse health effects in children and adults [46]. It is a persistent metal in all parts of the environment, in air, water and soil, and is primarily derived from a variety of manufactured products like leaded gasoline, paints, ceramics, solders, water pipes, hair dye, cosmetics, airplanes, farm equipment, shielding for X-ray machines [47]. And it is very toxic to the nervous system [46].
Exposure occurs through ingestion of Pb-contaminated substances and inhalation of Pb particles that come from the burning of Pb-containing materials, such as leaded gasoline and residential paint, are the primary route of exposure to Pb [47,48]. And exposure to Pb plays a major role in exacerbating respiratory diseases [47], including COPD, pulmonary dysfunction, antioxidant activity [49], asthma [50], and neurodevelopmental impacts [48]. Correspondingly, soil and water Pb distribution have been shown to be associated with patterns of respiratory disease burden in Iran [51]. Pb-induced asthma includes effects on immune balance, oxidative stress, and inflammatory responses [50], resulting in seizures, headache, coma, and even death [52]. While air levels of Pb have been dramatically reduced in the US, it is still a problem at some specific sites. However, there is little release of Pb from point sources in NYS. Since Pb exposure was very low and variable, we decided not to include it in the study analysis.

4.4. Particulate Matter and Respiratory Diseases

PM is of great public health concern because smaller particulates can penetrate deep into the lungs and reach the pulmonary alveolar region. This is particularly the case for PM2.5 and ultrafine particulates (PM0.1) [53,54].
Studies have shown correlations between PM0.1 and different respiratory diseases in different parts of the world. For example, Bergmann et al. [54] examined associations between short-term exposure to PM0.1 and mortality and hospitalizations in Copenhagen, Denmark. The results showed significant associations between exposure to PM0.1 and hospitalizations for asthma and mortality for COPD. One IQR increase in PM0.1 was associated with an OR = 1.04 (0.01, 1.07), lag 0–4, and 1.02 [1.00, 1.04], lag 0–1, was associated with COPD mortality [OR = 1.13 (1.01, 1.26)] and asthma hospitalization [OR = 1.08 (1.00, 1.16)] at lag 0–1. The study findings showed that short-term exposure to PM0.1 can trigger respiratory disease mortality and morbidity.
PM2.5 has also been associated in multiple epidemiological studies with ER visits for respiratory diseases [55,56] and has also been found to cause lung function reduction and airway inflammation [57], COPD, and asthma exacerbations [58,59,60]. A multicity time-series study involving 112 cities in the US, conducted by Zanobetti & Schwartz [61], showed that a 10-μg/m3 increase in 2-day averaged PM2.5 resulted in a 1.68% increase (1.04–2.33) in respiratory deaths.
It has been suggested by multiple studies that PM may exacerbate asthma symptoms and increase risk of asthma attacks [62,63]. The global burden of outdoor air pollution on asthma ER visits in 2015 alone was estimated to be between 5 and 10 million globally. This was attributable to PM, where 12% of these estimates were observed in China [16]. Duan et al. [64] indicated that for every 10μg/m3 increase in PM2.5 concentration, the risk of hospitalization increases by 1.61% in COPD patients in the US, and 0.82% in Beijing, China.
Although most studies focus on the smaller particulates, thinking the larger particles are usually removed from the respiratory tracts and do not enter the alveoli, some studies have found associations between larger particulates and respiratory diseases. Kang et al. [65] in their nationwide retrospective cohort study of 121,423 adults in South Korea found associations between PM10 exposure and mortality for severe exacerbation of respiratory diseases. But if one only measures PM10, that measure will include smaller particulates that may, in fact, be the responsible factor.
Another study on PM10 was conducted in London, United Kingdom, by Canova et al. [66]. This was a case-crossover study to investigate PM10-induced hospital admissions for asthma and COPD. The study found that every 10μg/m3 increase in PM10 was related to an increase in asthma or COPD admission rate, especially in lag 0–3 days [OR = 1.35 (1.04–1.76)].

4.5. Sulfur Dioxide and Respiratory Diseases

SO2 is emitted from natural and anthropogenic sources [67]. SO2 is generated from the burning of sulfur-containing fuel like coal and is one of the prevalent air pollutants released from natural sources such as volcanoes or anthropogenically from burning of fossil fuel and biomass at large industrial plants such as oil refineries and power stations [68]. Recent studies have shown SO2 is also a biological gas in various mammalian tissues [69], and people with asthma are especially susceptible to its effects [25]. Short term exposures of asthmatic individuals to elevated levels of SO2 while exercising at a moderate level may result in breathing difficulties, wheezing, chest tightness, and shortness of breath [70]. Orellano et al. [71] conducted a systematic review and meta-analysis to evaluate the effect of short-term exposure to ambient SO2 on all-cause and respiratory mortality. The study found that every 10 µg/m3 in acute SO2 exposure was significantly associated with all-cause mortality [RR = 1.0059 (1.0046–1.0071)], and respiratory mortality [RR = 1.0067 (1.0025–1.0109)]. The authors concluded that there were positive associations between short-term exposure to ambient SO2 and all-cause and respiratory mortality.
A cohort study comprised 351 asthmatic and 327 non-asthmatic children in Puerto Rico from 2009 to 2010 was conducted by Rosser et al. [72]. The study evaluated the effects of the annual average 1 h daily maximum SO2 on asthma, atopy, total IgE, and lung function. Results showed annual SO2 exposure (per 1 ppb) was significantly associated with asthma [OR = 1.42 (1.05–1.91)] and atopy [OR = 1.35 (1.02–1.78)]. The conclusion was that SO2 exposure is linked to asthma and atopy, and long-term SO2 exposure also showed an association with reduced FEV1/FVC, particularly in asthmatics.
SO2 exposure has been correlated with increased overall ER visits for asthma, COPD, upper respiratory infection, pneumonia, dysrhythmia, hypertension, abdominal pain, depression, and headache [73]. Health effects and symptoms related to this pollutant include burning in the nose and throat, sore throat, difficulty inhaling deeply, altered sense of smell, and increased susceptibility to respiratory infections. SO2 combines with water in the respiratory tract to form sulfuric acid [67], which is likely responsible for some of the symptoms. SO2 has been linked to an accelerated decline in lung function, which is a special concern for developing children and people who have underlying COPD, asthma, or other chronic respiratory diseases [73].
Madaniyazi & Xerxes [16] indicated that the association between SO2 exposure and exacerbation of asthma has been investigated extensively, and it has been confirmed to be a key risk factor for asthma even at low levels. They performed a meta-analysis on the short-term exposure to SO2 and the mortality of asthma in East Asian countries reported that hospital utilization for asthma among children increased by 5.7% for every 10 μg/m3 increase in the daily mean concentration of SO2. Like NO2 and O3, SO2 has also been strongly associated with asthma and exacerbations. Elevated SO2 levels can cause coughing, mucus secretion, and aggravation of asthma [21,32,74].

4.6. Nitrogen Oxides and Respiratory Diseases

NOX are produced from natural sources such as volcanic activity, biomass burning, and bacterial activity [75], or from anthropogenic sources such as burning fossil fuels in stationary sources like industrial plants, or in motor vehicles [76]. NOx causes respiratory irritation and can trigger cell damage and inflammatory processes throughout the respiratory system, from the nose to the pulmonary alveoli [77]. Nitric oxide (NO), nitrous oxide (N2O) and nitrogen dioxide (NO2) generate nitrogen oxides (NOx), which are considered primary air pollutants [78]. NO is a free radical that produces oxidants with low water solubility and can trigger cell damage and inflammatory processes throughout the respiratory system, from the nose to the pulmonary alveoli [79,80]. NOx causes respiratory problems such as coughing, dyspnea, wheezing, bronchospasm, and pulmonary edema at high concentrations [81]. NOx is a free radical-producing oxidant with low water solubility and is a deep lung irritant [68]. It is a precursor to ground-level ozone and can participate in the secondary formation of PM2.5. Nitric oxide has diverse roles in the immune system, from innate resistance to suppression of Th1 functions to induction of oxidative injury [82]. A longitudinal study was conducted by Ghosh et al. [77] in the Czech Republic to assess ambient NOx exposure and early childhood respiratory illnesses. Children were followed from birth to 4.5 years of age. For the first 2 years of life, an IQR increase in the 30-day average of NOx resulted in an OR = 1.31 (1.07, 1.61) for bronchitis and OR = 1.23 (1.01–1.49) for two- to 4.5-year-olds. Results from this longitudinal study demonstrate associations between NOx and respiratory illnesses, especially for bronchitis.
Many studies have reported the effects of short-term exposure to NOX on human morbidity and mortality [83]. Meng et al. [84] in their multilocation analysis in 398 cities found that a 10 μg/m3 increase in NO2 concentration on lag 1 day was associated with 0.47% (0.21% to 0.72%) increases in respiratory mortality. The authors therefore concluded that NO2 is associated with considerable health risks even at levels below health-based standards and guidelines, including the current WHO air quality guidelines.
NOx exposures can exacerbate existing respiratory disease by impairing the functions of epithelial cells and alveolar macrophages, contributing to airway inflammation [24]. Increased levels of NOX have been correlated with increased use of ER visits, specifically for asthma, COPD, respiratory infections, otitis media, cardiovascular diseases, hypertension, dysrhythmia, abdominal pain, depression, and headache [73]. A recent study was conducted by Kowalska et al. [85] to assess the risk related to NOx and NO2 concentration increase, and daily hospital visits due to bronchitis and asthma exacerbation in Poland. Results showed a significant association between outpatient visits and hospitalizations for bronchitis and asthma exacerbation and daily NOx concentrations. The strongest relationship was observed in the case of NO2, and outpatient visits due to bronchitis, RR = 1.434 (1.308–1.571). In addition to traffic-related air pollution, evidence from previous studies has shown that people who live near contaminated sites known as point sources show abnormalities of serum immunoglobulins and suffer from more frequent hospitalization for respiratory infections, chronic bronchitis, and COPD [86]. Power plants account for approximately 16% of NOx emissions in the US [70].

4.6.1. Point Sources Emissions of Criteria Air Pollutants and Asthma

Studies have indicated that air pollution contributes to increased asthma prevalence and symptom onset [28,87,88] and asthma exacerbations [71]. This study adds to the many research studies that report that exposure to the CAPs increases the risk of ER visits for asthma, and that among the pollutants in this study, NOx and CO have the largest effects, followed by SO2. PM2.5, however, did not show any significant association with asthma. This may be because the amount of PM2.5 coming from point sources is very small relative to the amount coming from other sources, because there is other evidence showing clearly that PM2.5 does contribute to asthma attacks. It was a surprise to find a significant association with PM10 but not PM2.5. However, similar results have been previously reported, as mentioned above. Even though most larger particulates are trapped and removed by ciliary action and mucosa, they still may trigger irritation and inflammation. The effects of all these pollutants on the onset and or exacerbation of asthma were confirmed in previous epidemiologic studies. For instance, Gorai et al. [49] in their GIS-based approach for assessing the association between air pollution and asthma in NYS, found significant associations between exposure to CAPs with asthma prevalence rate in NYS, US.

4.6.2. Point Source Emissions of Criteria Air Pollutants and COPD

COPD is a common respiratory disease, affecting 5–10% of the US population. Smoking is known to be a major cause of the development of COPD, and when an individual already has impaired respiratory function, it is not surprising that superimposed exposure to CAPs increases the need for treatment in the ER. COPD-related death has continued to increase, and it is one of the leading health burdens worldwide that accounts for almost 3 million deaths annually. Outdoor air pollution has contributed to its increased incidence and prevalence [89,90]. From the results in Table 2 of this study, there is a strong positive and statistically significant association between the pollutants and ER visits. As was the case with asthma, the associations were strongest with the gaseous pollutants, which were also the largest component of pollutants coming from point sources. For COPD, both PM10 and PM2.5 showed significant associations. These associations are confirmed by published associations between exposure to these air pollutants and ER visits for COPD [25].
Air pollution is a major environmental issue affecting respiratory health globally. This study complements our earlier VOC-focused analysis [88] by examining point source criteria air pollutants, which differ in sources, atmospheric behavior, exposure profiles, and regulatory relevance. Although both studies use NEI point source data and similar zip code-level modeling frameworks, the scientific question here is distinct, namely whether CAP emissions from local point sources, even as a small fraction of overall air pollution, are associated with elevated asthma and COPD ER visits after accounting for key confounders and co-pollutants (including PM2.5 and VOCs). The observed pollutant-specific associations support the interpretation that local CAP point sources contribute modestly but significantly to respiratory morbidity, underscoring the importance of evaluating multiple pollutant classes when assessing community-level health impacts and informing targeted mitigation near emitting facilities.

4.6.3. Significance of These Results

The goal of this study was to assess associations between point source CAPs and ER visits for asthma and COPD at zip code levels in NYS from 2010 to 2018, and to identify which of these pollutants increases the risk of an ER visit for both diseases. The respiratory system is very vulnerable to the hazardous effects of air pollution, and respiratory diseases are significant causes of ER visits. Air pollution, including CAPs, has been extensively studied and proven to be a major risk factor that leads to significant adverse health outcomes. Both short- and long-term exposures to air pollutants can adversely affect respiratory health, leading to ER visits, hospitalization, and in some cases even death by inducing airway inflammation, even at very low concentrations [89,90,91]. ER visits for asthma and COPD in this study showed significant adjusted associations with CAPs exposure when considering CAPs exposure as just point sources. This association was observed for all years, even after adjusting for poverty and smoking in mixed effects regression models that allow for county-level variation. Single pollutant adjusted regressions showed that CO, NOx, and SO2 contributed the largest to both disease outcomes. These are also the pollutants that contribute the largest amount of pollution from point sources. The results of this study are consistent with findings in the literature cited, suggesting that exposure to CAPs is a risk factor associated with an increase in the number of ER visits for both asthma [92] and COPD [93].

4.6.4. Strengths and Limitations

Strengths of this study include its temporal length (2010–2018) and use of NEI data to provide source and magnitude information for spatially distributed Criteria Air Pollutants.
However, our study has several limitations. First, ecologic design does not permit assessment of causal relationships between point source exposures and emergency room visits, so we report adjusted single pollutant associations. Second, reporting air pollution is mandatory but patchy, so the NEI data may represent only a fraction of actual emissions. Finally, the criteria air pollutants were sampled on just three time points during our 9-year study period (years 2011, 2014, 2017) and include just known point source outdoor pollution emission sources. To address this limitation, we adjusted our models at the county level for pollution from all sources.

5. Conclusions

Most pollutants in the study were positive and statistically significant with asthma, indicating a detrimental effect for relatively local point sources of pollution. All pollutants showed associations with asthma ER visits except PM2.5. For COPD, all the pollutants showed significant positive associations with the outcome. The gaseous pollutants (CO, NOx, and SO2) showed consistent positive associations and showed the largest effects. For the particulates, PM10 showed positive associations with asthma and COPD, but with a smaller effect size, while PM2.5 also showed a positive association with COPD but not asthma. Ambient air levels of SO2 and NOx were related positively and significantly with a substantial increase in asthma and COPD ER visits. The amounts of gaseous CAPs emitted from point sources is much larger than that for particulates, and we cannot distinguish whether the greater toxicity of the gaseous CAPs is due to their quantity or relative toxicity.
While point source emissions of CAPs are small relative to total emissions coming from traffic, building heating, and other sources of fossil fuel combustion, our study shows that these point source emissions are associated with more frequent ER visits among those living in the same zip code. Furthermore, we find that the gaseous pollutants SO2, NOX and CO have a stronger impact on morbidity than particulates. Whether this is due to the relative amount of emissions from the different point sources or to relative respiratory toxicity remains to be determined.

Author Contributions

Conceptualization: T.S.L. and D.O.C.; investigation: T.S.L.; data curation: L.E.J., T.S.L. and N.A.M.; methodology: L.E.J.; software: L.E.J., T.S.L. and N.A.M.; validation: L.E.J.; formal analysis: L.E.J.; resources: D.O.C.; writing, original draft: T.S.L., L.E.J., N.A.M. and D.O.C.; writing—review and editing: T.S.L., L.E.J., N.A.M. and D.O.C.; supervision: D.O.C. and L.E.J. This work was a part of the PhD dissertation of T.S.L. All authors have read and agreed to the published version of the manuscript.

Funding

This study was supported by internal funds from the Institute for Health and the Environment, University at Albany, SUNY.

Institutional Review Board Statement

Ethical review and approval were waived for this study due to the fact that use of SPARCS data contains no unique identifiers.

Informed Consent Statement

Informed consent is not relevant to this study which relies upon ER visits of individuals with no identifying information.

Data Availability Statement

The original contributions presented in this study are included in the article. Further inquiries can be directed to the corresponding author.

Conflicts of Interest

All authors declare that they do not have conflicts of interest related to this manuscript. D.O.C. has served as an expert witness in cases regarding the health effects of air pollution, but does not see any conflict regarding this study.

References

  1. Madani, N.A.; Jones, L.E.; Carpenter, D.O. Different volatile organic compounds in local point source air pollution pose distinctive elevated risks for respiratory disease-associated emergency room visits. Chemosphere 2023, 344, 140403. [Google Scholar] [CrossRef] [Scilit] [PubMed]
  2. Khatri, K.L.; Tamil, L.S. Early Detection of Peak Demand Days of Chronic Respiratory Diseases Emergency Department Visits Using Artificial Neural Networks. IEEE J. Biomed. Health Inform. 2018, 22, 285–290. [Google Scholar] [CrossRef] [Scilit]
  3. Li, X.; Cao, X.; Guo, M.; Xie, M.; Liu, X. Trends and risk factors of mortality and disability adjusted life years for chronic respiratory diseases from 1990 to 2017: Systematic analysis for the Global Burden of Disease Study 2017. BMJ 2020, 368, m234. [Google Scholar] [CrossRef] [Scilit]
  4. Silva, G.E.; Sherrill, D.L.; Guerra, S.; Barbee, R.A. Asthma as a risk factor for COPD in a longitudinal study. Chest 2004, 126, 59–65. [Google Scholar] [CrossRef] [Scilit]
  5. Zeki, A.A.; Schivo, M.; Chan, A.; Albertson, T.E.; Louie, S. The asthma-COPD overlap syndrome: A common clinical problem in the elderly. J. Allergy 2011, 2011, 861926. [Google Scholar] [CrossRef] [Scilit] [PubMed]
  6. Green, C.E.; Turner, A.M. The role of the endothelium in asthma and chronic obstructive pulmonary disease (COPD). Respir. Res. 2017, 18, 20. [Google Scholar] [CrossRef] [Scilit]
  7. Morissette, M.; Godbout, K.; Côté, A.; Boulet, L.P. Asthma COPD overlap: Insights into cellular and molecular mechanisms. Mol. Aspects Med. 2022, 85, 101021. [Google Scholar] [CrossRef] [Scilit]
  8. Barnes, P.J. Cellular and molecular mechanisms of asthma and COPD. Clin. Sci. 2017, 131, 1541–1558. [Google Scholar] [CrossRef] [Scilit]
  9. Simkovich, S.M.; Goodman, D.; Roa, C.; Crocker, M.E.; Gianella, G.E.; Kirenga, B.J.; Wise, R.A.; Checkley, W. The health and social implications of household air pollution and respiratory diseases. npj Prim. Care Respir. Med. 2019, 29, 12. [Google Scholar] [CrossRef] [Scilit] [PubMed]
  10. Szyszkowicz, M.; Kousha, T.; Castner, J.; Dales, R. Air pollution and emergency department visits for respiratory diseases: A multi-city case crossover study. Environ. Res. 2018, 163, 263–269. [Google Scholar] [CrossRef] [Scilit] [PubMed]
  11. Castner, J.; Guo, L.; Yin, Y. Ambient air pollution and emergency department visits for asthma in Erie County, New York 2007–2012. Int. Arch. Occup. Environ. Health 2018, 91, 205–214. [Google Scholar] [CrossRef] [Scilit]
  12. Nsemo, A.D. Health problems associated with urbanization and industrialization. Int. J. Innov. Res. Adv. Stud. 2019, 6, 149–157. [Google Scholar]
  13. Sonnoh, F.; Khwaja, H.A.; Fatmi, Z.; Rizvi, N.A.; Turabi, A.; Hussain, M.M.; Siddique, A.; Carpenter, D.O. Gaseous pollutants linked to pulmonary diseases: East meets West. Air Qual. Atmos. Health 2024, 17, 2879–2897. [Google Scholar] [CrossRef] [Scilit]
  14. Nayebare, S.R.; Aburizaiza, O.S.; Siddique, A.; Carpenter, D.O.; Hussain, M.M.; Zeb, J.; Aburiziza, A.K.; Khwaja, H.A. Exposure to black carbon (BC) and the secondary aerosol (p-SO42 and p-NO3−) components of fine particulate matter (PM2.5) and cardiopulmonary morbidity in Jeddah, Saudi Arabia. Atmosphere 2025, 16, 168. [Google Scholar] [CrossRef] [Scilit]
  15. Shin, S.; Bai, L.; Burnett, R.T.; Kwong, J.C.; Hystad, P.; van Donkelaar, A.; Laavigne, E.; Wiechenthal, S.; Copes, R.; Martin, R.A.; et al. Air Pollution as a Risk Factor for Incident Chronic Obstructive Pulmonary Disease and Asthma. A 15-Year Population-based Cohort Study. Am. J. Respir. Crit. Care Med. 2021, 203, 1138–1148. [Google Scholar] [CrossRef] [Scilit]
  16. Madaniyazi, L.; Xerxes, S. Outdoor air pollution and the onset and exacerbation of asthma. Chronic Dis. Transl. Med. 2021, 7, 100–106. [Google Scholar] [CrossRef] [Scilit] [PubMed]
  17. Samoli, E.; Nastos, P.T.; Paliatsos, A.G.; Katsouyanni, K.; Priftis, K.N. Acute effects of air pollution on pediatric asthma exacerbation: Evidence of association and effect modification. Environ. Res. 2011, 111, 418–424. [Google Scholar] [CrossRef] [Scilit]
  18. Mahler, B.; Băiceanu, D.; Panciu, T.C. Air Pollutants and Their Impact on Chronic Diseases—A Retrospective Study in Bucharest, Romania. Atmosphere 2023, 14, 867. [Google Scholar] [CrossRef] [Scilit]
  19. Zheng, X.-Y.; Ding, H.; Jiang, L.-N.; Chen, S.-W.; Zheng, J.-P.; Oiu, M.; Zhou, Y.S.; Chen, Q.; Guan, W.J. Association between Air Pollutants and Asthma Emergency Room Visits and Hospital Admissions in Time Series Studies: A Systematic Review and Meta-Analysis. PLoS ONE 2015, 10, e0138146. [Google Scholar] [CrossRef] [Scilit]
  20. Strickland, M.J.; Darrow, L.A.; Klein, M.; Flanders, W.D.; Sarnat, J.A.; Muholland, J.A.; Tolbert, P.E. Short-term associations between ambient air pollutants and pediatric asthma emergency department visits. Am. J. Respir. Crit. Care Med. 2010, 182, 307–316. [Google Scholar] [CrossRef] [Scilit]
  21. Byers, N.; Ritchey, M.; Vaidyanathan, A.; Brandt, A.J.; Yip, F. Short-term effects of ambient air pollutants on asthma-related emergency department visits in Indianapolis, Indiana, 2007–2011. J. Asthma 2016, 53, 245–252. [Google Scholar] [CrossRef] [Scilit]
  22. Alhanti, B.A.; Chang, H.H.; Winquist, A.; Mulholland, J.A.; Darrow, L.A.; Samat, S.E. Ambient air pollution and emergency department visits for asthma: A multi-city assessment of effect modification by age. J. Expo. Sci. Environ. Epidemiol. 2016, 26, 180–188. [Google Scholar] [CrossRef] [Scilit]
  23. Lavigne, E.; Villeneuve, P.J.; Cakmak, S. Air pollution and emergency department visits for asthma in Windsor, Canada. Can. J. Public Health 2012, 103, 4–8. [Google Scholar] [CrossRef] [Scilit]
  24. DeVries, R.; Kriebel, D.; Sama, S. Outdoor air pollution and COPD-related emergency department visits, hospital admissions, and mortality: A meta-analysis. COPD J. Chronic Obstr. Pulm. Dis. 2017, 14, 113–121. [Google Scholar] [CrossRef] [Scilit]
  25. Li, J.; Sun, S.; Tang, R.; Qiu, H.; Huang, Q.; Mason, T.G.; Tian, L. Major air pollutants and risk of COPD exacerbations: A systematic review and meta-analysis. Int. J. Chron. Obstruct. Pulmon. Dis. 2016, 11, 3079–3091. [Google Scholar] [CrossRef] [Scilit] [PubMed]
  26. DeVries, R.; Krieber, D.; Sma, S. Low level air pollution and exacerbation of existing COPD: A case crossover analysis. Environ. Health 2016, 15, 98. [Google Scholar] [CrossRef] [Scilit] [PubMed]
  27. Faustini, A.; Stafoggia, M.; Cappai, G.; Forastiere, F. Short-term effects of air pollution in a cohort of patients with chronic obstructive pulmonary disease. Epidemiology 2012, 23, 861–879. [Google Scholar] [CrossRef] [Scilit]
  28. Delfino, R.J.; Wu, J.; Tjoa, T.; Gullesserian, S.K.; Nickerson, B.; Gillen, D.L. Asthma morbidity and ambient air pollution: Effect modification by residential traffic-related air pollution. Epidemiology 2014, 25, 48–57. [Google Scholar] [CrossRef] [Scilit] [PubMed]
  29. Sinclair, A.H.; Melly, S.; Tolsma, D.; Spengler, J.; Perkins, L.; Rohr, A.; Wyzga, R. Childhood asthma acute primary care visits, traffic, and traffic-related pollutants. J. Air Waste Manage. Assoc. 2014, 64, 561–567. [Google Scholar] [CrossRef] [Scilit]
  30. Hendryx, M.; Luo, J.; Chojenta, C.; Byles, J.E. Air pollution exposures from multiple point sources and risk of incident chronic obstructive pulmonary disease (COPD) and asthma. Environ. Res. 2019, 179, 108783. [Google Scholar] [CrossRef] [Scilit] [PubMed]
  31. Labelle, R.; Brand, A.; Buteau, S.; Smargiassi, A. Hospitalizations for respiratory problems and exposure to industrial emissions in children. Environ. Pollut. 2015, 4, 77. [Google Scholar] [CrossRef] [Scilit]
  32. Smargiassi, A.; Kosatsky, T.; Hicks, J.; Plante, C.; Armstrong, B.; Villeneuve, P.J.; Goudreau, S. Risk of asthmatic episodes in children exposed to sulfur dioxide stack emissions from a refinery point source in Montreal, Canada. Environ. Health Perspect. 2009, 117, 653–659. [Google Scholar] [CrossRef] [Scilit]
  33. Saxena, P.; Sonwani, S. Primary Criteria Air Pollutants: Environmental Health Effects. In Criteria Air Pollutants and Their Impact on Environmental Health; Springer: Singapore, 2019. [Google Scholar] [CrossRef] [Scilit]
  34. Shen, F.; Zhang, L.; Jiang, L.; Tang, M.; Gai, X.; Chen, M.; Ge, X. Temporal variations of six ambient criteria air pollutants from 2015 to 2018, their spatial distributions, health risks and relationships with socioeconomic factors during 2018 in China. Environ. Int. 2020, 137, 105556. [Google Scholar] [CrossRef] [Scilit]
  35. Viegi, G.; Maio, S.; Fasola, S.; Baldacci, S. Global burden of chronic respiratory diseases. J. Aerosol Med. Pulm. Drug Deliv. 2020, 33, 171–177. [Google Scholar] [CrossRef] [Scilit]
  36. Wang, Y.; Yao, C.; Xu, C.; Zeng, X.; Zhou, M.; Ln, Y.; Zhang, P.; Yin, P. Carbon monoxide and risk of outpatient visits due to cause-specific diseases: A time-series study in Yichang, China. Environ. Health 2019, 18, 36. [Google Scholar] [CrossRef] [Scilit] [PubMed]
  37. Liu, D.; Vonwiller, M.; Li, J.; Liu, J.; Szidat, S.; Zhang, Y. Fossil and non-fossil fuel sources of organic and elemental carbonaceous aerosol in Beijing, Shanghai, and Guangzhou: Seasonal carbon source variation. Aerosol Air Qual. Res. 2020, 20, 2495–2506. [Google Scholar] [CrossRef] [Scilit]
  38. Hoyt, G.L. Cigarette smoking: Nicotine, carbon monoxide, and the physiological effects on exercise responses. Sport Sci. Rev. 2013, 22, 5. [Google Scholar] [CrossRef] [Scilit]
  39. Rochette, L.; Cottin, Y.; Zeller, M.; Vergely, C. Carbon monoxide: Mechanisms of action and potential clinical implications. Pharmacol. Ther. 2013, 137, 133–152. [Google Scholar] [CrossRef] [Scilit] [PubMed]
  40. Hess, D.R. Inhaled carbon monoxide: From toxin to therapy. Respir. Care 2017, 62, 1333–1342. [Google Scholar] [CrossRef] [Scilit]
  41. Lee, J.S.; Kim, T.Y.; Bae, K.S.; Kim, H. Usefulness of a modified poisoning severity score for predicting prognosis in acute carbon monoxide poisoning. Am. J. Emerg. Med. 2022, 51, 156–162. [Google Scholar] [CrossRef] [Scilit]
  42. Evans, K.A.; Halterman, J.S.; Hopke, P.K.; Fagnano, M.; Rich, D.Q. Increased ultrafine particles and carbon monoxide concentrations are associated with asthma exacerbation among urban children. Environ. Res. 2014, 129, 11–19. [Google Scholar] [CrossRef] [Scilit]
  43. Song, J.; Qiu, W.; Huang, X.; Guo, Y.; Chen, W.; Wang, D.; Zhang, X. Association of ambient carbon monoxide exposure with hospitalization risk for respiratory diseases: A time series study in Ganzhou, China. Front. Public Health 2023, 11, 1106336. [Google Scholar] [CrossRef] [Scilit]
  44. Raji, H.; Riahi, A.; Borsi, S.H.; Masoumi, K.; Khanjani, N.; AhmaffiAngali, K.; Goudarzi, G.; Dastoorpoor, M. Acute Effects of Air Pollution on Hospital Admissions for Asthma, COPD, and Bronchiectasis in Ahvaz, Iran. Int. J. Chron. Obstruct. Pulmon. Dis. 2020, 15, 501–514. [Google Scholar] [CrossRef] [Scilit]
  45. Zhao, Y.; Hu, J.; Tan, Z.; Liu, T.; Zeng, W.; Li, X.; Huang, C.; Wang, S.; Huang, Z.; Ma, W. Ambient carbon monoxide and increased risk of daily hospital outpatient visits for respiratory diseases in Dongguan, China. Sci. Total Environ. 2019, 668, 254–260. [Google Scholar] [CrossRef] [Scilit]
  46. Dlgado, C.F.; Ullery, M.A.; Jordan, M.; Duclos, C.; Rajagopalan, S.; Scott, K. Lead exposure and developmental disabilities in preschool-aged children. J. Public Health Manag. Pract. 2018, 24, e10–e17. [Google Scholar] [CrossRef] [Scilit]
  47. Boskabady, M.; Marefati, N.; Farkhondeh, T.; Shakeri, F.; Fafshbaf, A.; Boskabady, M.-H. The effect of environmental lead exposure on human health and the contribution of inflammatory mechanisms, a review. Environ. Int. 2018, 120, 404–420. [Google Scholar] [CrossRef] [Scilit] [PubMed]
  48. Al Osman, M.; Yang, F.; Massey, I.Y. Exposure routes and health effects of heavy metals on children. Biometals 2019, 32, 563–573. [Google Scholar] [CrossRef] [Scilit]
  49. Gorai, A.; Tuluri, F.; Tchounwou, P. A GIS Based Approach for Assessing the Association between Air Pollution and Asthma in New York State, USA. Int. J. Environ. Res. Public Health 2014, 11, 4845–4869. [Google Scholar] [CrossRef] [Scilit]
  50. Farkhondeh, T.; Samarghandian, S.; Sadighara, P. Lead exposure and asthma: An overview of observational and experimental studies. Toxin Rev. 2014, 34, 6–10. [Google Scholar] [CrossRef] [Scilit]
  51. Skalny, A.V.; Lima, T.R.R.; Ke, T.; Zhou, J.C.; Bornhorst, J.; Alekseenko, S.; Aaseth, J.; Anesti, O.; Sarigiannis, D.A.; Tssatakis, A.; et al. Toxic metal exposure as a possible risk factor for COVID-19 and other respiratory infectious diseases. Food Chem. Toxicol. 2020, 146, 111809. [Google Scholar] [CrossRef] [Scilit] [PubMed]
  52. Pfadenhauer, L.M.; Burns, J.; Rohwer, A.; Rehfuess, E.A. A protocol for a systematic review of the effectiveness of interventions to reduce exposure to lead through consumer products and drinking water. Syst. Rev. 2014, 3, 36. [Google Scholar] [CrossRef] [Scilit]
  53. Harrison, R.M.; Yin, J. Particulate matter in the atmosphere: Which particle properties are important for its effects on health? Sci. Total Environ. 2000, 249, 85–101. [Google Scholar] [CrossRef] [Scilit]
  54. Bergmann, M.L.; Andersen, Z.J.; Massling, A.; Kindler, P.A.; Loft, S.; Amini, H.; Hunter, T.C.; Guo, Y.; Maric, M.; Nordstrom, C.; et al. Short-term exposure to ultrafine particles and mortality and hospital admissions due to respiratory and cardiovascular diseases in Copenhagen, Denmark. Environ. Pollut. 2023, 336, 122396. [Google Scholar] [CrossRef] [Scilit] [PubMed]
  55. Shukla, A.; Bunkar, N.; Kumar, R.; Bhargava, A.; Tiwari, R.; Chadbury, K.; Goryacheva, I.; Mishra, P.E. Air pollution associated epigenetic modifications: Transgenerational inheritance and underlying molecular mechanisms. Sci. Total Environ. 2019, 656, 760–777. [Google Scholar] [CrossRef] [Scilit] [PubMed]
  56. Kyung, S.Y.; Jeong, S.H. Particulate-Matter Related Respiratory Diseases. Tuberc. Respir. Dis. 2020, 83, 116–121. [Google Scholar] [CrossRef] [Scilit]
  57. Gauderman, W.J.; Avol, E.; Gilliland, F.; Vora, H.; Thomas, D.; Berhane, K.; McConnell, R.; Kuenzili, N.; Lumann, F.; Rappaport, H.M.; et al. The Effect of Air Pollution on Lung Development from 10 to 18 Years of Age. N. Engl. J. Med. 2004, 351, 1057–1067. [Google Scholar] [CrossRef] [Scilit]
  58. Pope, C.A.; Ezzati, M.; Dockery, D.W. Fine-particulate air pollution and life expectancy in the United States. N. Engl. J. Med. 2009, 360, 376–386. [Google Scholar] [CrossRef] [Scilit]
  59. Nachman, K.E.; Parker, J.D. Exposures to fine particulate air pollution and respiratory outcomes in adults using two national datasets: A cross-sectional study. Environ. Health 2012, 11, 25. [Google Scholar] [CrossRef] [Scilit] [PubMed]
  60. Tsai, S.S.; Chiu, H.F.; Weng, H.H.; Yang, C.Y. Short-Term Effects of Fine Particulate Air Pollution on Emergency Room Visits for Cardiac Arrhythmias: A Case-Crossover Study in Taipei. J. Toxicol. Environ. Health Part A 2013, 76, 614–623. [Google Scholar] [CrossRef] [Scilit]
  61. Zanobetti, A.; Schwartz, J. The effect of fine and coarse particulate air pollution on mortality: A national analysis. Environ. Health Perspect. 2009, 117, 898–903. [Google Scholar] [CrossRef] [Scilit]
  62. Deng, Q.; Lu, C.; Norbäck, D.; Bornehag, C.G.; Zhang, Y.; Liu, W.; Yuan, H.; Sundell, J. Early life exposure to ambient air pollution and childhood asthma in China. Environ. Res. 2015, 143, 83–92. [Google Scholar] [CrossRef] [Scilit]
  63. Matthews, N.C.; Pfeffer, P.E.; Mann, E.H.; Kelly, F.J.; Corrigan, C.J.; Hawrylowicz, C.M.; Lee, T.H. Urban particulate matter–activated human dendritic cells induce the expansion of potent inflammatory Th1, Th2, and Th17 effector cells. Am. J. Respir. Cell Mol. Biol. 2016, 54, 250–262. [Google Scholar] [CrossRef] [Scilit]
  64. Duan, R.R.; Hao, K.; Yang, T. Air pollution and chronic obstructive pulmonary disease. Chronic Dis. Transl. Med. 2020, 6, 260–269. [Google Scholar] [CrossRef] [Scilit]
  65. Kang, S.; Hong, Y.S.; Park, J.; Kang, D.; Kim, H.; Lee, J.; Kim, W.; Kang, W.K.; Guallar, E.; Cho, J.; et al. Air pollution and mortality in patients with chronic obstructive pulmonary disease: A cohort study in South Korea. Ther. Adv. Chronic Dis. 2023, 14, 20406223231176175. [Google Scholar] [CrossRef] [Scilit]
  66. Canova, C.; Dunster, C.; Kelly, F.J.; Minelli, C.; Shah, P.L.; Caneja, C.; Tumilty, M.K.; Burney, P. PM10-induced hospital admissions for asthma and chronic obstructive pulmonary disease: The modifying effect of individual characteristics. Epidemiology 2012, 23, 607–615. [Google Scholar] [CrossRef] [Scilit]
  67. Khalaf, E.; Mohammadi, M.; Sulistiyani, S.; Ramírez-Coronel, A.; Kiani, F.; Jalil, A.T.; Almulla, A.F.; Ashan, P.; Farhadi, M.; Derikondi, M. Effects of sulfur dioxide inhalation on human health: A review. Rev. Environ. Health 2022, 39, 331–337. [Google Scholar] [CrossRef] [Scilit] [PubMed]
  68. Bălă, G.P.; Râjnoveanu, R.M.; Tudorache, E.; Motișan, R.; Oancea, C. Air pollution exposure-the (in)visible risk factor for respiratory diseases. Environ. Sci. Pollut. Res. 2021, 28, 19615–19628. [Google Scholar] [CrossRef] [Scilit]
  69. Huang, Y.; Zhang, H.; Lv, B.; Tang, C.; Du, J.; Jin, H. Sulfur dioxide: Endogenous generation, biological effects, detection, and therapeutic potential. Antioxid. Redox Signal. 2022, 36, 256–274. [Google Scholar] [CrossRef] [Scilit] [PubMed]
  70. Sims, J.N.; Leggett, S.S.; Myla, A. Industrial Emissions and Asthma Prevalence. Eur. J. Environ. Public Health 2020, 4, em0046. [Google Scholar] [CrossRef] [Scilit] [PubMed]
  71. Orellano, P.; Reynoso, J.; Quaranta, N. Short-term exposure to Sulphur dioxide (SO2) and all-cause and respiratory mortality: A systematic review and meta-analysis. Environ. Int. 2021, 150, 106434. [Google Scholar] [CrossRef] [Scilit]
  72. Rosser, F.; Forno, E.; Kurland, K.S.; Han, Y.Y.; Mair, C.; Perez, E.A.; Canino, G.; Celedon, J.C. Annual SO2 exposure, asthma, atopy, and lung function in Puerto Rican children. Pediatr. Pulmonol. 2020, 55, 330–337. [Google Scholar] [CrossRef] [Scilit]
  73. Castner, J.; Gittere, S.; Seo, J.Y. Criteria air pollutants and emergency nursing. J. Emerg. Nurs. 2015, 41, 186–192. [Google Scholar] [CrossRef] [Scilit] [PubMed]
  74. Brand, A.; McLean, K.E.; Henderson, S.B.; Fournier, M.; Liu, L.; Kosatsky, T.; Smargiassi, A. Respiratory hospital admissions in young children living near metal smelters, pulp mills and oil refineries in two Canadian provinces. Environ. Int. 2016, 94, 24–32. [Google Scholar] [CrossRef] [Scilit]
  75. Ghaly, A.E.; Ramakrishnan, V.V. Nitrogen sources and cycling in the ecosystem and its role in air, water and soil pollution: A critical review. J. Pollut. Eff. Control 2015, 3, 1000136. [Google Scholar] [CrossRef]
  76. César, A.C.G.; Carvalho, J.A., Jr.; Nascimento, L.F.C. Association between NOx exposure and deaths caused by respiratory diseases in a medium-sized Brazilian city. Braz. J. Med. Biol. Res. 2015, 48, 1130–1135. [Google Scholar] [CrossRef] [Scilit]
  77. Ghosh, R.; Joad, J.; Benes, I.; Dostal, M.; Sram, R.J.; Hertz-Picciotto, I. Ambient nitrogen oxides exposure and early childhood respiratory illnesses. Environ. Int. 2012, 39, 96–102. [Google Scholar] [CrossRef] [Scilit]
  78. César, A.C.G.; De Carvalho, J.A., Jr.; Nascimento, L.F.C. Exposure To Nitrogen Oxides And Hospitalizations From Cardiovascular Diseases In Piracicaba, SP. ISEE Conf. Abstr. 2015, 27, 1157. [Google Scholar] [CrossRef] [Scilit]
  79. Theodorakidou, M.; Lambrou, G.I. Public health issues from the exposure to nitrogen oxides: A brief review. ARC J. Public Health Community Med. 2017, 2, 44–56. [Google Scholar]
  80. Gorguner, M.; Akgun, M. Acute inhalation injury. Eurasian J. Med. 2010, 42, 28–35. [Google Scholar] [CrossRef] [Scilit] [PubMed]
  81. Ihedike, C.; Ling, J. Effects of Ozone, Particulate Matter10 and Oxides of Nitrogen on Respiratory Health (COPD and asthma) in Nigeria: A Systematic Review. Lupine Online J. Nurs. Health Care 2022, 3, 364–371. [Google Scholar]
  82. Solomon, C.; Christian, D.L.; Chen, L.L.; Welch, B.S.; Kleinman, M.T.; Dunham, E.; Erle, D.J.; Balmes, J.R. Effect of serial-day exposure to nitrogen dioxide on airway and blood leukocytes and lymphocyte subsets. Eur. Respir. J. 2000, 15, 922–928. [Google Scholar] [CrossRef] [Scilit]
  83. Sun, J.; Barnes, A.J.; He, D.; Wang, M.; Wang, J. Systematic review and meta-analysis of the association between ambient nitrogen dioxide and respiratory disease in China. Int. J. Environ. Res. Public Health 2017, 14, 646. [Google Scholar] [CrossRef] [Scilit]
  84. Meng, X.; Liu, C.; Chen, R.; Sera, F.; Vicedo-Cabrera, A.M.; Miloevic, Q.; Tuo, Y.; Tong, S.; Coelho, M.S.Z.S.; Saldiva, O.P.H.N.; et al. Short term associations of ambient nitrogen dioxide with daily total, cardiovascular, and respiratory mortality: Multilocation analysis in 398 cities. BMJ 2021, 372, n534. [Google Scholar] [CrossRef] [Scilit]
  85. Kowalska, M.; Skrzypek, M.; Kowalski, M.; Cyrys, J. Effect of NOx and NO2 concentration increase in ambient air to daily bronchitis and asthma exacerbation, Silesian Voivodeship in Poland. Int. J. Environ. Res. Public Health 2020, 17, 754. [Google Scholar] [CrossRef] [Scilit]
  86. Carpenter, D.O.; Ma, J.; Lessner, L. Asthma and infectious respiratory disease in relation to residence near hazardous waste sites. Ann. N. Y. Acad. Sci. 2008, 1140, 201–208. [Google Scholar] [CrossRef] [Scilit] [PubMed]
  87. Madani, N.A.; Carpenter, D.O. Patterns of emergency room visits for respiratory disease in New York State in relation to air pollution, poverty and smoking. Int. J. Environ. Res. Public Health 2023, 20, 3267. [Google Scholar] [CrossRef] [Scilit] [PubMed]
  88. Maio, S.; Fasola, S.; Marcon, A.; Angino, A.; Baldacci, S.; Bilo, M.B.; Bono, R.; La Gutta, S.; Marchetti, P.; Sarno, G.; et al. Relationship of long-term air pollution exposure with asthma and rhinitis in Italy: An innovative multipollutant approach. Environ. Res. 2023, 224, 115455. [Google Scholar] [CrossRef] [Scilit] [PubMed]
  89. Eisner, M.D.; Anthonisen, N.; Coultas, D.; Kuenzli, N.; Perez-Padilla, R.; Postina, D.; Romieu, I.; Silverman, E.; Balmes, J.R.; Committee on Nonsmoking COPD; et al. An official American Thoracic Society public policy statement: Novel risk factors and the global burden of chronic obstructive pulmonary disease. Am. J. Respir. Crit. Care Med. 2010, 182, 693–718. [Google Scholar] [CrossRef] [Scilit]
  90. Song, Q.; Christiani, D.; Wang, X.; Ren, J. The Global Contribution of Outdoor Air Pollution to the Incidence, Prevalence, Mortality and Hospital Admission for Chronic Obstructive Pulmonary Disease: A Systematic Review and Meta-Analysis. Int. J. Environ. Res. Public Health 2014, 11, 11822–11832. [Google Scholar] [CrossRef] [Scilit]
  91. Tiotiu, A.I.; Novakova, P.; Nedeva, D.; Chong-Neto, H.J.; Novakova, S.; Steiropoulos, P.; Kowal, K. Impact of Air Pollution on Asthma Outcomes. Int. J. Environ. Res. Public Health 2020, 17, 6212. [Google Scholar] [CrossRef] [Scilit]
  92. Khreis, H.; Cirach, M.; Mueller, N.; de Hoogh, K.; Hoek, G.; Nieuwenhuijsen, M.J.; Rojas-Rudeda, D. Outdoor air pollution and the burden of childhood asthma across Europe. Eur. Respir. J. 2019, 54, 1802194. [Google Scholar] [CrossRef] [Scilit] [PubMed]
  93. Moore, E.; Chatzidiakou, L.; Kuku, M.O.; Jones, R.L.; Smeeth, L.; Beevers, S.; Kelly, F.; Barratt, B.; Quint, J.K. Global associations between air pollutants and chronic obstructive pulmonary disease hospitalizations. A systematic review. Ann. Am. Thorac. Soc. 2016, 13, 1814–1827. [Google Scholar] [CrossRef] [Scilit] [PubMed]
Atmosphere 17 00322 g001
Figure 1. Effect sizes for estimated associations for criteria pollutants and asthma.
Figure 1. Effect sizes for estimated associations for criteria pollutants and asthma.
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Figure 2. Effect sizes for estimated associations of criteria pollutants and COPD.
Figure 2. Effect sizes for estimated associations of criteria pollutants and COPD.
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Table 1. Total emissions for each criteria pollutant in NYS for the study period, based on NEI exposure data for 2011, 2014, 2017, given in tons.
Table 1. Total emissions for each criteria pollutant in NYS for the study period, based on NEI exposure data for 2011, 2014, 2017, given in tons.
PollutantsExposure in Tons
Carbon monoxide (CO)186,081
Nitrogen oxides (NOx)145,773
Lead (Pb)5067
Fine particulate matter (PM2.5)13,074
Coarse particulate matter (PM10)18,868
Sulfur dioxide (SO2)126,752
Table 2. β Estimate, lower and upper CIs, and p-values for the CAPs and asthma ER visits.
Table 2. β Estimate, lower and upper CIs, and p-values for the CAPs and asthma ER visits.
OutcomePollutantEstimate95% CIp-Value *
AsthmaCO0.0240.017, 0.031<0.0001
NOx0.0320.017, 0.047<0.0001
PM2.50.001−0.012, 0.0140.898
PM100.01670.0, 0.0340.057
SO20.11690.096, 0.138<0.0001
* p-values give significance of adjusted associations between outcome and zip code-level pollutant exposure.
Table 3. Estimates, CIs and p-values for CAPs and ER visits for COPD.
Table 3. Estimates, CIs and p-values for CAPs and ER visits for COPD.
OutcomePollutantβ Estimate95% CIp-Value *
COPDCO0.0290.022, 0.037<0.0001
NOx0.0410.029, 0.053<0.0001
PM2.50.0090.002, 0.0180.0145
PM100.0120.004, 0.0210.0024
SO20.0290.021, 0.037<0.0001
* p-values give the significance of adjusted associations between outcome and zip code-level pollutant exposure.
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Lebbie, T.S.; Jones, L.E.; Madani, N.A.; Carpenter, D.O. Associations Between Emergency Room Visits for Respiratory Diseases and Exposure to Zip Code-Level Criteria Air Pollutants in New York State. Atmosphere 2026, 17, 322. https://doi.org/10.3390/atmos17030322

AMA Style

Lebbie TS, Jones LE, Madani NA, Carpenter DO. Associations Between Emergency Room Visits for Respiratory Diseases and Exposure to Zip Code-Level Criteria Air Pollutants in New York State. Atmosphere. 2026; 17(3):322. https://doi.org/10.3390/atmos17030322

Chicago/Turabian Style

Lebbie, Tamba S., Laura E. Jones, Najm Alsadat Madani, and David O. Carpenter. 2026. "Associations Between Emergency Room Visits for Respiratory Diseases and Exposure to Zip Code-Level Criteria Air Pollutants in New York State" Atmosphere 17, no. 3: 322. https://doi.org/10.3390/atmos17030322

APA Style

Lebbie, T. S., Jones, L. E., Madani, N. A., & Carpenter, D. O. (2026). Associations Between Emergency Room Visits for Respiratory Diseases and Exposure to Zip Code-Level Criteria Air Pollutants in New York State. Atmosphere, 17(3), 322. https://doi.org/10.3390/atmos17030322

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