With less decline and greater attributable impact than PM2.5, NO2 is increasingly important for measuring morbidity impacts from local sources (i.e., traffic and buildings) in New York City.
Abstract
Background: Air quality in New York City has improved substantially in the past 2 decades due to reductions in both transported aerosols and local emissions. We estimated the short-term risk changes for three criteria air pollutants and corresponding attributable burdens. Methods: Trends in percent excess risk (PER) per same pollution increment and attributable counts and fractions for fine particles (PM2.5), nitrogen dioxide (NO2), and ozone (warm season only) were examined for Emergency Department (ED) visits (2005–2019) and hospitalizations (2000–2019) for youth asthma (ages 5–17), adult cardiovascular disease (CVD) (ages 40+), and older adult respiratory causes (ages 65+). Time-series models considered up to 3-day lag, adjusted for seasonal trends, day of week, holidays, and concurrent and delayed temperature. Results: Most pollutant-outcome pairs did not exhibit trends in PERs over time. NO2-attributable burden was higher than PM2.5 burden for asthma and CVD outcomes. We estimated about 4500 (17%) youth asthma ED visits and 1000 (2%) CVD hospitalizations on average annually (2005–2019) attributable to NO2 compared with 1900 (7%) youth asthma ED visits and 450 (1%) CVD hospitalizations attributable to PM2.5. NO2- and PM2.5-attributable health impacts declined about 50%–70%, driven by decreasing pollution levels and total morbidity burden depending on outcome, pollutant, and season. Ozone-attributable burden was mostly unchanged over time. Conclusion: With less decline and greater attributable impact than PM2.5, NO2 is increasingly important for measuring morbidity impacts from local sources (i.e., traffic and buildings) in New York City. Ozone impacts from regional source emissions persist.
Novel evidence is provided that short-term absolute increases in air pollution levels are associated with elevated risks of depression, which is worth consideration in future disease prevention practices.
Yating Ma, Chen-Lu Yang, Lijun Bai et al.· Ecotoxicology and Environmen...· 0 citations
Introduction: Traffic-Related Air Pollution (TRAP) is a major source of urban air pollution, with vehicular emissions releasing Particulate Matter (PM₂.₅ and PM₁₀), Nitrogen dioxide (NO₂) and Carbon monoxide (CO) into the atmosphere . Short-term exposure to these pollutants has been linked to adverse cardiovascular effects, including increased blood pressure, reduced Heart Rate Variability (HRV) and arterial stiffness . However, evidence on the immediate cardiovascular responses of healthy young adults following roadside exposure remains limited. This study evaluated the acute cardiovascular effects of short-term exposure to TRAP. Materials and methods: Sixty healthy volunteers aged 18-25 years participated in a 45-min roadside exposure study at a busy urban location. Ambient PM₂.₅, PM₁₀, NO₂, and CO concentrations were continuously monitored using validated portable air quality sensors and integrated monitoring techniques . Cardiovascular parameters, including systolic and diastolic blood pressure, HRV (RMSSD and SDNN) and arterial stiffness, were measured before and after exposure using standardized non-invasive instruments . Pre- and post-exposure differences were analyzed using paired t-tests and correlation analysis was performed to examine associations between pollutant concentrations and cardiovascular responses. Results: PM₂.₅ concentrations ranged from 92–118 μg/m³ and NO₂ concentrations from 58–72 ppb, exceeding the World Health Organization air quality guideline values. Following exposure, systolic blood pressure increased by 4–6 mmHg, HRV indices decreased by 10–20% and arterial stiffness increased. PM₂.₅ concentrations were significantly associated with increased blood pressure and reduced HRV, consistent with previous studies. Conclusion: Short-term exposure to traffic-related air pollution produced measurable cardiovascular changes in healthy young adults, including elevated blood pressure, reduced HRV, and increased arterial stiffness. These findings
Manikandan S, S. N, M. Selvaraj· Journal of air pollution and...· 0 citations
Short-term exposure to PM2.5, PM10, SO2, NO2, and CO was associated with increased AECOPD hospitalization risk, with nonlinear, lagged, and cumulative effects, and older adults and females may be more susceptible to ambient air pollution.
Huixia Shi, Jiajun Li, Bo-Yan Li et al.· Medicine· 0 citations
This study examines the long-term associations between ambient air pollutants and the burden of major respiratory and infectious diseases in this geographically sensitive region. A retrospective analysis was conducted using ICD-10-coded hospital records of patients diagnosed with asthma, chronic obstructive pulmonary disease (COPD), bronchitis, and tuberculosis from January 2020 to June 2026. These data were integrated with in situ air quality measurements, including PM10, PM2.5, and SO2, as well as satellite-derived Aerosol Optical Depth (AOD) from MODIS. Disease incidence was stratified by year, sex, and age groups (0–85+ years) to assess demographic susceptibility patterns. Respiratory diseases constituted a substantial public health burden over the study period. Asthma showed a marked female predominance (≈29,700 females vs. ≈16,000 males) and a bimodal age distribution with peaks in early childhood (0–5 years) and mid-adulthood (35–50 years). COPD was predominantly observed in males (≈8300 males vs. ≈5500 females), with a higher median age range (≈67–70 years). Bronchitis exhibited a similar bimodal pattern, disproportionately affecting both pediatric and elderly populations, while overall case numbers declined over time. Tuberculosis incidence was approximately threefold higher in males than females, with notable age-related divergence, affecting younger females (≈30–32 years) and middle-aged males (≈42–45 years). The findings suggest a spatial–temporal correspondence between elevated pollutant concentrations and respiratory disease prevalence in the Iğdır Basin. The observed sex- and age-specific disparities underscore the potential value of region-specific environmental health strategies, strengthened air quality management, and continuous epidemiological surveillance in enclosed basin environments.
Melahat Batu Ağırkaya, Fatma Şencan, Mehmet Ali Çelik· Pollutants· 0 citations
Air pollution at least 4 years before hospitalization may increase the odds of hospitalization with Parkinson’s Disease, and reducing air pollution exposure may have long-term effects on PD prevention.
Scott W. Delaney, Lauren Mock, Veronica A. Wang et al.· Environmental Epidemiology· 0 citations
Exposure to fine particulate matter (PM2.5) increases paediatric respiratory morbidity, but its impact on the intensity and economic burden of care in early childhood remains unclear. Here we link nationwide health records for 3,210,381 South Korean children (99,261,945 child-month observations, 2015-2019) and exploit quasi-random variation in PM2.5 induced by thermal inversions to estimate its causal effects on respiratory care and expenditure. A 1-standard-deviation increase in monthly PM2.5 (7.23 micrograms per cubic metre) raises respiratory visits broadly, peaking at age 1 (0.29 additional visits per child-month) and remaining significant through age 6. In contrast, expenditures rise disproportionately among children under 3, increasing by 46.7%, 43.0%, and 35.4% at ages 0, 1, and 2 and becoming indistinguishable from zero beyond age 4. This shift towards higher-intensity emergency care translates into a 32.2% increase in annual respiratory spending among children under 5. Air pollution thus imposes a dual burden, amplifying both the frequency and severity of illness among the youngest infants.
H. Kim, J. Suh, J. Shin et al.· medRxiv· 0 citations
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