Aug 2026· Environmental Epidemiology· Vol 10· 0 citations· 43 references
Medicine
TL;DR
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.
Abstract
Background: Parkinson’s Disease (PD) prevention and treatment are complicated because biological processes underlying PD may begin several years before diagnosis. Previous studies suggest that increased exposure to fine particulate matter (PM2.5) and nitrogen dioxide (NO2) air pollution increases PD morbidity. Methods: We analyzed data from 10,366,083 Medicare fee-for-service beneficiaries (age 65+) in the contiguous United States from 2000 to 2016. We defined “hospitalization with PD” as a beneficiary’s first hospitalization claim with diagnosis codes indicating PD. We linked 10-year exposure histories for PM2.5, NO2, and summer ozone (O3). In a discrete-time survival analysis, we fitted distributed lag models and estimated the lagged associations between air pollution and the odds of first hospitalization with PD. Results: Increased PM2.5 and NO2 exposure at least 4 years before hospitalization was associated with increased odds of hospitalization with PD. Accounting for nonlinearities in exposure-response and 10 years of continuous exposure to PM2.5 at the 90th versus the 0.5th percentile (i.e., 11.8 μg/m3 vs. 3.0 μg/m3), the odds ratio for hospitalization with PD was 1.634 (95% CI: 1.489, 1.792). Similarly, for 10 years of continuous exposure to NO2 at the 90th versus the 0.5th percentile (i.e., 31.7 ppb vs. 3.7 ppb), the odds ratio for hospitalization with PD was 1.474 (95% CI: 1.379, 1.575). Evidence of a relationship between O3 exposure and odds for hospitalization with PD was more limited. Conclusions: Air pollution at least 4 years before hospitalization may increase the odds of hospitalization with PD. Reducing air pollution exposure may have long-term effects on PD prevention.
A marginally increased risk for PD is observed after higher levels of exposure to O 3 (OR 1.03, 95% CI 1.00-1.06 per IQR) for exposure 6–16 years before the index date, suggesting a possible role of ozone in PD development even at low exposure levels, which requires further studies.
I. Rumrich, A. Korhonen, L. Frohn et al.· npj Parkinson's Disease· 0 citations
Positive associations between long-term exposure to NO2 and CKD incidence were greater in never smokers than in ever-smokers, and stronger associations among never-smokers suggest that environmental exposures may independently influence kidney health.
Gonzalo Hevia-Ramos, Jiawei Zhang, Stephane Tuffier et al.· Journal of Exposure Science...· 0 citations
Short-term absolute changes in ambient air pollution levels may result in disease events such as depression, whereas evidence from large-scale epidemiological studies has been insufficient. A time-stratified case-crossover study was performed to investigate the associations between air pollution increases between neighboring days (APINs, generated as the differences in absolute air pollution concentrations on the current days minus those on the previous days) and morbidity risks of depression based on hospital admission and outpatient visit data from 239 Chinese cities of prefecture-level or above during 2013-2017. Daily absolute concentrations of particulate matter with an aerodynamic diameter ≤ 2.5 μm (PM2.5), particulate matter with an aerodynamic diameter ≤ 10 μm (PM10), nitrogen dioxide (NO2), sulfur dioxide (SO2), carbon monoxide (CO) and ozone (8 h O3) were obtained, and conditional logistic regression models were used to evaluate the associations between absolute concentrations and APINs of major air pollutants with morbidity risks of depression. A total of 330,610 hospital admissions and 3,726,390 outpatient visits for depression were included. Per interquartile range (IQR) increase in APINs of major air pollutants at lag 0-3 were associated with increases ranging from 0.59% (0.06%, 1.13%) (8 h O3) to 1.66% (1.09%, 2.22%) (NO2) in hospital admissions for depression; and with increases ranging from 0.42% (0.15%, 0.68%) (8 h O3) to 0.85% (0.56%, 1.14%) (NO2) in outpatient visits for depression, which were robust to adjustments for absolute concentrations of major air pollutants (with the exception of 8 h O3). This study provides novel evidence 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, Chenlu Yang, Lijun Bai et al.· Ecotoxicology and Environmen...· 0 citations
Fine particulate air pollution (PM2.5) in the United States has fallen by roughly half since 2000, yet linked health outcomes such as diabetes and childhood ADHD have not improved in parallel. One reconciling possibility is that pollution exposure in early life produces health effects that emerge only years or decades later, after pollution itself has declined. Using two decades of U.S. county-level data, we relate annual PM2.5 estimates to birth outcomes, diabetes prevalence, and small-area estimates of childhood attention-deficit/hyperactivity disorder (ADHD) across short and long time scales. Within counties, changes in low birth weight rates are associated with changes in PM2.5 during the same year and the year prior to birth. At longer time scales, cross-county comparisons show that PM2.5 exposure is associated with higher prevalence of adult diabetes and ADHD after approximately a decade. Together, these patterns suggest that population-level health risks from air pollution may persist over decades, even as pollution itself declines.
R. A. Bentley, L. Ozeryansky· medRxiv· 0 citations
Emerging evidence links air pollution exposure to metabolic dysfunction; however, few studies have examined diabetes-related mortality in relation to ambient air pollutants using high-resolution exposure data at the population level. In the United States, particularly in large and geographically diverse states such as California, exposure contrasts and population heterogeneity provide an important setting to evaluate these associations.
We conducted a matched case–control analysis using California Department of Public Health (CDPH) Vital Records (2010–2021). Diabetes-related mortality events (ICD-10 E11) were identified as primary or contributory causes. Decedents (cases) were geocoded to residential addresses, and one-year rolling averages of fine particulate matter (PM
2.5
) before death were assigned as individual exposures. Each death record was matched to its selected controls based on month and year of birth and race-ethnicity. Controls were identified from the same statewide CDPH mortality database and were eligible because they had not died by the corresponding case’s date of death. Because the number of eligible controls varied across matched strata, controls were randomly sampled within each matched stratum to achieve an overall control-to-case ratio of approximately 2:1 for the study population. The final dataset included 60,824 diabetes-related deaths and 119,053 controls. Exposures were standardized by their interquartile range (IQR) and conditional logistic regression models estimated associations between 1 year rolling average fine particulate matter (PM
2.5
) exposure and odds of diabetes-related mortality, adjusting for age, sex, race-ethnicity, marital status, and education. Nitrogen dioxide (NO
2
) was included as a co-pollutant for confounding control.
PM
2.5
exposure (per 2.65 μg/m
3
IQR increase) was associated with a 18% higher odds of diabetes-related mortality (OR = 1.18; 95% CI: 1.15–1.22) before traffic indicator NO
2
adjustment and showed a stronger association with 21% higher odds (OR = 1.21; 95% CI: 1.17–1.25) after NO
2
adjustment. Health economics analysis estimated that reducing PM
2.5
exposure by its IQR could avoid losses of $31.2 million per 100,000 people.
Higher ambient PM
2.5
exposure was associated with increased odds of diabetes-related mortality in California even after adjustment for NO
2
and other impact factors. These findings support the need for continued strengthening of ambient air quality regulations.
Richy Zheng, Jason G. Su, E. Shahriary et al.· Frontiers in Public Health· 0 citations
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.
A. Spira-Cohen, Rebecca Goldberg, Sarah Johnson et al.· Environmental Epidemiology· 0 citations
