Skip to content
Open access

Long-term exposure to air pollution and chronic kidney disease incidence in adults: The Danish Nurse Cohort.

Jul 2026 · Journal of Exposure Science and Environmental Epidemiology · 0 citations · 20 references
Medicine

TL;DR

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.

Abstract

Background

Air pollution is an established risk factor for cardiovascular and metabolic diseases, but evidence on chronic kidney diseases (CKD) remains limited.

Objective

We aim to examine the association between long-term exposure to air pollutants and CKD incidence.

Methods

We followed 24,581 female nurses from the Danish Nurse Cohort, recruited in 1993 or 1999, for their first-ever hospital contact with a primary or secondary CKD diagnosis until 2018. We estimated annual mean levels of particulate matter with a diameter < 2.5 µm (PM2.5) and 10 µm (PM10), nitrogen dioxide (NO2), and black carbon (BC) at nurses' residential addresses using the DEHM/UBM/AirGIS modeling system. We used Cox regression models to examine the association of 14-year running means of air pollutants with CKD incidence and to explore the effect modification of this association by lifestyles.

Results

Over 521,211 person-years of follow-up, 429 nurses developed CKD. We found positive associations of modest magnitude between long-term exposure to air pollutants and CKD, with hazard ratios (95% confidence intervals) per interquartile range: 1.18 (0.93-1.50) per 2.86 µg/m3 for PM2.5, 1.14 (0.93-1.40) per 3.33 µg/m3 for PM10, 1.13 (0.99-1.28) per 8.09 µg/m3 for NO2, and 1.09 (1.00-1.20) per 0.34 µg/m3 for BC. The associations between long-term exposure to NO2 and CKD incidence were greater in never smokers than in ever-smokers. Associations with NO2 and BC remained unchanged in two-pollutant models, whereas those with PM10 and PM2.5 attenuated.

Significance

Our study adds important new findings to the growing evidence suggesting that air pollution may be associated with CKD incidence. IMPACT STATEMENT This study provides longitudinal evidence that long-term exposure to ambient air pollution contributes to chronic kidney disease (CKD) incidence, even in a relatively healthy occupational cohort and at comparatively low pollution levels. Although effect sizes were modest, consistent positive associations, particularly for NO2 and black carbon, highlight traffic-related pollution as a potential renal risk factor. Stronger associations among never-smokers suggest that environmental exposures may independently influence kidney health. These findings reinforce the need to integrate air pollution into CKD risk assessment and prevention strategies. Strengthening air quality policies and reducing long-term residential exposure could help lower CKD burden and protect kidney health at the population level.

Read PDF

Similar papers

Open access Jul 2026

Short-term exposure to ambient air pollutants increases the mortality risk of chronic kidney disease: a time-stratified case-crossover study in Zhejiang Province.

A significant association between short-term exposure to air pollutants and CKD mortality in the population of Zhejiang Province is revealed and a need for governmental authorities to enhance the monitoring and control of air pollution to mitigate the health burden on the elderly is suggested.

Pin-Yuan Dai, Xiao-Yan Zhou, Wei-Wei Gong et al. · 0 citations
Open access Aug 2026

Long-Term Air Pollution Exposure, Cardiovascular Disease, and Cardiometabolic Risk Factors in Middle-Aged and Older Chinese Adults: A Prospective Cohort Study

The substantial burden of cardiovascular disease (CVD) attributable to air pollution remains a critical public health challenge, yet its combined effect with cardiometabolic factors is not fully understood. This study leveraged data from the Global Burden of Disease Study (GBD) and the China High Air Pollutants (CHAP) database to evaluate the CVD burden attributable to air pollution, which was found to increase progressively with age. We conducted a cross-sectional analysis using baseline (2011) data from 7420 participants aged ≥ 45 years in the China Health and Retirement Longitudinal Study (CHARLS), and a prospective cohort analysis in 8792 participants followed through 2020. In the longitudinal analysis, long-term exposure to PM2.5 (HR = 1.09, 95% CI: 1.03–1.16) and PM10 (HR = 1.07, 95% CI: 1.04–1.10) was significantly associated with an elevated risk of incident CVD, whereas the association for NO2 was nominally significant (HR = 1.12, 95% CI: 1.00–1.24) and that for O3 was not statistically significant (HR = 1.08, 95% CI: 0.93–1.27). Furthermore, prolonged exposure to these pollutants was associated with a higher prevalence of hypertension, diabetes, dyslipidemia, and obesity, and with adverse levels of metabolic indicators, including the TyG, TyG-BMI, and TyG-WC indices. A random forest model showed modest discrimination for incident CVD (AUC = 0.656), identifying PM10 and PM2.5 as the most important predictors. In conclusion, long-term exposure to ambient air pollution, particularly particulate matter, is associated with an increased risk of CVD and cardiometabolic disorders in middle-aged and older Chinese adults.

Xue-Hua Wang, Zhaohui Wang, Yan Wang · 0 citations
Open access Aug 2026

Long-term cumulative associations of annual air pollution exposure and hospitalization with Parkinson’s Disease

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. · 0 citations
Open access Jul 2026

Long-term exposure to six gaseous air pollutants and risk of Parkinson’s Disease

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. · 0 citations
Open access Aug 2026

Association between Long-Term Ambient PM2.5 Exposure and Hypertension and Metabolic Syndrome among Ghanaian Adults.

INTRODUCTION Air pollution is a leading environmental risk factor for cardiovascular disease (CVD), yet its relationship with metabolic syndrome (MetS) and its components in sub-Saharan Africa are unclear. This study aimed to examine the association between long-term PM2.5 exposure and MetS (and its component conditions) in a Ghanaian adult cohort. METHODS We performed a cross-sectional analysis of 1,833 adults (40-60 years) from the Awi-Gen study. Long-term PM2.5 exposure (2007-2015) was estimated via a satellite-based model. MetS was defined using harmonized criteria. We used multivariable logistic regression with sequential adjustment for covariates. RESULTS A positive association was observed between PM2.5 and hypertension, while no association was found for MetS overall or its component conditions. Each 1 μg/m3 increase in PM2.5 was associated with 6% higher odds of hypertension (OR: 1.06, 95% CI: 1.02-1.11). PM2.5 quartiles also showed a dose-response relationship with hypertension (p-trend=0.003), with the highest exposure linked to a 50% greater likelihood of hypertension. The calculated population attributable fraction for PM2.5 and hypertension was 18.6%. INTERPRETATION In this rural Ghanaian population, long-term PM2.5 exposure was associated with hypertension but not with metabolic syndrome or its other components. These findings provide important evidence from an understudied sub-Saharan African population and support the integration of air quality management into cardiovascular disease prevention strategies.

Ali Moro, E. Nonterah, Godfred Agongo et al. · 0 citations

We use cookies to run the site and, with your consent, for analytics and to show ads. See our Cookie Policy.