Aug 2026· Reviews on Environmental Health· 0 citations· 53 references
Medicine
TL;DR
Current evidence suggests that exposure to fine particulate matter may contribute to early-life elevation in blood pressure; however, given the paucity of longitudinal data and the complexity of multipollutant exposures, further research employing standardized exposure metrics, harmonized outcome definitions, and multipollutant models are needed to clarify independent pollutant effects.
Abstract
Abstract Introduction Ambient air pollution is a modifiable environmental exposure that may contribute to early cardiovascular risk. Although long-term exposure has been linked to blood pressure (BP) dysregulation, research on its effects in children remains limited, despite their particular vulnerability during critical periods of cardiovascular development. This updated systematic review and meta-analysis aimed to estimate pollutant-specific associations of long-term air pollution exposure with BP and hypertension in children and adolescents. Content Following PRISMA guidelines, studies were identified from prior systematic reviews and meta-analyses as well as an updated PubMed and Web of Science searches through March 27, 2025. Twenty-one studies, including 990,157 participants, were included in the systematic review evaluating air pollutants, including PM1, PM2.5, PM10, NO, NO2, NOx, SO2, O3, and CO. Meta-analysis was limited to PM2.5, PM10, and NO2 because cohort data for other pollutants were limited, and exposure increments and hypertension definitions varied across studies. Summary Long-term PM2.5 exposure showed the most consistent association with higher systolic BP (0.59 mmHg per 10 μg/m3; 95 % CI: 0.28–0.90). PM10 was initially associated with higher systolic (0.28 mmHg per 10 μg/m3; 95 % CI: 0.25–0.31) and diastolic (0.27 mmHg; 95 % CI: 0.24–0.30) BP, but these associations were not sustained in sensitivity analyses. NO2 showed no significant association with systolic or diastolic BP. Several pollutants, including PM2.5, PM10, SO2, O3, and CO, were associated with increased odds of hypertension. Outlook Current evidence suggests that exposure to fine particulate matter may contribute to early-life elevation in blood pressure; however, given the paucity of longitudinal data and the complexity of multipollutant exposures, further research employing standardized exposure metrics, harmonized outcome definitions, and multipollutant models are needed to clarify independent pollutant effects.
Collectively, the available evidence supports a plausible role of PM 2.5 and PM 10 in elevating essential HTN risk; however, the association with GH remains inconclusive due to the limited studies.
OBJECTIVES
Evidence suggests that ambient air pollution contributes to metabolic dysregulation, including hyperuricemia. However, previous studies were limited to specific groups or regions with relatively high air pollutant concentrations. This study examined the association between long-term exposure to ambient air pollutants and hyperuricemia in a general population exposed to relatively low pollution concentrations.
METHOD
This cross-sectional study analyzed 20,117 adults who underwent health screenings in the Republic of Korea (2015-2019). Annual mean concentrations of PM2.5, PM10, NO2, SO2, and CO were estimated at residential addresses using the Community Multiscale Air Quality model. Hyperuricemia was defined as serum uric acid level > 7.0 mg/dL (males) or > 6.0 mg/dL (females). Multivariable logistic regression estimated odds ratios (ORs) per interquartile range (IQR) increase in pollutant exposure, adjusting for confounders including estimated glomerular filtration rate.
RESULTS
Among 20,117 participants, 3,078 (15.3%) had hyperuricemia. All five pollutants were significantly associated with hyperuricemia. The ORs (95% CIs) per IQR increase were 1.06 (1.01-1.10) for PM2.5, 1.15 (1.08-1.21) for PM10, 1.07 (1.00-1.14) for NO2, 1.13 (1.07-1.19) for SO2, and 1.06 (1.01-1.11) for CO. Associations were stronger among current smokers, older adults, and individuals with dyslipidemia or central obesity (all P for interaction < 0.05).
CONCLUSIONS
Long-term exposure to air pollutants was significantly associated with hyperuricemia, independent of renal function and even at low concentrations. These findings suggest that air pollution is an important environmental risk factor for metabolic disease, emphasizing the need for stricter regulations to protect vulnerable populations. Key Points • Long-term exposure to major ambient air pollutants is significantly associated with an increased risk of hyperuricemia, even at relatively low concentrations. • The association between air pollution and hyperuricemia persists independent of renal function, suggesting a potential role in systemic metabolic dysregulation. • Vulnerable populations, including older adults, current smokers, and individuals with metabolic conditions, exhibit stronger associations between air pollution exposure and hyperuricemia.
S. Cho, Hyun Jin Kim, Soontae Kim et al.· Clinical Rheumatology· 0 citations
Evidence linking long-term multipollutant exposure with incident pulmonary hypertension (PH) and circulating metabolic profiles is limited. We investigated individual and joint air pollution exposures in relation to incident PH, characterized pollution-related circulating metabolic signatures, and evaluated their potential mediating roles. This prospective cohort included 444,346 participants without PH at baseline who had air pollution exposure estimates and nuclear magnetic resonance metabolomics data. PM2.5, PM10, NO2, and NOx were assessed as individual pollutants and jointly summarized using an air pollution score (APS). Exposure-related metabolic signatures were derived by elastic-net regression, and their associations with incident PH and potential mediating contributions were evaluated using Cox proportional hazards models and mediation analyses. During 13.58 years of median follow-up, 2328 participants developed PH. Higher APS was associated with increased PH risk (hazard ratio [HR] per 1-SD increment, 1.12; 95% confidence interval [CI], 1.08-1.17). Individual pollutants were also positively associated with PH, with HRs ranging from 1.06 to 1.93 per 10-μg/m3 increment. Elastic-net regression yielded 105 metabolites for the APS signature and 52-123 metabolites for pollutant-specific signatures, mainly involving lipoprotein-related measures, fatty acids, and amino acids. These signatures were also associated with incident PH (HRs per 1-SD increment, 1.12-1.24). The overall metabolic signature mediated 11.74% (95% CI, 7.91%-18.95%) of the APS-PH association, whereas pollutant-specific signatures mediated 11.38%-26.00% of the corresponding pollutant-PH associations. Both individual pollutants and the weighted APS were positively associated with incident PH, with circulating metabolic alterations potentially contributing to these associations.
Ling Kuang, Er-La Huang, Bing-Yun Zhang et al.· Ecotoxicology and Environmen...· 0 citations
BACKGROUND
Ambient air pollution is an established cardiovascular risk factor, but its relation to arrhythmia-related outcomes has been synthesised less comprehensively than other cardiovascular endpoints.
OBJECTIVE
We conducted a systematic review and meta-analysis of studies examining ambient air pollution and arrhythmia-related outcomes.
METHODS
Primary meta-analyses were restricted to short-term particulate matter associations standardised to 10 μg/m3. Secondary analyses examined broader short-term models on the original study scale, long-term models were analysed separately, and an exploratory global multilevel model was used to account for multiple effect estimates within studies.
RESULTS
Thirty-two studies represented over 34 million participants or analysed cases across designs. In the primary analyses, short-term PM2.5 exposure standardised to 10 μg/m3 was associated with atrial fibrillation (4 studies; pooled relative risk [RR] 1.045, 95% CI 1.025-1.066; I2=0.66%) and with sudden cardiac arrest or sudden cardiac death (7 studies; RR 1.052, 1.031-1.075; I2=49.0%). Short-term PM10 exposure standardised to 10 μg/m3 was associated with sudden cardiac arrest or sudden cardiac death (3 studies; RR 1.024, 1.012-1.036; I2=0%). Expanded short-term analyses yielded similar pooled estimatesLong-term PM2.5-AF estimates were highly heterogeneous (pooled ratio 1.077, 95% CI 1.002-1.158; I2=99.9%), limiting interpretation. Additional sensitivity models yielded directionally consistent estimates.
CONCLUSIONS
Short-term exposure to particulate air pollution was associated with risks of atrial fibrillation and sudden cardiac arrest/sudden cardiac death. Given the observational evidence base, findings should be interpreted cautiously and viewed as consistent with, rather than definitive evidence of, an association between particulate exposure and arrhythmia-related events.
Andrea Matteucci, Luca Sgarra, M. Bonanni et al.· Heart Rhythm· 1 citation
BACKGROUND AND AIMS
The interaction between air pollutants and lifestyles on heart failure (HF) and its variation by age of HF onset remains unclear. We aim to assess the joint association of air pollutants and lifestyles with HF and examine whether it differs between early- and late-onset HF.
METHODS
: A cohort of 233,341 UK Biobank participants (2006-2010 baseline, followed up until 2023) was analyzed. Air pollution (NO2, NOx, PM10, PM2.5, PM2.5-10) and lifestyle (physical activity, smoking, sleep, diet, drinking, BMI) scores were computed, where higher scores indicated exposure to heavier air pollution or more unhealthy lifestyles. Cox models evaluated their associations with HF risk, and interactions were tested multiplicatively and additively.
RESULTS
: High air pollution (scores in top tertile) and unfavourable lifestyle (scores up to 5∼6) were associated with higher HF risk independently. Joint-exposure analyses revealed that unfavourable lifestyle and high air pollution were jointly linked to HF, which appeared stronger for early-onset HF [relative excess risk due to interaction: 0.44 (95%CI:0.14∼0.74) for all HF, 1.33 (95%CI:0.03∼2.62) for early-onset HF, 0.39 (95%CI:0.08∼0.70) for late-onset HF; p-value for the early-versus-late interaction contrast=0.08]. In turn, lifestyle differences [between unfavourable (5∼6) and favourable (0∼2)] were associated with larger HF incidence differences in high than low air pollution group, especially for early-onset HF [1.62-fold (95%CI:1.42∼1.84) for all HF, 3.35-fold (95%CI:1.76∼9.79) for early-onset HF, 1.52-fold (95%CI:1.33∼1.74) for late-onset HF].
CONCLUSIONS
: Air pollutants and lifestyles are jointly associated with HF risk, with young adults in air-polluted areas potentially gaining greater benefits from lifestyle differences.
Xing-Jie Fang, Meng-Dan Liang, Yao-Wei Sun et al.· European Journal of Preventi...· 0 citations
This systematic review investigates the mediating factors in the relationship between ambient air pollution exposure and cognitive aging. We identified 16 studies examining 72 unique exposure-mediator-outcome associations for six pollutants (PM2.5, PM10, NO2, NOX, black carbon, and PM1 components). The most studied pollutant was PM2.5 (65% of analyses). Cognitive outcomes included memory, cognitive processing speed, and clinically diagnosed conditions such as dementia incidence. Potential mediators spanned mental health outcomes (depression, anxiety, stress), lung function (FEV1, FVC, PEF), vascular diseases (stroke, hypertension), inflammation (CRP), metabolic factors (type 2 diabetes), sleep, and neuroanatomical changes. The quality of mediation analysis reporting was generally good, but most studies had some risk of bias, particularly in outcome assessment and confounding adjustment. Cardio and Cerebro-vascular diseases emerged as a potential key mediator. Mental health outcomes, sleep, and lung function also showed mediating potential, but further research is needed to confirm these findings. This review highlights the need for rigorous causal mediation analyses and standardized reporting to better understand the complex pathways linking air pollution to cognitive aging, in order to identify targeted preventive measures to reduce the negative impact of ambient air pollution on cognitive health.
M. Z. Sakhvidi, E. Burte, A. Mehrparvar et al.· Ageing Research Reviews· 0 citations
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