Evidence suggests a possible modest association between long-term PM2.5 exposure and VTE; however, considerable between-study variability and sensitivity to exposure harmonization limit definitive conclusions.
Abstract
Background
Ambient air pollution is associated with cardiovascular morbidity and mortality, but its relationship with venous thromboembolism (VTE) remains uncertain. We performed an updated systematic review and meta-analysis evaluating particulate matter exposure and VTE risk.
Methods
PubMed, Embase, Web of Science, and the Cochrane Library were searched for observational studies evaluating PM2.5 or PM10 exposure and venous thrombotic outcomes. Studies were stratified by pollutants, exposure duration, and effect measure. Estimates were harmonized to 10 μg/m³, and random-effects models using restricted maximum-likelihood estimation and Hartung-Knapp adjustment were applied.
Results
Nineteen studies representing >4.5 million participants met the inclusion criteria. Overall long-term analyses showed no significant association for PM2.5 (HR 1.42, 95% CI 0.88-2.28; I²=97.0%) or PM10 (HR 1.18, 95% CI 0.85-1.64; I²=96.2%). However, sensitivity analyses restricted to studies natively reporting effects per 10 μg/m³ showed an association between PM2.5 and VTE (HR 1.070, 95% CI 1.010-1.135; I²=0%), while PM10 showed a borderline association (HR 1.023, 95% CI 1.000-1.047; I²=0%). Short-term PM2.5 and PM10 exposures were not significantly associated with venous thrombotic risk.
Conclusions
Evidence suggests a possible modest association between long-term PM2.5 exposure and VTE; however, considerable between-study variability and sensitivity to exposure harmonization limit definitive conclusions. Standardized exposure metrics and consistent VTE definitions are needed to clarify this association.
This study systematically evaluates the association between trace metal exposure and hypertension risk, explores dose-response patterns, and investigates underlying molecular mechanisms. A systematic review was conducted according to PRISMA guidelines, including 39 high-quality observational studies retrieved from PubMed, Web of Science, Embase, and the Cochrane Library. Meta-analysis results showed a significant positive association between blood lead exposure and hypertension (OR = 1.16, 95% CI: 1.02-1.31) as well as gestational hypertension (OR = 1.56, 95% CI: 1.21-2.02). Conversely, blood manganese demonstrated a potential protective effect, showing a monotonically declining linear trend with hypertension risk and a significantly reduced risk of gestational hypertension (OR = 0.40, 95% CI: 0.25-0.65). Dose-response analysis based on restricted cubic splines revealed nonlinear patterns: blood cadmium exhibited a U-shaped dose-response relationship (P non-linear = 0.005) with risk rising markedly above 3.5 µg/L, and dietary zinc showed a J-shaped curve (P non-linear = 0.004) peaking around 22 mg/day. Urinary biomarkers (cadmium, lead, arsenic, zinc, vanadium, and cobalt) generally showed stronger associations with hypertension than blood biomarkers. However, for several metals - including vanadium, cobalt, chromium, and nickel - the available evidence was limited to one to three studies, and the corresponding risk estimates should therefore be interpreted with caution and require confirmation in future larger-scale studies. Bioinformatics analysis highlighted that trace metal exposure may promote hypertension through mechanisms such as oxidative stress, inflammatory responses (e.g., TNF signaling), and disruption of the AGE-RAGE pathway. The findings suggest that lead exhibits threshold-free linear toxicity, while manganese may have a protective effect. Pregnant women were identified as a particularly sensitive population to environmental metal exposure. This study provides epidemiological evidence and explores molecular mechanisms, supporting preventive strategies for environmentally induced hypertension. The image summary is shown in the Graphical Abstract.
Yunzhen Lei, J. Diao, Ming Xu et al.· Ecotoxicology and Environmen...· 0 citations
The increased risk after adjustment for smoking and the suggestion of a dose-response, are consistent with the hypothesis of an association between benzene exposure and lung cancer risk.
M. S. Seyyedsalehi, Mattia Bonetti, Darshi Shah et al.· European Journal of Epidemio...· 0 citations
Occupational PAH exposure is modestly associated with upper gastrointestinal cancer risk, particularly esophageal cancer, with higher risk estimates observed in high-exposure occupations.
M. S. Seyyedsalehi, Anna Vrtev, M. Lanza et al.· European Journal of Cancer P...· 0 citations
Exposure to heavy metals is regarded as a potential contributor to the development of hyperuricemia (HU). However, related research findings are inconsistent. This systematic review and meta-analysis aimed to explore the association between blood concentrations of heavy metals (such as lead, cadmium, manganese, mercury) and HU. PubMed, EMBASE, Web of Science, and Cochrane Library databases were searched to collect related studies up to June 2024. The pooled odds ratio (OR) and 95% confidence interval (CI) were calculated utilizing a random-effects model or a fixed-effects model. Sensitivity analysis was conducted, while publication bias was assessed using funnel plots and Egger's test. A total of 19 eligible studies were included. The meta-analysis indicated a significant association between blood lead levels and the risk of HU (OR: 1.88; 95% CI: 1.22-2.92; P<0.005). Blood levels of cadmium (OR: 1.31; 95% CI: 0.68-2.52; non-significant), manganese (OR: 1.04; 95% CI: 0.88-1.22; non-significant), and mercury (OR: 1.55; 95% CI: 0.70-3.44; non-significant) were not significantly associated with the risk of HU. In conclusion, this study demonstrates a significant positive association between blood lead levels and the risk of HU. No significant association is found between blood levels of cadmium, manganese, and mercury and the risk of HU.
Yanxia Gan, Xi Yu, Puhui Zhou· Joint Bone Spine· 0 citations
BACKGROUND
Tetrachloroethylene (PCE) is a ubiquitous chlorinated solvent with documented placental transfer. Despite widespread environmental and occupational exposure, no prior systematic review has synthesized evidence on prenatal PCE exposure and adverse birth outcomes.
METHODS
We conducted a systematic review and meta-analysis of observational studies. PubMed, Web of Science, PsycINFO, EMBASE, and CINAHL were searched from inception to July 13, 2026. Eligible studies reported associations between prenatal PCE exposure (drinking water or inhalation) and adverse birth outcomes. Study quality was assessed using the Newcastle-Ottawa Scale (NOS) and Agency for Healthcare Research and Quality (AHRQ) criteria. Random-effects meta-analyses were performed using risk ratios (RRs) with 95% confidence intervals (CIs), with Knapp-Hartung adjustments and Paule-Mandel τ2 estimation.
RESULTS
Twenty one studies (1987-2023) met inclusion criteria. Prenatal PCE exposure was associated with spontaneous abortion (8 studies; RR = 1.28, 95% CI 1.00-1.63; I2 = 64.2%). Analyses of stillbirth, central nervous system defects, oral clefts, neural tube defects, preterm birth, low birthweight, and small-for-gestational-age (SGA) yielded positive but statistically non-significant pooled estimates. The certainty of evidence ranged from very low to low across outcomes (GRADE).
CONCLUSIONS
Prenatal PCE exposure may be associated with spontaneous abortion, particularly at higher exposure levels, and with SGA. Findings support ongoing regulatory efforts to limit PCE in occupational and environmental settings, particularly for pregnant individuals. Future prospective studies with biological monitoring and confounder-adjusted designs are needed.
Pallavi Menon, K. Patel, Jordan Kaplan et al.· Environmental Research· 0 citations
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.
H.C. Culpan, Y. Gözderesi, Nur Canpolat et al.· Reviews on Environmental Hea...· 0 citations
