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BACKGROUND: A recently developed urinary peptidomics biological aging clock can be used to study accelerated human aging. From 1990 to 2019, exposure to airborne particulate matter (PM) became the leading environmental risk factor worldwide. OBJECTIVES: This study investigated whether air pollution exposure is associated with accelerated urinary peptidomic aging, independent of calendar age, and whether this association is modified by other risk factors. METHODS: In a Flemish population, the urinary peptidomic profile (UPP) age (UPP-age) was derived from the urinary peptidomic profile measured by capillary electrophoresis coupled with mass spectrometry. UPP-age-R was calculated as the residual of the regression of UPP-age on chronological age, which reflects accelerated aging predicted by UPP-age, independent of chronological age. A high-resolution spatial-temporal interpolation method was used to assess each individual's exposure to P[M.sub.10], P[M.sub.2.5], black carbon (BC), and nitrogen dioxide (N[O.sub.2]). Associations of UPP-age-R with these pollutants were investigated by mixed models, accounting for clustering by residential address and confounders. Effect modifiers of the associations between UPP-age-R and air pollutants that included 18 factors reflecting vascular function, renal function, insulin resistance, lipid metabolism, or inflammation were evaluated. Direct and indirect (via UPP-age-R) effects of air pollution on mortality were evaluated by multivariable-adjusted Cox models. RESULTS: Among 660 participants (50.2% women; mean age: 50.7 y), higher exposure to P[M.sub.10], P[M.sub.2.5], BC, and N[O.sub.2] was associated with a higher UPP-age-R. Studying effect modifiers showed that higher plasma levels of desphospho-uncarboxylated matrix Gla protein (dpucMGP), signifying poorer vitamin K status, steepened the slopes of UPP-age-R on the air pollutants. In further analyses among participants with dpucMGP [greater than or equal to] 4.26 [micro]g/L (median), an interquartile range (IQR) higher level in P[M.sub.10], P[M.sub.2.5], BC, and N[O.sub.2] was associated with a higher UPP-age-R of 2.03 [95% confidence interval (CI): 0.60, 3.46], 2.22 (95% CI: 0.71, 3.74), 2.00 (95% CI: 0.56, 3.43), and 2.09 (95% CI: 0.77, 3.41) y, respectively. UPP-age-R was an indirect mediator of the associations of mortality with the air pollutants [multivariable-adjusted hazard ratios from 1.094 (95% CI: 1.000, 1.196) to 1.110 (95% CI: 1.007, 1.224)] in participants with a high dpucMGP, whereas no direct associations were observed. DISCUSSION: Ambient air pollution was associated with accelerated urinary peptidomics aging, and high vitamin K status showed a potential protective effect in this population. Current guidelines are insufficient to decrease the adverse health effects of airborne pollutants, including healthy aging trajectories. https://doi.org/10.1289/EHP13414, Introduction Over the past 20 y, global life expectancy at birth increased from 67.2 to 73.5 y. (1) In line with this remarkable increase in longevity, global exposure to harmful [...]

Background Estimating the burden of hypertension in Nigeria hitherto relied on clinic blood pressure (BP) measurement alone. This excludes individuals with masked hypertension (MH), i.e. normotensive clinic but hypertensive out-of-clinic BP. Methods In a nationally representative sample of adult Nigerians, we obtained clinic BP using auscultatory method and out-of-clinic BP by self-measured home BP with semi-automated oscillometric device. Clinic BP was average of 5 consecutive measurements and home BP was average of 3 days duplicate morning and evening readings. MH was clinic BP <140 mm Hg systolic and 90 mm Hg diastolic and home BP ≥135 mm Hg systolic and/or 85 mm Hg diastolic. Results Among 933 participants, the prevalence of sustained hypertension, MH, and white-coat hypertension was 28.3%, 7.9%, and 11.9%, respectively. Among subjects whose clinic BP were in the normotensive range (n = 558), the prevalence of MH was 13%; 12% among untreated and 27% among treated individuals. The mutually adjusted odds ratios of having MH among all participants with normotensive clinic BP were 1.33 (95% confidence interval, 1.10–1.60) for a 10-year higher age, 1.59 (1.09–2.40) for a 10 mm Hg increment in systolic clinic BP, and 1.16 (1.08–1.28) for a 10 mg/dl higher random blood glucose. The corresponding estimates in the untreated population were 1.24 (1.03–1.51), 1.56 (1.04–2.44), and 1.16 (1.08–1.29), respectively. Conclusions MH is common in Nigeria and increasing age, clinic systolic BP, and random blood glucose are the risk factors. [ABSTRACT FROM AUTHOR]

Purpose: Previous studies that addressed whether left ventricular hypertrophy is more closely associated with central than peripheral blood pressure (BP) have been inconsistent. Radial artery wave generated by applanation tonometry and calibrated with brachial BP in 162 adult Nigerians were analysed by using generalized transfer function to derive central BP. Materials and methods: We compared the associations of ECG voltages and left ventricular hypertrophy (ECG-LVH) as continuous and binary variables respectively with central and brachial BP indices. Results: In a multivariable adjusted analysis, 1 standard deviation (SD) increase in brachial systolic, diastolic, pulse and mean arterial pressures increased the Sokolow–Lyon QRS voltage by 0.34 (CI, 0.21–0.48; p < 0.0001), 0.21 (CI, 0.07–0.36; p < 0.05); 0.22 (CI, 0.9–0.34; p < 0.001) and 0.29 (CI, 0.14–0.43) similar to (p > 0.05) corresponding Sokolow–Lyon QRS increase of 0.26 (0.12–0.40, p < 0.001); 0.14 (0.00–0.28, p < 0.05); 0.24 (0.11–0.39; p < 0.001) and 0.19 (0.05–0.34, p < 0.05) respectively observed for 1 SD increment in central pressures. The odds ratio (OR) relating ECG-LVH to 1 SD increase in brachial systolic, pulse, and mean arterial pressures were 2.62 (CI, 1.49–4.65, p < 0.001); 1.88 (CI, 1.19–2.95, p < 0.01) and 2.16 (CI, 1.22–3.82, p < 0.01) was similar to (p > 0.05) corresponding OR of 2.41 (1.33–4.36, p < 0.01); 2.04 (1.23–3.37, p < 0.01); 2.00 (1.11–3.63, p < 0.001) observed for I SD increment in central pressures. Conclusion: Central and peripheral BP are similarly associated with Sokolow–Lyon ECG voltage and hypertrophy. [ABSTRACT FROM AUTHOR]

Blacks are more prone to salt-sensitive hypertension than Whites. This cross-sectional analysis of a multi-ethnic cohort aimed to search for proteins potentially involved in the susceptibility to salt sensitivity, hypertension, and hypertension-related complications. The study included individuals enrolled in African Prospective Study on the Early Detection and Identification of Cardiovascular Disease and Hypertension (African-PREDICT), Flemish Study of the Environment, Genes and Health Outcomes (FLEMENGHO), Prospective Cohort Study in Patients with Type 2 Diabetes Mellitus for Validation of Biomarkers (PROVALID)-Austria, and Urinary Proteomics Combined with Home Blood Pressure Telemonitoring for Health Care Reform Trial (UPRIGHT-HTM). Sequenced urinary peptides detectable in 70% of participants allowed the identification of parental proteins and were compared between Blacks and Whites. Of 513 urinary peptides, 300 had significantly different levels among healthy Black (n = 476) and White (n = 483) South Africans sharing the same environment. Analyses contrasting 582 Blacks versus 1731 Whites, and Sub-Saharan Blacks versus European Whites replicated the findings. COL4A1, COL4A2, FGA, PROC, MGP, MYOCD, FYXD2, and UMOD were identified as the most likely candidates underlying the racially different susceptibility to salt sensitivity, hypertension, and related complications. Enriched pathways included hemostasis, platelet activity, collagens, biology of the extracellular matrix, and protein digestion and absorption. Our study suggests that MGP and MYOCD being involved in cardiovascular function, FGA and PROC in coagulation, FYXD2 and UMOD in salt homeostasis, and COL4A1 and COL4A2 as major components of the glomerular basement membrane are among the many proteins potentially incriminated in the higher susceptibility of Blacks compared to Whites to salt sensitivity, hypertension, and its complication. Nevertheless, these eight proteins and their associated pathways deserve further exploration in molecular and human studies as potential targets for intervention to reduce the excess risk of hypertension and cardiovascular complications in Blacks versus Whites., (© 2024 The Author(s). PROTEOMICS published by Wiley‐VCH GmbH.)

Objectives: Greater vulnerability of Black vs. White individuals to cardiovascular disease (CVD) and chronic kidney disease (CKD) is well charted in the United States, but studies involving sub-Saharan blacks are scarce., Methods: Baseline data (2021-2024) were collected in 168 sub-Saharan Blacks and 93 European Whites in an ongoing clinical trial (NCT04299529), using standardized patient selection criteria. Data included clinical and biochemical risk factors, ECG and echocardiographic traits, Framingham CVD risk, CKD grades (KDIGO 2024), self-assessed symptoms (WHO questionnaire), and urinary proteomic profiles predictive of left ventricular dysfunction (LVD) and CKD, HF1, and CKD273, respectively. Racial comparisons rested on unadjusted and multivariable-adjusted analyses., Results: Despite being younger (60.4 vs. 68.3 years), blacks had a worse risk profile, as evidenced by higher diabetes prevalence, higher BMI, faster heart rate, unfavourable serum cholesterol fractions, lower estimated glomerular filtration rate, microalbuminuria, and sedentary lifestyle. This resulted in blacks having higher 10-year CVD risk, higher heart age (index of vascular ageing with chronological age as reference), and a worse CKD grades. In both races, CKD273 increased with CKD grade, but CKD273 and HF1 were not different by race. These observations were robust in subgroup and adjusted analyses., Conclusion: This study did not differentiate host (genetic, molecular, and pathogenic) from environmental drivers of disease. Nonetheless, the findings call for a multipronged and comprehensive implementation of innovative health policies in sub-Saharan countries. Education, research, empowerment of stakeholders, and international learned societies connecting experts from a wide array of disciplines should vigorously sustain this effort., (Copyright © 2024 The Author(s). Published by Wolters Kluwer Health, Inc.)