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Central hemodynamics in relation to low-level environmental lead exposure

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posted on 2019-12-13, 10:49 authored by Cai-Guo Yu, Fang-Fei Wei, Zhen-Yu Zhang, Lutgarde Thijs, Wen-Yi Yang, Blerim Mujaj, Ying-Mei Feng, José Boggia, Harry A. Roels, Harry A. J. Struijker-Boudier, Tim S. Nawrot, Peter Verhamme, Jan A. Staessen

Purpose: Arterial stiffness predicts cardiovascular complications. The association between arterial stiffness and blood lead (BL) remains poorly documented. We aimed to assess the association of central hemodynamic measurements, including pulse wave velocity (aPWV), with blood lead in a Flemish population.

Materials and Methods: In this Flemish population study (mean age, 37.0 years; 48.3% women), 267 participants had their whole BL and 24-h urinary cadmium (UCd) measured by electrothermal atomic absorption spectrometry in 1985–2005. After 9.4 years (median), they underwent applanation tonometry to estimate central pulse pressure (cPP), the augmentation index (AI), pressure amplification (PA), and aPWV. The amplitudes of the forward (Pf) and backward (Pb) pulse waves and reflection index (RI) were derived by a pressure-based wave separation algorithm.

Results: BL averaged 2.93 μg/dL (interquartile range, 1.80–4.70) and UCd 4.79 µg (2.91–7.85). Mean values were 45.0 ± 15.2 mm Hg for cPP, 24.4 ± 12.4% for AI, 1.34 ± 0.21 for PA, 7.65 ± 1.74 m/s for aPWV, 32.7 ± 9.9 mm Hg for Pf, 21.8 ± 8.4 mm Hg for Pb, and 66.9 ± 18.4% for RI. The multivariable-adjusted association sizes for a 2-fold higher BL were: +3.03% (95% confidence interval, 1.56, 4.50) for AI; −0.06 (−0.08, −0.04) for PA; 1.02 mm Hg (0.02, 2.02) for Pb; and 3.98% (1.71, 6.24) for RI (p ≤ .045). In 206 participants never on antihypertensive drug treatment, association sizes were +2.59 mm Hg (0.39, 4.79) for cPP and +0.26 m/s (0.03, 0.50) for aPWV. Analyses adjusted for co-exposure to cadmium were consistent.

Conclusion: In conclusion, low-level environmental lead exposure possibly contributes to arterial stiffening and wave reflection from peripheral sites.

Funding

The European Union [HEALTH-F7-305507 HOMAGE] and the European Research Council [Advanced Researcher Grant 2011-294713-EPLORE and Proof-of-Concept Grant 713601-uPROPHET], the European Research Area Net for Cardiovascular Diseases [JTC2017-046-PROACT], and the Research Foundation Flanders, Ministry of the Flemish Community, Brussels, Belgium [G.0881.13] supported the Research Unit Hypertension and Cardiovascular Research.

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