Blood Cadmium Levels in Nonexposed Male Subjects Living in the Rome Area: Relationship to Selected Cardiovascular Risk Factors

Blood and Urine Cadmium, Blood Pressure, and Hypertension: A Systematic Review and Meta-analysis

“…These three cross-sectional studies used the following number of subjects: 2,853 ( Kurihara et al 2004 ), 1,902 ( Eum et al 2008 ), and 1,223 ( Menditto et al 1998 ). Outcome measures included categorical measures of HTN, that is, SBP ≥ 140 mmHg and/or DBP > 90 mmHg or taking anti-HTN drugs ( Kurihara et al 2004 ) or SBP ≥ 140 mmHg or DBP ≥ 90 mmHg or self-reported HTN in medical examination ( Eum et al 2008 ); continuous SBP and DBP ( Eum et al 2008 ; Menditto et al 1998 ); and mean BP, that is, DBP + pulse pressure ÷ 3 ( Eum et al 2008 ) and DBP + 1 / 3 × (SBP – DBP) ( Menditto et al 1998 ).…”

“…These three cross-sectional studies used the following number of subjects: 2,853 ( Kurihara et al 2004 ), 1,902 ( Eum et al 2008 ), and 1,223 ( Menditto et al 1998 ). Outcome measures included categorical measures of HTN, that is, SBP ≥ 140 mmHg and/or DBP > 90 mmHg or taking anti-HTN drugs ( Kurihara et al 2004 ) or SBP ≥ 140 mmHg or DBP ≥ 90 mmHg or self-reported HTN in medical examination ( Eum et al 2008 ); continuous SBP and DBP ( Eum et al 2008 ; Menditto et al 1998 ); and mean BP, that is, DBP + pulse pressure ÷ 3 ( Eum et al 2008 ) and DBP + 1 / 3 × (SBP – DBP) ( Menditto et al 1998 ). Exposure measures included BCd tertiles (0.18–1.28 μg/L, 1.29–1.86 μg/L, 1.87–5.52 μg/L ( Eum et al 2008 ); 84% upper cutoff dichotomized BCd and UCd, that is, geometric means × geometric SDs: UCd, men, 1.8 × 2.5 = 4.5 μg/g; UCd, women, 2.4 × 2.8 = 6.72 μg/g; BCd, men, 2.2 × 1.9 = 4.18 μg/L; BCd, women, 2.3 × 1.8 = 4.14 μg/L ( Kurihara et al 2004 ); and continuous log-transformed BCd ( Menditto et al 1998 ).…”

“… Kurihara et al (2004) used multivariable analysis to control for smoking status but did not separate former smokers from nonsmokers. Eum et al (2008) controlled for former, current, and never-smokers, and Menditto et al (1998) controlled for number of cigarettes smoked per day. Each of these studies statistically adjusted for smokers and nonsmokers but did not present the results separately for these two groups.…”

Lead effect on blood pressure in moderately lead‐exposed male workers

“…Hypertension status appears to be better associated with biomarkers of cumulative Pb exposure, such as bone Pb and chelatable Pb excreted in urine, in active Pb workers [Lee et al, 2001] as well as in the general population [Batuman et al, 1983;Hu et al, 1996;Korrick et al, 1999]. The influences of body mass index (BMI), hematocrit (Hct), age, dietary habits, smoking, and alcohol consumption appear to impair or diminish any significant quantitative relationship between blood pressure and biomarkers of Pb and Cd, according to the results of multiple regression analysis [Elwood et al, 1988;Harlan, 1988;Pocock et al, 1988;Victery et al, 1988;Grandjean et al, 1989;Morris et al, 1990;Staessen et al, 1990Staessen et al, , 1991Staessen et al, , 1996Whittemore et al, 1991;Menditto et al, 1994Menditto et al, , 1998Micciolo et al, 1994]. However, both Pb and Cd are pervasive in the human environment and accumulate in the human body over a lifetime, and it is known that age, smoking habit, and alcohol consumption contribute to the increase in cumulative exposure to Pb and Cd in the individual [Grandjean et al, 1981;Shaper et al, 1982;Telišman et al, 1986Telišman et al, , 1997Telišman et al, , 2001Berglund and Vahter, 1998].…”

Renoprotective effect of myricetin restrains dyslipidemia and renal mesangial cell proliferation by the suppression of sterol regulatory element binding proteins in an experimental model of diabetic nephropathy

“…Several epidemiological and experimental studies also suggest that STZ and chronic exposure of Cd caused alterations of lipid metabolism leads to diabetic nephropathy (Wen et al, 2012;Menditto et al, 1998;Satarug and Moore, 2004). The dyslipidemia accompanying insulin resistance is characterized by decreases in plasma levels of HDL with elevated plasma FFAs, TC and TGs associated with elevated VLDL production, a concomitant increase in plasma levels of small LDL.…”