Maternal Blood Lead Levels and the Risk of Pregnancy-Induced Hypertension
Maternal Blood Lead Levels and the Risk of Pregnancy-Induced Hypertension
Background: Prior studies revealed associations of environmental lead exposure with risks of hypertension and elevated blood pressure.
Objective: We examined the effect of blood lead levels on blood pressure and the incidence of pregnancy-induced hypertension (PIH) in the second and third trimesters of pregnancy.
Methods: One thousand seventeen pregnant women were enrolled in two French municipalities between 2003 and 2005 for the EDEN (Etude des Déterminants pré et post natals du développement et de la santée de l' Enfant) cohort study. Blood lead concentrations were measured by atomic absorption spectrometry in mothers between 24 and 28 weeks of gestation.
Results: PIH was diagnosed in 106 subjects (10.9%). Age, parity, weight gain, alcohol, smoking habits, and calcium supplementation were comparable between hypertensive and nonhypertensive women. Lead levels were significantly higher in PIH cases (mean ± SD, 2.2 ± 1.4 µg/dL) than in normotensive patients (1.9 ± 1.2 µg/dL; p = 0.02). Adjustment for potential confounder effects slightly attenuated but did not eliminate the significant association between blood lead levels and the risk of PIH (adjusted odds ratio of PIH = 3.3; 95% confidence interval, 1.1–9.7). We also observed geographic differences in lead exposure and in the incidence of PIH and found significant correlations between blood lead levels and unadjusted as well as adjusted systolic and diastolic blood pressures after 24 weeks of gestation.
Conclusions: These findings confirm the relationship between blood lead levels at mid-pregnancy and blood pressure and suggest that environmental lead exposure may play an etiologic role in PIH.
Lead is one of the most extensively studied reproductive toxicants. Several epidemiologic studies have demonstrated a positive association between blood lead levels and blood pressure among nonpregnant adults (Nawrot et al. 2002; Schwartz 1995). The evidence is sufficient to infer a causal relationship of lead exposure with hypertension (Navas-Acien et al. 2007). However, the role of lead in pregnancy-induced hypertension (PIH) remains unclear.
PIH is characterized by an increase in systolic blood pressure (SBP ≥ 140 mmHg) and/or diastolic blood pressure (DBP ≥ 90 mmHg) after 20 weeks of gestation. This disorder can be complicated by proteinuria, a condition corresponding to preeclampsia. PIH is encountered in 10% of pregnancies and is an important cause of morbidity for both mother and fetus (National High Blood Pressure Education Program 2000).
Environmental factors may have a role in this disease occurrence. Although some studies failed to find a relationship between lead concentrations in cord blood and preeclampsia (Angell and Lavery 1982), several authors demonstrated higher blood levels of lead, cadmium, and manganese in hypertensive or preeclampsia patients compared with normotensive women (Dawson et al. 2000; Kosanovic et al. 2002; Rothenberg et al. 1999; Vigeh et al. 2004). Other elements such as zinc and selenium were reported to be reduced in hypertensive pregnant women (Dawson et al. 1999; Rayman et al. 2003).
Blood lead levels increase during pregnancy, from 24 weeks of gestation until delivery, because of increased gastrointestinal absorption and because of an increase in bone turnover in this period (Hertz-Picciotto et al. 2000; O'Flaherty et al. 1995). Several mechanisms may contribute to the pathogenesis of lead-induced hypertension: increases in endothelin and thromboxane production, inhibition of vascular smooth muscle ATPases, oxidation of endogenous nitric oxide by reactive oxygen species, and a decrease in glomerular filtration rate of the kidneys with increase in the renin–angiotensin II–aldosterone activity (Gonick and Behari 2002; Vaziri and Khan 2007; Vaziri and Sica 2004). Interactions between lead and other elements are possible because oxidative stress produced by lead, cadmium, or manganese may be counterbalanced by the antioxidative properties of manganese or selenium (Anastasakis et al. 2008; Campagna et al. 2000; Huel et al. 2000; Vaziri and Sica 2004; Verity 1999).
In the present study, we examined the relationship between PIH and circulating blood lead, cadmium, manganese, and selenium concentrations in a nonselected population of pregnant women.
Abstract and Introduction
Abstract
Background: Prior studies revealed associations of environmental lead exposure with risks of hypertension and elevated blood pressure.
Objective: We examined the effect of blood lead levels on blood pressure and the incidence of pregnancy-induced hypertension (PIH) in the second and third trimesters of pregnancy.
Methods: One thousand seventeen pregnant women were enrolled in two French municipalities between 2003 and 2005 for the EDEN (Etude des Déterminants pré et post natals du développement et de la santée de l' Enfant) cohort study. Blood lead concentrations were measured by atomic absorption spectrometry in mothers between 24 and 28 weeks of gestation.
Results: PIH was diagnosed in 106 subjects (10.9%). Age, parity, weight gain, alcohol, smoking habits, and calcium supplementation were comparable between hypertensive and nonhypertensive women. Lead levels were significantly higher in PIH cases (mean ± SD, 2.2 ± 1.4 µg/dL) than in normotensive patients (1.9 ± 1.2 µg/dL; p = 0.02). Adjustment for potential confounder effects slightly attenuated but did not eliminate the significant association between blood lead levels and the risk of PIH (adjusted odds ratio of PIH = 3.3; 95% confidence interval, 1.1–9.7). We also observed geographic differences in lead exposure and in the incidence of PIH and found significant correlations between blood lead levels and unadjusted as well as adjusted systolic and diastolic blood pressures after 24 weeks of gestation.
Conclusions: These findings confirm the relationship between blood lead levels at mid-pregnancy and blood pressure and suggest that environmental lead exposure may play an etiologic role in PIH.
Introduction
Lead is one of the most extensively studied reproductive toxicants. Several epidemiologic studies have demonstrated a positive association between blood lead levels and blood pressure among nonpregnant adults (Nawrot et al. 2002; Schwartz 1995). The evidence is sufficient to infer a causal relationship of lead exposure with hypertension (Navas-Acien et al. 2007). However, the role of lead in pregnancy-induced hypertension (PIH) remains unclear.
PIH is characterized by an increase in systolic blood pressure (SBP ≥ 140 mmHg) and/or diastolic blood pressure (DBP ≥ 90 mmHg) after 20 weeks of gestation. This disorder can be complicated by proteinuria, a condition corresponding to preeclampsia. PIH is encountered in 10% of pregnancies and is an important cause of morbidity for both mother and fetus (National High Blood Pressure Education Program 2000).
Environmental factors may have a role in this disease occurrence. Although some studies failed to find a relationship between lead concentrations in cord blood and preeclampsia (Angell and Lavery 1982), several authors demonstrated higher blood levels of lead, cadmium, and manganese in hypertensive or preeclampsia patients compared with normotensive women (Dawson et al. 2000; Kosanovic et al. 2002; Rothenberg et al. 1999; Vigeh et al. 2004). Other elements such as zinc and selenium were reported to be reduced in hypertensive pregnant women (Dawson et al. 1999; Rayman et al. 2003).
Blood lead levels increase during pregnancy, from 24 weeks of gestation until delivery, because of increased gastrointestinal absorption and because of an increase in bone turnover in this period (Hertz-Picciotto et al. 2000; O'Flaherty et al. 1995). Several mechanisms may contribute to the pathogenesis of lead-induced hypertension: increases in endothelin and thromboxane production, inhibition of vascular smooth muscle ATPases, oxidation of endogenous nitric oxide by reactive oxygen species, and a decrease in glomerular filtration rate of the kidneys with increase in the renin–angiotensin II–aldosterone activity (Gonick and Behari 2002; Vaziri and Khan 2007; Vaziri and Sica 2004). Interactions between lead and other elements are possible because oxidative stress produced by lead, cadmium, or manganese may be counterbalanced by the antioxidative properties of manganese or selenium (Anastasakis et al. 2008; Campagna et al. 2000; Huel et al. 2000; Vaziri and Sica 2004; Verity 1999).
In the present study, we examined the relationship between PIH and circulating blood lead, cadmium, manganese, and selenium concentrations in a nonselected population of pregnant women.
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