Maternal Cadmium Levels During Pregnancy and the Relationship with Preeclampsia and Fetal Biometric Parameters

Abstract

Preeclampsia, which is caused by multiple factors, still remains one of the most serious complications of pregnancy. This study was designed to determine cadmium levels in women with preeclampsia compared to those of normotensive women. In this case-control study, maternal blood, umbilical cord blood, and placental cadmium levels were measured by an inductively coupled plasma mass spectrometry system in 51 women presenting consecutively with preeclampsia and 51 normotensive pregnant women. Groups were matched for maternal age, parity, and gestational age. Birth outcomes were recorded, such as gestational age at delivery, birth weight, and Apgar score. Median (interquartile range [IQR]) blood cadmium concentration was 1.21 μg/L (0.76-1.84 μg/L) and 1.09 μg/L (0.72-1.31 μg/L) in women with preeclampsia and normotensive, respectively; values for placental cadmium levels of women with preeclampsia and normotensive were 3.61 μg/kg (2.19-4.37 μg/kg) and 4.28 μg/kg (3.06-5.71 μg/kg), respectively. We observed a statistically significant increase in blood and placental cadmium levels in women with preeclampsia compared to healthy pregnant women. After adjusting for pre-pregnancy body mass index, maternal age, parity, gestational age at sample collection, and maternal calcium and magnesium levels, the odds ratio of having preeclampsia in the high tertile was markedly increased (odds ratio, 7.83 [95% CI, 1.64-37.26]) compared with the low tertile. Interestingly, there was no difference in the cadmium level in umbilical cord blood between the groups. Within the preeclamptic group, higher cadmium status was significantly associated with decreased birth weight. Our study suggested that elevated cadmium level in the maternal circulation could potentially increase the risk of preeclampsia. The results also demonstrate that higher cadmium status may contribute to fetal growth restriction in preeclamptic patients.

Environmental contaminants and preeclampsia: a systematic literature review

“…Briefly, the 28 investigations were published between 2006–2018 with sample sizes ranging from 58 to 1.21 million women. There were 6 studies on POP (Eslami et al 2016; Murray et al 2018; Savitz et al 2012; 2014; Stein et al 2009; Starling et al 2014), one study on water contaminants (Carwile et al 2014), 11 investigations on air pollutants (Dadvand et al 2014; Lee et al 2013; Madsen et al 2017; Mendola et al 2016; Nahidi et al 2014; Pedersen et al 2017; Savitz et al 2015; Wang et al 2018b; Wesselink et al 2017; Wu et al 2016; Yorifuji et al 2015), 6 examining metals (Elongi Moyene et al 2016; Maduray et al 2017; Sandoval-Carrillo et al 2016; Laine et al 2015; Wang et al 2018a; Vigeh et al 2006), and 4 investigations evaluating non-persistent organic pollutants (Cantonwine et al 2016; Leclerc et al 2014; Ye et al 2017; Shaw et al 2018).…”

“…A 2018 case-control study conducted in a Chinese medical center identified an elevated risk of preeclampsia with elevated maternal blood concentrations of Cd, when metal levels were measured between the 28 th -40 th week of pregnancy (Wang et al 2018a). In this study, Wang et al (2018a) defined preeclampsia using the hypertension guidelines of ACOG, and proteinuria defined in any of the following ways: urine protein greater than 300 mg/24 hr; one positive dipstick; or a protein/creatinine ratio >0.3.…”

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“…Many previous studies have demonstrated that a higher level of Cd is present in the peripheral blood of preeclamptic women than that of women undergoing normal pregnancies. 13 The most conclusive evidence that links Cd with hypertensive disorders came from an animal experiment launched in 1965 by Henry, who successfully replicated the hypertensive model by injecting pregnant rats with the aqueous solution of Cd. 12 The toxic effects of Cd share strikingly similar features to many of clinical manifestations of PE, such as hypertension, proteinuria, and lesion of the liver and kidney.…”

“…12 Recently, many studies showed a close relationship between Cd and PE. 13,14 The toxic effects of Cd share similar features with the clinical manifestations of PE, such as hypertension, proteinuria, decreased placental perfusion, fetal growth restriction, convulsions, and dysfunction of liver and kidney. 15 Although the placenta has a certain barrier to Cd, it is still an important target organ for Cd.…”

Silencing of Annexin A1 suppressed the apoptosis and inflammatory response of preeclampsia rat trophoblasts

“…Severe PE can advance to eclampsia, leading to complications, such as HELLP syndrome (involving hemolysis, increased liver enzyme levels and thrombocytopenia), coagulation dysfunction, cardiopulmonary syndrome and cardiorenal syndrome, which directly threaten the safety of pregnant women ( 3 , 4 ). PE not only produces adverse effects on the maternal body, but also leads to fetal hypoxic-ischemic injury, resulting in intrauterine growth retardation and even fetal death ( 5 - 7 ). Although numerous efforts have been made in order to fully understand PE, the pathogenesis of PE remains unclear.…”