Maternal Low-Level Lead Exposure and Fetal Growth

Zhu, Motao; Fitzgerald, Edward F.; Gelberg, Kitty H.; Lin, Shao; Druschel, Charlotte M.

doi:10.1289/ehp.0901561

Cited by 185 publications

(140 citation statements)

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“…26 Maternal lead exposure during pregnancy was reported to negatively affect gestational length and to increase the risk of preterm and small-for-gestational age infants. 1,11,12,14,25,27 However, in these studies, the lead levels in maternal blood were .5 mg/dL, thus the effects of the very low levels currently observed in developed countries are still to be thoroughly evaluated. In addition, environmental constraints on fetal growth may not only affect birth outcomes, but also have lasting effects on postnatal growth.…”

Section: Discussionmentioning

confidence: 98%

“…However, low-level exposure to lead still continues because of the widespread use of lead and its persistent nature. 1,2 The mean blood lead level among childbearing women in the United States was 1.2 mg/dL according to the national survey conducted in [2003][2004], and the level in childbearing Korean women was 1.6 mg/dL by the national survey conducted in 2008-2009. 3,4 Exposure to low-level lead is known to induce a wide range of adverse health effects, 5 and children are particularly sensitive to its effects because of the ongoing development of body organs and the nervous system.…”

mentioning

confidence: 99%

“…8,9 Although the sensitive period remains undetermined, prenatal exposure to lead is of particular concern because lead is known to cross the placenta and cause adverse birth outcomes, such as preterm birth, low birth weight, and small for gestational age. 1,[10][11][12][13][14][15] Schell et al 12 found that maternal blood lead levels of $3 mg/dL during the second trimester were associated with reduced head circumference at 6 and 12 months, but had no significant effects at ,3 mg/dL. Afeiche et al, 16 in a follow-up study of attained child weight, found that prenatal maternal bone lead was associated with lower weight over time among girls up to 5 years of age.…”

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confidence: 99%

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Postnatal Growth Following Prenatal Lead Exposure and Calcium Intake

Hong¹,

Kulkarni

Lim

et al. 2014

Pediatrics

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WHAT'S KNOWN ON THIS SUBJECT:Lead is an ubiquitous environmental pollutant, and no safe threshold for blood lead level in children has been discovered yet. Prenatal lead exposure affects growth of children.WHAT THIS STUDY ADDS: Low level of prenatal lead exposure of ,5.0 mg/dL affects postnatal children' s growth, which was further intensified by low calcium intake. abstract BACKGROUND: The effects on postnatal growth of maternal exposure to low levels of lead during pregnancy have not been well established. In addition, information is limited regarding the protective effect of dietary calcium intake during pregnancy against the effect of lead for fetal and postnatal growth. We investigated the relationship between prenatal exposure to lead and growth at birth and 6, 12, and 24 months postnatal, and evaluated the role of calcium intake against the effect of lead. METHODS:A total of 1150 pregnant women, and their subsequent offspring, enrolled in a prospective birth cohort study (Mothers and Children' s Environmental Health Study), were evaluated. Multivariable regression analysis was conducted to estimate the effects of prenatal maternal blood lead levels on growth at each follow-up. RESULTS:The blood lead levels of participating mothers were ,5.0 mg/dL and mean levels were 1.25 mg/dL during the early (before 20 gestational weeks) and late (at delivery) gestational periods. Prenatal exposure to lead, particularly in late pregnancy, was significantly associated with a reduction in infantile growth at 24 months. When pregnant women had dietary calcium intake at mean or upper level, the association was not significant. In contrast, lower than mean level of calcium intake intensified the adverse effect of prenatal lead exposure on growth in children.CONCLUSIONS: Prenatal lead exposure ,5.0 mg/dL adversely affects postnatal growth and low calcium intake aggravates the effect, indicating more stringent control of lead and sufficient intake of calcium are necessary to help children' s health.

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Section: Discussionmentioning

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confidence: 99%

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Postnatal Growth Following Prenatal Lead Exposure and Calcium Intake

Hong¹,

Kulkarni

Lim

et al. 2014

Pediatrics

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“…However, in a large cohort involving more than 34 000 live births, investigators found that a 5-μg/dL (50-ppb) increase in blood lead concentrations was associated with a 61-g decrement in birth weight. 26 The National Toxicology Program concluded that maternal blood lead concentrations <5 μg/dL (<50 ppb) are associated with lower birth weight.…”

Section: Scope Of the Problemmentioning

confidence: 99%

Prevention of Childhood Lead Toxicity

Lanphear¹,

Lowry²,

Ahdoot³

et al. 2016

Pediatrics

182

140

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Blood lead concentrations have decreased dramatically in US children over the past 4 decades, but too many children still live in housing with deteriorated lead-based paint and are at risk for lead exposure with resulting lead-associated cognitive impairment and behavioral problems. Evidence continues to accrue that commonly encountered blood lead concentrations, even those below 5 µg/dL (50 ppb), impair cognition; there is no identified threshold or safe level of lead in blood. From 2007 to 2010, approximately 2.6% of preschool children in the United States had a blood lead concentration ≥5 µg/dL (≥50 ppb), which represents about 535 000 US children 1 to 5 years of age. Evidence-based guidance is available for managing increased lead exposure in children, and reducing sources of lead in the environment, including lead in housing, soil, water, and consumer products, has been shown to be cost-beneficial. Primary prevention should be the focus of policy on childhood lead toxicity.

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“…Hg exposure occurs in the daily intake of rice in China [6]. Prenatal exposure to environmental chemicals such as organophosphate insecticides, tobacco smoke, heavy metals and perfluorinated compounds (PFCs) is associated with fetal growth restriction and low birth weight of infants [7][8][9][10]. The concentration of chemicals detected in the fetal environment is, however, relatively low (around 0.1-10 ppb level) and far from the levels reported in pharmacological studies.…”

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Epigenetic Assessment of Environmental Chemicals Detected in Maternal Peripheral and Cord Blood Samples

et al. 2011

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Abstract. Epigenetic alteration is an emerging paradigm underlying the long-term effects of chemicals on gene functions. Various chemicals, including organophosphate insecticides and heavy metals, have been detected in the human fetal environment. Epigenetics by DNA methylation and histone modifications, through dynamic chromatin remodeling, is a mechanism for genome stability and gene functions. To investigate whether such environmental chemicals may cause epigenetic alterations, we studied the effects of selected chemicals on morphological changes in heterochromatin and DNA methylation status in mouse ES cells (ESCs). Twenty-five chemicals, including organophosphate insecticides, heavy metals and their metabolites, were assessed for their effect on the epigenetic status of mouse ESCs by monitoring heterochromatin stained with 4′,6-diamino-2-phenylindole (DAPI). The cells were surveyed after 48 or 96 h of exposure to the chemicals at the serum concentrations of cord blood. The candidates for epigenetic mutagens were examined for the effect on DNA methylation at genic regions. Of the 25 chemicals, five chemicals (diethyl phosphate (DEP), mercury (Hg), cotinine, selenium (Se) and octachlorodipropyl ether (S-421)) caused alterations in nuclear staining, suggesting that they affected heterochromatin conditions. Hg and Se caused aberrant DNA methylation at gene loci. Furthermore, DEP at 0.1 ppb caused irreversible heterochromatin changes in ESCs, and DEP-, Hg-and S-421-exposed cells also exhibited impaired formation of the embryoid body (EB), which is an in vitro model for early embryos. We established a system for assessment of epigenetic mutagens. We identified environmental chemicals that could have effects on the human fetus epigenetic status. Key words: DNA methylation, Embryoid body, Epigenetic mutagens, ES cells, Heterochromatin (J. Reprod. Dev. 57: [507][508][509][510][511][512][513][514][515][516][517] 2011) any chemicals have been widely used in the household, agricultural and urban environment, and there are various environmental chemicals in the fetal growth environment: organophosphate insecticides (chlorpyrifos), perfluorooctane sulfonate (PFOS), di(2-ethylhexyl)phthalate (DEHP), elements of tobacco smoke (nicotine and cotinine) and heavy metals (lead (Pb), cadmium (Cd) and mercury (Hg)) [1][2][3][4][5]. Hg exposure occurs in the daily intake of rice in China [6]. Prenatal exposure to environmental chemicals such as organophosphate insecticides, tobacco smoke, heavy metals and perfluorinated compounds (PFCs) is associated with fetal growth restriction and low birth weight of infants [7][8][9][10]. The concentration of chemicals detected in the fetal environment is, however, relatively low (around 0.1-10 ppb level) and far from the levels reported in pharmacological studies. Such a low concentration may accumulate in the fetus and placenta and affect fetal growth [11][12][13][14], and alternatively, some chemicals may have long-term effects on gene functions and stability even at a low concentration ...

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Maternal Low-Level Lead Exposure and Fetal Growth

Cited by 185 publications

References 26 publications

Postnatal Growth Following Prenatal Lead Exposure and Calcium Intake

Postnatal Growth Following Prenatal Lead Exposure and Calcium Intake

Prevention of Childhood Lead Toxicity

Epigenetic Assessment of Environmental Chemicals Detected in Maternal Peripheral and Cord Blood Samples

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