Talk:Abnormal Development - Heavy Metals
Environmental cadmium exposure is associated with elevated risk of chronic otitis media in adults
Occup Environ Med. 2018 Mar 26. pii: oemed-2017-104631. doi: 10.1136/oemed-2017-104631. [Epub ahead of print]
Lee DW1, Oh SH2, Park MK2, Lim YH3,4, Hong YC1,3,4.
OBJECTIVES: Chronic otitis media (COM) is caused by an infection of the middle ear, although it may also be associated with environmental pollutants. Recent reports found that cadmium exposure could be toxic to middle ear cell lines, but the role of cadmium in the development of COM in humans has not been examined to date. We hypothesised that environmental cadmium exposure was associated with an increased risk of COM in the general population. METHODS: We analysed cross-sectional data for 5331 adults of 20 years of age or above, obtained from the Korea National Health and Nutrition Examination Survey 2010-2012. We examined the association between blood cadmium levels and COM diagnosed by an otolaryngologist. RESULTS: The highest quartile group of cadmium blood concentration was associated with an OR of 3.33 (95% CI 1.78 to 7.53) for COM, after adjusting for potential confounding factors. Doubling blood cadmium concentration resulted in an OR of 1.58 (95% CI 1.19 to 2.08) for COM. These associations were robust on sensitivity analyses after excluding current smokers and former smokers and after excluding subjects with a potential history of occupational exposure to cadmium. CONCLUSIONS: The results of our study suggest that environmental cadmium exposure is associated with increased risk of COM, and further studies are warranted to understand the pathogenetic mechanism by which COM is caused by cadmium exposure. © Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.
KEYWORDS: cadmium; chronic otitis media; environmental exposure PMID: 29581150 DOI: 10.1136/oemed-2017-104631
Acute effects of lead on porcine neonatal Sertoli cells in vitro
Toxicol In Vitro. 2018 Apr;48:45-52. doi: 10.1016/j.tiv.2017.12.013. Epub 2017 Dec 19.
Mancuso F1, Arato I2, Lilli C2, Bellucci C2, Bodo M2, Calvitti M2, Aglietti MC3, dell'Omo M4, Nastruzzi C5, Calafiore R6, Luca G7, Marinucci L2.
Environmental pollution is one of the main factors responsible for reducing fertility in males. Lead is one of the major heavy metal contaminants that impairs several organs; it preferentially accumulates in male reproductive organs and alters sperm quality both in vivo and in vitro. However, the underlying mechanisms remain unclear. Sertoli cells (SCs) provide structural and physiological support to spermatogenic cells within seminiferous tubules. Therefore, changes in SCs affect the developing germ cells and alter spermatogenesis. This study aimed to assess whether exposure to subtoxic doses of adversely affects SC functioning in higher mammals. Purified and functional porcine neonatal SCs were exposed to lead acetate at three different concentrations. Lead exposure decreased the mRNA expression and protein levels of inhibin B and anti-Mullerian hormone (AMH) compared to control, indicating loss of FSH-r integrity in terms of 17-β-oestradiol production under FSH stimulation. In addition, we observed an increase in the mRNA levels of Akt and mTOR, and the phosphorylation of p38 and Akt in SCs exposed to lead at all concentrations compared to unexposed control SCs. In conclusion, lead is toxic to SCs, even at low concentrations, and is expected to alter spermatogenesis. KEYWORDS: Lead acetate; Sertoli cells; Toxicity PMID: 29273543 DOI: 10.1016/j.tiv.2017.12.013
Prenatal Exposure to Cadmium, Placental Permeability and Birth Outcomes in Coastal Populations of South Africa
PLoS One. 2015 Nov 6;10(11):e0142455. doi: 10.1371/journal.pone.0142455. eCollection 2015.
Röllin HB1,2, Kootbodien T2, Channa K3, Odland JØ4,1.
BACKGROUND: The impact of prenatal exposure to cadmium (Cd) on birth outcomes is an area of concern. This study aimed to assess an impact of prenatal Cd exposure on birth outcomes in distinct coastal populations of South Africa. METHODS: Cadmium was measured in maternal blood (CdB) (n = 641), cord blood and in maternal urine (n = 317). This investigation assessed the associations between CdB (non-transformed) and birth outcomes across the 25th, 50th, and 75th percentile for birth weight, birth length and head circumference, to test for a linear trend. Associations between natural log-transformed maternal CdB, size at birth and other factors were further evaluated using linear mixed-effects modelling with random intercepts. RESULTS: The average gestational age in the total sample was 38 weeks; 47% of neonates were female, average birth weight was 3065 g and 11% were of low birth weight (< 2500 g). The geometric mean (GM) of the maternal CdB level was 0.25 μg/L (n = 641; 95% CI, 0.23-0.27). The cord blood Cd level was 0.27 μg/L (n = 317; 95% CI, 0.26-0.29) and urine (creatinine-corrected) Cd level was 0.27 μg/L (n = 318; 95% CI, 0.24-0.29). The CdB cord:maternal ratio in the sub-cohort was 1, suggesting that the placenta offers no protective mechanism to the foetus. An inverse association was found between CdB and the lower birth weight percentile in female neonates only (β = - 0.13, p = 0.047). Mothers who reported eating vine vegetables daily had lower levels of CdB (β = - 0.55, p = 0.025). Maternal smoking was associated with an elevation in natural log-transformed CdB levels in both male and female cohorts. DISCUSSION: Significant inverse associations between prenatal Cd exposure and birth anthropometry were found in female neonates but not in male neonates, suggesting potential sex differences in the toxico-kinetics and toxico-dynamics of Cd.
Maternal-infant biomarkers of prenatal exposure to arsenic and manganese
J Expo Sci Environ Epidemiol. 2015 Aug 26. doi: 10.1038/jes.2015.45. [Epub ahead of print]
Rodrigues EG1, Kile M2, Dobson C1, Amarasiriwardena C3, Quamruzzaman Q4, Rahman M4, Golam M4, Christiani DC1.
Because arsenic (As) and manganese (Mn) are able to pass the placenta, infants among exposed populations may be exposed to considerable levels in utero. The main objective of this paper is to evaluate infant toenails, hair, and cord blood as biomarkers of prenatal exposure to As and Mn and determine the relationship between maternal and infant As and Mn concentrations in these biomarkers. Of the 1196 pregnant women in Bangladesh who were monitored throughout pregnancy until 1 month post-partum and completed all study visits, we included 711 mother-infant pairs who had at least one maternal and one infant biomarker of exposure available for analysis. Toenail and hair samples were collected from the women during the first trimester and 1 month post-partum and from the infants at the age of 1 month. Cord blood was collected at the time of delivery. Maternal toenail concentrations were correlated with infant toenail concentrations for As and Mn (n=258, r=0.52, 95% CI: 0.43-0.60, P<0.0001 and r=0.39, 95% CI: 0.28-0.49, P<0.0001), respectively. Similarly, maternal hair concentrations were correlated with infant hair As (n=685, r=0.61, 95% CI: 0.56-0.65, P<0.0001) and infant hair Mn (n=686, r=0.21, 95% CI: 0.14-0.28, P<0.0001). Cord blood As was correlated with infant toenail and hair As, although cord blood Mn was only correlated with infant toenail. Toenails and cord blood appear to be valid biomarkers of maternal-fetal transfer of As and Mn, whereas hair may not be a suitable biomarker for in utero exposure to Mn.Journal of Exposure Science and Environmental Epidemiology advance online publication, 26 August 2015; doi:10.1038/jes.2015.45.
Lead Exposure during Early Human Development and DNA Methylation of Imprinted Gene Regulatory Elements in Adulthood
Environ Health Perspect. 2015 Jun 26. [Epub ahead of print]
Li Y1, Xie C2, Murphy SK, Skaar D, Nye M, Vidal AC, Cecil KM, Dietrich KN, Puga A, Jirtle RL, Hoyo C.
BACKGROUND: Lead exposure during early development causes neurodevelopmental disorders by unknown mechanisms. Epidemiologic studies have focused recently on determining associations between lead exposure and global DNA methylation; however, such approaches preclude the identification of loci that may alter human disease risk. OBJECTIVES: The objective of this study was to determine if maternal, postnatal and early childhood lead exposure alter the differentially methylated regions (DMRs) that control the monoallelic expression of imprinted genes involved in metabolism, growth and development. METHODS: Questionnaire data and serial blood lead levels were obtained from 105 participants (64 females, 41 males) of the Cincinnati Lead Study from birth to 78 months. During adulthood, peripheral blood DNA was used to quantify CpG methylation in peripheral blood leukocytes at DMRs of 22 human imprinted genes using Sequenom EpiTYPER assays. Statistical analyses were conducted using linear regression. RESULTS: Mean blood lead concentration from birth to 78 months was associated with a significant decrease in PEG3 DMR methylation, (β=-0.0014, 95% CI:-0.0023, -0.0005, p=0.002), stronger in males, (β=-0.0024, 95% CI:-0.0038, -0.0009, p=0.003) than females (β=-0.0009, 95% CI:-0.0020, 0.0003, p=0.1). Elevated mean childhood blood lead concentration was also associated with a significant decrease in IGF2/H19 (β=-0.0013, 95% CI:-0.0023, -0.0003, p=0.01) DMR methylation, but primarily in females, (β=-0.0017, 95% CI:-0.0029, -0.0006, p=0.005) than males, (β=-0.0004, 95% CI:-0.0023, 0.0015, p=0.7). Elevated blood lead concentration during the neonatal period was associated with higher PLAGL1/HYMAI DMR methylation regardless of sex, (β=0.0075, 95% CI:0.0018, 0.0132, p=0.01). The magnitude of associations between cumulative lead exposure and CpG methylation remained unaltered from 30 to 78 months. CONCLUSIONS: Our findings provide evidence for early childhood lead exposure resulting in sex-dependent and gene-specific DNA methylation differences in the DMRs of PEG3, IGF2/H19 and PLAGL1/HYMAI in adulthood.
Environmental toxicants and autism spectrum disorders: a systematic review
Transl Psychiatry. 2014 Feb 11;4:e360. doi: 10.1038/tp.2014.4.
Rossignol DA1, Genuis SJ2, Frye RE3. Author information
Although the involvement of genetic abnormalities in autism spectrum disorders (ASD) is well-accepted, recent studies point to an equal contribution by environmental factors, particularly environmental toxicants. However, these toxicant-related studies in ASD have not been systematically reviewed to date. Therefore, we compiled publications investigating potential associations between environmental toxicants and ASD and arranged these publications into the following three categories: (a) studies examining estimated toxicant exposures in the environment during the preconceptional, gestational and early childhood periods; (b) studies investigating biomarkers of toxicants; and (c) studies examining potential genetic susceptibilities to toxicants. A literature search of nine electronic scientific databases through November 2013 was performed. In the first category examining ASD risk and estimated toxicant exposures in the environment, the majority of studies (34/37; 92%) reported an association. Most of these studies were retrospective case-control, ecological or prospective cohort studies, although a few had weaker study designs (for example, case reports or series). Toxicants implicated in ASD included pesticides, phthalates, polychlorinated biphenyls (PCBs), solvents, toxic waste sites, air pollutants and heavy metals, with the strongest evidence found for air pollutants and pesticides. Gestational exposure to methylmercury (through fish exposure, one study) and childhood exposure to pollutants in water supplies (two studies) were not found to be associated with ASD risk. In the second category of studies investigating biomarkers of toxicants and ASD, a large number was dedicated to examining heavy metals. Such studies demonstrated mixed findings, with only 19 of 40 (47%) case-control studies reporting higher concentrations of heavy metals in blood, urine, hair, brain or teeth of children with ASD compared with controls. Other biomarker studies reported that solvent, phthalate and pesticide levels were associated with ASD, whereas PCB studies were mixed. Seven studies reported a relationship between autism severity and heavy metal biomarkers, suggesting evidence of a dose-effect relationship. Overall, the evidence linking biomarkers of toxicants with ASD (the second category) was weaker compared with the evidence associating estimated exposures to toxicants in the environment and ASD risk (the first category) because many of the biomarker studies contained small sample sizes and the relationships between biomarkers and ASD were inconsistent across studies. Regarding the third category of studies investigating potential genetic susceptibilities to toxicants, 10 unique studies examined polymorphisms in genes associated with increased susceptibilities to toxicants, with 8 studies reporting that such polymorphisms were more common in ASD individuals (or their mothers, 1 study) compared with controls (one study examined multiple polymorphisms). Genes implicated in these studies included paraoxonase (PON1, three of five studies), glutathione S-transferase (GSTM1 and GSTP1, three of four studies), δ-aminolevulinic acid dehydratase (one study), SLC11A3 (one study) and the metal regulatory transcription factor 1 (one of two studies). Notably, many of the reviewed studies had significant limitations, including lack of replication, limited sample sizes, retrospective design, recall and publication biases, inadequate matching of cases and controls, and the use of nonstandard tools to diagnose ASD. The findings of this review suggest that the etiology of ASD may involve, at least in a subset of children, complex interactions between genetic factors and certain environmental toxicants that may act synergistically or in parallel during critical periods of neurodevelopment, in a manner that increases the likelihood of developing ASD. Because of the limitations of many of the reviewed studies, additional high-quality epidemiological studies concerning environmental toxicants and ASD are warranted to confirm and clarify many of these findings.
Birth outcome measures and maternal exposure to heavy metals (lead, cadmium and mercury) in Saudi Arabian population
Int J Hyg Environ Health. 2014 Mar;217(2-3):205-18. doi: 10.1016/j.ijheh.2013.04.009. Epub 2013 May 9.
Al-Saleh I1, Shinwari N2, Mashhour A2, Rabah A3. Author information
This cross-sectional study was conducted to assess the association between exposure to heavy metals (lead, cadmium and mercury) during pregnancy and birth outcomes in 1578 women aged 16-50 years who delivered in Al-Kharj hospital, Saudi Arabia, in 2005 and 2006. The levels of lead, cadmium and mercury were measured in umbilical cord blood, maternal blood and the placenta. Outcome variables were anthropometric measures taken at birth, along with the risk of being small-for-gestational age (SGA). We selected the 10th percentile as the cutoff for dichotomizing measures of birth outcome. Cadmium, despite its partial passage through the placenta had the most prominent effect on several measures of birth outcome. After adjustment for potential confounders, logistic regression models revealed that crown-heel length (p=0.034), the Apgar 5-minute score (p=0.004), birth weight (p=0.015) and SGA (p=0.049) were influenced by cadmium in the umbilical cord blood. Significant decreases in crown-heel length (p=0.007) and placental thickness (p=0.022) were seen with higher levels of cadmium in maternal blood. As placental cadmium increased, cord length increased (p=0.012) and placental thickness decreased (p=0.032). Only lead levels in maternal blood influenced placental thickness (p=0.011). Mercury in both umbilical cord and maternal blood was marginally associated with placental thickness and placental weight, respectively. Conversely, placental mercury levels significantly influenced head circumference (p=0.017), the Apgar 5-minute score (p=0.01) and cord length (p=0.026). The predictions of these models were further assessed with the area under the curve (AUC) of the receiver operating curves (ROCs), which were modest (larger than 0.5 and smaller than 0.7). The independence of gestational age or preterm births on the observed effect of metals on some measures of birth outcome, suggested detrimental effects of exposure on fetal development. The magnitude of the estimated effects might not necessarily be of clinical significance for infants but may have a considerable public-health relevance given the high prevalence of exposure to heavy metals. Further research should be conducted to confirm these findings and to evaluate their long-term risks, if any. Copyright © 2013 Elsevier GmbH. All rights reserved. KEYWORDS: Anthropometric measures, Birth outcome, Cadmium, Lead, Maternal blood, Mercury, Placenta, Saudi Arabia, Small-for-gestational age, Umbilical cord blood
Mercury levels in an urban pregnant population in Durham County, North Carolina
Int J Environ Res Public Health. 2011 Mar;8(3):698-712. Epub 2011 Mar 1.
Miranda ML, Edwards S, Maxson PJ. Source Children's Environmental Health Initiative, Nicholas School of the Environment, Duke University, Box 90328, Durham, NC 27708, USA. email@example.com
The adverse effects of prenatal mercury exposure, most commonly resulting from maternal fish consumption, have been detected at very low exposure levels. The omega-3 fatty acids found in fish, however, have been shown to support fetal brain and vision development. Using data from a prospective, cohort study of pregnant women from an inland area in the US South, we sought to understand the fish consumption habits and associated mercury levels across subpopulations. Over 30% of women had at least 1 μg/L of mercury in their blood, and about 2% had blood mercury levels above the level of concern during pregnancy (≥ 3.5 μg/L). Mercury levels were higher among Asian/Pacific Islander, older, higher educated, and married women. Fish consumption from any source was reported by 2/3 of the women in our study, with older women more likely to consume fish. Despite eating more fish meals per week, lower income, lower educated women had lower blood mercury levels than higher income, higher educated women. This suggests the different demographic groups consume different types of fish. Encouraging increased fish consumption while minimizing mercury exposure requires careful crafting of a complex health message.
Simultaneous removal of chromium and arsenate from contaminated groundwater by ferrous sulfate: batch uptake behavior
J Environ Sci (China). 2011;23(3):372-80. Guan X, Dong H, Ma J, Lo IM. Source State Key Laboratory of Urban Water Resource and Environment, Harbin Institute of Technology, Harbin 150090, China. firstname.lastname@example.org
Chromium and/or arsenate removal by Fe(II) as a function of pH, Fe(II) dosage and initial Cr(VI)/As(V) ratio were examined in batch tests. The presence of arsenate reduced the removal efficiency of chromium by Fe(II), while the presence of chromate significantly increased the removal efficiency of arsenate by Fe(II) at pH 6-8. In the absence of arsenate, chromium removal by Fe(II) increased to a maximum with increasing pH from 4 to 7 and then decreased with a further increase in pH. The increment in Fe(II) dosage resulted in an improvement in chromium removal and the improvement was more remarkable under alkaline conditions than that under acidic conditions. Chromium removal by Fe(II) was reduced to a larger extent under neutral and alkaline conditions than that under acidic conditions due to the presence of 10 micromol/L arsenate. The presence of 20 micromol/L arsenate slightly improved chromium removal by Fe(II) at pH 3.9-5.8, but had detrimental effects at pH 6.7-9.8. Arsenate removal was improved significantly at pH 4-9 due to the presence of 10 micromol/L chromate at Fe(II) dosages of 20-60 micromol/L. Elevating the chromate concentration from 10 to 20 micromol/L resulted in a further improvement in arsenate removal at pH 4.0-4.6 when Fe(II) was dosed at 30-60 micromol/L.
PMID: 21520805 http://www.ncbi.nlm.nih.gov/pubmed/21520805
Nickel toxicity in embryos and larvae of the South American toad: effects on cell differentiation, morphogenesis, and oxygen consumption
Environ Toxicol Chem. 2011 May;30(5):1146-52. doi: 10.1002/etc.484. Epub 2011 Feb 25.
Sztrum AA, D'Eramo JL, Herkovits J. Source Instituto de Ciencias Ambientales y Salud, Fundación Pro Salud y Medio Ambiente, Buenos Aires, Argentina.
Nickel, a widely distributed heavy metal in the biosphere, produces systemic, carcinogenic, and teratogenic effects. The objectives of the present study are to report the acute, short-term chronic, and chronic toxicity of Ni in Rhinella arenarum embryos as well as the stage-dependent susceptibility to this heavy metal, including oxygen consumption, teratogenesis, and adverse effects on cell differentiation processes. The stages evaluated were blastula (S.7), gastrula (S.11), tail bud (S.17), fin circulation (S.22), and complete operculum (S.25), in this last case by means of toxicity profile curves. Nickel increases its adverse effects gradually, with a maximum value after 96 h. The 50% lethal concentrations (LC50s) for 96, 168, and 240 h at S.25 were 1.14, 0.60, and 0.48 mg Ni²(+) /L, respectively; S.11 and S.22 were the least and most susceptible to Ni with, LC50s 96 h of 6.12 and 0.19 mg Ni²(+) /L, respectively. A reduction of approximately 25% in oxygen consumption anticipates lethal effects from S.17 onward. The main teratogenic effects were retarded growth and development, extremely severe axis incurvations, persistent yolk plug, asymmetry, microcephaly and mouth and gill agenesia, and limited neuromuscular activity. Ciliated cells were not functional. The possibility of associating the remarkable stage-dependent susceptibility to Ni with environmental changes during the evolutionary process is also considered.
Copyright © 2011 SETAC.
PMID: 21312246 http://www.ncbi.nlm.nih.gov/pubmed/21312246
Cadmium-induced teratogenicity in lizard embryos: correlation with metallothionein gene expression
Comp Biochem Physiol C Toxicol Pharmacol. 2011 Jan;153(1):119-27. Epub 2010 Oct 1.
Simoniello P, Motta CM, Scudiero R, Trinchella F, Filosa S. Source Department of Biological Sciences, Evolutionary and Comparative Section, University Federico II, Naples, Italy.
Cadmium teratogenic effects and metallothionein expression were studied in tissues of lizard embryos at different stages of development. Incubation of eggs in cadmium contaminated soil had no effect on embryo survival, but strongly affected cranial morphogenesis. Cytological analyses demonstrated abnormalities in the development of proencephalic vesicles, mesencephalon and eyes. No defects were observed in somite or limb development. Northern blot analysis demonstrated that MT expression was much stronger in embryos developed in cadmium contaminated soil. In situ hybridization showed an early induction of MT gene expression in developing liver and gut, whereas in brain and eyes the spatial and temporal localization of MT transcripts did not change. A possible correlation between inability to induce MT expression and abnormalities observed in the head region of lizard developing embryos is suggested.
Copyright © 2010 Elsevier Inc. All rights reserved.
PMID: 20888429 http://www.ncbi.nlm.nih.gov/pubmed/20888429
Embryotoxicity of cobalt ferrite and gold nanoparticles: a first in vitro approach
Reprod Toxicol. 2010 Sep;30(2):271-6. Epub 2010 Jun 8.
Di Guglielmo C, López DR, De Lapuente J, Mallafre JM, Suàrez MB. Source UTOX-PCB, Unit of Experimental Toxicology and Ecotoxicology, Parc Científic Barcelona, Barcelona, Spain. email@example.com
Nanoparticles (NPs) are emerging as promising biomedical tools thanks to their peculiar characteristics. Our purpose was to investigate the embryotoxicity of cobalt ferrite and gold NPs through the Embryonic Stem Cell Test (EST). The EST is an in vitro standard assay, which permits to classify substances as strongly, weakly or non-embryotoxic. Due to the particular physical-chemical nature of nanoparticles, we introduced a modification to the standard protocol exposing the Embryonic Stem Cells (ES-D3) to nanoparticles only during the first 5 days of the assay. Moreover, we proposed a method to discriminate and compare the embryotoxicity of the substances within the weakly embryotoxic range. Our ID(50) results permit to classify cobalt ferrite nanoparticles coated with gold and silanes as non-embryotoxic. The remaining nanoparticles have been classified as weakly embryotoxic in this decreasing order: gold salt (HAuCl(4).3H(2)O)>cobalt ferrite salt (CoFe(2)O(4))>cobalt ferrite nanoparticles coated with silanes (Si-CoFe)>gold nanoparticles coated with hyaluronic acid (HA-Au).
Copyright 2010 Elsevier Inc. All rights reserved.
PMID: 20566333 http://www.ncbi.nlm.nih.gov/pubmed/20566333
Blood lead changes during pregnancy and postpartum with calcium supplementation
Environ Health Perspect. 2004 Nov;112(15):1499-507.
Gulson BL, Mizon KJ, Palmer JM, Korsch MJ, Taylor AJ, Mahaffey KR. Source Graduate School of the Environment, Macquarie University, Sydney, New South Wales, Australia. firstname.lastname@example.org
Pregnancy and lactation are times of physiologic stress during which bone turnover is accelerated. Previous studies have demonstrated that there is increased mobilization of lead from the maternal skeleton at this time and that calcium supplementation may have a protective effect. Ten immigrants to Australia were provided with either calcium carbonate or a complex calcium supplement (approximately 1 g/day) during pregnancy and for 6 months postpartum. Two immigrant subjects who did not conceive acted as controls. Sampling involved monthly venous blood samples throughout pregnancy and every 2 months postpartum, and quarterly environmental samples and 6-day duplicate diets. The geometric mean blood lead at the time of first sampling was 2.4 microg/dL (range, 1.4-6.5). Increases in blood lead during the third trimester, corrected for hematocrit, compared with the minimum value observed, varied from 10 to 50%, with a geometric mean of 25%. The increases generally occurred at 6-8 months gestation, in contrast with that found for a previous cohort, characterized by very low calcium intakes, where the increases occurred at 3-6 months. Large increases in blood lead concentration were found during the postpartum period compared with those during pregnancy; blood lead concentrations increased by between 30 and 95% (geometric mean 65%; n = 8) from the minimum value observed during late pregnancy. From late pregnancy through postpartum, there were significant increases in the lead isotopic ratios from the minimum value observed during late pregnancy for 3 of 8 subjects (p < 0.01). The observed changes are considered to reflect increases in mobilization of lead from the skeleton despite calcium supplementation. The identical isotopic ratios in maternal and cord blood provide further confirmation of placental transfer of lead. The extra flux released from bone during late pregnancy and postpartum varies from 50 to 380 microg lead (geometric mean, 145 microg lead) compared with 330 microg lead in the previous cohort. For subjects replete in calcium, the delay in increase in blood lead and halving of the extra flux released from bone during late pregnancy and postpartum may provide less lead exposure to the developing fetus and newly born infant. Nevertheless, as shown in several other studies on calcium relationships with bone turnover, calcium supplementation appears to provide limited benefit for lead toxicity during lactation.
PMID: 15531434 [PubMed - indexed for MEDLINE] PMCID: PMC1247613
Interrelations of lead levels in bone, venous blood, and umbilical cord blood with exogenous lead exposure through maternal plasma lead in peripartum women
Environ Health Perspect. 2001 May;109(5):527-32.
Chuang HY, Schwartz J, Gonzales-Cossio T, Lugo MC, Palazuelos E, Aro A, Hu H, Hernandez-Avila M. Source Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA. Abstract Recent research has raised the possibility that fetal lead exposure is not estimated adequately by measuring lead content in maternal whole blood lead because of the variable partitioning of lead in whole blood between plasma and red blood cells. Lead in maternal plasma may derive in large part from maternal bone lead stores. In this study we aimed to estimate the contribution of maternal whole blood lead, maternal bone lead levels, and environmental lead to umbilical cord blood lead levels (as a measure of fetal lead exposure). In the model, we assumed that lead from all of these sources reaches the fetus through the maternal plasma lead pathway. In 1994-1995, we recruited 615 pregnant women for a study of lead exposure and reproductive outcomes in Mexico City. We gathered maternal and umbilical cord blood samples within 12 hr of each infant's delivery and measured maternal lead levels in cortical bone and trabecular bone by a K-X-ray fluorescence (K-XRF) instrument within 1 month after delivery. We administered a questionnaire to assess use of lead-glazed ceramics (LGC) to cook food and we obtained data on regional air lead levels during the 2 months before delivery. We used structural equation models (SEMs) to estimate plasma lead as the unmeasured (latent) variable and to quantify the interrelations of plasma lead, the other lead biomarkers, and environmental lead exposure. In the SEM analysis, a model that allowed plasma lead to vary freely from whole blood lead explained the variance of cord blood lead (as reflected by a total model R(2); R(2) = 0.79) better than did a model without plasma lead (r(2) = 0.67). Cortical bone lead, trabecular bone lead, use of LGC, and mean air lead level contributed significantly to plasma lead. The exchange of lead between plasma and red blood cells was mostly in the direction of plasma to cells. According to the final model, an increase in trabecular bone lead and cortical bone lead was associated with increases in cord blood lead of 0.65 and 0.25 microg/dL, respectively. An increase of 0.1 microg/m(3) in air lead was associated with an increase in the mean level of fetal cord blood lead by 0.67 microg/dL. With one additional day of LCG use per week in the peripartum period, the mean fetal blood lead level increased by 0.27 microg/dL. Our analyses suggested that maternal plasma lead varies independently from maternal whole blood lead and that the greatest influences on maternal plasma lead are maternal bone lead stores, air lead exposures, and recent cooking with LGC. The contributions from endogenous (bone) and exogenous (environmental) sources were relatively equal. Measurement of plasma and bone lead may be important in accurately assessing fetal lead exposure and its major sources, particularly if exogenous exposures decline.
Chromium III histidinate exposure modulates gene expression in HaCaT human keratinocytes exposed to oxidative stress
Hazane-Puch F, Benaraba R, Valenti K, Osman M, Laporte F, Favier A, Anderson RA, Roussel AM, Hininger-Favier I. Biol Trace Elem Res. 2010 Oct;137(1):23-39. Epub 2009 Nov 10. PMID: 19902159
Chromium effects on free radical processes in goldfish tissues: comparison of Cr(III) and Cr(VI) exposures on oxidative stress markers, glutathione status and antioxidant enzymes
Kubrak OI, Lushchak OV, Lushchak JV, Torous IM, Storey JM, Storey KB, Lushchak VI. Comp Biochem Physiol C Toxicol Pharmacol. 2010 Sep;152(3):360-70. Epub 2010 Jun 12. PMID: 20547245
Lactational hexavalent chromium exposure-induced oxidative stress in rat uterus is associated with delayed puberty and impaired gonadotropin levels
Samuel JB, Stanley JA, Roopha DP, Vengatesh G, Anbalagan J, Banu SK, Aruldhas MM. Hum Exp Toxicol. 2010 Mar 4. [Epub ahead of print] PMID: 20203132
Reproductive toxicity of chromium in adult bonnet monkeys (Macaca radiata Geoffrey). Reversible oxidative stress in the semen
Subramanian S, Rajendiran G, Sekhar P, Gowri C, Govindarajulu P, Aruldhas MM. Toxicol Appl Pharmacol. 2006 Sep 15;215(3):237-49. Epub 2006 May 6. PMID: 16678873
Maternal iron status influences iron transfer to the fetus during the third trimester of pregnancy.
Am J Clin Nutr. 2003 Apr;77(4):924-30. O'Brien KO, Zavaleta N, Abrams SA, Caulfield LE.
Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205-2179, USA. email@example.com Abstract BACKGROUND: The effect of maternal iron status on fetal iron deposition is uncertain. OBJECTIVE: We used a unique stable-isotope technique to assess iron transfer to the fetus in relation to maternal iron status. DESIGN: The study group comprised 41 Peruvian women. Of these women, 26 received daily prenatal supplements containing iron and folate (n = 11; Fe group) or iron, folate, and zinc (n = 15; Fe+Zn group) from week 10-24 of pregnancy to 1 mo postpartum. The remaining 15 women (control group) received iron supplementation only during the final month of pregnancy. During the third trimester of pregnancy (+/- SD: 32.9 +/- 1.4 wk gestation) oral 57Fe (10 mg) and intravenous 58Fe (0.6 mg) stable iron isotopes were administered to the women, and isotope enrichment and iron-status indicators were measured in cord blood at delivery. RESULTS: The net amount of 57Fe in the neonates' circulation (from maternal oral dosing) was significantly related to maternal iron absorption (P < 0.005) and inversely related to maternal iron status during the third trimester of pregnancy: serum ferritin (P < 0.0001), serum folate (P < 0.005), and serum transferrin receptors (P < 0.02). Significantly more 57Fe was transferred to the neonates in non-iron-supplemented women: 0.112 +/- 0.031 compared with 0.078 +/- 0.042 mg in the control group (n = 15) and the Fe and Fe+Zn groups (n = 24), respectively (P < 0.01). In contrast, 58Fe tracer in the neonates' circulation was not significantly related to maternal iron status. CONCLUSION: The transfer of dietary iron to the fetus is regulated in response to maternal iron status at the level of the gut.
Tohoku J Exp Med. 2003 Sep;201(1):1-9. Behavioral teratology of mercury and its compounds. Satoh H.
Environmental Health Sciences, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan. firstname.lastname@example.org Abstract Mercury and its compounds have a wide spectrum of toxicities depending upon the chemical forms and modes of exposure. Among the various chemical forms, mercury vapor and methylmercury are well known and established as neurotoxic agents. Since the disasters in Minamata and Iraq, in which fetuses were more susceptible than adults to methylmercury exposure, much attention has been focused on prenatal exposure to mercury and its consequence. Recently postnatal effects of in utero exposure to methylmercury through fish (and marine mammals) consumption by mothers have been concerned and several epidemiological studies have been conducted. Therefore, one of the most seriously concerned issues is the postnatal effects of in utero exposure to methylmercury. Because of these observations in humans, animal experiments have been conducted employing prenatal exposure to low levels of mercury. This paper reviews the animal (rodents) experiments concerning "behavioral teratology" of mercury for better understanding of effects of prenatal exposure to mercury and its compounds in addition to commentary on history and framework of behavioral teratology.
For chemical page - formaldehyde
Embryo toxicity and teratogenicity of formaldehyde
Thrasher JD, Kilburn KH. Arch Environ Health. 2001 Jul-Aug;56(4):300-11. Review. PMID: 11572272
"C-14 formaldehyde crosses the placenta and enters fetal tissues. The incorporated radioactivity is higher in fetal organs (i.e., brain and liver) than in maternal tissues. The incorporation mechanism has not been studied fully, but formaldehyde enters the single-carbon cycle and is incorporated as a methyl group into nucleic acids and proteins. Also, formaldehyde reacts chemically with organic compounds (e.g., deoxyribonucleic acid, nucleosides, nucleotides, proteins, amino acids) by addition and condensation reactions, thus forming adducts and deoxyribonucleic acid-protein crosslinks. "