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Estimation of health effects of prenatal methylmercury exposure using structural equation models
Esben Budtz-J?rgensen, Niels Keiding, Philippe Grandjean, Pal Weihe
Environmental Health , 2002, DOI: 10.1186/1476-069x-1-2
Abstract: Structural equation models were developed for assessment of the association between biomarkers of prenatal mercury exposure and neuropsychological test scores in 7 year old children. Eleven neurobehavioral outcomes were grouped into motor function and verbally mediated function. Adjustment for local dependence and item bias was necessary for a satisfactory fit of the model, but had little impact on the estimated mercury effects. The mercury effect on the two latent neurobehavioral functions was similar to the strongest effects seen for individual test scores of motor function and verbal skills. Adjustment for contaminant exposure to poly chlorinated biphenyls (PCBs) changed the estimates only marginally, but the mercury effect could be reduced to non-significance by assuming a large measurement error for the PCB biomarker.The structural equation analysis allows correction for measurement error in exposure variables, incorporation of multiple outcomes and incomplete cases. This approach therefore deserves to be applied more frequently in the analysis of complex epidemiological data sets.Observational studies in epidemiology often involve several sources of uncertainty, such as measurement error, proxy variables of unknown validity, confounder adjustment, and multiple comparisons with outcome variables. Standard statistical methods are poorly suited to deal with these problems, especially when all of them occur at the same time. During the past decade or so, the technique of structural equation analysis has been advanced and made more easily available through software packages. Studies in environmental epidemiology have started to incorporate this approach [1,2], although most studies have focused on estimating the relative importance of exposure sources, e.g., with regard to lead concentrations in the body [3]. New user-friendly software offers opportunities that we have explored in a complex data set from an environmental epidemiology study on the effects of develop
Impact on fetal growth of prenatal exposure to pesticides due to agricultural activities: a prospective cohort study in Brittany, France
Claire Petit, Cécile Chevrier, Ga?l Durand, Christine Monfort, Florence Rouget, Ronan Garlantezec, Sylvaine Cordier
Environmental Health , 2010, DOI: 10.1186/1476-069x-9-71
Abstract: A prospective birth cohort recruited 3421 pregnant women in a French agricultural region (Brittany, 2002-2006) through gynecologists, ultrasonographers, and maternity hospitals during routine prenatal care visits before 19 weeks of gestation. The national agricultural census in 2000 provided the percentages of the municipality area devoted to cultivation of corn, wheat, colza, peas, potatoes, and fresh vegetables.Birth weight and the risk of fetal growth restriction were not associated with agricultural activities in the municipality of residence in early pregnancy. Children whose mother lived in a municipality where peas were grown had a smaller head circumference at birth than those in municipalities not growing peas (-0.2 cm, p = 0.0002). Head circumference also tended to be lower when wheat was grown, but not to a statistically significant degree (p-trend = 0.10). Risk of an infant with a small head circumference was higher for mothers living in a municipality where peas (OR = 2.2; 95% CI = 1.2-3.6) or potatoes (OR = 1.5; 95% CI = 0.9-2.4) were grown.Agricultural activities in the municipality of residence may have negative effects on cranial growth. Cultivation of pea crops and, to a lesser degree, potato and wheat crops, may negatively affect head circumference. Insecticides, including organophosphate insecticides, were applied to most of the area devoted to pea and potato crops; this was less true for corn and wheat crops. These results must be interpreted in light of the study's limitations, in particular, the scale at which we could assess pesticide exposure.Pesticides are used principally and massively in agriculture. After application, they enter the various environmental compartments: ground and surface water, soil, plants, and the atmosphere [1]. Several studies [2-4] have shown that pesticides used in agricultural fields and volatilized into the atmosphere contaminate the domestic environment and may therefore be an important source of pesticide exposu
Low level methylmercury exposure affects neuropsychological function in adults
Edna M Yokoo, Joaquim G Valente, Lynn Grattan, Sérgio Schmidt, Illeane Platt, Ellen K Silbergeld
Environmental Health , 2003, DOI: 10.1186/1476-069x-2-8
Abstract: A cross-sectional study was conducted in six villages on the Cuiaba River. Participants included 129 men and women older than 17 years of age. They were randomly selected in proportion to the age range and number of inhabitants in each village. Questionnaire information was collected on demographic variables, including education, occupation, and residence history. Mercury exposure was determined by analysis of hair using flameless atomic absorption spectrophotometry. The neurocognitive screening battery included tests from the Wechsler Memory Scale and the Wechsler Adult Intelligence Scale, Concentrated Attention Test of the Toulouse-Pierron Factorial Battery, the Manual Ability Subtests of the Tests of Mechanical Ability, and the Profile of Mood States.Mercury exposures in this population were associated with fish consumption. The hair mercury concentration in the 129 subjects ranged from 0.56 to 13.6 μg/g; the mean concentration was 4.2 ± 2.4 micrograms/g and the median was 3.7 μg/g. Hair mercury levels were associated with detectable alterations in performance on tests of fine motor speed and dexterity, and concentration. Some aspects of verbal learning and memory were also disrupted by mercury exposure. The magnitude of the effects increased with hair mercury concentration, consistent with a dose-dependent effect.This study suggests that adults exposed to MeHg may be at risk for deficits in neurocognitive function. The functions disrupted in adults, namely attention, fine-motor function and verbal memory, are similar to some of those previously reported in children with prenatal exposures.In recent years there has been a growing appreciation for acquired risk factors for neurologic disease and neuropsychological dysfunction, including exposures to environmental neurotoxicants such as the heavy metals. In this investigation, we studied the effects of environmental exposures to methylmercury (MeHg) via diet on neurocognitive status in adults. This study is of crit
Methylmercury Exposure and Health Effects from Rice and Fish Consumption: A Review  [PDF]
Ping Li,Xinbin Feng,Guangle Qiu
International Journal of Environmental Research and Public Health , 2010, DOI: 10.3390/ijerph7062666
Abstract: Methylmercury (MeHg) is highly toxic, and its principal target tissue in humans is the nervous system, which has made MeHg intoxication a public health concern for many decades. The general population is primarily exposed to MeHg through consumption of contaminated fish and marine mammals, but recent studies have reported high levels of MeHg in rice and confirmed that in China the main human exposure to MeHg is related to frequent rice consumption in mercury (Hg) polluted areas. This article reviews the progress in the research on MeHg accumulation in rice, human exposure and health effects, and nutrient and co-contaminant interactions. Compared with fish, rice is of poor nutritional quality and lacks specific micronutrients identified as having health benefits (e.g., n-3 long chain polyunsaturated fatty acid, selenium, essential amino acids). The effects of these nutrients on the toxicity of MeHg should be better addressed in future epidemiologic and clinical studies. More emphasis should be given to assessing the health effects of low level MeHg exposure in the long term, with appropriate recommendations, as needed, to reduce MeHg exposure in the rice-eating population.
Exposure to Prenatal Infection and Risk of Schizophrenia  [PDF]
Alan S. Brown
Frontiers in Psychiatry , 2011, DOI: 10.3389/fpsyt.2011.00063
Abstract: We provide a brief review of findings supporting a role for prenatal infection in the etiology of schizophrenia. Our group and others have conducted birth cohort studies to address whether in utero exposure to infectious agents, prospectively documented by biomarker assays of archived maternal sera, and by detailed obstetric records, confer an increased risk of schizophrenia in adult offspring. Prenatal exposure to influenza, elevated toxoplasma antibody, rubella, genital–reproductive infections, and other infections have been associated with an increased risk of schizophrenia among offspring. Animal models have supported these epidemiologic findings by revealing that maternal immune activation causes phenotypes analogous to those found in patients with schizophrenia. Given that exposure to microbial agents are preventable or treatable, they suggest that interventions to diminish the incidence of infection during pregnancy have the potential to prevent an appreciable proportion of schizophrenia cases. Given the clear genetic component to schizophrenia, future studies should include investigations of interactions between prenatal infection and susceptibility genes in the pathogenesis of schizophrenia.
Prenatal cocaine exposure alters alpha2 receptor expression in adolescent rats
Rosemarie M Booze, David R Wallace, Janelle M Silvers, Barbara J Strupp, Diane M Snow, Charles F Mactutus
BMC Neuroscience , 2006, DOI: 10.1186/1471-2202-7-33
Abstract: Sex-specific alterations of α2-AR were found in the hippocampus and amygdala of the cocaine-exposed animals, as well as an upregulation of α2-AR in parietal cortex.These data suggest that prenatal cocaine exposure results in a persistent alteration in forebrain NE systems as indicated by alterations in receptor density. These neurochemical changes may underlie behavioral abnormalities observed in offspring attentional processes following prenatal exposure to cocaine.Recently, noradrenergic systems have been identified as a potential teratogenic target underlying the functional effects of prenatal cocaine [1-3]. However, information regarding the consequences of prenatal cocaine on the development of noradrenergic receptors is relatively sparse. NE is present early in brain development and regulates important aspects of prenatal brain development, including neural migration and synaptogenesis [4,5]. Thus, the ability of cocaine to inhibit NE reuptake has potentially profound effects on the developing nervous system and function of NE systems.Previous investigations into the effects of prenatal cocaine exposure on catecholaminergic receptors have, for the most part, focused on the long-term effects of exposure on dopaminergic [6-10] and serotonergic [11-14] receptor systems. Fewer studies have examined the noradrenergic receptor family following prenatal cocaine exposure. The neurophysiological effects of NE are mediated by three types of receptors: α1, α2 and β. The α2 adrenergic receptors are present very early in development, in some brain areas as early as E15 [4]. Prenatal exposure to cocaine has been found to elevate the density of α2 adrenergic receptors in the cerebellum and forebrain [15]. Henderson et al [16] reported that cortical α2 adrenergic receptor density was unchanged in male rat pups following prenatal cocaine exposure. However, these studies did not differentiate between male and female offspring and used homogenate binding techniques. Moreover, co
La exposición prenatal a andrógenos como factor de reprogramación fetal Prenatal exposure to androgens as a factor of fetal programming  [cached]
Sergio E. Recabarren,Teresa Sir-Petermann,Manuel Maliqueo,Alejandro Lobos
Revista médica de Chile , 2006,
Abstract: Both epidemiological and clinical evidence suggest a relationship between the prenatal environment and the risk of developing diseases during adulthood. The first observations about this relationship showed that prenatal growth retardation or stress conditions during fetal life were associated to cardiovascular, metabolic and other diseases in later life. However, not only those conditions may have lasting effects after birth. Growing evidence suggests that prenatal exposure to steroids (either of fetal or maternal origin) could be another source of prenatal programming with detrimental consequences during adulthood. We have recently demonstrated that pregnant women with polycystic ovary syndrome exhibit elevated androgen levels compared to normal pregnant women, which could provide an androgen excess for both female or male fetuses. We have further tested this hypothesis in an animal model of prenatal androgenization, finding that females born from androgenized mothers have a low birth weight and high insulin resistance, that starts at an early age. On the other hand, males have low testosterone and LH secretion in response to a GnRH analogue test compared to control males and alterations in seminal parameters. We therefore propose that our efforts should be directed to modify the hyperandrogenic intrauterine environment to reduce the potential development of reproductive and metabolic diseases during adulthood
Estimating uncertainty in observational studies of associations between continuous variables: example of methylmercury and neuropsychological testing in children
Goodman Michael,Barraj Leila M,Mink Pamela J,Britton Nicole L
Epidemiologic Perspectives and Innovations , 2007, DOI: 10.1186/1742-5573-4-9
Abstract: Background: We suggest that the need to account for systematic error may explain the apparent lack of agreement among studies of maternal dietary methylmercury exposure and neuropsychological testing outcomes in children, a topic of ongoing debate. Methods: These sensitivity analyses address the possible role of systematic error on reported associations between low-level prenatal exposure to methylmercury and neuropsychological test results in two well known, but apparently conflicting cohort studies: the Faroe Islands Study (FIS) and the Seychelles Child Development Study (SCDS). We estimated the potential impact of confounding, selection bias, and information bias on reported results in these studies using the Boston Naming Test (BNT) score as the outcome variable. Results: Our findings indicate that, assuming various degrees of bias (in either direction) the corrected regression coefficients largely overlap. Thus, the reported effects in the two studies are not necessarily different from each other. Conclusion: Based on our sensitivity analysis results, it is not possible to draw definitive conclusions about the presence or absence of neurodevelopmental effects due to in utero methylmercury exposure at levels reported in the FIS and SCDS.
Nuclear and Mitochondrial DNA Alterations in Newborns with Prenatal Exposure to Cigarette Smoke  [PDF]
Francesca Pirini,Elisa Guida,Fahcina Lawson,Andrea Mancinelli,Rafael Guerrero-Preston
International Journal of Environmental Research and Public Health , 2015, DOI: 10.3390/ijerph120201135
Abstract: Newborns exposed to maternal cigarette smoke (CS) in utero have an increased risk of developing chronic diseases, cancer, and acquiring decreased cognitive function in adulthood. Although the literature reports many deleterious effects associated with maternal cigarette smoking on the fetus, the molecular alterations and mechanisms of action are not yet clear. Smoking may act directly on nuclear DNA by inducing mutations or epigenetic modifications. Recent studies also indicate that smoking may act on mitochondrial DNA by inducing a change in the number of copies to make up for the damage caused by smoking on the respiratory chain and lack of energy. In addition, individual genetic susceptibility plays a significant role in determining the effects of smoking during development. Furthermore, prior exposure of paternal and maternal gametes to cigarette smoke may affect the health of the developing individual, not only the in utero exposure. This review examines the genetic and epigenetic alterations in nuclear and mitochondrial DNA associated with smoke exposure during the most sensitive periods of development (prior to conception, prenatal and early postnatal) and assesses how such changes may have consequences for both fetal growth and development.
Depression-Like Effect of Prenatal Buprenorphine Exposure in Rats  [PDF]
Chih-Jen Hung, Chih-Cheng Wu, Wen-Ying Chen, Cheng-Yi Chang, Yu-Hsiang Kuan, Hung-Chuan Pan, Su-Lan Liao, Chun-Jung Chen
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0082262
Abstract: Studies indicate that perinatal opioid exposure produces a variety of short- and long-term neurobehavioral consequences. However, the precise modes of action are incompletely understood. Buprenorphine, a mixed agonist/antagonist at the opioid receptors, is currently being used in clinical trials for managing pregnant opioid addicts. This study provides evidence of depression-like consequence following prenatal exposure to supra-therapeutic dose of buprenorphine and sheds light on potential mechanisms of action in a rat model involving administration of intraperitoneal injection to pregnant Sprague-Dawley rats starting from gestation day 7 and lasting for 14 days. Results showed that pups at postnatal day 21 but not the dams had worse parameters of depression-like neurobehaviors using a forced swimming test and tail suspension test, independent of gender. Neurobehavioral changes were accompanied by elevation of oxidative stress, reduction of plasma levels of brain-derived neurotrophic factor (BDNF) and serotonin, and attenuation of tropomyosin-related kinase receptor type B (TrkB) phosphorylation, extracellular signal-regulated kinase (ERK) phosphorylation, protein kinase A activity, cAMP response element-binding protein (CREB) phosphorylation, and CREB DNA-binding activity. Since BDNF/serotonin and CREB signaling could orchestrate a positive feedback loop, our findings suggest that the induction of oxidative stress, reduction of BDNF and serotonin expression, and attenuation of CREB signaling induced by prenatal exposure to supra-therapeutic dose of buprenorphine provide evidence of potential mechanism for the development of depression-like neurobehavior.
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