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At least 19 recordsLinked to original sources
PubMed2005

[The relationship between early neo-maternal exposure, and maternal attachment, maternal self-esteem and postpartum depression in the mothers of NICU infants].

PURPOSE: This study was performed to investigate the quantities of three neo-maternal exposures; visiting frequency, auditory contact and physical contact, and to examine the relationship between the quantities of each exposure and maternal attachment, maternal self-esteem and postpartum depression in 40 mothers of NICU babies during the first week in the NICU. METHOD: Each neo-maternal exposure was counted at every mother's visit to the newborn and maternal attachment, maternal self-esteem and postpartum depression were measured using the maternal attachment inventory, the maternal self-report inventory and Edinburgh Postpartum Depression Scale (EPDS) on the first and seventh day in the NICU. RESULT: The Mean of each neo-maternal exposure was 8.77(2.81) for the visiting frequency, 5.82(3.66) for the auditory contact and 5.60(2.89) for the physical contact during 7 days in the NICU. No significant changes were found in the scores of maternal attachment, maternal self-esteem and postpartum depression between the first and the seventh day in the NICU. The quantities of neo-maternal exposures were positively related to the scores of maternal attachment and maternal self-esteem but not related to postpartum depression. CONCLUSION: The results of the study suggest the lack of early neo-maternal exposure in cases of NICU hospitalization negate its beneficial effects on maternal psychological well-being in increasing maternal attachment and self-esteem. More efforts are needed for the neo-maternal interaction and the reevaluation of NICU visitation hours in order to promote maternal-infant interaction.

Adult↗
PubMed2004

Sensitivity of offspring to chronic 3,4-dichloroaniline exposure varies with maternal exposure.

Many anthropogenic pollutants are present in aquatic systems for extended periods of time. Populations in the field may be exposed to toxicants for several generations, which may affect their sensitivity to toxicants. Ceriodaphnia cf. dubia mass cultures were maintained for four generations in various concentrations of 3,4-dichoroaniline (0, 2.5, 5, 10, and 15 microg/L) and were reestablished every generation using fourth-brood neonates. Each generation, chronic toxicity tests were initiated using fourth-brood neonates from each mass culture treatment. Significantly (P < 0.05) reduced sensitivity to 3,4-dichloroaniline compared to control animals was shown by F1 offspring from mothers exposed to 15 microg/L, F2 offspring from mothers exposed to 5, 10, and 15 microg/L, F3 offspring from mothers exposed to 10 and 15 microg/L, and F4 offspring from mothers exposed to all 3,4-dichloroaniline treatments (2.5, 5, 10, and 15 microg/L). Possible explanations for the development of tolerance, and the possible implications of tolerance, are discussed.

Adaptation, Physiological↗
PubMed2004

Induction of calbindin-D9k messenger RNA and protein by maternal exposure to alkylphenols during late pregnancy in maternal and neonatal uteri of rats.

Environmental chemicals are proposed to possess hormone-like properties, such as mimicking natural hormones, inhibiting the action of hormones, and inducing abnormal gene expression. Among environmental chemicals, the alkylphenol products (APs), octylphenol (OP) and nonylphenol (NP), are derived from alkylphenol ethoxylates and have been reported to be environmentally persistent. Thus, in the present study, we examined the effect of two APs, OP and NP, on the expression of Calbindin-D(9k) (CaBP-9k) following maternal exposure during late pregnancy in maternal and fetal uteri. Treatment with a high dose (600 mg/kg body weight [BW]) of OP and NP resulted in an induction of CaBP-9k mRNA at Day 5 of lactation, as did a single treatment with diethylstilbestrol (DES) and 17beta-estradiol (E2) in maternal uteri. The expression of CaBP-9k mRNA was also induced following treatment with a high dose (600 mg/kg BW) of OP, transferred from the mother, exposed to fetuses during late pregnancy, and persisted through Day 5 of lactation. It is of interest that treatments with high doses of OP (400 and 600 mg/kg BW) reduced the expression of maternal estrogen receptor alpha (ERalpha) mRNA, as E2 did. However, all doses of NP resulted in an inhibition of neonatal ERalpha, while only the high does of OP (600 mg/kg BW) induced the reduction of neonatal ERalpha mRNA expression, as E2 did. Parallel to mRNA, the expression of CaBP-9k protein was significantly induced by treatment with a high dose of OP and NP. In conclusion, maternal exposure to APs, OP and NP, during late pregnancy increased the expressions of CaBP-9k mRNA and protein in maternal and neonatal uteri. These results suggest that the absorption and distribution of environmental estrogenic compounds in maternal and neonatal uteri are extremely rapid, and these chemicals can easily pass though the placenta during pregnancy to affect functions of neonatal reproductive tissues.

Animals↗
PubMed1989

A toxicology evaluation of postnatal maternal exposure to cesium.

The effect of postnatal maternal exposure to CsCl on the newborn was studied in the mouse. Maternal ingestion of 1 mEq CsCl solution as the only drinking fluid began immediately after birth and the offspring were breast-fed until weaning. They were then separated from the nursing dams and remained Cs free for a subsequent 2 weeks prior to sacrifice. Maternal Cs exposure decreased the weanling body weight from controls and they attained normal body weight after 2 weeks of Cs-free period during development. Maternal Cs ingestion caused a reduction in offspring brain weight of both sexes compared to controls. The kidney weight of the developing female, but not male, offspring was also decreased from controls as a consequence of maternal Cs exposure. The offspring's hepatic alcohol and aldehyde dehydrogenase were not altered from controls as a function of maternal exposure to Cs salt. Little changes occurred in offspring heart lactate dehydrogenase by the maternal Cs treatment. The results suggest that maternal Cs exposure during breast-feeding affected body weight and the CNS of the offspring. The change noted in weanling kidney weight was sex dependent. These gross pathological changes in weanling organ weight were not apparent when maternal breast-feeding was eliminated. The data indicates that Cs adversely affected the newborn which was eliminated after cessation of the Cs exposure.

Alcohol Dehydrogenase↗
PubMed2006

Maternal exposure to low levels of ambient air pollution and preterm birth in Brisbane, Australia.

BACKGROUND: [corrected] There is evidence that maternal exposure to ambient air pollution during pregnancy is associated with adverse birth outcomes. OBJECTIVE: To assess preterm birth (PTB) in relation to maternal exposure to ambient air pollution. DESIGN: Retrospective cohort. SETTING: Brisbane, Australia. POPULATION: A total of 28,200 singleton live births for the period of 1 July 2000 to 30 June 2003. METHODS: Average maternal exposure estimates for ambient particulate matter (PM(10) and bsp), ozone (O(3)) and nitrogen dioxide were calculated over the first 3 months after last menstrual period (LMP) and the last 3 months prior to birth (individually and combined as trimesters). MAIN OUTCOME MEASURES: PTB was defined as gestation <37 weeks and odds ratios (OR) were calculated for PTB per interquartile range increase in the maternal exposure estimate for each pollutant. Various covariates were controlled for, including season of birth. RESULTS: Exposure to PM(10) and O(3) during trimester one was associated with an increased risk of PTB (OR = 1.15, 95% CI 1.06-1.25 and OR = 1.26, 95% CI 1.10-1.45, respectively). The PM(10) exposure effect associated with trimester one was strongly related to exposure during the first month post-LMP (PM(10), month one; OR = 1.19, 95% CI 1.13-1.26). CONCLUSION: These results suggest that maternal exposure to low levels of ambient air pollution is associated with PTB.

Air Pollutants↗
PubMed2005

Maternal exposure to bisphenol a during late pregnancy resulted in an increase of Calbindin-D9k mRNA and protein in maternal and postnatal rat uteri.

It has been reported that Calbindin-D9k (CaBP-9k) is rapidly and strongly induced by environmental estrogenic compounds, possibly through estrogen receptors (ERalpha) in the uterus of mammals. CaBP-9k can be evaluated as an early gene marker for assaying estrogenic effects of putative environmental chemicals in the rat uterus. This study was undertaken to investigate CaBP-9k mRNA and protein expression in the postnatal rat uterus following maternal exposure to 17beta-estradiol (E2) and bisphenol A (BPA) during the neonatal period. Treatment with a high dose of BPA (600 mg/kg body weight (BW) per day) resulted in a 3-fold increase in CaBP-9k mRNA expression for 3 days, while a single dose of E2 (40 microg/kg BW per day) induced 2-fold increase of this gene in the maternal uterus. In an agreement with maternal CaBP-9k mRNA, postnatal CaBP-9k mRNA in the uterus increased 4-fold when treated with BPA (600 mg/kg BW per day). In addition, treatment with increasing concentrations of BPA resulted in significant increases in CaBP-9k protein in the maternal rat uterus. It is of interest that increasing doses of BPA induced a significant ERalpha mRNA increase in the postnatal uterus. Furthermore, immunohistochemistry revealed that treatment with BPA induced CaBP-9k protein in the maternal uterus. We demonstrated that maternal exposure to BPA during late pregnancy induced CaBP-9k mRNA and protein in maternal and postnatal rat uteri. These results suggest that rapid absorption and distribution of environmental estrogenic compounds occurs in maternal and neonatal rat uteri and these chemicals can easily pass though the placenta during pregnancy to affect postnatal reproductive functions.

Animals↗
PubMed2000

Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion, testis size, and sertoli cell number.

We have tested the hypothesis that maternal exposure to octylphenol, a putative endocrine disrupting chemical, will suppress gonadotropin secretion with a concomitant decrease in testis size and Sertoli cell number during fetal life in the lamb. In Exp 1, pregnant ewes received a continuous iv infusion of diethylstilbestrol (DES; 50 microg/kg x day), octylphenol (1000 microg/kg x day), or vehicle (1:4, alcohol-saline) from days 110-115 of gestation. The fetuses were chronically catheterized in utero, and blood samples were collected every 8 h to monitor gonadotropin secretion. In Exp 2, pregnant ewes received twice weekly sc injections of DES (0.5 microg/kg x day), octylphenol (1000 microg/kg x day), or corn oil from day 70 of gestation to birth. The pituitary gland and testes were collected from the lambs at the end of the treatment period. In Exp 1, maternal exposure to octylphenol suppressed (P < 0.05) FSH concentrations without any effect (P > 0.05) on LH concentrations compared with those in control fetuses. In Exp 2, long-term maternal exposure to octylphenol or a 1000-fold lower dose of DES suppressed (P < 0.05) FSH, messenger RNA levels and the number of FSHbeta-immunopositive cells in the pituitary gland and reduced testis weight and the number of Sertoli cells in the testis compared with those in control lambs. We conclude that maternal exposure to octylphenol inhibits the secretion of FSH in the fetus with a concomitant decrease in testis size and Sertoli cell number at birth.

Animals↗
PubMed2006

Maternal exposure to estradiol and endocrine disrupting compounds alters the sensitivity of sea urchin embryos and the expression of an orphan steroid receptor.

Endocrine disrupting compounds (EDCs) are known to affect reproduction and development in marine invertebrates. In previous work, we have shown that developing sea urchin embryos were sensitive to estradiol and estrogenic EDCs at environmentally relevant concentrations in a tamoxifen-sensitive manner (Roepke et al. 2005. Aquat Toxicol 71:155-173). In this study, we report the effects of maternal exposure to EDCs on embryo sensitivity and regulation of an orphan steroid receptor in sea urchin eggs. Maternal exposures were conducted by injecting female Strongylocentrotus purpuratus sea urchins initiating oogenesis with two concentrations of estradiol, octylphenol, tributyltin and o, p-DDD for 8 weeks with an induced spawning before and after the injection cycle. Developing embryos were less sensitive to estradiol following maternal exposure to estradiol, octylphenol and DDD. The steroidogenesis inhibitor, spironolactone, and the aromatase inhibitor, formestane, affected normal sea urchin development with EC50 values of 18 and 2 microM, respectively. Binding of estradiol was demonstrated in homogenates supernatants of sea urchin embryos by filtration centrifugation and column chromatography, but saturation was not reached until 4-6 hr and was highly variable. Analysis of eggs from pre- and post-injection spawns using real-time Q-PCR for the mRNA of an orphan steroid receptor, SpSHR2, shows that receptor mRNA increased in eggs with estradiol, octylphenol and tributyltin but decreased with DDD. RIA showed that estradiol may be present during gastrulation. In summary, maternal exposure to estradiol and EDCs alters embryo sensitivity and regulates the expression of an orphan steroid receptor in the egg.

Animals↗
PubMed1995

Behavioural consequences of maternal exposure to natural cannabinoids in rats.

Cannabis sativa preparations (hashish, marijuana) are the most widely used illicit drugs during pregnancy in Western countries. The possible long-term consequences for the child of in utero exposure to cannabis derivatives are still poorly understood. Animal models of perinatal cannabinoid exposure provide a useful tool for examining the developmental effects of cannabinoids. Behavioral consequences of maternal exposure to either cannabis preparations or to its main psychoactive component, delta 9-tetrahydrocannabinol (THC) in rat models are reviewed in this paper. Maternal exposure to cannabinoids resulted in alteration in the pattern of ontogeny of spontaneous locomotor and exploratory behavior in the offspring. Adult animals exposed during gestational and lactational periods exhibited persistent alterations in the behavioral response to novelty, social interactions, sexual orientation and sexual behavior. They also showed a lack of habituation and reactivity to different illumination conditions. Adult offspring of both sexes also displayed a characteristic increase in spontaneous and water-induced grooming behavior. Some of the effects were dependent on the sex of the animals being studied, and the dose of cannabinoid administered to the mother during gestational and lactational periods. Maternal exposure to low doses of THC sensitized the adult offspring of both sexes to the reinforcing effects of morphine, as measured in a conditioned place preference paradigm. The existence of sexual dimorphisms on the developmental effects of cannabinoids, the role of sex steroids, glucocorticoids, and pituitary hormones, the possible participation of cortical projecting monoaminergic systems, and the mediation of the recently described cannabinoid receptors are also analyzed. The information obtained in animal studies is compared to the few data available on the long-term behavioral and cognitive effects on in utero exposure to cannabis in humans.

Abnormalities, Drug-Induced↗
PubMed1997

Transgenerational effects of maternal exposure to chemicals on the functional development of the brain in the offspring.

In order to prevent health risk from environmental chemicals, particularly for progeny, we have been performing a risk assessment for various chemicals including therapeutic agents. This paper reports the functional effects of maternal exposure to psychoactive drugs, anticancer drugs, or herbicides on the offspring of rats. Maternal exposure to imipramine in a dose equivalent to the therapeutic dose per unit body weight induced hyperthermic response to chlorpromazine in the male offspring, while normal control rats showed a marked hypothermia. Exposure to ethosuximide resulted in an increase in play fighting behavior in young offspring that was fostered by lactating normal mothers. Single exposures to nimustine or cisplatin, anticancer drugs, at a different gestational stage resulted in an acceleration of growth when exposed at the earlier stage of gestation. Moreover, cisplatin-exposed rats were emotionally unstable, showing a short latent time to the first line-crossing in an open-field during infantile period. The rats exposed to glufosinate ammonium, an herbicide, during the time of neurogenesis in the hippocampus showed a decrease in the wet-dog shakes response to kainic acid at six weeks of age. These results suggest that maternal exposure to chemicals during pregnancy induces a variety of functional abnormalities in the brain of the offspring dependent on the pharmacologic action of chemicals and the stage of gestation even with a single exposure.

Aggression↗
PubMed2005

Maternal exposure to the antiepileptic drug vigabatrin affects postnatal development in the rat.

The objective was to investigate, in the rat, the effects of maternal exposure to vigabatrin (VGB) on the postnatal motor-cognitive behaviour of the offspring. We used an experimental evaluator-blind, placebo-controlled study in the rat. Ten pregnant rats were divided into five groups and treated with different doses of VGB (250, 500, 750, 1000 mg/kg/day) or placebo from gestation day (GD) 6 to GD10. After delivery, 56 pups (40 pups prenatally exposed to VGB and 16 pups exposed to placebo) were evaluated for motor-cognitive behaviour throughout postpartum day 40. At the end of testing sessions the animals were sacrificed and brain tissues processed for biochemical analysis of GABA levels. Body weight of pups and young rats whose mothers were treated with a dose of 750 mg/kg/day were significantly lower both at birth and during the whole postnatal life with respect to the control groups. Young rats of this group exhibited impaired performance in both the open-field and water maze tasks. Brain GABA contents were dramatically increased in this group of rats. No other significant nutritional, biochemical or behavioural changes were observed after treatments with doses of VGB lower than 750 mg/kg/day. The exposure to a dose of 1000 mg/kg caused abortion. Maternal exposure to VGB at relatively high doses (750 mg/kg/day) is likely to cause some important changes of the nutritional status during the pre- and postnatal life. Thus, the biochemical and cognitive abnormalities observed in this study could be related to some disturbances of brain development induced by malnutrition and/or to a disturbance of neuronal programming of the gabaergic system.

Animals↗
PubMed2001

Association of transposition of the great arteries in infants with maternal exposures to herbicides and rodenticides.

The Baltimore-Washington Infant Study, a case-control study of congenital heart defects in liveborn infants conducted in 1981--1989, interviewed parents about a wide range of environmental exposures that occurred during and before the pregnancy. In the period 1987--1989, the questionnaire was expanded to include a detailed inquiry about exposures to pesticides. An analysis of these latter data revealed an association of maternal exposure to any pesticides during the first trimester with transposition of the great arteries in their infants (TGA; n = 66 infants), relative to 771 control infants, with an odds ratio of 2.0 (95% confidence interval (CI): 1.2, 3.3). No other heart defects were associated with pesticides. When analyzed by type of pesticide and adjusted for covariates, there were associations of TGA with maternal exposures to herbicides (odds ratio (OR) = 2.8; 95% CI: 1.3, 7.2) and to rodenticidal chemicals (OR = 4.7; 95% CI: 1.4, 12.1) but not to insecticides (OR = 1.5; 95% CI: 0.9, 2.6). No data were collected on specific chemicals or brand names. These results raise new questions about the possible epidemiologic association of TGA with some classes of pesticides and warrant new, carefully targeted investigations.

Adult↗
PubMed2004

Maternal exposure to nicotine and chlorpyrifos, alone and in combination, leads to persistently elevated expression of glial fibrillary acidic protein in the cerebellum of the offspring in late puberty.

We previously showed that maternal exposure to nicotine, alone or in combination with chlorpyrifos, caused an increase in glial fibrillary acidic protein (GFAP) immunostaining in the CA1 subfield of hippocampus and cerebellum in postnatal day (PND) 30 offspring. In the present study, PND 60 offspring were evaluated for histopathological and cholinergic effects following maternal exposure to nicotine and chlorpyrifos, alone and in combination. Timed-pregnant Sprague-Dawley rats (300-350 g) were treated daily with nicotine (1 mg/kg, s.c., in normal saline) or chlorpyrifos (0.1 mg/kg, dermal, in ethanol) or a combination of nicotine and chlorpyrifos from gestational days (GD) 4 to 20. Control animals were treated with saline and ethanol. On PND 60, the offspring were evaluated for cholinergic changes and pathological effects. Plasma butyrylcholinesterase (BChE) activity in the female offspring from chlorpyrifos treated mothers showed a significant increase (approximately 183% of control). Male offspring from mothers treated with either chlorpyrifos or nicotine alone showed a significant increase in the acetylcholinesterase (AChE) activity in the brainstem while female offspring from mothers treated with either nicotine or a combination of nicotine and chlorpyrifos showed a significant increase (approximately 134 and 126% of control, respectively) in AChE activity in the brainstem. No significant changes were observed in the ligand binding densities for alpha4beta2 and alpha7 nicotinic acetylcholine receptors in the cortex. Histopathological evaluation using cresyl violet staining showed a significant decrease in surviving Purkinje neurons in the cerebellum of the offspring from nicotine treated mothers. An increase in GFAP immunostaining in cerebellar white matter was observed in the offspring from the mothers treated with nicotine. These results suggest that maternal exposure to real-life levels of nicotine and/or chlorpyrifos causes differential regulation of brainstem AChE activity. Also, nicotine caused a decrease in the surviving neurons and an increased expression of GFAP in cerebellar white matter of the offspring on PND 60. These changes can lead to long-term neurological adverse health effects later in life.

Alkaloids↗
PubMed2006

A review of nitrates in drinking water: maternal exposure and adverse reproductive and developmental outcomes.

In this review we present an update on maternal exposure to nitrates in drinking water in relation to possible adverse reproductive and developmental effects, and also discuss nitrates in drinking water in the United States. The current standard for nitrates in drinking water is based on retrospective studies and approximates a level that protects infants from methemoglobinemia, but no safety factor is built into the standard. The current standard applies only to public water systems. Drinking water source was related to nitrate exposure (i.e., private systems water was more likely than community system water to have nitrate levels above the maximum contaminant limit). Animal studies have found adverse reproductive effects resulting from higher doses of nitrate or nitrite. The epidemiologic evidence of a direct exposure-response relationship between drinking water nitrate level and adverse reproductive effect is still not clear. However, some reports have suggested an association between exposure to nitrates in drinking water and spontaneous abortions, intrauterine growth restriction, and various birth defects. Uncertainties in epidemiologic studies include the lack of individual exposure assessment that would rule out confounding of the exposure with some other cause. Nitrates may be just one of the contaminants in drinking water contributing to adverse outcomes. We conclude that the current literature does not provide sufficient evidence of a causal relationship between exposure to nitrates in drinking water and adverse reproductive effects. Future studies incorporating individual exposure assessment about users of private wells--the population most at risk--should be considered.

Abortion, Spontaneous↗
PubMed2004

Induction of hypospadias in a murine model by maternal exposure to synthetic estrogens.

We tested the hypothesis that maternal exposure to synthetic estrogen can cause hypospadias in male offspring and defined the morphological changes in the disrupted urethral seam. Timed pregnant C57/6 mice were exposed to synthetic estrogens. The genital tubercles were examined for the presence of hypospadias using histology, three-dimensional computer reconstruction, and plastic cast injection molds of the urethra. Microscopic serial analysis confirmed the presence of hypospadias, which occurred in approximately 50% of the synthetic-estrogen-treated male fetuses. No effect was seen in the female embryos. Plastic cast injection showed that affected males had a shorter total urethral length and loss of male anatomic features such as the prostatic utricle. Exposure to synthetic estrogens during pregnancy affects the normal development of the urethra in the mouse. We conclude that endocrine disrupters play an important role in genital tubercle anomalies.

Animals↗
PubMed1989

Analyses of transplacentally induced sister chromatid exchanges and micronuclei in mouse fetal liver cells following maternal exposure to cigarette smoke.

The effect of maternal exposure to cigarette smoke on the fetus was studied by analyses of sister chromatid exchange (SCE) and formation of micronuclei with fetal liver cells. Fetal tissues were obtained from pregnant ICR/Jcl mice at the 16th day of gestation. Mice were exposed to mainstream or sidestream cigarette smoke with or without passage through filter (gas phase smoke or whole smoke). Each stream of smoke was used for three exposure schedules, i.e., short-term (two exposures at 15th and 16th day of gestation), long-term (exposure started at 4 wk before mating and stopped at 16th day of gestation), and prepregnant term (exposed for 4 wk before mating). The number of SCEs of fetal liver cells was significantly increased in all exposed groups. In the mainstream experiments, the long-term group showed a significant increase in the number of SCEs in comparison with that in the short-term group. Exposure to sidestream smoke increased the number of SCEs more than in groups exposed to mainstream smoke. This tendency was also recognized in the experiments with filtered smoke. On the contrary, no significant changes were observed by the micronucleus test. The transplacental genotoxic effect of maternally inhaled cigarette smoke was accurately detected by analysis of SCEs with fetal liver cells.

Animals↗
PubMed2004

Maternal exposure to low doses of bisphenol a has no effects on development of female reproductive tract and uterine carcinogenesis in Donryu rats.

Effects of maternal exposure to low doses of bisphenol A (BPA), including those comparable with human exposure levels, on growth and development of the female reproductive system and uterine carcinogenesis in Donryu rats were investigated. Dams were administered BPA (0, 0.006 and 6 mg/kg/day) daily by gavage from gestation day 2 up to the day before weaning (postnatal day 21 at offspring). The serum levels of BPA were significantly elevated in the dams receiving 6 mg/kg/day, however, BPA levels in the milk of dams, and those in the serum and liver of offspring were similar between control and treated groups. The treatment did not exert any influences on uterine development including weight, gland genesis and estrogen receptor alpha expression, vaginal opening and gonadotropin secretion in the female offspring up to puberty. After maturation, no effects were evident with regard to estrous cyclicity in female offspring treated with BPA. In addition, the treatment had no effects on age-related morphological changes of the reproductive and endocrine organs and uterine carcinogenesis until 15 months of age. The results demonstrate that maternal exposure to BPA at levels comparable to human exposure did not have any effects on the female reproductive system of offspring in rats. In addition, BPA was also found in the serum, milk and liver of control dams and pups, and low levels of BPA were detected in drinking water and pellet diet. The present study showed that the experimental animals were also exposed to environmental BPA in the animal room.

Animals↗
PubMed1997

Maternal exposure to influenza and cold in pregnancy and electrodermal activity in offspring: the Mauritius Study.

Data are in conflict concerning whether a mother's exposure to influenza in pregnancy gives rise to an increased probability that her offspring will develop schizophrenia. In Northern Hemisphere studies, exposure to influenza and cold tend to be confounded. The present study, carried out in Mauritius, examines the effect of maternal exposure to the virus and separately to cold on aspects of electrodermal activity that have been shown in other studies to be related to schizophrenia. The findings are that maternal exposure to influenza in the second and third trimesters gives rise to children who at the age of 3 years show electrodermal hyperresponsivity, whereas exposure to cold in the same periods gives rise to children who tend to be hyporesponsive. In both instances, exposure tends to produce lower levels of tonic activity than in those not exposed to the virus or to cold.

Child, Preschool↗