Prenatal Chemical Exposures https://greenmedinfo.com/category/keywords/Prenatal%20Chemical%20Exposures en Commonly taken analgesics could decrease germ cell number and ovarian size in F1 offspring in rats. https://greenmedinfo.com/article/commonly-taken-analgesics-could-decrease-germ-cell-number-and-ovarian-size-f1- n/a PMID:  Sci Rep. 2016 Jan 27 ;6:19789. Epub 2016 Jan 27. PMID: 26813099 Abstract Title:  Analgesic exposure in pregnant rats affects fetal germ cell development with inter-generational reproductive consequences. Abstract:  Analgesics which affect prostaglandin (PG) pathways are used by most pregnant women. As germ cells (GC) undergo developmental and epigenetic changes in fetal life and are PG targets, we investigated if exposure of pregnant rats to analgesics (indomethacin or acetaminophen) affected GC development and reproductive function in resulting offspring (F1) or in the F2 generation. Exposure to either analgesic reduced F1 fetal GC number in both sexes and altered the tempo of fetal GC development sex-dependently, with delayed meiotic entry in oogonia but accelerated GC differentiation in males. These effects persisted in adult F1 females as reduced ovarian and litter size, whereas F1 males recovered normal GC numbers and fertility by adulthood. F2 offspring deriving from an analgesic-exposed F1 parent also exhibited sex-specific changes. F2 males exhibited normal reproductive development whereas F2 females had smaller ovaries and reduced follicle numbers during puberty/adulthood; as similar changes were found for F2 offspring of analgesic-exposed F1 fathers or mothers, we interpret this as potentially indicating an analgesic-induced change to GC in F1. Assuming our results are translatable to humans, they raise concerns that analgesic use in pregnancy could potentially affect fertility of resulting daughters and grand-daughters. https://greenmedinfo.com/article/commonly-taken-analgesics-could-decrease-germ-cell-number-and-ovarian-size-f1-#comments Acetaminophen (Tylenol) Toxicity Infertility: Female Prenatal Chemical Exposures Acetaminophen Analgesic: Non-opioid Indomethacin Paracetamol Acetaminophen (Tylenol) Toxicity Infertility: Female Prenatal Chemical Exposures Transgenerational Epigenetic Modification Animal Study Mon, 26 Jun 2017 19:23:53 +0000 greenmedinfo 149599 at https://greenmedinfo.com Early paracetamol exposure produces major changes in serotonergic and dopaminergic neurotransmission in the prefrontal cortex and striatum. https://greenmedinfo.com/article/early-paracetamol-exposure-produces-major-changes-serotonergic-and-dopaminergi n/a PMID:  Behav Brain Res. 2017 Apr 14 ;323:162-171. Epub 2017 Feb 3. PMID: 28163096 Abstract Title:  Paracetamol - Effect of early exposure on neurotransmission, spatial memory and motor performance in rats. Abstract:  In the present study we examined the effect of prenatal and early life paracetamol exposure on neurotransmission and its behavioural manifestation in rat male pups. In order to assess the ability of spatial learning and memory consolidation and the level of physical and exploratory activity we conducted a series of behavioural tests: Staircase Test, Hole Board Test and Water Maze. The concentrations of monoamines, metabolites and amino acids were determined using High Performance Liquid Chromatography in the prefrontal cortex, hippocampus and striatum. The effect on spatial memory and exploratory behaviour was most pronounced in animals treated with the lower dose of paracetamol. In this group we have observed a much lower motor activity and decreased head-dipping behaviour. Simultaneously, the number of crossings in the Water Maze under the previous platform position during the probe trial was significantly higher in rats treated with paracetamol at the dose of 5mg/kg. There was also a preference for a new location of a platform to the original position of the platform in the reversal probe trial of this group. These results indicate that early paracetamol exposure produces major changes in serotonergic and dopaminergic neurotransmission in the prefrontal cortex and striatum. At the same time, administration of the drug in early life results in the spectacular change in the amino acid level, in particular in the hippocampus and cortex. This has been reflected in the behaviour of animals in the Water Maze and Hole Board Test (without any noticeable impact on the Staircase Test). https://greenmedinfo.com/article/early-paracetamol-exposure-produces-major-changes-serotonergic-and-dopaminergi#comments Acetaminophen (Tylenol) Toxicity Prenatal Chemical Exposures Acetaminophen Paracetamol Acetaminophen Acetaminophen (Tylenol) Toxicity paracetamol Prenatal Chemical Exposures Animal Study Mon, 26 Jun 2017 21:17:54 +0000 greenmedinfo 149614 at https://greenmedinfo.com Exposure to nonylphenol and BPA and possibly inflammation in increasing oxidative stress and decreasing antioxidant activity during pregnancy. https://greenmedinfo.com/article/exposure-nonylphenol-and-bpa-and-possibly-inflammation-increasing-oxidative-st n/a PMID:  Environ Sci Technol. 2017 May 11. Epub 2017 May 11. PMID: 28490175 Abstract Title:  Prenatal nonylphenol and bisphenol A exposures and inflammation are determinants of oxidative/nitrative stress: A Taiwanese cohort study. Abstract:  Prenatal exposure to nonylphenol (NP) and/or bisphenol A (BPA) has been reported to be associated with adverse birth outcomes; however, the underlying mechanisms remain unclear. The primary mechanism is endocrine disruption of the binding affinity for the estrogen receptor, but oxidative stress and inflammation might also play a contributory role. We aimed to investigate urinary NP and BPA levels in relation to biomarkers of oxidative/nitrative stress and inflammation and to explore whether changes in oxidative/nitrative stress are a function of prenatal exposure to NP/BPA and inflammation in 241 mother-fetus pairs. Third-trimester urinary biomarkers of oxidative/nitrative stress were simultaneously measured, including products of oxidatively and nitratively damaged DNA (8-hydroxy-2'-deoxyguanosine (8-OHdG) and 8-nitroguanine (8-NO2Gua)) as well as products of lipid peroxidation (8-iso-prostaglandin F2α (8-isoPF2α) and 4-hydroxy-2-nonenal-mercapturic acid (HNE-MA)). The antioxidant glutathione peroxidase (GPx) and inflammation biomarkers, including C-reactive protein (CRP) and a panel of cytokines (interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α)), were analyzed in maternal and umbilical cord plasma samples. In adjusted models, we observed significant positive associations between NP exposure and 8-OHdG and 8-NO2Gua levels, between BPA and 8-isoPF2α levels, and between maternal CRP levels and HNE-MA levels. Additionally, BPA and TNF-α levels in cord blood were inversely associated with maternal and GPx levels in cord blood as well as maternal TNF-α levels were inversely associated with maternal GPx levels. These results support a role for exposure to NP and BPA and possibly inflammation in increasing oxidative/nitrative stress and decreasing antioxidant activity duringpregnancy. https://greenmedinfo.com/article/exposure-nonylphenol-and-bpa-and-possibly-inflammation-increasing-oxidative-st#comments Bisphenol Toxicity Inflammation Prenatal Chemical Exposures Bisphenol A Nonylphenol Bisphenol A Bisphenol Toxicity Inflammation Nonylphenol Prenatal Chemical Exposures Risk Factors Animal Study Mon, 15 May 2017 21:49:43 +0000 greenmedinfo 147797 at https://greenmedinfo.com Intake of fisetin during pregnancy in rats ameliorated in utero mercury exposure induced neurotoxicity outcomes. https://greenmedinfo.com/article/intake-fisetin-during-pregnancy-rats-ameliorated-utero-mercury-exposure-induce n/a PMID:  Biol Trace Elem Res. 2017 Jun ;177(2):297-315. Epub 2016 Nov 4. PMID: 27815688 Abstract Title:  Effect of Gestational Intake of Fisetin (3,3',4',7-Tetrahydroxyflavone) on Developmental Methyl Mercury Neurotoxicity in F1 Generation Rats. Abstract:  Methyl mercury (MeHg) is a developmental neurotoxin that causes irreversible cognitive damage in offspring of gestationally exposed mothers. Currently, no preventive drugs are established against MeHg developmental neurotoxicity. The neuroprotective effect of gestational administration of a flavanoid against in utero toxicity of MeHg is not explored much. Hence, the present study validated the effect of a bioactive flavanoid, fisetin, on MeHg developmental neurotoxicity outcomes in rat offspring at postnatal weaning age. Pregnant Wistar rats were simultaneously given MeHg (1.5 mg/kg b.w.) and two doses of fisetin (10 and 50 mg/kg b.w. in two separate groups) orally from gestational day (GD) 5 till parturition. Accordingly, after parturition, on postnatal day (PND) 24, weaning F1 generation rats were studied for motor and cognitive behavioural changes. Biochemical and histopathological changes were also studied in the cerebral cortex, cerebellum and hippocampus on PND 25. Administration of fisetin during pregnancy prevented behavioural impairment due to transplacental MeHg exposure in weaning rats. Fisetin decreased the levels of oxidative stress markers, increased enzymatic and non-enzymatic antioxidant levels and increased the activity of membrane-bound ATPases and cholinergic function in F1 generation rats. In light microscopic studies, fisetin treatment protected the specific offspring brain regions from significant morphological aberrations. Between thetwo doses of fisetin studied, 10 mg/kg b.w. was found to be more satisfactory and effective than 50 mg/kg b.w. The present study shows that intake of fisetin during pregnancy in rats ameliorated in utero MeHg exposure-induced neurotoxicity outcomes in postnatal weaning F1 generation rats. https://greenmedinfo.com/article/intake-fisetin-during-pregnancy-rats-ameliorated-utero-mercury-exposure-induce#comments Fisetin Flavonoids Mercury Poisoning Neurodegenerative Diseases Oxidative Stress Prenatal Chemical Exposures Mercury Neuroprotective Agents Fisetin Flavonoids Mercury Poisoning Methylmercury Neurodegenerative diseases oxidative stress Prenatal Chemical Exposures Animal Study Wed, 19 Jul 2017 22:44:08 +0000 greenmedinfo 150696 at https://greenmedinfo.com Maternal acetaminophen use during pregnancy was associated with lower performance IQ in 5-year olds. https://greenmedinfo.com/article/maternal-acetaminophen-use-during-pregnancy-was-associated-lower-performance-i n/a PMID:  Epidemiology. 2016 Nov ;27(6):912-8. PMID: 27479646 Abstract Title:  Prenatal Use of Acetaminophen and Child IQ: A Danish Cohort Study. Abstract:  BACKGROUND: Acetaminophen (paracetamol) is the most commonly used pain and fever medication during pregnancy, and recently has been linked to hyperactivity and behavioral problems in children. We examine whether prenatal use of acetaminophen affects children's intelligence quotient (IQ). METHODS: We studied 1,491 mothers and children enrolled in the Danish National Birth Cohort (DNBC; 1996-2002). Acetaminophen use in pregnancy was prospectively recorded in three telephone interviews. Child IQ was assessed at age 5 with the Wechsler Primary and Preschool Scales of Intelligence-Revised (WPPSI-R) administered by trained psychologists. We employed linear regression analysis, adjusting for maternal IQ and other confounding factors, and assessed interactions between acetaminophen and indications for use. RESULTS: Both maternal fever in pregnancy and acetaminophen use were associated with child IQ. Children born to mothers using acetaminophen without reporting fever scored on average 3.4 points lower (95% confidence interval [CI]: 0.30 to 6.6 points) on performance IQ compared with offspring of mothers who neither experienced fever nor took acetaminophen. Estimated effects for acetaminophen were stronger for first or second trimester use. Children born to mothers reporting fever without using acetaminophen also scored lower on verbal (2.7 points, 95% CI: -0.19, 5.6) and performance IQ (4.3 points, 95% CI: 0.30, 8.3); IQ scores were not affected if mothers with fever used acetaminophen. CONCLUSIONS: Maternal acetaminophen use during pregnancy was associated with lower performance IQ in 5-year olds. However, acetaminophen treatment of maternal fever in pregnancy showed an apparent compensatory association with child IQ scores. (See video abstract at http://links.lww.com/EDE/B87.). https://greenmedinfo.com/article/maternal-acetaminophen-use-during-pregnancy-was-associated-lower-performance-i#comments Acetaminophen (Tylenol) Toxicity Prenatal Chemical Exposures Acetaminophen Paracetamol Acetaminophen Acetaminophen (Tylenol) Toxicity paracetamol Prenatal Chemical Exposures Human Study Mon, 26 Jun 2017 19:39:13 +0000 greenmedinfo 149600 at https://greenmedinfo.com Maternal folate supplementation counteracts bisphenol A induced Igf2 DNA hypermethylation in the offspring. https://greenmedinfo.com/article/maternal-folate-supplementation-counteracts-bisphenol-induced-igf2-dna-hyperme n/a PMID:  J Appl Toxicol. 2017 Feb 6. Epub 2017 Feb 6. PMID: 28165156 Abstract Title:  Pancreatic impairment and Igf2 hypermethylation induced by developmental exposure to bisphenol A can be counteracted by maternal folate supplementation. Abstract:  Increasing evidence indicates that bisphenol A (BPA), a widely manufactured environmental pollutant, can induce changes in DNA methylation paatterns, which is a potential mechanism linking this environmental exposure to disease development. We investigated the influence of developmental exposure to BPA on pancreatic DNA methylation patterns and whether maternal folate supplementation can modify the epigenetic status and pancreatic impairment induced by BPA. Our results showed that maternal dietary folate supplementation in rats exposed to BPA counteracted the observed BPA-induced pancreatic impairments in the offspring, which included disrupted insulin secretion and glucose intolerance, and impaired morphology and ultrastructure ofβ cells. Moreover, these pancreatic dysfunctions were shown to be associated with low expression and DNA hypermethylation of insulin-like growth factor-2 (Igf2) in islets induced by exposure to BPA during the developmental period. Importantly, maternal dietary folate supplementation was demonstrated to negate this Igf2 DNA hypermethylation in the offspring, which was consistent with the upregulation of Igf2 expression. Overall, our results suggest that early developmental exposure to BPA alters the DNA methylation of Igf2, that these altered methylation patterns are associated with impaired β-cell function in the offspring and that these effects can be counteracted by maternal folate supplementation. Copyright © 2017 John Wiley&Sons, Ltd. https://greenmedinfo.com/article/maternal-folate-supplementation-counteracts-bisphenol-induced-igf2-dna-hyperme#comments Bisphenol Toxicity Folate Folate: Dietary Prenatal Chemical Exposures Bisphenol A Pancreato Protective Agents Bisphenol A Bisphenol Toxicity Folate Prenatal Chemical Exposures Risk Reduction Animal Study Thu, 09 Feb 2017 01:38:13 +0000 greenmedinfo 143247 at https://greenmedinfo.com Maternal paracetamol use during pregnancy could be associated with poorer attention and executive function in 5-year-olds. https://greenmedinfo.com/article/maternal-paracetamol-use-during-pregnancy-could-be-associated-poorer-attention n/a PMID:  Int J Epidemiol. 2016 Dec 1 ;45(6):2009-2017. PMID: 28031314 Abstract Title:  Paracetamol use during pregnancy and attention and executive function in offspring at age 5 years. Abstract:  Methods: We studied 1491 mothers and children enrolled in the Danish National Birth Cohort (DNBC; 1996-2002). Prenatal paracetamol use was prospectively recorded in three telephone interviews. Trained psychologists assessed child's attention function using the Test of Everyday Attention for Children at Five (TEACh-5). Parents and preschool teachers completed Behaviour Rating Inventory of Executive Function (BRIEF) to assess executive functions. We estimated the differences of composite mean outcome scores, and odds ratios (OR) for subnormal attention or executive function (defined as 1 standard deviation below the mean), adjusting for maternal IQ, maternal mental health, indications for paracetamol use and other potential confounders. Results: First trimester use of paracetamol was associated with poorer attention scores in childhood [mean difference -0.34, 95% confidence interval (CI) -0.63, -0.05 for overall attention, and -0.25, 95% CI -0.50, 0.01 for selective attention]. Children prenatally exposed to paracetamol were also at a higher risk for subnormal overall attention (OR = 1.5, 95% CI 1.0, 2.5), selective attention difficulties (OR = 1.5, 95% CI 1.0, 2.4), and parent-rated subnormal executive function (metacognition index, OR = 1.5, 95% CI 0.9, 2.3). The risks for subnormal overall attention or executive function were elevated with longer duration of paracetamol use in pregnancy. Conclusions: We found some evidence that maternal paracetamol use during pregnancy was associated with poorer attention and executive function in 5-year-olds. https://greenmedinfo.com/article/maternal-paracetamol-use-during-pregnancy-could-be-associated-poorer-attention#comments Acetaminophen (Tylenol) Toxicity Prenatal Chemical Exposures Acetaminophen Paracetamol Acetaminophen Acetaminophen (Tylenol) Toxicity paracetamol Prenatal Chemical Exposures Human Study Mon, 26 Jun 2017 21:47:59 +0000 greenmedinfo 149616 at https://greenmedinfo.com Occurrence of eczema in early childhood may be influenced by prenatal exposure to certain phthalates in boys. https://greenmedinfo.com/article/occurrence-eczema-early-childhood-may-be-influenced-prenatal-exposure-certain- n/a PMID:  Environ Health Perspect. 2018 Feb 2 ;126(2):027002. Epub 2018 Feb 2. PMID: 29398652 Abstract Title:  Prenatal Exposure to Phthalates and the Development of Eczema Phenotypes in Male Children: Results from the EDEN Mother-Child Cohort Study. Abstract:  BACKGROUND: Contradictory results exist regarding the importance of early-life exposure to phthalates for development of childhood eczema. OBJECTIVES: We evaluated the association between maternal urinary concentrations of phthalate metabolites between the 24th and 28th week of gestation and occurrence of eczema in their sons up to 5 y of age, according to allergic sensitization as assessed by total immunoglobulin E (IgE) in a subsample of individuals. METHODS: Data on health outcomes and background factors were collected using five standardized annual questionnaires completed by parents at the children's ages of 1-5 y, and their associations with phthalate metabolite urinary concentrations were assessed in 604 mother-son pairs with adjusted multiple logistic regression and Cox's survival model. Several eczema phenotypes were considered. Atopic status was assessed at 5 y of age in 293 boys through total IgE assessment. RESULTS: At 5 y of age, the prevalence of ever eczema was 30.4%. Metabolites of di-isobutyl phthalate (DiBP) and di-isononyl phthalate (DiNP) were positively associated with early-onset (0-24 mo of age) eczema (15.7%) and late-onset (24-60 mo of age) eczema (14.7%). Applying the Cox's model showed a significant association of occurrence of eczema in the first 5 y of life with DiBP and DiNP metabolites. Among IgE-sensitized boys, metabolites of di-n-butyl phthalate (DBP) and DiBP were significantly associated with ever eczema {hazard ratio (HR)=1.67 [95% confidence interval (CI): 1.10, 2.54], p=0.01 and HR=1.87 (95% CI: 1.01, 3.48), p=0.04, respectively}. CONCLUSIONS: Occurrence of eczema in early childhood may be influenced by prenatal exposure to certain phthalates in boys. Further investigations are needed to confirm this observation. https://doi.org/10.1289/EHP1829. https://greenmedinfo.com/article/occurrence-eczema-early-childhood-may-be-influenced-prenatal-exposure-certain-#comments Eczema Phthalate Toxicity Prenatal Chemical Exposures Phthalates eczema Phthalate Toxicity Phthalates Prenatal Chemical Exposures Human Study Thu, 08 Feb 2018 02:09:57 +0000 greenmedinfo 159471 at https://greenmedinfo.com Prenatal and postnatal paracetamol exposure results in modulation of cerebellar neurotransmission with changes concerning mainly 5-HIAA and MHPG levels. https://greenmedinfo.com/article/prenatal-and-postnatal-paracetamol-exposure-results-modulation-cerebellar-neur n/a PMID:  Pharmacol Rep. 2016 Dec ;68(6):1159-1164. Epub 2016 Sep 7. PMID: 27611980 Abstract Title:  Cerebellar level of neurotransmitters in rats exposed to paracetamol during development. Abstract:  BACKGROUND: The present study was designed to clarify the effect of prenatal and postnatal paracetamol administration on the neurotransmitter level and balance of amino acids in the cerebellum. METHODS: Biochemical analysis to determine the concentration of neurotransmitters in this brain structure was performed on two-month-old Wistar male rats previously exposed to paracetamol in doses of 5 (P5, n=10) or 15mg/kg (P15, n=10) throughout the entire prenatal period, lactation and until the completion of the second month of life, when the experiment was terminated. Control animals were given tapped water (Con, n=10). The cerebellar concentration of monoamines, their metabolites and amino acids were assayed using High Performance Liquid Chromatography (HPLC). RESULTS: The present experiment demonstrates that prenatal and postnatal paracetamol exposure results in modulation of cerebellar neurotransmission with changes concerning mainly 5-HIAA and MHPG levels. CONCLUSION: The effect of paracetamol on monoaminergic neurotransmission in the cerebellum is reflected by changes in the level of catabolic end-products of serotonin (5-HIAA) and noradrenaline (MHPG) degradation. Further work is required to define the mechanism of action and impact of prenatal and postnatal exposure to paracetamol in the cerebellum and other structures of the central nervous system (CNS). https://greenmedinfo.com/article/prenatal-and-postnatal-paracetamol-exposure-results-modulation-cerebellar-neur#comments Acetaminophen (Tylenol) Toxicity Prenatal Chemical Exposures Acetaminophen Neurotoxic Paracetamol Acetaminophen Acetaminophen (Tylenol) Toxicity paracetamol Prenatal Chemical Exposures Animal Study Mon, 26 Jun 2017 22:38:06 +0000 greenmedinfo 149621 at https://greenmedinfo.com Prenatal exposure to BPA may potentially increase the risk of allergic diseases at very early life in female infants. https://greenmedinfo.com/article/prenatal-exposure-bpa-may-potentially-increase-risk-allergic-diseases-very-ear n/a PMID:  Pediatr Res. 2017 Jan 31. Epub 2017 Jan 31. PMID: 28141789 Abstract Title:  Prenatal exposure to bisphenol A and risk of allergic diseases in early life. Abstract:  BACKGROUND: Prenatal exposure to bisphenol A (BPA) affects immune system and promotes allergy and asthma in mice, but findings in human studies are limited. We investigated whether prenatal exposure to BPA is associated with increased risk of allergic diseases in infants. METHODS: We measured BPA concentrations in maternal urine samples collected at delivery from 412 women in Wuhan, China. The occurrence of allergic diseases including eczema and wheeze were assessed at age 6 months through questionnaires. We used logistic regression to evaluate the association between urinary BPA levels and the risk of allergic diseases. RESULTS: Mothers of infants with allergic diseases had significantly higher urinary BPA levels than those of infants without allergic diseases (median: 2.35 vs. 4.55µg/l, P = 0.03). Increased risk of infant allergic diseases was associated with creatinine-adjusted maternal urinary BPA concentrations. And this association was limited to females (OR = 1.36; 95% CI: 1.10-1.79) rather than males. After stratification by maternal age, the association was only significant in infants of mothers who were younger than 25 years old (OR = 1.90; 95% CI: 1.09-3.29). CONCLUSION: Prenatal exposure to BPA may potentially increase the risk of allergic diseases at very early life in female infants.Pediatric Research (2017); doi:10.1038/pr.2017.20. https://greenmedinfo.com/article/prenatal-exposure-bpa-may-potentially-increase-risk-allergic-diseases-very-ear#comments Allergies Bisphenol Toxicity Prenatal Chemical Exposures Bisphenol A allergies Bisphenol Toxicity Increased Risk Prenatal Chemical Exposures Human Study Thu, 09 Feb 2017 01:49:22 +0000 greenmedinfo 143250 at https://greenmedinfo.com Prenatal exposures and the development of childhood wheezing illnesses. https://greenmedinfo.com/article/prenatal-exposures-and-development-childhood-wheezing-illnesses n/a PMID:  Curr Opin Allergy Clin Immunol. 2017 Apr ;17(2):110-115. PMID: 28079560 Abstract Title:  Prenatal exposures and the development of childhood wheezing illnesses. Abstract:  PURPOSE OF REVIEW: To critically evaluate and summarize studies published between July 2015 and June 2016 linking prenatal exposures and the onset of childhood wheezing illnesses and to discuss future research directions in this field. RECENT FINDINGS: The aggregated evidence indicates a consistent detrimental effect of prenatal exposure to parental smoking, outdoor air pollution, and maternal stress on childhood wheezing illnesses. Less consistent evidence suggests an adverse impact of maternal obesity during pregnancy and prenatal exposure to antibiotics on these outcomes. There is insufficient evidence to support an association between in-utero exposure to acetaminophen or prenatal levels of specific nutrients (such as vitamin D, folic acid, or polyunsaturated fatty acids) and childhood wheezing illnesses. SUMMARY: Several common potentially modifiable prenatal exposures appear to be consistently associated with childhood wheezing illnesses (e.g. parental smoking, outdoor air pollution, and maternal stress). However, the effect of many other prenatal exposures on the onset of childhood wheezing illnesses remains unclear. The existing scientific evidence from the past year does not allow us to make any new recommendations on primary prevention measures. Intervention studies will best demonstrate whether changing the prenatal environment can prevent childhood wheezing illnesses and asthma. https://greenmedinfo.com/article/prenatal-exposures-and-development-childhood-wheezing-illnesses#comments Acetaminophen (Tylenol) Toxicity Prenatal Chemical Exposures Wheezing: Infants Acetaminophen (Tylenol) Toxicity Environmental Factors Prenatal Chemical Exposures Risk Factors Wheezing: Infants Review Mon, 26 Jun 2017 20:18:19 +0000 greenmedinfo 149606 at https://greenmedinfo.com Prenatal organophosphate insecticide exposure effects infant sensory function. https://greenmedinfo.com/article/prenatal-organophosphate-insecticide-exposure-effects-infant-sensory-function n/a PMID:  Int J Hyg Environ Health. 2018 Feb 2. Epub 2018 Feb 2. PMID: 29402694 Abstract Title:  Prenatal organophosphate insecticide exposure and infant sensory function. Abstract:  BACKGROUND: Occupational studies suggest that exposure to organophosphate insecticides (OPs) can lead to vision or hearing loss. Yet the effects of early-life exposure on visual and auditory function are unknown. Here we examined associations between prenatal OP exposure and grating visual acuity (VA) and auditory brainstem response (ABR) during infancy. METHODS: 30 OPs were measured in umbilical cord blood using gas chromatography tandem mass spectrometry in a cohort of Chinese infants. Grating visual acuity (VA) (n = 179-200) and auditory brainstem response (ABR) (n = 139-183) were assessed at 6 weeks, 9 months, and 18 months. Outcomes included VA score, ABR wave V latency and central conduction time, and head circumference (HC). Associations between sensory outcomes during infancy and cord OPs were examined using linear mixed models. RESULTS: Prenatal chlorpyrifos exposure was associated with lower 9-month grating VA scores; scores were 0.64 (95% CI: -1.22, -0.06) points lower for exposed versus unexposed infants (p = 0.03). The OPs examined were not associated with infant ABR latencies, but chlorpyrifos and phorate were both significantly inversely associated with HC at 9 months; HCs were 0.41 (95% CI: 0.75, 0.6) cm and 0.44 (95% CI: 0.88, 0.1) cm smaller for chlorpyrifos (p = 0.02) and phorate (p = 0.04), respectively. CONCLUSIONS: We found deficits in grating VA and HC in 9-month-old infants with prenatal exposure to chlorpyrifos. The clinical significance of these small but statistically significant deficits is unclear. However, the disruption of visual or auditory pathway maturation in infancy could potentially negatively affect downstream cognitive development. https://greenmedinfo.com/article/prenatal-organophosphate-insecticide-exposure-effects-infant-sensory-function#comments Pesticide Toxicity Prenatal Chemical Exposures Pesticides Pesticide Toxicity pesticides Prenatal Chemical Exposures Human Study Thu, 08 Feb 2018 02:31:58 +0000 greenmedinfo 159473 at https://greenmedinfo.com The consumption of energy drinks during pregnancy and lactation has a negative impact on the newborns. https://greenmedinfo.com/article/consumption-energy-drinks-during-pregnancy-and-lactation-has-negative-impact-n n/a PMID:  Biomed Pharmacother. 2018 Mar 29 ;102:798-811. Epub 2018 Mar 29. PMID: 29605768 Abstract Title:  Perinatal exposure to energy drink induces oxidative damage in the liver, kidney and brain, and behavioral alterations in mice offspring. Abstract:  The worldwide consumption of energy drinks (EDs) has increased in recent years. EDs have several side effects and can be linked to liver injury, kidney damage and risk-seeking behavior. The impact of perinatal consumption of EDs on the newborns has not been previously investigated. In this study, we evaluated the effects of perinatal exposure to a caffeinated ED on the liver, kidney, brain, locomotor activity and anxiety in mice newborns. Pregnant mice received 2.5 or 5 ml ED by oral gavage from the first day of pregnancy until day 15 after birth. Perinatal exposure to the ED induced a significant increase in lipid peroxidation and declined antioxidant defenses in the liver, kidney, cerebrum, cerebellum and medulla oblongata of the newborns at days 21 and 35 after birth. ED induced several histological alterations, including vacuolations and lipid infiltration of hepatocytes, developing and degenerated glomeruli and dilated urinary spaces in the renal cortex, pyknosis and chromatolysis of the cerebral and medullary neurons, and degenerated and abnormal Purkinje cells in the cerebellum. In addition, ED increased the locomotion and induced anxiety-like behavior in mice newborns. In conclusion, perinatal exposure to EDs induces oxidative stress, tissue injury and behavioral alterations in the mice newborns. Therefore, the consumption of EDs during pregnancy and lactation has a negative impact on the newborns and should be treated as a significant health problem that warrants attention. https://greenmedinfo.com/article/consumption-energy-drinks-during-pregnancy-and-lactation-has-negative-impact-n#comments Prenatal Chemical Exposures Energy Drinks Energy Drinks Prenatal Chemical Exposures Transgenerational Epigenetic Modification Animal Study Tue, 10 Apr 2018 16:41:44 +0000 greenmedinfo 162408 at https://greenmedinfo.com This data provide strong evidence that prenatal acetaminophen interferes with maternal immune and endocrine adaptation to pregnancy. https://greenmedinfo.com/article/data-provide-strong-evidence-prenatal-acetaminophen-interferes-maternal-immu-0 n/a PMID:  Am J Pathol. 2015 Oct ;185(10):2805-18. Epub 2015 Aug 5. PMID: 26254283 Abstract Title:  Prenatal acetaminophen affects maternal immune and endocrine adaptation to pregnancy, induces placental damage, and impairs fetal development in mice. Abstract:  Acetaminophen (APAP; ie, Paracetamol or Tylenol) is generally self-medicated to treat fever or pain and recommended to pregnant women by their physicians. Recent epidemiological studies reveal an association between prenatal APAP use and an increased risk for asthma. Our aim was to identify the effects of APAP in pregnancy using a mouse model. Allogeneically mated C57Bl/6J females were injected i.p. with 50 or 250 mg/kg APAP or phosphate-buffered saline on gestation day 12.5; nonpregnant females served as controls. Tissue samples were obtained 1 or 4 days after injection. APAP-induced liver toxicity was mirrored by significantly increased plasma alanine aminotransferase levels. In uterus-draining lymph nodes of pregnant dams, the frequencies of mature dendritic cells and regulatory T cells significantly increased on 250 mg/kg APAP. Plasma progesterone levels significantly decreased in dams injected with APAP, accompanied by a morphologically altered placenta. Although overall litter sizes and number of fetal loss remained unaltered, a reduced fetal weight and a lower frequency of hematopoietic stem cells in the fetal liver were observed on APAP treatment. Our data provide strong evidence that prenatal APAP interferes with maternal immune and endocrine adaptation to pregnancy, affects placental function, and impairs fetal maturation and immune development. The latter may have long-lasting consequences on children's immunity and account for the increased risk for asthma observed in humans. https://greenmedinfo.com/article/data-provide-strong-evidence-prenatal-acetaminophen-interferes-maternal-immu-0#comments Acetaminophen (Tylenol) Toxicity Asthma Prenatal Chemical Exposures Acetaminophen Immunotoxic Paracetamol Acetaminophen Acetaminophen (Tylenol) Toxicity Asthma paracetamol Prenatal Chemical Exposures Animal Study Mon, 26 Jun 2017 19:14:23 +0000 greenmedinfo 149597 at https://greenmedinfo.com