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Prenatal mercury exposure and features of autism: a prospective population study / J. GOLDING in Molecular Autism, 9 (2018)
[article]
Titre : Prenatal mercury exposure and features of autism: a prospective population study Type de document : Texte imprimé et/ou numérique Auteurs : J. GOLDING, Auteur ; D. RAI, Auteur ; S. GREGORY, Auteur ; G. ELLIS, Auteur ; A. EMOND, Auteur ; Y. ILES-CAVEN, Auteur ; J. HIBBELN, Auteur ; C. TAYLOR, Auteur Article en page(s) : 30p. Langues : Anglais (eng) Mots-clés : Adult Autistic Disorder/epidemiology Child Female Fish Products/standards Food Contamination Humans Male Maternal Nutritional Physiological Phenomena Mercury/blood Pregnancy Prenatal Exposure Delayed Effects/epidemiology alspac Autism Autistic traits Dental amalgam Fish consumption Prenatal mercury Social cognition Index. décimale : PER Périodiques Résumé : Background: Mercury (Hg) has been suspected of causing autism in the past, especially a suspected link with vaccinations containing thiomersal, but a review of the literature shows that has been largely repudiated. Of more significant burden is the total quantity of Hg in the environment. Here, we have used the Avon Longitudinal Study of Parents and Children (ALSPAC) to test whether prenatal exposure from total maternal blood Hg in the first half of pregnancy is associated with the risk of autism or of extreme levels of autistic traits. This is the largest longitudinal study to date to have tested this hypothesis and the only one to have considered early pregnancy. Methods: We have used three strategies: (1) direct comparison of 45 pregnancies resulting in children with diagnosed autism from a population of 3840, (2) comparison of high scores on each of the four autistic traits within the population at risk (n~2800), and (3) indirect measures of association of these outcomes with proxies for increased Hg levels such as frequency of fish consumption and exposure to dental amalgam (n > 8000). Logistic regression adjusted for social conditions including maternal age, housing circumstances, maternal education, and parity. Interactions were tested between risks to offspring of fish and non-fish eaters. Results: There was no suggestion of an adverse effect of total prenatal blood Hg levels on diagnosed autism (AOR 0.89; 95% CI 0.65, 1.22) per SD of Hg (P = 0.485). The only indication of adverse effects concerned a measure of poor social cognition when the mother ate no fish, where the AOR was 1.63 [95% CI 1.02, 2.62] per SD of Hg (P = 0.041), significantly different from the association among the offspring of fish-eaters (AOR = 0.74 [95% CI 0.41, 1.35]). Conclusion: In conclusion, our study identifies no adverse effect of prenatal total blood Hg on autism or autistic traits provided the mother ate fish. Although these results should be confirmed in other populations, accumulating evidence substantiates the recommendation to eat fish during pregnancy. En ligne : https://dx.doi.org/10.1186/s13229-018-0215-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=371
in Molecular Autism > 9 (2018) . - 30p.[article] Prenatal mercury exposure and features of autism: a prospective population study [Texte imprimé et/ou numérique] / J. GOLDING, Auteur ; D. RAI, Auteur ; S. GREGORY, Auteur ; G. ELLIS, Auteur ; A. EMOND, Auteur ; Y. ILES-CAVEN, Auteur ; J. HIBBELN, Auteur ; C. TAYLOR, Auteur . - 30p.
Langues : Anglais (eng)
in Molecular Autism > 9 (2018) . - 30p.
Mots-clés : Adult Autistic Disorder/epidemiology Child Female Fish Products/standards Food Contamination Humans Male Maternal Nutritional Physiological Phenomena Mercury/blood Pregnancy Prenatal Exposure Delayed Effects/epidemiology alspac Autism Autistic traits Dental amalgam Fish consumption Prenatal mercury Social cognition Index. décimale : PER Périodiques Résumé : Background: Mercury (Hg) has been suspected of causing autism in the past, especially a suspected link with vaccinations containing thiomersal, but a review of the literature shows that has been largely repudiated. Of more significant burden is the total quantity of Hg in the environment. Here, we have used the Avon Longitudinal Study of Parents and Children (ALSPAC) to test whether prenatal exposure from total maternal blood Hg in the first half of pregnancy is associated with the risk of autism or of extreme levels of autistic traits. This is the largest longitudinal study to date to have tested this hypothesis and the only one to have considered early pregnancy. Methods: We have used three strategies: (1) direct comparison of 45 pregnancies resulting in children with diagnosed autism from a population of 3840, (2) comparison of high scores on each of the four autistic traits within the population at risk (n~2800), and (3) indirect measures of association of these outcomes with proxies for increased Hg levels such as frequency of fish consumption and exposure to dental amalgam (n > 8000). Logistic regression adjusted for social conditions including maternal age, housing circumstances, maternal education, and parity. Interactions were tested between risks to offspring of fish and non-fish eaters. Results: There was no suggestion of an adverse effect of total prenatal blood Hg levels on diagnosed autism (AOR 0.89; 95% CI 0.65, 1.22) per SD of Hg (P = 0.485). The only indication of adverse effects concerned a measure of poor social cognition when the mother ate no fish, where the AOR was 1.63 [95% CI 1.02, 2.62] per SD of Hg (P = 0.041), significantly different from the association among the offspring of fish-eaters (AOR = 0.74 [95% CI 0.41, 1.35]). Conclusion: In conclusion, our study identifies no adverse effect of prenatal total blood Hg on autism or autistic traits provided the mother ate fish. Although these results should be confirmed in other populations, accumulating evidence substantiates the recommendation to eat fish during pregnancy. En ligne : https://dx.doi.org/10.1186/s13229-018-0215-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=371 A biomarker-based study of prenatal smoking exposure and autism in a Finnish national birth cohort / K. CHESLACK-POSTAVA in Autism Research, 14-11 (November 2021)
[article]
Titre : A biomarker-based study of prenatal smoking exposure and autism in a Finnish national birth cohort Type de document : Texte imprimé et/ou numérique Auteurs : K. CHESLACK-POSTAVA, Auteur ; A. SOURANDER, Auteur ; S. HINKKA-YLI-SALOMÄKI, Auteur ; I. W. MCKEAGUE, Auteur ; H. M. SURCEL, Auteur ; A. S. BROWN, Auteur Article en page(s) : p.2444-2453 Langues : Anglais (eng) Mots-clés : Autism Spectrum Disorder Autistic Disorder Biomarkers Case-Control Studies Child Female Finland/epidemiology Humans Maternal Exposure Pregnancy Prenatal Exposure Delayed Effects/epidemiology Smoking autism cotinine prenatal exposure delayed effects smoking Index. décimale : PER Périodiques Résumé : Maternal exposure to tobacco smoke during pregnancy is a common and persistent exposure linked to adverse neurodevelopmental outcomes in the offspring. However, previous studies provide mixed evidence regarding the relationship between prenatal smoking and offspring autism. This study used cotinine level, a biomarker for nicotine, to investigate the relationship between prenatal smoking and autism. The authors conducted a population-based case-control study nested in a national cohort of all births in Finland from 1987 to 2005. Cases diagnosed with childhood autism (ICD-10/9 code F84.0/299.0) through 2007 were identified using data from linked national registers. Each case was matched with a control on date of birth (±30?days), sex, and place of birth (N =?962 pairs). Maternal serum cotinine levels were prospectively measured in first- to early second-trimester serum samples archived in a national biobank using a quantitative immunoassay. Data were analyzed using conditional logistic regression. Prenatal maternal levels of serum cotinine were not associated with the odds of autism, whether cotinine was classified continuously, by deciles, or using previously defined categories corresponding to probable maternal smoking status. After adjusting for maternal age, paternal age, previous births, and any history of parental psychiatric disorder, the odds ratio for categorical high versus low cotinine, using a 3-level exposure variable, was 0.98 (95% CI = 0.76, 1.26; p = 0.88). In conclusion, this national birth cohort-based study does not provide evidence for an association between maternal cotinine, a biomarker of maternal smoking, and risk of autism. LAY SUMMARY: This study explored whether prenatal exposure to tobacco smoke in mothers is related to the diagnosis of autism in their children, by measuring the levels of cotinine, a biomarker for tobacco exposure, in stored serum samples drawn from mothers during pregnancy. The levels of cotinine in the mothers of children diagnosed with autism were similar to those in the mothers of control children of similar age and gender distribution. En ligne : http://dx.doi.org/10.1002/aur.2608 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=450
in Autism Research > 14-11 (November 2021) . - p.2444-2453[article] A biomarker-based study of prenatal smoking exposure and autism in a Finnish national birth cohort [Texte imprimé et/ou numérique] / K. CHESLACK-POSTAVA, Auteur ; A. SOURANDER, Auteur ; S. HINKKA-YLI-SALOMÄKI, Auteur ; I. W. MCKEAGUE, Auteur ; H. M. SURCEL, Auteur ; A. S. BROWN, Auteur . - p.2444-2453.
Langues : Anglais (eng)
in Autism Research > 14-11 (November 2021) . - p.2444-2453
Mots-clés : Autism Spectrum Disorder Autistic Disorder Biomarkers Case-Control Studies Child Female Finland/epidemiology Humans Maternal Exposure Pregnancy Prenatal Exposure Delayed Effects/epidemiology Smoking autism cotinine prenatal exposure delayed effects smoking Index. décimale : PER Périodiques Résumé : Maternal exposure to tobacco smoke during pregnancy is a common and persistent exposure linked to adverse neurodevelopmental outcomes in the offspring. However, previous studies provide mixed evidence regarding the relationship between prenatal smoking and offspring autism. This study used cotinine level, a biomarker for nicotine, to investigate the relationship between prenatal smoking and autism. The authors conducted a population-based case-control study nested in a national cohort of all births in Finland from 1987 to 2005. Cases diagnosed with childhood autism (ICD-10/9 code F84.0/299.0) through 2007 were identified using data from linked national registers. Each case was matched with a control on date of birth (±30?days), sex, and place of birth (N =?962 pairs). Maternal serum cotinine levels were prospectively measured in first- to early second-trimester serum samples archived in a national biobank using a quantitative immunoassay. Data were analyzed using conditional logistic regression. Prenatal maternal levels of serum cotinine were not associated with the odds of autism, whether cotinine was classified continuously, by deciles, or using previously defined categories corresponding to probable maternal smoking status. After adjusting for maternal age, paternal age, previous births, and any history of parental psychiatric disorder, the odds ratio for categorical high versus low cotinine, using a 3-level exposure variable, was 0.98 (95% CI = 0.76, 1.26; p = 0.88). In conclusion, this national birth cohort-based study does not provide evidence for an association between maternal cotinine, a biomarker of maternal smoking, and risk of autism. LAY SUMMARY: This study explored whether prenatal exposure to tobacco smoke in mothers is related to the diagnosis of autism in their children, by measuring the levels of cotinine, a biomarker for tobacco exposure, in stored serum samples drawn from mothers during pregnancy. The levels of cotinine in the mothers of children diagnosed with autism were similar to those in the mothers of control children of similar age and gender distribution. En ligne : http://dx.doi.org/10.1002/aur.2608 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=450 Prenatal maternal infection and risk for autism in offspring: A meta-analysis / N. TIOLECO in Autism Research, 14-6 (June 2021)
[article]
Titre : Prenatal maternal infection and risk for autism in offspring: A meta-analysis Type de document : Texte imprimé et/ou numérique Auteurs : N. TIOLECO, Auteur ; A. E. SILBERMAN, Auteur ; K. STRATIGOS, Auteur ; Sharmila BANERJEE-BASU, Auteur ; M. N. SPANN, Auteur ; A. H. WHITAKER, Auteur ; J. Blake TURNER, Auteur Article en page(s) : p.1296-1316 Langues : Anglais (eng) Mots-clés : Autism Spectrum Disorder Autistic Disorder/epidemiology Causality Female Humans Pregnancy Pregnancy Complications Prenatal Exposure Delayed Effects/epidemiology Risk Factors autism infections pregnancy prenatal risk factors Index. décimale : PER Périodiques Résumé : While prenatal maternal infection has received attention as a preventable and treatable risk factor for autism, findings have been inconsistent. This paper presents the results of a meta-analysis to determine whether the weight of the evidence supports such an association. Studies with a categorical diagnosis of autism as the outcome and an assessment of its association with prenatal maternal infection or fever (or the data necessary to compute this association) were included. A total of 36 studies met these criteria. Two independent reviewers extracted data on study design, methods of assessment, type of infectious agent, site of infection, trimester of exposure, definition of autism, and effect size. Analyses demonstrated a statistically significant association of maternal infection/fever with autism in offspring (OR = 1.32; 95% CI = 1.20-1.46). Adjustment for evident publication bias slightly weakened this association. There was little variation in effect sizes across agent or site of infection. Small differences across trimester of exposure were not statistically significant. There was some evidence that recall bias associated with status on the outcome variable leads to differential misclassification of exposure status. Nonetheless, the overall association is only modestly reduced when studies potentially contaminated by such bias are removed. Although causality has not been firmly established, these findings suggest maternal infection during pregnancy confers an increase in risk for autism in offspring. Given the prevalence of this risk factor, it is possible that the incidence of autism would be reduced by 12%-17% if maternal infections could be prevented or safely treated in a timely manner. LAY SUMMARY: This study is a meta-analysis of the association of maternal infection during pregnancy and subsequent autism in offspring. In combining the results from 36 studies of this association we find that a significant relationship is present. The association does not vary much across the types of infections or when they occur during pregnancy. We conclude that the incidence of autism could be substantially reduced if maternal infections could be prevented or safely treated in a timely manner. En ligne : http://dx.doi.org/10.1002/aur.2499 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=449
in Autism Research > 14-6 (June 2021) . - p.1296-1316[article] Prenatal maternal infection and risk for autism in offspring: A meta-analysis [Texte imprimé et/ou numérique] / N. TIOLECO, Auteur ; A. E. SILBERMAN, Auteur ; K. STRATIGOS, Auteur ; Sharmila BANERJEE-BASU, Auteur ; M. N. SPANN, Auteur ; A. H. WHITAKER, Auteur ; J. Blake TURNER, Auteur . - p.1296-1316.
Langues : Anglais (eng)
in Autism Research > 14-6 (June 2021) . - p.1296-1316
Mots-clés : Autism Spectrum Disorder Autistic Disorder/epidemiology Causality Female Humans Pregnancy Pregnancy Complications Prenatal Exposure Delayed Effects/epidemiology Risk Factors autism infections pregnancy prenatal risk factors Index. décimale : PER Périodiques Résumé : While prenatal maternal infection has received attention as a preventable and treatable risk factor for autism, findings have been inconsistent. This paper presents the results of a meta-analysis to determine whether the weight of the evidence supports such an association. Studies with a categorical diagnosis of autism as the outcome and an assessment of its association with prenatal maternal infection or fever (or the data necessary to compute this association) were included. A total of 36 studies met these criteria. Two independent reviewers extracted data on study design, methods of assessment, type of infectious agent, site of infection, trimester of exposure, definition of autism, and effect size. Analyses demonstrated a statistically significant association of maternal infection/fever with autism in offspring (OR = 1.32; 95% CI = 1.20-1.46). Adjustment for evident publication bias slightly weakened this association. There was little variation in effect sizes across agent or site of infection. Small differences across trimester of exposure were not statistically significant. There was some evidence that recall bias associated with status on the outcome variable leads to differential misclassification of exposure status. Nonetheless, the overall association is only modestly reduced when studies potentially contaminated by such bias are removed. Although causality has not been firmly established, these findings suggest maternal infection during pregnancy confers an increase in risk for autism in offspring. Given the prevalence of this risk factor, it is possible that the incidence of autism would be reduced by 12%-17% if maternal infections could be prevented or safely treated in a timely manner. LAY SUMMARY: This study is a meta-analysis of the association of maternal infection during pregnancy and subsequent autism in offspring. In combining the results from 36 studies of this association we find that a significant relationship is present. The association does not vary much across the types of infections or when they occur during pregnancy. We conclude that the incidence of autism could be substantially reduced if maternal infections could be prevented or safely treated in a timely manner. En ligne : http://dx.doi.org/10.1002/aur.2499 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=449