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Croen L.A.,Kaiser Permanente | Grether J.K.,Environmental Health Investigations Branch | Yoshida C.K.,Kaiser Permanente | Odouli R.,Kaiser Permanente | Hendrick V.,University of California at Los Angeles
Archives of General Psychiatry | Year: 2011

Context: The prevalence of autism spectrum disorders (ASDs) has increased over recent years. Use of antidepressant medications during pregnancy also shows a secular increase in recent decades, prompting concerns that prenatal exposure may contribute to increased risk of ASD. Objective: To systematically evaluate whether prenatal exposure to antidepressant medications is associated with increased risk of ASD. Design: Population-based case-control study. Medical records were used to ascertain case children and control children and to derive prospectively recorded information on mothers' use of antidepressant medications, mental health history of mothers, and demographic and medical covariates. Setting: The Kaiser Permanente Medical Care Program in Northern California. Participants: A total of 298 case children with ASD (and their mothers) and 1507 randomly selected control children (and their mothers) drawn from the membership of theKaiser Permanente Medical Care Program in Northern California. Main Outcome Measures: ASDs. Results: Prenatal exposure to antidepressant medications was reported for 20 case children (6.7%) and 50 control children (3.3%). In adjusted logistic regression models, we found a 2-fold increased risk of ASD associated with treatment with selective serotonin reuptake inhibitors by the mother during the year before delivery (adjusted odds ratio, 2.2 [95% confidence interval, 1.2-4.3]), with the strongest effect associated with treatment during the first trimester (adjusted odds ratio, 3.8 [95% confidence interval, 1.8-7.8]). No increase in risk was found for mothers with a history of mental health treatment in the absence of prenatal exposure to selective serotonin reuptake inhibitors. Conclusion: Although the number of children exposed prenatally to selective serotonin reuptake inhibitors in this population was low, results suggest that exposure, especially during the first trimester, may modestly increase the risk of ASD. The potential risk associated with exposure must be balanced with the risk to the mother or fetus of untreated mental health disorders. Further studies are needed to replicate and extend these findings. ©2011 American Medical Association. All rights reserved.

Salinas D.B.,University of Southern California | Sosnay P.R.,Johns Hopkins University | Azen C.,Clinical Translational Science Institute | Young S.,The Sequoia Foundation | And 3 more authors.
Journal of Cystic Fibrosis | Year: 2015

Background: The Clinical and Functional Translation of CFTR project (CFTR2) classified some cystic fibrosis transmembrane conductance regulator (. CFTR) gene variants as non-cystic fibrosis (CF)-causing. To evaluate this, the clinical status of children carrying these mutations was examined. Methods: We analyzed CF disease-defining variables over 2-6 years in two groups of California CF screen- positive neonates born from 2007 to 2011: (1) children with two CF-causing variants and (2) children with one CF-causing and one non-CF-causing variant, as defined by CFTR2. Results: Children carrying non-CF-causing variants had significantly higher birth weight, lower immunoreactive trypsinogen and sweat chloride values, higher first year growth curves, and a lower rate of persistent Pseudomonas aeruginosa colonization compared to children with two CF-causing variants. Conclusions: The outcomes in children 2-6 years of age with the L997F, G576A, R1162L, V754M, R668C, R31C, and S1235R variants are consistent with the CFTR2 non-CF-causing classification. © 2015 European Cystic Fibrosis Society..

Zerbo O.,Kaiser Permanente | Yoshida C.,Kaiser Permanente | Grether J.K.,Kaiser Permanente | Van de Water J.,University of California at Davis | And 5 more authors.
Journal of Neuroinflammation | Year: 2014

Background: Biologic markers of infection and inflammation have been associated with Autism Spectrum Disorders (ASD) but prior studies have largely relied on specimens taken after clinical diagnosis. Research on potential biologic markers early in neurodevelopment is required to evaluate possible causal pathways and screening profiles.Objective: To investigate levels of cytokines and chemokines in newborn blood specimens as possible early biologic markers for autism.Methods: We conducted a population-based case-control study nested within the cohort of infants born from July 2000 to September 2001 to women who participated in the prenatal screening program in Orange County, California, USA. The study population included children ascertained from the California Department of Developmental Services with Autism Spectrum Disorder (ASD, n = 84), or developmental delay but not ASD (DD, n = 49), and general population controls randomly sampled from the birth certificate files and frequency matched to ASD cases on sex, birth month and birth year (GP, n = 159). Cytokine and chemokine concentrations were measured in archived neonatal blood specimens collected for routine newborn screening.Results: Cytokines were not detected in the vast majority of newborn samples regardless of case or control status. However, the chemokine monocyte chemotactic protein-1 (MCP-1) was elevated and the chemokine Regulated upon Activation Normal T-Cell Expressed and Secreted (RANTES) was decreased in ASD cases compared to GP controls. The chemokines macrophage inflammatory protein-1alpha (MIP-1α) and RANTES were decreased in children with DD compared to GP controls.Conclusion: Measurement of immune system function in the first few days of life may aid in the early identification of abnormal neurodevelopment and shed light on the biologic mechanisms underlying normal neurodevelopment. © 2014 Zerbo et al.; licensee BioMed Central Ltd.

Goines P.E.,University of California at Davis | Croen L.A.,Kaiser Permanente | Braunschweig D.,University of California at Davis | Yoshida C.K.,Kaiser Permanente | And 5 more authors.
Molecular Autism | Year: 2011

Background: Immune anomalies have been documented in individuals with autism spectrum disorders (ASDs) and their family members. It is unknown whether the maternal immune profile during pregnancy is associated with the risk of bearing a child with ASD or other neurodevelopmental disorders. Methods. Using Luminex technology, levels of 17 cytokines and chemokines were measured in banked serum collected from women at 15 to 19 weeks of gestation who gave birth to a child ultimately diagnosed with (1) ASD (n = 84), (2) a developmental delay (DD) but not autism (n = 49) or (3) no known developmental disability (general population (GP); n = 159). ASD and DD risk associated with maternal cytokine and chemokine levels was estimated by using multivariable logistic regression analysis. Results: Elevated concentrations of IFN-, IL-4 and IL-5 in midgestation maternal serum were significantly associated with a 50% increased risk of ASD, regardless of ASD onset type and the presence of intellectual disability. By contrast, elevated concentrations of IL-2, IL-4 and IL-6 were significantly associated with an increased risk of DD without autism. Conclusion: The profile of elevated serum IFN-, IL-4 and IL-5 was more common in women who gave birth to a child subsequently diagnosed with ASD. An alternative profile of increased IL-2, IL-4 and IL-6 was more common for women who gave birth to a child subsequently diagnosed with DD without autism. Further investigation is needed to characterize the relationship between these divergent maternal immunological phenotypes and to evaluate their effect on neurodevelopment. © 2011 Goines et al; licensee BioMed Central Ltd.

Wagner J.,Environmental Health Laboratory Branch | Naik-Patel K.,Centers for Disease Control and Prevention | Wall S.,Environmental Health Laboratory Branch | Harnly M.,Environmental Health Investigations Branch
Atmospheric Environment | Year: 2012

Computer-controlled scanning electron microscopy and energy-dispersive X-ray spectroscopy were used to obtain ambient PM mass concentrations, elemental size distributions, morphologies, and particle types during four Bermuda grass burn events in Imperial Valley, California. Passive PM samplers were deployed to three to six locations surrounding each burn for durations of 24-120 h. Average PM 2.5 and PM 10 levels were modestly but significantly higher at locations less than 3.2 km (two miles) from the nearest burn (n = 37). During one monitored burn, higher winds caused an intense ground-level plume to envelop two samplers mounted on telephone poles very close to the field. For this event, 24-h PM 2.5 exposures downwind were up to 17 times higher than that measured upwind. Particles were classified into five distinct chemical types consistent with local area sources. Burn-related particle types, primarily submicron carbonaceous particles, contributed 95% of the PM 2.5 in the location directly impacted by the ground-level plume, compared to only 12% in the upwind location. Downwind PM 10-2.5 particles were enriched in potassium, phosphorus, chlorine, calcium, silicon, and sulfur, consistent with analyses of bulk and partially-burned Bermuda grass. The accuracy and precision of passive sampler PM measurements were all within 4 μg m -3, though low median values caused high percent differences for PM 2.5. The use of electron microscopy and passive sampling in this study enabled detailed PM characterizations, spatial comparisons, and rapid deployment in often dynamic sampling scenarios. © 2012 Elsevier Ltd.

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