Environmental Health Investigations Branch

Richmond, CA, United States

Environmental Health Investigations Branch

Richmond, CA, United States
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Hallmayer J.,Stanford University | Cleveland S.,Stanford University | Torres A.,Stanford University | Phillips J.,Stanford University | And 13 more authors.
Archives of General Psychiatry | Year: 2011

Context: Autism is considered the most heritable of neurodevelopmental disorders, mainly because of the large difference in concordance rates between monozygotic and dizygotic twins. Objective: To provide rigorous quantitative estimates of genetic heritability of autism and the effects of shared environment. Design, Setting, and Participants: Twin pairs with at least 1 twin with an autism spectrum disorder (ASD) born between 1987 and 2004were identified through the California Department of Developmental Services. Main Outcome Measures: Structured diagnostic assessments (Autism Diagnostic Interview-Revised and Autism Diagnostic Observation Schedule) were completed on 192 twin pairs. Concordance rates were calculated and parametric models were fitted for 2 definitions, 1 narrow (strict autism) and 1 broad (ASD). Results: For strict autism, probandwise concordance for male twins was 0.58 for 40 monozygotic pairs (95% confidence interval [CI], 0.42-0.74) and 0.21 for 31 dizygotic pairs (95% CI, 0.09-0.43); for female twins, the concordance was 0.60 for 7 monozygotic pairs (95% CI, 0.28-0.90) and 0.27 for 10 dizygotic pairs (95% CI, 0.09-0.69). For ASD, the probandwise concordance for male twins was 0.77 for 45 monozygotic pairs (95% CI, 0.65-0.86) and 0.31 for 45 dizygotic pairs (95% CI, 0.16-0.46); for female twins, the concordance was 0.50 for 9 monozygotic pairs (95% CI, 0.16-0.84) and 0.36 for 13 dizygotic pairs (95% CI, 0.11-0.60). A large proportion of the variance in liability can be explained by shared environmental factors (55%; 95% CI, 9%-81% for autism and 58%; 95% CI, 30%-80% for ASD) in addition to moderate genetic heritability (37%; 95% CI, 8%-84% for autism and 38%; 95% CI, 14%-67% for ASD). Conclusion: Susceptibility to ASD has moderate genetic heritability and a substantial shared twin environmental component. ©2011 American Medical Association. All rights reserved.


Hoshiko S.,Environmental Health Investigations Branch | English P.,Environmental Health Investigations Branch | Smith D.,Environmental Health Investigations Branch
International Journal of Public Health | Year: 2010

Objectives: To characterize excess mortality during a major heat wave in California and its regions; to assess the validity of a simple method. Methods: We calculated mortality rate ratios for the heatwave period, using a reference period of the same number of days from the same summer. We conducted alternative analyses and compared our results with those from a timeseries model. Results: We estimated 655 excess deaths, a 6% increase (95% confidence interval, 3-9%), impacting varied geographic/ climate regions. Alternate analyses supported model validity. Conclusions: California experienced excess heat-wave related mortality not restricted to high heat regions. As climate change is anticipated to increase heat events, public health efforts to monitor effects assume greater importance. © Birkhäuser Verlag, Basel/Switzerland 2009.


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 4 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.


Dickenson C.A.,University of California at San Francisco | Woodruff T.J.,University of California at San Francisco | Stotland N.E.,University of California at San Francisco | Dobraca D.,Environmental Health Investigations Branch | Das R.,Environmental Health Investigations Branch
American Journal of Obstetrics and Gynecology | Year: 2013

Mercury exposure during pregnancy can have serious health effects for a developing fetus including impacting the child's neurologic and cognitive development. Through biomonitoring in a low-income Latina population in California, we identified a patient with high levels of mercury and traced the source to face creams purchased in a pharmacy in Mexico. © 2013 Mosby, Inc. All rights reserved.


Wagner J.,Environmental Health Laboratory Branch | Naik-Patel K.,Centers for Disease Control and Prevention | Naik-Patel K.,Environmental Health Investigations Branch | 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.


Hoffmann T.J.,University of California at San Francisco | Windham G.C.,Environmental Health Investigations Branch | Anderson M.,Environmental Health Investigations Branch | Croen L.A.,Kaiser Permanente | And 3 more authors.
JAMA Psychiatry | Year: 2014

IMPORTANCE Few studies have examined the curtailment of reproduction (ie, stoppage) after the diagnosis of a child with autism spectrum disorder (ASD). OBJECTIVE To examine stoppage in a large, population-based cohort of families in which a child has received a diagnosis of ASD. DESIGN, SETTING, AND PARTICIPANTS Individuals with ASD born from January 1, 1990, through December 31, 2003, were identified in the California Department of Developmental Services records, which were then linked to state birth certificates to identify full sibs and half-sibs and to obtain information on birth order and demographics. A total of 19 710 case families in which the first birth occurred within the study period was identified. These families included 39 361 individuals (sibs and half-sibs). Control individuals were randomly sampled from birth certificates and matched 2:1 to cases by sex, birth year, and maternal age, self-reported race/ethnicity, and county of birth after removal of children receiving services from the California Department of Developmental Services. Using similar linkagemethods as for case families, 36 215 pure control families (including 75 724 total individuals) were identified that had no individuals with an ASD diagnosis. EXPOSURES History of affected children. MAIN OUTCOMES AND MEASURES Stoppagewas investigated by comparing the reproductive behaviors of parents after the birth of a child with ASD vs an unaffected child using a survival analysis framework for time to next birth and adjusting for demographic variables. RESULTS For the first few years after the birth of a child with ASD, the parents' reproductive behavior was similar to that of control parents. However, birth rates differed in subsequent years; overall, families whose first child had ASD had a second child at a rate of 0.668 (95% CI, 0.635-0.701) that of control families, adjusted for birth year, birth weight, maternal age, and self-reported maternal race/ethnicity. Results were similar when a later-born child was the first affected child in the family. Reproductive curtailment was slightly stronger among women who changed partners (relative rate for second-born children, 0.553 [95%CI, 0.498-0.614]). CONCLUSIONS AND RELEVANCE These results provide the first quantitative assessment and convincing statistical evidence of reproductive stoppage related to ASD. These findings have implications for recurrence risk estimation and genetic counseling. Copyright © 2014 American Medical Association. All rights reserved.


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..


Hoshiko S.,Environmental Health Investigations Branch | Smith D.,Environmental Health Investigations Branch | Fan C.,Environmental Health Investigations Branch | Jones C.R.,Environmental Health Investigations Branch | And 2 more authors.
Pediatric Radiology | Year: 2014

Background: Radiation exposure from medical sources now equals or exceeds that from natural background sources, largely attributable to a 20-fold increase in CT use since 1980. Increasing exposure to children and fetuses is of most concern due to their heightened susceptibility. More recently, CT use may be leveling or decreasing, but it is unclear whether this change is widespread or varies by type of institution. Objective: We sought to characterize trends in CT utilization in California hospitals and emergency departments among children and pregnant women, looking at different types of facilities, such as teaching, private, public and nonprofit institutions. Materials and methods: We examined frequency of CT examinations by year from 229 facilities reporting CT usage in routinely collected California statewide data for 2005–2012. We modeled trends overall and by facility type. Results: CT scans for pediatric and pregnant patient visits in the emergency department increased initially, then started to decline after 2008. Among hospital admissions, rates declined or leveled after 2005. In the emergency department, CT rates varied between types of facilities, with teaching hospitals reducing use sooner and more sharply than other types of facilities. Conclusion: CT utilization in California among children and pregnant women has begun to level or decline. Still, population exposure remains at historically high levels, warranting consideration of potential public health implications. Further examination of reasons for trends among hospital types, particularly how teaching hospitals have reduced rates of CT utilization, may help identify strategies for CT reduction without compromising patient care. © 2014, Springer-Verlag Berlin Heidelberg.


Hoshiko S.,Environmental Health Investigations Branch | Grether J.K.,Environmental Health Investigations Branch | Windham G.C.,Environmental Health Investigations Branch | Smith D.,Environmental Health Investigations Branch | Fessel K.,Environmental Health Investigations Branch
Autism Research | Year: 2011

Thyroid hormones substantially influence central nervous system development during gestation. We hypothesized that perturbations of early thyroid profiles may contribute to the development of autism spectrum disorders (ASD). Thyroid pathways could provide a mechanism by which environmental factors that affect the thyroid system may impact autism occurrence or phenotypic expression. We investigated whether thyroxine (T4) levels at birth are associated with subsequent ASD, using two existing California study groups in multivariate analysis. One study group included children born in the San Francisco Bay Area in 1994, with cases identified through the California Department of Developmental Services (DDS) and/or the Kaiser Permanente Medical Care Program of Northern California (244 cases, 266 controls); the other included children born in California in 1995, with cases identified through DDS (310 cases, 518 controls). Matched controls were selected from birth certificate records. This exploratory analysis suggested that infants with very low T4 (<3rd percentile) may have higher ASD risk, although results reached statistical significance only for the 1995 study group (1995: OR = 2.74 (95% CI 1.30-5.75; 1994: OR = 1.71 (95% CI 0.57-5.19). A variety of alternate analyses were conducted with available data, without further resolution of the difference between the two study groups. The results of our study indicate that further studies are warranted to investigate whether thyroid hormone perturbations play a role in the development of ASD by evaluating additional potential confounders and genotype or phenotype in larger studies. © 2011, International Society for Autism Research, Wiley-Liss, Inc.

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