2015 Progress Report: CHAMACOS Cohort Project: Pesticides and PBDE on Neurobehavior and Puberty

EPA Grant Number: R834513C001
Subproject: this is subproject number 001 , established and managed by the Center Director under grant R834513
(EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).

Center: Center for the Health Assessment of Mothers and Children of Salinas - UC Berkeley School of Public Health: CHAMACOS Office, Berkeley, CA
Center Director: Eskenazi, Brenda
Title: CHAMACOS Cohort Project: Pesticides and PBDE on Neurobehavior and Puberty
Investigators: Eskenazi, Brenda , Arora, Manish , Bradman, Asa , Chevrier, Jonathan , Harley, Kim , Holland, Nina T. , Johnson, Caroline , Lustig, Robert , Sjodin, Andreas , Smith, Donald
Institution: University of California - Berkeley , Centers for Disease Control and Prevention , Mount Sinai School of Medicine , University of California - San Francisco , University of California - Santa Cruz
EPA Project Officer: Louie, Nica
Project Period: August 1, 2009 through July 31, 2014 (Extended to July 31, 2016)
Project Period Covered by this Report: June 1, 2014 through May 31,2015
RFA: Children's Environmental Health and Disease Prevention Research Centers (with NIEHS) (2009) RFA Text |  Recipients Lists
Research Category: Children's Health , Health

Objective:

In Project A, we are examining the association of DDT, Mn, and PBDEs with neurodevelopment and onset of puberty in boys in the CHAMACOS cohort. This study directly addresses worldwide concerns that changes in onset of sexual maturation may be related to endocrine disruptors in the environment and fills a large data gap in research for boys. It also addresses concerns that exposure to DDT/E, PBDEs, and Mn may compromise neurodevelopment.

Progress Summary:

1. To maintain and expand the CHAMACOS cohort as children begin the critical transition to puberty, assessing neurodevelopment and pubertal development in 300 boys from 9 to 13 years of age.

We have successfully met our goal of expanding the CHAMACOS cohort to 300 boys. We assessed 326 boys at age 9 years, 310 boys at age 10½, and 304 boys at age 12. To date, we have assessed 225 boys at the final visit point of this project, age 12¾, and plan to assess an additional 40 boys by the end of this visit point in late July.

2. To determine whether prenatal and childhood exposure to DDT/E, PBDEs, and Mn are associated with neurobehavioral functioning at age 9, 10½, and 12 years.

Note: This Center grant includes the follow-up of boys only. We received an NIEHS grant (ES017054) to assess the girls in the CHAMACOS cohort. To increase statistical power we have combined boys and girls from the CHAMACOS cohort for all analyses of neurobehavioral functioning, though we have assessed for heterogeneous associations by sex 1 (i.e., interaction). For both DDT/E and PBDEs, measured maternal pregnancy serum concentrations were used as the exposure variable for the majority of CHAM1 participants (i.e., members of the original CHAMACOS cohort followed since pregnancy), while back-extrapolated pregnancy concentrations were used for all CHAM2 participants (i.e., members of the CHAMACOS cohort enrolled at child age 9) as well as for CHAM1 participants who were missing pregnancy or delivery serum samples. Prenatal concentrations were back-extrapolated from DDT/E and/or PBDE levels measured in maternal serum collected when the child was 9 years old using the SuperLearner algorithm, which is an ensemble machine learning technique that uses the weighted combination of algorithms to return a prediction function that minimizes the cross-validated mean squared error (see Project B). In validation models, which used maternal serum concentrations to back-extrapolate values in women for whom measured pregnancy values were also available, the model R2 for models comparing extrapolated and measured values was 0.95 for both p,p’-DDT and p,p’-DDE, and ranged from 0.58-0.84 for the four highest detected PBDE congeners in this population (PBDE-47, 99, 100, 153; see Verner, et al., 2015).

DDT/E: Generalized estimating equation (GEE) models and multivariable linear models were used to test relationships between prenatal p,p’-DDT/E and children’s WISC full scale IQ as well as four composite scales (verbal comprehension, perceptual reasoning, working memory, and processing speed. In sex-combined analyses, GEE models revealed significant inverse associations between DDT/E and processing speed scores only, though separate linear models by age indicated that this association was present at 7 but not 10½ years of age. Our analyses suggest heterogeneous associations by sex, with girls exhibiting more negative associations between in utero DDT/E exposure and age 7 outcomes in particular. At age 10½, however, boys but not girls exhibited borderline-significant inverse associations between in utero DDT/E exposure and working memory scores. A manuscript by Gaspar, et al., regarding associations between prenatal p,p’-DDT/E serum concentrations and children’s Wechsler Intelligence Scales for Children-IV (WISC) scores at ages 7 and 10½ is undergoing minor revisions for publication in the journal Environment International.

PBDEs: GEE models and multivariable linear models were used to test relationships between prenatal and childhood concentrations of the sum of four congeners (PBDE-47, 99, 100, 153) and multiple indicators of attention and executive functioning. Key attention indicators included the Conners’ Continuous Performance Test (CPT), completed by children at ages 9 and 12, the WISC processing speed scale, completed by children at age 10½, and the Conners’ ADHD/DSM-IV Scales (CADS), completed by parents at child ages 9 and 12. Key executive function indicators included, but were not limited to, the Wisconsin Card Sort Task (WCST), completed by children at ages 9 and 12, the WISC working memory scale, completed by children at age 10½, and the Behavior Rating Inventory of Executive Function, completed by parents at child ages 9 and 12.

Attention GEE analyses showed borderline-significant adverse associations between prenatal PBDE concentrations and parent-reported (CADS) attention problems, as well as significant increase in CPT hit rate standard error across blocks, indicating a shortcoming in maintaining attention and consistent responding over the duration of a low-interest task. Linear models by age indicated that parent-report (CADS) associations were present at age 9 but not 12, whereas CPT associations were relatively consistent at both time points. Linear models also showed a statistically significant adverse association between prenatal PBDE concentrations and WISC processing speed scores at age 10½ (β:-4.2; 95% CI:-7.1,-1.3). Executive function GEE models showed adverse associations between prenatal PBDE concentrations and parent-reported (BRIEF) executive function problems, as well as increased errors on the WCST. Associations were more pronounced in the subset of participants with measured prenatal PBDE serum concentrations than in the full sample which included back extrapolated values. In the subset with measured PBDE values, statistically significant associations were seen for parent-reported emotional control and working memory subscales of the BRIEF, as well as for perseverative and overall errors on the WCST. Linear models by age indicated that parent-report (BRIEF) associations were present at age 9 but absent or attenuated at age 12, whereas WCST associations were relatively consistent at both time points. WISC working memory at age 10½ and other indicators of executive functioning were not associated with PBDE concentrations. Though child age 9 PBDE concentrations were not associated with attention or executive function measures in any sex-combined models, there was evidence of differential associations of child age 9 PBDE concentrations with parent reported attention (CADS) and executive function (BRIEF) problems by child sex, with more adverse associations seen for girls than for boys. Prenatal PBDE models showed little evidence of interaction by sex. A manuscript by Sagiv, et al., regarding associations between prenatal and child age 9 PBDE serum concentrations and children’s attention and executive functioning between ages 9 and 12 has been accepted pending minor revisions with the journal Neurotoxicology and Teratology.

Mn: As described in previous progress reports and publications (e.g., Gunier, et al., 2013), Mn was measured in dentine from children’s shed teeth, with the neonatal line used to distinguish prenatal (~13-16 weeks gestation through delivery) from early postnatal exposure (birth- ~10-11 months old). In Project A, GEE models and multivariable linear models were used to test relationships between prenatal and early postnatal Mn exposure and neurobehavioral, cognitive, memory, and motor tests. Key behavior and attention indicators included teacher-report CADs at age 7 and parent-report CADs at ages 7 and 9; teacher-report Behavior Assessment System for Children (BASC) scores at age 7, parent-report BASC at ages 7 and 10½, and youth self report BASC at age 10½; and child CPT scores at age 9. Cognition indicators included WISC full scale IQ and subscale scores from ages 7 and 10½. Memory indicators included the NEPSY-II Memory for Designs test completed at age 9 and the Children’s Auditory Verbal Learning Test, 2nd edition (CAVLT-2) completed at age 10½. Motor indicators included finger tapping and pegboard tasks completed at age 7, plus select subtests of the Luria Nebraska Motor Battery completed at ages 9 and 10½.

Results of these analyses suggested heterogeneous exposure-outcome associations by sex. With regards to behavior/attention measures, prenatal Mn exposure showed adverse associations with maternally-reported internalizing, externalizing, and hyperactivity problems at age 10½ for boys but not girls, whereas postnatal Mn exposure was associated with these outcomes for both boys and girls. Cognition, memory, and motor analyses indicated positive associations between both prenatal and postnatal Mn exposure for performance outcomes in boys, that is, improved performance as a function of Mn exposure; by contrast, girls tended to show null associations between either prenatal or postnatal Mn exposure and performance in these domains. For cognitive and memory measures, an interaction between prenatal Mn and prenatal lead levels was also detected. Children of mothers with above-median (≥ 0.8 µg/dL) prenatal lead levels demonstrated poorer performance in these domains as a function of increasing prenatal Mn exposure.

A manuscript by Mora, et al., regarding associations between prenatal and early postnatal Mn exposure and children’s behavior/attention, cognition, memory, and motor functioning at ages 7, 9, and/or 10½ years has been accepted pending minor revision by the journal Environment International.

As part of dissertation research, Gunier, et al., examined the relationship of Mn in dentine and CHAMACOS children’s performance on the Bayley Scales of Infant Development and found that postnatal Mn levels were associated with small decreases in MDI at 6-months and 12-months of age with stronger associations among girls for both MDI and PDI. In addition, girls whose mothers had lower hemoglobin levels experienced larger decreases in MDI and PDI associated with prenatal Mn levels than girls whose mothers had higher hemoglobin levels. This paper is being revised for publication in Environmental Research.

In preliminary analyses, we did not observe an association between hair Mn concentrations and 10.5 year IQ or behavior in models adjusted for child’s exact age, maternal education, poverty status, language of assessment and HOME score. We are currently preparing a manuscript for publication using the Mn hair analyses.

3. To determine whether prenatal and childhood exposure to DDT/E, PBDEs, and Mn are associated with timing of pubertal development in boys between age 9 and 13 years.

DDT/E and PBDEs: We are currently preparing a manuscript regarding prenatal and child age 9 PBDE, DDT/E, and hexachlorobenzene (HCB) exposure levels in association with timing of pubertal onset. Though these analyses will not be finalized until we have completed data collection at 12¾, we nonetheless have a significant body of longitudinal data on which to base initial analyses. Our analyses indicate statistically significant earlier onset of male puberty in association with each family of compounds investigated. We present results for CHAM1 boys, whose more accurate maternal pregnancy exposure measures showed statistically significant associations with puberty outcomes. In boys from the CHAM1 cohort, maternal prenatal PBDE concentrations were significantly associated with earlier onset of pubic hair development for ΣPBDEs, BDE-99, BDE-100, and BDE-153. BDE-47 concentrations were marginally associated with earlier development. Prenatal HCB concentrations were also associated with earlier pubic hair development. Prenatal concentrations of DDT and DDE were associated with earlier genital development, as was prenatal BDE-153. Boys' serum PBDE and organochlorine pesticide concentrations at 9 years were not associated with age of pubertal onset.

Our analysis also assesses associations between these chemicals and timing of pubertal onset in girls, for whom we gathered data under separate funding (NIH grant number ES017054). In girls, PBDE concentrations were not associated with the onset of puberty for either breast or pubic hair development, although the non-significant results suggested later puberty. In the CHAM1 cohort, higher prenatal maternal PBDEs were associated with later menarche for ΣPBDEs, BDE-47, and BDE-99, and marginally associated for BDE-100 and BDE-153. For girls in both cohorts, prenatal DDE concentrations were associated with earlier menarche. Age 9 BDE-153 concentrations were associated with late menarche, with marginal associations for ΣPBDEs and BDE-99.

Mn: To date, we have only run preliminary analyses of prenatal and postnatal Mn exposure in association with pubertal onset. Among 103 boys with available exposure and outcome data, our preliminary analyses indicate a marginally significant association of prenatal Mn with later onset of genital development. Among girls (N = 113), higher postnatal (i.e., infancy) Mn exposure was associated with significantly earlier onset of pubic hair development.

4. To determine whether prenatal and childhood exposure to DDT/E, PBDEs, and Mn are associated with hormone levels in boys at age 12.

DDT/E and PBDEs: We are currently preparing a manuscript regarding prenatal PBDE, DDT/E, and polychlorinated biphenyls (PCB) exposure levels in association with luteinizing hormone (LH), testosterone (T), and follicle stimulating hormone (FSH) in boys at age 12. Concentrations of FSH, LH, and T were measured in first-morning blood samples collected from 229 boys at age 12. All hormones and exposures were log10-transformed for statistical analysis; exposures were lipid-adjusted as well. Linear regression models were adjusted for child age, BMI, cohort, gestational age at birth, smoking, and alcohol use. In utero exposure to certain PBDEs and PCBs but not DDT/E was associated with elevations in sex hormones suggestive of earlier onset of puberty. Specifically, BDE-153 was associated with significant increases in FSH, LH, and T. BDE-100 was also positively associated with LH, and total PCBs was positively associated with FSH. Analyses are complete and we expect to submit this manuscript by the end of the summer.

Mn: To date, we have only run preliminary analyses of prenatal and postnatal Mn exposure in association with hormones in boys. Among 78 boys included in these preliminary analyses, we observed no association between either prenatal or postnatal Mn exposure and LH, T, or FSH at age 12. These data have been presented at scientific conferences but given the small numbers of boys with Mn measured, we will likely not submit this as a separate manuscript.

Significance:
This portion of our Center grant set out to assess effects on boys’ neurodevelopment and pubertal development of prenatal and early life exposure to three environmental exposures with wide U.S. and global relevance. PBDE exposure is nearly ubiquitous in the United States; Mn is widely used as a fuel additive, in fungicides, and emitted industrially; and DDT is used globally, primarily for malaria control. Our Center was well poised to address societal concerns that environmental exposures could contribute to apparent increases in neurobehavioral issues like attention problems and a shifting age at puberty. The research we proposed promised to address important data gaps, including the role of exposures experienced in utero and effects on male puberty, which had hitherto received less attention than female puberty.

We have made important progress towards these aims. Though not yet published, our near-complete analyses on male puberty offer compelling evidence that prenatal exposure to PBDEs and DDT/E contribute to an earlier onset of puberty in boys. For PBDEs, clinical Tanner staging and measurement of sex hormones in 12-year-old boys’ blood both support this point, whereas for DDT/E, associations are evident in Tanner stage but not hormone assessments. Our neurodevelopmental analyses completed to date (all undergoing minor revision prior to publication) suggest that each of our three exposures of primary interest may well contribute to attention and/or executive function difficulties in this age range (9 to 12 years), sometimes for boys more so than girls. Specifically, we found evidence that PBDEs and Mn may contribute to attention problems including hyperactivity, and that PBDEs and DDT/E may contribute to executive function deficits including impaired working memory. Overall, our findings to date support the conclusions that prenatal exposure and possibly exposures during infancy are more critical to later development than those occurring later in childhood (e.g., age 9 exposure levels), and that each of the exposures of interest – all of which are known or suspected endocrine disruptors – exert gender-specific impacts. Finally, our overall findings suggest that while reasonably precise back-extrapolation of persistent chemical exposure over a relatively long time period (in this case, 9 years) is achievable, the loss of accuracy in the exposure measure significantly inhibits the ability to detect associations with health and development outcomes. In our research, this has manifested as a fairly consistent pattern of stronger and more significant exposure-outcome associations for participants with measured versus back-extrapolated prenatal exposure values. This latter observation underlines the critical importance of pre-birth cohorts with measured in utero exposures in quantifying the true human health effects of environmental exposures.

Future Activities:

In the next 4 months, we will complete Year 12¾ visits as well as data entry and cleaning of Tanner data collected from the final ~100 boys seen at this visit, so that we can finalize puberty analyses that rely on these data. Over the next year, we anticipate publishing all manuscripts noted above that are currently in preparation or under revision, and preparing a manuscript related to Mn and pubertal development.


Journal Articles on this Report : 26 Displayed | Download in RIS Format

Other subproject views: All 137 publications 67 publications in selected types All 67 journal articles
Other center views: All 666 publications 138 publications in selected types All 137 journal articles
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Journal Article Audelo J, Kogut K, Harley KG, Rosas LG, Stein L, Eskenazi B. Maternal depression and childhood overweight in the CHAMACOS Study of Mexican-American children. Maternal and Child Health Journal 2016;20(7):1405-1414. R834513 (2014)
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  • Journal Article AugsJoost B, Jerman P, Deardorff J, Harley K, Constantine NA. Factors associated with parent support for condom education and availability. Health Education & Behavior 2014;41(2):207-215. R834513 (2014)
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  • Journal Article Chevrier J, Warner M, Gunier RB, Brambilla P, Eskenazi B, Mocarelli P. Serum dioxin concentrations and thyroid hormone levels in the Seveso Women’s Health Study. American Journal of Epidemiology 2014;180(5):490-498. R834513 (2014)
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  • Journal Article Dannemiller KC, Mendell MJ, Macher JM, Kumagai K, Bradman A, Holland N, Harley K, Eskenazi B, Peccia J. Next-generation DNA sequencing reveals that low fungal diversity in house dust is associated with childhood asthma development. Indoor Air 2014;24(3):236-247. R834513 (2014)
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  • Journal Article Engel SM, Bradman A, Wolff MS, Rauh VA, Harley KG, Yang JH, Hoepner LA, Barr DB, Yolton K, Vedar MG, Xu Y, Hornung RW, Wetmur JG, Chen J, Holland NT, Perera FP, Whyatt RM, Lanphear BP, Eskenazi B. Prenatal organophosphorus pesticide exposure and child neurodevelopment at 24 months: an analysis of four birth cohorts. Environmental Health Perspectives 2016;124(6):822-830. R834513 (2014)
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  • Journal Article Erkin-Cakmak A, Harley KG, Chevrier J, Bradman A, Kogut K, Huen K, Eskenazi B. In utero and childhood polybrominated diphenyl ether exposures and body mass at age 7 years: the CHAMACOS Study. Environmental Health Perspectives 2015;123(6):636-642. R834513 (2015)
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  • Journal Article Eskenazi B, Kogut K, Huen K, Harley KG, Bouchard M, Bradman A, Boyd-Barr D, Johnson C, Holland N. Organophosphate pesticide exposure, PON1, and neurodevelopment in school-age children from the CHAMACOS study. Environmental Research 2014;134:149-157. R834513 (2014)
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  • Journal Article Gaspar FW, Harley KG, Kogut K, Chevrier J, Mora AM, Sjodin A, Eskenazi B. Prenatal DDT and DDE exposure and child IQ in the CHAMACOS cohort. Environment International 2015;85:206-212. R834513 (2014)
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  • Journal Article Gomez N, Guendelman S, Harley KG, Gomez SL. Nativity and neighborhood characteristics and cervical cancer stage at diagnosis and survival outcomes among Hispanic women in California. American Journal of Public Health 2015;105(3):538-545. R834513 (Final)
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  • Journal Article Gunier RB, Arora M, Jerrett M, Bradman A, Harley KG, Mora AM, Kogut K, Hubbard A, Austin C, Holland N, Eskenazi B. Manganese in teeth and neurodevelopment in young Mexican-American children. Environmental Research 2015;142:688-695. R834513 (2014)
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  • Journal Article Gunier RB, Bradman A, Harley KG, Kogut K, Eskenazi B. Prenatal residential proximity to agricultural pesticide use and IQ in 7-year-old children. Environmental Health Perspectives 2017;125(5):057002 (8 pp.). R834513 (Final)
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  • Journal Article Harley KG, Engel SM, Vedar MG, Eskenazi B, Whyatt RM, Lanphear BP, Bradman A, Rauh VA, Yolton K, Hornung RW, Wetmur JG, Chen J, Holland NT, Barr DB, Perera FP, Wolff MS. Prenatal exposure to organophosphorous pesticides and fetal growth: pooled results from four longitudinal birth cohort studies. Environmental Health Perspectives 2016;124(7):1084-1092. R834513 (Final)
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  • Journal Article Harley KG, Rauch SA, Chevrier J, Kogut K, Parra KL, Trujillo C, Lustig RH, Greenspan LC, Sjodin A, Bradman A, Eskenazi B. Association of prenatal and childhood PBDE exposure with timing of puberty in boys and girls. Environment International 2017;100:132-138. R834513 (2014)
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  • Journal Article Heggeseth B, Harley K, Warner M, Jewell N, Eskenazi B. Detecting associations between early-life DDT exposures and childhood growth patterns: a novel statistical approach. PLoS ONE 2015;10(6):e0131443 (13 pp.). R834513 (2015)
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  • Journal Article Huen K, Yousefi P, Bradman A, Yan L, Harley KG, Kogut K, Eskenazi B, Holland N. Effects of age, sex, and persistent organic pollutants on DNA methylation in children. Environmental and Molecular Mutagenesis 2014;55(3):209-222. R834513 (2012)
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  • Journal Article Huen K, Harley K, Kogut K, Rauch S, Eskenazi B, Holland N. DNA methylation of LINE-1 and Alu repetitive elements in relation to sex hormones and pubertal timing in Mexican-American children. Pediatric Research 2016;79(6):855-862. R834513 (2014)
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  • Journal Article Lopez-Espinosa M-J, Mondal D, Armstrong BG, Eskenazi B, Fletcher T. Perfluoroalkyl substances, sex hormones, and insulin-like growth factor-1 at 6-9 years of age: a cross-sectional analysis within the C8 Health Project. Environmental Health Perspectives 2016;124(8):1269-1275. R834513 (2014)
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  • Journal Article Mora AM, van Wendel de Joode B, Mergler D, Cordoba L, Cano C, Quesada R, Smith DR, Menezes-Filho JA, Eskenazi B. Maternal blood and hair manganese concentrations, fetal growth, and length of gestation in the ISA cohort in Costa Rica. Environmental Research 2015;136:47-56. R834513 (2014)
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  • Journal Article Mora AM, Arora M, Harley KG, Kogut K, Parra K, Hernandez-Bonilla D, Gunier RB, Bradman A, Smith DR, Eskenazi B. Prenatal and postnatal manganese teeth levels and neurodevelopment at 7, 9, and 10.5 years in the CHAMACOS cohort. Environment International 2015;84:39-54. R834513 (2014)
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  • Journal Article Quiros-Alcala L, Mehta S, Eskenazi B. Pyrethroid pesticide exposure and parental report of learning disability and attention deficit/hyperactivity disorder in U.S. children: NHANES 1999-2002. Environmental Health Perspectives 2014;122(12):1336-1342. R834513 (2014)
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  • Journal Article Raanan R, Harley KG, Balmes JR, Bradman A, Lipsett M, Eskenazi B. Early-life exposure to organophosphate pesticides and pediatric respiratory symptoms in the CHAMACOS cohort. Environmental Health Perspectives 2015;123(2):179-185. R834513 (2010)
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  • Journal Article Raanan R, Balmes JR, Harley KG, Gunier RB, Magzamen S, Bradman A, Eskenazi B. Decreased lung function in 7-year-old children with early-life organophosphate exposure. Thorax 2016;71(2):148-153. R834513 (2015)
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  • Journal Article Rowe C, Gunier R, Bradman A, Harley KG, Kogut K, Parra K, Eskenazi B. Residential proximity to organophosphate and carbamate pesticide use during pregnancy, poverty during childhood, and cognitive functioning in 10-year-old children. Environmental Research 2016;150:128-137. R834513 (2015)
    R834513 (Final)
    R834513C001 (2015)
  • Abstract from PubMed
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  • Abstract: ScienceDirect-Abstract
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  • Other: ScienceDirect-Full Text-PDF
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  • Journal Article Sagiv SK, Kogut K, Gaspar FW, Gunier RB, Harley KG, Parra K, Villasenor D, Bradman A, Holland N, Eskenazi B. Prenatal and childhood polybrominated diphenyl ether (PBDE) exposure and attention and executive function at 9-12 years of age. Neurotoxicology and Teratology 2015:52(Pt B):151-161. R834513 (2014)
    R834513 (2015)
    R834513 (Final)
    R834513C001 (2014)
    R834513C001 (2015)
  • Full-text from PubMed
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  • Associated PubMed link
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  • Abstract: ScienceDirect-Abstract
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  • Other: ScienceDirect-Full Text-PDF
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  • Journal Article Stein LJ, Gunier RB, Harley K, Kogut K, Bradman A, Eskenazi B. Early childhood adversity potentiates the adverse association between prenatal organophosphate pesticide exposure and child IQ: the CHAMACOS cohort. Neurotoxicology 2016;56:180-187. R834513 (2015)
    R834513 (Final)
    R834513C001 (2015)
  • Abstract from PubMed
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  • Abstract: Science Direct-Abstract
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  • Other: Science Direct-Full Text-PDF
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  • Journal Article Verner M-A, Gaspar FW, Chevrier J, Gunier RB, Sjodin A, Bradman A, Eskenazi B. Increasing sample size in prospective birth cohorts:back-extrapolating prenatal levels of persistent organic pollutants in newly enrolled children. Environmental Science & Technology 2015;49(6):3940-3948. R834513 (2014)
    R834513 (2015)
    R834513 (Final)
    R834513C001 (2015)
    R834513C002 (2014)
    R834513C002 (2015)
  • Full-text from PubMed
  • Abstract from PubMed
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  • Supplemental Keywords:

    DDT, DDE, PBDEs, flame retardants, manganese, maneb, PCbs, HCB, puberty, neurodevelopment, behavior, children's health, CHAMACOS, RFA, Health, Scientific Discipline, INTERNATIONAL COOPERATION, Health Risk Assessment, Biochemistry, Children's Health, Environmental Policy, Biology, farmworkers, pesticide exposure, flame retardants, PBDE, children's vulnerablity, neurochemical effects, harmful environmental agents, biological markers, agricultural community

    Relevant Websites:

    http://cerch.org Exit Exit

    Progress and Final Reports:

    Original Abstract
  • 2010 Progress Report
  • 2011 Progress Report
  • 2012 Progress Report
  • 2013 Progress Report
  • 2014 Progress Report
  • Final

  • Main Center Abstract and Reports:

    R834513    Center for the Health Assessment of Mothers and Children of Salinas - UC Berkeley School of Public Health: CHAMACOS Office, Berkeley, CA

    Subprojects under this Center: (EPA does not fund or establish subprojects; EPA awards and manages the overall grant for this center).
    R834513C001 CHAMACOS Cohort Project: Pesticides and PBDE on Neurobehavior and Puberty
    R834513C002 Project B: Exposure Project: Mn, DDT/E and PBDE Exposure to Farmworker Children
    R834513C003 Epigenetics Project
    R834513C004 Community Outreach and Translation Core