2014 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 , University of California - Santa Cruz
Current 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: August 1, 2009 through July 31,2014
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 on 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 319 boys at age 9 years and 309 boys at age 10 1/2. To date, 287 boys have been assessed at age 12 and we are on track to complete visits with at least 300 boys by September 2014. We are approximately halfway through the final visit point of this project, with 160 boys assessed to date at age 12 3/4.

2. To determine whether prenatal and childhood exposure to DDT/E, PBDEs, and Mn are associated with neurobehavioral functioning at age 9, 10 1/2, and 12 years.

DDT/E: To increase statistical power, we combined boys and girls from the CHAMACOS cohort in all analyses of neurodevelopment, after confirming that there was no heterogeneity in associations by sex. For CHAM1 (the original CHAMACOS cohort followed since in utero), prenatal DDT/E concentrations were measured in maternal serum collected during pregnancy. For CHAM2 (participants enrolled at age 9), prenatal DDT/E concentrations were back-extrapolated from DDT/E 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.

Multivariable linear models and generalized estimating equation (GEE) models were used to test the relationship between prenatal p,p’-DDT/E serum concentrations with full scale IQ and 4 subtests (working memory, perceptual reasoning, verbal comprehension, and processing speed) assessed at the 7-year (CHAM1 only) and 10 1/2-year (CHAM1 and CHAM2) visits. No significant associations were seen between prenatal p,p’-DDT/E and IQ or any of the 4 subtests when age 7 (n = 316) and 10 1/2 (n = 595) outcomes were examined individually. However, as shown in Table 1, the longitudinal GEE analysis (n = 619) found a significant decrease in processing speed for every 10-fold increase in prenatal p,p’-DDT (β = -1.6, CI 95% = -2.9,-0.3) and p,p’-DDE (β = -2.0, CI 95% = -3.7,-0.3) serum concentrations.

Table 1. Change in cognitive scores in children tested at 7 years and/or 10.5 years for each 10-fold increase in prenatal p,p’-DDT/E using GEE modelsa

   

p,p’-DDT

p,p’-DDE

Cognitive test

n

β (95% CI)

β (95% CI)

WISC-IV subscale

Working memory

616

-0.5 (-1.8,0.8)

0.1 (-1.7,1.9)

Perceptual reasoning

619

-0.3 (-1.9,1.3)

0.2 (-2,2.4)

Verbal comprehension

617

-0.8 (-2,0.4)

0.0 (-1.6,1.6)

Processing speed

616

-1.6 (-2.9,-0.3)*

-2.0 (-3.7,-0.3)*

Full-scale IQ

616

-0.9 (-2.2,0.4)

-0.3 (-2,1.4)

a Adjusted for maternal education, maternal intelligence, maternal depression, language of WISC testing, maternal birth country, years in the United States prior to delivery, HOME z-score, and household poverty

* p-value < 0.05

PBDEs: As with DDT, measured prenatal PBDE concentrations were used for CHAM1 children and back-extrapolated prenatal concentrations were used for CHAM2 children. Measured PBDE concentrations at age 9 were available for both CHAM1 and CHAM2 children. Prenatal and 9-year PBDE concentrations were associated with decrements in memory at 9 and 10 1/2 years. Each 10-fold increase in prenatal ΣPBDE concentrations was associated with decrements in scores on the NEPSY-II Memory for Designs test at age 9 (β = -0.6, p = 0.22 for immediate recall; β = -1.1, p = 0.04 for delayed recall) and each 10-fold increase in 9-year ΣPBDE concentrations was associated with lower scores on the California Auditory Verbal Learning Task (CAVLT) at age 10 1/2 (β = -4.8, p = 0.04 for immediate recall; β = -3.9, p = 0.06 for delayed recall). Non-significant decrements were seen in WISC full scale IQ and subscales at age 10 1/2.

DDT/E and PBDEs: We found evidence of interaction between prenatal DDT/E and PBDEs on child behavior. Maternal DDT/E appeared to potentiate the association of PBDEs and teacher report of internalizing problems (βInter = 4.9; 95% CI = 0.8, 9.1), particularly for anxiety (βInter = 4.5; 95% CI = 0.4, 8.7) and somatization (βInter = 6.7; 95% CI = 2.1, 11.3). For instance, maternal PBDE concentrations were associated with an 8.2-point (95% CI: 0.4, 16.1) increase in scores on the BASC somatization problems scale at the 95th percentile of maternal DDT but no significant association was observed at the 50th percentile of maternal DDT (β = -4.6; 95% CI = -9.2, 0.1; Figure 1). We found no evidence of interaction for postnatal exposure.

Figure 1. Teacher report of somatization problems and interaction between prenatal DDT and PBDEs.

https://cfpub.epa.gov/ncer_abstracts/images/fckimages/index.cfm?imgid=8055

Mn: We measured prenatal and postnatal dentine Mn concentrations in shed teeth. We examined the relationship between prenatal and postnatal exposure and children’'s performance at 6, 12 and 24-months of age on the Bayley Scales of Infant Development mental and psychomotor development indices. We explored the possibility of an inverted U-shaped association with neurodevelopment because Mn is an essential nutrient. We also evaluated potential interactions between Mn exposure and blood lead concentrations as well as maternal iron status during pregnancy. We observed a negative association between postnatal Mn levels in dentin and psychomotor development at 6 months of age. The relationship followed an inverse U-shaped association with the strongest effect observed when comparing the highest tertile of Mn levels in teeth to the middle tertile of Mn levels in teeth (-3.6 points; 95% CI: -6.9, -0.2). Prenatal Mn levels in dentin were associated with mental and psychomotor development at 6 months only among children whose mothers’ were iron deficient during pregnancy. We did not observe a significant interaction with prenatal or postnatal blood lead concentrations in this cohort.

We assessed the association of Mn levels in teeth with cognition, attention, memory, and motor functioning in the CHAMACOS children at age 7, 9, and 10.5 years. We used generalized linear models and generalized additive models to test for linear and non-linear associations, and generalized estimating equation models to assess longitudinal effects. We observed a significant increase of 0.7 and 0.9 points in NEPSY-II Memory for Designs immediate and delayed memory scaled scores (95% CI = 0.2-1.3, and 0.3-1.4, respectively) per two-fold increase in postnatal dentine Mn concentrations. We also found an increase of 0.2 (95% CI = 0-0.3) in Dominant Hand Finger tapping scores with the dominant hand per two-fold increase in postnatal dentine Mn concentrations. We did not observed any association between postnatal Mn exposure and WISC-IV scores at 7 years, but we observed a weak and positive linear association between postnatal dentine Mn and WISC-IV Perceptual Reasoning IQ and Working Memory IQ at 10.5 years (β for a two-fold increase in concentrations = 2.6, 95% CI = 0.3-4.8; and β for a two-fold increase in concentrations = 1.6, 95% CI = 0-3.2; respectively). We also observed positive associations between postnatal dentine Mn and WISC-IV Perceptual Reasoning IQ, Working Memory IQ, and Full Scale IQ in longitudinal models (β for a two-fold increase in concentrations = 2.4, 95% CI = 0.3-4.5; β = 1.5, 95% CI = 0-3.0; and β = 1.8, 95% CI = 0.1-3.4; respectively).

Finally, in preliminary analyses of Mn hair concentrations we did not observe an association with 10.5 year IQ in models adjusted for child’'s exact age, maternal education, poverty status and HOME score.

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

Pubertal assessments at 12 and 12 3/4 are not yet complete. However, we have conducted preliminary analyses of time to onset of puberty using interval censored survival analysis to evaluate the association of the onset of puberty in girls at 9 years of age and boys at 10.5 years of age with prenatal and childhood exposures to DDT/E, PBDEs and Mn.

DDT/E and PBDEs: We did not observe associations of between prenatal or 9 year PBDE or DDT/E blood concentrations and onset of puberty in boys with the CHAM1 and 2 cohorts combined (Table 2). However, among boys from the original CHAM1 cohort (i.e., with more accurately measured prenatal serum concentrations), we found that prenatal DDT and DDE serum concentrations were associated with earlier onset of genital development (HR = 1.7; 95% CI = 1.1, 2.7 for each 10-fold increase in DDE; HR = 1.5; 95% CI = 1.1, 2.1 for each 10-fold increase in DDT). Concentrations of all prenatal PBDE congeners were associated with earlier onset of pubic hair development in CHAM1 boys (HR = 3.1, 95% CI = 1.3, 7.3 for each 10-fold increase in ΣPBDEs) and BDE-153 also was associated with earlier genital development.

Mn: We had prenatal and postnatal measurements of Mn levels in tooth dentin for 219 participants for whom we also had Tanner staging information available at 9 years of age in girls and at 10.5 years of age in boys. We observed an earlier onset of pubic hair development in girls that had higher prenatal Mn teeth levels, with a HR = 1.73 (1.12, 2.68) for every two-fold increase in prenatal Mn tooth dentin.

Table 2.  Association of prenatal and 9-year-old lipid-adjusted PBDE and DDT/E concentrations (log10) with pubertal development in boys.

 
 

Genital Development

Pubic Hair Development

 

HR (95% CI)

HR (95% CI)

Prenatal Exposure (CHAM1 only, n = 105)

BDE-47

1.8 (0.9, 3.6)

2.7 (1.2, 6.0)*

BDE-99

1.7 (0.9, 3.4)

2.5 (1.2. 5.4)*

BDE-100

2.2 (0.9, 4.9)

3.2 (1.3, 8.0)*

BDE-153

2.4 (1.0, 5.7)*

4.8 (1.8, 13.0)*

ΣPBDEs

2.0 (1.0, 4.3)

3.1 (1.3, 7.3)*

DDE

1.7 (1.1, 2.7)*

0.9 (0.5, 1.5)

DDT

1.5 (1.1, 2.1)*

0.9 (0.6, 1.4)

Prenatal Exposure (CHAM1 & CHAM2, n = 255)

BDE-47

1.0 (0.4, 1.5)

1.4 (0.8, 2.5)

BDE-99

1.0 (0.7, 1.6)

1.5 (0.8, 2.6)

BDE-100

1.1 (0.7, 1.7)

1.3 (0.7, 2.5)

BDE-153

1.1 (0.7, 1.8)

1.4 (0.7, 2.9)

ΣPBDEs

1.0 (0.7, 1.6)

1.5 (0.8, 2.7)

DDE

1.2 (0.8, 1.6)

0.9 (0.6, 1.4)

DDT

1.1 (0.9, 1.4)

0.9 (0.7, 1.3)

9-Year Exposure (CHAM1 & CHAM2, n = 256)

BDE-47

1.3 (0.8, 1.9)

1.1 (0.6, 2.1)

BDE-99

1.1 (0.8, 1.7)

1.1 (0.6, 1.9)

BDE-100

1.2 (0.7, 2.0)

1.2 (0.6, 2.3)

BDE-153

1.7 (1.0, 3.0)

1.2 (0.5, 2.8)

ΣPBDEs

1.3 (0.8, 2.1)

1.2 (0.6, 2.4)

DDE

1.3 (0.9, 1.9)

1.1 (0.7, 1.7)

DDT

1.2 (0.8, 1.8)

0.8 (0.4, 1.5)

Controlling for maternal education, years in the United States, birth order, family income, CHAM1 vs. CHAM2, duration of exclusive breastfeeding, BMI at 9Y, child examiner, child exact age at assessment.

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

We collected early morning blood samples from 145 boys (113 CHAM1, 32 CHAM2) and laboratory analysis has been completed by Esoterix laboratory in Calabasas Hills, CA, for testosterone (T), luteinizing hormone (LH), and follicle stimulating hormone (FSH). We conducted preliminary analyses of hormone levels in boys at age 12 and exposure to DDT/E, PBDEs and Mn in models adjusted for child’'s exact age and BMI at the 12-year visit. We did not observe a relationship with measured prenatal concentrations of DDT/E and any hormone measurement. For measured prenatal concentrations of PBDEs, we found significant associations between levels of BDE-153 and LH and testosterone. A ten-fold increase of BDE-153 concentration in prenatal blood resulted in a 160% increase in LH (p = 0.003) and a 200% increase in testosterone (p = 0.01). Results were similar and remained significant using back-extrapolated BDE-153 concentrations in CHAM2 participants. There were no associations between DDT/E or PBDEs measured in children at 9 years of age and hormone levels in boys at age 12. Prenatal Mn levels measured in tooth dentin were not related to hormone levels in boys. However, a two-fold increase in postnatal Mn dentin levels was associated with a 15% increase in FSH (p = 0.04). In future analyses, we will include Tanner stage at the 12-year assessment in the models and will explore non-linear relationships using generalized additive models.

Other Studies

  • OPs Pooling Project
  • DAPs and Respiratory
  • Sulfur and Respiratory
  • BPA and Behavior/Obesity

Future Activities:

In the next year, we will complete as many 12 3/4 visits as we are able before funding expires. We will complete data entry and cleaning of the 12 year questionnaire and neurodevelopment data, as well as for age 12 and 12 3/4 Tanner data. Statistical analyses of prenatal PBDEs and DDT/E exposure in CHAM2 study participants (Aims 2 and 3) will begin now that back-extrapolated levels for CHAM2 are available.


Journal Articles on this Report : 28 Displayed | Download in RIS Format

Other subproject views: All 137 publications 67 publications in selected types All 67 journal articles
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Journal Article Alkon A, Boyce WT, Tran L, Harley KG, Neuhaus J, Eskenazi B. Prenatal adversities and Latino children's autonomic nervous system reactivity trajectories from 6 months to 5 years of age. PLoS One 2014;9(1):e86283. R834513 (2012)
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  • Journal Article Alkon A, Harley KG, Neilands TB, Tambellini K, Lustig RH, Boyce WT, Eskenazi B. Latino children's body mass index at 2-3.5 years predicts sympathetic nervous system activity at 5 years. Childhood Obesity 2014;10(3):214-224. R834513 (2012)
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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 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 Chopra V, Harley K, Lahiff M, Eskenazi B. Association between phthalates and attention deficit disorder and learning disability in U.S. children, 6-15 years. Environmental Research 2014;128:64-69. 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, Warner M, Sirtori M, Fuerst T, Rauch SA, Brambilla P, Mocarelli P, Rubinacci A. Serum dioxin concentrations and bone density and strucure in the Seveso Women’s Health Study. Environmental Health Perspectives 2014;122(1):51-57. R834513 (2014)
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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 Gemmill A, Gunier RB, Bradman A, Eskenazi B, Harley KG. Residential proximity to methyl bromide use and birth outcomes in an agricultural population in California. Environmental Health Perspectives 2013;121(6):737-743. R834513 (2013)
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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 Harley KG, Gunier RB, Kogut K, Johnson C, Bradman A, Calafat AM, Eskenazi B. Prenatal and early childhood bisphenol A concentrations and behavior in school-aged children. Environmental Research 2013;126:43-50. R834513 (2014)
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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 organophosphate pesticides and fetal growth: pooled results from four longitudinal birth cohort studies. Environmental Health Perspectives 2016;124(7):1084-1092. R834513 (2014)
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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 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, Lundh T, Lindh CH, Bradman A, Eskenazi B. Blood and hair manganese concentrations in pregnant women from the Infants’ Environmental Health Study (ISA) in Costa Rica. Environmental Science & Technology 2014;48(6):3467-3476. 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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  • Abstract: EHP-Abstract & Full Text-HTML
  • 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)
    R834513 (Final)
    R834513C001 (2014)
    R834513C001 (2015)
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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)
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  • Journal Article Sermondade N, Faure C, Fezeu L, Shayeb AG, Bonde JP, Jensen TK, Van Wely M, Cao J, Martini AC, Eskandar M, Chavarro JE, Koloszar S, Twigt JM, Ramlau-Hansen CH, Borges Jr. E, Lotti F, Steegers-Theunissen RPM, Zorn B, Polotsky AJ, La Vignera S, Eskenazi B, Tremellen K, Magnusdottir EV, Fejes I, Hercberg S, Levy R, Czernichow S. BMI in relation to sperm count: an updated systematic review and collaborative meta-analysis. Human Reproduction Update 2013;19(3):221-231. R834513 (2014)
    R834513C001 (2014)
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  • Journal Article Volberg V, Harley K, Calafat AM, Dave V, McFadden J, Eskenazi B, Holland N. Maternal bisphenol A exposure during pregnancy and its association with adipokines in Mexican-American children. Environmental and Molecular Mutagenesis 2013;54(8):621-628. R834513 (2014)
    R834513C001 (2014)
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  • Abstract: Wiley-Abstract
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  • Journal Article Warner M, Mocarelli P, Brambilla P, Wesselink A, Samuels S, Signorini S, Eskenazi B. Diabetes, metabolic syndrome, and obesity in relation to serum dioxin concentrations: the Seveso Women's Health Study. Environmental Health Perspectives 2013;121(8):906-911. R834513 (2013)
    R834513 (2014)
    R834513 (Final)
    R834513C001 (2013)
    R834513C001 (2014)
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  • Journal Article Warner M, Schall RA, Harley KG, Bradman A, Barr D, Eskenazi B. In utero DDT and DDE exposure and obesity status of 7-year-old Mexican-American children in the CHAMACOS cohort. Environmental Health Perspectives 2013;121(5):631-636. R834513 (2013)
    R834513 (2014)
    R834513 (Final)
    R834513C001 (2013)
    R834513C001 (2014)
    R834513C003 (2013)
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  • Journal Article Warner M, Wesselink A, Harley KG, Bradman A, Kogut K, Eskenazi B. Prenatal exposure to dichlorodiphenyltrichloroethane and obesity at 9 years of age in the CHAMACOS Study cohort. American Journal of Epidemiology 2014;179(11):1312-1322. R834513 (2014)
    R834513C001 (2014)
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  • Abstract: Oxford Journals-Abstract
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  • Journal Article Wesselink A, Warner M, Samuels S, Parigi A, Brambilla P, Mocarelli P, Eskenazi B. Maternal dioxin exposure and pregnancy outcomes over 30 years of follow-up in Seveso. Environment International 2014;63:143-148. R834513 (2014)
    R834513C001 (2014)
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  • Supplemental Keywords:

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

    Relevant Websites:

    Center for Environmental Research and Children's Health Exit

    Progress and Final Reports:

    Original Abstract
  • 2010 Progress Report
  • 2011 Progress Report
  • 2012 Progress Report
  • 2013 Progress Report
  • 2015 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