Kimberly  Yolton

Dr. Kimberly Yolton

orcid

Research Focus & Metrics

Academic Career Length

36Years (1991-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 January 2005 in Environmental Health Perspectives
Verified
Journal Article
Open access
KYKimberly Yolton
Kimberly Yolton
KDKim Dietrich
Kim Dietrich
PAPeggy Auinger
Peggy Auinger
BLBruce P. Lanphear
Bruce P. Lanphear
RHRichard Hornung
Richard Hornung
We used the Third National Health and Nutrition Examination Survey (NHANES III), conducted from 1988 to 1994, to investigate the relationship between environmental tobacco smoke (ETS) exposure and cognitive abilities among U.S. children and adolescents ...

1 September 2011 in Neurotoxicology and Teratology
Verified
Journal Article
Closed access
KYKimberly Yolton
Kimberly Yolton
YXYingying Xu
Yingying Xu
DSDonna Strauss
Donna Strauss
MAMekibib Altaye
Mekibib Altaye
ACAntonia M. Calafat
Antonia M. Calafat
JKJane Khoury
Jane Khoury

22 March 2016 in International Journal of Epidemiology
Verified
Journal Article
Open access
PDF file
JBJoseph Braun
Joseph Braun
GKGeetika Kalloo
Geetika Kalloo
ACAimin Chen
Aimin Chen
KDKim N. Dietrich
Kim N. Dietrich
SLStacey Liddy-Hicks
Stacey Liddy-Hicks
BLBruce P. Lanphear
Bruce P. Lanphear
Early life environmental factors may increase the risk of disease in childhood or adulthood. Well-established examples of early life environmental factors affecting later life health include the increased risk of vaginal clear cell carcinoma and several reproductive disorders following in utero diethylstilbestrol exposure, and cognitive decrements in children with prenatal mercury or childhood lead exposure.1–4 These studies indicate that the effect of some environmental factors may depend on the timing of exposure relative to sensitive developmental windows.

28 May 2015 in Environmental Health
Verified
Journal Article
Open access
PDF file
MSMelissa Lynne Wagner Schuman
Melissa Lynne Wagner Schuman
Jason RichardsonJason Richardson
Jason Richardson
PAPeggy Auinger
Peggy Auinger
JBJoseph Braun
Joseph Braun
BLBruce Lanphear
Bruce Lanphear
TFTanya E. Froehlich
Tanya E. Froehlich
Pyrethroid pesticides cause abnormalities in the dopamine system and produce an ADHD phenotype in animal models, with effects accentuated in males versus females. However, data regarding behavioral effects of pyrethroid exposure in children is limited. We examined the association between pyrethroid pesticide exposure and ADHD in a nationally representative sample of US children, and tested whether this association differs by sex. Data are from 8–15 year old participants (N = 687) in the 2001–2002 National Health and Nutrition Examination Survey. Exposure was assessed using concurrent urinary levels of the pyrethroid metabolite 3-phenoxybenzoic acid (3-PBA). ADHD was defined by either meeting Diagnostic and Statistical Manual of Mental Disorders-Fourth Edition criteria on the Diagnostic Interview Schedule for Children (DISC) or caregiver report of a prior diagnosis. ADHD symptom counts were determined via the DISC. Multivariable logistic regression examined the link between pyrethroid exposure and ADHD, and poisson regression investigated the link between exposure and ADHD symptom counts. Children with urinary 3-PBA above the limit of detection (LOD) were twice as likely to have ADHD compared with those below the LOD (adjusted odds ratio [aOR] 2.42; 95 % confidence interval [CI] 1.06, 5.57). Hyperactive-impulsive symptoms increased by 50 % for every 10-fold increase in 3-PBA levels (adjusted count ratio 1.50; 95 % CI 1.03, 2.19); effects on inattention were not significant. We observed possible sex-specific effects: pyrethroid biomarkers were associated with increased odds of an ADHD diagnosis and number of ADHD symptoms for boys but not girls. We found an association between increasing pyrethroid pesticide exposure and ADHD which may be stronger for hyperactive-impulsive symptoms compared to inattention and in boys compared to girls. Given the growing use of pyrethroid pesticides, these results may be of considerable public health import.

17 September 2015 in Environmental Health
Verified
Journal Article
Open access
PDF file
EWErika F. Werner
Erika F. Werner
JBJoseph M. Braun
Joseph M. Braun
KYKimberly Yolton
Kimberly Yolton
JKJane C. Khoury
Jane C. Khoury
BLBruce P. Lanphear
Bruce P. Lanphear
Exposure to phthalates, a class of endocrine disrupting chemicals, is ubiquitous. We examined the association of urinary phthalate metabolite concentrations during pregnancy with maternal blood pressure and risk of pregnancy-induced hypertensive diseases. We used data from the Health Outcomes and Measures of the Environment Study, a prospective birth cohort of low-risk pregnant women recruited between March 2003 and January 2006. We analyzed maternal urine samples collected at 16 and 26 weeks gestation for 9 phthalate monoester metabolites reflecting exposure to 6 phthalate diesters. Outcomes included maternal blood pressure at <20 and ≥20 weeks gestation and pregnancy induced hypertensive diseases (gestational hypertension, preeclampsia, eclampsia, and HELLP syndrome). Data were available for 369 women who gave birth to singleton, live-born infants without congenital anomalies. Of the phthalate metabolites evaluated, only mono-benzyl phthalate (MBzP) concentrations were significantly associated with maternal diastolic blood pressure at <20 weeks gestation. Women in the third MBzP tercile at 16 weeks gestation had diastolic blood pressure 2.2 (95 % CI: 0.5–3.9) mm Hg higher at <20 weeks gestation and 2.8 (95 % CI: 0.9–4.7) mm Hg higher at ≥20 weeks gestation compared to women in the first tercile. Compared to women in the first tercile, women in the top MBzP tercile at 16 weeks had an increased risk of developing pregnancy-induced hypertensive diseases (RR = 2.92, 95 % CI 1.15–7.41, p-value for trend = 0.01). MBzP concentrations at 26 weeks gestation were not as strongly associated with blood pressure at ≥20 weeks gestation or risk of pregnancy-induced hypertensive diseases. This study suggests that maternal urinary MBzP concentrations may be associated with increased diastolic blood pressure and risk of pregnancy-induced hypertensive diseases.

1 February 2010 in Pediatrics
Verified
Journal Article
Closed access
PDF file
KYKimberly Yolton
Kimberly Yolton
YXYingying Xu
Yingying Xu
JKJane Khoury
Jane Khoury
PSPaul Succop
Paul Succop
BLBruce Lanphear
Bruce Lanphear
JOJudith Owens
Judith Owens
OBJECTIVES: The objective of this study was to investigate the relationship between exposure to secondhand smoke (SHS) and child sleep patterns among a group of children with asthma who were exposed regularly to tobacco smoke at home. METHODS: We studied 219 children who were enrolled in an asthma intervention trial and were exposed regularly to SHS. Serum cotinine levels were used to measure exposure to tobacco smoke, and sleep patterns were assessed through parent reports using the Children9s Sleep Habits Questionnaire. Covariates in adjusted analyses included gender, age, race, maternal marital status, education, and income, prenatal tobacco exposure, maternal depression, Home Observation for Measurement of the Environment total score, household density, asthma severity, and use of asthma medications. RESULTS: Exposure to SHS was associated with sleep problems, including longer sleep-onset delay (P = .004), sleep-disordered breathing (P = .02), parasomnias (P = .002), daytime sleepiness (P = .022), and overall sleep disturbance (P = .0002). CONCLUSIONS: We conclude that exposure to SHS is associated with increased sleep problems among children with asthma.