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By Author</option><option value="asc">Date Ascending</option><option value="desc">Date Descending</option></select></div><div class="o-input__droplist1 c-sort__page-input"><label for="c-sort2">Show:</label><select name="rows" id="c-sort2" form="facetForm"><option selected="" value="10">10</option><option value="20">20</option><option value="30">30</option><option value="40">40</option><option value="50">50</option><option value="100">100</option></select></div></div><input type="hidden" name="start" form="facetForm" value="0"/><nav class="c-pagination--next"><ul><li><a href="" aria-label="you are on result set 1" class="c-pagination__item--current">1</a></li><li><a href="" aria-label="go to result set 2" class="c-pagination__item">2</a></li><li><a href="" aria-label="go to result set 3" class="c-pagination__item">3</a></li><li><a href="" aria-label="go to result set 4" class="c-pagination__item">4</a></li><li><a href="" aria-label="go to result set 25" class="c-pagination__item">25</a></li><li class="c-pagination__next"><a href="" aria-label="go to Next result set">Next</a></li></ul></nav></div><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-thesis">Thesis</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/113291w9"><div class="c-clientmarkup">Factors of susceptibility to dioxin in the Seveso Women’s Health Study</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AAmes%2C%20Jennifer">Ames, Jennifer</a> </li><li class="c-authorlist__begin"><span class="c-authorlist__heading">Advisor(s):</span> <a href="/search/?q=author%3AEskenazi%2C%20Brenda">Eskenazi, Brenda</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucb_etd">UC Berkeley Electronic Theses and Dissertations</a> (2018)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><p>Evidence of inter-individual differences in toxicant response has necessitated heavy editing of Paracelsus’ famous toxicological maxim “the dose makes the poison” to include factors such as age, sex, and timing of exposure. This dissertation takes advantage of a unique multigenerational, long-term cohort and advances in molecular technology to examine whether life stage and genetic factors also modify human sensitivity to toxic exposures, particularly with respect to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a persistent organic pollutant with well-documented carcinogenic and endocrine-disrupting effects in humans. Although increasing animal evidence supports the hypothesis that in utero exposure to endocrine disrupting compounds can have a long-term impact on the health of the 2nd and subsequent generations, the evidence in humans is limited. In addition, individuals may have differences in susceptibility to chemical exposure based on their genetic make-up. </p><p> On July 10, 1976, an explosion at a chemical plant near Seveso, Italy resulted in a toxic plume that exposed nearby residents to high levels of TCDD. The Seveso Women’s Health Study (SWHS), an ambidirectional cohort study, was initiated in 1996 to investigate the health of 981 women who were newborn to age 40 years in 1976, had resided in the immediate vicinity of the plant, and had archived samples of blood collected soon after the explosion. The SWHS is the only comprehensive study of the health effects of TCDD exposure in a female population, and has the unique benefit of measurements of individual-level TCDD in blood collected near the time of the explosion. In 2014, 611 offspring of the SWHS who were born after the accident, and potentially exposed to their mother’s TCDD body burdens in utero were enrolled.</p><p> The first two chapters examine the neurotoxic effects of TCDD during windows of susceptibility in utero and later in life when hormonal processes potentially sensitive to TCDD’s estrogenic influence are driving brain changes. In particular, chapter 1 investigates TCDD and cognitive and physical functioning in SWHS women decades after their direct exposure to the accident and the modifying effects of menarche and menopause. Chapter 2 addresses the relation between neuropsychological function in 7-17 year old offspring (n=161) with respect to their mother’s 1976 exposures and maternal levels estimated at the time of pregnancy. Lastly, Chapter 3 examines genetic susceptibility in the aryl hydrocarbon receptor (AhR), a key transcription factor in the metabolism of TCDD and other xenobiotics in humans. Specifically, we conducted a gene-by-environment (GxE) analysis to evaluate the modifying effect of genetic polymorphisms in maternal AhR on the relationship between maternal TCDD levels and child birthweight, an indicator of a restricted fetal environment. The SWHS Second Generation Study in conjunction with the parent SWHS offers a rich dataset in which to explore windows of neurotoxic and genetic susceptibility to TCDD across the lifecourse and test the fetal origins of disease hypothesis.</p></div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/113291w9"><img src="/cms-assets/a0c5c014e30e9459f0b8952b692795433cac99730ff29abef7c74be6f714e362" alt="Cover page: Factors of susceptibility to dioxin in the Seveso Women’s Health Study"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-thesis">Thesis</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/5g23b6bm"><div class="c-clientmarkup">Prenatal Insecticide Exposure and Children's Cognitive Development</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AGaspar%2C%20Fraser%20William">Gaspar, Fraser William</a> </li><li class="c-authorlist__begin"><span class="c-authorlist__heading">Advisor(s):</span> <a href="/search/?q=author%3AEskenazi%2C%20Brenda">Eskenazi, Brenda</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucb_etd">UC Berkeley Electronic Theses and Dissertations</a> (2014)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><p>Although approximately 123 million people may be exposed to high levels of insecticides through the use of indoor residual spraying (IRS) for malaria control, very little data exists on exposure levels and risk to residents. In addition, certain populations may be more susceptible to the unintended health effects of insecticide exposure from IRS including the developing fetus. The aims of this dissertation were as follows: 1) build indoor transport and fate models to estimate insecticide exposure and risk to individuals living in homes sprayed for malaria control, 2) measure the serum levels of dichlorodiphenyl-trichloroethane (DDT) and its breakdown product dichlorodiphenyl-dichloroethylene (DDE) in a community where IRS occurs and test for intervenable characteristics to reduce exposure, and 3) evaluate the relationship between prenatal DDT and DDE exposure and children's cognitive development.</p><p>Of the 12 insecticides recommended for IRS by the World Health Organization (WHO), only DDT and deltamethrin have been measured longitudinally after IRS to assess exposure to residents of sprayed homes. In Chapter 2, we developed two dynamic indoor fugacity models, representing two of the common building types of homes in rural Africa, to track insecticide transport and fate in indoor compartments. For three age groups (birth to < 1 year old, 6 to 11 years old, and > 21 years old), we calculated insecticide uptake via inhalation, dust ingestion, and dermal absorption of dust and compared dose estimates with chronic and acute health-based benchmark doses set by the Food and Agriculture Organization and WHO. We accounted for model variability and uncertainty with Latin hypercube sampling. We found simulated indoor air concentrations, dust concentrations, and loading levels generally agreed with longitudinal measurements previously reported in homes sprayed with DDT and deltamethrin. While indoor air concentrations typically peaked on the day of IRS, dust concentrations often peaked days after IRS. At least one simulation of the average daily dose over the year after IRS for DDT, fenitrothion, pirimiphos-methyl, bendiocarb, and propoxur exceeded the Acceptable Daily Intake (ADI). The use of fenitrothion and DDT for IRS posed the greatest risk to residents of sprayed homes. For example, 67% and 33% of the simulated average dose estimates for fenitrothion and DDT exceeded the ADI in children less than one year old, respectively. None of the daily dose estimates exceeded the Acute Reference Doses. Results from this chapter indicate the feasibility and utility of using fugacity models to estimate exposure and risk to insecticides from IRS. In addition, model results indicate long-term home contamination from IRS and residents of IRS homes may be exposed to insecticides at levels that exceed chronic health-based benchmark doses. Given that dust concentrations often peaked days after IRS, residents should be informed that contact with the floor should be avoided during this period, especially for children with high hand-to-mouth behavior. </p><p>The use of DDT as an IRS insecticide has contributed to uniquely high DDT and DDE body burden in residents of sprayed homes. In Chapter 3, we described the Venda Health Examination of Mothers, Babies, and their Environment (VHEMBE) cohort and presented data on DDT and DDE serum concentrations measured in VHEMBE mothers. In addition, we applied targeted maximum likelihood estimation (TMLE) procedures to understand the change in marginal p,p'-DDT and p,p'-DDE body burden given seven hypothetical exposure interventions. A total of 751 mothers completed a baseline questionnaire and provided a serum sample. The majority of mothers enrolled in the VHEMBE cohort study were between 18 and 24 years of age (50.2%), completed at least grade 12 education (68.3%), lived below the South African poverty line of $40 per household member per month (58.3%), and were multiparous (56.8%). p,p'-DDT and p,p'-DDE serum concentrations were above the limit of quantification (LOQ) in 90.7 and 97.2% of the blood samples, respectively, while o,p'-DDT and o,p'-DDE serum concentrations were above the LOQ in 43.3 and 17.2% of the blood samples, respectively. Median (inter-quartile range) p,p'-DDT and p,p'-DDE serum concentrations were 56.8 (19.6-261.1) and 76.5 (27.9-271.5) ng/g-lipid, respectively. Of the seven interventions tested, three significantly reduced DDT and DDE exposures. If all VHEMBE mothers never lived in a DDT sprayed home, they would have 69.4% (95% CI: -76.3, -60.4) and 67.1% (95% CI: -73.6, -58.9) lower marginal p,p'-DDT and p,p'-DDE serum concentrations, respectively, than if all mothers ever lived in a DDT sprayed home. If all mothers lived in a household that wet mopped their floors at least seven times per week, they would have 25.2% (95% CI: -40.4, -6.1) and 21.9% (95% CI: -36.1, -4.6) lower marginal p,p'-DDT and p,p'-DDE serum concentrations, respectively, than if all mothers lived in a household that wet mops their floors less than seven times per week. In addition, if all mothers lived in a household with piped water, they would have 22.1% (95% CI: -38.0, -2.0) lower marginal p,p'-DDT serum concentrations than if all mothers lived in a household without piped water. Our findings suggest that DDT/E exposure is decreasing in IRS areas and several intervenable factors may exist to reduce DDT/E exposure in IRS communities.</p><p>Animal studies have shown DDT and DDE to be neurodevelopmental toxicants, but epidemiological studies have reported inconsistent findings between prenatal DDT and DDE exposure and child neurodevelopment. In Chapter 4, we investigated the association between prenatal DDT and DDE exposure and child neurodevelopment in the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS) cohort study. We combined the original prospective CHAMACOS cohort with a retrospective cohort of mother/child pairs and estimated prenatal DDT and DDE exposure with measured or predicted maternal concentrations during pregnancy. Using generalized estimating equation and linear regression models, we evaluated the relationship of prenatal DDT and DDE exposure with Full Scale Intelligence Quotient (IQ) and 4 subtests (Working Memory, Perceptual Reasoning, Verbal Comprehension, and Processing Speed) assessed in children 7 and 10.5-years after birth using the Wechsler Intelligence Scale for Children (WISC). In the longitudinal analyses (n = 619), we found an inverse association between prenatal DDT and DDE exposure and Processing Speed scores (p-value < 0.05). In the cross sectional analyses when the children were 7 and 10.5 years old, prenatal DDT exposure was inversely associated with Processing Speed at age 7 years (n = 316), but prenatal DDT and DDE exposure were not associated with Full Scale IQ or any of the WISC subscales at age 10.5 years (n = 595). We found evidence for effect modification by sex as prenatal DDE exposure was inversely associated with Processing Speed in the longitudinal analysis and both Full Scale IQ and Processing Speed at age 7 years in females, but not males. We conclude that prenatal DDT and DDE exposure may be associated with delayed Processing Speed in school-aged children, but with no other intelligence metric, and that the child's sex may modify this relationship.</p></div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/5g23b6bm"><img src="/cms-assets/a605a766403c571d4b292b2963973ee59f734568edf3311cc512338d60d6d2c9" alt="Cover page: Prenatal Insecticide Exposure and Children's Cognitive Development"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-thesis">Thesis</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/2fw8s6s3"><div class="c-clientmarkup">Exposure to manganese, fetal growth, and neurodevelopment in children living in agricultural communities in Costa Rica and California</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AMora%2C%20Ana%20Maria">Mora, Ana Maria</a> </li><li class="c-authorlist__begin"><span class="c-authorlist__heading">Advisor(s):</span> <a href="/search/?q=author%3AEskenazi%2C%20Brenda">Eskenazi, Brenda</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucb_etd">UC Berkeley Electronic Theses and Dissertations</a> (2014)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><p>There is a growing concern about excess manganese (Mn) exposure in pregnant women and children. Recent studies have reported adverse health effects in children living near Mn mining and/or transformation plants or drinking water contaminated with Mn. This dissertation focuses on environmental exposures to Mn in pregnant women and children living near agricultural fields treated with Mn-containing fungicides in Costa Rica and California, and their effects on fetal growth, length of gestation, and children's neurodevelopment.</p><p>Chapter 1 provides a general introduction to human exposure to Mn and highlights the background, significance and specific aims for each study/chapter.</p><p>Chapter 2 focuses on the environmental and lifestyle factors associated with Mn concentrations in pregnant women living near banana plantations with extensive aerial spraying of Mn-containing fungicide mancozeb in Costa Rica. For these analyses, Mn concentrations were measured in repeated blood and hair samples collected from 449 pregnant women enrolled in the Infants' Environmental Health Study (ISA). Mean blood Mn and geometric mean hair Mn concentrations were 24.4 μg/L (8.9-56.3) and 1.8 μg/g (0.05-53.3), respectively. Blood Mn concentrations were positively associated with gestational age at sampling (β = 0.2; 95% CI: 0.1, 0.2), number of household members (β = 0.4; 95% CI: 0.1, 0.6), and living in a house made of permeable and difficult-to-clean materials (β = 2.6; 95% CI: 1.3, 4.0); and inversely related to smoking (β = -3.1; 95% CI: -5.8, -0.3). Hair Mn concentrations were inversely associated with gestational age at sampling (% change = 0.8; 95% CI: -1.6, 0.0); and positively associated with living within 50 meters of a plantation (% change = 42.1; 95% CI: 14.2, 76.9) and Mn concentrations in drinking water (% change = 17.5; 95% CI: 12.2, 22.8). Findings from these analyses suggest that pregnant women living near banana plantations aerially sprayed with mancozeb may be environmentally exposed to Mn.</p><p>In Chapter 3 the association of prenatal blood and hair Mn concentrations with fetal growth and length of gestation in pregnant women and children living near banana plantations sprayed with mancozeb in Costa Rica was examined. Data on blood or hair Mn concentrations and birth outcomes were collected from 380 mother-infant pairs from the ISA study. Linear regression and generalized additive models were used in these analyses to test for linear and nonlinear associations. Mean (± SD) blood Mn concentration was 24.4 ± 6.6 μg/L and geometric mean (geometric SD) hair Mn concentration was 1.8 (3.2) μg/g. Hair Mn concentrations during the 2nd trimester and averaged over pregnancy were positively related to infant chest circumference (β for 10-fold increase = 0.6 cm; 95%CI: 0.2, 1.1; and β = 0.7 cm; 95%CI: 0.2, 1.2). Similarly, mean maternal hair Mn concentrations during pregnancy were associated with increased chest circumference (β for 10-fold increase = 1.32 cm; 95% CI: 0.54, 2.09) in infants whose mothers did not have gestational anemia but not in infants of mothers who had gestational anemia (β = 0.24 cm; 95% CI: -0.57, 1.05; p<sub>INT</sub> = 0.09). Mean maternal blood Mn concentrations during pregnancy were associated with decreased chest circumference in infants whose mothers were living below the poverty line (β for one-unit increase = -0.06 cm; 95% CI: -0.12, -0.01), but not in those living above poverty (β = 0.02 cm; 95% CI: -0.06, 0.09; p<sub>INT</sub> = 0.08). Mean maternal hair Mn concentrations were positively associated with length of gestation in infants born to women living below the poverty line (β for 10-fold increase = 4.11 days; 95% CI: 0.47, 7.75) but negatively associated in those living above poverty (β = -3.17 days; 95% CI: -7.93, 1.58; p<sub>INT</sub> = 0.03). In contrast to findings from previous studies, no linear or nonlinear associations of Mn concentrations with lowered birth weight or head circumference were observed. Nevertheless, hair Mn concentrations were related to larger chest circumference in infants born to women without gestational anemia and longer gestational durations in women living below the poverty line, while blood Mn concentrations were associated with smaller chest circumferences. The clinical significance of larger chest circumference, in the absence of an association between hair Mn concentrations and other measures of fetal growth in this study, is unknown. Inconsistencies between studies could be due to differences in the study population, sample size, time of biological sampling, and sources of Mn exposure.</p><p>In Chapter 4 the neurodevelopmental effects of early life exposure to Mn, indicated by prenatal and postnatal dentine Mn levels in children's deciduous teeth, were examined in school-age children living near agricultural fields treated with Mn-containing fungicides in California. Participants in these analyses included 247 children enrolled in the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS) study, a prospective cohort study in an agricultural area of California. Data on attention, cognition, memory, and motor functioning were collected from children at ages 7, 9, and 10.5 years. Generalized linear models and generalized additive models were used to test for linear and nonlinear associations, and generalized estimating equation models to assess longitudinal effects. Higher prenatal and postnatal dentine Mn levels were associated with improved cognitive abilities and fine motor coordination at 7, 9, and 10.5 years. Higher prenatal dentine Mn levels were associated with poorer attention at ages 7, 9, and 10.5 but only in boys and children born to mothers with higher lead exposure during pregnancy or gestational anemia. Higher postnatal dentine Mn levels were associated with better immediate and delayed memory at 9 and 10.5 years. Longitudinal models showed a weak association between postnatal dentine Mn levels and better cognitive outcomes at 7 and 10.5 years. These associations were all linear, and no threshold was observed. Previous studies have reported associations between childhood Mn exposure and negative neurodevelopmental effects, but in this study, small and positive relationships between postnatal dentine Mn and fine motor coordination, memory, and cognition were observed in children aged 7, 9, and 10.5 years. Disparities in findings between studies could be due to differences in the study design, timing of Mn measurements, exposure pathways, and/or exposure matrix.</p><p>Finally, Chapter 5 highlights the major findings for each chapter/study, conclusion, and future directions.</p></div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/2fw8s6s3"><img src="/cms-assets/3e7c5407ddea9722682bf148dd4c9a4771368ab13c59e852e2e2911283af58e7" alt="Cover page: Exposure to manganese, fetal growth, and neurodevelopment in children living in agricultural communities in Costa Rica and California"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-thesis">Thesis</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/2qj341v3"><div class="c-clientmarkup">Periconceptional and prenatal maternal glucose levels: immediate and long-term effects on offspring</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AEhrlich%2C%20Samantha%20Frances">Ehrlich, Samantha Frances</a> </li><li class="c-authorlist__begin"><span class="c-authorlist__heading">Advisor(s):</span> <a href="/search/?q=author%3AEskenazi%2C%20Brenda">Eskenazi, Brenda</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucb_etd">UC Berkeley Electronic Theses and Dissertations</a> (2011)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><p>Although the obesity epidemic in the United States appears to be leveling off, over half of all reproductive aged women in the U.S. are overweight [defined as body mass index (BMI) ≥25 kg/m<sup>2</sup>] or obesity [defined as body mass index (BMI) ≥30 kg/m<sup>2</sup>]. Overweight and obese women are more likely to suffer from a variety of reproductive complications, including adverse perinatal outcomes; overweight and obesity are also well-established risk factors for gestational diabetes and type 2 diabetes. Gestational diabetes mellitus (GDM), defined as carbohydrate intolerance leading to hyperglycemia with first onset or recognition during pregnancy, complicates 7% to 10% of pregnancies in the U.S. Type 2 diabetes mellitus (T2DM) is emerging as a leading cause of death and disability in the U.S. and currently straining the health care system.</p><p>This goal of this dissertation is to investigate the effects of periconceptual and prenatal maternal glucose levels on immediate and longer-term offspring outcomes. Three studies were undertaken, comprising three chapters, to complete this dissertation; all utilize a cohort study design, with data obtained from several sources. The study described in the first chapter examines the association between periconceptual maternal glycaemia and newborn sex ratio in a large data set from Kaiser Permanente Northern California. Women were categorized into the following groups: overt pregravid diabetes, gestational diabetes, mild pregnancy hyperglycemia and normoglycemic pregnancies. It has long been hypothesized that natural selection would favor a reproductive strategy biased towards females under adverse circumstances and males under favorable conditions in order to maximize the number of surviving grandchildren. Thus, I hypothesized that women with overt pregravid diabetes would exhibit the lowest newborn sex ratio (ratio of males to females at birth, i.e. more girls) due to the unfavorable state of chronic disease and women with gestational diabetes would exhibit the highest sex ratio (i.e. more boys) due to the presence of excessive fuel substrates early in pregnancy. </p><p>The study described in the second chapter explores programming for childhood obesity by maternal pregnancy glucose levels in women without recognized diabetes or gestational diabetes; the study comprising the third chapter considers the association between pregnancy glucose levels in these same women and cardiometabolic risk factors in their children at 7 years of age. Data for chapters 2 and 3 come from the CHAMACOS (Center for the Health Assessment of Mothers and Children of Salinas) longitudinal birth cohort. Several studies have demonstrated an increased risk for childhood obesity and adverse cardiometabolic profiles among children exposed to maternal diabetes or gestational diabetes in utero. Yet no study has considered the risk of childhood obesity across several ages or examined the childhood growth trajectory associated with increasing maternal glucose levels among children who were not exposed to maternal diabetes or gestational diabetes in utero. Likewise, little is known regarding the association between increasing maternal glucose levels and childhood cardiometabolic risk factors among children who were not exposed to maternal diabetes or gestational diabetes in utero. There appears to be a continuous association between increasing maternal glucose levels and the risk of several perinatal complications in infants born to women whose pregnancies were not complicated by diabetes, thus it is plausible that increasing pregnancy glucose levels below those diagnostic of disease could also be associated with longer-term adverse outcomes in the offspring.</p><p>In the first study, examination of the crude sex ratio across categories of maternal glycemia suggested a trend consistent with my hypothesis, but the odds ratio estimates did not attain statistical significance. The second study found a significant association between maternal pregnancy glucose levels in women without recognized diabetes or gestational diabetes and increased BMI z-score at 7 years of age in their children. The third study discovered that maternal pregnancy glucose levels in the same population were significantly associated with increased cardiometabolic risk in the children, specifically increased blood pressure and waist circumference. The results of studies two and three extend upon research in women with overt, recognized diabetes or gestational diabetes during pregnancy and lend additional support to the developmental origins of disease hypothesis. The findings of this dissertation indeed suggest that periconceptual and prenatal maternal glucose levels effect immediate and longer-term offspring outcomes. Of particular concern are the findings of studies two and three, which suggest programming for adverse childhood outcomes in women without recognized, overt disease. Given the epidemic of obesity in the U.S. and the relationship between obesity and increased levels of glycemia, these findings suggest the need for lifestyle interventions targeting maternal pregravid obesity and mildly increased levels of pregnancy glycemia in order to improve the health of the next generation.</p></div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/2qj341v3"><img src="/cms-assets/9a04ebaccb13ed5b12a0843754dd00354a6cca04c3cfe384f57c05e64a6f93d1" alt="Cover page: Periconceptional and prenatal maternal glucose levels: immediate and long-term effects on offspring"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/6gz4h75b"><div class="c-clientmarkup">Pyrethroid Pesticide Exposure and Parental Report of Learning Disability and Attention Deficit/Hyperactivity Disorder in U.S. Children: NHANES 1999–2002</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AQuir%C3%B3s-Alcal%C3%A1%2C%20Lesliam">Quirós-Alcalá, Lesliam</a>; </li><li><a href="/search/?q=author%3AMehta%2C%20Suril">Mehta, Suril</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AEskenazi%2C%20Brenda">Eskenazi, Brenda</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucb_postprints">UC Berkeley Previously Published Works</a> (2014)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><h3>Background</h3>Use of pyrethroid insecticides has increased dramatically over the past decade; however, data on their potential health effects, particularly on children, are limited.<h3>Objective</h3>We examined the cross-sectional association between postnatal pyrethroid exposure and parental report of learning disability (LD) and attention deficit/hyperactivity disorder (ADHD) in children 6-15 years of age.<h3>Methods</h3>Using logistic regression, we estimated associations of urinary metabolites of pyrethroid insecticides with parent-reported LD, ADHD, and both LD and ADHD in 1,659-1,680 children participating in the National Health and Nutrition Examination Survey (1999-2002).<h3>Results</h3>The prevalence rates of parent-reported LD, ADHD, and both LD and ADHD were 12.7%, 10.0%, and 5.4%, respectively. Metabolite detection frequencies for 3-PBA [3-phenoxybenzoic acid], cis-DCCA [cis-(2,2-dichlorovinyl)-2,2-dimethylcyclopropane-1-carboxylic acid], and trans-DCCA [trans-(2,2-dichlorovinyl)-2,2-dimethylcyclopropane-1-carboxylic acid] were 77.1%, 35.6%, and 33.9%, respectively. The geometric mean 3-PBA concentration was 0.32 μg/L (median = 0.31 μg/L; interquartile rage = 0.10-0.89 μg/L). cis- and trans-DCCA 75th-percentile concentrations were 0.21 μg/L and 0.68 μg/L, respectively. Log10-transformed 3-PBA concentrations were associated with adjusted odds ratios (ORs) of 1.18 (95% CI: 0.92, 1.51) for parent-reported LD, 1.16 (95% CI: 0.85, 1.58) for ADHD, and 1.45 (95% CI: 0.92, 2.27) for both LD and ADHD. Adjusted ORs remained nonsignificant and decreased after controlling for creatinine and other environmental chemicals previously linked to altered neurodevelopment. Similarly, no significant associations were observed for cis- and trans-DCCA.<h3>Conclusions</h3>Postnatal pyrethroid exposure was not associated with parental report of LD and/or ADHD. Given the widespread and increasing use of pyrethroids, future research should evaluate exposures at current levels, particularly during critical windows of brain development.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/6gz4h75b"><img src="/cms-assets/48cdb714c37a14cebd3aa9d93122f6cda12fe41ac63ac2f8efa50b8e845748c8" alt="Cover page: Pyrethroid Pesticide Exposure and Parental Report of Learning Disability and Attention Deficit/Hyperactivity Disorder in U.S. Children: NHANES 1999–2002"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-thesis">Thesis</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/3mj0844w"><div class="c-clientmarkup">Environmental and epigenetic determinants of child adipokines in a Mexican-American population.</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AVolberg%2C%20Vitaly%20Alexander">Volberg, Vitaly Alexander</a> </li><li class="c-authorlist__begin"><span class="c-authorlist__heading">Advisor(s):</span> <a href="/search/?q=author%3AHolland%2C%20Nina">Holland, Nina</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AEskenazi%2C%20Brenda">Eskenazi, Brenda</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucb_etd">UC Berkeley Electronic Theses and Dissertations</a> (2013)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><p>In the last 30 years there has been a sharp increase in obesity among children, and minority populations are particularly vulnerable. Although etiology of obesity is thought to be multifactorial with causes stemming from diet, environment, genetics and their interaction, no clear molecular pathways have been identified. Underlying obesity development are changes in critical energy balance hormones, adiponectin and leptin (adipokines), however their development and determinants over the childhood period remain poorly understood. </p><p>Previous studies indicate that certain features of the early life environment may have lasting effects on future child metabolic health and highlight the potential obesogenic role of Bisphenol A (BPA) - a high volume production chemical detectable in 93% of the United States population. Mechanisms of BPA action remain uncertain however a leading hypothesis argues that BPA exposure may result in epigenetic changes, such as altered deoxyribonucleic acid (DNA) methylation, affecting expression of adipogenic genes. </p><p>To address these data gaps, we proposed the following specific aims: </p><p>(1) To measure plasma adiponectin and leptin in Mexican-American children from the Center for Health Assessment of Mothers and Children of Salinas (CHAMACOS) cohort at birth and again at 2, 5, and 9 years, examining heterogeneity in adipokine growth patterns and their association with candidate perinatal factors.</p><p>(2) To determine whether maternal or concurrent urinary BPA concentrations are associated with adiponectin and/or leptin levels in children.</p><p>(3) To characterize DNA methylation structure of peroxisome proliferator-activated receptor gamma (PPARy) - the master regulator gene in adipogenesis, determine whether PPARy methylation is associated with child adipokines and/or body size and whether prenatal or concurrent BPA may influence PPARy methylation.</p><p>Our results highlight several developmental differences in adiponectin vs. leptin over the childhood period. While leptin levels closely and positively correlated with child body size at all ages, adiponectin had inverse and weaker associations with body mass index (BMI) at 2, 5, and 9 years. Further, adjusting for BMI, adiponectin reflected an improved lipid profile while leptin was directly related to systolic and diastolic blood pressure in 9-year-old children. </p><p>Of the candidate perinatal factors examined, we identified maternal consumption of sugar-sweetened beverages (SSB) during pregnancy and increased rate of growth during the first 6 months of life as significant risk factors for altered adiponectin levels during childhood. Further, children with greater birth weight had rapidly-rising leptin levels over the birth to 9-year period and highest BMI and waist circumference at 9 years. </p><p>Our BPA analyses indicated sexually dimorphic responses similar to those previously reported in animal studies. While BPA concentrations during early pregnancy were directly associated with adiponectin levels in 9-year-old girls (b=3.71, P=0.03, N=131), BPA concentrations during late pregnancy were associated with increased plasma leptin in 9-year-old boys (b=0.06, P=0.01, N=179), controlling for sociodemographics, dietary variables and child BMI.</p><p> </p><p>Finally, using the Infinium Illumina 450K Array, we examined DNA methylation in 23 sites spanning the PPARy promoter and gene body region in discovery (N=117 at birth, N=108 at 9 years) and validation (N=116 at birth, N=131 at 9 years) sets of children. We report that methylation in site 1 was significantly and negatively associated with child size at birth (b=-2.5, P=0.04) and at 9 years (b=-4.8, P<0.001) in the discovery set, and these relationships were replicated in the validation set. Overall our research adds evidence in support of the hypothesis the children's metabolic health may be programmed during early life and suggests that epigenetic mechanisms may play an important role in determining child size.</p></div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/3mj0844w"><img src="/cms-assets/4fe6c5d8e51a21c5dbbab1a9306421d7645c2d57ff7a7729057db0a1a5c9e8c6" alt="Cover page: Environmental and epigenetic determinants of child adipokines in a Mexican-American population."/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-thesis">Thesis</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/8g93p2fx"><div class="c-clientmarkup">In utero exposure to personal care product and plasticizing chemicals and childhood immune dysfunction</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3ABerger%2C%20Kimberly">Berger, Kimberly</a> </li><li class="c-authorlist__begin"><span class="c-authorlist__heading">Advisor(s):</span> <a href="/search/?q=author%3AHarley%2C%20Kim">Harley, Kim</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AEskenazi%2C%20Brenda">Eskenazi, Brenda</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucb_etd">UC Berkeley Electronic Theses and Dissertations</a> (2018)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><p>Recent studies suggest that phthalates, parabens, and other phenols found in personal care products and plastics may be related to immunologic diseases. This dissertation focuses on in utero exposure to these chemicals and the development of asthma, aeroallergies, and eczema in childhood, as well as lung function and relative concentrations of immune system biomarkers in childhood. We explored measurements of immune system functioning and atopic disease in children in the Center for the Health Assessment of Mothers and Children in Salinas (CHAMACOS) study, a prospective cohort of pregnant women and their children, from age six months to seven years and describes data collection and data consistency across ages. We determined classifications of cases of probable asthma, aeroallergies, and eczema at age seven in this population and found that, at age seven, 36 children out of 353 with relevant data (10%) had probable asthma, 87 children of 339 with relevant data (26%) had aeroallergies, and 23 children of 338 with relevant data (7%) had eczema. Lung function measurements were similar to national averages, and cytokine measurements changed with age in expected patterns.</p><p>We analyzed associations of prenatal urinary concentrations of high molecular weight phthalates and bisphenol A, commonly found in some plastics, with probable asthma, aeroallergies, eczema, and spirometry at age seven, and with blood cytokine measurements at ages two, five, and seven. Logistic and linear regressions were conducted for 392 children, and Bayesian Model Averaging (BMA) was used to identify a select number of additional personal care product and plasticizing chemicals to be controlled for in the models, in order to account for confounding by joint chemical exposure to all phthalates, parabens, and phenols studied in this dissertation. We found that concentrations of monocarboxyisooctyl phthalate (MCOP) were associated with increased odds of having probable asthma (OR: 1.54, 95% CI: 1.12, 2.12) and poorer lung function (RR for forced expiratory volume in one second [FEV1]: -0.09, 95% CI: -0.15, -0.03; RR for forced expiratory flow from 25–75% of FVC [FEF25-75%]: -6.98, 95% CI: -10.95, -2.84). MCOP (OR: 1.28, 95% CI: 1.02, 1.62), MCPP (OR: 1.36, 95% CI: 1.07, 1.73), and BPA (OR: 1.35, 95% CI: 1.06, 1.73) were associated with aeroallergies, in crude models and models adjusting for demographic factors, but not in models adjusting further for additional chemical concentrations.</p><p>We also examined associations between prenatal urinary concentrations of low molecular weight phthalates, parabens, triclosan, 2,4-dichlorophenol, 2,5-dichlorophenol, and benzophenone-3, all commonly found in personal care products, and the outcomes described above. Similar methods were used, including selection of additional chemical covariates using BMA. We found that concentrations of propyl paraben (OR: 0.84, 95% CI: 0.73, 0.97) and 2,5-dichlorophenol (OR: 0.63, 95% CI: 0.47, 0.86) were associated with decreased odds of having probable asthma. We also found that concentrations of monoethyl phthalate (MEP) were associated with lower spirometry measurements (RR for FEV1: -0.03, 95% CI: -0.07, 0.00; RR for FEF25-75%: -3.23, 95% CI: -5.87, -0.52), but that concentrations of mono-n-butyl phthalate (MBP) were associated with higher spirometry measurements (RR for FEV1: 0.06, 95% CI: 0.01, 0.11; RR for FEF25-75%: 4.29, 95% CI: 0.04, 8.71). We also found that MBP concentrations were longitudinally associated with higher T helper cell 2 percentage (Th2%) across ages two, five, and seven (RR: 8.40, 95% CI: 1.95, 15.26) and that mono-isobutyl phthalate (MiBP) concentrations were longitudinally associated with lower T helper 1:T helper 2 cell ratio (RR: -6.19, 95% CI: -11.70, -0.32).</p><p>We explored novel methods to analyze joint exposure to the chemicals studied in this dissertation, as people are typically exposed to mixtures of chemicals, rather than to a single chemical. We chose to analyze probable asthma and allergies, but not eczema, with these methods because eczema showed no associations in our regression analyses above. We also included only FEV1 out of the four spirometry measures, though results for other spirometry measures were similar. We chose not to include cytokine measurements because associations in the above analyses were not consistent and would likely not yield results useful for the demonstration of these new methods. Bayesian Profile Regression was used to cluster children into groups based on their patterns of joint prenatal exposure to phthalates, parabens, and other phenols. Clusters were then evaluated for their relationship to probable asthma, aeroallergies, and FEV1. We found that participants clustered into seven exposure groups, characterized by high and low levels of chemicals consistent with expected patterns of product use. However, these clusters were not related to the three immune outcomes. Bayesian Kernel Machine Regression (BKMR) was used to determine associations of each chemical, in the context of joint exposure to the other chemicals, with probable asthma, aeroallergies, and FEV1. We found that BKMR associations were similar to those found via logistic and linear regressions, and that strong associations of some chemicals had additive effects on associations of other chemicals.</p><p>We found evidence that in utero urinary concentrations of high molecular weight phthalates appear to be associated with asthma and adverse respiratory function in childhood, and possibly with aeroallergies in childhood. In utero urinary concentrations of low molecular weight phthalates appear to be associated with altered cytokine levels in early childhood, and concentrations of parabens and other phenols show limited or no association with respiratory or immune function in childhood.</p></div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/8g93p2fx"><img src="/cms-assets/a9b90924f6f9344aa69d0bcac2a88526df7cc83cad4c527daf3364b977d6a32f" alt="Cover page: In utero exposure to personal care product and plasticizing chemicals and childhood immune dysfunction"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-thesis">Thesis</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/9rh7m44q"><div class="c-clientmarkup">Children's residential exposures to flame retardants, pesticides and pesticide degradation products, and the relationship of pesticides with autonomic nervous system functioning</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AQuiros%20Alcala%2C%20Lesliam">Quiros Alcala, Lesliam</a> </li><li class="c-authorlist__begin"><span class="c-authorlist__heading">Advisor(s):</span> <a href="/search/?q=author%3AEskenazi%2C%20Brenda">Eskenazi, Brenda</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3ANicas%2C%20Mark">Nicas, Mark</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucb_etd">UC Berkeley Electronic Theses and Dissertations</a> (2010)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><p>Protecting children's environmental health is a significant public health challenge given children's unique exposure pathways and special vulnerabilities to environmental contaminants compared to adults. This dissertation focused on topics surrounding children's environmental health research with an emphasis on exposure assessment and application in an epidemiologic investigation. The environmental contaminants that this work focused on included pesticides and polybrominated diphenyl ether (PBDE) flame retardants.</p><p>Chapter 1 provides a general introduction to children's environmental health and highlights the background and significance and specific aims for each study/chapter. </p><p>Chapter 2 focuses on children's residential exposures via house dust to pesticides and PBDEs in low-income homes. House dust was used to assess indoor residential exposures to these environmental contaminants given that for young children this medium serves as a reservoir for contaminants tracked-in or used indoors and a source of non-dietary ingestion. Additionally, the contaminants of interest have been routinely measured in this medium. In this study, concentrations for 24 pesticides, one pesticide synergist, and three PBDE congeners (major constituents of the pentaBDE flame retardant commercial mixture commonly used on furniture) were measured in house dust samples from farmworker and urban homes in California. Pesticides frequently detected in most homes included: organophosphates (chlorpyrifos and diazinon) which were voluntarily phased-out for residential uses prior to this study by the urging of the United States Environmental Protection Agency (EPA); pyrethroids such as permethrins, allethrins, cypermethrins; and the synergist piperonyl butoxide. Interestingly, chlorthal-dimethyl was detected solely in farmworker homes, suggesting contamination due to regional agricultural use. All three PBDE congeners were detected in all homes and maximum concentrations for each of these congeners are the highest reported to date in house dust (BDE-47: 125 632 ng/g, BDE-99: 218 768 ng/g, BDE-100: 41 149 ng/g). Possible explanations for the high PBDE concentrations observed include California's stringent flammability standards and the presence of poorly constructed or deteriorating furniture treated with PBDEs as previously hypothesized by other researchers. Additionally, diazinon and chlorpyrifos concentrations in Salinas farmworker homes were lower than concentrations reported in samples from Salinas farmworker homes studied between 2000-2002, suggesting a temporal reduction after the U.S. Environmental Protection Agency's voluntary residential phase-out. Lastly, for some resident children, estimated non-dietary PBDE but not pesticide intake exceeded U.S. EPA recommended chronic reference doses (RfDs). </p><p>In chapter 3 the presence in the environment of dialkylphosphates (DAPs), non-specific urinary OP pesticide metabolites, and their relation to children's urinary DAP metabolites was investigated. Although DAPs were found to be present in the environment, as assessed in house dust, this medium may not play a significant contribution to the DAPs observed in children's urine. The non-dietary ingestion exposure route for environmental DAPs was estimated to be <5% of the dose calculated from DAP levels in children's urine. The distribution of concentrations of diethyl and dimethyl DAPs in dust differed from those observed in children's urine, a finding suggesting that DAPs behave differently in the environment and in the body. However, if humans excrete DAPs unchanged then it is possible for urinary DAPs to reflect exposure to both OP pesticides and DAPs present in one's environment and/or food. Results from this study indicate other sources and pathways, such as DAPs in food, may impact urinary DAP levels more significantly than DAPs in dust. More research is needed on the pharmacokinetics and toxicodynamics of preformed DAPs and other specific OP metabolites to determine the extent of their contribution to urinary biomarkers in humans.</p><p>In chapter 4 the effects of early life exposures to OP pesticides, as assessed by urinary DAP metabolites, on children's autonomic dysregulation (concomitant sympathetic activation and parasympathetic withdrawal) were assessed at several time points (i.e., when children were 6 months and 1, 3 ½ and 5 years of age). This is the first study to use ANS response measures as outcomes to investigate the association between OP pesticide exposures in children and ANS regulation. The study population was part of the Center for Children's Environmental Health Research longitudinal birth cohort study (CHAMACOS). Children in this cohort live in the Salinas Valley, an agricultural region in California with intense OP pesticide use and were predominantly from Mexico or Mexican-American. Children's autonomic nervous system (ANS) function was assessed using resting and reactivity measures of respiratory sinus arrhythmia (RSA), pre-ejection period (PEP), and heart rate (HR), while OP pesticide exposures were assessed in utero and postnatally by using urinary DAPs. Although the results suggest that OP pesticides at the exposure levels observed are not associated with children's ANS dysregulation, the study focused on a relatively demographically and ethnically homogeneous study population; thus, the results may not be generalizable to other populations. Future investigations in this population will involve evaluating what factors predict ANS regulation and whether ANS resting and reactivity measures of HR, RSA, and PEP are related to later physical and mental problems as observed in prior studies.</p><p>Finally, chapter 5 highlights the major findings, public health implications and future directions for each chapter/study.</p></div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/9rh7m44q"><img src="/cms-assets/0efa91e5fdf11c5cf933cc99fbae1242e52829241fcf4c2215712d409b8dabef" alt="Cover page: Children's residential exposures to flame retardants, pesticides and pesticide degradation products, and the relationship of pesticides with autonomic nervous system functioning"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-thesis">Thesis</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/1908k2m0"><div class="c-clientmarkup">Exposure to Manganese from Agricultural Pesticide Use and Neurodevelopment in Young Children</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AGunier%2C%20Robert%20Bruce">Gunier, Robert Bruce</a> </li><li class="c-authorlist__begin"><span class="c-authorlist__heading">Advisor(s):</span> <a href="/search/?q=author%3AEskenazi%2C%20Brenda">Eskenazi, Brenda</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AJerrett%2C%20Michael">Jerrett, Michael</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucb_etd">UC Berkeley Electronic Theses and Dissertations</a> (2013)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><p>Using data from the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS) study, this dissertation shows that agricultural use of fungicides that contain manganese (Mn) results in higher levels of Mn in children's homes and teeth, and that higher Mn levels in children's teeth are associated with a modest deficit in neurodevelopment at 6-months of age. In Chapter 2, predictors of Mn concentrations and loadings in house dust samples are evaluated. The fungicides maneb and mancozeb are approximately 21% Mn by weight and more than 150,000 kg are applied each year to crops in the Salinas Valley, California. It is not clear whether agricultural use of these fungicides increases Mn levels in homes. In this study, predictors of Mn levels in house dust samples are evaluated. House dust samples were collected from 378 residences enrolled in the CHAMACOS study with a second sample collected nine months later from 90 residences. House dust samples were analyzed for Mn using inductively coupled plasma optical emission spectroscopy. Information from interviews, home inspections, and pesticide use reporting data was used to identify potential predictors of Mn dust concentrations and loadings. Linear mixed-effects models were used to identify significant predictors. Mn was detectable in dust samples from all homes. The median Mn concentration was 171 µg/g and median Mn loading was 1,908 µg/m2 at first visit. In multivariable models, Mn dust concentrations and loadings increased with the number of farmworkers in the home and the amount of agricultural Mn fungicides applied within three kilometers of the residence. Dust concentrations and loadings were higher in residences located on Antioch Loam soil than other soil types, in homes with poor or average compared to excellent housekeeping practices, and residences located in the southern Salinas Valley compared those located in the town of Salinas or the northern part of the Salinas Valley. In summary, agricultural use of Mn containing fungicides were found to contribute to Mn dust concentrations and loadings in nearby residences and farmworker homes.</p><p>Chapter 3 presents an analysis that identifies determinants of Mn in prenatal dentin from children's shed teeth. Mn is an essential nutrient, but over-exposure can be neurotoxic. Over 800,000 kilograms of Mn-containing fungicides are applied each year in California. Manganese levels in teeth are a promising biomarker of perinatal exposure. Participants in this analysis included 207 children enrolled in the CHAMACOS study, a longitudinal birth cohort study in an agricultural area of California. Mn was measured in teeth using laser-ablation-inductively coupled plasma-mass spectrometry. The purpose of this analysis was to determine environmental and lifestyle factors related to prenatal Mn levels in shed teeth. Storage of farmworkers' shoes in the home, maternal farm work, agricultural use of Mn-containing fungicides within 3 km of the residence, residence built on Antioch Loam soil and Mn dust loading (µg/m2 of floor area) during pregnancy were associated with higher Mn levels in prenatal dentin (p<0.05). Maternal smoking during pregnancy was inversely related to Mn levels in prenatal dentin (p<0.01). Multivariable regression models explained 22 - 29% of the variability of Mn in prenatal dentin. These results suggest that Mn measured in prenatal dentin provides retrospective and time specific levels of exposure to the fetus resulting from environmental and occupational sources.</p><p>Chapter 4 evaluates the association between Mn in prenatal and postnatal dentin of children's shed teeth and early neurodevelopment. Previous studies have observed associations between Mn exposure and children's neurodevelopment, primarily using concurrent exposure measurements in blood or hair. Prenatal and postnatal Mn exposures have not been evaluated together in a prospective study of neurodevelopment in young children. Mn levels in prenatal and postnatal dentin were measured from children's shed teeth. 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 was examined. The possibility of an inverted U-shaped association with neurodevelopment was explored since Mn is an essential nutrient. Potential interactions between Mn exposure and blood lead concentrations were also evaluated as well as effect modification by maternal iron status during pregnancy. An inverse association between postnatal Mn levels in dentin and psychomotor development at 6-months of age was observed with a modest decrease in psychomotor development scores, which followed an inverse U-shape, with the strongest effect observed when comparing the highest tertile of Mn levels in teeth to the middle tertile of Mn levels in teeth (-4.6 points; 95% Confidence Interval: -8.0, -1.3). Among children whose mothers' were iron deficient during pregnancy, prenatal Mn levels in dentin were associated with both mental and psychomotor development at 6-months. No interactions with prenatal or postnatal blood lead concentrations were observed in this cohort. In conclusion, a modest decrease in psychomotor development at 6-months of age was associated with postnatal Mn levels in dentin from a mean score of 96 for the middle tertile compared to 94 at the highest tertile. Iron status during pregnancy appeared to be a potentially important effect modifier of prenatal Mn exposure and neurodevelopment at 6-months of age.</p></div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/1908k2m0"><img src="/cms-assets/e94c79929174525286bfaa0906eba24d52b623b99304fe015077ef4005adb330" alt="Cover page: Exposure to Manganese from Agricultural Pesticide Use and Neurodevelopment in Young Children"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-thesis">Thesis</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/32v8g97t"><div class="c-clientmarkup">Examining Pesticide Exposure, Dose, and Neurobehavioral Effects among Children and Adolescents Living in California’s Salinas Valley</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AHyland%2C%20Carly">Hyland, Carly</a> </li><li class="c-authorlist__begin"><span class="c-authorlist__heading">Advisor(s):</span> <a href="/search/?q=author%3AEskenazi%2C%20Brenda">Eskenazi, Brenda</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3ABradman%2C%20Asa">Bradman, Asa</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucb_etd">UC Berkeley Electronic Theses and Dissertations</a> (2021)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><p>Prenatal organophosphate (OP) pesticide exposure has been associated with adverse neurodevelopment, including decreased cognition, increased hyperactivity and inattention, and higher risk for autism-related traits in multiple studies. However, OP pesticide use has decreased in recent decades and data gaps exist regarding the neurodevelopmental impacts of current-use pesticides, such as neonicotinoids, glyphosate, and pyrethroids. Moreover, most people, particularly those living in agricultural areas, are exposed to multiple pesticides and research is needed to examine the effects of these mixtures that may interact synergistically to adversely impact health and neurodevelopment. Mounting evidence also suggests that the effects of environmental toxicants are due in part to causal interactions with social stressors and biologic factors, e.g., genetics, however studies investigating the neurodevelopmental impacts of environmental exposures have typically treated social factors as confounders. Failure to account for potential effect modification by these factors may underestimate the impact of environmental neurotoxicants, particularly among the most vulnerable populations where exposures to environmental and non-chemical stressors are likely to co-occur. Additionally, previous exposure assessment and epidemiology studies investigating pesticide exposures and subsequent health effects have largely relied on the analysis of dialkylphosphate (DAPs) metabolites, non-specific biomarkers of OP pesticide exposure, from random spot urine samples. DAPs have higher inter- and intra-individual variability and data gaps exist regarding the extent to which concentrations from spot samples may approximate internal dose from the “gold standard” 24-hour urine samples, which has implications for pesticide risk assessment and the establishment of regulatory guidelines. This dissertation aims to examine the validity of using DAPs assessed from random spot urine samples to estimate cumulative OP pesticide dose, the associations between applications of mixtures of agricultural pesticides near the home during pregnancy and early childhood with adolescent neurobehavioral functioning, and the joint effects of use of mixtures of agricultural pesticides near the home during pregnancy and adverse childhood experiences (ACEs) on adolescent neurobehavioral outcomes. Chapter 1 provides a general introduction to human exposure to agricultural pesticides and highlights the background, significance, and specific aims for each study/chapter. Chapter 2 examines the validity of using first morning void (FMV) and random non-FMV urine samples to estimate cumulative 24-hr OP pesticide dose among participants in the Child Validation Study (CVS). For this study, investigators collected urine samples over seven consecutive days, including two 24-hr samples, from 25 children living in the agricultural Salinas Valley, California. These analyses employed measurements of urinary DAP metabolites, data on nearby agricultural pesticide applications, and daily dietary intake data to estimate internal dose from exposure to a mixture of OP pesticides according to the United States (US) Environmental Protection Agency (EPA) Cumulative Risk Assessment guidelines. Dose estimates from volume- and creatinine-adjusted same-day FMV and non-FMV spot urine samples were compared to the “gold standard” estimates from 24-hr samples. Non-FMV samples had relatively weak ability to predict 24-hr dose (R2=0.09-0.38 for total DAPs) and tended to underestimate the percentage of samples exceeding regulatory guidelines. Models with FMV samples or the average of an FMV and non-FMV sample were similarly predictive of 24-hr estimates (R2 for DAPs=0.40-0.68 and 0.40-0.80, respectively, depending on volume adjustment method). Findings for these analyses suggest that reliance on non-FMV samples for risk assessments may underestimate daily OP dose and the percentage of children with dose estimates exceeding regulatory guidelines. Chapter 3 examines associations of applications of mixtures of agricultural pesticides within 1 kilometer (km) of the home during pregnancy and early childhood (ages 0-5 years) and adolescent internalizing and externalizing behaviors in the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS) cohort. These analyses employed linear mixed effects Bayesian Hierarchical Models (BHM) to examine associations with maternal- and youth-reported behavioral and emotional problems from the Behavior Assessment System for Children, 2nd edition (BASC-2) at ages 16 and 18 years (n=593). Associations between pesticide applications and neurobehavioral outcomes were largely null. There were some trends of modestly increased internalizing behaviors and attention problems in association with OP insecticide use near the home during the prenatal period. In the postnatal period, a two-fold increase in glyphosate applications was associated with more youth-reported depression (β=1.2; 95% Credible Interval (CrI): 0.2, 2.2) and maternal-reported internalizing behaviors (β=1.23; 95% CrI: 0.2, 2.3) and anxiety (β=1.2; 95% CrI: 0.2, 2.3). There were some protective associations with imidacloprid, a neonicotinoid, during the prenatal period, particularly in sex-specific analyses. This study extends previous work by considering the neurobehavioral effects of potential exposure to mixtures of pesticides. Chapter 4 examines interactions of applications of pesticide mixtures near the home during pregnancy and childhood adversity with adolescent neurobehavioral outcomes among CHAMACOS participants. These analyses employed linear mixed effects BHM to examine the joint effect of applications of 11 agricultural within 1 km of maternal homes during pregnancy and youth-reported Adverse Childhood Experiences (ACEs) with maternal and youth-reported internalizing behaviors, hyperactivity, and attention problems at ages 16 and 18 years. Overall, there was little evidence of modification of exposure-outcome associations by ACEs. Malathion use near the home during pregnancy with associated with increased internalizing behaviors among those with high ACEs from both maternal report (β = 1.9; 95% CrI: 0.2, 3.7 for high ACEs [3+] vs. β = -0.1; 95% (CrI): -1.2, 0.9 for low ACEs [0-2]) and youth report (β = 2.1; 95% CrI: 0.4, 3.8 for high ACEs vs. β = 0.2; 95% CrI: -0.8, 1.2 for low ACEs). Results were stronger among males for both maternal and youth report of internalizing behaviors. Applications of malathion and dimethoate were also associated with higher youth-reported hyperactivity and/or inattention among those with high ACEs. There was no evidence of effect modification by ACEs for any other pesticides. This analysis builds upon previous studies by considering co-exposure to mixtures of agricultural pesticides and social adversity. It is the first to examine interactions of chemical and non-chemical stressors on neurobehavioral development assessed during adolescence or early adulthood. Chapter 5 highlights the major findings for each chapter/study, conclusion, and future directions. </p></div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/32v8g97t"><img src="/cms-assets/fb878e4142d6542bd8c0e54578a5116eadbbfc6e4b70122e5bdf12a02087a196" alt="Cover page: Examining Pesticide Exposure, Dose, and Neurobehavioral Effects among Children and Adolescents Living in California’s Salinas Valley"/></a></div></section><nav class="c-pagination--next"><ul><li><a href="" aria-label="you are on result set 1" class="c-pagination__item--current">1</a></li><li><a href="" aria-label="go to result set 2" class="c-pagination__item">2</a></li><li><a href="" aria-label="go to result set 3" class="c-pagination__item">3</a></li><li><a href="" aria-label="go to result set 4" class="c-pagination__item">4</a></li><li><a href="" aria-label="go to result set 25" class="c-pagination__item">25</a></li><li class="c-pagination__next"><a href="" aria-label="go to Next result set">Next</a></li></ul></nav></section></main></form></div><div><div class="c-toplink"><a href="javascript:window.scrollTo(0, 0)">Top</a></div><footer class="c-footer"><nav class="c-footer__nav"><ul><li><a href="/">Home</a></li><li><a href="/aboutEschol">About eScholarship</a></li><li><a href="/campuses">Campus Sites</a></li><li><a href="/ucoapolicies">UC Open Access Policy</a></li><li><a href="/publishing">eScholarship Publishing</a></li><li><a href="https://www.cdlib.org/about/accessibility.html">Accessibility</a></li><li><a href="/privacypolicy">Privacy Statement</a></li><li><a href="/policies">Site Policies</a></li><li><a href="/terms">Terms of Use</a></li><li><a href="/login"><strong>Admin Login</strong></a></li><li><a href="https://help.escholarship.org"><strong>Help</strong></a></li></ul></nav><div class="c-footer__logo"><a href="/"><img class="c-lazyimage" data-src="/images/logo_footer-eschol.svg" alt="eScholarship, University of California"/></a></div><div class="c-footer__copyright">Powered by the<br/><a href="http://www.cdlib.org">California Digital Library</a><br/>Copyright © 2017<br/>The Regents of the University of California</div></footer></div></div></div></div> <script src="/js/vendors~app-bundle-7424603c338d723fd773.js"></script> <script src="/js/app-bundle-63f992b6abba5f8338a3.js"></script> </body> </html>