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Your Environment. Your Health.

Goal 2 – Individual Susceptibility Across the Lifespan

Implementation Highlights and Accomplishments

Woman looking into test tube

Understand individual susceptibility across the life span to chronic, complex diseases resulting from environmental factors, in basic and population-based studies, to facilitate prevention and decrease public health burden.

  1. Using a life-span approach, identify critical windows of susceptibility to the effects of environmental exposures.
  2. Deepen our understanding of dose-response relationships to environmental factors across the life span.
  3. Study the factors that determine individual susceptibility to environmental stressors across the life span.

Research Funding

The Preconception Exposure Window and Health of the Offspring (R01)
The purpose of this Funding Opportunity Announcement (FOA) is to encourage grant applications from the scientific community that use animal models to investigate whether environmental exposures to male or female germ cells during the preconception time period (pre-fertilization) can cause molecular alterations that lead to later-life traceable phenotypic outcomes in the first generation offspring. ES-16-007

Using Omics to Define Human Placental Development and Function Across Pregnancy (R21)
This Funding Opportunity Announcement (FOA) invites grant applications for research directed at the development of omics profiles reflecting human placental development and function across gestation.  A goal of this FOA is to create a community resource of research resources that are broadly available and shared with the research community for providing a foundation for further integration with other novel technologies being developed to advance safe, real time placental assessment in vivo, as well as for providing large amounts of complex data and associated metadata to the research community to further advance and accelerate research in the field. RFA-HD-16-037

Environmental influences on Placental Origins of Development (ePOD) R01
The purpose of this FOA is to stimulate multidisciplinary research projects from the scientific community that use a combination of animal/cell models and non-invasive human placenta tissues or biomarkers to investigate how early life exposures affect placental growth, development, and function, and the subsequent health of the offspring. RFA-ES-17-005

Children's Health Exposure Analysis Resource (CHEAR)
NIEHS is establishing an infrastructure, the Children's Health Exposure Analysis Resource (CHEAR), to provide the extramural research community access to laboratory and statistical analyses to add or expand the inclusion of environmental exposures in their research.  CHEAR is being solicited through three FOAs, this FOA solicits a network of laboratories providing a comprehensive suite of laboratory-based analytical services for samples derived from extant or ongoing children's health studies in the extramural research community. Each laboratory center (defined in this FOA as a Hub) within the network will provide analysis of environmental and endogenous exposures through both targeted and untargeted approaches.  Each Hub will also provide analyses of biological response indicators such as DNA damage, oxidative stress, immune/inflammation indicators and other molecular markers.  Hubs will incorporate a developmental core to develop novel measures for exposures and responses, expanding the number of current, commonly measured analytes, and developing new methods for detecting analytes in other biological matrices, in addition to serum, plasma or urine.

The Children's Health Exposure Analysis Resource (CHEAR) is a multi-unit infrastructure to provide access to comprehensive exposure analysis that can be performed using biological samples collected in studies of children's health.  The network has three units, a National Exposure Assessment Laboratory Network and an Exposure Data Repository and Resource for Statistical Analysis and Methods Development, as well as a coordinating center. ES-15-009, ES-15-010, ES-15-011

Environmental Influences during Windows of Susceptibility in Breast Cancer Risk (U01)
This funding opportunity will support transdisciplinary research projects to investigate the influence of environmental exposures during specific time windows of susceptibility on breast cancer risk. Applicants must propose transdisciplinary research project that addresses one or more potential windows of susceptibility and facilitates the integration of experimental model and human studies to accelerate understanding of the contribution of environmental factors to breast cancer risk, the underlying mechanisms, and potential prevention strategies. ES-14-011, ES-14-012

Children's Environmental Health and Disease Prevention Research Centers (P50)
This Funding Opportunity Announcement (FOA) encourages grant applications to support a transdisciplinary program of basic and applied research to examine the effects of environmental factors on children’s health and well-being. Research conducted through the Centers should include substantive areas of science in children’s health while incorporating innovative technologies and approaches and links to the environment. This program encourages strong links between disciplines in the basic, applied, clinical and public health sciences to prevent disease and promote health of all children ES-14-002

The Role of Environmental Exposures in the Development of Autoimmune Disease (R21)
This announcement encourages exploratory research applications aimed at investigating the role environmental exposures play in the development and/or the exacerbation of autoimmune disease. Of particular interest are projects that will identify and characterize critical windows of exposure susceptibility, projects that explore mechanisms responsible for gender differences in response and development of autoimmune disease, and studies that can produce potential biomarkers for use in subsequent human surveillance studies. ES-13-011

Research Linking Environmental Exposure to Alzheimer's Disease (R01)
The purpose of this funding opportunity announcement (FOA) is to support research establishing a link between environmental exposure and the risk for Alzheimer’s disease (AD). Research is encouraged ranging from basic mechanistic exposure studies to human-based studies. This new effort seeks to promote work to further the understanding of the combined roles of exposure and processes implicated in AD such as inflammation and genetic susceptibility. This FOA is intended to support the broad research goals of the 2012-2017 Strategic Plan for NIEHS. ES-13-006, ES-13-006

Selected Programs and Awards

2017 NIEHS Outstanding New Environmental Scientist (ONES) Awardee James Roede, Ph.D., from the University of Colorado, Denver, will use cellular and animal models to investigate the impact of the fungicide Maneb on the cellular mechanisms involved in brain cell development.

NIH High Risk High Reward Awards
Manish Arora, Ph.D., an environmental scientist and dentist at the Icahn School of Medicine at Mount Sinai, won the New Innovator Award for Reconstructing Fetal Toxicant Exposure and Homeostatic Disruptions. Arora and his colleagues developed and validated this innovative use of baby teeth with NIEHS support. They previously showed that the amount of lead in dentine formed around the time of birth was strongly correlated with lead levels in umbilical cord blood.

2016 Outstanding New Environmental Scientist (ONES) Awardees Michele La Merrill, Ph.D., from the University of California, Davis, will explore whether exposure to the pesticide DDT during pregnancy causes insulin resistance, by interfering with the production of body heat.

Maitreyi Mazumdar, M.D., from Harvard Medical School, the Harvard T.H. Chan School of Public Health, and Boston Children’s Hospital (BCH), will research whether prenatal exposure to arsenic may increase the risk of infant neural tube defects.

Selected Scientific Advances

2017

  • Taylor KW (NTP), DD Baird (DIR), AH Herring, LS Engel, HB Nichols, DP Sandler (DIR) and MA Troester. 2017. Associations among personal care product use patterns and exogenous hormone use in the NIEHS Sister Study. J Expo Sci Environ Epidemiol 27:458-464. [Abstract]
    This study used a data-centered approach to classify complex patterns of exposure to personal care products and to understand how these patterns vary according to use of exogenous hormone exposures, oral contraceptives, and post-menopausal hormone therapy.
  • Williams CJ (DIR), A Chu, WN Jefferson (DIR), D Casero, D Sudhakar, N Khurana, CP Hogue, C Aryasomayajula, P Patel, P Sullivan, E Padilla-Banks (DIR), S Mohandessi, C Janzen and M Wadehra. 2017. Epithelial membrane protein 2 (EMP2) deficiency alters placental angiogenesis, mimicking features of human placental insufficiency. J Pathol 242(2):246-259. [Abstract]
    To test the role of Epithelial membrane protein-2 (EMP2) in pregnancy, mice lacking EMP2 were generated and their fertility was examined. To determine if these results translated to human pregnancy, placentas from normal, term deliveries or those complicated by placental insufficiency resulting in intrauterine growth restriction (IUGR) were stained for EMP2.
  • Cisse YM, Russart KL, Nelson RJ. 2017. Parental Exposure to Dim Light at Night Prior to Mating Alters Offspring Adaptive Immunity. Sci Rep 7:45497. [Abstract]
    This study explored the relationship between parental exposure to dim light at night and cell-mediated and humoral immunity in their offspring.
  • Stanko JP (NTP), GE Kissling (DIR), VA Chappell (NTP) and SE Fenton (NTP). 2016. Differences in the Rate of in Situ Mammary Gland Development and Other Developmental Endpoints in Three Strains of Female Rat Commonly Used in Mammary Carcinogenesis Studies: Implications for Timing of Carcinogen Exposure. Toxicol Pathol 44(7):1021-33. [Abstract]
    In this study, in situ mammary gland development was assessed in females of the Harlan Sprague-Dawley (Hsd:SD), Charles River Sprague-Dawley (Crl:SD), and Charles River Long-Evans (Crl:LE) rat strains at postnatal days 25, 33, and 45.
  • Grau-Perez M, Kuo CC, Spratlen M, Thayer KA (NTP), Mendez MA, Hamman RF, Dabelea D, Adgate JL, Knowler WC, Bell RA, Miller FW (DIR), Liese AD, Zhang C, Douillet C, Drobna Z, Mayer-Davis EJ, Styblo M, Navas-Acien A. 2017. The Association of Arsenic Exposure and Metabolism with Type 1 and Type 2 Diabetes in Youth: The SEARCH Case-Control Study. Diabetes Care 40(1):46-53. [Abstract]
    Researchers examined the association of arsenic with type 1 and type 2 diabetes in the SEARCH for Diabetes in Youth Case-Control (SEARCH-CC) study.
  • Bernardi LA, Carnethon MR, de Chavez PJ, Ikhena DE, Neff LM, Baird DD (DIR), Marsh EE. 2017. Relationship between obesity and anti-Mullerian hormone in reproductive-aged African American women. Obesity (Silver Spring) 25(1):229-235. [Abstract]
    Using data form women participating in an ongoing National Institute of Environmental Health Sciences study, the authors aimed to determine whether there is an association between obesity and anti-Müllerian hormone (AMH) among reproductive-aged African American women (AAW).
  • Zuccolo L, DeRoo LA, Wills AK, Davey Smith G, Suren P, Roth C, Stoltenberg C, Magnus P. 2016. Pre-conception and prenatal alcohol exposure from mothers and fathers drinking and head circumference: results from the Norwegian Mother-Child Study (MoBa). Sci Rep 7:39535. [Abstract]
    Using data from 68,244 mother-father-offspring trios from the Norwegian Mother and Child Cohort Study (MoBa) (1999-2009), this study investigated the association of maternal and paternal alcohol drinking before and early in pregnancy with infant head circumference.
  • Reid NM, Proestou DA, Clark BW, Warren WC, Colbourne JK, Shaw JR, Karchner SI, Hahn ME, Nacci D, Oleksiak MF, Crawford DL, Whitehead A. 2016. The genomic landscape of rapid repeated evolutionary adaptation to toxic pollution in wild fish. Science 354(6317):1305-1308. [Abstract]
    Through analysis of 384 whole killifish genome sequences and comparative transcriptomics in four pairs of sensitive and tolerant populations, the authors identify the aryl hydrocarbon receptor-based signaling pathway as a shared target of selection.
  • Renzetti S, Just AC, Burris HH, Oken E, Amarasiriwardena C, Svensson K, Mercado-Garcia A, Cantoral A, Schnaas L, Baccarelli AA, Wright RO, Tellez-Rojo MM. 2017. The association of lead exposure during pregnancy and childhood anthropometry in the Mexican PROGRESS cohort. Environ Res 152:226-232. [Abstract]
    The objective of this study was to determine how lead exposure during pregnancy is associated with children's growth parameters, including height, weight, body mass index and percentage body fat measured between ages 4-6 years old in a Mexico City pregnancy cohort.

2016

  • Eckel SP, Cockburn M, Shu YH, Deng H, Lurmann FW, Liu L, Gilliland FD. 2016. Air pollution affects lung cancer survival. Thorax 71(10):891-898. [Abstract]
    This study aimed to determine whether ambient air pollutant exposures are associated with the survival of patients with lung cancer.
  • Dunaway KW, Islam MS, Coulson RL, Lopez SJ, Vogel Ciernia A, Chu RG, Yasui DH, Pessah IN, Lott P, Mordaunt C, Meguro-Horike M, Horike SI, Korf I, LaSalle JM. 2016. Cumulative Impact of Polychlorinated Biphenyl and Large Chromosomal Duplications on DNA Methylation, Chromatin, and Expression of Autism Candidate Genes. Cell Rep 17(11):3035-3048. [Abstract]
    Using whole-genome bisulfite sequencing in brain tissue and a neuronal cell culture model carrying a 15q11.2-q13.3 maternal duplication, this study describes how significant global DNA hypomethylation is enriched over autism candidate genes and affects gene expression.
  • Buckley JP, Engel SM, Braun JM, Whyatt RM, Daniels JL, Mendez MA, Richardson DB, Xu Y, Calafat AM, Wolff MS, Lanphear BP, Herring AH, Rundle AG. 2016. Prenatal phthalate exposures and body mass index among 4 to 7 year old children: A pooled analysis. Epidemiology 27(3):449-58. [Abstract]
  • Bell MR, Thompson LM, Rodriguez K, Gore AC. 2016. Two-hit exposure to polychlorinated biphenyls at gestational and juvenile life stages: 1. Sexually dimorphic effects on social and anxiety-like behaviors. Horm Behav 78:168-77. [Abstract]
  • Bell MR, Hart BG, Gore AC. 2016. Two-hit exposure to polychlorinated biphenyls at gestational and juvenile life stages: 2. Sex-specific neuromolecular effects in the brain. Mol Cell Endocrinol 420:125-37. [Abstract]
  • Markunas CA (DIR), AJ Wilcox (DIR), Z Xu (DIR), BR Joubert (DIR), S Harlid (DIR), V Panduri (DIR), SE Haberg, W Nystad, SJ London (DIR), DP Sandler (DIR), RT Lie, PA Wade (DIR) and JA Taylor (DIR). 2016. Maternal Age at Delivery Is Associated with an Epigenetic Signature in Both Newborns and Adults. PLoS ONE 11(7):e0156361 [Abstract]
  • Rowe C, Gunier R, Bradman A, Harley KG, Kogut K, Parra K, Eskenazi B. 2016. Residential proximity to organophosphate and carbamate pesticide use during pregnancy, poverty during childhood, and cognitive functioning in 10-year-old children. Environ Res 150:128-137.   [Abstract]
  • McGuinn LA, Voss RW, Laurent CA, Greenspan LC, Kushi LH, Windham GC. 2016. Residential proximity to traffic and female pubertal development. Environ Int 94:635-641. [Abstract]
  • Glicksberg BS, Li L, Badgeley MA, Shameer K, Kosoy R, Beckmann ND, Pho N, Hakenberg J, Ma M, Ayers KL, Hoffman GE, Dan Li S, Schadt EE, Patel CJ, Chen R, Dudley JT. 2016. Comparative analyses of population-scale phenomic data in electronic medical records reveal race-specific disease networks. Bioinformatics 32(12):i101-i110. [Abstract]
  • Jusko TA, Oktapodas M, Palkovičová Murinová L, Babinská K, Babjaková J, Verner MA, DeWitt JC, Thevenet-Morrison K, Čonka K, Drobná B, Chovancová J, Thurston SW, Lawrence BP, Dozier AM, Järvinen KM, Patayová H, Trnovec T, Legler J, Hertz-Picciotto I, Lamoree MH. 2016. Dietary Determinants of Perfluorooctane Sulfonic (PFOS) and Perfluorooctanoic Acid (PFOA) Concentrations in Human Colostrum. Environ Sci Technol 50(13):7152-62. [Abstract]
  • O'Brien KM (DIR), Shi M (DIR), Sandler DP (DIR), Taylor JA (DIR), Zaykin DV (DIR), Keller J, Wise AS (DIR), Weinberg CR (DIR). 2016. A family-based, genome-wide association study of young-onset breast cancer: inherited variants and maternally mediated effects. Eur J Hum Genet 24(9):1316-23. [Abstract]
  • Parks CG (DIR), AA D'Aloisio (DIR) and DP Sandler (DIR). 2016. Early Life Factors Associated with Adult-Onset Systemic Lupus Erythematosus in Women. Front Immunol 7(103):1-7. [Abstract]
  • Stingone JA, McVeigh KH, Claudio L. 2016. Association between prenatal exposure to ambient diesel particulate matter and perchloroethylene with children's 3rd grade standardized test scores. Environ Res 148:144-153. [Abstract]
  • Huen K, Calafat AM, Bradman A, Yousefi P, Eskenazi B, Holland N. 2016. Maternal phthalate exposure during pregnancy is associated with DNA methylation of LINE-1 and Alu repetitive elements in Mexican-American children. Environ Res 148:55-62. [Abstract]
  • Mora-Zamorano FX, Klingler R, Murphy C, Basu N, Head JH, Carvan Iii MJ. 2016. Parental whole life cycle exposure to dietary methylmercury in zebrafish (Danio rerio) affects the behavior of offspring. Environ Sci Technol 50(9):4808-16. [Abstract]
  • James P, Hart JE, Banay RF, Laden F. 2016. Exposure to Greenness and Mortality in a Nationwide Prospective Cohort Study of Women. Environ Health Perspect 124(9):1344-52. [Abstract]

2015

  • Fannin RD (DIR), K Gerrish (DIR), SO Sieber (DIR), PR Bushel (DIR), PB Watkins and RS Paules (NTP). 2015. Blood transcript immune signatures distinguish a subset of people with elevated serum ALT from others given acetaminophen. Clin Pharmacol Ther 99:432-441. [Abstract]
  • White AJ, Nichols HB, Bradshaw PT, Sandler DP (DIR). 2015. Overall and central adiposity and breast cancer risk in the Sister Study. Cancer 121(20):3700-8. [Abstract]
  • Upson K (DIR), Harmon QE (DIR), Baird DD (DIR). 2015. Soy-Based Infant Formula Feeding and Ultrasound-Detected Uterine Fibroids among Young African-American Women with No Prior Clinical Diagnosis of Fibroids. Environ Health Perspect 124(6):769-75. [Abstract]
  • Sen A, Heredia N, Senut MC, Land S, Hollocher K, Lu X, Dereski MO, Ruden DM. 2015. Multigenerational epigenetic inheritance in humans: DNA methylation changes associated with maternal exposure to lead can be transmitted to the grandchildren. Sci Rep 5:14466. [Abstract]
  • 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. 2015. Prenatal Exposure to Organophosphorous Pesticides and Fetal Growth: Pooled Results from Four Longitudinal Birth Cohort Studies. Environ Health Perspect 124(7):1084-1092. [Abstract]
  • Hewitt Fenton SE (NTP) and LS Birnbaum (OD). 2015. Timing of Environmental Exposures as a Critical Element in Breast Cancer Risk. J Clin Endocrinol Metab 100(9):3245-3250. [Abstract]
    Examining reports from the 2009 President’s Cancer Panel, 2012 Institute of Medicine, 2013 Interagency Breast Cancer and the Environment Coordinating Committee as well as research publications dating back to 2012, scientists provided evidence for a lack of data in early life exposures and the risk of breast cancer over a lifetime despite evidence suggesting some chemicals have a more pronounced increase in breast cancer risk when exposure occurs early in life.
  • Tyler CR, Hafez AK, Solomon ER, Allan AM. 2015. Developmental exposure to 50 parts-per-billion arsenic influences histone modifications and associated epigenetic machinery in a region- and sex-specific manner in the adult mouse brain. Toxicol Appl Pharmacol 288(1):40-51. [Abstract]
    This work exposes potential mechanisms of arsenic toxicity and the long-term impact of fetal exposures to environmentally relevant levels of arsenic that may affect susceptibility to disease in adulthood.
  • Debes F, Weihe P, Grandjean P. 2015. Cognitive deficits at age 22 years associated with prenatal exposure to methylmercury. Cortex 74:358-369. [Abstract]
    Using a birth cohort in the Faroe Islands, this work extends previous findings of persistent cognitive effects after developmental exposure to adulthood using multiple cognitive tests and statistical modeling analyses suggesting prenatal exposure to methylmercury impacts cognition irreversibly.
  • Li Y, Xie C, Murphy SK, Skaar D, Nye M, Vidal AC, Cecil KM, Dietrich KN, Puga A, Jirtle RL, Hoyo C. 2015. Lead Exposure during Early Human Development and DNA Methylation of Imprinted Gene Regulatory Elements in Adulthood. Environ Health Perspect 124(5):666-73. [Abstract]
    This research examined epigenetic changes, which alter gene activity without changing DNA sequence, in blood samples taken from women of the Cincinnati Lead cohort 30 years ago and compared the results to babies born to these women finding lead concentrations were associated with the epigenetic state of more than half of the genes examined suggesting early childhood exposure to lead may result in epigenetic changes which could alter gene activity.
  • Yeramaneni S, Dietrich KN, Yolton K, Parsons PJ, Aldous KM, Haynes EN. 2015. Secondhand Tobacco Smoke Exposure and Neuromotor Function in Rural Children. J Pediatr 167(2):253-9.e1. [Abstract]
    This community-based participatory research study of 404 children and their families in Ohio assessed the association of second hand smoke exposure and increased risk of neuromotor effects in children finding exposure to secondhand smoke was significantly associated with poor fine motor and gross motor development in children highlighting the need for intervention to reduce childhood exposure and prevent adverse effects in children.
  • Stansfield KH, Ruby KN, Soares BD, McGlothan JL, Liu X, Guilarte TR. 2015. Early-life lead exposure recapitulates the selective loss of parvalbumin-positive GABAergic interneurons and subcortical dopamine system hyperactivity present in schizophrenia. Transl Psychiatry 5:e522. [Abstract]
  • Cantoral A, Téllez-Rojo MM, Ettinger AS, Hu H, Hernández-Ávila M, Peterson K. 2015. Early introduction and cumulative consumption of sugar-sweetened beverages during the pre-school period and risk of obesity at 8-14 years of age. Pediatr Obes 11(1):68-74. [Abstract]
    Research found Mexican children with the highest cumulative sugar-sweetened beverage consumption had almost three times the odds of developing obesity at age 8-14 suggesting sugar-sweetened beverage intake should be limited in the pre-school lifestage to prevent the likelihood of obesity in pre-pubertal and pubertal lifestages.
  • Teitelbaum SL, Belpoggi F, Reinlib L. 2015. Advancing research on endocrine disrupting chemicals in breast cancer: expert panel recommendations. Reprod Toxicol 54:141-147. [Abstract]
    This paper outlines recommendations made by an expert panel to highlight areas where research is needed and describes effective approaches for advancing research on the environmental origins of breast cancer across the lifespan.
  • French, JE (NTP), Gatti, DM, Morgan, DL (NTP), Kissling, GE (DIR), Shockley, KR (DIR), Knudsen, GA (OD), Shepard, KG, Price, HC, King, D (NTP), Witt, KL (NTP), Pedersen, LC (DIR), Munger, SC, Svenson, KL and Churchill, GA. 2014. Diversity Outbred Mice Identify Population-Based Exposure Thresholds and Genetic Factors that Influence Benzene-Induced Genotoxicity. Environ Health Perspect 123:237-245. [Abstract]
    Using a mouse model of genetic diversity to more closely mimic a human population, this work identified differences in individual susceptibility to benzene exposure and found specific genes that may play a role in this susceptibility.
  • House, JS (DIR), Li, H (DIR), DeGraff, LM (DIR), Flake, G (NTP), Zeldin, DC (DIR) and London, SJ (DIR). 2014. Genetic variation in HTR4 and lung function: GWAS follow-up in mouse. FASEB J 29(1):323-335. [Abstract]
    Using a genetically modified mouse model, this work followed up on human genome-wide association studies that identified associations between noncoding mutations and pulmonary function and found mutations altered lung function and increased airway hyperresponsiveness in mutant mice suggesting genetic variation identified in human genome-wide association studies may be the cause of altered lung function.
  • Cho, HY (DIR), Jedlicka, AE, Gladwell, W (DIR), Marzec, J (DIR), McCaw, ZR (DIR), Bienstock, R (DIR) and Kleeberger, SR (DIR). 2014. Association of Nrf2 polymorphism haplotypes with acute lung injury phenotypes in inbred strains of mice. Antioxid Redox Signal 22(4):325-338. [Abstract]
    Using multiple, genetically diverse inbred mouse strains classified by DNA sequence, authors uncovered differential susceptibilities to acute lung injury which may provide insight into the genetic variation of same DNA region of humans and its role in oxidative lung disorders.
  • Young, MT, Sandler, DP (DIR), DeRoo, LA (DIR), Vedal, S, Kaufman, JD and London, SJ (DIR). 2014. Ambient Air Pollution Exposure and Incident Adult Asthma in a Nationwide Cohort of U.S. Women. Am J Respir Crit Care Med 190(8):914-921. [Abstract]
    The Sister Study, a cohort of ~50,000 sisters of women who have had breast cancer, found air pollution exposure increases the risk of developing asthma in women or increased the risk of developing wheeze (asthma symptom) in women.

2014

  • Ekenga CC (DIR), CG Parks (DIR), AA D'Aloisio (DIR), LA DeRoo (DIR) and DP Sandler (DIR). 2014. Breast Cancer Risk after Occupational Solvent Exposure: the Influence of Timing and Setting. Cancer Res 74(11):3076-3083. [Abstract]
    The Sister Study, a cohort of ~50,000 sisters of women who have had breast cancer, examined the relationship between occupational exposure to solvents and breast cancer finding the life stage between puberty and first birth in a woman (critical period of breast development) may be an important window of susceptibility for estrogen receptor-positive invasive breast cancer.
  • Markunas CA (DIR), Xu Z (DIR), Harlid S (DIR), Wade PA (DIR), Lie RT, Taylor JA (DIR), Wilcox AJ (DIR). 2014. Identification of DNA Methylation Changes in Newborns Related to Maternal Smoking during Pregnancy. Environ Health Perspect 122(10):1147-1153. [Abstract]
    The Norway Facial Clefts Study identified epigenetic changes in the DNA of children born to smoking mothers vs. nonsmokers lending weight to the hypothesis that maternal behaviors during pregnancy can affect fetal DNA.
  • Liu J, Liu X, Wang W, McCauley L, Pinto-Martin J, Wang Y, Li L, Yan C, Rogan WJ (DIR). 2014. Blood lead concentrations and children's behavioral and emotional problems: A Cohort Study. JAMA Pediatr 168(8):737-45. [Abstract]
    Research indicates blood lead levels in children are associated with an increased risk of behavioral and emotional problems providing more evidence that there is no safe lead level.
  • Furlong MA, Engel SM, Barr DB, Wolff MS. 2014. Prenatal exposure to organophosphate pesticides and reciprocal social behavior in childhood. Environ Int 70:125-31. [Abstract]
    Adding to the literature that supports potential adverse neurobehavioral outcomes result from prenatal organophosphate pesticide exposure, this work also highlights a potential health disparity in blacks and boys exposed to specific pesticides.
  • Chen A, Yolton K, Rauch SA, Webster GM, Hornung R, Sjödin A, Dietrich KN, Lanphear BP. 2014. Prenatal Polybrominated Diphenyl Ether Exposures and Neurodevelopment in U.S. Children through 5 Years of Age: The HOME Study. Environ Health Perspect 122(8):856-62. [Abstract]
    Research in the Health Outcomes and Measures of the Environment (HOME) Study between March 2003 and February 2006 in Cincinnati suggests prenatal exposures to PBDE flame retardants leads to lower IQs and increased hyperactivity in children.
  • Shelton JF, Geraghty EM, Tancredi DJ, Delwiche LD, Schmidt RJ, Ritz B, Hansen RL, Hertz-Picciotto I. 2014. Neurodevelopmental Disorders and Prenatal Residential Proximity to Agricultural Pesticides: The CHARGE Study. Environ Health Perspect 122(10):1103-9. [Abstract]
    The Childhood Autism Risk from Genetics and the Environment (CHARGE) Study provided additional evidence that autism spectrum disorders are linked to prenatal pesticide exposures and highlights a risk of autism spectrum with pyrethroid exposure, a chemical that is supposed to be a safe alternative to organophosphates that were shown to increase risk of autism spectrum disorder by 60%.
  • Chrysovergis K (DIR), X Wang (DIR), J Kosak (DIR), SH Lee, J Sik Kim (DIR), JF Foley (NTP), G Travlos (NTP), S Singh (DIR), S Joon Baek and TE Eling(DIR). 2014. NAG-1/GDF15 prevents obesity by increasing thermogenesis, lipolysis and oxidative metabolism. Int J Obes (Lond) 38:1555-1564.
    [Abstract]

    This work suggests the human gene NAG1 protects against obesity and colon cancer, in part, via epigenetic regulation.
  • Ciencewicki, JM (DIR), Wang, X (DIR), Marzec, J (DIR), Serra, ME, Bell, DA (DIR), Polack, FP and Kleeberger, SR (DIR). 2014. A genetic model of differential susceptibility to human respiratory syncytial virus (RSV) infection. FASEB J 28(4):1947-1956. [Abstract]
    This work identified individual susceptibility to human RSV using a human cell model of genetic variation which may help understand RSV disease severity in children.
  • Weinberg, CR, Shi, M, Deroo, LA, Taylor, JA, Sandler, DP and Umbach, DM. 2014. Asymmetry in family history implicates nonstandard genetic mechanisms: application to the genetics of breast cancer. PLoS Genet 10(3):e1004174. [Abstract]
    The Sister Study, a cohort of ~50,000 sisters of women who have had breast cancer, identified nonstandard genetic mechanisms that may be important contributors of breast cancer risk.
  • Salo PM (DIR), SJ Arbes, Jr., R Jaramillo, A Calatroni, CH Weir, ML Sever, JA Hoppin (DIR), KM Rose, AH Liu, PJ Gergen, HE Mitchell and DC Zeldin (DIR). 2014. Prevalence of allergic sensitization in the United States: Results from the National Health and Nutrition Examination Survey (NHANES) 2005-2006. J Allergy Clin Immunol 134(2):350-359. [Abstract]
    Scientists investigated the prevalence of allergies in children through adults across US and found regional differences in the prevalence of specific types of allergies and show that prevalence of allergies is the same across the US except in children age 5 and younger
  • Richardson JR, Roy A, Shalat SL, von Stein RT, Hossain MM, Buckley B, Gearing M, Levey AI, German DC. 2014. Elevated serum pesticide levels and risk for Alzheimer disease. JAMA Neurol 71(3):284-90. [Abstract]
    This epidemiology study described an association between increased levels of pesticide in the serum and an increased risk for Alzheimer’s disease and also points toward an individual susceptibility in genetic carriers of the APOE ε4 allele suggesting a possible early detection method for the disease.
  • Skinner MK, Manikkam M, Tracey R, Guerrero-Bosagna C, Haque M, Nilsson EE. 2013. Ancestral dichlorodiphenyltrichloroethane (DDT) exposure promotes epigenetic transgenerational inheritance of obesity. BMC Med 11:228. [Abstract]
    Using a rodent model of ancestral dichlorodiphenyltrichloroethane exposure, this work described over 50% of the “great-grandchildren” of pregnant rodents exposed were obese and the great-grandchild generation mutations  in a number of genes associated with obesity.
  • Davis DA, Bortolato M, Godar SC, Sander TK, Iwata N, Pakbin P, Shih JC, Berhane K, McConnell R, Sioutas C, Finch CE, Morgan TE. 2013. Prenatal exposure to urban air nanoparticles in mice causes altered neuronal differentiation and depression-like responses.  PLoS One 8(5):e64128. [Abstract]
    Using a mouse model for prenatal exposure to urban freeway nanoparticulate matter, scientists found prenatal exposure can affect brain development with males exhibiting increased depression-like responses in behavioral tests.
  • Perera FP, Wang S, Rauh V, Zhou H, Stigter L, Camann D, Jedrychowski W, Mroz E, Majewska R. 2013. Prenatal exposure to air pollution, maternal psychological distress, and child behavior. Pediatrics 132(5):e1284-94. [Abstract]
    Scientists studied a birth cohort in the coal-burning region of Poland and found mothers who exhibited psychological distress gave birth to children who were more severely affected by prenatal exposure to air pollution resulting in adverse affects on neurobehavioral development.
  • Stapleton PA, Minarchick VC, Yi J, Engels K, McBride CR, Nurkiewicz TR. 2013. Maternal engineered nanomaterial exposure and fetal microvascular function: does the Barker hypothesis apply? Am J Obstet Gynecol 209(3):227.e1-11. [Abstract]
    This research investigated the effect of maternal engineered nanomaterial inhalation and found evidence that this exposure adversely impacts fetal blood vessel function.

Other Implementation Activities

Zika in Infants and Pregnancy Study

Zika in Infants and Pregnancy (ZIP) Study - The National Institutes of Health (NIH) and Fundacao Oswaldo Cruz (the Oswaldo Cruz Foundation, also known as Fiocruz), a scientific research organization based in Rio de Janeiro, have begun a study to evaluate the magnitude of health risks that Zika virus infection poses to pregnant women and their developing fetuses, as well as infants. The study will begin in Puerto Rico and expand to several locations in Brazil, Colombia, and other areas experiencing active local transmission of the virus.

The Zika in Infants and Pregnancy (ZIP) Study aims to enroll as many as 10,000 pregnant women, ages 15 and older, at 15 locations. The participants, who must be in their first trimester of pregnancy when joining, will be followed throughout their pregnancies to determine if they become infected with the virus and, if so, what outcomes result for both mother and child. The infants will be carefully followed for at least one year after birth.

Clinical Studies:

NIH Roadmap Epigenomics Program Integrative Analysis of 111 Reference Human Epigenomes

This effort, which is co-led by NIEHS, has now mapped more than 100 types of human cells and tissues. The resulting comprehensive catalog of epigenomic data provides a first-of-its-kind resource that will help researchers make direct comparisons across cell types and tissues. The researchers expect that the data, which is freely available, will be of broad use to scientists for studies of gene regulation, cellular differentiation, genome evolution, genetic variation, and human disease. Integrative analysis of 111 reference human epigenomes.

Electronic Waste and Children’s Health

The World Health Organization (WHO) convened a working meeting on e-waste and child health on June 11-12, 2013 in Geneva, sponsored by NIEHS and the German Federal Ministry for the Environment, Nature Conservation, and Nuclear Safety. NIEHS-supported researchers were deeply involved in planning and participating in the sessions. In addition, NIEHS provided funds so that researchers from lower- and middle-income countries where unregulated e-waste recycling is most prevalent, including China, India, Vietnam, and countries in West Africa, could attend. The meeting resulted in a training guide for physicians on the topic. NIEHS spurs investigation into the health effects of e-waste recycling.

WHO CC Network for Children's Environmental Health (Network)

The NIEHS-WHO Collaborating Centre for Environmental Health Sciences is providing development support to a network of designated WHO Collaborating Centres (WHO CC). The WHO CC Network for Children's Environmental Health (Network) is working to address children's environmental health issues at the local, regional, national, and international levels. The network is comprised of more than 10 research institutes around the world. Each acts as a hub to strengthen national or regional capacity to advance children's environmental health. At the same time, collaboration and the sharing of services and expertise among Centres in the Network builds global children's environmental health capacity. WHO Collaborating Centres Network for Children's Environmental Health.

President’s Task Force on Environmental Health Risks and Safety Risks to Children

This task force, which comprises representatives of 17 federal departments and White House offices, is charged with: identifying priority issues of environmental health and safety risks to children that are best addressed through interagency efforts; developing strategies to protect children’s environmental health and safety; recommending and implementing interagency actions; and communicating information to federal, state, and local decision makers for use in protecting children from environmental health and safety risks. NIEHS staff engages on this task force as members of the Steering Committee and co-chairs of the Subcommittees on Chemical Exposures and on Climate Change. President's Task Force on Environmental Health and Safety Risks to Children