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Your Environment. Your Health.

Goal 3 – Exposure Science and the Exposome

Implementation Highlights and Accomplishments

Boy holding a basketball and a girl

Transform exposure science by enabling consideration of the totality of human exposures and links to biological pathways, and create a blueprint for incorporating exposure science into human health studies.

  1. Advance characterization of environmental exposures through improved exposure assessment, at both the individual and population levels.
  2. Define and disseminate the concept of the exposome.
  3. Create tools and technologies and the research capacity needed to characterize the exposome.

Research Funding

Powering Research through Innovative Methods for mixtures in Epidemiology (PRIME)(R01)
Developed to stimulate the development of innovative statistical, data science, or other quantitative approaches to studying the health effects of complex chemical mixtures in environmental epidemiology. RFA-ES-17-001

Novel Assays for Screening the Effects of Chemical Toxicants on Cell Differentiation (R43/R44)
The purpose of this SBIR FOA was to support development of assays that will provide information on mechanisms of chemically-induced biological activity, help to prioritize chemicals for more extensive toxicological evaluation, support more predictive models of in vivo biological response, and potentially inform the role of genetic diversity in toxicological effects. RFA-ES-17-007

Novel Technologies for Rapid and Sensitive Biomonitoring in Humans (R43/R44)
The purpose of this SBIR FOA was to develop point-of-care or benchtop instruments, or other laboratory-based approaches for the characterization of major classes of analytes that include known and suspected toxicants and their major metabolites in human biological samples, including blood, urine, and saliva, which are likely to be available from both prospective and retrospective epidemiological cohorts. RFA-ES-14-005

Validation and Demonstration of Devices for Environmental Exposure Assessment (R21/R33)
The purpose of this RFA was to facilitate the translation of prototype devices for characterization of personal exposures into field use by supporting a phased validation effort involving a partnership between tool developers and environmental epidemiologists. Seven grants were awarded (FY15 funding). RFA-ES-13-013

The Preconception Exposure Window and Health of the Offspring (R01)
This Funding Opportunity Announcement (FOA) is intended to encourage grant applications that use animal models to investigate whether environmental chemical exposures during the preconception time period (pre-fertilization) to germ cells can be mechanistically linked to later-life traceable phenotypic outcomes in the first generation offspring. ES-16-007

Nanomaterials Health Implications Research (NHIR): Comprehensive Evaluation of Interactions between Engineered Nanomaterials and Biological System (U01)
The interaction of Engineered Nanomaterials (ENMs) and biological systems is guided by their material properties; thousands of ENMs have been generated with subtle changes in these physicochemical properties. Developing comprehensive biological response profiles for a large number of ENMs present in diverse nanoenabled products is a difficult task.  The NIEHS Nanotechnology Health Implications Research (NHIR) program is being established to gain a better understanding of ENMs-biological interactions to guide development of benign ENMs and support safe and sustainable use of nanotechnology. ES-15-013

Nanomaterials Health Implications Research (NHIR): Engineered Nanomaterials Resource and Coordination Core (U24)
Nanotechnology, once restricted to 'clean rooms,' has become a major industry generating thousands of engineered nanomaterials (ENMs) that are incorporated into everyday products ranging from personal care products to packaging, construction, water filtration, and children's clothes and toys. This widespread production and use of ENMs present opportunities for unintended human exposure, while their impact on biological systems is not clearly understood. To address these concerns, the NIEHS initiated a nanotechnology environmental health and safety (Nano EHS) program in 2004 and participated in national efforts through the National Nanotechnology Initiative Environmental, Health, and Safety (NNI EHS) Research Strategy (http://www.nano.gov/nni-pca).

The overarching goal of the NIEHS Nano EHS program is to gain a fundamental understanding of the molecular and pathological pathways involved in mediating the response to ENMs. Towards this goal, comprehensive profiles are needed to gain detailed molecular understanding of the interactions between ENM and biological systems.   Such knowledge will in turn allow in silico hazard assessment of ENMs and guide the development of benign, next generation, ENMs.  ES-15-012

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

Centers of Excellence on Environmental Health Disparities Research (P50)
This Funding Opportunity Announcement (FOA) encourages grant applications to support Centers of Excellence on Environmental Health Disparities Research to stimulate basic and applied research on environmental health disparities. The proposed research is expected to develop innovative approaches to understand environmentally-driven health disparities and improve access to healthy environments for vulnerable populations and communities. ES-14-010

Biogeochemical Interactions Affecting Bioavailability for in situ Remediation of Hazardous Substances (R01)
Contaminants in the environment are affected by complex biological, geological and chemical processes that have implications for both remediation effectiveness as well as exposure risk to humans.  By understanding the mechanisms of these complex interactions, we are better equipped to optimize remediation strategies and, therefore, improve science-based decision making for site management, priority-setting, and remedy selection.  This funding opportunity announcement (FOA) will support problem-solving research on the mechanisms of biogeochemical interactions affecting bioavailability in the context of in situ remediation of contaminated soil, sediment, surface water, or groundwater. ES-13-010

Selected Programs and Awards

New Centers

  • The Emory Health and Exposome Research Center: Understanding Lifetime Exposures (HERCULES) was funded in May 2013 for $4.5 million over four years. HERCULES received a $7.5 million renewal in funding in 2017. HERCULES will provide key infrastructure and expertise to develop and refine new tools and technologies. Key among these are the Integrated Health Sciences Facility Core and the Systems Biology Core which we can develop the needed tools to assess the exposome. The former will help generate exposure data, improve metabolomic approaches, and facilitate clinical studies, while the latter will help synthesize the data into comprehensive computational models.
  • The Center for Translational Environmental Health Research is a collaboration of Texas A&M University, Baylor College of Medicine, and the University of Houston. The research base of the new center will focus on five thematic areas impacting human environmental health: early life exposures, chronic disease, metabolism, emerging technologies, and the microbiome. Centers of excellence adds Texas consortium.
  • The Center for Urban Responses to Environmental Stressors (CURES) at Wayne State University places special emphasis on understanding how environmental exposures, during life windows of heightened susceptibility, can adversely affect health, particularly in vulnerable persons, such as children and adults of low socioeconomic status, older adults, first responders, and refugees. NIEHS-funded center focuses on urban environmental stressors.
  • The NC State Center for Human Health and the Environment will collaborate with researchers at the East Carolina University Brody School of Medicine, North Carolina Central University, North Carolina Department of Health and Human Services, and Research Triangle Institute NIH Eastern Regional Comprehensive Metabolomics Resource Core. Leveraging the technical expertise of CHHE and its partners, the center will focus on how environmental stressors interact with biomolecular signaling pathways, the genome, and the epigenome. NC State and UC Davis join NIEHS environmental health sciences research centers.
  • The UC Davis center comprises a team of scientists from 19 departments, across four schools and colleges. The center will focus on exposures such as particles and volatile organic compounds in ambient air, pollutants in drinking water and food, and household or personal care products. NC State and UC Davis join NIEHS environmental health sciences research centers.

Selected Scientific Advances

2017

  • O' Lenick CR, Chang HH, Kramer MR, Winquist A, Mulholland JA, Friberg MD, Sarnat SE. 2017. Ozone and childhood respiratory disease in three US cities: evaluation of effect measure modification by neighborhood socioeconomic status using a Bayesian hierarchical approach. Environ Health 16(1):36. [Abstract]
    Researchers evaluated individual and area-level factors as modifiers of the association between warm-season (May-Sept.) temperature and pediatric respiratory morbidity in Atlanta.
  • Xiao S, JR Coppeta, HB Rogers, BC Isenberg, J Zhu, SA Olalekan, KE McKinnon, D Dokic, AS Rashedi, DJ Haisenleder, SS Malpani, CA Arnold-Murray, KW Chen, MY Jiang, L Bai, CT Nguyen, JY Zhang, MM Laronda, TJ Hope, KP Maniar, ME Pavone, MJ Avram, EC Sefton, S Getsios, JE Burdette, JJ Kim, JT Borenstein and TK Woodruff. 2017. A microfluidic culture model of the human reproductive tract and 28-day menstrual cycle. Nature Communications 8:14584. [Abstract]
    This study shows that a microfluidic system supports murine ovarian follicles to produce the human 28-day menstrual cycle hormone profile, which controls human female reproductive tract and peripheral tissue dynamics in single, dual and multiple unit microfluidic platforms.

2016

  • Grau-Perez M, CC Kuo, M Spratlen, KA Thayer (NTP), MA Mendez, RF Hamman, D Dabelea, JL Adgate, WC Knowler, RA Bell, FW Miller (DIR), AD Liese, C Zhang, C Douillet, Z Drobna, EJ Mayer-Davis, M Styblo and A Navas-Acien. 2016. 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.
  • 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.
  • Dunaway K, Goorha S, Matelski L, Urraca N, Lein PJ, Korf I, Reiter LT, LaSalle JM. 2016. Dental Pulp Stem Cells Model Early Life and Imprinted DNA Methylation Patterns. Stem Cells 35(4):981-988. [Abstract]
    Using whole genome bisulfite sequencing, the authors show that dental pulp stem cells (DPSCs), derived from baby teeth and cultured in serum-containing media, have partially methylated domains (PMDs) and mimic the inner cell mass (ICM) and placental methylome more closely than induced pluripotent stem cells (iPSCs) and embryonic stem cells (ESCs).
  • 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.
  • 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.
  • Ho SM, Rao RC, To S, Schoch E, Tarapore P. 2016. Bisphenol A and its analogues disrupt centrosome cycle and microtubule dynamics in prostate cancer. Endocr Relat Cancer 24(2):83-96. [Abstract]
    Researchers examine whether exposure of prostate cancer cells (LNCaP, C4-2) to low-dose BPA and its structural analogues (BPS, BPF, BPAF, TBBPA, DMBPA and TMBPA) affects centrosome amplification (CA), a hallmark of cancer initiation and progression.
  • 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]
  • Mendelsohn E, Hagopian A, Hoffman K, Butt CM, Lorenzo A, Congleton J, Webster TF, Stapleton HM. 2016. Nail polish as a source of exposure to triphenyl phosphate. Environ Int 86:45-51. [Abstract]
  • Reese SE (DIR), S Zhao (DIR), MC Wu, BR Joubert (DERT), CL Parr (DIR), SE Haberg, PM Ueland, RM Nilsen, O Midttun, SE Vollset, SD Peddada (DIR), W Nystad and SJ London (DIR). 2016. DNA Methylation Score as a Biomarker in Newborns for Sustained Maternal Smoking during Pregnancy. Environ Health Perspect 125(4):760-766. [Abstract]
  • Bonner MR, LE Beane Freeman, JA Hoppin, S Koutros, DP Sandler (DIR), CF Lynch, CJ Hines, K Thomas, A Blair and MC Alavanja. 2016. Occupational Exposure to Pesticides and the Incidence of Lung Cancer in the Agricultural Health Study. Environ Health Perspect 125(4):544-551. [Abstract]
  • Parks CG (DIR), JA Hoppin, AJ DeRoos, KH Costenbader, MC Alavanja and DP Sandler (DIR). 2016. Rheumatoid Arthritis in Agricultural Health Study Spouses: Associations with Pesticides and Other Farm Exposures. Environ Health Perspect 124(11):1728-1734. [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]
  • Paquette AG, Houseman EA, Green BB, Lesseur C, Armstrong DA, Lester B, Marsit CJ. 2016. Regions of variable DNA methylation in human placenta associated with newborn neurobehavior. Epigenetics. 11(8):603-13. [Abstract]
  • Hu XC, Andrews DQ, Lindstrom AB, Bruton TA,  Schaider LA, Grandjean P, Lohmann R, Carignan CC, Blum A, Balan SA, Higgins CP, Sunderland EM. 2016. Detection of Poly- and Perfluoroalkyl Substances (PFASs) in U.S. Drinking Water Linked to Industrial Sites, Military Fire Training Areas, and Wastewater Treatment Plants. Environ Sci Technol Lett 3(10):344-350. [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]

2015

  • 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):1084-92. [Abstract]
  • Thayer KA (NTP), DR Doerge, D Hunt (DIR), SH Schurman (DIR), NC Twaddle, MI Churchwell, S Garantziotis (DIR), GE Kissling (DIR), MR Easterling, JR Bucher (NTP) and LS Birnbaum (OD). 2015. Pharmacokinetics of bisphenol A in humans following a single oral administration. Environ Int 83:107-115. [Abstract]
    This work described a human pharmacokinetic clinical study, out of the NIEHS Clinical Research Unit, to characterize BPA levels in blood and urine using more sensitive analytical methods than previously described.
  • Lebov JF, LS Engel, D Richardson, SL Hogan, JA Hoppin and DP Sandler (DIR). 2015. Pesticide use and risk of end-stage renal disease among licensed pesticide applicators in the Agricultural Health Study. Occup Environ Med 73(1):3-12. [Abstract]
    This work examined environmental risk factors for kidney disease in male pesticide applicators participating in the Agricultural Health Study and found the risk of end-stage kidney disease was significantly greater for pesticide applicators that were hospitalized and had multiple medical visits due to pesticide use.
  • Hewitt SC (DIR), W Winuthayanon (DIR), B Pockette (DIR), RT Kerns (DIR), JF Foley (NTP), N Flagler (NTP), E Ney (NTP), A Suksamrarn, P Piyachaturawat, PR Bushel (DIR) and KS Korach(DIR). 2015. Development of Phenotypic and Transcriptional Biomarkers to Evaluate Relative Activity of Potentially Estrogenic Chemicals in Ovariectomized Mice. Nat. Biotechnol. Environ. Health Perspect 123(4):344-352. [Abstract]
    Scientists used a mouse model of prepubertal girls and postmenopausal women and to build a screen to identify estrogenic activity of chemicals and classify the relative strength of endocrine disruptors.
  • Harvey JB (DNTP), Hong HH (DNTP), Bhusari S, Ton TV (DNTP), Wang Y (DNTP), Foley JF (DNTP), Peddada SD (DIR), Hooth M (DNTP), DeVito M (DNTP), Nyska A, Pandiri AR (DNTP), Hoenerhoff MJ (DNTP). 2015. F344/NTac Rats Chronically Exposed to Bromodichloroacetic Acid Develop Mammary Adenocarcinomas With Mixed Luminal/Basal Phenotype and Tgfβ Dysregulation. Veterinary pathology 53(1):170-181. [Abstract]
    This work describes the results for a rodent model exposed to a disinfection by-product in drinking water and found exposed animals expressed more genes associated with human breast cancer and multiple genes in a single signaling pathway suggesting this exposure may activate a pathway involved in mammary tumor development.
  • Person RJ (DNTP), Olive Ngalame NN (DNTP), Makia NL (DIR), Bell MW (DNTP), Waalkes MP (DNTP), Tokar EJ (DNTP). 2015. Chronic inorganic arsenic exposure in vitro induces a cancer cell phenotype in human peripheral lung epithelial cells. Toxicology and applied pharmacology 286(1):36-43. [Abstract]
    This work suggests a chronically exposed human lung cell line develops similar characteristics as lung cancer cells and may serve as a model for arsenic-induced lung cancer.
  • Verner MA, Gaspar FW, Chevrier J, Gunier RB, Sjödin A, Bradman A, Eskenazi B. 2015. Increasing sample size in prospective birth cohorts: back-extrapolating prenatal levels of persistent organic pollutants in newly enrolled children. Environ Sci Technol 49(6):3940-8. [Abstract]
    This work evaluated different models to back-extrapolate prenatal levels of POPs in newly enrolled children to increase sample size in prospective birth cohorts of prenatal exposure and found the Super Learner model outperformed the others tested and could reliably back-extrapolate from levels 9 years after birth suggesting this approach may be useful for increasing sample size when examining exposure to persistent chemicals.
  • 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.
  • Rojas D, Rager JE, Smeester L, Bailey KA, Drobná Z, Rubio-Andrade M, Stýblo M, García-Vargas G, Fry RC. 2015. Prenatal Arsenic Exposure and the Epigenome: Identifying Sites of 5-methylcytosine Alterations that Predict Functional Changes in Gene Expression in Newborn Cord Blood and Subsequent Birth Outcomes. Toxicol Sci 143(1):97-106. [Abstract]
    Scientists identified epigenetic changes that predict functional changes in gene expression and birth outcomes in newborn cord blood.

2014

  • Patel CJ, Ioannidis JP. 2014. Placing epidemiological results in the context of multiplicity and typical correlations of exposures. J Epidemiol Community Health 68(11):1096-100. [Abstract]
    This work proposes a method to report exposome and epidemiological data.
  • Whitworth KW, RM Bornman, JI Archer, MO Kudumu, GS Travlos (NTP), RE Wilson (NTP) and MP Longnecker (DIR). 2014. Predictors of Plasma DDT and DDE Concentrations among Women Exposed to Indoor Residual Spraying for Malaria Control in the South African Study of Women and Babies (SOWB). Environ. Health Perspect 122(6):545-552. [Abstract]
    Researchers analyzed the blood of women across eight villages in South Africa and found higher levels of DDT in women whose indoor walls were likely to have been sprayed with the pesticide. A potential exposure reduction strategy found women who took a series of steps to prepare their home before spraying had lower blood levels of DDT.
  • 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.
  • Prins GS, Hu WY, Shi GB, Hu DP, Majumdar S, Li G, Huang K, Nelles JL, Ho SM, Walker CL, Kajdacsy-Balla A, van Breemen RB. 2014. Bisphenol A promotes human prostate stem-progenitor cell self-renewal and increases in vivo carcinogenesis in human prostate epithelium. Endocrinology 155(3):805-17. [Abstract]
    Using a mouse model of embryonic exposure to BPA, scientists describe the effects of BPA exposure on human prostate stem-like cells.
  • Vaughan JM, Garrett BJ, Prophete C, Horton L, Sisco M, Soukup JM, Zelikoff JT, Ghio A, Peltier RE, Asgharian B, Chen LC, Cohen MD. 2014. A novel system to generate WTC dust particles for inhalation exposures. Journal of Exposure Science and Environmental Epidemiology 24(1):105-112. [Abstract]
    This work describes a new model system to assess health effects on World Trade Center first responder exposures.
  • Ji JS, Schwartz J, Sparrow D, Hu H, Weisskopf MG. 2014. Occupational Determinants of Cumulative Lead Exposure: Analysis of Bone Lead Among Men in the VA Normative Aging Study. J Occup Environ Med 56(4):435-40. [Abstract]
    Using the Normative Aging Study, this work examined the bone lead concentration in 1,320 men across 14 occupation categories and found service workers, construction workers, extractive craft workers, installation, maintenance, and repair craft workers had the highest bone lead concentrations suggesting occupation is a good predictor of lead exposure.
  • 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.
  • 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.
  • Zota AR, Linderholm L, Park JS, Petreas M, Guo T, Privalsky ML, Zoeller RT, Woodruff TJ. 2013. Temporal comparison of PBDEs, OH-PBDEs, PCBs, and OH-PCBs in the serum of second trimester pregnant women recruited from San Francisco General Hospital, California. Environ Sci Technol 47(20):11776-84. [Abstract]
    This study assessed levels of flame retardants and other persistent chemicals in blood samples from low-income pregnant women in California and found a decrease in flame retardant levels over time which supports the impact of legislation that banned the production of certain flame retardants in California.

Other Implementation Activities

Exposure Science and the Exposome webinar series
NIEHS launched the Exposure Science and the Exposome Webinar Series on April 4, 2014 to foster discussions on international efforts in advancing exposure science and the exposome concept as well as challenges and opportunities in incorporating this concept in environmental health research.

Transform Tox Testing Challenge
Innovative thinkers are sought for a new federal challenge that will help advance the field of predictive toxicology. The Transform Tox Testing Challenge: Innovating for Metabolism, issued on Jan. 8, will provide up to $1 million in total prizes for modifications to existing high throughput screening (HTS) designs and prototypes that allow both chemicals and their metabolite products to be evaluated.

The National Toxicology Program (NTP) has joined with the National Center for Advancing Translational Sciences, also part of the National Institutes of Health, and the U.S. Environmental Protection Agency (EPA) to issue this new challenge. The goal is to improve the relevance and accuracy of toxicity data generated by automated chemical screening technology.

One Bioregion/One Health
This new framework provides an approach to transboundary regional planning that considers relationships between people and nature in the quest for healthier living spaces. The One Health concept acknowledges that human health is interconnected and dependent on the health of animals and the environment. A bioregion is a territory that is socially and culturally defined by its people rather than borders on a map. Bioregions are shaped by global trends, including climate change, food and water issues, economic crisis, large-scale natural disasters, and widespread increases in preventable diseases. The framework, funded in part by NIEHS and developed by researchers at the University of California-San Diego Superfund Research Center, merges regional planning and ecosystem management as a way to improve public and environmental health.

Chemical Screening Data. On 17 December 2013, the U.S. Environmental Protection Agency (EPA) released new chemical screening information on 1,800 chemicals found in industrial and consumer products, food additives, and drugs. These data were gathered through the NTP-led, interagency Tox21 collaboration.

Comparative Toxicogenomics Database. Funded in part by NIEHS, scientists at the pharmaceutical corporation Pfizer Inc. and academic researchers affiliated with the Comparative Toxicogenomics Database (CTD) have integrated information about the toxicity of more than 1,200 pharmaceuticals into this publicly available research resource. The database provides chemical-gene-disease information and associated functional and pathway data to connects mechanisms of chemical action to potential impacts on human health. The Pfizer collaboration specifically added data for chemicals that may be involved in cardiovascular, neurological, kidney, and liver disorders. Molecular toxicologist Carolyn Mattingly, Ph.D., associate professor at North Carolina State University is lead researcher on the study and has been directing the development of the CTD with NIEHS support since 2001. According to Mattingly, this is the only database out there that connects mechanisms of chemical action to potential impacts on human health. Comparative Toxicogenomics Database.