Exposure to high doses of arsenic-contaminated drinking water has been shown to have a significant adverse impact on prenatal growth and childhood cognitive development. Much less is known about the child health effects of the lower doses of arsenic exposure typical of U:S. populations despite evidence of adverse effects such as increased cancer risk at such levels in adults. Recent research suggests that diet may be the most significant source of exposure to arsenic for the general U.S. population, particularly children. Understanding the roles of diet and water as sources of arsenic is vital to assessing exposure risk especially in young children for whom developmental toxicant exposure can be highly deleterious. The New Hampshire Birth Cohort (NHBC) recruits from a population where about 15% of households have private wells with arsenic concentrations above the current maximum contaminant level of 10 pg/L. Thus, it provides a unique opportunity to evaluate early childhood arsenic exposure via drinking water and diet and to quantify physical growth and neurodevelopmental effects of such exposure. To characterize early childhood arsenic intake, we will combine consumption data from repeated dietary assessments with arsenic concentrations measured in each child's drinking water and foods. We will then explore how intake through water and diet are associated with urinary and toenail biomarkers of arsenic exposure. These arsenic biomarkers will then be evaluated for their association with altered growth (weight, length/height), and adiposity (body mass index, waist circumference, skinfold thicknesses) during the first five years of life, as well as impairment in behavioral skills and executive function at ages 3 and 5 years, and decrements in cognitive ability and motor proficiency at age 5 years, all neurodevelopment skills for which prior research supports likely arsenic sensitivity. The in utero and early childhood periods are windows of heightened vulnerability to environmental contaminants because of lower body mass and rapid development. Children also have specific dietary patterns that often include foods high in arsenic, especially rice and rice-based products. This innovative project will combine detailed longitudinal assessment of arsenic exposure and growth and neurological development to better understand critical children's health impacts of this common contaminant.
Exposure to low doses of arsenic through water and food is pervasive, yet the sources and consequences of such exposure are poorly understood. This study will help to identify foods commonly consumed during the first five years of life that contain arsenic and elucidate if there are important growth and developmental consequences of arsenic exposure for young children. Results of this research could help inform decisions about food safety policies and the establishment of dietary guidelines to reduce arsenic-related health risks to children.
|Winterbottom, Emily F; Koestler, Devin C; Fei, Dennis Liang et al. (2017) The aquaglyceroporin AQP9 contributes to the sex-specific effects of in utero arsenic exposure on placental gene expression. Environ Health 16:59|
|Everson, Todd M; Kappil, Maya; Hao, Ke et al. (2017) Maternal exposure to selenium and cadmium, fetal growth, and placental expression of steroidogenic and apoptotic genes. Environ Res 158:233-244|
|Nachman, Keeve E; Ginsberg, Gary L; Miller, Mark D et al. (2017) Mitigating dietary arsenic exposure: Current status in the United States and recommendations for an improved path forward. Sci Total Environ 581-582:221-236|
|Taylor, Vivien; Goodale, Britton; Raab, Andrea et al. (2017) Human exposure to organic arsenic species from seafood. Sci Total Environ 580:266-282|
|Demidenko, Eugene; Glaholt, S P; Kyker-Snowman, E et al. (2017) Single toxin dose-response models revisited. Toxicol Appl Pharmacol 314:12-23|
|Kaushal, Akhilesh; Zhang, Hongmei; Karmaus, Wilfried J J et al. (2017) Genome-wide DNA methylation at birth in relation to in utero arsenic exposure and the associated health in later life. Environ Health 16:50|
|Thompson, Jeffrey A; Marsit, Carmen J (2017) A METHYLATION-TO-EXPRESSION FEATURE MODEL FOR GENERATING ACCURATE PROGNOSTIC RISK SCORES AND IDENTIFYING DISEASE TARGETS IN CLEAR CELL KIDNEY CANCER. Pac Symp Biocomput 22:509-520|
|Breton, Carrie V; Marsit, Carmen J; Faustman, Elaine et al. (2017) Small-Magnitude Effect Sizes in Epigenetic End Points are Important in Children's Environmental Health Studies: The Children's Environmental Health and Disease Prevention Research Center's Epigenetics Working Group. Environ Health Perspect 125:511-526|
|Patel, Chirag J; Kerr, Jacqueline; Thomas, Duncan C et al. (2017) Opportunities and Challenges for Environmental Exposure Assessment in Population-Based Studies. Cancer Epidemiol Biomarkers Prev 26:1370-1380|
|Appleton, Allison A; Jackson, Brian P; Karagas, Margaret et al. (2017) Prenatal exposure to neurotoxic metals is associated with increased placental glucocorticoid receptor DNA methylation. Epigenetics 12:607-615|
Showing the most recent 10 out of 103 publications