1999 Progress Report: Environmental Exposures Related to Early PubertyEPA Grant Number: R825816
Title: Environmental Exposures Related to Early Puberty
Investigators: Wolff, Mary S. , Berkowitz, Gertrud S. , Britton, Julie , Forman, Joel , Godbold, James , Hochman, Sarah , Kabat, Geoffrey , Kadlubar, Fred F. , Kase, Nathan , Larson, Signe , Leleiko, Neal
Current Investigators: Wolff, Mary S. , Berkowitz, Gertrud S. , Britton, Julie , Forman, Joel , Godbold, James , Hochman, Sarah , Kabat, Geoffrey , Kadlubar, Fred F. , Kase, Nathan , Larson, Signe , Leleiko, Neal , Serra, Nicole , Wetmur, James G.
Institution: Mount Sinai School of Medicine
EPA Project Officer: Hahn, Intaek
Project Period: January 16, 1998 through January 15, 2001
Project Period Covered by this Report: January 16, 1998 through January 15, 1999
Project Amount: $380,482
RFA: Issues in Human Health Risk Assessment (1997) RFA Text | Recipients Lists
Research Category: Economics and Decision Sciences , Health Effects , Human Health Risk Assessment , Health
The goal of this research is to investigate the potential effect of cumulative, multiple environmental exposures on onset of puberty; in particular, early breast and hair development, which may be associated with estrogenic exposures. A secondary goal is to characterize the role of environmental exposures in racial/ethnic differences among girls as these exposures affect onset of puberty.
Our main hypothesis is that hormonally active exposures hasten onset of puberty (specifically, high levels of organochlorines and low levels of dietary isoflavones). Ancillary hypotheses are that environmental exposures are higher among girls from minority groups and that such exposures are mitigated by hormone-metabolizing enzymes.
Healthy 9-year-old girls from the Mount Sinai Pediatric Outpatient Clinic and the nearby Uptown Pediatric Practice were recruited from each of three ethnic groups (54 African-American, 66 Caucasian, 72 Hispanic). Both recent and usual dietary intake of phytoestrogen-containing foods, and potential confounders (height, weight, physical activity) were recorded. A blood sample was obtained to be analyzed for organochlorines (DDE, PCBs) and hormone-metabolizing genes, and spot urine samples to be analyzed for isoflavones were collected. We collected limited information on early life events (i.e., birth weight, mother's weight at birth); and further birth information was obtained from our hospital's neonatal data base and from birth certificates. The outcomes, pubertal stages of breast and hair development, are being modeled in relation to dietary factors, including food and nutrient intake and phytoestrogens. We have established a unique phytonutrient database to estimate phytoestrogen intake from the dietary questionnaire. Obesity and physical activity are also being examined as risk factors for puberty. Organochlorine analyses are still under way, but preliminary data show low levels (i.e., DDE in serum <2 ng/mL), but some variability in both DDE and PCBs.
Results to date show strong positive associations of pubertal onset with body mass index and African-American ethnicity. There is no effect of phytoestrogens (as lignans, isoflavones, flavonoids, and phytosterols) on pubertal onset; there is a significant effect of a very few food items and of three nutrients (vitamin C, saturated fat, magnesium) with pubertal onset, but the meaning of these associations is not yet clear. Analysis of phytoestrogens in urine has been completed, and there are some differences among ethnic groups. Relationships of urinary metabolites with pubertal onset are being examined. Differences are evident in physical activity among ethnic groups, but relationships with pubertal onset are not statistically significant. We have not yet completed the statistical analyses for birth outcomes and organochlorines. We have assessed variants in two hormone-metabolizing enzymes, and analyses are still under way for two additional enzymes.