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Early Life Exposure to Endocrine Disrupting Chemicals: Epigenomic and Transcriptomic Networks and RAGE in Liver Disease

Award Number: R01ES034793
ORGANIZATION: NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 04/17/2024
PERIOD OF PERFORMANCE END DATE: 03/31/2027

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Early Life Exposure to Endocrine Disrupting Chemicals: Epigenomic and Transcriptomic Networks and RAGE in Liver Disease - PROJECT SUMMARY Bisphenol S (BPS), bisphenol F (BPF), and diisononylphthalate (DINP) are increasingly replacing the endocrine disrupting chemicals bisphenol A (BPA) and di-2-ethylhexylphthalate (DEHP), respectively. However, BPS, BPF, and DINP have not undergone safety testing. Perinatal exposures (in utero and during lactation) to BPA and DEHP are associated with the development of non-alcoholic fatty liver disease (NAFLD). NAFLD, a common disease in children, is being diagnosed at increasingly younger ages and its prevalence is increasing in late adolescence. While BPA and DEHP have been extensively studied in this context, BPS/BPF and DINP have not. BPS exposure promoted NAFLD progression in zebrafish, and BPF serum levels are higher in NAFLD patients than in controls. BPS and BPF levels were associated with increased prevalence of obesity in children, a risk factor for NAFLD. DINP caused lipidomic disruption in neonatal mice, while phthalate exposure caused hepatic steatosis in adult mice. Thus, like BPA and DEHP, early-life BPS/BPF and DINP exposure may promote NAFLD development/progression. To date, the mechanisms by which bisphenols and phthalates, particularly as a mixture, trigger these long-term metabolic consequences are elusive. Here, we will test the hypothesis that early life exposure to a bisphenol/phthalate mixture activates RAGE signaling pathways, triggers a trained immune response in peripheral monocytes, and reprograms the epigenome/transcriptome in liver and in peripheral monocytes, thereby priming offspring for exaggerated metabolic dysfunction upon exposure to Western diet. This ViCTER consortium will address this novel hypothesis through integrated studies in mice and in human subjects.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $767,661 )
2026	2026	BECKMAN RESEARCH INSTITUTE OF THE CITY OF HOPE	1500 DUARTE RD	DUARTE	CA	91010	LOS ANGELES	USA	Environmental Health	000	3	4/10/2026	NON-COMPETING CONTINUATION	$767,661
														Subtotal = $767,661

Issue Date FY: 2025 ( Subtotal = $767,661 )
2025	2025	BECKMAN RESEARCH INSTITUTE OF THE CITY OF HOPE	1500 DUARTE RD	DUARTE	CA	91010	LOS ANGELES	USA	Environmental Health	000	2	3/27/2025	NON-COMPETING CONTINUATION	$767,661
														Subtotal = $767,661

Issue Date FY: 2024 ( Subtotal = $767,662 )
2024	2024	BECKMAN RESEARCH INSTITUTE OF THE CITY OF HOPE	1500 DUARTE RD	DUARTE	CA	91010	LOS ANGELES	USA	Environmental Health	000	1	4/17/2024	NEW	$767,662
														Subtotal = $767,662

Grand Total All Awards = $2,302,984

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Early Life Exposure to Endocrine Disrupting Chemicals: Epigenomic and Transcriptomic Networks and RAGE in Liver Disease

Award Number: R01ES034793

ORGANIZATION: NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 04/17/2024

PERIOD OF PERFORMANCE END DATE: 03/31/2027

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