Many common disorders have been linked with early gestational exposures or environmental insults (14). Because of the known role of the chromatin accessibility landscape in mediating responses to cellular exposures such as hormones (15), we examined if DHSs harboring GWAS variants were active during fetal developmental stages. Of 2,931 noncoding disease- and trait-associated SNPs within DHSs globally, 88.1% (2,583) lie within DHSs active in fetal cells and tissues. 57.8% of DHSs containing disease-associated variation are first detected in fetal cells and tissues and persist in adult cells (‘fetal origin’ DHSs), while 30.3% are fetal stage-specific DHSs (Fig. 1D). GWAS variants in adult stage-specific DHSs localize chiefly in mature hematopoietic cells, connective tissue, endothelial cells, and malignant cells (fig. S6).
