United States

Many population projections used by international and government agencies assume that, in today's low-fertility societies, future fertility rates will stop declining and roughly stabilize. This paper assesses the evidence for an equilibrium point or rebound from low levels. We show that there is no robust evidence for a systematic fertility rebound, or for a stable equilibrium point at any fertility level conventionally assumed. Instead, where and when fertility has fallen low, it has tended to keep falling. This is true across a range of data sources, time periods, and fertility measures: United Nations data on period total fertility rates for all country-years from 1950 to 2023; Human Fertility Database data on completed fertility for cohorts born between 1935 and 1975 in 31 countries; and fertility rates in subnational geographies in Japan, India, and the United States. We reconcile these results with a prior literature that documented fertility reversals among some low-fertility countries in the early 2000s. Our findings provide an empirical basis for re-examining the equilibrium and rebound assumptions embedded in widely used population projections.

We show how fertility delays compound across generations to raise age at first grandmotherhood. Under the 1960 first-birth schedule median grandmotherhood came at 44. Under the 2024 schedule it is 57, cutting the healthy years with grandchildren from 28 to 15. Longer life does not make up the loss of years when the grandmother is healthy enough to supply money and care. Delay is most pronounced among the college-educated, with reproductive-control access accounting for over half the fall in grandmotherhood by age 55 among White college graduates. When a daughter times her first birth to maximize her own payoff, the loss her choice imposes on her mother is external to her calculation. We call this the Rotten Adult Kid Problem. Delay raises both the price of a grandmother's care and wealth per grandchild.

This paper sets up a model with endogenous fertility and urban migration. Children are costly in terms of both goods and space. Incomes depend on population density through an agglomeration effect. An increase in the strength of the agglomeration effect can set in motion a process whereby urban migration increases, and fertility rates fall in both urban and rural locations, similar to U.S. data. Urban fertility falls due to rising rents while rural fertility falls because incomes fall. The rural population vanishes in the long run but the urban location rebounds, ending up with the same population density that it started off with.

Child poverty under the Supplemental Poverty Measure fell 20 percentage points between 1967 and 2024, a decline conventionally credited to income growth and changing taxes and transfers. I show that 5.4 points—27% of the decline or 3.7 million fewer children in poverty in 2024—instead reflect a fertility dividend: smaller families spread finite resources across fewer children. Because equivalence scales and decompositions condition on family size, standard accounting records demographic change as income growth. I quantify the dividend with a rank-preserving transport of the family-size distribution, and corroborate the mechanism by showing that twin-induced parity transitions still raise child poverty 3–7 points.

In the late nineteenth century, Americans feared that crowded immigrant neighborhoods were spreading disease through industrial cities. We study this claim using newly constructed town-level panel data from Massachusetts, 1860 to 1915, a setting uniquely suited to this exercise because its early vital registration system allows consistent measurement of mortality before national registration became widespread. Using a shift-share instrumental variable strategy based on historical settlement patterns, we estimate the effect of local exposure to immigration on mortality. The relevant question is not whether immigrant families themselves experienced higher mortality, but whether immigration altered the local disease environment more broadly. We find that increases in the foreign-born share significantly raised infant and child mortality, with the infant effect falling disproportionately on the post-neonatal period. Mechanical changes in the composition of births by parent nativity account for only a portion of the estimated effect, implying that the results are not driven primarily by higher mortality among immigrant births. Instead, the evidence is consistent with increased exposure to immigrants, communicable disease, and spillovers to children of native-born parents. These findings highlight immigration as one factor shaping the mortality transition in crowded high-mortality environments.