An interesting paper by Douglas Almond (2006) examines whether or not influenza infections of pregnant mothers can influence long-term outcomes of the in utero babies. Almond uses the 1918 “Spanish flu” pandemic in the United States as a source of exogenous variation to test the fetal origins hypothesis. The fetal origins hypothesis states that “certain chronic health conditions can be traced to the course of fetal development.”
The influenza outbreak of 1918 was brief (lasting only about 4 months), but deadly, killing more Americans than all combat deaths in the twentieth century. There were, however, 25 million individuals who contracted the deadly influenza strain and survived. Almond seeks to compare individuals born to pregnant mothers with the Spanish flu with a control group of individuals who were born from pregnant mothers without the virus. This is done two ways: using a dummy variable for being born in 1919 and using variation in one’s state of birth.
Using the 1919 dummy variable and comparing it to cohorts born between 1912 and 1922, Almond finds that the 1919 cohort had reduced educational attainment, increased rates of physical disability, lower income, lower socioeconomic status, and received more transfer payment than the surround cohorts.
In his secondary specification, the author examines 1960, 1970, and 1980 census data. Because census data include the state of birth for each person, Almond can trace use cross-state variation in infection rates from the 1919 Spanish flu. The author concludes that outcomes are worse for individuals born in 1919 in states with higher Spanish flu infection rates than for individuals born in 1919 in states with lower infection rates.
One may worry that the Spanish flu killed the less healthy or less ‘genetically endowed’ children in the 1918 cohort while the 1919 cohort survived because they were in utero. If this was the case, the 1918 cohort mean outcomes would be inflated and any differences may not be due to fetal development issues in the 1919 cohort, but the fact that the 1918 cohort may be more genetically endowed than usual. Almond finds that this is not the case, since the 1918 and 1920 birth cohorts have similar outcomes to the other birth cohorts in the 1912 to 1922 groups.
This paper gives robust evidence to support the fetal origins hypothesis. Prior epidemiological studies looked at famines, which tended to be more long-lasting and thus did not provide as much of a sharp, exogenous source of variation.
- Almond, Douglas (2006) “Is the 1918 Influenza Pandemic Over? Long-Term Effects of In Utero Influenza Exposure in the Post-1940 U.S. Population,” Journal of Political Economy, v. 114, pp. 672–712.