The Covid-19 pandemic is poised to kill people on a global scale not witnessed since the 1918 influenza pandemic. Because the influenza pandemic killed an estimated 50 million people worldwide and 675,000 in the United States, it stands out among scholars as a uniquely catastrophic event. But less well-known is that the typical rate of death from infectious disease among urban nonwhites in the early twentieth century was just as catastrophic — even in non-pandemic years.
With Elizabeth Wrigley-Field and Chris Muller (my un-bylined guest co-authors for this post), we’ve calculated these rates:
We find that the rate of death from infectious disease that urban nonwhites experienced in every year leading up to the 1918 influenza pandemic was greater than what urban whites experienced during the pandemic itself. To construct these rates, we digitized cause-specific, racial-group-specific death counts from 1906-1942 (excluding 1938)–all years such data were available in the U.S. Vital Statistics from 1900 to 1950. In the Vital Statistics, “Mexicans” were included in the white counts (except in 1930-1934, when they were classified as non-white). Non-whites included Blacks, Native Americans, and Asian Americans, but given the racial composition of American cities in the first half of the 20th century, African Americans accounted for the vast majority of the non-white population. We then combined those death counts with population estimates derived from the U.S. Census (Ruggles et al. 2020) to produce death rates for individual cities. The rates shown above are median rates across cities. Infectious deaths were deaths to causes such as tuberculosis, influenza, pneumonia, and diarrhea. For a full list of causes and more detail about the mortality dataset, see Feigenbaum et al. 2019.
Southerners living in cities suffered from far higher infectious mortality rates than their city-dwelling counterparts in the North and Midwest. But these regional differences, as we documented previously, are nearly completely explained by extreme racial disparities. Simply put, African American mortality in the early 20th century was terribly high and this combined with the disproportionate share of African Americans living in the South—more than 90% in 1900 and still 77% in 1940—made Southern cities look deadly. But Southern cities were not differentially deadly for everyone, only their Black residents.
The reasons for Blacks’ extreme rates of death from infectious disease in the early twentieth century have not received the attention they deserve, but previous research has proposed some explanations. As Alexandra Cirone noted last month on Broadstreet, pandemics are political. Can the same be said for the inequality in infectious death rates in non-pandemic years? The answer, like most answers in social science, is likely complicated and we think more research is vital. We have a few candidates, based on our reading of the historical mortality literature, but we are eager to see scholars search for explanations in many different directions.
Segregation and Living Conditions
Living conditions are an obvious culprit for disparities. African Americans were pushed into segregated and extremely crowded neighborhoods with poor housing stock, where infectious diseases are likely to spread (Du Bois 1908, Roberts 2009, Zelner et al. 2017). African Americans were sometimes confined to areas whose topography exposed them to sewage in the years before universal sewage and water treatment (Roberts 2009: 72).
Now, for those of you looking for precisely identified causal estimates of living conditions or density or segregation on mortality or black-white mortality disparities, you’ll be disappointed. Much more work still needs to be done. Still, studies of the political economy of zoning from Shertzer et al. suggests city planners in Chicago used the racial geography of the city when deciding which neighborhoods in Chicago would be zoned for residential, commercial, or industrial uses and that these zoning choices in the 1920s had century-long consequences.
Public Health Investments
Many large American cities began filtering and chlorinating their water supplies in the early 20th century. Somehow, scholars 100 years later are still debating the magnitudes of the effects of clean water and good sewage on mortality. The standard wisdom, dating to Cutler and Miller (2005) was that these interventions had dramatically large effects on mortality. Recent work from Anderson et al. (2019) is more skeptical of the effect of clean water, narrowing past estimates, and focusing more on specific water-born illnesses like typhoid. There has been some nice scholarly back and forth between the sets of authors about, among other things, properly calculating population denominators, but we digress.
Ultimately, clean water seems unlikely to account for the racial disparities we document in the early 20th century. If anything, such investments shrunk mortality gaps. In another paper, Anderson et al (2020) find support for an old claim of Werner Troesken’s that public investments in clean water would disproportionately benefit African Americans because even in a segregated city it is hard to completely exclude part of the population from city-level public health interventions. Specifically, Anderson et al. show that adding chlorine to city water shrunk black-white infant mortality gaps by 13 percent and reduced the gap in mortality from diarrhea under age 2.
Poverty
African Americans in cities also had extremely high poverty rates during the early 20th century (Ewbank 1987), a brutal lived reality in both the South and the rest of the country. Such poverty could imply a level of malnutrition that can hamper disease resistance.
In research demonstrating the long-term consequences of the 1918 pandemic for its survivors, scholars commonly treat 1918 as an exceptional, unprecedented event (e.g., Almond 2006). But it should be more widely known that, at least judged by their rate of death from infectious disease, Blacks living in cities experienced a pandemic in every documented year prior to 1918.
