IJE Advance Access originally published online on January 25, 2007
International Journal of Epidemiology 2007 36(1):248-257; doi:10.1093/ije/dyl302
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Did clean water reduce black–white mortality inequalities in the United States? Water, Race, And Disease.
E-mail: sam.harper{at}mcgill.ca
Did clean water reduce black–white mortality inequalities in the United States? Water, Race, And Disease. Werner Troesken, Cambridge, MA: MIT Press, 2004. £22.95, ISBN 0-262-20148-8.
The first attempt at a nationwide census of mortality in the United States occurred in 1850, and though it was of mixed quality and there was substantial under-coverage of reporting, the best estimates suggest that life expectancy was around 40 years for whites and as low as 23 years for blacks—an astonishing 17 year difference.1,2 At that time, given the prevailing social and economic conditions among blacks, this observation was not likely to have been particularly surprising. Yet, the mortality and life expectancy advantage for whites has remained throughout the 20th century, despite the enormous improvements in overall health and life expectancy over the next 150 years. The persistence of this health inequality has occupied the attention of a variety of scholars throughout the century—epidemiologists, physicians, historians, economists—so much so that the issue has now come with some urgency to occupy a prominent place in discussions of US health policy.
One way of viewing this historical pattern is to ask, why is it that, despite massive health improvements among all groups, this inequality remains? That is, what explains the persistence of this inequality, which has been continually reproduced over generations? It is this persistence that continues to drive much of the concern for race-ethnic inequalities in health today, and there is no shortage of literature to remind us of this fact.3–6 For example, Levine et al.7 recently stated that ‘We have seen no sustained decrease in black–white disparities in either age-adjusted mortality or overall life expectancy at birth at the national level since the end of World War II, despite decades of funding for social, health-related, and other programmes designed to reduce racial disparities (p. 480).’ Similarly sober assessments have also found their way into the mainstream press, where one columnist recently stated that ‘black males live seven years less than white males. Hispanics live five years less. That basic gap hasn't changed in half a century.’8 Yet, despite black life expectancy being persistently lower than white life expectancy, others have noted that the size of this gap has changed considerably over time—increasing in some periods while decreasing in others—as a result of changes in age-, gender- and cause-specific mortality.9–11 A more nuanced way to view the problem of black–white inequalities in health is not only to ask why the gap persistently favours whites but also why the size of the gap rises or falls during particular historical periods. A better understanding of why the size of the gap changes may provide insight to potential solutions for the problem of its persistence.
It is exactly this question of the historical changes in the magnitude of race-ethnic inequalities in health that motivates a fascinating new book, Water, Race and Disease, by University of Pittsburgh historian Werner Troesken.12 The book probes the question of why, from 1900 to 1940, life expectancy among US blacks dramatically improved, in both absolute terms and relative to whites. This was a period of intense racial animosity, when discrimination against blacks was occurring in virtually every facet of social and economic life and was being written into US law, especially in the areas of education and housing.13 How is it possible that in the context of such an overtly hostile social environment black mortality could be improving at a faster rate than whites. Troesken's answer, most succinctly, is clean water. Using various lines of qualitative and quantitative evidence and a variety of data sources, he argues that the central factor responsible for the health improvement among blacks during this period was the introduction of clean water in US cities. In doing so, he attempts to show that while racial discrimination was indeed pervasive in social life and many institutions (including public health), there was far less discrimination in the provision of urban public water and sewers, and this lead to reductions in mortality from waterborne diseases such as typhoid and diarrhoea.
The purpose of Troesken's investigation was not, however, to deliberately investigate the causes of US mortality change. As an economic historian who has written largely on the development of public utilities in the United States, he is more interested in what racial differences in disease rates suggest about discrimination in access to public goods—a topic that resonates with contemporary discussions of race-ethnic inequalities in health.14 On this view, he finds the fact that black–white differences in mortality dramatically declined in the first half of the 20th century difficult to square with the received wisdom of contemporary historians, many of whom argue that blacks and foreign-born whites were discriminated against in the provision of public health and medical services. If discrimination was indeed pervasive, then it would seem to follow either that technological developments in public health and medicine bear little relationship to disease trends during this period—for how could the systematic denial of the benefits of public health to minority groups reduce health inequalities?—or that discrimination was perhaps less systematic than previously thought. And while there remains ongoing discussion of the former,15,16 Troesken comes down quite firmly on the latter, and makes a strong case that there was far less discrimination in the provision of public water than in other dimensions of US society. While the main purpose of his book is to investigate the extent to which US cities and towns discriminated against blacks in the provision of public water and sewer facilities, his findings also have implications for understanding historical patterns of race-ethnic inequalities in health.
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To make the case that improvements in access to clean water were the driving force in declining overall mortality and narrowing black–white mortality inequalities, Troesken provides evidence for three historical developments: first, that reductions in waterborne disease mortality played a substantial role in overall mortality improvements; second, that improvements in waterborne disease mortality were driven primarily through the introduction of clean water, as opposed to other pathways and third, that blacks disproportionately benefited from the introduction of clean water. On balance, the evidence he brings to bear is more convincing on the last of these assertions than the first two. He makes a convincing case that there was limited discrimination in access to public water and that this benefited blacks in terms of typhoid mortality, but his larger argument about the role of clean water in reducing the overall mortality burden among blacks is more difficult to accept without some reservations.
To what extent did reductions in waterborne disease mortality contribute to overall mortality improvement between 1900 and 1940? Using published vital statistics data, Troesken estimates that the direct effect of waterborne (typhoid and diarrhoeal diseases) mortality reductions lowered overall mortality by 24%; an impressive contribution, but probably insufficient on its own to account for the overall declines in black–white mortality inequalities. To further bolster his case he argues that exposure to waterborne illnesses also had important indirect effects that worked by increasing the risk of death from numerous other causes, including heart disease, tuberculosis, pneumonia, liver and kidney disease. He estimates that in the early 20th century around half the US population was likely to have been exposed to either typhoid or diarrhoeal disease at some point in their lives, so if such exposures had lingering effects for other diseases the cumulative effect could be substantial. To get a more precise estimate of the indirect effects of eliminating waterborne mortality, he cites a relatively obscure concept called the Mills–Reincke phenomenon, which was based in late 19th and early 20th century observations by public health and sanitary experts of mortality trends in cities before and after they began filtering the water supply.17 They were surprised to find that not only did the introduction of clean water reduce mortality from waterborne diseases, it also reduced overall mortality by much more than would be expected based on improvements in waterborne disease alone (i.e. it also seemed to reduce non-waterborne disease mortality). Though the mechanism was the subject of much speculation, the impact of improved water quality on mortality was so strong that the ‘phenomenon’ implied that after the introduction of clean water each death saved from typhoid also prevented ‘two to four additional deaths from such causes as pneumonia, heart disease or tuberculosis (p. 50).’12 Troesken uses this indirect relationship between waterborne and non-waterborne disease mortality to calculate that roughly another 20% of the US mortality decline from 1900 to 1940 was indirectly due to the effect of improved water on non-waterborne mortality. Thus, if we take the direct and indirect effects to be distinct, Troesken's estimates approach explaining almost half of the overall mortality decline during this period.
The second argument that Troesken makes, and one that turns out to be crucial for explaining the disproportionate benefits of clean water for blacks, is that the improvements in waterborne disease rates were in fact due to the construction and implementation of large-scale public works projects rather than through other potential pathways, such as improved living standards, behavioural changes or the development of medical treatments. In general, he does not substantively address the issue of rising living standards other than a passing reference to Thomas McKeown's focus on improved nutrition as the major driver of mortality change18 and to the subsequent historical work which has generally shown McKeown to have overstated his case.19 Rather, he is content to simply note that his evidence is consistent with a large and important contribution of the installation of water and sewer systems to reducing overall mortality, a finding in line with at least some historical investigations in other countries.20 As to the role of medicine, it is well-known that despite the development of a vaccine for typhoid in the late 19th century it was not generally available for public use due to difficulties of administration, adverse reactions and storage problems, which makes it difficult to argue that medical improvements could be an important part of the story he tells. Finally, in terms of personal health practices, Troesken does not deny that behavioural changes may have occurred with the spread of the germ theory of disease and the identification of microorganisms as the culprits behind communicable diseases. Indeed, he points out that in the absence of effective treatments for waterborne diseases households could protect themselves by adopting certain practices to reduce their exposure, such as testing water for microorganisms, boiling water and buying bottled water or household filters. However, he argues that the resources and knowledge necessary for household prevention were probably more available to economically advantaged households, which were far more likely to be white. Thus, the differential ability of white and black households to avoid exposure to waterborne illnesses by other means provides Troesken with a plausible mechanism for hypothesizing that clean water would have a larger benefit for blacks. He provides some limited evidence on this using data from the US Department of Labor's 1915 study of infant mortality in Baltimore. Taking the non-diarrhoeal infant death rate as a proxy for a households ‘healthfulness’ (including health habits), he shows that in households without sewers diarrhoeal death rates were strongly correlated with non-diarrhoeal death rates, but weakly correlated in households with sewers. Access to sewers, he argues, provided a kind of buffer for household behaviours that might otherwise increase the risk of infection, and to the extent that blacks were less likely to be able to take individual precautions, sewers would have been particularly beneficial.
The heart of his analysis is the last third of the book, which is devoted to demonstrating quantitatively that blacks benefited disproportionately from clean water. He analyses typhoid mortality in a panel of 33 US cities over the period 1910–20, during which some cities began filtering their water supply and some did not. This particular econometric strategy is useful as it allows him to identify the effect of filtration while controlling for potentially confounding factors such as national mortality trends and persistent differences in social and economic characteristics of cities. Overall he estimates that water filtration reduced mean typhoid mortality rates by 53% among blacks but only a statistically insignificant 16% for whites. By virtue of its disproportionate effects on blacks the installation of water filters thus reduced black–white typhoid mortality inequality, which he also tests formally by modelling both the black–white mortality difference and the mortality ratio as outcomes. There is clear and consistent evidence that filtration reduced the black–white difference, but the results for the ratio are less robust. In addition, the pattern of results was similar in both cities of the South and the non-South, though the inclusion of pre-filtration city-specific time trends diminishes the effects in southern cities.
Importantly, Troesken also finds that the benefits of filtration were larger in cities that were more racially integrated with respect to housing. Overall he finds that higher levels of racial segregation did not eliminate the mortality benefit of water filtration, but did appear to make it less effective. In cities below the median level of segregation water filtration reduced black mortality by nearly 60%, whereas in more segregated cities the reduction was only 20%. This focus on segregation may strike some readers as an odd line of investigation, but it is crucial for explaining why there was less discrimination in the provision of water than in provision of other public goods. In contrast to the image associated with the hyper-segregated US cities of the 1970s and 1980s—vast stretches of the urban landscape identifiable with a single race-ethnic group—residential segregation occurred on a much smaller scale in the early 20th century.21 White families usually lived in the prominent houses lining broad avenues whereas black families, often employed as servants, lived on smaller streets nearby. This of course led to residential segregation, but of a different character than contemporary patterns, at the level of streets or blocks rather than entire neighbourhoods. One reason this more ‘local’ pattern of residential segregation might have led to less discrimination in the provision of public water is because water and sewer lines were connected through a series of mains, and the factors that dictated their placement were primarily technical (soil quality, elevation, drainage, etc.). As it happens, the features of the landscape important for providing clean water did not necessarily line up with the boundaries that might separate black and white neighbourhood enclaves. As Troesken says, for the designers of modern water and sewer systems ‘basic engineering concerns overrode all other considerations (p. 38).’12 This meant that in relatively more integrated cities blacks and whites were more likely to be serviced by the same infrastructure, and because levels of segregation as a whole were lower during this historical period this benefited blacks more generally. Thus, in spite of pervasive discriminatory attitudes, early 20th century residential patterning made it difficult to deny water and sewer service to black families without also doing so for some white families; a risk white politicians were not eager to take.
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Relatively lower levels of segregation were one factor that led to less discrimination in water provision; another was fear, both of disease and, somewhat more perversely, of racial ‘contamination.’ In the southern city of Memphis, Tennessee Troesken shows that the lingering effects of a severe yellow fever epidemic in 1878 combined with anti-contagionist rhetoric implicating ‘sewer gas’ as the culprit drove city officials to develop a new, more sophisticated, sewer system. US Census micro data from 1880 mapped to Memphis neighbourhoods demonstrates that both blacks and whites gained relatively equal access to redesigned sewer service in this less-segregated city, leading quite rapidly to declines in black–white mortality inequality from waterborne diseases. Even more interesting is Troesken's discussion of the experience of Jacksonville, Florida, where he demonstrates how pervasive individual and institutional racism during this period may be reconciled with the equitable provision of public water. He quotes at length the city's municipal health officer, Dr Charles Terry, who argued in no uncertain terms that blacks were unfit to care for themselves and were a serious threat to the health of whites, primarily through the dissemination of disease via flies and open privies. This combination of the fear of ‘contamination’ and racial superiority led Terry to advocate ‘bringing water and sewers to black neighbourhoods and households, not despite the race of the people who lived there, but because of it (p. 88).’12 As a result, the passage of a stern anti-typhoid act requiring fly-proof privy screens (subsidized for the poor) and the segregation of typhoid cases reduced the black–white typhoid mortality gap from 50 to 4 deaths per 100 000 in just 3 years, and the subsequent introduction of water chlorination continued to keep this gap low.
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Troesken's quantitative evidence on typhoid is the strongest part of his argument and is surprising enough to provoke some scrutiny. Toward the end, he devotes two chapters of his book to exploring the reliability of his data and his statistical assumptions—different ways of controlling for prior disease trends, modelling absolute vs relative mortality differences, the reliability of typhoid mortality rates, etc. It is worth noting that he finds some evidence that typhoid was more often misdiagnosed as malaria among blacks, which would tend to underestimate the extent to which blacks disproportionately benefited from water filtration. In addition, he provides here more evidence for his primary assertion—that there was less discrimination in the provision of water—by analysing changes in the growth of water mains in response to black and white population changes. This tends to support his overall conclusion that, ‘Holding everything else constant, there were only trivial differences in the rates at which black and white households connected to public water and sewer lines (p. 115).’12 While this in-depth exploration of statistical assumptions may not make for compelling reading, it is helpful for placing some bounds on the size of his effects and it is also somewhat refreshing to see an author attempt to provide justification for his statistical assumptions. By and large, his analysis of water filtration and typhoid is generally convincing and robust to a number of alternative specifications, which lends considerable support to his larger argument about the role of clean water in reducing overall mortality inequality. But there are reasons to suspect he overstates his case.
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Some questions and potential limitations |
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While Troesken is keen to make the case that declines in absolute and relative black–white inequality in overall mortality were due primarily to the introduction of clean water, he does not present any specific evidence to quantify this phenomenon. Rather, he demonstrates sequentially that black–white mortality inequality declined, that waterborne disease reductions accounted for an important part of the decline in mortality in the overall population, and, most convincingly, that clean water benefited blacks more than whites with respect to typhoid mortality in a sample of US cities. Given the strength of the evidence he presents on typhoid, the larger story he tells is plausible, but one difficulty with his case comes from his first premise: that the period from 1900 to 1940 saw declines in absolute and relative overall mortality inequality between blacks and whites. In perhaps the clearest expression of his hypothesis, Troesken says that among blacks the ‘rapid absolute and relative improvements in health and life expectancy that occurred during the early 20th century were driven in large part by the installation of water and sewer systems’ (italics in original) (p. 10).12 This is a bold statement and stands in contrast to most contemporary assessments of black–white mortality patterns during this period. Most observers have interpreted early 20th century US mortality trends as indicative of whites benefiting more than blacks from public health innovation,22,23 evidenced by absolute mortality gains for blacks but not relative to whites. One could of course argue that a decline in the absolute gap in mortality rates represents a meaningful decline in inequality even if relative inequality increased, but most have used the relative frame and concluded that, at the very least, inequalities were not narrowing during this period. For example, in his review of pre-1940 black mortality trends Ewbank writes: ‘between 1900 and 1940 the child mortality rate among blacks remained about 70% above that of whites. Despite substantial declines in infant and child mortality, blacks did not succeed in reducing their risks relative to whites (p. 108).’24
Why does Troesken get a different answer than others? Using the same data as Troesken,25 in Figure 1 I have reproduced the ‘puzzling’ phenomenon with which he begins his study, i.e. the rapid decline in black–white mortality inequality (the data are for whites and non-whites, virtually all of whom were black during this period25). The question is whether the data seen in Figure 1 actually represent the phenomenon Troesken describes. He says that ‘most of the improvement in black life expectancy that occurred between 1900 and 1940 was concentrated among blacks living in urban areas (p. 4),’12 as can be seen in the series marked ‘urban’ in Figure 1. And while he is quite clear that the arguments in his book are applicable only to urban-dwelling blacks, the series labelled ‘non-white urban’ in Figure 1 is not wholly accurate. The estimates for the ‘urban’ series come from deaths recorded in the US Death Registration Area (DRA), an expanding area for which the registration of deaths was at least 90% complete.26 The DRA expanded from 10 states and the District of Columbia in 1900 and covered the entire United States by 1933. Importantly, in 1900 the DRA contained only 5% of the US black population, 85% of whom lived in urban areas. It is possible that this provides a reasonable estimate of black urban mortality in 1900, but it has been noted that this sample was unlikely to be even representative of all urban blacks.27 But even assuming the estimate is reasonable, by 1910 another 12 states were added to the DRA, increasing the coverage of the black population to 18%, but less than half (48%) of this expanded population now lived in urban areas.28 This of course reflects the fact that only a small proportion of blacks lived in urban areas at this time. It is, therefore, difficult to characterize this data series as truly ‘urban’ even by 1910 and this suggests that the declines in mortality Troesken attributes to improved water may be overestimated or partly an artefact of an expanding DRA which increasingly included non-urban blacks.
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Because this is one of the central conclusions of his analysis, it is worth considering in more detail. Table 1 shows the changes in mortality in the DRA for whites and non-whites in cities (population 10 000 or more) and rural areas from 1910 to 1920.29 Similar to what is seen in Figure 1, the total mortality rate declined by 25% for non-whites and only 14% for whites, producing observed declines in absolute and relative black–white inequality. Yet when disaggregated to urban and rural areas, three things become clear. First, the relative mortality improvement was similar in urban and rural areas for both whites and non-whites, which is not exactly consistent with Troesken's evidence on cities; second, the ‘urban penalty’ was much worse for non-whites, as death rates were roughly 50% higher in cities than rural areas, compared with only 20% higher for whites; and third, the fraction of the non-white population in rural areas ‘increased’ dramatically as coverage among non-whites improved, from 26% in 1910 to 64% in 1920. Taken together, these three changes suggest that a non-trivial part of the apparent improvement in non-white mortality Troesken attributes to clean water is driven by the expansion of the DRA to include non-whites living in rural areas, where mortality was lower.30 A simple decomposition31 of the mortality change is given at the bottom of Table 1, showing that the shift in urban/rural composition accounted for <10% of the decline in white mortality, but 51% of the non-white decline. Thus, a sizeable portion of the rapid overall improvement in life expectancy shown in Figure 1 and noted by Troesken is a consequence of improved ascertainment of mortality for US blacks, most of whom still lived in rural areas during this period. This does not suggest he is necessarily wrong about mortality improvement among urban blacks as a result of clean water, but it does make clear that the contribution of such improvement to resolving the ‘puzzle’ of black mortality change is difficult to measure using US historical vital statistics data.
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The compositional effect of the expanding US registration area also leads to potential difficulties with Troesken's estimate for the contribution of declines in waterborne mortality to overall mortality improvement, which serves as the basis for the link between his evidence in US cities and the declines in black–white mortality inequalities. It has been noted that the estimated trends using this data are likely to approximate national trends,32 but when attempting to quantify the contribution of particular diseases to mortality decline, compositional issues are more difficult to ignore. Figure 2 shows trends in all-cause and waterborne (typhoid plus diarrhoeal diseases) mortality rates stratified by the decade during which US states were admitted to the DRA. For all-cause mortality it is clear that states admitted later, as the registration area expanded, already had lower mortality than the existing states, though this does not appear to be the case for diarrhoeal disease and typhoid mortality. For example, Table 2 shows that in 1910 the combined death rate in states that existed in the DRA in 1900 was 1562.4/100 000, but was only 1285.2 among states that were admitted between 1901 and 1910. Table 2 also quantifies this compositional effect on total mortality decline, demonstrating that roughly 50% of the observed decline in US total mortality from 1900 to 1910 and 30% of the decline from 1910 to 1920 was not due exclusively to declining mortality rates, but to adding states to the DRA where all-cause mortality rates were already lower. However, the compositional effect is much smaller for waterborne mortality, indicating that newly added states had higher waterborne disease mortality but lower mortality from other causes. It is hard to know what the net effect of the changing DRA would be on Troesken's estimates of the direct contribution of clean water to health improvement, but based on Figure 2 it appears that the compositional effect of adding more states to the expanding DRA leads to overestimates of the decline in overall mortality while potentially underestimating the contribution of typhoid and diarrhoeal diseases.
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Issues related to understanding the components of mortality change using US historical data complicate the story Troesken tells about the role of clean water in improving overall US population health and health inequalities, but have less bearing on his quantitative work in US cities. While he presents a compelling case that the introduction of clean water had important health benefits for the urban population, it was not the only thing changing that may have affected mortality from waterborne diseases. In virtually all the cities he studies, rates of typhoid mortality were decreasing prior to the introduction of clean water technology. Troesken is well-aware of this and controls for prior disease trends to isolate the specific effects of water filtration, but the strength of the declines in all cities raises questions about the absolute effect of clean water in reducing mortality. Troesken says that the declines in these non-filtering cities were ‘less dramatic (p. 120),’12, which is true, but this relative comparison obscures just how fast typhoid rates were falling everywhere, with or without clean water. Even among the cities that did not install water filters during the period 1910–20 crude typhoid mortality rates declined by 60% among blacks and 67% among whites; the same reductions were 80 and 83% in cities that did install filters. Clearly filtering has a sizeable effect, but the general declines implicate other potential determinants, such as improved nutrition, rising standards of living, and changes in personal and household hygienic behaviour, and they are likely to play a stronger role than Troesken suggests. For example, historical studies by Preston and colleagues33,34 show that important changes in personal health care practices, health behaviours, medical advice and ideas about disease transmission mechanisms were all likely to have made important contributions to mortality declines during the first decades of the 20th century. Thus, while I do not doubt that Troesken's estimates of the health effects of clean water are real, his assumption that ‘waterborne diseases were eliminated solely through improvements in public water and sewer systems (p. 46–7)’12 likely overestimates their impact on reducing overall mortality.
A final area of difficulty with Troesken's broader argument has to do with extrapolating his analyses of typhoid to make larger claims about the role of clean water in reducing mortality. Mortality from typhoid has never been a major cause of death, which begs the question of how an improved water supply could have such a drastic effect on declines in overall black–white mortality inequality. Far more deaths were generated by tuberculosis, pneumonia, cardiovascular diseases and particularly among infants, diarrhoeal diseases. Table 3 shows death rates from specific causes of death for the US in 1900–04 and 1940 and the contribution of each cause to the decline in overall mortality. The declines in typhoid mortality are impressive, but only account for 5% of the decline in mortality observed from 1900 to 1940. In terms of waterborne disease, diarrhoeal diseases made a much larger contribution to mortality decline. Troesken, therefore, has to assume that the effects of clean water were similar for typhoid and diarrhoeal diseases, yet there is some evidence to suggest that the two diseases may have different determinants, and may therefore be responsive to different interventions. In the US, rates of typhoid mortality were typically highest among young adults, whereas the vast majority of diarrhoeal disease mortality affected those under 2 years of age,29 and Troesken does not consider age-specific mortality in his analyses. Some studies that have attempted to look at the effects of water filtration on both typhoid and diarrhoeal diseases found the effects were either specific to, or else much stronger for, typhoid.35,36 In addition, Condran and Cheney found little relationship between rates of typhoid and diarrhoeal diseases among US cities37 or Philadelphia wards38 in the early 20th century, as did Harmon39 in comparing mortality patterns in US cities in 1916. Troesken's case would therefore be strengthened if he found similar results using diarrhoeal disease mortality for the same sample of cities, but inconsistencies in disease-specific mortality reporting across cities appear to make this difficult.
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Troesken also suggests that exposure to waterborne diseases increased the risk of death from other causes later in life, such as heart and respiratory diseases. This allows for the possibility that clean water may have also affected causes of death like pneumonia and tuberculosis which were quantitatively more important to US mortality improvement (Table 3). This is intriguing, but the evidence he cites for this is not particularly persuasive. For example, he cites favourably Costa's study that found US military recruits who had typhoid were more likely to have an ‘irregular pulse’ and valvular heart disease in later life,40 but in her subsequent work typhoid exposure was not predictive of death for any cause and diarrhoeal disease was actually protective of respiratory mortality.41 Other studies also suggest the role of childhood infections in heart disease is at best mixed,42,43 though few studies have looked at typhoid and diarrhoeal diseases in particular (in part due to the dramatic decline in typhoid mortality that has occurred in more developed countries in the first half of the 20th century). However, in more recent work by Clay and Troesken44 they use a similar panel of cities to demonstrate some plausibility that declines in typhoid mortality were associated with lower rates of heart disease 15 years later. Cutler and Miller45 also recently found in 12 US cities that the combined effects of water filtration and chlorination not only virtually eliminated typhoid mortality from 1900 to 1936, but also accounted for 43% of the overall reduction of total mortality in this period, 74% of the infant mortality decline and 62% of the decline in childhood mortality. Importantly, in cause-specific analyses they also show that the additional mortality declines were for other communicable diseases—pneumonia, meningitis, tuberculosis and diphtheria—with virtually no effect on non-communicable diseases such as cancer and diabetes. This certainly suggests clean water may have wide ranging effects on health, but this remains an area of future research. It may be worth looking for evidence of lifecourse effects in other places that have experienced particularly severe outbreaks of typhoid in the past, such as Tokyo in 1923–24.46
To conclude, while I have some reservations about Troesken's broader argument about the role of clean water in reducing overall black–white mortality differentials, on the whole I find Water, Race, And Disease an important, fascinating and generally convincing study. I highly recommend it to anyone interested in the historical intersection between race, politics and public health in the United States. His book shows not only that public health efforts to improve the disease environment have had an enormous health impact, but that when implemented without discrimination such interventions can also reduce social inequalities in health, even in the presence of persistent discrimination in the allocation of other public goods.
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John Lynch made thoughtful contributions to this article, for which I am grateful.
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