Abstract

Iodine deficiency is the leading cause of preventable mental retardation in the world today. The condition, which was common in the developed world until the introduction of iodized salt in the 1920s, is connected to low iodine levels in the soil and water. We examine the impact of salt iodization on cognitive outcomes in the US by taking advantage of this natural geographic variation. Salt was iodized over a short period of time beginning in 1924. We use military data collected during WWI and WWII to compare outcomes of cohorts born before and after iodization in localities that were naturally poor and rich in iodine. We find that for the one quarter of the population most deficient in iodine this intervention raised IQ by approximately one standard deviation. Our results can explain roughly one decade’s worth of the upward trend in IQ in the US (the Flynn Effect). We also document a large increase in thyroid-related deaths following the countrywide adoption of iodized salt, which affected mostly older individuals in localities with high prevalence of iodine deficiency.

1. Introduction

Deficiencies in the consumption of micronutrients, the vitamins and minerals required in trace amounts for proper metabolic functioning, are a major contributor to poor health in developing countries.¹ Elimination of deficiencies in micronutrients such as vitamin A, zinc, iron, and iodine has been a major focus of development efforts around the world. Nutritional supplementation programs are widely seen as cost-effective interventions with potentially large effects on human capital, though their impact can be hard to evaluate, since their benefits may not be observable for several decades.² Until the second half of the 20th century micronutrient deficiencies were a problem in currently developed countries as well. This paper focuses on the historical experience of the United States and the impact of its successful eradication of iodine deficiency.

The World Health Organization estimates that nearly 50 million people suffer some degree of mental impairment due to iodine deficiency, and that this is the leading cause of preventable mental retardation in the world. Eliminating iodine deficiency around the globe is an ongoing project, largely through the introduction of iodized salt.³ In the US iodine deficiency was a significant problem in the early part of the 20th century with rates of deficiency similar to those faced by the worst afflicted developing countries today. The United States virtually eliminated iodine deficiency with the introduction of iodized salt in 1924.⁴

The most important detrimental effects of iodine deficiency are on the cognitive development of fetuses in utero, and these effects are not reversible later on in life. Eradication of iodine deficiency is thus a candidate explanation for part of the Flynn Effect, the gradual rise in measured IQ that has been observed in developed countries over the course of the twentieth century. As we show below, the benefits of iodization were large, but there were also very significant health costs (several thousand premature deaths) associated with it.

We exploit the interaction of pre-existing geographic variation in iodine deficiency with a national program of salt iodization to identify the program impact. Iodine deficiency is linked directly to geography through the food and water supply. In adults, the most noticeable symptom of iodine deficiency is goiter, the enlargement of the thyroid gland. Prior to salt iodization, endemic goiter was present in regions of the US where the iodine content of the soil and water was low. In 1924 iodized salt was introduced in the United States explicitly to reduce the goiter rate. Since there are large in utero effects of iodine deficiency, we expect to see a significant difference in cognitive ability between those born before and after the introduction of iodized salt in locations with low levels of environmental iodine. Those living in high-iodine regions provide a control group.

We use two unique data sources to look at the effects of iodine deficiency eradication on cognitive ability. From World War I draft physicals we know the incidence of goiter in recruits for 151 geographic regions before the introduction of iodized salt. This provides us with a measure of spatial variation in iodine deficiency prior to treatment.⁵ Our outcome measure is provided by an extensive data set of men who enlisted in the Army during World War II. Upon enlistment, each recruit took the Army General Classification Test (AGCT), a forerunner to the Armed Forces Qualification Test (AFQT). The Air Force was assigned draftees with significantly higher average test scores than the Ground Forces. The probability of assignment to the Air Force rises significantly for those born in high-goiter (i.e. low-iodine) locations in the years after the introduction of iodized salt. Using information about average scores of Air and Ground Force recruits we infer a one standard deviation increase in average test scores in these regions. Our results explain roughly one decade’s worth of the Flynn Effect in the US.

In addition to the positive cognitive effects of iodizing salt we document a significant negative side effect. Chronic iodine deficiency followed by a sudden large intake of iodine can cause iodine-induced hyperthyroidism, which can be fatal. We find a large rise in thyroid-related deaths in iodine deficient regions following the introduction of iodized salt. We estimate that at least 10,000 deaths over the period 1925–1942 were the result of iodization.

The paper proceeds as follows:Section 2 provides some background on iodine deficiency disorders.Section 3 outlines the history of salt iodization in the US.Section 4 describes our data and provides some background on their collection. InSection 5 we present previously undocumented evidence on the spike of thyroid-related mortality following iodization.Section 6 explains our identification strategy andSection 7 presents our results. InSection 8 we present two robustness checks which corroborate our main findings.Section 9 puts our results in the context of related research on the effects of iodization on cognitive ability.Section 10 concludes.

2. Iodine Deficiency Disorders

Recent work has shown that the quality of maternal health and nutrition during pregnancy has persistent effects on adult health outcomes.⁶ Iodine is one of the “big three” micronutrients, deficiencies in which are a major source of ill health in developing countries (the other two are vitamin A and iron). Iodine deficiency is the leading cause of preventable mental retardation in the world. Nearly one third of the world’s population are at risk, in the sense that their iodine intake is considered insufficient. 241 million school-age children receive inadequate amounts of iodine in their diet (Andersson et al. (2012)).

Iodine Deficiency Disorders is a term used to describe a set of conditions that result from inadequate intake of iodine. The thyroid gland contains 70–80% of the total iodine content in the human body (Fleischer et al. (1974)). The thyroid gland uses iodine to produce thyroxin, a hormone that regulates metabolism. When there is too little iodine in the diet, the thyroid compensates for the shortage by enlarging in order to produce more thyroxin per unit of iodine. When dietary iodine is only slightly inadequate, the enlarged thyroid will be able to produce sufficient thyroxin for normal body functioning. This enlargement is known as euthyroid goiter. At lower levels of dietary iodine, the enlarged thyroid will produce inadequate thyroxin, a condition known as hypothyroid goiter, characterized by slow metabolism, lethargy, and weight gain.

Goiters due to iodine deficiency are often reversible after an increase in dietary iodine. However, in some people with this condition, increased iodine consumption results in the thyroid gland producing excessive quantities of thyroxin, resulting in hyperthyroidism: an overly accelerated metabolism, with symptoms including rapid heartbeat, weight loss, temperature elevation, nervousness, and irritability. This “iodine-induced thyrotoxicosis” is most likely to occur in individuals who have experienced long periods of iodine deficiency.⁷

Iodine deficiency early in pregnancy causes irreversible brain damage to the foetus. Severe iodine deficiency can result in cretinism, which is characterized by “profound mental deficiency, dwarfism, spastic dysplasia and limited hearing” (Scrimshaw (1998, p.364)). In endemic areas cretinism can affect up to 15% of the population (de Benoist et al., eds (2004)). However, as Scrimshaw points out, “even in areas where cases of cretinism due to iodine deficiency in the mother are few, the linear growth of the infant, its intellectual capacity, and certain other of its neurological functions are permanently compromised to varying degrees.”⁸ In other words, even if iodine deficiency does not result in cretinism, an iodine-deficient population will experience a continuum of cognitive impairment. Deficient populations typically see a leftward shift in the entire IQ distribution.⁹ In a meta-analysis of 18 studiesBleichrodt and Born (1994) estimate that the average IQ of iodine-deficient groups is 13.5 points lower than non-deficient groups. While widely cited, this result is based primarily on cross-sectional comparisons of observational data, which makes the identification of a causal effect questionable.

Historically, the geographical characteristics of an area determined the endemicity of iodine deficiency. Ocean water is rich in iodine, which is why endemic goiter is not observed in coastal areas. Iodine is transferred from the ocean to the soil by rain. Heavy rainfall can cause soil erosion, in which case the iodine-rich upper layers of soil are washed away. The last glacial period had the same effect: iodine-rich soil was substituted by iodine-poor soil from crystalline rocks (Koutras et al. (1980)). This explains the prevalence of endemic goiter in regions that were marked by intense glaciation, such as Switzerland and the Great Lakes region of the USA. Iodine, when present in the soil, is absorbed by plants and can reach humans through the food chain. Iodine is also present in subsurface water in some locations. Finally, deposits of mineral salt (the remains of evaporated seawater) contain iodine, but this is lost when the salt is refined.

Iodine was first isolated in 1811 by Courtois. Over a century of clinical research proved iodine’s essential role in prophylaxis against iodine deficiency disorders. Doctors and public health officials have used different methods of iodine supplementation. Salt iodization has emerged as the cheapest and widest-reaching way to protect a population from iodine deficiency.¹⁰

3. Salt Iodization in the United States

Salt iodization was the first step in the systematic fortification of food for public health reasons. It was made possible by the nearly simultaneous discovery of a widespread health problem and of its underlying cause. In the First World War draft a little more than 2.5 million draftees were examined for various physical and mental shortcomings. Statistics from these physicals showed the geographic distribution of many diseases and defects, among them goiter, across the United States (Love and Davenport (1920)).

According to the draft examinations almost 12,000 men had goiter and a third of these were judged unfit for service because the size of their neck was too big for the military tunic to be buttoned (Kelly and Snedden (1960, p.34)). Most of them came from states in the Northwest (Washington, Oregon, Idaho, Montana) and the area around the Great Lakes. In Northern Michigan, for instance, more draftees were judged unfit for service “for large and toxic goiters than for any other medical disorder” (Markel (1987, p.221)). On the other hand, goiter was rare in people coming from coastal areas.

This led to multiple surveys of goiter, which confirmed the geographical variation in the prevalence of the disease. By that time there was medical and veterinary evidence showing that goiters could be reduced by adding iodine to the diet.¹¹ These observations prompted a public debate on whether and how to provide iodine prophylaxis to the American population. Although there was discussion of possible negative side effects in the form of hyperthyroidism, the medical consensus was that small amounts of iodine in the diet were beneficial for the vast majority of iodine-deprived populations.

Public health authorities in Michigan, one of the worst-afflicted states, held a symposium on thyroid disease in 1922. The idea of salt iodization (first implemented in Switzerland in 1922) was introduced by David Murray Cowie, M.D. as a cheap and effective means of providing iodine to all population groups, regardless of social status. The Iodized Salt Committee, chaired by Cowie, was set up to investigate the matter further. The Committee agreed upon the launch of a statewide educational campaign on goiter and its prevention through iodized salt, sponsored by the Michigan State Medical Society.

The Committee also contacted the state’s salt manufacturers. The actions of the Michigan salt producers were important, because Michigan was the largest producer of salt for human consumption in the country.¹² The salt producers, although convinced about the public-service character of the project, had initial qualms about its economic feasibility and profitability; it would be financially impossible to separate the salt intended for the Michigan market and then add iodine to it. Instead, the Salt Producers Association decided to launch iodized salt nationwide. Through aggressive advertising of the “new salt,” salt companies contributed to the educational campaign throughout the country (Markel (1987, p. 224)).Figure 1 shows two newspaper advertisements from this period.

Michigan was the first state to introduce iodized salt in May 1924. Morton Salt Company, the largest producer in the country at the time, began selling iodized salt on a nationwide basis in the fall of 1924.¹³ At the same time public awareness of the problem, especially in those areas that were worst afflicted, was gaining momentum. Articles in newspapers and magazines around the country advocated the use of the new salt for all cooking and eating purposes, making references to successful goiter prophylaxis in Switzerland. In advertisements for iodized salt the new commodity bore the endorsement of state or national medical associations, and educational booklets were provided by the salt companies upon demand. Many newspaper sources show the generalized availability and use of iodized salt from 1924 onwards. In addition, as we show inSection 5, the rapid rise in thyroid-related mortality, not only in Michigan but throughout the country, further indicates that iodine supplementation diffused quite rapidly.

4. Data Sources

To implement our identification strategy we need data on the prevalence of iodine deficiency before 1924, as well as data on outcomes of individuals born in these areas both before and after 1924. Our primary data sources take advantage of two previously unused surveys of prime age American males in the early part of the twentieth century.

5. The Rise in Thyroid-Related Deaths

As discussed earlier, the treatment designed to help goiter sufferers sometimes ended up killing them. In Europe, the potential negative side-effects of iodine treatment had been discussed as early as the nineteenth century (McClure (1934) andCarpenter (2005)) and made universal iodine prophylaxis a controversial public health measure. In this Section, we document a large increase in deaths linked to the adoption of iodized salt, which we have not seen previously discussed in the literature.

Figure 7 shows the annual rate of deaths in the US over the period 1910–1960 due to exophthalmic goiter, which accounted for the overwhelming majority of deaths due to thyroid disease over this period.²⁸ There is an extremely large rise in the death rate at the time of iodization. Between 1921 and 1926 the death rate nearly doubled from 2.1 to 4 per 100,000. Deaths due to goiter remained elevated for at least a decade. There was also a large gender disparity in death rates. In 1926 death rates were over 6 times as high for women as for men.²⁹ The population of the United States in 1926 was 117 million, and so the rise of approximately two deaths per 100,000 people represented an extra 2,340 deaths in that year. Over the period 1925–1942 there appear to be at least 10,000 excess deaths that resulted from the introduction of iodized salt. We have found little discussion in the literature of what appears to be a high short-term price the country paid for long-run benefits resulting from this public health intervention.³⁰

The medical literature suggests that iodine-induced hyperthyroidism is most common among those with long-standing iodine deficiency. Consistent with this, the rise in the death rate was highest, and persisted the longest, among older age groups. Deaths in the 25–34 age category less than doubled from 1921 to 1926, and had fallen below their 1921 level by 1935. In the 65–74 age category, deaths more than tripled between 1921 and 1926, and were still three times their 1921 level in 1935. The link between iodine deficiency and the rise in deaths at the time of iodization is also apparent looking across states.Figure 8 plots goiter deaths over the period of salt iodization separately for high- and low-goiter states. We label a state as high-goiter if its goiter prevalence inDefects is higher than 5 cases per 1,000.³¹ The trends between the two state groups are similar except for the period from 1925 to 1932. There is a sharp rise in deaths in high-goiter states in 1925 and 1926, which we do not observe for low-goiter states. As expected, large increases in mortality all took place in states that had high levels of goiter due to iodine deficiency. In addition, the rise in goiter deaths occurs sharply after 1924, which is when salt iodization began in Michigan. The evidence from mortality rates suggests, therefore, that iodization spread quickly around the country after its introduction in Michigan in 1924.

6. Identification

Our identification strategy relies on spatial variation in the extent of pre-existing iodine deficiency along with temporal variation arising from the introduction and rapid spread of iodized salt. High-goiter areas provide the treatment group and low-goiter areas the control group. Years before 1924 are pre-treatment and years after 1924 are post-treatment.

Our baseline regression specification is the following Linear Probability Model:

wherey_iste is an indicator variable equal to 1 if an individuali born in yeart in locality s and joining the Army at timee was assigned to the Air Force, and equal to 0 otherwise.³²

The goiter rate interacted with a set of birth year dummies provides the main coefficients of interest. We choose 1924 as the excluded category, so that the coefficients of interest correspond to differences relative to the 1924 cohort. Iodized salt first became available in May 1924, and take-up, while rapid, was not instantaneous.Field et al. (2009) provide evidence that the first trimester of gestation is the most relevant period for the cognitive impact of iodine deficiency. Thus the majority of those born in 1924 would not have been treated at all. The pattern of coefficients on the interaction of goiter and birth year dummies will show how the relationship between the geologically determined level of iodine deficiency and cognitive ability changes over time. The iodization of salt in 1924 should make these coefficients significantly larger for the later cohorts. Note, however, that we do not impose any particular pattern in the coefficients of interest; we let the data tell the story of whether and how the probability of enlisting in the Air Force changed for cohorts born in affected areas, and we check whether that matches the introduction of iodized salt.

In all the regressions we include a full set ofDefects section fixed effects, as well as a set of state-specific trends. The latter control for gradual changes at the state level, which might affect each cohort’s probability of enlisting in the Air Force. In our first specification, we also include a full set of birth year fixed effects interacted with enlistment year indicator variables, to control for the changing demands of the war and the need for Air Force recruits. The interaction of birth year and enlistment year fixed effects also implicitly provides a control for enlistment age. In another specification, we include full sets of both birth year fixed effects and enlistment month fixed effects.

In our final sample we include all white males born between 1920 and 1928, who joined the Army between January 1940 and December 1946, who reside in their state of birth, and who were between 17 and 26 years old when they enlisted.³³ Since our identification relies on variation within a given birth - enlistment year cohort, we only use birth year - enlistment year cells with more than 100 observations.³⁴ Finally, because our theory relies on the Air Force getting preferential treatment, for most of the analysis we focus on the enlistment period up to November 1945, which is when positive selection for the Air Force ends.

We use two-way clustering for standard errors, at theDefects section level and the birth year level. To corroborate our findings, we conduct several robustness checks: first, we check that our estimates are not confounded by changes in demand for Air Force recruits. The enlistment year - birth year interactions should control for changing demand conditions, but we also show that our results hold for different parts of the distribution of demand. Second, we use an alternative measure of underlying iodine deficiency, the iodine content of drinking water, which is available for a few locations. The estimates from this check are consistent with the results using goiter as our measure of iodine deficiency. We also did a falsification exercise using all the other diseases that were measured at the section level inDefects, to show that our pattern of coefficients is not generally replicated with diseases that were not affected by iodization. Results from this falsification exercise can be found in anonline Appendix.³⁵

7. Results

Figure 9 is a first graphical preview of our results. We plot the probability of joining the Air Force for each cohort of recruits, by high-goiter and low-goiter group, according to the goiter level in their section of birth. The 95% confidence band around the means is very small, because our sample is large. The high-goiter group containsDefects sections which are at the top 25% of the distribution with a cutoff of 5.4 goiter cases per 1000.Figure 9 shows a jump in the probability of joining the Air Forces for the 1925 cohort coming from a high-goiter area relative to the same cohort coming from a low-goiter area. The jump is even more pronounced for the 1926 cohort. Note that half of the 1927 cohort and all of the 1928 cohort only enlisted after the Air Force stopped receiving preferential treatment among Army commands.

Figure 10 is a regression-adjusted graphical presentation of our results.Figure 10 plots the average residuals for each cohort - goiter group combination, after regressing an Air Force indicator variable on enlistment month fixed effects for each birth cohort separately. The 95% confidence band is, again, very narrow.Figure 10 accounts for changing demand conditions over the course of the war, and it shows that those cohorts born after iodization in a previously high-goiter area had a sudden increase in their probability of joining the Air Force (as long as they enlisted when there was positive selection into the Air Force), as opposed to those coming from low-goiter areas.Figure 10 also shows evidence ofnegative selection into the Air Force for the 1928 cohort, who enlisted during the final phase of the war.

Table 3 displays estimates from a linear probability model of assignment to the Air Force. The dependent variable is an indicator switching on if the individual entered the Army Air Force (AAF). The regressors of interest are the interactions of birth year dummy variables with a continuous measure of goiter in the section where the recruit was born. The excluded year is 1924, which is when iodized salt was introduced. The coefficients correspond to changes in percentage points in the probability of joining the Air Force. Columns (1) and (2) ofTable 3 use all enlistment months in the estimation. In columns (3) and (4) we focus on the positive selection period, which ends in November 1945. Our theory relies on the Air Force getting preferential treatment in the cognitive ability of its enlistees, so we focus on this enlistment period in all other specifications. Columns (1) and (3) include interactions of birth year and enlistment year fixed effects. Columns (2) and (4) include birth year fixed effects and enlistment month fixed effects as controls.

The pattern of coefficients suggests a clear break before and after 1924. Cohorts born after 1924 in high-goiter sections are more likely to join the Air Force compared to other recruits. The 1923 cohort, which was the last cohort born before iodization in high-goiter areas, was less likely to be assigned to the Air Force compared to the cohorts that would have enlisted at the same time. The positive effect disappears for the 1928 cohort. This is consistent with the fact that the 1928 cohort enlisted when positive selection into the Air Force was largely over, as can be seen inFigure 6.

The effects that we estimate are large in high-goiter areas. The coefficients for 1925, 1926, and 1927 are between 0.4 and 0.8 percentage points. The most affected areas in our sample have goiter levels of roughly 30 per 1000 cases. Multiplying the coefficients by 30 indicates that themost affected areas saw a 12–24 percentage point increase in the likelihood of joining the AAF if they were born after 1924.

InTable 4 we run a specification similar to column (3) ofTable 3, but instead of using a continuous measure of goiter, we separate the sample into high- and low-goiter sections, and include interactions of birth year dummy variables with a high-goiter indicator as our regressors of interest. We define high-goiter to correspond to the top 20% (column (1)), the top 25% (column (2)) and the top 30% (column (3)) of the population-weighted goiter distribution.³⁶

The results ofTable 4 echo the earlier results, but they are easier to interpret. Depending on how we define “high-goiter” and which cohort we are looking at, individuals born post-iodization in high-goiter areas see a 3.8–10 percentage point increase in the probability that they enter the Air Forces compared to earlier cohorts. Given that the average rate of assignment to the Air Force is roughly 14% for the entire sample, this is a large effect.

In summary, the pattern of coefficients from the linear probability model suggests a big, sudden increase in the probability of assignment to the Air Force for later cohorts born in high-goiter areas. The timing of the change corresponds to the introduction of iodized salt, and is consistent with cognitive gains in utero for the treated populations.

8. Robustness checks

9. Interpretation of Coefficients

In this Section we translate the results of our regressions inSection 7 into a measure of the implied intelligence increases in the population following iodine supplementation. To do so, we construct a simple model of the selection in to the Army Air Forces. We write the model in terms of IQ scores, which are a more conventional measure than the AGCT scores that were actually used in the selection of recruits.

Consider a pool of recruits composed of two populations. A fraction (1 −ϕ) of recruits are from regions in which there is no iodine deficiency. Let their intelligence be represented by a random variable IQ that is distributed normally with mean of 100 and standard deviation of 15. A fractionϕ of recruits are from iodine deficient regions. Prior to treatment, their intelligence is given by the random variableIQ_d, distributed normally with a mean of X and a standard deviation of 15. The average level of IQ in the population would be$\overline{IQ}=\varphi X+(1-\varphi )100$. After treatment, the distributions are assumed to be identical.

As discussed above, a specific fraction of AAF recruits scored above the mean on the AGCT. Given this, we wish to examine how the probability of entering the AAF differs between the two populations before and after treatment. Letψ be the fraction of recruits entering the AAF that had AGCT scores above the mean, and letθ be the fraction of the overall pool of recruits that entered the AAF.

The sources that we have available do not describe the exact process by which the target percentage of above-average recruits in the AAF was achieved. Here we consider a simple and robust algorithm that would have produced this result. Suppose that initially, the AAF draws randomly from the pool of recruits until it has filled its quota for recruitsbelow the mean. Since half the distribution is below the mean, this would fill a fraction 2(1 −ψ) of the allotted slots. To fill the remaining available slots, the AAF would draw randomly from the pool of recruits with AGCT score above the mean.

Under such an algorithm, we can calculate the probability of someone from a low-iodine region entering the AAF as the sum of the initial draw from the entire distribution and the secondary draw where only the top half of the distribution is considered.

Similarly, the probability of someone from a non-deficient region entering the AAF is:

The difference between these two probabilities corresponds to the regression coefficient in our specification. The difference is the increase in the probability of entering the AAF resulting from iodization³⁹:

We apply this model to our setting as follows. First,Figure 4 suggests that, on average, across all the different recruitment periods (the 75% rule period, the period with no rule, and the period with two rules), about 70% of Air Force recruits had an AGCT score above the median. Thus we setψ = 0.70. Second, according to our data the fraction of all recruits going to the Air Force was 14%. We use this value forθ. Finally, we need a measure of the fraction of recruits coming from iodine-deficient regions. In practice, there was a range of iodine deficiency as recorded in theDefects data. In column ( 2)Table 4 we defined our “high-goiter” dummy as corresponding to the one-quarter of sections with the highest prevalence of goiter. Thus we use a value ofϕ = 0.2 5, and evaluate the coefficient from the regression that used this dummy variable.

Using these parameters,Table 7 shows the implied effect of iodization on the probability of entry into the AAF for a range of possible values ofX, the mean level of IQ in the iodine-deficient regions. The estimated coefficient on the high-goiter dummy inTable 4 is in the range 3.8–10 percentage points. Comparing these estimates toTable 7, we see that the lower range of these estimates are consistent with iodization raising IQ by 15 points (that is,X = 85), which is a reasonable expectation given the work of (Bleichrodt and Born 1994). However, the higher range of estimates is larger than any reasonable estimate of the increase in IQ that would have resulted from iodization. Given the uncertainty surrounding the selection process and prior literature on iodization we do not consider the larger results plausible. In any case, our results are consistent with a substantial effect, in line with the existing literature.⁴⁰

Our estimates and their interpretation are based on a sample of male recruits. However, there is evidence suggesting that females are more prone to the development of iodine deficiency disorders than males.Field et al. (2009) discuss experimental evidence that, in animals, females are more likely to suffer cognitive damage in utero as a result of iodine deficiency. BothField et al. (2009) andPoliti (2010) find larger effects of iodization programs on graduation rates for females than for males. Therefore, the effect of iodization on the general population might well be larger than our estimates suggest.

10. Conclusion

Iodization of salt in the United States was one of the first instances of broad-based food fortification, a practice that continues in wealthy countries to this day and is spreading rapidly to the developing world. The experience of the US offers a useful natural experiment for identifying the long-term effects of an important micronutrient deficiency that many developing countries still struggle with today. Prior to iodization, there was significant geographic variation in iodine deficiency, resulting from identifiable soil and water conditions. This variation can be measured using data on the prevalence of goiter, allowing us to clearly distinguish between treatment and control groups. Iodization of salt was national in scope and implemented rapidly. The key period in which iodine deficiency affects cognitive development is a narrow window during gestation. Thus we are able to easily differentiate treated from non-treated cohorts.

We find that cognitive abilities of men born in iodine-deficient regions rose relative to those born in non-deficient regions for cohorts in utero after the advent of iodization. Our measure of cognitive ability is the probability of a man being assigned to the Army Air Forces, entry into which was partially based on performance on a standardized intelligence test. Interpreting our measure in terms of IQ, our finding is that in iodine-deficient regions, iodization raised IQ scores by roughly one standard deviation, or 15 points. Given that one- quarter of the population lived in such regions, this implies a nationwide increase in average IQ of 3.5 points. In developed countries, average IQ rose at a rate of roughly three points per decade for much of the twentieth century. This is the Flynn Effect, which is thought to be largely attributable to reduced health and nutrition insults in utero and among children. Thus our results are consistent with the elimination of iodine deficiency in the United States accounting for roughly one decade’s worth of the Flynn Effect.

From the few pre-iodization surveys of goiter prevalence in the general population⁴¹, we know that iodine deficiency in the worst-afflicted parts of the United States was of a magnitude similar to that encountered in goitrous areas of developing countries and considered a serious public health concern many decades later.⁴² Therefore, our results are relevant for current iodine supplementation efforts around the world.

Supplementary Material

Acknowledgments

We would like to thank Hoyt Bleakley, Kenneth Chay, Andrew Clausen, Joseph Ferrie, seminar participants at Tel Aviv University, Boston College, Brown University, Northwestern University, and conference participants at the NBER’s Cohort Studies Meeting, AEA Meetings and SIRE’s Young Researchers Forum for helpful comments. Desislava Byanova, Federico Droller, Bryce Millett Steinberg, and Young Min Kim provided excellent research assistance.

Footnotes

References

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