
Redlining and Lead Poisoning:Causes and Consequences
In 1934, the Federal Housing Authority precluded mortgage loans to residents of neighborhoods with non-White families or where housing was deteriorated; these were declared "hazardous" and labeled red on maps. In 1962 three redlined north Brooklyn neighborhoods had 41 children, all Black and Puerto Rican, with lead levels >60ug/dL. A review of public polices in the U.S. from 1898 to the present revealed that lead poisoning followed an income gradient with multiple disproportionate effects on non-White children in redlined neighborhoods. The poisonings diminished when federal and local regulations prevented lead exposure. While redlining had profound influences on both likelihood and severity of lead poisoning and its consequences, it was a mediator of effects. The principal causes were federal policies failing to prevent environmental contamination and local governments failing to prevent exposure.
In 1962 Harold Jacobziner and Harry Raybin, epidemiologists with the New York City Department of Health provided a map showing neighborhoods where children had blood lead levels greater than 60µg/dl, the upper limit of normality at that time.1,2 Jacobziner and Raybin countered a false assumption that differences in lead poisoning by race were a result of biologic factors. As they wrote,
The majority of cases occur in the Puerto Rican and non-white, not because of any genetic predetermined factors but chiefly because the above ethnic groups live in areas where substandard housing prevail, i.e., the "lead belt."1
A second false assumption, that poisoning was due to negligent parenting and characteristics of poisoned children prior to their poisoning, was challenged in 1956 by J. Julian Chisholm Jr. and Harold Harrison,3 who asserted that
no mother can reasonably be expected to prevent the repetitive ingestion of a few paint chips when these are readily accessible. … Where housing has been permitted to deteriorate, exposure to lead may be of such intensity as to outweigh such individual variables as mental retardation and emotional maladjustments in the child.3
Subsequent research suggests that these lead belt neighborhoods arose in part because of restrictions by race on affordable mortgages provided by the Home Owners Loan [End Page 431] Corporation (HOLC) and the Federal Housing Authority (FHA).4[p64],5–7,8[pp54–55] An FHA directive stated that "if a neighborhood is to retain stability, it is necessary that properties shall continue to be occupied by the same social and racial classes."4[p.65],8[p.54],9[p.204] Neighborhoods were therefore ranked on color-coded maps that were distributed to lenders; the colors ranged from green for those considered "best" to red for those considered "hazardous."4[p.65],10 "A neighborhood earned a red color," wrote Richard Rothstein, "if African American families lived in it, even if it was a solid middle-class neighborhood of single-family homes"4[p.64]—thus the term "redlining."4[pp.vii–vii],5
Three redlined neighborhoods in north Brooklyn—Crown Heights, Bedford-Stuyvesant, and Fort Greene—were in the lead belt identified by Jacobziner and Raybin.1 In the first nine months of 1961, at least 41 children in these neighborhoods were found to have had blood lead levels greater than 60µg/dl. Thirteen children in the five boroughs of New York City, all of African American or Puerto Rican ancestry, died of lead poisoning in those nine months.1
This commentary will identify factors affecting the consequences of lead poisoning for children living in redlined neighborhoods, with the objective of clarifying relationships between redlining and the prevalence, severity, and consequences of the lead poisoning experienced by resident children. Documents were reviewed from 1898 to the present highlighting public policies that affected exposure to environmental lead; the epidemiology of lead poisoning by race, income, and location; and the impact of race-based policies affecting vulnerability to exposure and consequences that followed. This commentary also considered limitations placed on lead content of paint and gasoline, rules for lead inspection and mitigation prior to sale or rental, racial biases in sale and rental of residences, and legal expectations for landlords and how they were enforced.
The Demographics of Lead Poisoning, 1961 to 1980
Jacobziner and Raybin provided a map highlighting neighborhoods where children with blood lead levels greater than 60µg/dl lived.1 A comparison of their map with those provided by the FHA to lenders shows that three lead belt neighborhoods in north Brooklyn—Crown Heights, Bedford-Stuyvesant, and Fort Greene—were also redlined. This is shown in Figure 1.
Jacobziner and Raybin's observations also coincide with data on lead levels of children from the Second National Health and Nutrition Examination Survey collected between 1976 and 1980.11 Mahaffey et al. found that Black children six months to two years of age had significantly higher mean lead levels (20.9+/–0.96) than White children of the same age (15.0+/–0.56µgm/dL; t=95.9, p<.001).11 Similarly, for children two to five years of age, Black children had significantly higher mean lead levels (20.8+/–0.55µgm/dL) than White children (14.9+/–0.41µgm/dL; t= 203, p<0.001). Overall, they report a "prevalence of elevated lead levels [greater than 30µg/dL] of 12.2 per cent in black children and 2.0 per cent in white children."11
With respect to income differentials, Mahaffey et al. report that "among whites and blacks, preschool children from families with annual income under $6,000 had significantly higher prevalence of elevated lead levels than those of higher income families." [End Page 432]
Through the 1960s and 1970s the Fort Greene, Bedford-Stuyvesant, and Crown Heights neighborhoods were populated by low-income families of color.
[End Page 433]
Data are from the Second Health and Nutrition Examination Survey conducted between 1976 and 1980.11
Also noted was "a stronger relation among blacks than among whites between income and the proportion of children with elevated blood lead levels."11 As shown in Figure 2, there are substantial racial and economic gradients in susceptibility to lead poisoning, with all children in low-income families having higher lead levels than non-lowincome and all children in Black families having higher lead levels than children in White families. The greatest risk was for children in families that were low-income and Black. When differentiated by race or by income, all comparisons showed significant differences in lead levels with a probability less than .05.
With respect to location of housing, Mahaffey et al. expressed caution about making comparisons of data by race for children living in rural areas because of the small number42 of rural Black children in their study.11 With that caveat, they reported that "the relation between the percentage of children with elevated blood lead levels and the degree of urbanization was apparently stronger in blacks than in whites. In the central cities the percentage of children with elevated blood lead levels was significantly higher among blacks than among whites (p<0.01)."11 Their data suggest that low-income Black children living in central cities were at the highest risk for lead poisoning while those who lived outside of cities or had higher incomes had some protection. Low-income white families also had greater access to housing outside of neighborhoods restricted to Blacks, but low-income Black families had none.8[p.54]
In investigating whether redlining was the cause for the heightened incidence of lead poisoning among non-White children in these neighborhoods,4[p.230],12 it became [End Page 434] clear that a cause-and-effect relationship did not exist between redlining and lead poisoning. According to Merwyn Susser, a causal relationship requires association, time order, and "direction" (the process of occurrence), as well as a severity of outcomes.13 In these Brooklyn neighborhoods, however, exposure and poisoning likely occurred prior to the onset of redlining, representing a failure of Susser's time order requirement.14,15 With proper regulation of lead in gasoline and paint, exposure would have been diminished substantially.15–18 The role of redlining, therefore, was as a mediator between exposure and the consequences of redlining. This suggests that the primary causes of lead exposure in these redlined neighborhoods were, first, at the federal level, a failure to address the toxicity of lead in industrial products and wastes14–18 and, second, at local levels, failures to protect children from exposure to flaking lead-based paint in debilitated housing.1,15–20
Prior to the setting of strict standards for exposure to environmental lead,21–23 redlining restricted low-income and non-White families to neighborhoods where children were exposed to flaking and peeling lead-based paints in debilitated apartments1,3,18 and to gasoline fumes from proximate street and highway traffic.19–21,24–26 Lead contamination of urban drinking water followed a similar pattern.18 Redlining of neighborhoods affected levels of exposure to fumes; however, this happened only when there were high levels of ambient pollution for children in society taken as a whole, a consequence of the lack of enforced standards.26
Low-income White children were also affected by exposures to environmental lead,11 but they were partially protected by the availability of affordable housing to White families in neighborhoods where Black families were not permitted residence.8[p.54] Additionally, there were some protections from lead poisoning for children from higher-income Black families,11 most likely due to greater selection opportunities within the limited pool of available housing for non-White families.27[p.27]
Questions remain about what contributed to these differences in lead levels in different children and how much can be ascribed to the policies of the HOLC and the FHA, how much to failures to regulate sources of and exposure to lead hazard, how much to poverty, and how much to pervasive elements of racial biases affecting multiple public policies in the United States at the time.
Public Policies Permitting Lead Exposure
In 1914, Alice Hamilton wrote that "the conditions under which the work is done in our factories are conducive of a very high rate of [lead] poisoning."14 Nevertheless, policies at the federal level permitted lead additives in gasoline until 199625 and in paint used for interior surfaces until 1979.15 The economic advantages from the addition of lead to products were substantial.15,22,25,28,29 Adding tetraethyl lead to gasoline increases octane level (fuel efficiency) at a lower cost than further refining.25 Similarly, as advertised to the public, there were substantial advantages in appearance and durability from using lead-based paint.28,29
In 1925, the Surgeon General of the United States temporarily suspended the production and sale of leaded gasoline and appointed a panel of experts to investigate recent fatalities that had "occurred in the manufacture and mixing of the concentrated [End Page 435] tetraethyl lead."25 An industry-dominated advisory committee in which Alice Hamilton was the only genuine environmental thinker advised against the use of tetraethyl lead in gasoline; their advice, however, was ignored.22
In 1969, Joel Alpert et al. expressed concern about environmental contamination from motor car exhausts,20 and in 1980 the U.S. Public Health Service concluded that lead in gasoline had become the predominant cause for lead poisoning in the United States.25 However, lead was not banned from gasoline until a decade later in 1990.16,25 The benefits of this ban on lead in gasoline were summarized by Herbert Needleman, who reported:
Between 1976 and 1994, the mean blood lead concentration in children dropped from 13.7µg/dL to 3.2µg/dL, in direct proportion to the amount of tetraethyl lead produced. One could want no clearer testimony to the efficacy of a well-conceived and consistently applied public health policy.
[emphasis added]16
The dynamic for putting lead into paint for interior spaces and later removing it is quite similar.15,30 Prior to limitations being placed on lead-based paint for interior surfaces, it could contain as much as 50% lead by weight (50gm of lead in 100gm of paint).30 Whereas most European countries banned such use by 1934,15 the United States did not begin to do so until 1955, at first as a voluntary standard. The contemporary standard is now 0.009gm of lead in 100gm of paint.31
Engaged health providers, through their advocacy efforts, played a role in ensuring that governments enacted these restrictions on the use of lead-based paint. In Baltimore, the first city to do so in 1950, Chisholm and Harrison were forceful advocates for restricting lead exposure.3,32 Similarly, Jacobziner and Raybin were advocates for preventive policies within the New York City Health Department, leading to the 1960 ban on lead in interior paint.1,23 Current New York regulations require inspection after a report from a tenant or a health provider of a child with a blood lead level >5.0µg/dL.23 Paint surfaces must be in good repair and lead-paint concentration, "tested by an x-ray fluorescence analyzer or accurately measured paint chip sample," must be less than 0.5mg/cm2, lowered from the 2004 standard of 1.0mg/cm2.23 That said, attention must be paid to persistent dangers from environmental lead.17,18
These observations document that the federal government's failure to prevent lead use in products likely created exposures to the public14–16,22,25 and municipal governments' failures to prevent exposure to children1,3,19 were the principal causes for lead poisoning and the consequences that followed. Lead poisoning would not have occurred in redlined neighborhoods had there been appropriate restrictions against exposure in place and enforced. This does not, however, diminish redlining's increasing the risk for lead exposure, the severity of poisonings, and the augmentation of consequences.
Redlining as a Mediator of Effects
Paula Braveman and Laura Gottlieb point to neighborhood social disadvantage as a social determinant of health.33 David Williams and Chiquita Collins describe, "racial residential segregation (as) the cornerstone on which black-white disparities in health status have been built in the U.S."34 Within the constructs of neighborhood social dis-advantage [End Page 436] and racial residential segregation, three elements of the redlining phenomenon mediate between exposure of urban non-White children to lead and heightened consequences: (1) limitations placed on Black families' ability to access resources of the dominant White society,34–37 (2) continued impoverishment of Black families,8p.132–137,34,38,39 and (3) iron deficiency as the subsequent consequence.40–42
Impact on Black families' ability to access resources of dominant White society
As with all race-based policies, with redlining there were assumptions of White superiority. Racially integrated housing would have undermined these assumptions. The redlining policies of 1934 codified extant racial biases that had restricted African American access to housing.43[p.305] Over the course of a century these biases had restricted residence choice of Black families long before the FHA and the HOLC issued their directives.4[p.xii],[pp.222–225],8[pp.17–19] The banking and real estate industries were fully cooperative with the racial restrictions for loans from the FHA and HOLC preceding, during and after the initiation of the redlining polices.4[p.9][p.109][p.274]
The historical antecedents of these racist protocols are apparent. Both long-standing private racism and public policies created disparities affecting African American residence in neighborhoods with higher-quality housing stock. W. E. B. Du Bois in The Philadelphia Negro, an historic ethnographic survey from 1899, described the origins of these racial restrictions there.43 Examples include the fact of "white people preferring not to live near Negros"43[p.295] lack of acceptance and safety outside restricted neighborhoods,43[p.297] and "all Negros, good, bad and indifferent," confined to Philadelphia's 7th ward and a few other localities.43[p305]
The discrimination in housing codified by the HOLC and the FHA continued even after redlining had been forbidden by the Fair Housing Act of 1968. As Douglas Massey and Nancy Denton write, "Rather than use these programs to promote fair housing goals, the FHA administered them in a manner that promoted segregation."8[p.205] They add that without ghettoization, the discriminatory practices affecting African Americans "would not have had the disastrous social and economic outcomes observed in inner cities."8[p.8]
As William Julius Wilson has pointed out, political, economic, and policy decisions that were at least partly influenced by race also affected the restrictions in housing that deprived African Americans of the stepping-stones, or ladders of opportunity, that could enable social and economic advancement:35–37
From a historical perspective, it is hard to overstate the importance of racialist structural factors. Aside from the enduring effects of slavery, Jim Crow segregation, public school segregation, legalized discrimination, residential segregation, the FHA's redlining of black neighborhoods in the 1940s and '50s [emphasis added]… there is the impact of political, economic and policy decisions that were at least partially influenced by race.35[pp.152–153]
Continued impoverishment of Black families
The 1934 redlining policies of the HOLC and the FHA codified extant racial biases to trap urban African Americans in a cycle of economic poverty.34–39 The cumulative effects of the discriminatory practices described have been an overwhelming concentration of wealth among White Americans and poverty among Black Americans,38 as well as the accentuation of income disproportions [End Page 437] that resulted in higher poverty rates for Black families compared with White ones.39 A cruel example of the economic effect of redlining on wealth disparities was the denial of FHA-supported mortgages to almost all Black veterans of World War II.7 As documented by Louis Lee Woods II, "Despite the fact that 1 in 13, or (7.69 percent) of all World War II veterans were African American, these former servicemen only received 0.7 percent of the VA-guaranteed mortgage loans."7
Transgenerational effects are illustrated by 2019 data from the U.S. Census Bureau that showed the median accumulated wealth for White families to be $139,000 "compared with $12,780 for black householders and $19,990 for Hispanic householders," an almost 11-fold White-to-Black advantage.38 The Annie E. Casey Foundation reported in 2018 that 32% of Black families had yearly incomes below the poverty level as opposed to 11.0% of White families and 36% of Hispanic ones.39
Poverty and iron deficiency
A consequence of poverty is an increased risk for malnutrition in childhood.40–42 Lack of sufficient income for necessities narrows the selection of foods to those containing the most energy at the lowest cost.40,41 Mengyao Zhang and Ghosh Debarchana documented "the disinclination of chain supermarkets to locate or pull out existing stores from impoverished neighborhoods," limiting availability of nutritious food.44 As described by Braveman and Gottlieb, "Neighborhood socioeconomic disadvantage and higher concentration of convenience stores [with] lower availability of fresh produce, combined with concentrated fast-food outlets and few recreational opportunities, can lead to poorer nutrition."33 These have all contributed to iron deficiency41,42 and pica,1,19,45 the persistent eating of substances that have no nutritional value, which in turn increases the risk for lead poisoning and its consequences.1,19,46–49 As a result, more expensive micronutrients such as iron are likely diminished in the diets of those living in redlined neighborhoods and their sequelae, resulting in iron deficiency and pica. This in turn increases the risk for lead poisoning and its consequences.1,19,45–49
A 1971 review of nutrition data from a predominantly African American community in New Haven by Vasquez-Sloane et al. showed a mean hemoglobin level of 11.1 gm/dL for children six to 36 months of age, with a fifth percentile at 7.7 gm/dL.49 As reported in the Ten-State Nutrition Survey, 1968–1970, "In all states the minority populations surveyed have substantially higher prevalence of abnormal hemoglobin levels than the White populations."50[p.18] In data from New York City, one of the 10 states, the survey found that 19.9% of all children younger than six years of age had hemoglobin levels below 10.0 gm/dL50[p.22] Notably, the current standard for hemoglobin level for children six months to two years of age is 12.0gm/dl.51 Studies conducted by Betsy Lozoff and colleagues have shown neurodevelopmental effects occurring in infants and toddlers with hemoglobin levels below 11.0g/dl that have long-term effects into adulthood.52,53
Three sets of research studies connect pica and iron deficiency with lead poisoning in childhood. First, Philip Lanzkowsky showed iron deficiency to be concomitant with pica.45 Chisholm reported, "Pica is particularly frequent among children among lower socioeconomic groups and is also a manifestation of iron deficiency anemia in some children."19[p.1486] From Jacobziner and Raybin we hear, "the existence of pica gives a higher correlation with an increased blood lead level than any other finding. … About 24% of the children who manifested pica were also found to have lead poisoning."1 [End Page 438]
Second, iron deficiency enhances lead absorption from the gastrointestinal tract because of common transport mechanisms.46 The data provided from the Ten-State Nutrition Survey suggest that the false conjecture of an increased susceptibility of Black children to lead poisoning referred to by Jacobziner and Raybin may have developed from the common occurrence of iron deficiency among low-income Black children.1,41,49,50
Finally, there is a commonality of the neurodevelopmental consequences of iron deficiency and those of lead poisoning that compound their effects.47,48 For both lead poisoning54–56 and iron deficiency,53 neurodevelopmental disabilities sustained in childhood last into adult life.
Causes and Consequences
While redlining is associated with dire consequences for affected families, and increases the risk for and severity of lead poisoning, the data provided do not follow a cause-and-effect model. Following Susser, association with lead poisoning in itself is not determinate.13 With proper regulation, lead poisoning could have been prevented.14–18 The underlying causes for the poisoning, therefore, were faulty public policies at all levels that permitted exposure to environmental lead,14–18,21–23 with the greatest impact on children who were both low-income and Black, those most likely to be exposed.1,11
Redlined neighborhoods were the milieu in which lead poisoning occurred and consequences followed. Theodore Wachs has described children's reaction to their environment as mediated by individual characteristics of a child.57 For example, a child with high reactivity and low self-regulation (also called a "difficult" temperament) will have a higher probability of poor social-emotional development when reared in environments containing high levels of developmental risk factors and low levels of developmental protective factors.58[pp.204–206] Thus, there are limits to how well one can predict how a unique environment will interact with the biologic influences on an individual child for specific outcomes.58[pp.178–181]
The environments of urban low-income and Black children have always been substantially different from those of White and income-sufficient ones.34–38 Differences in outcomes for groups of children from substantially different environments can be expected with regard to a similar biologic influence such as lead poisoning. The work of Urie Bronfenbrenner maintains that one must consider interactions of macrosocial environmental influences deriving from public policies and allocation of resources with microsocial ones of the family and community in which a child lives and grows.58[pp.178–181] Thus, the contribution of redlining to the consequences of lead poisoning was as a mediator of environmental effects rather than as a direct cause.
The influences of redlining in mediating between exposure and outcomes ranged from proximal to distal. The proximal effects were to codify racial segregation that forced "the Puerto Rican and non-white [to] … live in areas where substandard housing prevails"1 while at the same time denying opportunity for home improvement loans to maintain these facilities. The result, wrote Chisholm, was the "flaking of old lead contaminating paint to which small children have easy access."19[p.1486] Moreover, these neighborhoods were more likely to be in proximity to chemical and other industrial [End Page 439]
Public policy failures were the direct causative factors for the lead exposure described by Jacobziner and Raybin.1 The likelihood of exposure, severity of lead poisoning, and the consequences that followed were mediated by redlining.
plants where multiple exposures to toxic substances interacted with lead to worsen outcomes for the children living in them.4[pp.54–57],26
At an intermediate level, families became impoverished because they were unable to develop home equity4 and were denied opportunities within the society at large.33–37 Distal influences derived from the consequences of attending segregated schools in an era when limited educational development among non-White children was the common expectation.27 Figure 3 below provides a configuration for how primary and secondary phenomena mediate between public policies and the consequences of redlining, lead poisoning included.
Limitations
The cause-and-effect model for failure to regulate and thus not protect from environmental lead exposure meets Susser's criteria of association, time order, and direction.13 The plummeting of children's lead levels post-regulation from 1982 to the present confirms the model's validity.16–18 The role of redlining as a mediator, however, is one of many potential influences on exposure to and consequences from environmental lead. Each of the variables described (resources, income, and nutrition) interacts with all the others to give a myriad of outcomes in what Theodore Wachs describes as "specific organism-environment interactions."58p.152 For any single lead-poisoned child, susceptibility to an adverse experience and the likelihood of adverse outcomes can only be understood within the balance of supportive versus non-supportive life experiences.57 It is in this context that adverse social,33–37 economic,33,36–38 and nutritional33,40–42,44 consequences [End Page 440] of redlining-induced low-income, racialized segregation occur. The prevalence and severity of poisonings and the consequences that follow will be greater for children in families experiencing the cumulative indignities of redlining.
The role of redlining in creating and maintaining segregated African American communities has been challenged at the highest judicial level. In 2007, a five-to-four majority of the U.S. Supreme Court overruled federal judge Stephan Roth, who had ordered compensation for educational consequences of redlining at the divide between urban and suburban Detroit.4[pp.xii,xiii] Although, as justice Potter Stewart wrote for the majority opinion, "substantial evidence was provided to show governmental activity as a cause for the racial segregation," the court chose to ignore it.4[p.xiii] The differential in where Blacks and Whites lived, Stewart maintained, occurred because of "unknown, perhaps unknowable factors such as in-migration, birth rates, economic changes or cumulative acts of private racial fears."4[p.xii]
The last of these, racial fears, was undoubtedly true. When Black families had tried to overcome obstacles by renting or buying homes in White enclaves, they faced social exclusion and at times violence.8[p.35],42[pp.295–7],59 As a result, non-White families would, not surprisingly, segregate in protected enclaves.4[pp.215–217] Attempting residence in Levittown, New York, for example, Black families faced three levels of discrimination: they were excluded by racial criteria for sale,59 denied mortgages by the FHA9[p.204] and the GI Bill,7 and legitimately feared violence if they did succeed in purchasing property.59
Conclusions
The substantial racial and economic gradients in susceptibility to lead poisoning shown by Mahaffey et al. documented that the greatest risk was for children in low-income and Black families.11 Redlining by the FHA and the HOLC increased the risk of exposure of these children to environmental lead by codifying extant racial prejudices that had, a priori, created racially segregated, low-income areas8[pp.54–55],43[p.295] and, post priori, have continued them.8[p205] Multiple consequences of ghettoization have followed over generations to which attention must be paid.33–37 At the same time, addressing the needs of the most affected children required attention to the policies affecting all children. At the same time, addressing the needs of the most affected children required attention to the policies affecting all children.
It was the failure to limit the lead content of gasoline,16–18,21,22,25 paint,15–18,22 and drinking water18 that have put children in the United States at risk for lead poisoning11,16,18 until restrictions were placed on the inclusion of lead in industrial products21,22 and governments enacted protections from exposure.23,31 Effective policies for all children are necessary to address lead poisoning and concomitant issues of public health. As Herbert Needleman pointed out, there are no shortcuts or substitutes for "a well-conceived and consistently applied public health policy."16
ROBERT J. KARP is s Emeritus Professor of Pediatrics at SUNY-Downstate Medical Center, Brooklyn, NY.
Acknowledgments
The reviews and suggestions of Michelle Alperin, H. B. Karp, PhD, and Theodore Wachs, PhD are greatly appreciated. David Hampel ([email protected]) prepared the figures. The Library Service of the University of Richmond provided the colorcoded maps of the HOLC and FHA. Permission for reproduction of the figure from Jacobziner H, Raybin HW. The epidemiology of lead poisoning in children. Archives of Pediatrics. 1962;79(Feb):72–6 was graciously provided by SAGE Publications, holder of the copyright for Archives of Pediatrics.