Angle and McIntire Studied the Effects of Lead Aerosols
For this study Angle and McIntire focused on a battery plant in Omaha and the lead levels in black elementary age children’s blood based on how close their school was to the plant. In the study they monitored air levels of lead near the schools and near three industrial plants that were known to emit lead into the air from May to November of 1970. They also evaluated the children for their level of Glucose-6-Phosphate Dehydrogenase (G-6-PD) protein, finding that about 14.5% of males and 2.4% of females had a deficiency in the protein in a large sample size from suburban and urban areas (Angle and McIntire, 1972, p. 520). The schools they focused on for the rest of the study, however, were in the inner city near the industrial plants which they did not specify the locations of (Angle and McIntire, 1972, p. 520-521). Based on the map of the study sites in figure one and the distinctive outline of Carter Lake, however, we can tell that the general area of the study is Northeast Omaha just north of the downtown area (Angle and McIntire, 1972, p. 521).
The scientists then narrowed their sample size to 79 children and took their lead levels once in May the conventional way with whole blood and once in November by a “direct assay of the RBC lead, proposed by many as a more valid index of biotoxicity than whole blood lead” (Angle and McIntire, 1972, p. 520). In each sample about 45% of children were deficient in the G-6-PD enzyme. Of the children going to schools closest to the battery plant their blood lead was significantly higher when counted by RBC lead than those at the schools farther away as shown by the t-test statistical analysis (see Table 1), even when correcting for other variables like hemoglobin levels. However, the study was not able to establish a causal link between the higher blood lead and the air lead samples, simply the still-valuable correlation of proximity to emissions and higher lead levels.
But even the “circumstantial” evidence of higher RBC lead near emitters points to a distributive injustice, that children living in schools closer to emitters in urban centers are more likely to be affected strongly by their activities (Angle and McIntire, 1972, p. 522). The distributive injustice of lead poisoning, in addition to proximity to emitters and increased genetic vulnerability for some individuals, also has to do with housing conditions, as Dr. Sarah Royce noted in her 1990 monograph. “The prevalence of elevated levels, nevertheless, remains highest among inner-city, underprivileged children who live in deteriorating pre-1970s housing containing leaded-paint surfaces” (Royce and Needleman, 1990, p. 2). In addition, when compared to a population of college and professional students from rural Nebraska, who it is safe to assume were more socioeconomically advantaged than inner city school children, the average RBC lead of the school children was significantly higher (Angle and McIntire, 1972, p. 522).
The study supported the hypothesis that G-6-PD deficient individuals had a higher probability of having high RBC lead but lower lead levels in the serum, or fluid portion of the blood. Other studies had supported G-6-PD deficiency being linked to hemolytic crisis, which is a serious condition that occurs when too many red blood cells are destroyed (though this study did not have evidence for that). The authors noted that “If validated, the apparent increase in blood lead in G-6-PD deficient blacks is of potential significance to the 12 % of black males and the 1.4% of black females with this genetic variant, most of whom live in inner city areas of high ambient lead” (Angle and McIntire, 1972, p. 522). This simple statement acknowledges the reality that black people at the time, and even today, tended to live closer to the hazards of lead, and magnifies the problem of distributive injustice by recognizing that due to genetics some black people may be extra vulnerable to lead poisoning. Angle and McIntire also noted that this specific protein deficiency’s effects were not yet studied well in white people (Angle and McIntire, 1972, p. 522).
The discourse of lead toxicity has been heavily racialized, and was especially so in the mid-20th century when Angle and McIntire were writing. Nowadays we theorize that the reason those with African and Asian heritage have G-6-PD deficiency is because the trait gives protection against malaria, and developed alongside that disease although it has also been found in other areas of the world and is recognized as the most common enzyme defect (Cappellini and Fiorelli, 2008, p. 64). However, in Angle and McIntire's day, lead poisoning was heavily associated with poor housing and with the poor, who were disproportionately black, as in the 80s a national survey found that black children were 26 times more likely to have high blood lead levels than white children, and significantly four times the number of black children had been tested for lead previous to the study as white children (Warren, 2001, p. 228). This demonstrates how much more dangerous lead was for black American children than white children, and how more lead poisoning was associated with than the white population that so many more black children were tested.
Cappellini, M. D., & Fiorelli, G. (2008). Glucose-6-phosphate dehydrogenase deficiency. The Lancet, 371(9606), 64-74. https://https://doi.org/10.1016/S0140-6736(08)60073-2
McIntire, M. S., & Angle, C. R. (1972). Air Lead: Relation to Lead in Blood of Black School Children Deficient in Glucose-6-Phosphate Dehydrogenase. Science (American Association for the Advancement of Science), 177(4048), 520-522. https://10.1126/science.177.4048.520
Royce, S. E., & Needleman, H. L. (1990). United States. Agency for Toxic Substances and Disease Registry(Eds.), Lead toxicity. Atlanta, Ga.: U.S. Department of Health & Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry.
Warren, C. (2001). Brush with Death: A Social History of Lead Poisoning. Baltimore: Johns Hopkins University Press.