Abby Goodnough, Monical Davey, and Mitch Smith, "When the Water Turned Brown," The New York Times, January 23, 2016. http://www.nytimes.com/2016/01/24/us/when-the-water-turned-brown.html?_r=0 Nearly a year and a half after the city started using water from the long-polluted Flint River and soon after Dr. Hanna-Attisha’s news conference, the authorities reversed course, acknowledging that the number of children with high lead levels in this struggling, industrial city had jumped, and no one should be drinking unfiltered tap water. Residents had been complaining about the strange smells and colors pouring from their taps ever since the switch. Yet interviews, documents and emails show that as every major decision was made over more than a year, officials at all levels of government acted in ways that contributed to the public health emergency and allowed it to persist for months. The government continued on its harmful course even after lead levels were found to be rising, and after pointed, detailed warnings came from a federal water expert, a Virginia Tech researcher and others.
The EPA eventually raised concerns but not fast enough, nor aggressively enough, resulting in failures to redress the problem, thereby allowing children to bio-accumulate lead in their bones for over a year.
The children who are poisoned by lead today in Flint are disproportionately poor. Poor children are typically regarded by societal decision-makers as more disposable than wealthy ones (as argued in my book cited below).
Poor children have always been more vulnerable to lead poisoning and societal decision makers fought efforts to protect them for half a century.
Leaded gasoline and paint were the main sources of widespread lead contamination by the mid-twentieth century. Neither industry wanted to remove paint from their products.
The lead paint industry had their hired experts, just as the polluting industries do today. The paint industry experts declared that lead didn't cause mental problems beyond plumbism (acute lead poisoning) and that low-doses of lead were "safe," even for children.
The lead paint industry experts claimed that children with high levels of lead in their blood ate paint of their own volition. Thus, having high lead levels in your blood became a symptom among industry experts of mental retardation. Lead didn't cause cognitive problems, according to lead industry experts. Rather, children who were cognitively deficient were more likely to eat paint.
The story repeats over and over again, substitute your contaminant of choice.
Below find a narrative of callous industry experts pitted against childhood champions. Their battles over low dose effects and bioaccumulation remain relevant today.
Excerpted from Majia Nadesan (2010) Governing Childhood Into the Twenty-First Century. London: Palgrave (see book here). Excerpt drawn from Chapter Four, I chronicled the history of lead poisoning, examining how risks to children were systematically denied by polluting industries, particularly the paint industry.
Lead Poisoning and Childhood Risk: History
Poisoning by lead was known to effect industrial workers in the nineteenth century, but was believed to be limited to workers engaged in particular activities and particular industries. The first recorded instances of children’s exposure to lead poisoning in the home occurred in the nineteenth century; although, these cases were rare and occurred through lead poisoning of food (English 7-13). In 1904 ten children died in Queensland Australia from nibbling lead paint off their porch’s railings (Fee 575). This incident is widely cited as among the first recorded instance of childhood lead poisoning from paint.
Researchers published reports of lead poisoning of children in the 1920s and 1930s using case-by-case studies to document the adverse effects on children’s health posed by lead paint poisoning (Fee 576). Documented effects tended to be very overt and included symptoms such as comas and convulsions (573). More subtle symptoms reported include a change in disposition, abdominal pain, and anemia (575). These symptoms were all believed to derive from pica, the abnormal ingestion of non-food items, particularly paint. Pica was believed to occur most frequently in lower class populations, particularly African Americans (Washington 36). Rather than attributing pica to the probable medical cause of severe malnutrition, many medical authorities construed it as proof of individual and class degeneration.
Since public opinion held that only degenerate or deficient individuals were inclined to pica, political authorities saw little reason for regulating leaded paint. Leaded paint was considered to be superior to alternative paints and the paint industry actively resisted any efforts to curb lead content. Children were even incorporated in lead paint advertising to imply the product’s safety to children. The invention of leaded gasoline in the 1920s did raise some concern about potential public health effects. Ultimately, however, economic incentives outweighed health concerns (Rosner and Markowitz 344-352).
Despite the lack of political concern, a small group of medical doctors persevered in studying lead’s effects on childhood bodies. By the 1940s research published on lead paint poisoning in children had begun to develop a clinical picture of lead’s internal effects on young bodies. For instance, in 1942 Paul Reznikoff used case studies to document that lead absorption by infants and young children creates deposits on the bone, concentrated on where the bone grows most rapidly (1125). The resulting “dense area” could be detected using x-rays. This internal examination of the body offered another strategy for diagnosing lead poisoning in young children (1125).
Clinical doctors’ efforts to demonstrate lead’s harmful effects on children were challenged by the research of Robert Kehoe, whose research on lead was supported by the lead industry (Berney 7). Barbara Berney chronicles how Robert Kehoe combated lead legislation in the United States from the late 1920s through the 1940s (7). Kehoe argued that lead occurred naturally in human tissues and excreta and that the body did not store lead and therefore there was “no necessary relation between lead absorption and lead intoxication – no necessary connection between lead concentration in feces, urine, or tissues and lead poisoning” (cited in Berney 7). Kehoe’s arguments were widely accepted until medical researchers began undermining his claims with demographic and epidemiological evidence in the 1950s.
Kehoe’s arguments established the terrain upon which the adversaries battled. Accordingly, in order to prove that lead adversely affected children, researchers had to provide evidence for the following argumentative planks:
o Lead in the environment was a result of human use of lead in industry.
o Lead accumulated in the human body in proportion to the amount of lead found in the environment.
o Lead was absorbed by the body from the environment.
o Such absorption, measured in feces, urine, blood, and other tissues, was an indication of exposure and poisoning. (Berney 7-8)
The data generated from clinical case-by-case analyses provided insufficient evidence for supporting these claims’ relevance for the entire childhood population. Therefore, it was not until the late 1980s that epidemiologists were able to provide indisputable evidence that low levels of lead absorption in the absence of pica cause bodily and neurological harms for children.
Efforts to build a case supporting lead’s adverse effects can be traced to the proactive approach to health screening adopted by the city of Baltimore. In 1935 the city introduced a free diagnostic test for lead exposure. The test, used on people who were suspected of having lead poisoning, employed a new chemical method for detecting lead in blood called the “dithizone technique” (Fee 580). As the only city in the U.S. with a central diagnostic and reporting mechanism for lead poisoning, Baltimore’s data revealed lead poisoning as a frequent problem for children, particularly for those living in the city’s dilapidated areas (Fee 581). Of the 202 childhood deaths from lead poisoning reported to the U.S. Bureau of Census between 1931-1940, 24 percent came from Baltimore due to its enhanced reporting mechanisms (Fee 583).
Research by Randolph Byers, a medical doctor at Harvard Medical School, and Elizabeth Lord, a psychology PhD, also played in important role in efforts to accumulate the necessary evidence. Published in 1943, their collaborative analysis of 20 case study histories demonstrated how non-fatal lead poisoning adversely impacted children’s intellectual and emotional progress at school (479). At the time, blood levels of 70 to 80 μg/dL were commonly perceived to constitute poisoning while levels of 50 to 60 μg/dL were regarded as normal (Berney 9). Byers and Lord note in their study that blood levels as low as 40 μg/dL could cause poisoning and that lead accumulated in patients’ bodies and was retained after exposure stopped (475).
Bellinger and Bellinger observe that Byers’ and Lord’s study was significant for helping transform the prevailing “patient oriented” model of disease (855). The patient-oriented case-by-case medicine regarded poisoning to have occurred only when the child displayed specific and overt corporeal signs and symptoms of severe poisoning. This model presumed that children would recovery fully if they did not suffer from encephalopathy (855). Byers’ and Lords’ research challenged both assumptions. Some of the children followed in their case study approach were admitted to the hospital for relatively mild signs such as weakness, limping, irritability, and vomiting and did not exhibit the full range of symptoms of blood poisoning (476, 493). Yet, after following up on these cases, Byers and Lord found the children subsequently experienced marked academic and social problems. Intelligence tests administered by the researchers revealed relatively low scores ranging from 67-109; children with higher measured scores tended to exhibit impulsive behavior (477). Byers’ and Lord’s longitudinal case-study approach revealed previously unrecognized long-term risks to children posed by exposure to lead in the absence of overt poisoning, or plumbism.
Time magazine ran an article popularizing Byers’ and Lord’s findings. Titled “Paint Eaters,” the article informs parents, “If your child is slow with building blocks, but quick on tantrums, he may be a lead eater.” “One consequence of the plumbic passion in children may be stupidity,” the article warns. This warning expanded the public’s perception of the threat posed by lead exposure; lead didn’t simply kill; it could also impair. Despite Time’s warning, the public tended to regard lead poisoning as a problem restricted to poor children and children who engaged in the purportedly deviant practice of pica. Retrospective analyses of case studies of lead poisoning pointed to deteriorating living conditions as the primary factor affecting exposure. The tendency for cases to be reported by place of poisoning rather than age after 1951 reinforced the idea that lead poisoning was a disease of poverty (Warren 16).
The idea that lead poisoning was a disease of poverty shaped attitudes toward prevention. Public sentiment did not generally support eliminating lead from paint nor did the public support government-enforced clean-up of the dilapidated housing implicated in lead exposure. Instead, the poor were regarded as indirectly responsible for their poisoning through their careless housecleaning, negligent parenting, and/or deviant children.
In the late 1940s, Baltimore sent public health nurses to poor city neighborhoods to educate mothers of young children of the dangers of lead paint (Fee 586). Mothers were interpellated as responsible for preventing lead poisoning by repainting their homes and by carefully monitoring their children. These efforts to make mothers responsible for ensuring their children’s health through home hygiene extended decades of advice to mothers. For instance, in 1904 Adelaide Nutting of The John Hopkins Hospital published an article, “The Home and its Relation to the Prevention of Disease” arguing that proper home hygiene by mothers, including cleanliness from dust, ventilation, and sunlight, prevents a wide array of diseases including tuberculosis. Home hygiene, proper feeding of infants, and moral guidance together constituted the crux of responsible motherhood from the late nineteenth century onward through the mid twentieth century.
Public attitudes about the inadequate and irresponsible mothering skills of poor and ethnic mothers were reinforced by images of lead poisoned children in the popular media. For example, a 1957 article in the Saturday Evening Post titled, “Help for the Poisoned Child,” includes an illustration of a poisoned African American boy being treated by a white medical staff. The article’s text provides a stereotyped representation of “paint victims”:
Most paint victims are two- to three-year-olds and even younger crawlers a teething age. They nibble paint from toys, from crib railing, window sills; from scabrous walls in old tenements. The doctors call the paint eaters’ ailment ‘lead intoxication, or ‘pica,’ a term defined as, ‘depraved or perverted appetite or craving for unnatural foods, such as chalk, paint, clay. . . .’ (Berger 76-77)
The article reads ambiguously as to whether the “depraved or perverted appetite” derives from, or causes, the lead consumption. This representational framework no doubt contributed to a public unwillingness to regulate lead in paint because it indirectly cast children as responsible for their poisoning. In 1955 a voluntary standard for limiting indoor lead paint to 1 percent was passed yet outdoor paint continued to have high lead levels (Medley 69).
In 1958 Baltimore initiated the first large-scale screening for lead paint in order to evaluate the prevalence of lead paint in Baltimore homes (Berney 8). 70 percent of the 667 dwellings tested had lead in excess of 1 percent (8). Baltimore officials tabulated their lead poisoning statistics for children using race rather than income (Fee 584). Black children’s mortality from lead poisoning was found to be 5 times higher than white children’s (584). The researchers were aware that Black city residents lived in more dilapidated housing and that poor housing was the independent variable affecting mortality statistics. Still, rather than battling slum landlords, city health officials emphasized parent education and supervision. Poor mothers’ supposed negligent supervision of their children was ultimately cast in the public imagination as the determinant factor in childhood lead poisoning. The inner-city Black child emerged as the iconic victim of lead poisoning in popular media representations. This tragic figure garnered some public sympathy but few policy protections.
In 1959 Randolph Byers suggested that pica alone might not explain paint-based lead poisoning in children. He observed that normal mouthing behavior of children in environments with high levels of lead paint could cause poisoning, even when paint was intact (Berney 9). Byers’ observations would eventually help de-stigmatize lead poisoning as a disease of poverty and poor mothering. Epidemiological evidence played an important role in supporting Bryers’ supposition.
Declaration of the War on Poverty in 1964 made more money available for cities across the nation to implement city-wide screening programs for childhood lead exposure (Berney 11). Data collected in the 1960s showed high incidences of elevated blood levels; 25 to 45 percent of 1 to 6 year-olds living in high risk areas had blood lead levels exceeding 40 μg/dL, then considered the upper-limit of normal (Berney 13). More data allowed researchers to detect subtler effects. Each time screening guidelines were revised, researchers initiated new studies to determine whether the new level used to define “normal” was actually safe for children (Bellinger and Bellinger 253). Julian Chisholm’s work in the mid 1960s suggested that children were more vulnerable than adults to lead’s effects and that levels between 40 and 80 μg/dL might hold toxicological significance for children (English 147). In 1966 Harriet Hardy encouraged researchers to study infant exposure to lead, suggesting that infants might be particularly vulnerable to low levels of lead exposure (cited in Corn 107).
Field epidemiology and case findings reported in the 1950s and 1960s mobilized late 1960s and 1970s era activism around lead poisoning. Young epidemiologists in the 1960s and 1970s seized on lead poisoning as an issue that would bridge medical science and social activism: as Berney observes, “lead poisoning could be used to tie the emerging environmental movement (and the reemerging consciousness of the environment in public health) to civil rights issues” (11). The Black child poisoned by lead poisoning was increasingly cast as a victim of economic marginalization, environmental harm and injustice, and cultural stereotyping. Moreover, social activists could use growing epidemiological evidence of widespread lead poisoning among Black children to challenge racist popular sentiments that held them to be cognitively inferior to their white counterparts. Lead provided an environmental explanation for gaps in the measured IQ of Black and white children, deflecting both hereditary notions of inferiority and culturalist accounts of inferior parenting among poor Black families. Activists used the environmental-biological frame of lead poisoning to combat the moral taint of poverty and racism.....
Majia here: What happened to that energy, that movement to protect our most vulnerable persons from environmental toxins? The children of Flint Michigan are calling for a resurgence of resistance against greedy polluters and corrupted government officials who do not value child welfare. They are not the only ones being poisoned by lead, as this expert documents:
Uploaded on Jul 28, 2009Dr. Marc Edwards, professor of civil and environmental engineering at Virginia Tech, explains at the April 2009 Yale University Drinking Water Symposium that EPAs testing procedures fail to adequately detect lead in tap water.