Enenews today has a column on excess deaths in the US attributable to Fukushima. The research was conducted by Dr. Janette Sherman and epidemiologist Joseph Mangano, co-authors of the medical journal article on 14,000 excess U.S. deaths following Fukushima.
Download the program here: http://lhalevy.audioacrobat.com/deluge/NuclearHotseat-31_1-12-12.mp3
(enenews link http://enenews.com/study-authors-now-20000-excess-u-s-deaths-after-fukushima-not-14000-follow-up-article-looking-at-age-groups-cities-in-works)
Sherman and Mangano now see 20,000 excess deaths.
Their research is being challenged, particularly by scientists who claim that radiation could not be responsible for excess deaths since the only diseases and/or harms caused by radiation are cancer and radiation sickness.
A good example of this type of argument attempting to limit the attributable health effects of radiation is found here: http://www.acsh.org/factsfears/newsID.3313/news_detail.asp
It is very convenient to officially limit the number of diseases caused by an independent variable in order to reduce its overall significance in causing disease in a society.
The US paint industry used exactly this tactic in order to prevent leaded paint from being banned. The paint industry hired scientists who claimed the health effects of lead were limited to plumbism and that the correlation between lead and low IQ was confounded by the purported fact that only low-IQ children ate paint (pica) and that eating paint was the only vehicle for exposure. PLEASE SEE EXTENDED DISCUSSION BELOW
We know now that lead paint particles are inhaled and do not need to be deliberately ingested to cause health problems for all people, especially children.
We also know that low and mid-range levels of radiation cause a very wide array of health problems beyond cancer and radiation sickness.
The bird study and the study by Gould and Goldman established these low level effects after Chernobyl in the US
As stated by Dr. Janette Sherman, a toxicologist and contributing editor to the book Chernobyl: The Consequences of the Catastrophe for People and the Environment,[i] in an interviewed with Carl Grossman: “We’ve known about radioactive isotopes for decades…I worked for the Atomic Energy Commission in the 1950s and we knew about the effects then. To ignore the biology is to our peril. This is not new science. Cesium-137 goes to soft tissue. Strontium-90 goes to the bones and teeth. Iodine-131 goes to the thyroid gland.”[ii]
[i] Alexey Yablokov, Vassily B. Nesterenko, Alexey V. Nesterenko, and Janette D. Sherman-Nevinger Chernobyl: Consequences of the Catastrophe for the People and the Environment. New York: Annals of the New York Academy of Sciences 1141, 2009. http://www.strahlentelex.de/Yablokov%20Chernobyl%20book.pdf
FROM MY BOOK GOVERNING CHILDHOOD (2010) Palgrave.
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.
Managing Risk: Epidemiology, Environmentalism, and Social Welfare Biopolitics
Broader public receptivity to bio-environmental explanations was shaped by the growing environmentalist movement. Tracing the roots of the contemporary environmental movement is complicated but popular awareness of the role human contaminants play in adversely affecting animal and human populations can be attributed to Rachel Carson’s Silent Spring and to growing concerns about air pollution in major cities. Silent Spring explores the effects of DDT on natural environments and human populations. DDT was made available for civilian use in 1945 and was widely sprayed on agricultural crops. Carson’s book was serialized by The New Yorker, beginning in June of 1962, making it available to a wide audience and catalyzing concern about pesticides (National Resource Defense Council). Simultaneously, widespread concern was growing about air pollution. Although concerns about smog are hardly new, in the early 1960s articles began appearing in major newspapers providing scientific evidence of smog’s adverse effects on health. The Los Angeles Times ran quite a few of these articles, as illustrated by a 1961 article detailing the link between smog and lung cancer (Nelson I1) and another article describing a study in Los Angeles examining a possible link between blood lead levels and smog (Nelson B3). In 1963 Congress passed the first federal Clean Air Act, which allocated $95 million to the U.S. Health and Education and Welfare Department to study and support research on air pollution and control. This act funded more smog research which, in concert with Carson’s book, helped mobilize public concern about environmental risk.
Growing environmental concerns primed public receptivity to the results of the longitudinal data on lead poisoning and lead effects collected in the 1960s and 1970s. Drawing upon accumulating epidemiological evidence, public health authorities in the late 1960s and 1970s considered the possibility that lead exposure from a variety of sources over time could accumulate in the body, causing long term health effects (Corn 104-107). Sources of lead exposure broadened to include gasoline and aerosols in the air from smelters (Corn 106; Berney 20-21). Additionally, longitudinal epidemiological evidence collected in the 1960s and 1970s pointed to relatively subtle, but measurable, long term cognitive and behavioral effects from sub-clinical lead poisoning (Bellinger and Bellinger 855). The idea of “undue lead absorption” was created and disseminated as a way of talking about toxicological effects in the absence of overt, clinical symptoms of lead poisoning (i.e., plumbism) (English 151).
In 1970 the U.S. Surgeon General made lead poisoning an official health concern, orchestrating a shift in focus away from case findings and treatment of overt lead poisoning to prevention through mass screening and avoidance of undue exposure (Berney 14). The Center for Disease Control funded screening for approximately 4 million children from 1972 to 1981 using a newly developed finger stick technology (Berney 14). Data collected from these screenings supported the argument that exposure could occur through everyday activities and was not limited to pica (i.e., oral consumptions) (15). Simultaneously, the threshold for adverse effects from lead exposure for children was pushed ever lower as retrospective studies linked mental retardation and learning disabilities to lead exposure in children whose blood tested positively but whom displayed no overt features of poisoning (16). The U.S. Surgeon General reduced “undue exposure” of lead to 40 μg/dL (Berney 14).
Epidemiological data collected and analyzed in the 1970s called into question old stereotypes about childhood lead victims as the evidence gradually documented that all children, even those from affluent families, were vulnerable to sub-clinical lead poisoning. An article in The American Journal of Nursing in 1972 titled, “Lead Poisoning: Silent Epidemic and Social Crime” reports that “for every child treated annually for lead poisoning, 25 children are injured by lead but receive no treatment. Since 12,000 are treated annually, this suggests that nearly 300,000 children go untreated each year” (Reed 2181). The article cites pica as the mechanism for lead poisoning but claims that “studies have indicated that up to 50 percent of both middle-class and poor children demonstrate pica” (2182). The article provides two illustrations; one of a white child mouthing a windowsill and the other of an African-American child eating peeling paint from an exterior wall. The article concludes, “Lead poisoning is more a disease of the environment than of family neglect” (2184). While the article’s language encourages the reader to regard lead poisoning as affecting all children, the imagery and conclusion reinforce the historical supposition that lead poisoning is a disease of poverty, disproportionately affecting inner-city residents. Yet, unlike earlier representations, this article shifts responsibility from the victims of lead poisoning to the broader society. Accordingly, the conclusion reads: “The disease is the product of social and political conditions” and encourages nurses to perhaps “become directly involved in the political process” to “promote health and housing as high community priorities” (2184).
Lead poisoning had been transformed from an accidental occurrence afflicting suspect children to a “social crime.” Undue lead exposure was articulated as a social justice issue in left-leaning publications such as the Nation. A 1978 article titled, “Childhood’s Hidden Epidemic” (Huebner 242), quotes a health department staff member reporting on a Los Angeles community, “One must . . . consider the additional burden on these communities in their struggle for social and economic equality when, as a result of elevated blood levels, many of their youth cannot compete favorably in school or on the job” (cited on page 244).
Accumulating longitudinal data about the severity and scope of lead poisoning effects at low levels of exposure were used to mobilize popular support for regulating lead. In 1971 the Lead-Based Paint Poisoning Prevention Act was passed by Congress, which prohibited use of lead paint on toys, furniture, and food utensils and established guidelines for paint used on residential buildings or constructed with federal funds (Medley 70). In 1976 the Toxic Substances Control Act (TSCA) passed, enabling the EPA (established in 1970) to control chemicals known to pose unreasonable risks to human or environmental health. Lead was entirely banned from paint in 1978 and catalytic converters were introduced and lead was phased out of gasoline beginning in 1975. Exposure to lead was thus legitimized as a broad-scale concern necessitating market regulation.
However, the expansion of lead’s risk created confusion about the very definition of lead poisoning. Were children with elevated blood levels but no clinical symptoms really poisoned? Researchers in the 1970s debated whether epidemiological studies of sub-clinical effects such as school problems and failure were explained by blood level or confounding factors (Berney 17). Some critics of epidemiological work on lead poisoning insisted that children with neuro-behavioral problems such as low intelligence were likely to engage in pica, thereby confounding epidemiological conclusions that lead exposure caused the problems (17). Other researchers emphasized the mediating impact of diet and time spent in the home on lead absorption, implicating parental responsibility in moderating lead’s harms on children’s bodies. Old notions would not die that poor children were less closely supervised and were more likely to engage in deviant and developmentally inappropriate practices such as pica.
It was not until 1982 that researchers were able to use longitudinal epidemiological evidence to document unequivocally that undue lead exposure could “impede children’s overall developmental progress” in the absence of medical symptoms of lead poisoning, including lead encephalopathy, palsy, seizures, etc. (Medley 63). A study published by Herbert Needleman et al. in 1979 of low level lead exposure in Boston school children’s baby-teeth concludes that children with high concentrations of lead performed significantly poorer than their low-lead counterparts on the Wechsler Intelligence Scale for Children (Revised) on three measures of auditory and speech processing and on a measure of attention (689-693). The lead industry responded by attacking Needleman’s work, questioning his integrity (Rosner and Markowitz 330). Yet the lead industry’s efforts to discredit his work were eventually overwhelmed by the vast amount of research, including animal studies, establishing the diverse biological and behavioral effects of lead (Berney 18).
It had taken years to collect the longitudinal evidence to establish conclusively that undue lead exposure caused adverse health and cognitive effects in all populations, irrespective of economic status. During the 1970s, a primary decade for this type of research, children’s overall exposure to lead slowly declined as lead was banned from paint and from gasoline. Consequently, the threat to middle-class children declined as middle-class families moved into suburban homes built after lead was banned entirely from paint in 1978. Efforts from 1976 to 1980 by the National Center for Health Statistics to collect data on blood levels for the entire U.S. population using stratified random sampling produced a median result of 13μg/dL (Berney 21). Regulation was working. Lead concentrations in outdoor air declined about 96 percent from 1980 to 2005 (Berney 21). The effect was that lead’s relevance as a public-health concern for middle-class families declined at roughly the same time as indisputable evidence documented that all children were vulnerable to lead, even at low levels of exposure.
Middle-class parents were made aware of lead as a risk to their children’s cognitive development but were able to reduce exposure through “lifestyle” choices including where to live and how to avoid exposure through parenting practices. Unfortunately, working class populations had fewer choices and opportunities. On average, Black children ages 6 to 36 months were 6 times more likely to have blood lead level of 30-39 μg/dL and 8 times more likely to have over 40 μg/dL blood lead levels, as compared to white children in the period 1976-1980 (Nevin 326). Although undue lead absorption affected all children, the poor were disproportionately impacted.
As illustrated by an article published in October 1980 in The Saturday Evening Post titled “Suffer Little Children,” lead poisoning lingered in the public imagination as primarily a disease of poverty. The article cautions, “Rich or poor, a child living in any home built before World War II can be the victim of lead poisoning” but 6 of its 8 illustrations represent deteriorated housing and urban squalor. One illustration depicts a lead storage battery in a nondescript fireplace and another depicts a child playing in the snow with the warning that lead can accumulate in the ice of “heavily trafficked areas” (Frazier 73, 76). By implication, the article suggests that readers can reduce their exposure by careful selection of living conditions. Additionally, the article notes that “nutritional deficiency may also facilitate lead poisoning and increase its power to inflict damage,” presenting yet another step for parents to pursue to avoid undue lead exposure (76). The most interesting aspect of this article is its author’s conclusion:
It is my contention that, although it is yet unprovable, at least a portion of urban apathy, violence, vandalism and the decreased performance of school children could be a result of increasing levels of lead in the urban environment. It is also my contention that it is past time that we find out if this is so. (77)
By linking lead exposure to urban “apathy, violence, vandalism” the author reinforces the decades old idea that lead poisoning was a problem specific to poor, inner-city populations who failed to conform to “normal” standards of conduct; however, in an unusual twist, the author attributes lead exposure as the potential source of deviance rather than construing it as a byproduct of deviant behavior.
Despite the growing expression of medical concern about lead exposure, inadequate public support prevailed for legislatively enforcing clean-up of deteriorating paint in rental properties. Additionally, little support could be garnered for tighter regulation of lead in consumer products beyond paint and gasoline. The growing, suburban middle-class simply felt their children were largely safe from the perils of undue lead exposure. Suburban physicians bolstered this position by their failure to recognize symptoms of undue lead absorption in middle-class populations (Medley 63-64). Sara Medley therefore describes lead poisoning as a “paradox in modern industrial societies” because of its “neglect” by medical professionals and the public despite clear evidence of its harms.
Activists who remained concerned about lead poisoning in the 1980s tried to amplify the public perceptions of the scope of the problem. Lead was found to pervade both built and natural environments. Although concentrated in urban slums, lead in the environment was found to be ubiquitous, ranging from Greenland’s remote polar ice caps to rural areas (Medley 65). Lead was found in everyday household products ranging from newsprint to toothpaste (67). Research suggested that prolonged exposure to lead from multiple sources could be more detrimental than acute, severe exposure (68).
Research in the 1980s documented that detrimental effects could be found at ever lower levels of exposure. H. L. Needleman’s research during this timeframe used longitudinal prospective studies that measured blood levels from birth (from cord blood), tracked children across time, and controlled for confounding factors by collecting data from diverse demographic groups. Effects were documented below10 μg/dL (Berney 26). In 1985 the Center for Disease Control (CDC) lowered the level of concern to 25 μg/dL (Berney 28). By 1991 the level of concern had been lowered to 10 μg/dL (Bellinger and Bellinger). By 2003 government data were interpreted to indicate that “the threshold for harmful effects of lead remains unknown” (Meyer et al. 1). Childhood statistics collected by the U.S. federal government and released on-line in 2007 indicate that a child with a 10 µg/dL blood level experiences an average decrease in IQ of 6 points (Federal). In 2001-2004 approximately 1 percent of children ages 1 to 5 years exhibited blood levels in excess or equal to 10 micrograms per deciliter, a decline from approximately 88 percent of children in 1976-1980. Despite this decline, approximately 17 percent of Black non-Hispanic children and 4 percent of Mexican American children had blood levels at or above 5 μg/dL in 2001-2004. Lead may be the most toxicological hazard for U.S. children and lead from paint remains the most expensive sources of lead exposure and toxicity (Fee, 573).