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
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
http://enenews.com/huge-spike-in-us-infant-mortality-in-the-four-months-after-chernobyl-video
http://enenews.com/huge-spike-in-us-infant-mortality-in-the-four-months-after-chernobyl-video
bird study
http://www.youtube.com/watch?v=1hcBGSr9QGk
http://www.youtube.com/watch?v=1hcBGSr9QGk
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.
[ii] Cited in Grossman “Fukushima and the
Nuclear Establishment,” http://counterpunch.org/grossman06162011.html.
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).
That nuke hotseat is good stuff, eh?
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