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, 2009
Dr.
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.
There is a big difference between inorganic lead poisoning and teraethyl lead poisoning. Most of the lead poisoning attributed to paint in the cities in the 60s, 70s, and 80s was probably from tel in gasoline. Tel is a deadly and acutely lethal toxin like methyl mercury. The dust from lead paint breathed in does not take long to poison anyone.
ReplyDeleteThe inorganic lead in the water in Flint can lead to chronic poisoning but, the biotransformed organic lead and no doubt high concentrations of organic leads, are probably acutely poisoning people as I write.
Majia it might behoove you to contact Dr. F. Mazda Shirazi at the University of Arizona, or one of his associates and learn more abput the fundamentals of lead and heavy metal poisonings and toxicity.
I agree wez about the virus memes. Radioisotopes, heavy metals, and many other less toxic pollutants are ubiquitous in the envirnment. Especially in heavily industrialized nuclear nations like the United States.
ReplyDeleteI have for some time been attempting to get my small city to take the fluoride out of the water. Despite articles I sent the city council they wanted to do their own research which of course resulted in their doing nothing and mentioning the cavity prevention line. Recently I sent them an article regarding a study which proved that fluoride added to water did nothing by way of preventing caries. They will of course never do anything as it would be seen as too radical. A few dentists might attack them. They might have nightmares in which they were assaulted by decaying teeth and angry mothers. But who knows. Of course corporations have no consciences, no morals, no empathy, no consciousness as they are simply a kind of labor saving machine though their parts are human beings. We do not need to wait for evil predatory ET's or aliens as the corporations are doing a good job of destroying the human world. Now a specific diet might very well help detox the children though it is unlikely it will be broadcast. Naturopathic doctors know about these things. But since these are poor children it is probably not going to happen.
ReplyDeleteYou are so right William. Fluoride is from fluorine the most reactive halogen like chlorine, iodine, bromine. Big fraaud. Almost as bad as tetraethyl lead. Still not as bad as Nuclear power and nuclear waste. It is a byproduct of the nuclear industry as you and a lot of other peopke know. They got away with tetraethyl lead so long. Just 10 mls of tetraethyl lead can kill ya . A few mls gives you permanent brain damage. We all breathed tetraethyl lead till the 1990s
ReplyDeletehttp://www.cdc.gov/niosh/npg/npgd0601.html
They started using tel in the 30s.
Fluorine poisoning is one of the worse chemical poisonings possible. It sucks all the calcium out of your body. Pity those exposed to Hydrofluoric acid conaining ZAP aluminum wheel cleaner. To Those living in the bay area expised to the Perfluoric acid used to etch microchips all those years. Or those who live near chemical plants and petroleum distillation plants in new jersey, texas, louisiana where fluorine tanks have exploded! We have all been lied to so long.
http://emedicine.medscape.com/article/814774-overview#a3
It is ironic that we are the victims of scientific frqud that created and perpetuate this criminal activity but, we need aspects of that same science to know what to do about it.
Organolead compounds are compounds with carbon-lead bonds in their molecules. The first synthetic organic lead compound is hexaethyl diphosphate, synthesized in 1858, where the lead is tetravalent and bonded to three carbon atoms. organic lead compounds
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