HISTORY
OF LEAD POISONING IN THE WORLD
Dr.
Herbert L. Needleman
Introduction
The Center for Disease
Control classified the causes of disease and death as follows:
50 % due to unhealthy
life styles
25 % due to environment
25% due to innate
biology and
25% due to inadequate
health care.
Lead poisoning is
an environmental disease, but it is also a disease of life style. Lead
is one of the best-studied toxic substances, and as a result we know
more about the adverse health effects of lead than virtually any other
chemical. The health problems caused by lead have been well documented
over a wide range of exposures on every continent. The advancements
in technology have made it possible to research lead exposure down to
very low levels approaching the limits of detection. We clearly know
how it gets into the body and the harm it causes once it is ingested,
and most importantly, how to prevent it! Using advanced technology,
we can trace the evolution of lead into our environment and discover
the health damage resulting from its exposure.
Early History
Lead is a normal
constituent of the earth’s crust, with trace amounts found naturally
in soil, plants, and water. If left undisturbed, lead is practically
immobile. However, once mined and transformed into man-made products,
which are dispersed throughout the environment, lead becomes highly
toxic. Solely as a result of man’s actions, lead has become the most
widely scattered toxic metal in the world. Unfortunately for people,
lead has a long environmental persistence and never looses its toxic
potential, if ingested. The lead dispersed through gasoline exhausts,
smelter emissions, and peeling paint, etc. never fully disappears from
our environments nor has man evolved a good biological system to offer
any protection from it. In the course of evolutionary time, the global
contamination of this highly toxic substance into man’s environment
has been a very short and recent period.
It is believed that
mankind has used lead for over 6000 years. Lead mining probably predated
the Bronze or Iron Ages, with the earliest recorded lead mine in Turkey
about 6500 BC. The oldest artifact of smelted lead is a necklace found
in the ancient city site in Anatolia. The estimated age of this necklace
is 6,000 to 8,000 years ago. There were many reasons for lead’s use
other than its abundance and ease in obtaining it. Some of the properties
which make it commercially attractive include: easy workability, low
melting point, ability to form carbon metal compounds, hold pigments
well, very easily recycled, stands up well to the outside weather elements,
a high degree of corrosion resistance, it is inexpensive, etc. There
are also several habits and customs of cultures that contributed to
human exposure, such as using lead in medicines and cosmetics.
Lead’s toxicity
was recognized and recorded as early as 2000 BC and the widespread use
of lead has been a cause of endemic chronic plumbism in several societies
throughout history. The Greek philosopher Nikander of Colophon in 250
BC reported on the colic and anemia resulting from lead poisoning. Hippocrates
related gout to the food and wine, though the association between gout
and lead poisoning was not recognized during this period ( 450-380 BC).
Later during the Roman period, gout was prevalent among the upper classes
of Roman society and is believed to be a result of the enormous lead
intake.
Rome: The First
Mass Distributor of Lead:
The Romans conducted
lead mining on a massive scale and had several huge lead mine and smelter
sites. Lead was in big demand and was a byproduct of refining silver
and gold ore. One smelter site located in Spain required tens of thousands
of slaves to operate. Another large site was in Greece and the emissions
from these two sites would rise high into the atmosphere and get picked
up by the world’s air currents. Some lead would fall back to earth in
the snow and recently, scientists measured lead particles deposited
in Greenland’s ice to determine the history of lead production. The
massive mining and smelting of lead went on for hundreds of years and
the production of Roman lead was not surpassed till the period of the
Industrial Revolution.
In ancient Rome,
lead poisoning was a disease of the wealthy who used lead extensively:
leaden cooking utensils and pots, leaden wine urns, lead plumbing (also
to line the aqueducts) (Plumbing is derived from plumbum, Latin for
" Lead"), vessels used to concentrate grape juice, containers
used to store wine, and lead-based makeup. In those days there were
no substances ( like sulfites) to act as preservatives for the wines.
Lead is naturally sweet in taste and was found to enhance both the color
and bouquet of wine. The Romans shipped wines all over their empire,
as far way as northern Germany. A preservative was needed to prevent
bacteria from turning the wines into vinegar. The Greeks added pine
tree resin to their wines but the Romans preferred sweet Sapa, a boiled
down concentrate of grape juice. The problem with Sapa was that the
kettle used in boiling unfermented grape juice into a concentrate was
made of lead, which leaches into the liquid because of the high acidic
content of the grape juice. The final product, Sapa, is a sweet aromatic
syrup containing about one gram of lead per liter. Because of its sweet
taste, many Romans used it as a sweetening agent in many dishes. When
taken together, all the pathways of lead in Roman society, and the intake
of lead in Roman times is estimated to have varied from about 35 mg/day
to about 250 mg/day, compared to today’s daily intake of 0.3mg in the
United states in the 1980’s (National Academy of Sciences 1980).
There are many distinquished
historians who now believe that this high exposure to lead was a contributing
force in the decline of the Roman Empire. With the more recent scientific
research proving that lead is a highly neurotoxicant and analyzing the
strange behavior of most Roman leaders and the upper classes, a good
case can be made for lead’s role in a declining Roman society. What
is ironic is the fact the during Roman times lead poisoning was primarily
a disease of the affluent while today it is an affliction of primarily
the poorer communities.
The First Law
Banning Lead Was for Economic Reasons!
In the German city
of Ulm, during the late 1690’s, there was a severe outbreak of colic,
an illness characterized by a variety of symptoms, including excruciating
abdominal pain. Ulm’s official physician noted that at a local monastery
the monks who did not drink wine were healthy while those that did developed
colic. Since the monks lived together, ate the same food, and drank
the same wine, they provided the astute doctor with an ideal setting
for investigating the cause of the disease. Every time he visited the
monks he was offered a glass of wine until he too developed colic. Upon
a detailed investigation he found the culprit to be the agent used to
sweeten the wine, litharge, a white oxide of lead. When this
concentrated sweetener was added to sour wine it brought it back to
life and made it drinkable. The entire region depended upon the wine
export as a major source of revenue. If the word spread that the wine
from Ulm caused colic then the city's economy was threatened. In 1696,
Duke Ludwig issued a decree forbidding the use of lead-based additives
in any wine product. For anyone who violated this decree, the punishment
was death!
There were recordings
of Roman wine being banned by German tribes because of the sickness
which resulted. Surprisingly, many doctors of that period prescribed
preparations of mercury or litharge itself to cure colic! On and off
over the next centuries liquor would continue to be a source of lead
exposure. In 1763, a physician at the court of King George III, discovering
that lead fittings used to press cider caused an outbreak of colic.
The great gout epidemics of the eighteenth century in England were traced
to the popular port wines from Portugal which were heavily leaded (in
1825, 21 million liters of port was consumed in England). Poorly glazed
pottery used to store beers and wines resulted in chronic colic outbreaks
in Germany when the lead leached out into the brew. Even today, some
wine seals are made of lead and some leaded crystal decanters can leach
lead into the liquor. One of America’s first public health laws was
to ban the use of leaded coils due to the health problems it caused
to people who drank the spirits. In colonial America, the Massachusetts
Bay Colony banned lead from being added to wine and cider.
But it is not just
liquor products where lead can turn up. In Hungary, in 1994, a major
health problem occurred when red oxide lead was mixed into paprika to
brighten the color of the spice. Research has shown that stone mills,
which have lead pieces, can result in putting lead particles into the
flour. Lead has shown up in milk where cows have grazed on grasses growing
in soil with large lead accumulations from either industrial waste or
heavy auto traffic. Weather lead is puffed onto a 18th century
noble’s’ wig in the form of white lead litharge, innocently drunk with
wine made from grapes grown near a busy highway, or added as a filler
to ice cream being sold in India, man seems to create unusual pathways
for lead to enter the human system.
Occupational
Hazards
In the eighteenth,
nineteenth, and twentieth centuries the worst outbreaks of lead poisoning
of adults were occupational in origin. It became common knowledge that
to work in an industry where you handled lead was certain to make you
sick or worse. These workers absorbed lead from inhalation of fine lead
dust or fumes, contamination of food eaten at the workplace, or by absorption
through the skin. Charles Dickens describes in his essay "Star
of the East" the horrible effects of lead poisoning on women who
work in London’s infamous white lead mills, " her brain is coming
out her ear and it hurts her dreadful…". Benjamin Franklin in 1763
wrote about the "dry gripes" (colic) and "dangles"
(wrist drop) which affected tinkers, painters, and typesetters.
Lead’s hazards to
the reproductive process have been known for at least a century. British
factory inspectors at the turn of the twentieth century noted that women
who were exposed to lead through working in the cottage ceramic industry
tended to be barren and that children who were born to those women were
often short-lived. In most western countries during the 1930’s through
the 1970’s, awareness among health workers was associated with more
lead poisoning cases being reported, and laws protecting workers were
being enacted.
Today, occupational
exposure to lead remains a big problem in developing countries. Occupational
lead exposure is likely unregulated in these countries with little monitoring
of poisoning being done. What has become a growing concern among health
officials is the prevalence of home-based cottage industries in these
countries. These cottage industries are located in the where large numbers
of people live, especially children. They are of particular concern
since these non-regulated businesses deliver the lead right into the
homes or yards where children live or play. Children can also be exposed
when the working parent brings the lead dust home from work (on cloths,
in hair, or on shoes, etc.). With the enactment of worker safety regulations
and more accurate monoriting and reporting, the focus of lead research
began shifting towards children’s health.
Childhood Lead
Poisoning
Modern understanding
of lead poisoning in children has evolved through four stages.
First: when childhood
lead poisoning was first described in 1892 in Brisbane, Australia, its
very existence was disputed by elitist physicians in Sydney. A.J.
Turner, a house officer at the Brisbane Children’s Hospital, diagnosed
several children with lead intoxication who had been given a previous
diagnosis of meningitis. Also at Brisbane, J. Lockart Gibson , an ophthalmologist,
recognized lead poisoning in children with retinites and ophthalmoplegia.
They investigated and found the source of lead exposure to be paint
on rails in the children’s homes. Through their efforts, lead was eventually
banned from house paint in Australia in 1914. That same year, childhood
lead poisoning was first reported in America.
Second: After its
existence was accepted, the prevailing belief among pediatricians was
that children who did not die during the acute stage of the disease
suffered no lasting ill effects. In 1943, Byers demonstrated the persistence
of severe residue in children who had recovered from acute lead poisoning.
Dr. Randolph Byers, one of America’s first pediatric neurologists,
discovered that several children with learning or behavior disorders
had earlier been treated for lead poisoning. Along with Elizabeth Lord,
a psychologist at Boston Children’s Hospital, Byer conducted detailed
psychometric evaluations of 20 children who had reported previous lead
poisoning. They found that 19 of the 20 children were behavior disordered
or intellectually impaired. Dr. Byer’s studies in the early 1940’s were
the first to prove that children who survived acute intoxication were
often left with devastating deficits in intellectual function.
Third: The reality
of sequelae was then accepted, but sequelae were thought to afflict
only those patients who had had the most severe symptoms. In the late
1970s, 1980s, and early 90’s, the publication of papers from around
the world showing IQ and behavioral deficits at silent doses of lead,
the neuropsychological costs of asymptomatic lead exposure were established
to the satisfaction of the scientific community. This controversial
issue has now been effectively settled. With the release of extensive
research from numerous studies, each confirming the other, almost all
workers in the field agree that lead at silent doses produces deficits
in psychological function; these include intelligence, perception, attention,
language function, and perhaps social adjustment.
Fourth: Regulations
began to be shaped to accommodate the realization that lead at silent
doses damaged the brains of children. Mass public screening programs
were enacted to monitor the lead exposure of young children. For the
first time the focus of lead exposure was centered on primary prevention,
with many laws being enacted to eliminate lead sources in the environment.
Mandatory testing programs were being established in many states to
detect early identification of lead problems. In 1991 CDC devised a
strategic plan to prevent childhood lead toxicity. This was a historic
moment in lead poisoning prevention.
.
There were two important
sources of lead for children in America: paint and leaded gasoline.
lead in household paint was recognized as a danger early in the 20th
century; it was banned in Australia in 1914 and by international convention
in 1925. The United States was not a signatory to that agreement. It
was not until 1970 that a statute banning lead in household paint was
passed in the United States. Although in the early 1930s the city of
Baltimore recognized the widespread hazards of lead paint to children
and took steps to control its use, lead paint was not banned by statute
in this country until 1970.
Special Note
on the Evolution of the Most Widespread Toxin Ever Made!
Letting the "
Monster" loose: Propaganda, politics, and the "old boys club"
at work
No toxic substance
has been more widely distributed throughout man’s environment than the
lead additive Tel in gasoline. For over seven decades, millions of autos
of all descriptions have successfully dispersed this toxic substance
to all corners of the world. How did such a toxic substance ever gain
approval to expose hundred’s of millions of people?
In 1921, competition
in the expanding American automobile market was fierce. Ford's Model
T outsold all other manufacturers, and General Motor's flagship product,
the Cadillac, had a motor knock. The Model T was economical, dependable,
and easy to fix. Its performance, however, was unremarkable and it had
as much style as an orthopedic shoe. Charles F. Kettering, director
of research at General Motors, chafed in second place. He had a plan:
he would displace Ford with a high-performance engine in a fashionable
GM auto body. The best way to achieve high engine performance is to
increase compression in the cylinder. Squeeze the air-fuel mixture in
the cylinder into a smaller volume and it will detonate with much more
force. But when the gas volume is severely compressed, it acts like
diesel fuel and ignites prematurely. This is engine knock, and it causes
loss of power and eventual damage to the engine. Kettering set Thomas
Midgely, his close associate and principal chemist in GM's Dayton, Ohio,
research laboratory, to find an antiknock agent.
In December of that
year, after trying and discarding many compounds, Midgely tested an
old German patent, tetraethyl lead (TEL), in the laboratory engine,
which was knocking on ordinary gasoline. It immediately began to run
smoothly and silently. A new product was born, and a new firm, General
Motors Chemical Company, Kettering named the new fuel Ethyl Gas. Nowhere
was the word lead mentioned on the product label. That Memorial Day
the new fuel was used by some of the drivers in the Indianapolis 500.
This shrewd marketing step was a spectacular success: the first, second,
and third-place winners all ran on ethyl gasoline.
Shortly after production
began, workers in all three plants began to go crazy and die, often
in straightjackets. Somewhere between 13 and 15 known deaths occurred,
and over 300 men became psychotic. Workers called the product "looney
gas" and the place where it was fabricated "The House of Butterflies."
This last sobriquet was earned by the sight of psychotic workers trying
to brush phantom insects off of their arms.
A moratorium on
the use of TEL was called and the Surgeon General convened a meeting
of industrialists, public health specialists, and academic physicians
to determine if this new product was a serious enough threat to be banned
or whether it could be sold to the general public.
At the Surgeon General's
meeting, a young assistant professor of pathology at the University
of Cincinnati, Robert Kehoe, emerged as the principal industrial expert
and spokesman. When workers died in the Dayton plant in 1923, General
Motors asked Kehoe to consult and make preventive recommendations. He
made some measurements of lead levels in the plant and in workers directly
exposed to TEL. His control group was workers in the plant who had no
direct contact with the compound.
This assignment
marked the beginning of a major career shift for Kehoe. C. F. Kettering
would, with support from the Ethyl Corp., DuPont, and others, open the
Kettering Laboratory on the University of Cincinnati Medical campus
and name Kehoe as its director. Kehoe would also become Medical Director
of the Ethyl Corp. and a corporate officer at GM. In the Surgeon General's
meeting and others that followed his words were put forward as the final
opinion on lead by the industry representatives, and he was treated
with considerable deference. Kehoe was not burdened with a hypertrophied
sense of modesty. He spoke with great confidence that his data was the
best, if not the only, guide to the truth. Kehoe's sway in lead toxicology
held until the late 1960s. The durability of the extraordinary scientific
solecism that lead in the body was natural is a testament to the shielding
power of reputation. It pays to advertise.
There were no scientific
challengers to Kehoe until Clair Patterson. His methods and conclusions
could not have been more different. Patterson aimed his attack at Kehoe's
assertion that lead was a normal component of the human body, insisting
that what he called "normal" was in fact "typical." This was more than
a semantic quarrel. Patterson fundamentally altered the vocabulary with
which the debate over the health effects of lead was conducted. Most
people, following Kehoe's arguments, referred to "normal levels" of
lead in blood, soil, and air, meaning values near the average. They
assumed that because these levels were common, they were harmless. "Normal"
also carries some of the meaning "natural." Patterson argued that "normal"
should be replaced by "typical." Simply because a certain level of lead
was commonplace did not mean it was without harm. "Natural," he insisted,
was limited to concentrations of lead that existed in the body or environment
before contamination by man.
Kehoe and other
workers in lead completely missed this distinction because their reagents,
instruments, and the very air in their laboratories were freighted with
lead. As a result the baseline measurements of all their samples were
raised and their results blurred. In addition, the control subjects
in Kehoe's studies, the workers in the Dayton plant who did not directly
handle TEL, were nevertheless exposed to it. His second "unexposed"
group, the Mexican farmers, ate food that had been cooked in and served
from lead-containing ceramic pots and plates.
Patterson was able
to demonstrate and correct this fundamental error because of the extraordinary
measures he took to avoid contamination of his specimens. Because his
lab was cleaner than others, his measurements of isotopic ratios were
free of the contamination that confounded the findings of Kehoe and
others. Where Kehoe measured lead in "unexposed" workers in a TEL plant
and Mexican farmers, Patterson studied pre-iron age mummies and tuna
raised from pelagic waters.
Patterson stumbled
on the problem of global lead contamination while measuring the concentration
of mineral isotopes in his study of the age of the earth. He noticed
that the lead levels in his reagents and in soil and ice were much higher
than predicted by theory. It would have been understandable if he treated
the contamination of his reagents as a severe annoyance to be overcome
and then forgotten, but that was not his style. To him it was not a
nuisance but a clear signal of the contamination by lead of the biosphere.
This was an unrecognized danger, he believed, to everyone. In this regard,
he provided facts to flesh out the warnings 40 years earlier of Yandell
Henderson, David Edsall, and Alice Hamilton. Alice Hamilton of Harvard
Medical School, a pioneer in the study of occupational diseases and
a recognized expert in lead poisoning, spoke briefly at the hearings
to review TEL:
" I would like
to emphasize one or two points that have been brought out. One is the
fact that lead is a slow and cumulative poison and that it does not
usually produce striking symptoms that are easily recognized. The other
is that if this (as does seem to have been shown) is a probable danger,
shall we not say that it is going to be an extremely widespread one"?
She said that while it might be possible to educate a workforce on avoiding
lead poisoning, it would be impossible to control the behavior of a
whole country, and that TEL should be replaced with a less poisonous
antiknock agent.
These health scientists
predicted at the Surgeon General's 1925 meeting that tetraethyl lead
would lead to widespread increases in human lead burden. Patterson began
to divert a considerable proportion of his extraordinary mind and energy
away from pure geochemistry to the study of lead contamination. By conducting
his experiments in his ultra-clean chamber in which the air was filtered,
the experimenters gowned and masked, and the reagents and water supply
purified of any trace of lead, he was able to avoid contamination and
establish the true concentrations of lead in his samples. He showed
that technological activity had raised modern human body lead burdens
100 times that of our pretechnologic ancients. In addition to tuna caught
in the deep strata of the Pacific Ocean and brought to the surface with
great care to avoid contamination on the way up and pre-iron age mummies
buried in sandy soil, he sampled cores of the Greenland ice pack. By
slicing the ice cores he was able to precisely date the specimen and
show the time course of lead in the atmosphere.
The removal of lead
from gasoline in 1990, regarded by many as one of the major public health
triumphs of the 20th century, had an immediate impact. Between 1976
and 1994, the mean blood lead concentration in children dropped from
13.7 mcg/dL to 3.2 mcg/dL, in direct proportion to the amount of tetraethyl
lead produced. One could want no clearer testimony to the efficacy of
a well-conceived and consistently applied public health policy.
In 1993, the
National Academy of Sciences verified that lead at extremely low doses
caused neurobehavioural deficits.
Role of Lead
and Behavioral Toxicology
Behavioral toxicology,
the study of chemical toxicants and their influence on brain function,
is a young field. The notion that a chemical can affect the brain and
that the earliest expression of toxicity could be found in altered behavior,
thinking, or mood is not new; it was voiced at least 2000 years ago
by the Greek Dioscerides when he wrote, "Lead makes the mind give way."
Despite this early warning, the scientific community has until recently
paid little systematic attention to the impact of neurotoxicants on
behavior. The first textbook on this subject was published in 1975.
Behavioral teratology,
the study of the effect on behavior of chemical exposure of the
fetus in utero, is an even newer discipline. Until recently, the uterus
had been visualized as a time capsule with a 9-month lease, sheltering
the developing fetus from most adverse influences such as drugs, toxicants,
or nutritional deprivation. The thalidomide and Minamata disasters quickly
disabused scientists and laymen alike of this false comfort. It is now
clear that many chemicals cross the placenta and impinge on the developing
brain. Behavioral deficits have been shown for some agents at doses
well below those that cause anatomical alterations.
Three important
classes of neurotoxicants are metals, solvents, and pesticides. The
clearest data on the deleterious effects of prenatal exposure to toxicants
come from the study of two metals, lead and mercury, and from epidemiologic
investigations of the effects of alcohol taken during pregnancy. Less
complete data are available for two other groups of agents, solvents
and pesticides. What we do know about their effects on the fetal brain
is convincing enough to demand caution in their distribution.
In the late 1970s,
attention began to shift to the question of intrauterine exposure to
lead. Scanlon measured umbilical-cord blood lead concentrations in newborns
and showed that infants born to inner city mothers tended to have higher
blood lead levels than those born to suburban mothers. The observation
that lead crossed the placenta sparked studies of prenatal exposure
on infant development. The first study examined a large cohort of births
at the Boston Hospital for Women. Umbilical-cord bloods were obtained
from almost 12,000 births over a 2-year period. Lead was found to be
related to minor birth defects in a subsample of 5000 of these infants.
A subsample of these subjects that was evenly divided among low exposure
(< 3 ug/dl), medium exposure (6-7 ug/dl), and high exposure (>
10 ug/dl) was followed. Subjects were seen at 6, 12, 24, 57, and 120
months of age. Significant deficits in infant IQ scores were found in
children in the high cord blood lead group as late as 24 months of age.
At 57 and 120 months of age, the effect of umbilical-cord blood was
no longer significant, but the effect of the 24-month blood lead level
was statistically significant . Similar data have subsequently been
reported from studies in Cincinnati and Australia. It is clear that
lead exposure during pregnancy is a behavioral teratogen.
Conclusion
Winston Churchill
said: "Make no small plans". By this he meant that most enterprises
are not completely successful. To diminish one’s goals at the beginning
is to guarantee that success will be limited. Those who wish to end
childhood lead toxicity should aim high: make a large plan. They should
also be patient, and expect to spend a considerable amount of time in
the struggle to succeed.
References
1. Current Probl
Pediatric, (Dec.1988,) pp.703-706
2. American Journal
of Public Health , (Dec.1998), Vol. 88, No 12
3. Needleman-Environmental
Research, sec.a78, 79-85 (1998)
4. Needleman-Environmental
Research, 74, 95-103 (1997)
5. L.S. Ibels and
C.A. Pollock - Lead Intoxication- Medical Toxicology 1: 387-410
(1986)
6. Josef Eisinger-
Sweet Poison-Natural History Vol.105 no.7 pp48-53, (July 1996)
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