Fluoride: The Ultimate Cluster-Flux

And the Players Involved

A Compilation of Documents and Articles

Relating to Fluoride

This collection is dedicated to those who wrote the original works and
made them available on the internet. I have spent countless hours
searching for information on fluoride and it is my wish, by assembling
these works, to enable others to save time looking and make available
more time for them to ‘do’.

If you are sickened and appalled by the approved use of fluoride in

food, beverage and other consumer products then I ask that you spread
this knowledge on to others and contact your local representatives in the
hopes that one day fluoride will be more strictly regulated or, banned
altogether.

These documents are listed in roughly the order I found them. It would
be nearly impossible to group them in some kind of order since they are
all linked together – a cluster-flux of monumental proportions.

I would like to thank (or curse) Christopher Bryson whose excellent

book, The Fluoride Deception, opened my eyes to fluoride and started
me on this journey of uncovering the truth.

For more information on fluoride, I would recommend the Fluoride Action

Network (FAN) http://www.fluoridealert.org/ as a good place to start.

NOTICE

In accordance with Title 17 U.S.C., section 107, some material on this web site is provided without
permission from the copyright owner, only for purposes of criticism, comment, news reporting,
teaching, scholarship and research under the "fair use" provisions of federal copyright laws. These
materials may not be distributed further, except for "fair use" non-profit educational purposes,
without permission of the copyright owner.
 Dental Caries
Wiki: http://en.wikipedia.org/wiki/Dental_caries

Dental caries is a disease that damages tooth structures, resulting in what is commonly
called tooth decay or cavities, which are holes in the teeth.[1] This damage first affects the
hard tissues of the teeth (enamel, dentin and cementum). As the destruction progresses,
these tissues begin to break down, which can eventually lead to holes in the teeth. If left
untreated, the disease can lead to pain, tooth loss, infection, and, in severe cases, death.[2]
There is a long history of dental caries: over a million years ago, hominids such as
Australopithecus suffered from cavities. However, the incidence of cavities was very low
well into the Paleolithic and Mesolithic periods.[3] The largest increases in the prevalence
of caries have been associated with dietary changes.[3][4] Today, caries remains one of the
most common diseases throughout the world.

There are numerous ways to identify dental caries.[5] Although the presentation may
differ, the risk factors and development among distinct types of caries remain largely
similar. Initially, it may appear as a small chalky area but eventually develop into a large,
brown cavitation. Though sometimes caries may be seen directly, radiographs are
frequently needed to inspect less visible areas of teeth and to judge the extent of
destruction.

Tooth decay is caused by certain types of acid-producing bacteria (specifically

Lactobacillus species, Streptococcus mutans, and Actinomyces species) which cause
damage in the presence of fermentable carbohydrates such as sucrose, fructose, and
glucose.[6][7][8] The resulting high levels of acidity from lactic acid in the mouth affect
teeth because a tooth's special mineral content causes it to be sensitive to low pH.
Specifically, a tooth (which is primarily mineral in content) is in a constant state of back-
and-forth demineralization and remineralization between the tooth and surrounding
saliva. When the pH at the surface of the tooth drops below 5.5, demineralization
proceeds faster than remineralization (i.e. there is a net loss of mineral structure on the
tooth's surface). This results in the ensuing decay. Depending on the extent of tooth
destruction, various treatments can be used to restore teeth to proper form, function, and
aesthetics, but there is no known method to regenerate large amounts of tooth structure.
Instead, dental health organizations advocate preventive and prophylactic measures, such
as regular oral hygiene and dietary modifications, to avoid dental caries.[9]

History:
Archaeological evidence shows that tooth decay is an ancient disease dating far into
prehistory. Skulls dating from a million years ago through the neolithic period show signs
of caries, excepting those from the Paleolithic and Mesolithic ages.[3] The increase of
caries during the neolithic period may be attributed to the increase of plant foods
containing carbohydrates.[10] The beginning of rice cultivation in South Asia is also
believed to have caused an increase in caries.

A Sumerian text from 5000 BC describes a "tooth worm" as the cause of caries.[11]
Evidence of this belief has also been found in India, Egypt, Japan, and China.[4]

Unearthed ancient skulls show evidence of primitive dental work. In Pakistan, teeth
dating from around 5500 BC to 7000 BC show nearly perfect holes from primitive dental
drills.[12] The Ebers Papyrus, an Egyptian text from 1550 BC, mentions diseases of
teeth.[11] During the Sargonid dynasty of Assyria during 668 to 626 BC, writings from the
king's physician specify the need to extract a tooth due to spreading inflammation.[4] In
the Roman Empire, wider consumption of cooked foods led to a small increase in caries
prevalence.[13] The Greco-Roman civilization, in addition to the Egyptian, had treatments
for pain resulting from caries.[4]

The rate of caries remained low through the Bronze and Iron ages, but sharply increased
during the Medieval period.[3] Periodic increases in caries prevalence had been small in
comparison to the 1000 AD increase, when sugar cane became more accessible to the
Western world. Treatment consisted mainly of herbal remedies and charms, but
sometimes also included bloodletting.[14] The barber surgeons of the time provided
services that included tooth extractions.[4] Learning their training from apprenticeships,
these health providers were quite successful in ending tooth pain and likely prevented
systemic spread of infections in many cases. Among Roman Catholics, prayers to Saint
Apollonia, the patroness of dentistry, were meant to heal pain derived from tooth
infection.[15]

There is also evidence of caries increase in North American Indians after contact with
colonizing Europeans. Before colonization, North American Indians subsisted on hunter-
gatherer diets, but afterwards there was a greater reliance on maize agriculture, which
made these groups more susceptible to caries.[3]

In the medieval Islamic world, Muslim physicians such as al-Gazzar and Avicenna (in
The Canon of Medicine) provided the earliest known treatments for caries, though they
also believed that it was caused by tooth worms like what the ancients believed. This was
eventually proven false in 1200 by another Muslim dentist named Gaubari, who in his
Book of the Elite concerning the unmasking of mysteries and tearing of veils, was the first
to reject the idea of caries being caused by tooth worms, and he stated that tooth worms
in fact do not even exist. The theory of the tooth worm was thus no longer accepted in the
Islamic medical community from the 13th century onwards.[16]

During the European Age of Enlightenment, the belief that a "tooth worm" caused caries
was also no longer accepted in the European medical community.[17] Pierre Fauchard,
known as the father of modern dentistry, was one of the first to reject the idea that worms
caused tooth decay and noted that sugar was detrimental to the teeth and gingiva.[18] In
1850, another sharp increase in the prevalence of caries occurred and is believed to be a
result of widespread diet changes.[4] Prior to this time, cervical caries was the most
frequent type of caries, but increased availability of sugar cane, refined flour, bread, and
sweetened tea corresponded with a greater number of pit and fissure caries.

In the 1890s, W.D. Miller conducted a series of studies that led him to propose an
explanation for dental caries that was influential for current theories. He found that
bacteria inhabited the mouth and that they produced acids which dissolved tooth
structures when in the presence of fermentable carbohydrates.[19] This explanation is
known as the chemoparasitic caries theory.[20] Miller's contribution, along with the
research on plaque by G.V. Black and J.L. Williams, served as the foundation for the
current explanation of the etiology of caries.[4]

Main article: Fernando E. Rodriguez Vargas

In 1921, Major Fernando E. Rodriguez Vargas, DDS of the Army Dental Corps
discovered the bacteria which causes dental caries. According to his investigations, three
types of the Lactobacillus species, during the process of fermentation, are the causes of
cavities. [21] In December 1922, he published an original and fundamental work on the
specific bacteriology of dental caries. His findings were published in the December issue
of the Military Dental Journal titled "The Specific Study of the Bacteriology of Dental
Cavities". Rodríguez Vargas also developed the techniques and methods of analysis.[22]
On September 28, 1928, Rodriguez Vargas published in the "Journal of the American
Medical Association" his findings in the effectiveness of Iodine and other chemical
agents as disinfectants of the mucous membranes of the mouth.[23] Since then, other
scientists have used the findings of his investigations as the basis in the study of the
bacteriology of dental caries.

Epidemiology:

Worldwide, most children and an estimated ninety percent of adults have experienced
caries, with the disease most prevalent in Asian and Latin American countries and least
prevalent in African countries.[24] In the United States, dental caries is the most common
chronic childhood disease, being at least five times more common than asthma.[25] It is
the primary pathological cause of tooth loss in children.[26] Between 29% and 59% of
adults over the age of fifty experience caries.[27]

The number of cases has decreased in some developed countries, and this decline is
usually attributed to increasingly better oral hygiene practices and preventive measures
such as fluoride treatment.[28] Nonetheless, countries that have experienced an overall
decrease in cases of tooth decay continue to have a disparity in the distribution of the
disease.[27] Among children in the United States and Europe, twenty percent of the
population endures sixty to eighty percent of cases of dental caries.[13] A similarly skewed
distribution of the disease is found throughout the world with some children having none
or very few caries and others having a high number.[27] Australia, Nepal, and Sweden
have a low incidence of cases of dental caries among children, whereas cases are more
numerous in Costa Rica and Slovakia.[29]
The classic "DMF" (decay/missing/filled) index is one of the most common methods for
assessing caries prevalence as well as dental treatment needs among populations. This
index is based on in-field clinical examination of individuals by using a probe, mirror and
cotton rolls. Because the DMF index is done without X-ray imaging, it underestimates
real caries prevalence and treatment needs.[30]

Classification:
Caries can be classified by location, etiology, rate of progression, and affected hard
tissues.[5] These classification can be used to characterize a particular case of tooth decay
in order to more accurately represent the condition to others and also indicate the severity
of tooth destruction.

Location:
Generally, there are two types of caries when separated by location: caries found on
smooth surfaces and caries found in pits and fissures.[31] The location, development, and
progression of smooth-surface caries differ from those of pit and fissure caries. G.V.
Black created a classification system that is widely used and based on the location of the
caries on the tooth. The original classification distinguished caries into five groups,
indicated by the word, "Class", and a Roman numeral. Pit and fissure caries is indicated
as Class I; smooth surface caries is further divided into Class II, Class III, Class IV, and
Class V.[32] A Class VI was added onto Black's classification and also represents a
smooth-surface carious lesion.

Pit and fissure caries:

Pits and fissures are anatomic landmarks on a tooth where the enamel folds inward.
Fissures are formed during the development of grooves but the enamel in the area is not
fully fused. As a result, a deep linear depression forms in the enamel's surface structure,
which forms a location for dental caries to develop and flourish. Fissures are mostly
located on the occlusal (chewing) surfaces of posterior teeth and palatal surfaces of
maxillary anterior teeth. Pits are small, pinpoint depressions that are most commonly
found at the ends or cross-sections of grooves.[33] In particular, buccal pits are found on
the facial surfaces of molars. For all types of pits and fissures, the deep infolding of
enamel makes oral hygiene along these surfaces difficult, allowing dental caries to
develop more commonly in these areas.

The occlusal surfaces of teeth represent 12.5% of all tooth surfaces but are the location of
over 50% of all dental caries.[34] Among children, pit and fissure caries represent 90% of
all dental caries.[35] Pit and fissure caries can sometimes be difficult to detect. As the
decay progresses, caries in enamel nearest the surface of the tooth spreads gradually
deeper. Once the caries reaches the dentin at the dentino-enamel junction, the decay
quickly spreads laterally. Within the dentin, the decay follows a triangle pattern that
points to the tooth's pulp. This pattern of decay is typically described as two triangles
(one triangle in enamel, and another in dentin) with their bases conjoined to each other at
the dentino-enamel junction (DEJ). This base-to-base pattern is typical of pit and fissure
caries, unlike smooth-surface caries (where base and apex of the two triangles join).

Smooth-surface caries:
There are three types of smooth-surface caries. Proximal caries, also called interproximal
caries, form on the smooth surfaces between adjacent teeth. Root caries form on the root
surfaces of teeth. The third type of smooth-surface caries occur on any other smooth
tooth surface.

Proximal caries are the most difficult type to detect.[36] Frequently, this type of caries
cannot be detected visually or manually with a dental explorer. Proximal caries form
cervically (toward the roots of a tooth) just under the contact between two teeth. As a
result, radiographs are needed for early discovery of proximal caries.[37] Under Black's
classification system, proximal caries on posterior teeth (premolars and molars) are
designated as Class II caries.[38] Proximal caries on anterior teeth (incisors and canines)
are indicated as Class III if the incisal edge (chewing surface) is not included and Class
IV if the incisal edge is included.

Root caries, which are sometimes described as a category of smooth-surfaces caries, are
the third most common type of caries and usually occur when the root surfaces have been
exposed due to gingival recession. When the gingiva is healthy, root caries is unlikely to
develop because the root surfaces are not as accessible to bacterial plaque. The root
surface is more vulnerable to the demineralization process than enamel because
cementum begins to demineralize at 6.7 pH, which is higher than enamel's critical pH.[39]
Regardless, it is easier to arrest the progression of root caries than enamel caries because
roots have a greater reuptake of fluoride than enamel. Root caries are most likely to be
found on facial surfaces, then interproximal surfaces, then lingual surfaces. Mandibular
molars are the most common location to find root caries, followed by mandibular
premolars, maxillary anteriors, maxillary posteriors, and mandibular anteriors.

Lesions on other smooth surfaces of teeth are also possible. Since these occur in all
smooth surface areas of enamel except for interproximal areas, these types of caries are
easily detected and are associated with high levels of plaque and diets promoting caries
formation.[36] Under Black's classification system, caries near the gingiva on the facial or
lingual surfaces is designated Class V.[38] Class VI is reserved for caries confined to cusp
tips on posterior teeth or incisal edges of anterior teeth.

Other general descriptions:

Besides the two previously mentioned categories, carious lesions can be described further
by their location on a particular surface of a tooth. Caries on a tooth's surface that are
nearest the cheeks or lips are called "facial caries", and caries on surfaces facing the
tongue are known as "lingual caries". Facial caries can be subdivided into buccal (when
found on the surfaces of posterior teeth nearest the cheeks) and labial (when found on the
surfaces of anterior teeth nearest the lips). Lingual caries can also be described as palatal
when found on the lingual surfaces of maxillary teeth because they are located beside the
hard palate.

Caries near a tooth's cervix—the location where the crown of a tooth and its roots meet—
are referred to as cervical caries. Occlusal caries are found on the chewing surfaces of
posterior teeth. Incisal caries are caries found on the chewing surfaces of anterior teeth.
Caries can also be described as "mesial" or "distal." Mesial signifies a location on a tooth
closer to the median line of the face, which is located on a vertical axis between the eyes,
down the nose, and between the contact of the central incisors. Locations on a tooth
further away from the median line are described as distal.

Etiology:
In some instances, caries are described in other ways that might indicate the cause. "Baby
bottle caries", "early childhood caries", or "baby bottle tooth decay" is a pattern of decay
found in young children with their deciduous (baby) teeth. The teeth most likely affected
are the maxillary anterior teeth, but all teeth can be affected.[40] The name for this type of
caries comes from the fact that the decay usually is a result of allowing children to fall
asleep with sweetened liquids in their bottles or feeding children sweetened liquids
multiple times during the day. Another pattern of decay is "rampant caries", which
signifies advanced or severe decay on multiple surfaces of many teeth.[41] Rampant caries
may be seen in individuals with xerostomia, poor oral hygiene, methamphetamine use
(due to drug-induced dry mouth[42]), and/or large sugar intake. If rampant caries is a result
of previous radiation to the head and neck, it may be described as radiation-induced
caries. Problems can also be caused by the self destruction of roots and whole tooth
resorption when new teeth erupt or later from unknown causes.

Rate of progression:
Temporal descriptions can be applied to caries to indicate the progression rate and
previous history. "Acute" signifies a quickly developing condition, whereas "chronic"
describes a condition which has taken an extended time to develop. Recurrent caries, also
described as secondary, is caries that appears at a location with a previous history of
caries. This is frequently found on the margins of fillings and other dental restorations.
On the other hand, incipient caries describes decay at a location that has not experienced
previous decay. Arrested caries describes a lesion on a tooth which was previously
demineralized but was remineralized before causing a cavitation.

Affected hard tissue:

Depending on which hard tissues are affected, it is possible to describe caries as
involving enamel, dentin, or cementum. Early in its development, caries may affect only
enamel. Once the extent of decay reaches the deeper layer of dentin, "dentinal caries" is
used. Since cementum is the hard tissue that covers the roots of teeth, it is not often
affected by decay unless the roots of teeth are exposed to the mouth. Although the term
"cementum caries" may be used to describe the decay on roots of teeth, very rarely does
caries affect the cementum alone. Roots have a very thin layer of cementum over a large
layer of dentin, and thus most caries affecting cementum also affects dentin.

Signs and symptoms:

A person experiencing caries may not be aware of the disease.[43] The earliest sign of a
new carious lesion is the appearance of a chalky white spot on the surface of the tooth,
indicating an area of demineralization of enamel. This is referred to as incipient decay.
As the lesion continues to demineralize, it can turn brown but will eventually turn into a
cavitation ("cavity"). Before the cavity forms, the process is reversible, but once a cavity
forms, the lost tooth structure cannot be regenerated. A lesion which appears brown and
shiny suggests dental caries was once present but the demineralization process has
stopped, leaving a stain. A brown spot which is dull in appearance is probably a sign of
active caries.

As the enamel and dentin are destroyed, the cavity becomes more noticeable. The
affected areas of the tooth change color and become soft to the touch. Once the decay
passes through enamel, the dentinal tubules, which have passages to the nerve of the
tooth, become exposed and cause the tooth to hurt. The pain may worsen with exposure
to heat, cold, or sweet foods and drinks.[1] Dental caries can also cause bad breath and
foul tastes.[44] In highly progressed cases, infection can spread from the tooth to the
surrounding soft tissues. Complications such as cavernous sinus thrombosis and Ludwig's
angina can be life-threatening.[45] [46]

Diagnosis:
Primary diagnosis involves inspection of all visible tooth surfaces using a good light
source, dental mirror and explorer. Dental radiographs (X-rays) may show dental caries
before it is otherwise visible, particularly caries between the teeth. Large dental caries are
often apparent to the naked eye, but smaller lesions can be difficult to identify. Visual
and tactile inspection along with radiographs are employed frequently among dentists,
particularly to diagnose pit and fissure caries.[48] Early, uncavitated caries is often
diagnosed by blowing air across the suspect surface, which removes moisture and
changes the optical properties of the unmineralized enamel. This produces a white 'halo'
effect detectable to the naked eye.[citation needed] Fiberoptic transillumination, lasers and
disclosing dyes have been recommended for use as an adjunct when diagnosing smaller
carious lesions in pits and fissures of teeth.[citation needed]

Some dental researchers have cautioned against the use of dental explorers to find
caries.[36] In cases where a small area of tooth has begun demineralizing but has not yet
cavitated, the pressure from the dental explorer could cause a cavity. Since the carious
process is reversible before a cavity is present, it may be possible to arrest the caries with
fluoride and remineralize the tooth surface. When a cavity is present, a restoration will be
needed to replace the lost tooth structure.
At times, pit and fissure caries may be difficult to detect. Bacteria can penetrate the
enamel to reach dentin, but then the outer surface may remineralize, especially if fluoride
is present.[30] These caries, sometimes referred to as "hidden caries", will still be visible
on x-ray radiographs, but visual examination of the tooth would show the enamel intact
or minimally perforated.

Causes:
There are four main criteria required for caries formation: a tooth surface (enamel or
dentin); caries-causing bacteria; fermentable carbohydrates (such as sucrose); and
time.[49] The caries process does not have an inevitable outcome, and different individuals
will be susceptible to different degrees depending on the shape of their teeth, oral hygiene
habits, and the buffering capacity of their saliva. Dental caries can occur on any surface
of a tooth which is exposed to the oral cavity, but not the structures which are retained
within the bone.[50]

Teeth:
There are certain diseases and disorders affecting teeth which may leave an individual at
a greater risk for caries. Amelogenesis imperfecta, which occurs between 1 in 718 and 1
in 14,000 individuals, is a disease in which the enamel does not fully form or forms in
insufficient amounts and can fall off a tooth.[51] In both cases, teeth may be left more
vulnerable to decay because the enamel is not able to protect the tooth.[52]

In most people, disorders or diseases affecting teeth are not the primary cause of dental
caries. Ninety-six percent of tooth enamel is composed of minerals.[53] These minerals,
especially hydroxyapatite, will become soluble when exposed to acidic environments.
Enamel begins to demineralize at a pH of 5.5.[54] Dentin and cementum are more
susceptible to caries than enamel because they have lower mineral content.[55] Thus, when
root surfaces of teeth are exposed from gingival recession or periodontal disease, caries
can develop more readily. Even in a healthy oral environment, however, the tooth is
susceptible to dental caries.

The anatomy of teeth may affect the likelihood of caries formation. Where the deep
grooves of teeth are more numerous and exaggerated, pit and fissure caries are more
likely to develop. Also, caries are more likely to develop when food is trapped between
teeth.

Bacteria:
The mouth contains a wide variety of bacteria, but only a few specific species of bacteria
are believed to cause dental caries: Streptococcus mutans and Lactobacilli among
them.[6][8] Lactobacillus acidophilus, Actinomyces viscosus, Nocardia spp., and
Streptococcus mutans are most closely associated with caries, particularly root caries.
Bacteria collect around the teeth and gums in a sticky, creamy-coloured mass called
plaque, which serves as a biofilm. Some sites collect plaque more commonly than others.
The grooves on the biting surfaces of molar and premolar teeth provide microscopic
retention, as does the point of contact between teeth. Plaque may also collect along the
gingiva. In addition, the edges of fillings or crowns can provide protection for bacteria, as
can intraoral appliances such as orthodontic braces or removable partial dentures.[citation
needed]

Fermentable carbohydrates:
Bacteria in a person's mouth convert glucose, fructose, and most commonly sucrose
(table sugar) into acids such as lactic acid through a glycolytic process called
fermentation.[7] If left in contact with the tooth, these acids may cause demineralization,
which is the dissolution of its mineral content. The process is dynamic, however, as
remineralization can also occur if the acid is neutralized by saliva or mouthwash.
Fluoride toothpaste or dental varnish may aid remineralization.[56] If demineralization
continues over time, enough mineral content may be lost so that the soft organic material
left behind disintegrates, forming a cavity or hole.

Time:
The frequency of which teeth are exposed to cariogenic (acidic) environments affects the
likelihood of caries development.[57] After meals or snacks, the bacteria in the mouth
metabolize sugar, resulting in an acidic by-product which decreases pH. As time
progresses, the pH returns to normal due to the buffering capacity of saliva and the
dissolved mineral content of tooth surfaces. During every exposure to the acidic
environment, portions of the inorganic mineral content at the surface of teeth dissolves
and can remain dissolved for 2 hours.[58] Since teeth are vulnerable during these acidic
periods, the development of dental caries relies heavily on the frequency of acid
exposure. For example, when sugars are eaten continuously throughout the day, the tooth
is more vulnerable to caries for a longer period of time, and caries are more likely to
develop because the pH never returns to normal levels, thus the tooth surfaces cannot
remineralize or regain lost mineral content.[citation needed]

The carious process can begin within days of a tooth erupting into the mouth if the diet is
sufficiently rich in suitable carbohydrates. Evidence suggests that the introduction of
fluoride treatments have slowed the process.[59] Proximal caries take an average of four
years to pass through enamel in permanent teeth. Because the cementum enveloping the
root surface is not nearly as durable as the enamel encasing the crown, root caries tends
to progress much more rapidly than decay on other surfaces. The progression and loss of
mineralization on the root surface is 2.5 times faster than caries in enamel. In very severe
cases where oral hygiene is very poor and where the diet is very rich in fermentable
carbohydrates, caries may cause cavities within months of tooth eruption. This can occur,
for example, when children continuously drink sugary drinks from baby bottles. On the
other hand, it may take years before the process results in a cavity being formed.[citation
needed]

Other risk factors:

Reduced saliva is associated with increased caries since the buffering capability of saliva
is not present to counterbalance the acidic environment created by certain foods. As a
result, medical conditions that reduce the amount of saliva produced by salivary glands,
particularly the submandibular gland and parotid gland, are likely to lead to widespread
tooth decay. Examples include Sjögren's syndrome, diabetes mellitus, diabetes insipidus,
and sarcoidosis.[60] Medications, such as antihistamines and antidepressants, can also
impair salivary flow.[61] Moreover, sixty-three percent of the most commonly prescribed
medications in the United States list dry mouth as a known side effect.[60] Radiation
therapy of the head and neck may also damage the cells in salivary glands, increasing the
likelihood of caries formation.[62]

The use of tobacco may also increase the risk for caries formation. Some brands of
smokeless tobacco contain high sugar content, increasing susceptibility to caries.[63]
Tobacco use is a significant risk factor for periodontal disease, which can cause the
gingiva to recede.[64] As the gingiva loses attachment to the teeth, the root surface
becomes more visible in the mouth. If this occurs, root caries is a concern since the
cementum covering the roots of teeth is more easily demineralized by acids than
enamel.[39] Currently, there is not enough evidence to support a causal relationship
between smoking and coronal caries, but evidence does suggest a relationship between
smoking and root-surface caries.[65]

Pathophysiology:
Enamel:
Enamel is a highly mineralized acellular tissue, and caries act upon it through a chemical
process brought on by the acidic environment produced by bacteria. As the bacteria
consume the sugar and use it for their own energy, they produce lactic acid. The effects
of this process include the demineralization of crystals in the enamel, caused by acids,
over time until the bacteria physically penetrate the dentin. Enamel rods, which are the
basic unit of the enamel structure, run perpendicularly from the surface of the tooth to the
dentin. Since demineralization of enamel by caries generally follows the direction of the
enamel rods, the different triangular patterns between pit and fissure and smooth-surface
caries develop in the enamel because the orientation of enamel rods are different in the
two areas of the tooth .[66]

As the enamel loses minerals , and dental caries progress, they develop several distinct
zones, visible under a light microscope. From the deepest layer of the enamel to the
enamel surface, the identified areas are the: translucent zone, dark zones, body of the
lesion, and surface zone.[67] The translucent zone is the first visible sign of caries and
coincides with a 1-2% loss of minerals.[68] A slight remineralization of enamel occurs in
the dark zone, which serves as an example of how the development of dental caries is an
active process with alternating changes.[69] The area of greatest demineralization and
destruction is in the body of the lesion itself. The surface zone remains relatively
mineralized and is present until the loss of tooth structure results in a cavitation.

Dentin:
Unlike enamel, the dentin reacts to the progression of dental caries. After tooth
formation, the ameloblasts, which produce enamel, are destroyed once enamel formation
is complete and thus cannot later regenerate enamel after its destruction. On the other
hand, dentin is produced continuously throughout life by odontoblasts, which reside at
the border between the pulp and dentin. Since odontoblasts are present, a stimulus, such
as caries, can trigger a biologic response. These defense mechanisms include the
formation of sclerotic and tertiary dentin.[70]

In dentin from the deepest layer to the enamel, the distinct areas affected by caries are the
translucent zone, the zone of bacterial penetration, and the zone of destruction.[66] The
translucent zone represents the advancing front of the carious process and is where the
initial demineralization begins. The zones of bacterial penetration and destruction are the
locations of invading bacteria and ultimately the decomposition of dentin.

Sclerotic dentin:
The structure of dentin is an arrangement of microscopic channels, called dentinal
tubules, which radiate outward from the pulp chamber to the exterior cementum or
enamel border.[71] The diameter of the dentinal tubules is largest near the pulp (about
2.5 µm) and smallest (about 900 nm) at the junction of dentin and enamel.[72] The carious
process continues through the dentinal tubules, which are responsible for the triangular
patterns resulting from the progression of caries deep into the tooth. The tubules also
allow caries to progress faster.

In response, the fluid inside the tubules bring immunoglobulins from the immune system
to fight the bacterial infection. At the same time, there is an increase of mineralization of
the surrounding tubules.[73] This results in a constriction of the tubules, which is an
attempt to slow the bacterial progression. In addition, as the acid from the bacteria
demineralizes the hydroxyapatite crystals, calcium and phosphorus are released, allowing
for the precipitation of more crystals which fall deeper into the dentinal tubule. These
crystals form a barrier and slow the advancement of caries. After these protective
responses, the dentin is considered sclerotic.

Fluids within dentinal tubules are believed to be the mechanism by which pain receptors
are triggered within the pulp of the tooth.[74] Since sclerotic dentin prevents the passage
of such fluids, pain that would otherwise serve as a warning of the invading bacteria may
not develop at first. Consequently, dental caries may progress for a long period of time
without any sensitivity of the tooth, allowing for greater loss of tooth structure.

Tertiary dentin:
In response to dental caries, there may the production of more dentin toward the direction
of the pulp. This new dentin is referred to as tertiary dentin.[72] Tertiary dentin is
produced to protect the pulp for as long as possible from the advancing bacteria. As more
tertiary dentin is produced, the size of the pulp decreases. This type of dentin has been
subdivided according to the presence or absence of the original odontoblasts.[75] If the
odontoblasts survive long enough to react to the dental caries, then the dentin produced is
called "reactionary" dentin. If the odontoblasts are killed, the dentin produced is called
"reparative" dentin.

In the case of reparative dentin, other cells are needed to assume the role of the destroyed
odontoblasts. Growth factors, especially TGF-β,[75] are thought to initiate the production
of reparative dentin by fibroblasts and mesenchymal cells of the pulp.[76] Reparative
dentin is produced at an average of 1.5 µm/day, but can be increased to 3.5 µm/day. The
resulting dentin contains irregularly-shaped dentinal tubules which may not line up with
existing dentinal tubules. This diminishes the ability for dental caries to progress within
the dentinal tubules.

Treatment:
Destroyed tooth structure does not fully regenerate, although remineralization of very
small carious lesions may occur if dental hygiene is kept at optimal level.[1] For the small
lesions, topical fluoride is sometimes used to encourage remineralization. For larger
lesions, the progression of dental caries can be stopped by treatment. The goal of
treatment is to preserve tooth structures and prevent further destruction of the tooth.

Generally, early treatment is less painful and less expensive than treatment of extensive
decay. Anesthetics — local, nitrous oxide ("laughing gas"), or other prescription
medications — may be required in some cases to relieve pain during or following
treatment or to relieve anxiety during treatment.[77] A dental handpiece ("drill") is used to
remove large portions of decayed material from a tooth. A spoon is a dental instrument
used to remove decay carefully and is sometimes employed when the decay in dentin
reaches near the pulp.[78] Once the decay is removed, the missing tooth structure requires
a dental restoration of some sort to return the tooth to functionality and aesthetic
condition.

Restorative materials include dental amalgam, composite resin, porcelain, and gold.[79]
Composite resin and porcelain can be made to match the color of a patient's natural teeth
and are thus used more frequently when aesthetics are a concern. Composite restorations
are not as strong as dental amalgam and gold; some dentists consider the latter as the only
advisable restoration for posterior areas where chewing forces are great.[80] When the
decay is too extensive, there may not be enough tooth structure remaining to allow a
restorative material to be placed within the tooth. Thus, a crown may be needed. This
restoration appears similar to a cap and is fitted over the remainder of the natural crown
of the tooth. Crowns are often made of gold, porcelain, or porcelain fused to metal.

In certain cases, root canal therapy may be necessary for the restoration of a tooth.[81]
Root canal therapy, also called "endodontic therapy", is recommended if the pulp in a
tooth dies from infection by decay-causing bacteria or from trauma. During a root canal,
the pulp of the tooth, including the nerve and vascular tissues, is removed along with
decayed portions of the tooth. The canals are instrumented with endodontic files to clean
and shape them, and they are then usually filled with a rubber-like material called gutta
percha.[82] The tooth is filled and a crown can be placed. Upon completion of a root canal,
the tooth is now non-vital, as it is devoid of any living tissue.

An extraction can also serve as treatment for dental caries. The removal of the decayed
tooth is performed if the tooth is too far destroyed from the decay process to effectively
restore the tooth. Extractions are sometimes considered if the tooth lacks an opposing
tooth or will probably cause further problems in the future, as may be the case for
wisdom teeth.[83] Extractions may also be preferred by patients unable or unwilling to
undergo the expense or difficulties in restoring the tooth.

Prevention:
Oral hygiene:

Personal hygiene care consists of proper brushing and flossing daily.[9] The purpose of
oral hygiene is to minimize any etiologic agents of disease in the mouth. The primary
focus of brushing and flossing is to remove and prevent the formation of plaque. Plaque
consists mostly of bacteria.[84] As the amount of bacterial plaque increases, the tooth is
more vulnerable to dental caries. A toothbrush can be used to remove plaque on most
surfaces of the teeth except for areas between teeth. When used correctly, dental floss
removes plaque from areas which could otherwise develop proximal caries. Other adjunct
hygiene aids include interdental brushes, water picks, and mouthwashes.

Professional hygiene care consists of regular dental examinations and cleanings.

Sometimes, complete plaque removal is difficult, and a dentist or dental hygienist may be
needed. Along with oral hygiene, radiographs may be taken at dental visits to detect
possible dental caries development in high risk areas of the mouth.

Dietary modification:

For dental health, the frequency of sugar intake is more important than the amount of
sugar consumed.[57] In the presence of sugar and other carbohydrates, bacteria in the
mouth produce acids which can demineralize enamel, dentin, and cementum. The more
frequently teeth are exposed to this environment, the more likely dental caries are to
occur. Therefore, minimizing snacking is recommended, since snacking creates a
continual supply of nutrition for acid-creating bacteria in the mouth. Also, chewy and
sticky foods (such as dried fruit or candy) tend to adhere to teeth longer, and
consequently are best eaten as part of a meal. Brushing the teeth after meals is
recommended. For children, the American Dental Association and the European
Academy of Paediatric Dentistry recommend limiting the frequency of consumption of
drinks with sugar, and not giving baby bottles to infants during sleep.[85][86] Mothers are
also recommended to avoid sharing utensils and cups with their infants to prevent
transferring bacteria from the mother's mouth.[87]

It has been found that milk and certain kinds of cheese like cheddar can help counter
tooth decay if eaten soon after the consumption of foods potentially harmful to teeth.[57]
Also, chewing gum containing xylitol (wood sugar) is widely used to protect teeth in
some countries, being especially popular in the Finnish candy industry.[88] Xylitol's effect
on reducing plaque is probably due to bacteria's inability to utilize it like other sugars.[89]
Chewing and stimulation of flavour receptors on the tongue are also known to increase
the production and release of saliva, which contains natural buffers to prevent the
lowering of pH in the mouth to the point where enamel may become demineralised.[90]

Other preventive measures:

The use of dental sealants is a means of prevention. Sealants are thin plastic-like coating
applied to the chewing surfaces of the molars. This coating prevents the accumulation of
plaque in the deep grooves and thus prevents the formation of pit and fissure caries, the
most common form of dental caries. Sealants are usually applied on the teeth of children,
shortly after the molars erupt. Older people may also benefit from the use of tooth
sealants, but their dental history and likelihood of caries formation are usually taken into
consideration.

Fluoride therapy is often recommended to protect against dental caries. It has been
demonstrated that water fluoridation and fluoride supplements decrease the incidence of
dental caries. Fluoride helps prevent decay of a tooth by binding to the hydroxyapatite
crystals in enamel.[91] The incorporated fluoride makes enamel more resistant to
demineralization and, thus, resistant to decay.[92] Topical fluoride is also recommended to
protect the surface of the teeth. This may include a fluoride toothpaste or mouthwash.
Many dentists include application of topical fluoride solutions as part of routine visits.

Furthermore, recent research shows that low intensity laser radiation of argon ion lasers
may prevent the susceptibility for enamel caries and white spot lesions.[93] Also, as
bacteria are a major factor contributing to poor oral health, there is currently research to
find a vaccine for dental caries. As of 2004, such a vaccine has been successfully tested
on animals,[94] and is in clinical trials for humans as of May 2006.[95]

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Discussion H20: Spring Water, Drinking
Water, and Distilled Water
http://chetday.com/reverseosmosis.htm

by Josh Day

In my experience with home aquariums, I've learned a thing or two about water.
Fish, like us, benefit from "pure" water, and when the water contains toxins or other
contaminants, they don't do so well. The term pure should be used lightly because
oftentimes you don't want straight H20. Fish and plants need the trace elements
found in water, and we do too. So before you run to Sam's Club to buy that steam
distiller or deionizing filtration unit, let me share with you a few things I've
discovered about water.

Typically, you have three options for purchasing water at the grocery store. Drinking
water, natural spring water, and distilled water are the most common monikers on
plastic water jugs. You also have several brand names. These range from the generic
labels sold by the store, to popular, private names, to bottles of water sold by the
Coca Cola company which contain added sodium, among other less savory things.

Let's break it down:

• Drinking water is usually water straight from a government water authority

that is then further processed for the shelf. This process can range from
deionization to reverse osmosis. If you're looking for a "clean" kind of water
that is cheap and refreshing, drinking water is probably your best bet.
• Natural spring water is water pumped from, you guessed it, natural springs
in the earth. They often have cool names which make you think of a crystal
clear spring in the mountains, or a brown bear wading across a stream. This
water is rich in minerals and trace elements. It is tested for quality, but it is
usually not processed like drinking water because this would remove many of
its beneficial minerals.
• Distilled water has had all of its minerals and trace elements removed by
distillation, the act of steaming the water and then allowing the steam to cool
and turn back into water. Next to chlorinated tap water, this is probably the
worst choice for your long-term health. Please see this article on the dangers
of drinking distilled water for more information.

So what's the best choice of water for your health? The water we drink on a daily
basis can exhibit as wide a range as the food we consume. Say you wake up in the
morning and find all your bottled water gone, so you drink a glass of nasty, chlorine
and chloramine-rich tap water. You drink a 16 oz. bottle of spring water at work. You
have a sip of filtered tap water from a fountain at a public building. Finally, you
return home and try out your new Brita pitcher and drink water that's been purified
through activated carbon.
According to Dr. Zoltan P. Rona, "The ideal water for the human body should be
slightly alkaline and this requires the presence of minerals like calcium and
magnesium."

Please continue on with our next H2O discussion concerning processing methods.

Reverse Osmosis:

Discussion H20: From Tap to Reverse

Osmosis
by Josh Day

If you're on city or municipal water, what you're drinking goes through a maze of
processing and filtration before it ever reaches your tap. Raw, unclean water enters
the system and is then passed through a fibrous bed of either sand, fine gravel,
synthetic floss, or a combination of all three. This mechanical filtration removes
sediment and some cloudiness. Activated carbon and other substances then leech
harmful toxins out of the water in what is known as chemical filtration. A final stage
of filtration is biological filtration. Some treatment plants actually run their water
through plant life to absorb nitrates and other forms of nitrogen.

A similar occurrence is found in home aquariums. To clean your fish's water, some
form of filtration is necessary. The most common is what is known as a hang-on-the-
back (HOB) filter. Water is sucked through the intake tube and then pumped through
a layer of fine floss to remove visible particles and waste. There is then a layer of
activated carbon for chemical filtration. Finally, good bacteria called nitrobacters
exist on the filter floss, the gravel, and plants to consume the harmful ammonia and
nitrite which is produced from fish waste and uneaten food. Generally, a water
treatment plant is a macrocosm of this system.

The city usually adds chlorine or chloramine to the water to eradicate any pollutants
outside the treatment center on the water's path to your sink. Chlorine is like a
neutron bomb when it comes to killing everything in water. Chloramine is added as a
supplement in some municipal areas to add more oomph when distribution systems
are known to carry large tracts of bacteria. Both substances eradicate all bacteria.
They are also known poisons in larger volumes and quantities.

Home filters remove chlorine through activated carbon and other means. Bottled
water also is chlorine and chloramine free.

Now that we've discussed water treatment and basic filtration, let's get down to
brass tacks and talk about additional purification. Many filters offer multiple features
in purification, ranging from activated carbon, UV light, to reverse osmosis.

• Activated carbon is the most simple means of filtering tap water. As

mentioned above, granules of carbon remove harmful substances like
chlorine. With systems that utilize carbon there is often a secondary
mechanical filtration layer which eliminates sediments from the pipes. Some
 units often brag of multiple layers of filtration. This could include carbon,
floss, or a UV lamp.
• The next step in filtration is a process called KDF (Kinetic Degradation
Fluxion). Now, for those of you who are like me and never took a chemistry
class in college, here it is in layman terms: KDF uses oxidation and reduction
to remove chlorine and other substances from your water that carbon can't
touch. Ok, in English, this is basically another form of chemical filtration which
is more powerful than carbon. Many home filters a grade or so higher than
those that mainly use carbon utilize the KDF system.
• Onto ultraviolet light. UV light fries viruses and bacteria. A UV lamp is
placed in the center of a water passage, and the water surges through the
tunnel and is exposed to the bacteria-killing light. Though the light looks
really neat, unfortunately, it is only really effective at killing living germs and
bacteria and does nothing toward other contaminants.
• Deionized water is simply water with all the ions removed... this makes this
type of water very hungry, so to speak. Like distilled water which has no trace
elements or minerals whatsoever, D/I water actually seeks out its missing
ions. This water is largely used for laboratory experiments and saltwater
aquariums. It certainly should not be consumed on a long-term basis.
• The creme de la creme of filtration is water purified by reverse osmosis.
This process is so powerful that it's been called hyperfiltration. Water is
passed through a membrane so fine that it can remove pretty much anything.
There are also several stages of pre-filtration, as well as a storage tank for
purified water. Obviously, this system is costly and would take up some
amount of space... imagine having a miniature treatment plant under your
sink!

Many stores offer water purified through reverse osmosis. There are even vending
machines that allow you to buy R/O water as cheap as 25 cents a gallon! This is ideal
for me because I maintain a nano ten gallon reef aquarium and R/O water is perfect
because all the necessary trace elements are added when the salt is mixed.

However, if you're looking for water for you and your family, R/O water may not be
your best bet because of the loss of minerals. Contact your local water department
or run a google search to see if they have a website. You can obtain a report of your
water read-out, usually free of charge. You can find out if your water is fluoridated,
as well as see the level of phosphates, nitrates, and other bad things that comes
from the plant to your tap.

And if you're really concerned about the water you put in your body, consider
purchasing an aquarium pH test kit at a pet store. These are approximately five
dollars and can provide you with clues about the water you're drinking. If the water
is below 7.0 on the pH scale, it is acidic. If it is above, it is alkaline. Saltwater has a
pH of approximately 8.4. Reverse osmosis water generally has a pH of 6. Spring
water is supposed to be on the alkaline side due to its dissolved minerals. According
to many experts, acidic water is not good for you on a long-term basis and should
not be consumed.
 Drinking water quality and health1
Pat Kendall2

no. 9.307

from underground water tables (groundwater) and one-

Quick Facts half from surface water in rivers, lakes and reservoirs.

Water is our most essential nutrient. Hard vs. Soft Water

Water contains different amounts of dissolved
inorganic and organic compounds. The hardness of water relates to the amount of
The Environmental Protection Agency regulates calcium, magnesium and sometimes iron in the water.
public water systems. The more minerals present, the harder the water. Soft
The Colorado Department of Health regulates water may contain sodium and other minerals or
bottled or vended water if the water does not chemicals; however, it contains very little calcium,
leave Colorado. The Food and Drug magnesium or iron. Many people prefer soft water
Administration regulates if the water is because it makes soap lather better, gets clothes cleaner
involved in interstate commerce. and leaves less of a ring around the tub. Some
municipalities and individuals remove calcium and
magnesium, both essential nutrients, and add sodium in
an ion-exchange process to soften their water. The harder
Introduction the water, the more sodium that must be added in
exchange for calcium and magnesium ions to soften the
People can survive days, weeks or months without water. This process has drawbacks from a nutritional
food, but only about four days without water. The body standpoint.
uses water for digestion, absorption, circulation,
transporting nutrients, building tissues, carrying away
waste and maintaining body temperature. This information provided by:
The average adult consumes and excretes about 10
cups of water daily. Adults should drink six to eight cups
of liquids per day. Although most of this liquid should
come from beverages, food supplies some water. Our
bodies make water as a by-product in the breakdown of
fats, sugars and proteins to energy.
Water is always two parts hydrogen to one part
oxygen. Beyond that, its composition depends on where it
comes from, how it is processed and handled. Water can
be hard or soft, natural or modified, bottled or tap,
carbonated or still. About one-half of our water comes

1. Service in Action 9.307, Cooperative Extension, Colorado State University. Published May 1991. Revised October 1992. Copyright 1992. For more information,
contact your county Cooperative Extension office.
2. Colorado State University Cooperative Extension food science and human nutrition specialist and professor, food science and human nutrition.

Issued in furtherance of Cooperative Extension work, Acts of May 8 and June 30, 1914, in cooperation with the U.S. Department
of Agriculture, Milan Rewerts, interim director of Cooperative Extension, Colorado State University, Fort Collins, Colorado.
Cooperative Extension programs are available to all without discrimination. No endorsement of products named is intended nor
is criticism implied of products not mentioned.
Drinking water quality and health
First, soft water is more likely to dissolve certain
metals from pipes than hard water. These metals include
cadmium and lead, which are potentially toxic. Second,
soft water may be a significant source of sodium for
those who need to restrict their sodium intake for health
reasons. Approximately 75 milligrams of sodium is added
to each quart of water per 10 g.p.g. (grains per gallon)
hardness. Finally, there is epidemiological evidence to
suggest a lower incidence of heart disease in communities
with hard water. The Environmental Protection Agency
(EPA) doesn’t set a mandatory upper limit for sodium in
water, but suggests an upper limit of 20 milligrams per
liter (quart) to protect individuals on sodium-restricted
diets.
If you use a water softener, two ways to avoid excess
sodium in drinking water are: 1) use low sodium bottled
water, and 2) install a separate faucet in the kitchen for
unsoftened water.
Giardia and Other Microorganisms
Along with differences in mineral composition, water
contains different levels of microorganisms.
Bacteriological tests are available to determine if water is
bacteriologically safe for human consumption. Contact
the county health department for information on how and
where such tests are performed. Chlorination and
filtration are effective controls for most bacteria.
However, a tiny one-celled parasite not readily killed by
chlorination, Giardia lamblia, deserves special discussion.
Over the past several years, giardia has become an
increasingly common problem in rural and mountain
communities with inadequate filtration systems. Giardia is
mostly found in surface waters such as mountain streams
and lakes, not groundwater. Because one cannot see,
taste, or smell giardia, it is best not to drink water
directly from mountain streams or lakes.
Once ingested, the giardia cyst develops into a
trophozoite that attaches to the wall of the small intestine.
Disease symptoms usually include diarrhea with cramping
and gas, dehydration, weakness and loss of appetite.
Symptoms may take seven to 10 days to appear and last
up to six weeks. Most people are unaware at the time of
ingestion that they have been infected.
Laboratory identification can confirm the disease by
diagnosis of the organism in the stool. The disease is
curable with prescribed medication. If untreated, the
symptoms may disappear on their own and reoccur
intermittently over a period of months.
Treatment also can help prevent spread of the disease
between people and between pets and people. For
example, in a Colorado Department of Health study,
person-to-person contacts within families or between
small children in day care centers were responsible for 46
percent of the 360 cases investigated. In fact, only 15
Page 2
percent of the respondents had ingested stream or lake
water in the three weeks prior to the onset of symptoms.
Prevention is the best solution. Always wash your
hands after changing diapers and performing other
hygiene activities. Wash children’s hands frequently.
Thoroughly clean change surfaces after diapering.
It’s best to carry your own water on camping or
backpacking trips. If this is not practical, the next best
solution is to boil the water. Although giardia cysts are
killed at temperatures of 131 degrees F, boiling for one
minute at sea level and up to five minutes at 10,000 feet
is recommended to eliminate other microorganisms that
might be more heat resistant than giardia. Giardia also
will not survive in water held at 59 degrees F for 30
minutes if one iodine tablet has been added per quart.
Filters are available, but are expensive and inconvenient.
Furthermore, many products marketed for backpackers
are not effective in filtering out the tiny giardia cysts.
Protection is the key to the control of giardiasis.
Since feces can contain the organism, bury waste 8
inches deep and at least 100 feet away from natural
waters. Dogs, like people, can get infected with giardia.
Unless carefully controlled, dogs can contaminate the
water and continue the chain of infection from animals to
humans.
Fluoride
Fluoride is found naturally in Colorado water
supplies in different amounts. The dental benefits of
fluoridated water are well documented. Fluoride
concentrations of 1.0 milligrams per liter or greater will
reduce the incidence of dental cavities. However,
concentrations over 2.0 milligrams per liter can darken
tooth enamel causing fluorosis.
The American Dental Association and the American
Medical Association endorse fluoridation. Yet, after more
than 40 years of fluoridation, nearly 40 percent of tap
water remains unfluoridated. Opponents have long argued
that fluoridation violates individual rights, certain
religious beliefs that ban medications, and does not
prevent tooth decay. They also claim it promotes a
variety of ills. A recent study in which male (but not
female) rats given water with high levels of sodium
fluoride developed a rare bone cancer, added fuel to their
concerns. Proponents counter that fluoridation is not a
form of medication, but an adjustment of an essential
nutrient to a level favorable to health. What that level is
and whether or not it should come from fluoridated
drinking water will be at the crux of the next round of
debates.
Tooth decay is on the decline in the United States
(50 percent decline in the last 20 years). The decline is
occuring in fluoridated and to a lesser extent in non-
fluoridated areas. Fluoride treatments, fluoridated
Drinking water quality and health
toothpaste, better diets and improved oral hygiene are all
factors.
Like most elements, fluoride appears to be both
beneficial to health and potentially toxic. The goal is to
determine the optimum level and then decide how best to
achieve that level. The EPA currently sets the maximum
allowable level of sodium fluoride in drinking water
(natural or added) at 4 milligrams per liter (4 parts per
million) and the maximum recommended level at 2
milligrams per liter. The EPA reviews drinking water
standards every three years.
Lead
Lead is a toxic heavy metal known to turn up in
drinking water. Recent data indicate that levels formerly
safe may threaten health, especially among infants and
children. In an 1986 EPA survey, an estimated 40 million
Americans (one in five) were using drinking water that
contained potentially hazardous levels of lead.
Acute lead poisoning can cause severe brain damage
and death. The effects of chronic, low-level exposure,
however, are more subtle. The developing nervous
systems of fetuses, infants, and children are particularly
vulnerable. Recent studies show that lead exposure at a
young age can cause permanent learning disabilities and
hyperactive behavior. Low-level lead exposure also is
associated with elevated blood pressure, chronic anemia,
and peripheral nerve damage.
Natural water usually contains very little lead.
Contamination generally occurs in the water distribution
system or in the pipes of a home or facility. Lead pipes,
brass faucets and lead solder used to join copper pipes
are the culprits. If your home was built before 1986 when
a nation-wide ban on lead pipes and lead solder went into
effect, it is likely to have lead-soldered plumbing.
The severity of lead contamination depends in part on
how "corrosive" your water is. Soft or acidic water is
more likely to corrode plumbing and fixtures, leaching
out lead. According to the EPA, about 80 percent of
public water utilities deliver water that is moderately or
highly corrosive.
The EPA is changing the focus of its lead regulation
from a maximum contaminant level of 50 parts-per-
billion at the tap to imposed treatment if
Page 3
more than 10 percent of collected samples from a water
system exceed 15 parts-per-billion lead. Water systems
that exceed such levels will be required to implement
corrosion control measures to reduce leaching of lead into
water. Techniques such as adding lime (calcium oxide)
to reduce water acidity can greatly reduce lead levels at
the tap. A number of other simple practices also can help
reduce the level of lead at the tap.
1. Cook with and drink only cold water. Hot water
tends to dissolve more lead from pipes.
2. Don’t drink the first water out of your tap in the
morning. Let the water run for about one minute until
a change in temperature occurs.
3. For private wells, consider water treatment devices
such as calcite filters that reduce acidity and make
water less corrosive. Certain point-of-purchase
treatment devices (e.g., some ion-exchange filters,
reverse osmosis devices and distillation units) also
can remove lead.
4. If lead levels remain high, consider bottled water for
drinking and cooking purposes.
Nitrate
Nitrates may be found naturally in water or may
enter water supplies through a number of sources
(fertilizers, animal wastes, septic systems). High nitrate-
containing water is a serious health concern for pregnant
women and infants under the age of 6 months. Bacteria
in the infants’ digestive tracts may convert the relatively
harmless nitrate to nitrite. In turn, the nitrite combines
with some of the hemoglobin in blood to form
methemoglobin that cannot transport oxygen. To protect
those at risk, the Maximum Contaminant Level (MCL)
for nitrate in water is 45 mg/l as nitrate (NO3) or 10 mg/l
as nitrogen (N). The MCL for nitrite is 1 mg/l.
Sulfate
Sulfates occur naturally in groundwater combined
with calcium, magnesium and sodium as sulfate salts.
Sulfate content in excess of 250 to 500 ppm (mg/l) may
give water a bitter taste and have a laxative effect on
individuals not adapted to the water.
Water that smells like rotten eggs has a high level of
hydrogen sulfide gas. The gas may occur naturally in
water near oil or gas fields or as the result of bacterial
contamination. To test for bacterial contamination contact
the county health department or a commercial testing lab.
Drinking water quality and health
Organic Chemicals
The term "organic chemical" includes such products
as pesticides, herbicides, petroleum products and
industrial solvents. Although most have not been
routinely monitored, hundreds of different organic
chemicals have been found in drinking water from
accidental spills, improper disposal or non-point
movement through soils to groundwater. Today,
municipalities are required to monitor an increasing list
of organic chemicals under the Safe-Drinking-Water Act.
As with other contaminants, the danger from organic
chemicals in water is hard to assess. In high doses and
pure form some of these chemicals may promote cancer,
impair the nervous system or damage the heart. In low
doses, organic chemicals may have cumulative effects,
but so far not much is known about their nature or
magnitude.
Once groundwater is contaminated, cleanup of that
groundwater is extremely difficult. If the water is
unsuitable for human use, it also may be unsuitable for
agricultural uses and alternative sources of water may
need to be found. Organic chemicals and groundwater
contamination is an area where much research is needed.
In the meantime, the prudent use and disposal of all
chemicals (agricultural, industrial, home and garden) can
go a long way to protect the environment and
groundwater from contamination.
Radon
Radon is a radioactive gas, a decay product of
uranium, that can dissolve into water supplies. The gas
also is found in rocks and soils that contain granite,
shale, phosphate, and pitchblende. It is odorless, colorless
and tasteless.
The EPA considers radon to be a major potential
health threat, causing an estimated 10,000 to 40,000 lung-
cancer deaths each year. While most deaths are from
radon accumulated in houses from seepage through cracks
and holes in the foundation, 30 to 1,800 deaths per year
are attributed to radon from household water. Showering,
dish-washing and laundering agitate water and release
radon into the air. The EPA estimates that at least 8
million people may have high radon levels in their water
supply. Radon is most likely to be present in water from
private wells or from small community systems. Large
systems usually provide some kind of water treatment
that aerates the water and disperses any radon gas that
may be present.
Before you test your water for radon, test the air. If
your indoor radon level is high and you use groundwater,
test your water. If the air level is low, there is no need to
test your water. Test results are expressed in picocuries of
radon per liter of water (pCi/l). In general 10,000 pCi/l of
Page 4
radon in water contributes roughly 1 pCi/l of airborne
radon throughout the house. EPA currently advises
consumers to take action at total household air levels of 4
pCi/l. For waterborne radon, a simple step is to make
sure your bathroom, laundry and kitchen are well
ventilated. At moderate levels, this may adequately
reduce your exposure to waterborne radon. However if
you use a private well that has high levels of radon,
water treatment devices such as granular activated carbon
units and home aerators may be warranted.
Improving Water Quality
The growing uneasiness over the purity of tap water
has led many Americans to install waste treatment
devices, such as filters or distillers. See Service in Action
9.728 Drinking water treatment devices: filters and 9.729
Drinking water treatment devices: distillers.
Bottled vs Tap Water
Sales of bottled water have increased dramatically
over the last few years. Bottled-water companies and
public water systems often battle over the relative merits
of their products. EPA regulates public water systems.
FDA regulates bottled water that crosses state lines.
Bottled or vended water that stays in Colorado falls under
the jurisdiction of the Colorado State Department of
Health.
Public water systems generally are disinfected with
chlorine. Bottled water is commonly disinfected by ozone
treatment. Ozone is a high-strength oxygen that quickly
reverts to normal oxygen. It is a strong oxidant, like
chlorine, but does not add taste like chlorine does. The
length of time chlorine and ozone remain active in water
depends on many factors, including temperature. Chlorine
usually provides residual disinfection throughout the
public-water distribution system. Ozone provides a
residual disinfection for a limited time. However, bottled
water may be in distribution for several weeks and
storage conditions, especially temperature, may adversely
affect quality. In terms of bacterial content, it is
questionable as to whether bottled water is better than
most municipal tap water.
Bottled water often is purchased for its good taste.
However, taste does not always indicate safeness. At the
concentrations present in drinking water, most harmful
substances (including some disease-causing
microorganisms, nitrates, trace amounts of lead and
mercury, and some pesticides and organic materials) have
no taste. Differences in taste among bottled waters
generally are due to differing amounts of carbon dioxide,
calcium, iron compounds, sodium, and other minerals and
mineral salts. Differences also may be due to the amount
and type of processing.
Drinking water quality and health
Mineral-free water or distilled water is treated to
remove the minerals that occur naturally in water. Almost
all sodium is removed by these processes. The resulting
water is rather flat and tasteless for drinking because of
the lack of minerals.
Drinking water comes from municipal water
systems, wells or springs. It often is treated by reverse
osmosis to remove bacteria and other pathogens and most
pesticides. The resulting water is purified but still
contains some dissolved solids.
Natural water comes from unprotected well or
spring systems and is bottled without extensive treatment.
Because it is almost exclusively groundwater, it usually
contains a range of minerals and is, therefore, quite
flavorful. Spring water is ground water that has risen
naturally to the surface. Artesian spring water also rises
under its own pressure, but only after it has been reached
by drilling.
Mineral water is simply water that contains minerals
- which is true of virtually all water except distilled
water. Natural mineral water contains just the minerals
present in the water as it comes from the ground. Mineral
water can be still or sparkling. The carbon dioxide that
causes carbonation also can be natural or added during
bottling.
As for contaminants, bottled water generally rates as
good as but no better than municipal water supplies
Page 5
used for comparison purposes. If you do purchase bottled
or vended water, purchase from a quality retailer who
handles enough volume to rotate stock. If you have
concerns about locally vended water, contact your county
health department or the Colorado Department of Health,
(303) 692-2000.
References
E.P.A. Lead in Drinking Water: Should you be
concerned? Environmental Protection Agency, Public
Information Center, Waterside Mall, 410 M St., SW,
Washington D.C.
Follett, R.H. and J.R. Self. Domestic water quality
criteria. Colorado State University Cooperative
Extension, Service in Action, .513, Fort Collins, CO
1989.
Fundingsland, S. and D. Lundstrom. Drinking Water and
Health. Pub. 27, HEA, NDSU Extension Service,
North Dakota State University, Fargo, ND 58105,
June, 1988.
Shelton, T. Interpreting Drinking Water Quality Analysis
- What Do the Numbers Mean? Pub. E127, Rutgers
Cooperative Extension, Cook College, Rutgers
University, New Brunswick, NJ 08903, 1989.
Stewart, J., A. Lemley, S. Hogan, R. Weismiller. Health
Effects of Drinking Water Contaminants. Water
Quality Fact Sheet 2, Cornell University and
University of Maryland, Rev. 1988-89.
The Pollutants that Matter Most: Lead, Radon, Nitrate.
Consumer Reports, p. 30-32, January, 1990.
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4 JOINT FTC/DEPARTMENT OF JUSTICE HEARING

5 ON HEALTH CARE AND COMPETITION LAW AND POLICY

11 Thursday, June 12, 2003

12 9:15 a.m.

18 601 New Jersey Avenue, N.W.

19 Washington, D.C.

And I'm very grateful to Mr. Sfikas, who's next,

2 because I don't have to worry about his PowerPoint
3 presentation because he doesn't have one. Mr. Sfikas
argued
4 an advertising case a while ago before the Supreme Court,
5 California Dental, which was brought by the Federal Trade
6 Commission. Mr. Sfikas? Thanks for joining us today.
7 MR. SFIKAS: I would like to thank the Justice
8 Department and the Federal Trade Commission for inviting
me
9 as a representative of the American Dental Association to
10 speak to you today.
11 As it was indicated, I did represent the California
12 Dental Association in a case that went to the United
States
13 Supreme Court and thereafter was remanded to the Ninth
14 Circuit Court of Appeals.
15 In that case, the California Dental Association,
16 with reference to quality advertising, took the position
that
17 in order for a dentist in California who was a member of
the
18 association -- in order for that member to advertise
quality
19 claims, the claims had to be verifiable.
20 The FTC took the position that that was a restraint
21 of trade, interfering with both the consumer's right to
hear
22 that information and the dentist's right to utilize that
sort
23 of information. The case ended up that the California
Dental
24 Association prevailed and the case was dismissed against
the
25 California Dental Association.
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1 Now, I'd like to give you a little bit of
2 background, and then I will try to answer some of the
3 questions that appeared on the FTC website relating to
4 quality advertising.
5 Quality advertising is considered by many
6 inherently deceptive because it cannot be verified and it
7 cannot be precisely measured. The rationale for this
8 statement is the striking disparity between the knowledge
on
9 the other hand of the professional and the knowledge of
the
10 consumer.
11 Professionals, obviously, supplying information
12 have far greater knowledge regarding the quality than the
13 individual consumer who is buying that service. Thus, it
is
14 extremely difficult for a patient to discern whether he
or
15 she has had, let's say in this case, good dentistry.
16 If there is an individual who goes into a dentist
17 and has a tooth filled, it is very difficult for the
patient
18 to determine whether or not that restoration was a good
19 restoration. The same is obviously true for medicine and
the
20 other health care professionals that we saw with their
21 presentations today.
22 The quality of professional services tend to resist
23 evaluation by patients in part, as noted above, because
of
24 the specialized knowledge, but also with reference to
whether
25 or not that service was the type of outcome that was
expected
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1 as a result of what the health care professional did to
the
2 patient.
3 Many economists in this area and other experts have
4 come to the conclusion that the lay public is totally
5 incapable of evaluating the quality of medical services. A
6 patient's loyalty to his or her dentist also complicates
the
7 effectiveness of quality advertising.
8 In other words, there are bonds between patients
9 and dentists and patients and various physicians so that
10 irrespective of how you might rate that physician or
dentist,
11 they will continue to go to that dentist because they
have a
12 relationship with the dentist or the other health care
13 professional.
14 Now, as a result, the Supreme Court determined that
15 these various significant challenges to informed
decision16
making by the customers for professional services suggest
17 that advertising restrictions arguably protecting the
18 patient -- this is the requirement for verification of
the
19 quality advertising -- could not be looked upon in the
rather
20 cursory manner that the Federal Trade Commission had in
21 determining that there was an antitrust violation.
22 The Bates case has been mentioned by a couple of
23 speakers now, and that was the case that first introduced
24 advertising to the professions. But even in the Bates
case,
25 although it said advertising for routine services was
fine --
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1 and that was not an antitrust case; it was basically a
First
2 Amendment case -- nevertheless, the Chief Justice at the
3 time, who wrote the opinion, also noted that: "Claims
4 relating to the quality of legal services probably are not
5 susceptible of precise measurement or verification, and
under
6 some circumstances might well be deceptive or misleading
to
7 the public or even false."
8 Now, with this background, I'd like to try to
9 answer some of the questions that were posed on the
website
10 in introducing this hearing this afternoon.
11 What information regarding quality is available to
12 consumers? Well, of course, there is quality advertising.
13 However, we have all the cautions that not only I've
raised
14 here in the background but that the other speakers in
showing
15 various forms of advertising that were troubling.
16 But let me give you an illustration with reference
17 to dentistry. Let us suppose that Jane Jones, DDS, who
18 practices in the State of California, advertises herself
as
19 the best dentist in the West. Is this misleading? Is it
20 verifiable?
21 Well, in California and as a result of this Supreme
22 Court decision, Jane Jones would have to try to show that
she
23 is the best dentist in the West or she would not be
24 permitted, if she were a member of the association, to
run
25 this ad.
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1 Now, how are the ways that Jane Jones can show that
2 she is the best dentist in the West? I suppose if
something
3 like a magazine like Consumers Union did a study and
4 determined that she was the best dentist or among the very
5 best dentists, that would probably satisfy the fact that
this
6 advertisement had been verifiable.
7 What are the problems that might arise if this type
8 of advertising is permitted? Well, a patient may go to
Jane
9 Jones, believing that she is the best dentist in the State
of
10 California, and Jane Jones may not be the best dentist in
the
11 state and may, as a result, leave the patient with lips
that
12 are sore and a mouth that is sore as a result of this.
Well,
13 certainly this patient will not return to Jane Jones. She
14 will go on and look at other dentists, and it may be
trial
15 and error before she finds a dentist who she considers is
16 best for her.
17 Well, that trial and error constitutes search
18 costs, which would therefore interfere with the delivery
of
19 services. And one of the arguments in the California
Dental
20 Association case was that the elimination of those search
21 costs meant that this type of advertising would be pro22
competitive and, in fact, the Ninth Circuit Court of Appeals
23 found that to be the case.
24 What is the difference -- here's another
25 question -- what is the difference between dentists who
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1 advertise and those who do not advertise quality services?
2 Well, there may be no difference between them in terms of
3 training and skill. It's simply one is advertising that
she
4 is the best, and the other is not advertising. So it would
5 appear as if the advertisement might give the dentist who
was
6 advertising sort of the ability to say that they are
superior
7 to the other dentists in the community.
8 What role does comparative advertising play in
9 dental advertising? There is almost no comparative
10 advertising; at least, I've never come across comparative
11 advertising in dentistry.
12 Are there governmental and association limitations
13 on advertising? And yes, as you saw with Mr. Kelly
speaking,
14 the advertisement does have to be truthful. And in the
case
15 of the California Dental Association, it also has to be
16 verifiable.
17 And the question then is, is that -- what effect is
18 that on the marketplace? In my judgment, that's a
salutary
19 effect on the marketplace because consumers in
California,
20 for example, can rely on the fact that the professional
21 association of dentists in that state verify the
22 advertisements that are being run in the Yellow Pages or
in
23 newspaper columns or newspapers in general.
24 There's another question: What empirical evidence
25 supports this justification? Well, I'm really not aware
of
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1 any empirical evidence that supports this. However, I
2 suppose one way that you could determine that is to run a
3 study and see whether or not -- let's take California
again
4 as the illustration -- whether dentists in California who
are
5 not members of the California Dental Association run more
6 quality advertisements than members of the California
Dental
7 Association, who cannot run quality advertising unless
8 they're ready to verify those.
9 As a matter of fact, just as others have said here
10 with various physician-type advertising, advertising
among
11 dentists is flourishing. The last time the ADA survey
center
12 took a survey on advertising was in 1996 and I'm sure the
13 numbers would be much higher today. But in 1996, 65
percent
14 of all dentists were advertising. Now, that's not to say
15 they were advertising quality, but they were advertising
in
16 general.
17 And the survey further asked those dentists, did
18 they believe that their advertising was worthwhile? And
70
19 percent of the dentists of that 65 percent stated that
the
20 advertising was in fact worthwhile.
21 Now, the aftermath of the CDA litigation indicates
22 that probably the California victory was a pyrrhic
victory
23 because what has happened because of the expense of that
24 litigation, none of the state associations are enforcing
25 advertising principles of ethics.
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1 But it's even more significant: They are so
2 concerned about anything, any enforcement, any
disciplinary
3 actions, under the ADA principles of ethics that they are
not
4 moving forward to try to obtain discipline for any
violation
5 of the principles of ethics.
6 Now, I'd like to make one other statement for the
7 record. There was a dentist here yesterday, I guess during
8 the Noerr Pennington discussions, whose name -- I'll leave
9 his name out. But he made a statement which I would like
to
10 challenge.
11 His statement was that a dentist may not advertise
12 that he is a mercury-free dentist. And although the ADA
13 Judicial Council has never been called upon to resolve
that
14 issue, nor am I aware of any state association ever being
15 called upon to make a determination with reference to
this
16 ad, the likelihood is that that ad, without more --
mercury17
free dentist, John Smith is a mercury-free dentist -- that
18 would not violate the principles of ethics.
19 On the other hand, if that dentist went further and
20 stated that he or she were mercury-free dentists because
of
21 the toxicity of a certain type of restorative material,
that
22 very likely would violate the principles of ethics
because
23 that claim is untruthful and it's not verifiable.
24 In fact, the Food & Drug Administration, Health and
25 Human Services, has an extraordinarily large body of
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1 literature, that supports the notion that that form of
2 restorative is not harmful to patients and, in fact,
except
3 for a very small element of the population who may be
4 allergic to that restorative.
5 But with reference to history, that restorative has
6 been used for 150 years. All the governmental agencies,
the
7 scientific bodies, all conclude that it does not harm
8 patients. And therefore, if this dentist were to go
further
9 and say he is a mercury-free dentist because of the
toxicity
10 of a certain restorative, that probably would violate the
11 principles of ethics.
12 Let me conclude by telling you a joke that I used
13 to tell all of the dentists when I litigated with the
Federal
14 Trade Commission. And that litigation lasted for a number
of
15 years. And that was, how many lawyers does it take to
screw
16 in a light bulb? And the answer is, as many as you can
17 afford.
18 And I would tell the dentist that the United States
19 government has many, many lawyers that it affords who
work
20 for them in litigation with the FTC. Thank you very much
21 for permitting me to speak to you today about this
subject
22 matter.
23 MS. KOHRS: Thanks, Mr. Sfikas. I think we're just
24 going to take about a ten-minute break to give everybody
just
25 a chance to get up and stretch your legs and think a
little

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1 bit before we come back for the final speakers. So we'll
2 reconvene, actually, at about 4:00 by this clock here on
our
3 wall.
4 (A brief recess was taken.)
5 MS. KOHRS: It's 4:00 here. So I'm going to go
6 ahead and start with our next presenter, who is John
Gebhart.
7 MR. GEBHART: Thank you. Good afternoon, and I'd
8 like to express my appreciation to the FTC and the
Department
9 of Justice for inviting me here today. DoctorQuality is a
10 company that perhaps many of you do not know. We serve
11 anonymously or invisibly, in many cases. But I'm
interested
12 in giving you some background about what we do. No, I
don't
13 see where it fits with the agenda of today's discussions.
14 First, a word about myself. I'm actually trained
15 as a financial executive, financial and general
management,
16 although I've spent about the last 15 years in health
17 services in a variety of different activities.
18 I've worked in areas that pertain to health care
19 marketing, hospital marketing, demand and disease
management,
20 where we've delivered advice directly to consumers; also,
in
21 physician referral, physician practice management. I had
22 some brief involvement in providing information services
to
23 mental health professionals, and most recently have been
24 focusing on patient safety and physician quality with
25 DoctorQuality.
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1 Earlier this year as well, I had the opportunity to
2 serve on a panel at the NCQA that dealt with the issues of
3 provider referral and what kind of directory information
4 should be available to consumers. So hopefully I have some
5 insights onto some of the issues we're dealing with today.
6 I'm also going to talk a little bit about the
7 company. We provide a couple services, one of which I
think
8 is directly germane to today's discussions. And I would
9 submit the other one is as well, but perhaps not as
obvious.
10 And we're going to focus primarily on my Quality Coach,
which
11 is a provider service -- or a service that we provide to
12 health plans and large self-insured employers.
13 DoctorQuality was founded in 1999 during what I'd
14 like to refer to as the apex of the dotcom toga party. I
15 actually represent the second generation of management.
The
16 academic physicians who founded the company are back in
17 academic medicine, and doing so, they were able to double
18 their salaries and they now have 401(k) matching, to
which I
19 say God bless America.
20 Even though we have a very -- we're very young and
21 very new on the scene, we do have a very strong customer
base
22 made up of some reputable clients who have really helped
us
23 shape the platforms that we provide today.
24 We're also very fortunate to have the guidance of
25 some very prominent individuals on our board of
directors.
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1 One is a gentleman named Chuck Buck, who actually is a
member
2 of the Institute of Medicine, who published the frame3
breaking report in 1999, "To Err Is Human," which really
kind
4 of blew the covers off of medical errors. And the other is
5 Dr. David Nash. Dr. Nash heads up the Center for Health
6 Policy and Outcomes Research at Thomas Jefferson
University,
7 nationally known as one of the experts in quality and
patient
8 safety.
9 We are a company that uses health care technology
10 to improve quality and safety. We believe in the
transparent
11 marketplace. We believe that there's an opportunity to
get
12 more information into the right hands as people try to
either
13 monitor performance or make critical decisions.
14 To that end, we have a hospital and physician
15 selection tool that helps consumers choose resources
based on
16 performance and quality. We also have a hospital incident
17 and adverse event reporting tool which is used for
quality
18 assurance purposes, and from that activity we today house
the
19 largest database that we know of -- we've looked
everywhere
20 to find anything comparable, and we haven't been able to
--
21 we've got the largest database in existence for medical
22 errors and near-misses. And I'll talk a little bit about
23 that.
24 The two products that we offer are Risk Prevention
25 and Management, or RPM -- this is the hospital error
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1 collection tool. It's used for quality assurance purposes.
2 And we also have My Quality Coach, and that's the
physician
3 and hospital selection tool.
4 I'd like to emphasize, it's very important as we're
5 trying to provide information to consumers to make
informed
6 decisions. You must know that there is an impermeable wall
7 between these two platforms. The information that we
collect
8 in the conduct of the RPM program is private, confidential
9 information for quality assurance purposes only.
10 Frequently I get the question, so you collect
11 hospital error information and tell consumers who makes
the
12 most mistakes? That's not the objective of the program,
nor
13 will it ever be.
14 I want to start by talking about the hospital error
15 reduction program. I think it's important -- maybe not
16 directly in the context of today's discussions, but I
think
17 it's important in the context of: at some or another
every
18 one of us here is going to be a patient or has been a
19 patient.
20 Between 44,000 and 98,000 people are killed
21 annually in the United States as a result of an
unnecessary
22 medical error. Let's put that into context because 98,000
a
23 year is a big number. It's hard to really figure out what
24 that means. I've been given 15 minutes today. Three
people
25 will die while I'm up here. And that's a pretty sobering
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1 fact. So it's a very significant problem.
2 The other thing that's very interesting is of the
3 numerous medical errors that are made, it's been estimated
4 that only about 5 percent are actually reported, reported
in
5 the context of trying to analyze why the mistakes happened
so
6 preventive measures can be taken.
7 Not only is it a tragedy, but it costs a lot of
8 money, too. Medical errors cost this country about $140
9 billion a year, both in terms of repeated procedures and
the
10 costs for those procedures, and there's also a growing
11 concern, a crisis in many states, with respect to
malpractice
12 insurance. And this is a piece of it.
13 Now, it's very encouraging to see that many of the
14 states in this country are now requiring some form of
15 mandatory medical error reporting. About 20 states today
16 actually have some legislation on the books requiring
error
17 reporting.
18 I think two in particular are, I think, very near
19 and dear to DoctorQuality's heart. In New York, there's a
20 program called NYPORTS, and it might not be generally
known,
21 but every single hospital in New York has a dedicated
NYPORTS
22 terminal at which the hospital employees are required to
23 report certain errors to New York State.
24 Also, in Pennsylvania, I'm very proud to say that
25 yesterday our company submitted the bid to provide error
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1 reporting across the state to a new regulatory agency in
2 Pennsylvania known as the Patient Safety Authority. And
3 Pennsylvania is really going to be the first state of its
4 kind that is going to encourage not only what's known as
5 serious events -- in other words, the things that harm
6 patients -- but Pennsylvania wants to know about the near7
misses as well. And I think it's a big step forward in terms
8 of really being able to find ways to be proactive about
some
9 of these problems.
10 The problems that we see here are not necessarily
11 individual acts of negligence or incompetence. The
problems
12 that we see, we believe, most often are the result of a
13 system of care.
14 Here's a very startling statistic: From the time
15 that an individual is admitted to a hospital for what's
16 become a fairly routine procedure, coronary artery bypass
--
17 from the time that person is admitted to the time they're
18 discharged, about 400 people are going to be involved in
19 delivering care to that individual, 400.
20 Not all of these are going to be hands-on. Some of
21 these people are going to work in the lab, some in the
22 pharmacy, some in the kitchen. Some are going to work in
23 maintenance, and they're going to clean up the operating
room
24 after the fact.
25 But 400 employees of the hospital are involved in
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1 delivering service to one person. If each of them do three
2 things, that's more than a thousand opportunities for an
3 error someplace in the process.
4 So we believe that it's important to be able to
5 collect data and understand where in the system things
break
6 down. And we think this is a function of both variation
from
7 accepted medical practices, and it's also an important
8 element in trying to house the right kind of culture in
9 medical institutions.
10 And this might be the point where the service that
11 we provide internally and the service we provide
externally
12 overlap. And this might be the point that has the
greatest
13 relevance for today's discussion.
14 We start with trying to help our hospital clients
15 get an understanding of their culture, and someone in
public
16 relations told me a long time ago, public relations
starts at
17 home. You have to understand your own organization's
culture
18 if you're going to understand how you want to portray a
19 message or an image publicly.
20 One of the big problems in health care is that we
21 have not practiced an open and blame-free culture of
22 gathering information about mistakes. Whether if it's for
23 fear of reprimand or whether it's arrogance or something
in
24 between, a lot of these mistakes don't happen -- pardon
me,
25 they happen; they don't get reported. We'd like to be
able
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1 to change that, help our clients change that, and start to
2 gather the information to help them figure out where the
3 problems are.
4 So we start with culture. We move to data capture.
5 Once we know -- once we have the data, we can start to
6 analyze the data to figure out what the solutions are,
7 implement the solutions. And we find among a lot of our
8 clients, once we've nailed down one solution, another one
9 pops up. Health care technology changes constantly. Or
once
10 you've solved a problem on the surface, it might expose
11 several other problems underneath.
12 So we believe that it's important at every level,
13 and I think in particular with respect to health care
policy,
14 legislative policy, something has to be done to really
evolve
15 the culture of health care.
16 I mentioned a little bit earlier the database that
17 we have. Earlier this week we crossed the line. We now
have
18 a little more than 80,000 medical errors. Next week, it
will
19 be more than 81,000, collected from more than 150 health
care
20 facilities across the country.
21 You'll see that about two-thirds fall into either
22 the adverse clinical or medication areas. And I think the
23 statistics on the right-hand side are pretty telling as
well.
24 The one I like the most is that of all the items that are
25 reported to us, 43 percent involve a near-miss.
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1 You know, this might be a situation where in the
2 middle of the night you see the nurse come into your
hospital
3 room and say, "It's time for your pill," and she hands you
a
4 yellow pill. And maybe you're going to be awake enough to
5 say, "Wait a second. Mine is blue." That's a near-miss. It
6 was caught in time. And there could be about 15 people
7 someplace in the chain that somehow put a yellow pill on
that
8 tray for you instead of your blue one.
9 We've seen numerous cases where our clients being
10 able to quantify the recurrence of near-misses has led to
11 some very significant improvements in their procedures.
And
12 we were able to prevent similar recurrences in the
future.
13 I'm just going to say one more thing about the
14 medical error situation before we roll into the physician
and
15 provider selection tool that we provide. But I get a lot
of
16 questions very frequently about why should anyone really
want
17 to report a medical error?
18 The first one, you know, why should you want to do
19 it? Well, I believe that doctors went to medical school
to
20 learn how to do a good job. And there's a little bit of a
21 Pollyanna in me about that. I don't believe doctors go to
22 medical school so they can golf on Wednesday. There are
23 cheaper ways to golf on Wednesday.
24 I think that health care professionals try very
25 hard to do a good job, and I think it's harder and harder
to
228
For The Record, Inc.
Waldorf, Maryland
(301)870-8025
1 do a good job. And what we provide is an improvement tool
2 that helps people understand where their weaknesses are
and
3 be able to react to them.
4 Next question: Won't error reporting lead to
5 lawsuits? A very, very common misperception. And the
answer
6 is, in 49 states, no. In 49 states, any information that's
7 collected as part of a quality improvement is protected by
8 the peer review statutes, which means you cannot subpoena
it.
9 I'm sure that will be challenged, and it's probably a
10 question that we're going to have to wrestle for a long
time.
11 But I'm very pleased to say that at a policy level, in 49
12 states the answer is no. This does not lead to lawsuits.
13 This leads to better health care.
14 Who would want to report on a coworker? Well, let
15 me tell you about one of the programs that one of our
clients
16 has in place, which I think is just the perfect embrace
of
17 the kind of culture that we hope our clients are
promoting.
18 We have a client who has a program called the Plant a
Flag
19 program, and what happens is the hospital gives lapel
pins
20 and collar pins to the doctors and nurses that report an
21 error.
22 They take the attitude that the errors are like
23 potholes in the road. If you stepped in the pothole,
please
24 plant a flag so that your coworkers don't step into the
same
25 pothole. And we see hospitals give out gift certificates
for
229
For The Record, Inc.
Waldorf, Maryland
(301)870-8025
1 cookies in the cafeteria, movie tickets, anything to
promote
2 a culture of blame-free reporting.
3 And does this offend doctors? Well, it doesn't
4 offend doctors if they've embraced this culture of blame-
free
5 reporting. It's very important that we look at error
6 collection data in a non-punitive fashion. And I go back
to
7 my first point: 98,000 people die because of medical
errors.
8 It seems pretty apparent to me that blame has not worked.
We
9 need to try something else.
10 Let me turn to our second product, My Quality
11 Coach, which is an online consumer decision support
system
12 whereby consumers can choose physicians and hospitals
based
13 on quality and satisfaction data. With this program, we
14 encourage consumers to log on and prepare ratings on
their
15 doctors. And we also invite doctors and hospitals to
present
16 certain information about themselves.
17 Now, this information, we think, is pretty
18 important in the context of how resources are chosen, VHA
19 did -- the Voluntary Hospital Association, that is, did a
20 study last year and it seems pretty clear that health
care is
21 becoming more consumer-centric. I won't go ahead and read
22 all those, but you can probably them.
23 But in other words, this slide makes the point that
24 consumers are interested in finding out quality
information.
25 They would be very pleased to make decisions based on the
230
For The Record, Inc.
Waldorf, Maryland
(301)870-8025
1 standards of performance and the quality of care that's
2 delivered.
3 It's also becoming an increasing trend that
4 employers are very interested in this as well. It doesn't
5 cost more -- in fact, it actually costs less -- for the
6 employees to go to better quality doctors and better
quality
7 hospitals. And to the extent that this both is a way to
8 reduce health care cost and to bolster employee
satisfaction,
9 this is something that large employers in particular are
10 increasingly becoming very interested in.
11 This last point on the slide: Network size is
12 taking a back seat to network quality. Actually, that's
13 backwards, and the person who drafted that is going to be
in
14 big trouble tomorrow morning when I get back to the
office.
15 Network quality -- no. I'm sorry. I'm backwards.
16 Start again. Network size is taking a back seat to
network
17 quality. It used to be that when you'd get into a health
18 plan, you'd look at the book and say, is my doctor in
here?
19 Well, now people are increasingly trying to figure out,
is
20 the good doctor in here?
21 Just a snippet from the Philadelphia Business
22 Journal, where last year the Blue Cross organization in
town
23 has actually developed an incentive program based on
quality.
24 If institutions are delivering certain quality metrics,
25 they're paying bonuses, cash from a health plan, for
doing a
231
For The Record, Inc.
Waldorf, Maryland
(301)870-8025
1 good job.
2 We have a number of prominent clients -- I see the
3 two-minute sign is up, so -- we have big clients and we're
4 proud of them. I do want to point out that Patient Choice,
5 Luminos, and Destiny Health are all in the defined
6 contribution, defined consumer choice plans.
7 My Quality Coach has information on about 750,000
8 physicians and all of the hospitals in the country. And
it's
9 available via a secure password-protected site.
10 We offer our members an opportunity to rate
11 physicians. This is my -- one of my customs is to put up
on
12 slide that's just not legible. This is it. But you can
see
13 that there is a questionnaire that you can fill out, and
14 immediately upon completing the questionnaire, you can
see
15 satisfaction rankings for your physician compared to
other
16 physicians in the plan and other physicians in that same
17 specialty.
18 We, in addition to providing access to information
19 about how to find the best qualified physician and
hospital,
20 provide some personal health information tools, health
risk
21 assessments and health guides, that can help you better
22 understand your circumstances and prepare for your
23 interactions with the system.
24 Time is very short, so I'm going to go ahead and
25 skip over a couple of these. And I want to jump to, at
the
232
For The Record, Inc.
Waldorf, Maryland
(301)870-8025
1 very end here, a couple of things on -- the impact of this
2 kind of information on the providers and the hospitals
3 themselves.
4 We work very closely with the Pennsylvania Health
Care Cost Containment Council, or PHC45 . And they have
6 published a number of studies over the years. They got a
lot
7 of attention in 1998 around a study regarding coronary
artery
8 bypasses in Pennsylvania and the associated report cards
that
9 emanated from that study.
10 David Nash, prior to the formation of our company,
11 was quoted in the Wall Street Journal pointing out that
the
12 great thing about the report cards is it tells
institutions
13 where to start looking. It's a place to start looking at
14 performance and what to do about it. One of the surgeons
at
15 Lehigh Valley Hospital admits that they're under a
16 microscope, and says it's a good thing. It's causing them
to
17 move forward.
18 In the interest of time, we'll jump over these
19 statistics. But I do want to point out that the public
20 dissemination of performance data has had a very positive
21 impact in Pennsylvania. You can see that in the ten years
22 concluding in the year 2000, there's been a pretty
dramatic
23 decrease in mortality surrounding coronary artery
bypasses.
24 This has also been demonstrated in other disease
25 states and other procedures, where the impact of
revealing
233
For The Record, Inc.
Waldorf, Maryland
(301)870-8025
1 this performance data has had a very positive impact on
the
2 actual performance of the physicians themselves.
3 And I'll end with the last one from a fellow you
4 might know of, Dan Rather. "When it comes to choosing a
5 heart surgeon, Pennsylvania is on the cutting edge in
helping
6 consumers pick the right one."
7 So we like the idea of making information
8 available. We think it has a good impact on the
institutions
9 themselves. And we think it's a trend that consumers are
10 continuing to demand. Thank you very much.
11 MS. KOHRS: Thank you, John.
http://d.scribd.com/docs/1tgookcmufnftkinnmw4.pdf
 Environmental, Health, and Safety Guidelines
PHOSPHATE FERTILIZER PLANTSMANUFACTURING
WORLD BANK GROUP

Environmental, Health and Safety Guidelines

for Phosphate Fertilizer Manufacturing

Introduction capacity of the environment, and other project factors, are

The Environmental, Health, and Safety (EHS) Guidelines are
technical reference documents with general and industry-
specific examples of Good International Industry Practice
(GIIP) 1. When one or more members of the World Bank Group
are involved in a project, these EHS Guidelines are applied as
required by their respective policies and standards. These
industry sector EHS guidelines are designed to be used
together with the General EHS Guidelines document, which
provides guidance to users on common EHS issues potentially
applicable to all industry sectors. For complex projects, use of
multiple industry-sector guidelines may be necessary. A
complete list of industry-sector guidelines can be found at:
www.ifc.org/ifcext/enviro.nsf/Content/EnvironmentalGuidelines
taken into account. The applicability of specific technical
recommendations should be based on the professional opinion
of qualified and experienced persons.
When host country regulations differ from the levels and
measures presented in the EHS Guidelines, projects are
expected to achieve whichever is more stringent. If less
stringent levels or measures than those provided in these EHS
Guidelines are appropriate, in view of specific project
circumstances, a full and detailed justification for any proposed
alternatives is needed as part of the site-specific environmental
assessment. This justification should demonstrate that the
choice for any alternate performance levels is protective of
human health and the environment.

The EHS Guidelines contain the performance levels and Applicability

measures that are generally considered to be achievable in new
facilities by existing technology at reasonable costs. Application The EHS Guidelines for Phosphate Fertilizer Manufacturing
includes information relevant to facilities that produce
of the EHS Guidelines to existing facilities may involve the
phosphoric acid, single superphosphate (SSP),
establishment of site-specific targets, with an appropriate
triplesuperphosphate (TSP), and compound fertilizers (NPK).
timetable for achieving them.
Annex A contains a description of industry sector activities. This
The applicability of the EHS Guidelines should be tailored to document is organized according to the following sections:
the hazards and risks established for each project on the basis
Section 1.0 — Industry-Specific Impacts and Management
of the results of an environmental assessment in which site-
Section 2.0 — Performance Indicators and Monitoring
specific variables, such as host country context, assimilative Section 3.0 — References and Additional Sources
Annex A — General Description of Industry Activities
1
Defined as the exercise of professional skill, diligence, prudence and foresight
that would be reasonably expected from skilled and experienced professionals
engaged in the same type of undertaking under the same or similar
circumstances globally. The circumstances that skilled and experienced
professionals may find when evaluating the range of pollution prevention and
control techniques available to a project may include, but are not limited to,
varying levels of environmental degradation and environmental assimilative
capacity as well as varying levels of financial and technical feasibility.

APRIL 30, 2007 1

 Environmental, Health, and Safety Guidelines
PHOSPHATE FERTILIZER PLANTSMANUFACTURING
WORLD BANK GROUP

1.0 Industry-Specific Impacts fuels and resulting in significant generation of greenhouse

gases. The nitrophosphate production route requires the use of
and Management
CO2. Recommendations for the management of GHGs, in
The following section provides a summary of EHS issues
addition to energy efficiency and conservation, are addressed in
associated with phosphate fertilizer plants, which occur during
the General EHS Guidelines.
the operational phase, along with recommendations for their
management. Recommendations for the management of EHS
Process Emissions – Phosphoric Acid Production
issues common to most large industrial facilities during the
Two different production processes can be used in the
construction and decommissioning phases are provided in the
manufacture of phosphoric acid:
General EHS Guidelines.
• The wet process, which is the most commonly used in
1.1 Environment fertilizer plants, where phosphate rocks are digested with

Environmental issues associated with phosphate fertilizer plants an acid (e.g. sulfuric, nitric or hydrochloric acid). The tri-

include the following: calcium phosphate from the phosphate rock reacts with
concentrated sulfuric acid to produce phosphoric acid and
• Air emissions calcium sulfate (an insoluble salt); and
• Wastewater • The thermal process, where elemental phosphorous is
• Hazardous materials produced from phosphate rock, coke, and silica in an
• Wastes electrical resistance furnace and is then oxidized and
• Noise hydrated to form the acid. Thermal-generated acid is highly
purified, but also expensive, and hence produced in small
Air Emissions quantities, mainly for the manufacture of industrial
Combustion Source Emissions phosphates;
Exhaust gas emissions produced by the combustion of gas or
Process emissions include gaseous fluorides in the form of
diesel in turbines, boilers, compressors, pumps and other
hydrofluoric acid (HF) and silicon tetrafluoride (SiF4), released
engines for power and heat generation, are a source of air
during the digestion of phosphate rock, which typically contains
emissions from phosphate fertilizer manufacturing facilities.
2-4 percent fluorine.
Guidance for the management of small combustion source
emissions with a capacity of up to 50 megawatts thermal
The emissions typically associated with the thermal production
(MWth), including air emission standards for exhaust emissions,
process of phosphoric acid include phosphate, fluoride, dust,
is provided in the General EHS Guidelines. Guidance for the
cadmium (Cd), lead (Pb), zinc (Zn), and radionuclides (Po-210
management of energy conservation, which can significantly
and Pb-210). Dust emissions, containing water-insoluble
contribute to the reduction of emissions related to energy
fluoride, may occur during the unloading, storage, handling and
production, is also presented in the General EHS Guidelines.
Production of phosphate fertilizers is an energy intensive
process typically requiring significant use of energy from fossil

APRIL 30, 2007 2

 Environmental, Health, and Safety Guidelines
PHOSPHATE FERTILIZER PLANTSMANUFACTURING
grinding of the phosphate rock, which is transferred to storage
and grinding sections by conveyor belts or trucks2.
Recommended emission prevention and control measures
include the following:
• Properly select the phosphate rock (in terms of P2O5-
content, F-content, CaO/ P2O5 ratio, and physical quality)
to minimize the amount of acid required in the wet
production process, reduce emissions into the environment
and increase the possibility of phosphogypsum reuse;
• Select proper size of screens and mills (e.g. roller or chain
mills);
• Use covered conveyor belts and indoor storage;
• Apply good housekeeping measures (e.g. frequently
cleaning / sweeping facility surfaces and the quay);
• Recover dust from phosphate rock grinding through use of
properly operated and maintained fabric filters, ceramic
filters, and / or cyclones;
• Treat gaseous fluoride emissions using scrubbing systems
(e.g. void spray towers, packed beds, cross-flow venture,
and cyclonic column scrubbers). Fluorine is recovered as
fluosilicic acid, from which silica is removed through
filtration. A diluted solution of fluosilicic acid (H2SiF6) may
be used as the scrubbing liquid. Recovering of H2SiF6 is
an additional possibility for fluoride emission reduction.
Process Emissions – Superphosphate Phosphate
Fertilizer Production
Dust emissions may be generated during unloading, handling,
grinding, and curing of phosphate rock, in addition to granulation
and crushing of superphosphates. Emissions of gaseous
hydrofluoric acid (HF), silicon tetrafluoride (SiF4), and chlorides
may also generated from acidulation, granulation and drying.
Ammonia (NH3) and nitrogen oxides (NOx) may be generated
2 IPPC BREF (2006) and EFMA (2000a)
APRIL 30, 2007
WORLD BANK GROUP
during the drying and neutralization phases of ammonium nitrate
fertilizers. In addition, during the reaction of phosphate rock with
acid, limited amounts of organic compounds (including
mercaptans), present in the phosphate rock, are released and
may cause odor.3
Phosphate rock dust emissions should be prevented and
controlled through similar measures to those discussed in the
phosphoric acid production section. Additional emission
prevention and control measures include the following:
• Use of direct granulation may reduce the levels of fugitive
emissions compared with curing emissions from indirect
granulation. If indirect granulation is used, the curing
section should be an indoor system with vents connected
to a scrubbing system or to the granulation section;
• Use of plate bank product cooling systems to reduce air
flow requirements (e.g. instead of rotary drums or fluid bed
coolers);
• Consider use of fabric filters or high efficiency cyclones
and/or fabric filters rather than a wet scrubbing system to
treat exhaust air from neutralization, granulation, drying,
coating and product coolers and equipment vents, in order
to avoid creation of additional wastewater. Filtered air
should be recycled as dilution air to the dryer combustion
system;
• Emissions from granulation should be minimized through
application of surge hoppers to product size distribution
measurement systems for granulation recycle control.
Process Emissions – Compound Fertilizer Production
NPK fertilizers are typically produced from mixed acids or
nitrophosphate. Air emissions from NPK produced using the
mixed acids route include ammonia emissions from the
ammonization reactors; nitrogen oxides (NOX), mainly NO and
3 IPPC BREF. October 2006
3
 Environmental, Health, and Safety Guidelines
PHOSPHATE FERTILIZER PLANTSMANUFACTURING
NO2 with some nitric acid, from phosphate rock digestion in nitric
acid; fluorides from the phosphate rock reactions; aerosol
emissions, including ammonium nitrate (NH4NO3), ammonium
fluoride (NH4F), and ammonium chloride (NH4Cl), formed in the
gas-phase neutralization reaction between ammonia and acidic
components, as well as by sublimation from the boiling reaction
mixture; and fertilizer dust originating from drying and cooling
drums, and from other sources (e.g. screens, crushers, and
conveyors).
Air emissions from NPK produced using the nitrophosphate
route are similar to those discussed for the mixed acids route,
however they also include aerosol emissions (e.g. from the
dryer and granulator) of ammonium chloride (NH4Cl), originating
from the reaction of ammonia and hydrogen chloride (HCl) when
potassium chloride (KCl) is added to the powder.4 Other
significant air emissions include ammonia from the
neutralization of nitrophosphoric acid. Ammonia emissions may
also be generated from the calcium nitrate tetrahydrate (CNTH,
empirical formula: Ca(NO3)2*4H2O) conversion section, the
ammonium nitrate (AN, empirical formula: NH4NO3) evaporation
section, and the granulation or prilling sections. Aerosols of
ammonium nitrate may also be formed during the different
production steps, and emissions of hydrogen chloride (HCl) may
be present in the exhaust gases from drum granulators,
cyclones, and scrubber systems.5
Recommended measures to prevent and control air emissions
include the following:
• Reduce NOX emission from nitric acid use in phosphate
rock digestion by controlling the reactor temperature,6
optimizing the rock / acid ratio, and adding urea solution;
4 These emissions can cause the so-called “Tyndall-effect” creating a blue mist
at the stack.
5 EIPPCB BREF (2006) and EFMA (2000b,c)
6
High temperature leads to excessive NOX formation.
APRIL 30, 2007
WORLD BANK GROUP
• Treat gases from the digestion reactor in a spray tower
scrubber to recover NOX and fluorine compounds. The pH
may be adjusted by the addition of ammonia;
• Reduce NOx and odor emissions by selecting high grade
phosphate rock with low contents of organic compounds
and ferrous salts;
• Control particulate matter emissions, as discussed in the
phosphoric acid production section;
• Prevent and / or control emissions from granulation and
product cooling include:
o Scrubbing of gases from the granulator and the dryer
in venturi scrubbers with recirculating ammonium
phosphate or ammonium sulfo-phosphate solution;
o Discharge of scrubbed gases through cyclonic
columns irrigated with an acidic solution;
o Use of high efficiency cyclones to remove particulates
from dryer gases prior to scrubbing;
o Recycling of the air coming from the cooling
equipment as secondary air to the dryer after de-
dusting;
o Treating ammonia emissions by scrubbing with acidic
solutions;
• Fluoride emissions should be controlled through scrubbing
systems, as discussed for phosphoric acid production;
• Emissions to air from phosphate rock digestion, sand
washing and CNTH filtration should be reduced by applying
appropriate controls (e.g. multistage scrubbing, conversion
into cyanides);
• Ammonia in off-gases from the nitrophosphoric
neutralization steps should be removed through counter-
current scrubbers, with pH adjustment to most efficient
scrubbing condition (pH 3-4), with a mixture of HNO3
and/or H2SO4;
• Ammonia emissions from the granulation / drying sections
should be treated by scrubbing with acidic solutions;
4
 Environmental, Health, and Safety Guidelines
PHOSPHATE FERTILIZER PLANTSMANUFACTURING
• Minimize contact between wastes containing NOX and NH3
to prevent aerosol formation in NPK nitrophosphate route;
• Reduce aerosol emission by installing cyclones and
scrubbers;
• Reduce fluorides emissions by recycling of warm air.
Fugitive Emissions
Fugitive emissions are primarily associated with operational
leaks from tubing, valves, connections, flanges, packings, open-
ended lines, floating roof storage tank and pump seals, gas
conveyance systems, compressor seals, pressure relief valves,
tanks or open pits/containments, and loading and unloading
operations of products.
Recommended measures for reducing the generation of fugitve
emissions include:
• Selection of appropriate valves, flanges, fittings during
design, operation, and maintenance;
• Implementation of monitoring, maintenance, and repair
programs, particularly in stuffing boxes on valve stems and
seats on relief valves, to reduce or eliminate accidental
releases;
• Installation of leak detection and continuous monitoring in
all sensitive areas;
• Use of open vents in tank roofs should be avoided by
installing pressure relief valves. All storages and unloading
stations should be provided with vapor recovery units.
Vapor processing systems may consist of different
methods, such as carbon adsorption, refrigeration,
recycling collecting and burning.
Wastewater
Effluents – Phosphoric Acid Production
Effluents from phosphoric acid plants consist of discharges from
the vacuum cooler condensers and the gas scrubbing systems
APRIL 30, 2007
WORLD BANK GROUP
used for condensation and cleaning of vapors from process
operations. Condensed acidic vapors may contain fluorine and
small amounts of phosphoric acid. Water from the slurry used to
transport phosphogypsum, the by-product from wet phosphoric
acid production, may be released as effluent if it is not
recirculated back into the process. Emissions to water for the
disposal of gypsum may contain a considerable amount of
impurities, such as phosphorus and fluorine compounds,
cadmium and other heavy metals, and radionuclides. Drainage
from material stockpiles may contain heavy metals (e.g. Cd,
mercury [Hg], and Pb),fluorides, and phosphoric acid. Specific
emissions to water from the thermal process of phosphoric acid
production may include phosphorus and fluorine compounds,
dust, heavy metals, and radionuclides (e.g., Po-210 and Pb-
210). Recommended effluents management measures include
the following:7
• Select phosphate rock with low levels of impurities to
produce clean gypsum and reduce potential impacts from
disposal of gypsum;
• Consider dry systems for air pollution abatement (versus
wet scrubbing) to reduce wastewater generation. To
reduce fluoride emissions, the installation of scrubbers with
suitable scrubber liquids may be necessary;
• Recover fluorine released from the reactor and evaporators
as a commercial by-product (fluosilicic acid);
• Scrubber liquors should be disposed of after neutralization
with lime or limestone to precipitate fluorine as solid
calcium fluoride, if the fluorine is not to be recovered;
• Recycle water used for the transport of phosphogypsum
back into the process following a settling step;
• Where available, consideration should be given to use
seawater as scrubbing liquid, to facilitate reaction of
fluorine to harmless calcium fluoride;
7 IPPC BREF (2006) and EFMA (2000a)
5
 Environmental, Health, and Safety Guidelines
PHOSPHATE FERTILIZER PLANTSMANUFACTURING
• Minimize contamination of the scrubber effluent with
phosphorus pentoxide (P2O5) by conveying vapors from
vacuum flash coolers and vacuum evaporators to a
separator to remove phosphoric acid droplets;
• Minimize contamination of the scrubber effluent with
phosphorus pentoxide P2O5 using entrainment separators.
Additional phosphate removal can be achieved by applying
magnesium ammonium phosphate (struvite) or by calcium
phosphate precipitation;
• Consider decadmation of H3PO4 up to 95% by reactive
extraction with an organic solvent.
Effluents - Superphosphate Fertilizer Production
The main source of wastewater in phosphate fertilizer
production is the wet scrubbing systems to treat off-gases.
Contaminants may include filterable solids, total phosphorus,
ammonia, fluorides, heavy metals (e.g. Cd, Hg, Pb), and
chemical oxygen demand (COD). Recycling of scrubber liquids
back into the process should be maximized. Production of
acidulated phosphate rock (PAPR), a fertilizer product
consisting of a mixture of superphosphate and phosphate rock,
in addition to superphosphate (SSP), and triplesuperphosphate
(TSP) products can reduce wastewater volumes8.
Effluents - Compound Fertilizer Production
Effluents are usually limited from NPK mixed acids route
facilities, mainly consisting of wastewater from granulation and
exhaust gas scrubbing.
Effluent from NPK facilities employing the nitrophosphate route
may contain ammonia, nitrate, fluoride and phosphate.
Ammonia is found in the effluents of the condensates of the
ammonium nitrate evaporation or the neutralization of the nitro
phosphoric acid solution. Solutions containing ammonium nitrate
8 9
IPPC BREF (2006)
APRIL 30, 2007
WORLD BANK GROUP
must be pumped with care to limit the risks of explosions. The
main sources of nitrate and fluoride levels in effluent are the
scrubber liquors from phosphate digestion and sand (removed
from the process slurry) washing. Washing of sand also
generates phosphate content in the effluent.
Recommended effluent management measures include the
following9:
• Recycle the sand washing liquor to reduce phosphate
levels in wastewater effluents;
• Avoid co-condensation of vapors from ammonium nitrate
evaporation;
• Recycle NOX scrubber liquor to reduce ammonia, nitrate,
fluoride and phosphate levels;
• Recycle liquors resulting from scrubbing of exhaust gases
from neutralization;
• Consider reusing effluents as scrubber medium;
• Treat multi-stage scrubbing liquors, after circulation,
through settling (separation of solids), and recycle the
thickened portion back to the reactors.
• Consider combined treatment of exhaust gases from
neutralization, evaporation and granulation. This enables a
recycling of all scrubber liquids to the production process
and reduce waste water generation;
• Treat waste water through a biological treatment with
nitrification/denitrification and precipitation of phosphorous
compounds.
Process Wastewater Treatment
Techniques for treating industrial process wastewater in this
sector include filtration for separation of filterable solids; flow
and load equalization; sedimentation for suspended solids
reduction using clarifiers; phosphate removal using physical-
chemical treatment methods; ammonia and nitrogen removal
IPPC BREF (2006) and EFMA (2000b,c)
6
 Environmental, Health, and Safety Guidelines
PHOSPHATE FERTILIZER PLANTSMANUFACTURING
using physical-chemical treatment methods; dewatering and
disposal of residuals in designated waste landfills. Additional
engineering controls may be required for (i) fluoride removal and
(ii) advanced metals removal using membrane filtration or other
physical/chemical treatment technologies
Management of industrial wastewater and examples of
treatment approaches are discussed in the General EHS
Guidelines. Through use of these technologies and good
practice techniques for wastewater management, facilities
should meet the Guideline Values for wastewater discharge as
indicated in the relevant table of Section 2 of this industry sector
document.
Other Wastewater Streams & Water Consumption
Guidance on the management of non-contaminated wastewater
from utility operations, non-contaminated stormwater, and
sanitary sewage is provided in the General EHS Guidelines.
Contaminated streams should be routed to the treatment system
for industrial process wastewater. Recommendations to reduce
water consumption, especially where it may be a limited natural
resource, are provided in the General EHS Guidelines.
Hazardous Materials
Phosphate fertilizer manufacturing plants use, store, and
distribute significant amounts of hazardous materials (e.g. acids
and ammonia). Recommended practices for hazardous material
management, including handling, storage, and transport, are
presented in the General EHS Guidelines. Manufacture and
distribution of materials should be conducted according to
applicable international requirements where applicable.10
Wastes
Non-hazardous solid wastes may be generated from some
phosphate fertilizer manufacturing processes, including
10For example, the Rotterdam Convention on the Prior Informed Consent (PIC)
Procedure for Certain Hazardous Chemicals and Pesticides.
APRIL 30, 2007
WORLD BANK GROUP
phosphogypsum from wet phosphoric acid production, and
quartz sand from NPK production using the nitrophosphate
route. Quartz sand should be separated, washed, and recycled
as a building material. There is limited hazardous waste
generated from the phosphate fertilizer manufacturing
processes. In addition to the industry specific information
provided below, guidance on the management of hazardous and
non-hazardous wastes is provided in the General EHS
Guidelines.
Phosphogypsum
Phosphogypsum is the most significant by-product in wet
phosphoric acid production (approximately 4 - 5 tons of
phosphogypsum is produced for every ton of phosphoric acid,
as P2O5, produced11). Phosphogypsum contains a wide range of
impurities (residual acidity, fluorine compounds, trace elements
such as mercury, lead and radioactive components12). These
impurities and considerable amounts of phosphate might be
released to the environment (soil, groundwater and surface
water).Industry-specific pollution prevention and control
practices include13:
• Depending on its potential hazardousness (e.g. whether it
emits radon) phosphogypsum may be processed to
improve its quality and reused (e.g. as building material).
Possible options include:
o Production of cleaner phosphogypsum from raw
materials (phosphate rock) with low levels of
impurities
o Use of repulping
11 Gypsum contains a wide range of impurities (residual acidity, fluorine
compounds, trace elements such as mercury, lead and radioactive
components). IPPC BREF (2006)
12 Phosphate rock, phosphogypsum and the effluents produced from a
phosphoric acid plant have generally a lower radioac-tivity than the exemption
values given in the relevant international regulations and guidelines (for
example, EU Directive 96/26/EURATOM)
13 IPPC BREF (2006) and EFMA (2000a,b,c)
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• Use of di-hemihydrate recrystallization process with double prevention and control of physical, chemical, biological, and
stage filtration; radiological health and safety hazards described in the General
• If phosphogypsum can not be recycled due to the EHS Guidelines.
unavailability of commercially and technically viable
The most significant occupational health and safety hazards
alternatives, it should be managed as a hazardous or non-
occur during the operational phase of phosphate fertilizer
hazardous industrial waste, depending on its
manufacturing facilities and primarily include:
characteristics, according to the guidance in the General
EHS Guidelines.14 Additional management alternatives
• Process Safety
may include backfilling in mine pits, dry stacking15, and wet
• Chemical hazards
stacking.
• Decomposition, fires and explosions

Noise
Process Safety
Noise is generated from large rotating machines, including
Process safety programs should be implemented, due to
compressors and turbines, pumps, electric motors, air coolers,
industry-specific characteristics, including complex chemical
rotating drums, spherodizers, conveyors belts, cranes, fired
reactions, use of hazardous materials (e.g. toxic, reactive,
heaters, and from emergency depressurization. Guidance on
flammable or explosive compounds), and multi-step reactions.
noise management is provided in the General EHS Guidelines.
Process safety management includes the following actions:
1.2 Occupational Health and Safety
• Physical hazard testing of materials and reactions;
The occupational health and safety issues that may occur during
• Hazard analysis studies to review the process chemistry
the construction and decommissioning of phosphate fertilizer
and engineering practices, including thermodynamics and
manufacturing facilities are similar to those of other industrial
kinetics;
facilities, and their management is discussed in the General
• Examination of preventive maintenance and mechanical
EHS Guidelines.
integrity of the process equipment and utilities;
Facility-specific occupational health and safety issues should be • Worker training;
identified based on job safety analysis or comprehensive hazard • Development of operating instructions and emergency
or risk assessment, using established methodologies such as a response procedures.
hazard identification study [HAZID], hazard and operability study
[HAZOP], or a quantitative risk assessment [QRA]. As a general Chemical Hazards
approach, health and safety management planning should Ammonia and acids vapors, especially HF, are common toxic
include the adoption of a systematic and structured approach for chemicals in phosphate fertilizer plants. Threshold values
associated with specific health effects can be found in
14 The classification of phosphogypsum as a hazardous or non-hazardous internationally published exposure guidelines (see Monitoring
waste may depend on the level of radon emissions of the material. Removal of
this material from stack and subsequent disposal may be subject to specific below). In addition to guidance on chemical exposure provided
regulatory requirements depending on the jurisdiction.
15 It should be noted that dry stacking does not eliminate acid water seepage in the General EHS Guidelines, the following are
except in very arid climates.

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recommendations to prevent and control chemical exposure in
this sector:
• Avoid contact of acids with strong caustic substances. The
resulting reaction is exothermic and may cause splashes;
• Control fluoride gas build up in phosphoric acid storage
tanks;
• Install gas detectors in hazard areas;
• Provide adequate ventilation (e.g. air extraction and
filtration systems) in all areas where products are
produced, stored, and handled;
• Provide training and personal protection equipment for
personnel as described in the General EHS Guidelines.
Decomposition, Fire and Explosions
Decomposition16, fire and explosion hazards may be generated
from slurry pump explosions due to insufficient flow through the
pump or incorrect design; slurry decompositions due to low pH,
high temperature and contaminated raw materials; and
hydrogen gas generation due to phosphoric acid contact with
ferrous metals.
The risk of decomposition, fire and explosion can be minimized
by adopting measures such the following17:
• Inventory of ammonia, nitric and sulfuric acids should be
kept as low as possible. Supply by pipeline is
recommended in integrated chemical complexes;
• NPK fertilizer decomposition hazard should be prevented
through temperature control during production, adjustment
of formulations, and reduction of impurities. Compound
build–up on the inlet vanes in the dryer should be avoided
16 The manufacture, storage and transport of NPK fertilizers may generate a
hazard related to self-sustaining decomposition of fertilizer compounds with
ammonium nitrate at temperatures in excess of 130°C16. Decomposition is
dependant on product grades and formulations, and may release significant
amounts of toxic fumes.
17 EFMA. 2000b,c
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and uniform temperature profile of the air inlet should be
ensured;
• Segregating process areas, storage areas, utility areas,
and safe areas, and adopting of safety distances.
• Implementing well controlled operation and procedures in
avoiding hazardous gas and slurry mixtures;
• NPK storage should be designed according to
internationally recognized guidance and requirements18.
Adequate fire detection and fighting system should be
installed.
• Storage areas should be cleaned before any fertilizer is
introduced. Spillage should be cleared up as soon as
practicable. Fertilizer contamination with organic
substances during storage should be prevented; and
• Fertilizers should not be stored in proximity of sources of
heat, or in direct sunlight or in conditions where
temperature cycling can occur.
• Contact of phosphoric acid with ferrous metal component
should be prevented. Stainless steel should be used for
components possibly in contact with the acid.
1.3 Community Health and Safety
Guidance on the management of community health and safety
impacts during the construction and decommissioning phases
common to those of other large industrial facilities are discussed
in the General EHS Guidelines.
The most significant community health and safety hazards
during the operation of phosphate fertilizers facilities relate to
the management, storage and shipping of hazardous materials
and products, with potential for accidental leaks / releases of
toxic and flammable gases, and the disposal of wastes (e.g.
phosphogypsum, off-spec products, sludge). Plant design and
18 See for example the EC Fertilizer Directives EC 76/116 and EC 80/876 and
the COMAH Directive 96/82/EC.
9
 Environmental, Health, and Safety Guidelines
PHOSPHATE FERTILIZER PLANTSMANUFACTURING
operations should include safeguards to minimize and control
hazards to the community, including the following measures:
• Identify reasonable design leak scenarios;
• Assess the effects of potential leaks on surrounding areas,
including groundwater and soil pollution;
• Assess potential risks arising from hazardous material
transportation and select the most appropriate transport
routes to minimize risks to communities and third parties;
• Select plant location with respect to the inhabited areas,
meteorological conditions (e.g. prevailing wind directions),
and water resources (e.g., groundwater vulnerability).
Identify safe distances between the plant area, especially
the storage tank farms, and the community areas;
• Identify prevention and mitigation measures required to
avoid or minimize community hazards;
• Develop an Emergency Management Plan with the
participation of local authorities and potentially affected
communities.
Guidance on the transport of hazardous materials, the
development of emergency preparedness and response plans,
and other issues related to community health and safety is
discussed in the General EHS Guidelines.
2.0 Performance Indicators and
Monitoring
2.1 Environment
Emissions and Effluent Guidelines
Tables 1 and 2 present emission and effluent guidelines for this
sector. Guideline values for process emissions and effluents in
this sector are indicative of good international industry practice
as reflected in relevant standards of countries with recognized
regulatory frameworks. The guidelines are assumed to be
achievable under normal operating conditions in appropriately
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designed and operated facilities through the application of
pollution prevention and control techniques discussed in the
preceding sections of this document.
Effluent guidelines are applicable for direct discharges of treated
effluents to surface waters for general use. Site-specific
discharge levels may be established based on the availability
and conditions in use of publicly operated sewage collection and
treatment systems or, if discharged directly to surface waters,
on the receiving water use classification as described in the
General EHS Guidelines. These levels should be achieved,
without dilution, at least 95 percent of the time that the plant or
unit is operating, to be calculated as a proportion of annual
operating hours. Deviation from these levels in consideration of
specific, local project conditions should be justified in the
environmental assessment.
Combustion source emissions guidelines associated with
steam- and power-generation activities from sources with a
capacity equal to or lower than 50 MWth are addressed in the
General EHS Guidelines with larger power source emissions
addressed in the Thermal Power EHS Guidelines. Guidance
on ambient considerations based on the total load of emissions
is provided in the General EHS Guidelines.
Environmental Monitoring
Environmental monitoring programs for this sector should be
implemented to address all activities that have been identified to
have potentially significant impacts on the environment, during
normal operations and upset conditions. Environmental
monitoring activities should be based on direct or indirect
indicators of emissions, effluents, and resource use applicable
to the particular project. Monitoring frequency should be
sufficient to provide representative data for the parameter being
monitored. Monitoring should be conducted by trained
individuals following monitoring and record-keeping procedures
and using properly calibrated and maintained equipment.
10
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WORLD BANK GROUP

Monitoring data should be analyzed and reviewed at regular purposes only and individual projects should target continual
intervals and compared with the operating standards so that any improvement in these areas.
necessary corrective actions can be taken. Additional guidance
on applicable sampling and analytical methods for emissions Table 3. Resource and Energy Consumption
and effluents is provided in the General EHS Guidelines. Industry
Product Unit
Benchmark
Table 1. Air Emissions Guidelines for Phosphoric Ton phosphate 2.6-3.5 (1)
Phosphate Fertilizers Plants Acid rock/ton P2O5

Pollutant Units Guideline Value Ton H2SO4/ton P2O5 2.1-2.3 (1)

Phosphoric Acid Plants KWh/ton P2O5 120-180 (1)

Fluorides (gaseous) as HF mg/Nm 3 5 m3 cooling water/ton 100-150 (1)

Particulate Matter mg/Nm 3 50 P2O5

Phosphate Fertilizer Plants NPK A KWh/ton NPK 30-33 (1)(2)

Fluorides (gaseous) as HF mg/Nm 3 5
Total energy for drying 300-320 (1)(2)
Particulate Matter mg/Nm 3 50
MJ/ton NPK
Ammonia mg/Nm 3 50
HCl mg/Nm 3 30 NPK B KWh/ton NPK 50 (1)(2)
500 nitrophosphate unit
NOX mg/Nm 3
70 mix acid unit Total energy for drying 450 (1)(2)
MJ/ton NPK

NPK C KWh/ton NPK 50-109 (2)

Table 2. Effluents Guidelines for Phosphate
NPK C m3 cooling water/ton 17 (2)
Fertilizer Plants NPK

Pollutant Units Guideline Value NPK C Ton CO2 required/ton 1(1)(2)

P2O5
pH S.U. 6-9
Total Phosphorus mg/L 5 SSP KWh/ton SSP 19-34 (2)
mg/L 20
kg/ton NPK 0.03 SSP m3 water/ton SSP 0.1-2 (2)
Fluorides kg/ton
Phosphorus oxide 2 Notes:
(P2O5) NPK PLANTS A Granulation with a Pipe Reactor and Drum with ammoniation
NPK PLANTS B Mixed Acids Process
TSS mg/L 50
NPK PLANTS C Nitrophosphate Process
Cadmium mg/L 0.1 1. European Fertilizer Manufacturers Association (EFMA). 2000.
Total Nitrogen mg/L 15 2. EU IPPC - Reference Document on Best Available Tec hniques in Large Volume
Inorganic Chemicals – Ammonia, Acids and Fertilizers Industries. December
Ammonia mg/L 10
2006
Total Metals mg/L 10

Resource Use and Energy Consumption,

Emission and Waste Generation
Table 3 provides examples of resource consumption indicators
for energy and water in this sector. Table 4 provides examples
of emission and waste generation indicators in this sector.
Industry benchmark values are provided for comparative

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 Environmental, Health, and Safety Guidelines
PHOSPHATE FERTILIZER PLANTSMANUFACTURING
WORLD BANK GROUP

Governmental Industrial Hygienists (ACGIH),19 the Pocket

Table 4. Emissions, Effluents and Waste
Generation Guide to Chemical Hazards published by the United States

Industry National Institute for Occupational Health and Safety (NIOSH),20

Parameter Unit
Benchmark Permissible Exposure Limits (PELs) published by the

Phosphoric acid plants Occupational Safety and Health Administration of the United

Fluoride SO2 mg/Nm 3kg/ton HF 5–300.001 – 0.01 States (OSHA),21 Indicative Occupational Exposure Limit Values

Solid Waste Generation ton/ton P2O5 3.2/4-5 (1) published by European Union member states,22 or other similar
(phosphogypsum) sources.
(thermal/wet process)
NPK Production – Nitrophosphate Process
Accident and Fatality Rates
NH3 air emissions kg/ton P2O5 0.2
Projects should try to reduce the number of accidents among
NOX (as NO2) air kg/ton P2O5 1.0
emissions project workers (whether directly employed or subcontracted) to
Fluoride airFluorides air kg/ton P2O5 0.01 a rate of zero, especially accidents that could result in lost work
emissions
time, different levels of disability, or even fatalities. Facility rates
Total nitrogen effluents kg/ton P2O5 0.001 – 0.01
may be benchmarked against the performance of facilities in this
P2O5 effluents kg/ton P2O5 1.2
sector in developed countries through consultation with
Fluorides effluents kg/ton P2O5 0.7
published sources (e.g. US Bureau of Labor Statistics and UK
NPK Production – Mixed Acids Process
Health and Safety Executive)23.
NH3 emissions kg/ton NPK 0.2

NOX (as NO2) emissions kg/ton NPK 0.3

Occupational Health and Safety Monitoring
Fluorides emissions kg/ton NPK 0.02
The working environment should be monitored for occupational
Dust emissions kg/ton NPK 0.2
hazards relevant to the specific project. Monitoring should be
Total nitrogen effluents kg/ton NPK 0.2
designed and implemented by accredited professionals24 as part
Fluorides effluents kg/ton NPK 0.03
of an occupational health and safety monitoring program.
Fluorides air emissions mg/Nm 3 0.4-4
Facilities should also maintain a record of occupational
Dust air emissions mg/Nm 3 30-50 accidents and diseases and dangerous occurrences and
Chloride air emissions mg/Nm 3 19-20 accidents. Additional guidance on occupational health and
safety monitoring programs is provided in the General EHS
2.2 Occupational Health and Safety Guidelines.
Performance
Occupational Health and Safety Guidelines 19 Available at: http://www.acgih.org/TLV/ and http://www.acgih.org/store/
20 Available at: http://www.cdc.gov/niosh/npg/
Occupational health and safety performance should be 21 Available at:

evaluated against internationally published exposure guidelines, http://www.osha.gov/pls/oshaweb/owadisp.show_document?p_table=STANDAR

DS&p_id=9992
22 Available at: http://europe.osha.eu.int/good_practice/risks/ds/oel/
of which examples include the Threshold Limit Value (TLV®) 23 Available at: http://www.bls.gov/iif/ and

occupational exposure guidelines and Biological Exposure http://www.hse.gov.uk/statistics/index.htm

24 Accredited professionals may include Certified Industrial Hygienists,

Indices (BEIs®) published by American Conference of Registered Occupational Hygienists, or Certified Safety Professionals or their
equivalent.

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 Environmental, Health, and Safety Guidelines
PHOSPHATE FERTILIZER PLANTS
WORLD BANK GROUP

3.0 References and Additional Sources

European Commission. 2006. European Integrated Pollution Prevention and
Control Bureau (EIPPCB). Reference Document on Best Available Techniques
in Large Volume Inorganic Chemicals – Ammonia, Acids and Fertilizers. Seville:
EIPPCB. Available at http://eippcb.jrc.es/pages/FActivities.htm
European Fertilizer Manufacturer’s Association (EFMA). 2000a. Best Available
Techniques (BAT) Production of Phosphoric Acid (Booklet No. 4). Brussels:
EFMA. Available at http://www.efma.org/Publications/
EFMA. 2000b. BAT Production of NPK Fertilizers by the Nitrophosphate Route
(Booklet No. 7). Brussels: EFMA. Available at http://www.efma.org/Publications/
EFMA. 2000c. BAT Production of NPK Fertilizers by the Mixed Acid Route
(Booklet No. 8). Brussels: EFMA. Available at http://www.efma.org/Publications/
EFMA and International Fertilizer Industry Association (IFA). 1992. Handbook
for the Safe Storage of Ammonium Nitrate Based Fertilizers. Zurich/Paris:
EFMA/IFA. Available at http://www.efma.org/publications/
US EPA. 40 CFR Part 63, National Emission Standards for Hazardous Air
Pollutants for Source Categories: Subpart AA—National Emission Standards for
Hazardous Air Pollutants from Phosphoric Acid Manufacturing Plants.
Washington, DC: US EPA. Available at http://www.epa.gov/epacfr40/chapt-
I.info/
US EPA. 40 CFR Part 418 Fertilizer Manufacturing Point Source Category.
Subpart A—Phosphate Subcategory. Washington, DC: US EPA. Available at
http://www.epa.gov/epacfr40/chapt-I.info/
US EPA. 40 CFR Part 418 Fertilizer Manufacturing Point Source Category.
Subpart G—Mixed and Blend Fertilizer Production Subcategory. Washington,
DC: US EPA. Available at http://www.epa.gov/epacfr40/chapt-I.info/
US EPA. 40 CFR Part 422 Phosphate Manufacturing Point Source Category.
Washington, DC: US EPA. Available at http://www.epa.gov/epacfr40/chapt-
I.info/

German Federal Ministry for the Environment, Nature Conservation and Nuclear
Safety (BMU). 2004. Waste Water Ordinance – AbwV. (Ordinance on
Requirements for the Discharge of Waste Water into Waters). Promulgation of
the New Version of the Waste Water Ordinance of 17 June 2004. Berlin: BMU.
Available at
http://www.bmu.de/english/water_management/downloads/doc/3381.php

German Federal Ministry for the Environment, Nature Conservation and Nuclear
Safety (BMU). 2002. First General Administrative Regulation Pertaining to the
Federal Emission Control Act (Technical Instructions on Air Quality Control – TA
Luft). Berlin: BMU. Available at
http://www.bmu.de/english/air_pollution_control/ta_luft/doc/36958.php

United Kingdom (UK) Environmental Agency. 2002. Sector Guidance Note

Integrated Pollution Prevention and Control (IIPC) S4.03. Guidance for the
Inorganic Chem icals Sector. Bristol: Environment Agency. Available at
http://www.environment-
agency.gov.uk/business/444304/1290036/1290086/1290209/1308462/1245952/

International Fertilizer Industry Association (IFA) / United Nations Environment

Programmme (UNEP) / United Nations Industrial Development Organization
(UNIDO). 1998. The Fertilizer Industry's Manufacturing Processes and
Environmental Issues. (Technical Report No. 26, Part 1). Paris:
IFA/UNEP/UNIDO.

United States (US) Environmental Protection Agency (EPA). 1995. Office of

Compliance. Sector Notebook Project. Profile of the Inorganic Chemical
Industry. Washington, DC: US EPA. Available at
http://www.epa.gov/compliance/resources/publications/assistance/sectors/noteb
ooks/inorganic.html

US EPA. 40 CFR Part 60, Standards of Performance for New and Existing
Stationary Sources: Subpart T—Standards of Performance for the Phosphate
Fertilizer Industry: Wet-Process Phosphoric Acid Plants. Washington, DC: US
EPA. Available at http://www.epa.gov/epacfr40/chapt-I.info/

US EPA. 40 CFR Part 60, Standards of Performance for New and Existing
Stationary Sources: Subpart W—Standards of Performance for the Phosphate
Fertilizer Industry: Triple Superphosphate Plants. Washington, DC: US EPA.
Available at http://www.epa.gov/epacfr40/chapt-I.info/

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Annex A: General Description of Industry Activities
A modern phosphate fertilizer manufacturing complex is
characterized by large volume productions and is normally
highly integrated with upstream (e.g. ammonia, and acids such
as nitric, sulfuric, and phosphoric) and downstream (e.g.
ammonium nitrate and calcium ammonium nitrate) production
with the aim at optimizing production cost, logistics, safety and
environmental protection (Figure A.1). Phosphate fertilizer
plants may produce single (or normal) superphosphate (SSP)
and triple superphosphate (TSP); mixed fertilizers such as
Mono-Ammonium Phosphate (MAP) and Di-Ammonium
Phosphate (DAP); and all grades of compound fertilizers (NPK)
using the nitrophosphate / nitric acid route and the mixed acid /
sulfuric acid route. Facilities are usually equipped with an
integrated steam and electric power distribution grid servicing all
the plants and supplied by a central steam boiler and power
station. A waste water treatment plant is usually present.
Sulfuric Acid
Sulfuric acid (H2SO4) is used in the phosphate fertilizer industry
for the production of phosphoric acid. Sulfuric acid is
manufactured mainly from sulfur dioxide (SO2), produced
through the combustion of elemental sulfur. The exothermic
oxidation of sulfur dioxide over several layers of a suitable
catalyst (e.g. vanadium pentoxide) to produce sulfur trioxide
(SO3) is the most common process in sulfuric acid
manufacturing plants.25
Sulfuric acid is obtained from the absorption of SO3 and water
into H2SO4 (with a concentration of at least 98 percent) in
absorbers installed after multiple catalyst layers. The warm acid
produced is sparged with air in a column or in a tower to collect
25 IPPC BREF (2006)
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the remaining SO2 in the acid. The SO2 laden air is returned to
the process.
Phosphoric Acid
Phosphoric acid (H3PO4) is primarily used in the manufacture of
phosphate salts (e.g. for fertilizers and animal feed
supplements). Two different processes can be used in the
manufacture of phosphoric acid. In the first process, known as
the thermal process, elemental phosphorous is produced from
phosphate rock, coke, and silica in an electrical resistance
furnace and is then oxidized and hydrated to form the acid.
Thermal-generated acid is highly purified, but also expensive,
and hence produced in small quantities, mainly for the
manufacture of industrial phosphates.
The second type of process, known as the wet process, involves
digesting phosphate rocks with an acid (e.g. sulfuric, nitric or
hydrochloric acid). The tri-calcium phosphate from the
phosphate rock reacts with concentrated sulfuric acid to produce
phosphoric acid and calcium sulfate, which is an insoluble salt.
The operating conditions are generally designed so that the
calcium sulfate is precipitated as anhydrite, hemihydrate (HH)
and dihydrate (DH).
Different processes are needed because of different rocks and
gypsum disposal systems.26 The main production steps include
grinding of phosphate rock (if necessary); reaction with sulfuric
acid in a series of separate agitated reactors at a temperature of
70-80°C, filtration to separate the phosphoric acid from the
calcium sulfate; and concentration up to commercial phosphoric
acid with a concentration of 52-54 percent phosphorus
pentoxide (P2O5).
26 EIPPCB BREF (2006) and EFMA (2000a)
14
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PHOSPHATE FERTILIZER PLANTS
When the phosphoric acid plant is linked to a sulfuric acid plant,
the high-pressure steam produced in the waste heat recovery
boiler from the sulfuric acid is normally used to produce electric
power, and the low-pressure exhaust steam is used for
phosphoric acid vacuum concentration. The steam consumption
needed for the concentration can be reduced by using waste
heat originating in the sulfuric acid plant. This may be recovered
as heated water and used in the process of concentrating weak
acid to intermediate concentration. Phosphoric acid is most
commonly stored in rubber-lined steel tanks, although stainless
steel, polyester and polyethylene-lined concrete are also used.
Storage tanks are normally equipped to keep the solids in
suspension to avoid costly cleaning of the tank27.
Phosphate Fertilizers (SSP / TSP)
Phosphate fertilizers are produced by adding acid to ground or
pulverized phosphate rock. If sulfuric acid is used, single or
normal, superphosphate (SSP) is produced, with a phosphorus
content of 16–21 percent as phosphorous pentoxide (P2O5).
SSP production involves mixing the sulfuric acid and the rock in
a reactor. The reaction mixture is discharged onto a slow-
moving conveyor belt. If the reaction The mixture is directly fed
to a granulator, the process is the so called “direct” granulation.
In “indirect” granulation, the reaction mixture is stored for
“curing” for 4 to 6 weeks before bagging and then granulated.28
If phosphoric acid is used to acidulate the phosphate rock, triple
superphosphate (TSP) is produced with a phosphorus content
of 43–48 percent as P2O5. Two processes are used to produce
TSP fertilizers: run-of-pile and granulation. The run-of-pile
process is similar to the SSP process. Granular TSP uses
lower-strength phosphoric acid (40 percent, compared with 50
percent for run-of-pile method). The reaction mixture, a slurry, is
27 EFMA (2000a)
28 EIPPCB BREF (2006)
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sprayed onto recycled fertilizer fines in a granulator. Granules
grow and are then discharged to a dryer, screened, and sent to
storage.29
Compound Fertilizers (NPK)
Compound fertilizers are a large group of products, varying
based on the particular nitrogen / phosphorus / potassium
(N/P/K) ratios. Production processes are also numerous and
product types include PK, NP (e.g. DAP), NK and NPK. This
can be achieved by using two different routes, namely
production by the nitrophosphate route, and production by the
mixed acid route.
Nitrophosphate Route
The integrated nitrophosphate (NP) process produces
compound fertilizers (NPK) containing ammonium nitrate,
phosphate, and potassium salts (Figure A.2). The integrated
process starts with the dissolution of the phosphate rock in nitric
acid. Varying amounts of volatile compounds, such as carbon
dioxide (CO2), nitrogen oxides (NOX) and hydrogen fluoride
(HF), may be emitted, depending on the phosphate rock
characteristics. The resulting digestion solution contains
different amounts of suspended solids (e.g. quartz sand) that
are removed by centrifuges, hydrocyclones or, lamella
separators.30 After washing, the solids can be reused in the
building industry.
The liquor obtained from the process contains calcium ions in a
proportion that too high to guarantee the production of plant
available P2O5. The solution is therefore cooled so that calcium
nitrate tetrahydrate (CNTH) crystallizes out. The solution of
phosphoric acid, remaining calcium nitrate, and nitric acid,
called nitrophosphoric acid, can be separated from the CNTH
29 EIPPCB BREF (2006)
30 EFMA (2000b)
15
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PHOSPHATE FERTILIZER PLANTSMANUFACTURING
crystals by filtration. The nitrophosphoric acid is then neutralized
with ammonia, mixed with potassium / magnesium salts, sulfate
and/or micro-nutrients, and converted to NPK in a rotary
granulation drum, fluidized bed, prilling tower, or pug-mill to
obtain solid compound fertilizers.31
The separated calcium nitrate crystals are dissolved in an
ammonium nitrate solution and treated with an ammonium
carbonate solution. This solution is filtered to remove the
calcium carbonate crystals and it is used for the production of
granular calcium ammonium nitrate (CAN) fertilizer. The
resulting dilute ammonium nitrate solution is concentrated and
also used to produce CAN or NPK. The calcium nitrate solution
may also be neutralized and evaporated to obtain a solid
fertilizer.32
Three types of processes are normally used for the production
of NPK fertilizers from the NP liquor, namely prilling, drum or
pug-mill, and spherodizer granulation. In prilling, NP liquor,
mixed with the required salts and recycled product, overflows
into a rotating prill bucket from which the slurry is sprayed into
the prill tower. Fans at the top of the tower cause ambient air to
flow counter-current to the droplets formed by solidification.33
In drum or pug-mill granulation, the NP liquor, together with
required salts and recycled products, is sprayed into a rotating
drum granulator where granules formed are dried in a rotating
drying drum with hot air. The air leaving the drums contains
water vapor, dust, ammonia and combustion gases. The air
from the granulation and drying drums is treated in high
performance cyclones.34
31 Ibid.
32 Ibid
33 Ibid
34 Ibid
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In spherodizer granulation, the slurry is sprayed into a special
rotating drum, called a spherodizer, where warm air, heated to
300-400°C, flows co-currently thus evaporating the water
building up on granules.35
In all processes, the dry NPK granules are screened. The on-
size fraction passes to the conditioning process, and the over-
size fractions are taken out, crushed and recycled together with
the under-size fractions. The screen, crusher, and conveyor
discharges are de-dusted using the air required for granulation.
The commercial product from the drying and screening is cooled
in a fluidized bed, a bulk flow heat exchanger, or a rotating
drum. Off-gases from these latter stages, containing minor
amounts of dust, and generally no ammonia, are de-dusted in
cyclones. Finally, the product is cooled and coated before
storage, to minimize the subsequent caking of the material. The
coating consists of a treatment with an organic agent and
inorganic powder, added in a drum. The calcium nitrate crystals
from the nitrophosphate process can be processed to a solid
calcium nitrate (CN) fertilizer, using prilling or pan-granulation
technology, as an alternative to the combination of CNTH
conversion and subsequent processing to CAN.36
Mixed Acid Route
Processes applied in the mixed acid route of production are
numerous, the most common including granulation with a pipe
reactor system; drum granulation with ammoniation; and a
mixed acid process with phosphate rock digestion.37 A simplified
flow chart showing the three processes together is presented on
Figure A.3.
Granulation with a pipe reactor system works with a classical
granulation loop with one or two pipe reactors. One pipe reactor
35 Ibid
36 EFMA (2000b)
37
EFMA (2000c)
16
 Environmental, Health, and Safety Guidelines
PHOSPHATE FERTILIZER PLANTSMANUFACTURING
is fitted in the granulator and another may be used in the dryer.
Phosphoric acid or a mixture of phosphoric and sulfuric acids is
neutralized in the pipe reactors with gaseous or liquid ammonia.
A wide range of grades, including ammonium phosphates
(monoammonium phosphate – MAP, and diammonium
phosphate – DAP), can be produced.38 The required solid raw
materials such as potassium chloride, potassium sulfate,
superphosphate, secondary nutrients, micronutrients and filler
are fed into the granulator together with the recycled material.
The pipe reactor fitted in the granulator is designed to receive
phosphoric acid, part of the ammonia, and all the other liquid
feeds such as sulfuric acid and recycled scrubber liquor.
Concentrated ammonium nitrate solution may be added directly
into the granulator and ammoniation rates in the pipe reactor
vary according to the product. Further ammoniation may be
carried out in the granulator. A pipe reactor fitted in the dryer is
fed with phosphoric acid and ammonia.
Drum granulation with ammoniation consists of a classical
granulation loop using mainly solid raw materials. Ammonium
nitrate solution and / or steam is / are fed into the granulator.
The process is very flexible, and is able to produce a broad
spectrum of grades including products with low nitrogen content.
Ammonium nitrate solution is sprayed directly into the granulator
and sulfuric acid may be fed into the granulator followed by
ammoniation39. The granules obtained in both granulation
processes are dried in a drying section using a heated air
stream.40 The dry granules are managed as discussed for the
NP route.
Gases from the granulator and the dryer are scrubbed in venturi
scrubbers with recirculating ammonium phosphate or
ammonium sulfo-phosphate solution. The scrubber liquor which
38 Ibid.
39 EFMA (2000c)
40 Ibid.
APRIL 30, 2007
WORLD BANK GROUP
is being recycled is fed to the pipe reactor in the granulator.
Finally, the gases are vented through cyclonic columns irrigated
with an acidic solution. The gases coming from the dryer are de-
dusted in high efficiency cyclones to remove the majority of the
dust before scrubbing. The air coming from the cooling
equipment is generally recycled as secondary air to the dryer
after de-dusting.41
The mixed acid process with phosphate rock digestion is very
flexible and produces grades with varying degrees of phosphate
water solubility. The first step of the process is the exothermic
digestion of phosphate rock with nitric acid resulting in a solution
of phosphoric acid and calcium nitrate. Acid gases such as
oxides of nitrogen and fluorine compounds are formed during
the digestion, depending on the type of phosphate rock. Other
raw materials such as phosphoric, sulfuric, and nitric acids or
AN solution are added after the digestion. The acid slurry is
ammoniated with gaseous ammonia and after neutralization,
and other components such as ammonium phosphates,
superphosphates, ammonium sulfate, and compounds
containing potassium and magnesium are added. Most of these
materials may also be added before or during neutralization, but
if the raw material contains chloride, the pH of the slurry should
be 5 – 6 to avoid the production of hydrogen chloride. The
reactor battery ends with a buffer tank. The slurry granulation
can then be performed by different equipment such as drum,
blunger and spherodizer.42
The gases from the digestion reactors, where phosphate rock is
digested in nitric acid, are treated separately in a spray tower
scrubber to recover NOX and fluorine compounds. The pH is
adjusted by the addition of ammonia. The ammoniation reactor
gases are scrubbed in several stages of counter-current
41 Ibid.
42 Ibid.
17
 Environmental, Health, and Safety Guidelines
PHOSPHATE FERTILIZER PLANTSMANUFACTURING
WORLD BANK GROUP

scrubbing. The pH is adjusted to the most efficient scrubbing

condition, pH 3-4, with a mixture of HNO3 and/or H2SO4. The
first scrubbing stage ensures a saturation of the gases; the
second high pressure venturi stage is designed to remove
aerosols. The subsequent stages make the recovery efficiency
high and the final stage operates with the cleanest scrubbing
liquid. A droplet separator is installed in the stack or immediately
before it. The gases from the dryer (granulator / dryer) are led
through cyclones before entering the scrubber. The scrubber
consists of a variable throat venturi with subsequent two-stage
scrubbing. The last stage should be operated with the cleanest
liquid. A part of the liquor, after the circulation, goes to a settler
for the separation of solids. The thickened part is fed to the
reactors.43

Figure A.1: Integrated Phosphate Fertilizer Plants

Water Water Sulfur Water Air NH8

Phosphate
rock

H2SO4
Phosphoric Sulfuric Nitric acid
acid acid

H8PO4 NH8 HNO8

Phosphate H2SO4 Phosphate HNO8 Phosphate
rock rock H8PO4 K, rock
H2SO4 Mg, S
NH8

NPK NPK
TSP SSP Mixed acid route Nitrophosphate CO2
route

NPK,
TSP SSP NPK
AN/CAN

43 EFMA (2000c)

APRIL 30, 2007 18

 Environmental, Health, and Safety Guidelines
PHOSPHATE FERTILIZER PLANTSMANUFACTURING
WORLD BANK GROUP

Figure A.2: Compound Fertilizers: Nitrophosphate Route

K,
Mg, S H2SO4 NH8 HNO3 Phosphate NH8
rock

H8PO4
Complex HNO3 Nitrophosphoric
fertilizers acid

Ca(NO8)2

NH8
Calcium nitrate
CO2
conversion

CaCO3
NH4 NO3

Calcium
Calcium nitrate
ammonium
fertilizers nitrate fertilizers

NPK Ca(NO3)2 AN / CAN

APRIL 30, 2007 19

 Environmental, Health, and Safety Guidelines
PHOSPHATE FERTILIZER PLANTSMANUFACTURING
WORLD BANK GROUP

Figure A.3: Mixed Acid Route

Gas
HNO8 Digestion Scrubbing
Phosphate
reactors system Off-gas
rock

Scrubbing
liquid
Gas

AN Ammoniation /
solution Granulation & Cyclones /
NH3 Bag filters
H2SO4 / Pipe reactor /
H3PO4 Granulator
K, Mg, S

Off-spec
Dust

Dusty
Hot air, Dryer / Screener / air General
Coating Cooler & Coating dedusting system Off-gas
agents Gas /
dusty air

NPK

APRIL 30, 2007 20

 Journal of Applied Biomedicine
2: 141–150, 2004
ISSN 1214–0287

REVIEW

Fluorine in medicine
Anna Strunecká1, Jiří Patočka2, Paul Connett3
1
Department of Physiology and Developmental Physiology, Faculty of Sciences, Charles University, Praha,
Czech Republic
2
Department of Toxicology, Military Medical Academy, Hradec Králové and Faculty of Health and Social
Studies, University of South Bohemia, České Budějovice, Czech Republic
3
St. Lawrence University, Canton, New York, USA

Received 4th June 2004.

Published online 28th June 2004.

Summary
Fluoride has long been known to influence the activity of various enzymes in vitro. Latterly it has
been demonstrated that many effects primarily attributed to fluoride are caused by a synergistic
action of fluoride plus aluminum. Fluorinated chemicals are of growing importance, with
applications in medicine. Fluorine substitution has profound effects on the properties of organic
compounds. The very high electronegativity of fluorine can modify electron distribution in the
molecule, affecting its absorption, distribution and metabolism. Fluorine-containing drugs are used in
medicine as anesthetics, antibiotics, anti-cancer and anti-inflammatory agents,
psychopharmaceuticals, and in many other applications. The potential contribution of fluorinating
pharmaceuticals to human fluoride exposure is discussed.

Keywords: fluoride – aluminofluoride complexes – fluorine-containing drugs – health effects

INTRODUCTION Meyerhof, and their coworkers (McClure 1933). The

It is noteworthy that fluorine, which is the most
abundant halogen and the thirteenth most abundant
element in the earth’s crust, was not involved in the
ancient evolution of life on Earth as a regular
component of organic compounds of living
organisms (O'Hagan et al. 2002). All the known
naturally occurring fluoro-organic compounds are
poisonous (Patočka and Cabal 1999). The finding of
fluorine in teeth enamel, ash of blood, and the yolk
and shell of eggs stimulated the search for its
physiological role (McClure 1933, Waldbott et al.
1978). The effects of fluoride were reported in many
enzymatic reactions in research conducted by
prominent biochemists Embden, Lohman, Lipmann,
use of sodium fluoride helped in understanding the
mechanisms of enzyme catalysis in glycolytic and
Krebs-cycle pathways. Laboratory investigations
during the last several decades has produced
evidence that fluoride in the presence of trace
amounts of aluminum ions acts as an analogue of
phosphate groups and stimulates G proteins in cell
signalling cascades.
In addition to laboratory research using isolated
cells/tissues or animal models, many
epidemiological, ecological, and clinical studies
have shown the effects of fluoride on wildlife,
domestic animals, and humans. Most of the ill
effects caused by fluoride were first recognized
among workers in aluminum factories, where
 Strunecká et al.
fluoride and aluminum are present in high
concentrations. The levels of fluoride in the serum,
urine, and hair of these workers are higher than in
the control subjects. Osteoarthritis and related
disorders in industrial workers have been reported
since the 1930´s (McClure 1933, Roholm 1937,
Waldbott et al. 1978). Observation of industrial
fluorosis led to the use of fluoride in medicine as a
treatment to increase bone mass in osteoporosis
patients (Franke 1997).
Seventy years ago a dentist H. Trendley Dean,
working for the U.S. Public Health Service,
examined water from 345 communities in Texas and
claimed that there was a lower incidence of dental
caries in communities having about 1 ppm
(1 milligram per liter) fluoride in the water supply.
Dean's famous 21 City Study (Dean 1942) led to the
concept that fluoride ingestion will harden the
surface of teeth and make them less susceptible to
dental caries. In 1950, before any trials had been
completed, the US Public Health Service (PHS)
endorsed fluoridation of public water supplies. This
practice was initiated later also in many countries all
over the world as a way of preventing dental caries.
Numerous laboratory, clinical, and epidemiological
studies dealing with all aspects of the metabolism,
biological effects, pharmacology, and toxicology of
fluoride have published during the last 50 years. The
information already at hand, however, presents a
number of reasons for the serious assessment of the
risks of fluoride to the human body. Additionally,
people now get fluoride from many other sources,
including foods and beverages prepared with
fluoridated water, pesticide and fertilizer residues,
dental treatments and products. The past 50 years
have seen a dramatic increase in the volume of man-
made industrial fluoride compounds released into
the environment, so total fluoride intake has become
an issue of particular concern (Bryson 2004).
The development of new fluorinating agents and
advancement in organofluorine chemistry has
eminently increased the potential for synthesis of
novel fluorinated drugs and fluorine-containing
compounds with applications in medicine. These
include general anesthetics, antibiotics, antiviral and
antimalarial agents, anti-inflammatory drugs,
antidepressants, antipsychotics, and different bio-
compatible materials. Many of them release fluoride
into body fluids and tissues. Medical schools and
university texts seldom share the scientific details of
fluoride’s physiological and/or toxicological activity.
Because of this situation important questions remain
unanswered and many research avenues unexplored.
The aim of our article is to provide the first
foundation for the assessment of the safety, benefits
and/or risks of fluorine-containing drugs for human
health.
142
MECHANISM OF FLUORIDE EFFECTS IN
LIVING ORGANISMS
Fluoride interactions with enzymes
Fluoride has been found to inhibit the activity of
many important enzymes such as enolase, lipase,
phosphofructokinase, pyruvate kinase, glycogen
synthase, succinate dehydrogenase, cytochrom
oxidase, various phosphatases, ATP-ases, urease,
and cholinesterases, to name a few (Machoy 1981,
Strunecká and Patočka 2002, 2003). The Clinical
Toxicology of Commercial Products (FCDSW 1984)
accounts for the toxic action of fluoride by the fact
that fluoride ions act as enzymatic poisons,
inhibiting enzyme activities and, ultimately,
interrupting metabolic processes. Some enzymes,
such as adenylyl cyclase, lactate dehydrogenase,
glycogen phosphorylase, and many others, are
stimulated by fluoride in milimolar concentrations.
While fluoride in human organism will probably
not reach the concentrations used in laboratory
experiments with isolated cells/tissues, there may be
moments where fluoride ions reach
microenvironments where interference may occur,
especially at the active sites of certain enzymes.
In some cases the biological effects of fluoride
can be realized with the help of any metabolite of
fluoride, e.g. fluoroacetate (Arellano et al. 1997).
Fluoroacetate as well as some higher
ω-fluorocarboxylic acids have been described as the
toxic principle of some poisonous plants (Patocka
and Cabal 1999). Fluoroacetate is toxic because it is
converted in vivo in mitochondria to fluorocitrate,
which occurs through condensation of fluoroacetyl-
CoA with oxaloacetate by the enzyme citrate
synthase, which supplies acetyl-CoA into the citric
acid cycle. Fluorocitrate is a strong inhibitor of
aconitase. The vital biochemical pathway for energy
production in living organisms is thus frozen.
Fluoride synergistic effects with aluminum ions
Another concern is that fluoride forms complex ions
with aluminum ions. Fluoride anions, generally
introduced as NaF solutions, have long been known
to stimulate the activity of adenylyl cyclase and
GTP binding proteins (G proteins). It was later
demonstrated that the effects primarily attributed to
fluoride are caused by synergistic action with
aluminum (Sternweis and Gilman 1981). This fact
had at first been ignored because aluminum is a
normal component of glass from which it is etched
by a solution with fluoride.
In water solutions, aluminum forms in the excess
of fluoride aluminofluoride complexes (AlFx),
 Fluorine in medicine
whose average stoichiometry depends on the
fluoride concentration and the pH of the solution
(Chabre 1990, Strunecká et al. 2002). The ability of
these complexes to simulate phosphate groups in
many biochemical reactions has been documented
by numerous studies. AlFx can bind to proteins by
hydrogen bonds to the fluorine atom, just as to
oxygen atoms of a phosphate ion. Analogies
between the phosphate group and AlFx consist in
atomic and molecular similarities.
The transfer of phosphate groups is the basic
mechanism in the regulation of the activity of
numerous enzymes, energy metabolism, cell
signalling, and regulation of cell growth. In view of
the ubiquity of phosphate in cell metabolism, a
phosphoryl transfer transition state analog represents
a useful tool for laboratory investigations, but also a
strong potential danger for living organisms
including humans (Strunecká and Patočka 2002).
The low cost and availability of these
fluorometallic complexes probably contributed to the
fact that their use as a tool in laboratory studies of
G proteins is widely spread. Heterotrimeric G
proteins mediate the transfer of information from
heptahelical receptors in plasma membrane to
effector molecules (Gilman 1987, Morris and
Malbon 1999). Physiological agonists of G protein-
coupled receptors include neurotransmitters and
hormones, such as dopamine, epinephrine,
norepinephrine, serotonin, acetylcholine, glucagon,
vasopressin, melatonin, TSH, neuropeptides,
opioids, excitatory amino acids, prostanoids,
purines, photons, and odorants. The use of AlFx in
G protein studies brought a great deal of knowledge
about the role of G proteins in cell signalling
(Rodbell 1995). Numerous papers offer evidence
that AlFx influence various functions and
biochemical reactions of all cells and tissues of the
animal or human organisms with powerful
pharmacological efficacy. Fluoride in the presence
of trace amounts of aluminum affects all blood
elements, endothelial cells and blood circulation, the
function of lymphocytes and cells of the immune
system, bone cells, fibroblasts and lung cells, ion
transport in kidneys, calcium homeostasis, processes
of neurotransmission, metabolism of the liver,
growth and differentiation of cells, protein
phosphorylation, and cytoskeletal proteins
(Strunecká and Patočka 1999).
Such evidence is not surprising in respect to the
role of G proteins in signal transduction. It has been
demonstrated that AlFx may clone or potentiate the
action of numerous extracellular signals. Moreover,
the signal of every AlFx molecule is greatly
amplified during the processes of signal transduction
inside the cell. AlFx is therefore efficient in
extremely low (nM) concentrations. The
toxicological potential of fluoride is thus markedly
143
increased in the presence of trace amounts of
aluminum ions (Lubkowska et al. 2002).
FLUORIDE IN THE PREVENTION OF
TEETH CARIES AND DENTAL FLUOROSIS
In 1931, it was determined that the cause of
mottling tooth enamel, now called “dental fluorosis,”
was the presence of fluoride in the water. Because
some early researchers reported less tooth decay in
children with dental fluorosis (Dean 1942), it was
speculated that there might be a level at which
fluoride would protect teeth but not cause too much
fluorosis. However, the largest US survey and a
compilation of studies worldwide
(www.fluoridealert.org)) indicate that somewhere
between 30% and 50% of children in fluoridated
communities have dental fluorosis, and not all of it
in the very mild and mild categories. Thus, dental
fluorosis is now impacting 3–5 times as many
children as intended. There are many discussions
between proponents and opponents of water
fluoridation all over the world. While proponents,
including WHO, describe water fluoridation as “one
of the top ten public health achievements of the
twentieth century” and dismissed any notion of
health concerns, many scientists are concerned about
the risks of increased fluoride supplementation for
human health. Much evidence forces them to
consider whether any dental benefits could justify
potential health risks to so many people. One of the
reasons Dr. Arvid Carlsson (Nobel laureate in
medicine, 2000) gave for leading the successful
campaign against water fluoridation in Sweden was
his concern about what such increased fluoride
levels would do to the developing brain of newborn
infants (Carlsson 1978). In the light of recent
findings concerning fluoride’s potential
neurotoxicity, Carlsson’s concerns have gained
renewed significance (Strunecká and Patočka 2003).
Today, approximately 60–70% of American
people are supplied with fluoridated drinking water.
Worldwide, however, the vast majority of countries
do not support the practice and only Australia,
Columbia, Ireland, New Zealand, and Singapore
have more than 50% of their population drinking
fluoridated water (www.fluoridealert.org).
Nevertheless, the use of fluoride tablets
(0.5 mg NaF) as an efficient way for the prevention
of dental caries is commonly recommended by
official health and dental organizations (WHO,
EAPD).
While an analysis of discussions of fluoride
supplementation has not been the focus of this
review it seems that the reduction in tooth decay
attributed to water fluoridation is very small and
 Strunecká et al.
appears to be neither clinically nor statistically
significant (www.fluoridealert.org). WHO data
available online indicate the same declines in tooth
decay have occurred worldwide in both fluoridated
and non-fluoridated countries over the period from
the 1960’s to 1990’s. Unpurified hexafluorosilicic
acid is the primary chemical now used to fluoridate
public water supplies in the USA. Being able to
convert a hazardous waste material into a saleable
product is very attractive for the phosphate industry.
It would be extremely expensive to send this
material to hazardous waste sites.
Science has already accumulated evidence about
the detrimental effects of fluoride on the living
organism. Numerous published reports bring us at
least strong warnings and a challenge to increased
responsibility before prescription and
recommendation of endogenous administration of
fluoride in various drugs, particularly for children.
BONES AND SKELETAL FLUOROSIS
Caverzasio et al. (1998) have offered a very
plausible mechanism for fluoride’s ability to
stimulate the proliferation of osteoblasts, a
phenomenon exploited in the treatment of patients
with osteoporosis. When fluoride reaches calcified
tissues (like the teeth and bone) it rapidly exchanges
with the hydroxide ion on the calcium hydroxy
apatite crystals, forming calcium fluorapatite:
- -
Ca10(PO4)6(OH)2+2F = Ca10(PO4)6(F)2+2OH
Numerous authors have reported deterioration in the
mechanical properties of fluoride-containing bone
(Bohatyrewicz 1999, www.fluoridealert.org). It
seems that the effects of fluoride on bone quality are
dependent on the balance between the beneficial
effects and deleterious effects, which are influenced
by daily doses and the duration of treatment, and
actual content of fluoride in the bone. In examining
fluoride’s impact on bone in more detail, the
concern only deepens. Fluoride has different effects
on different parts of the bone. It tends to increase
the bone mineral density of trabecular bone (the
mesh-like interior of the bone, which is important
for weight bearing), but decreases the bone mineral
density of cortical bone, the outside layer of the
bone, which is important for resistance to torsional
and sheer stress.
The ability of fluoride to damage children’s
bones, even at low levels of water fluoridation
(1 ppm), was first observed in the 1945–55
fluoridation trial in the USA (Schlesinger et al.
1956). A higher incidence of cortical bone defects
144
was observed in the children in fluoridated
Newburgh (13.5%) than in non-fluoridated Kingston
(6.5%). In a survey of an area in Mexico, which had
naturally high levels of fluoride in the water, the
incidence of bone fractures in both children and
adults increased in a linear fashion with the severity
of dental fluorosis.
Since 1990, there have been at least seventeen
epidemiological studies that have examined whether
fluoridation influences the rate of hip fracture. Of
these, 10 have found a positive relationship and 7
have not (www.fluoridealert.org). Since the
Roholm’s classic study of cryolite workers in
Denmark (Roholm 1937), it has become apparent
that skeletal fluorosis impacts millions of people in
countries with regions of high endemic levels of
fluoride, like India and China. WHO (2002)
estimates indicate that for a total intake of
14 mg F/day, there is a clear risk of skeletal adverse
effects. There is suggestive evidence of an increased
risk of effects on the skeleton at total fluoride
intakes above about 6 mg/day.
FLUORINE-CONTAINING DRUGS
Artificial fluorine substitution of biologically active
molecules exercise an influence on their properties
and activities. The replacement of a hydrogen atom
and/or a hydroxyl group by a fluorine atom are
common strategies in drug development (Alkorta et
al. 2000). Fluorine substitution in a drug molecule
can influence not only pharmacokinetic properties,
such as absorption, tissue distribution, secretion, and
the route and rate of biotransformation but also its
pharmacodynamics and toxicology (Wakselman
1999). At present more than two hundred fluorinated
pharmaceuticals are available and others are
appearing. The benefit of fluorinated drugs for
human medicine is very well known; much less is
known about the danger of these compounds for
human health. The mechanism of fluorine
participation in their different undesirable effects has
not been fully explained. Defluorination of
fluorinated drugs can readily occur during
biotransformation, or may also occur spontaneously,
if a molecule is sufficiently electrophilic to undergo
direct reaction with a nucleophilic group present in
proteins and amino acids, such as the amino group
in lysine, the sulphydryl group in cysteine or the
hydroxyl group in serine (Park et al. 2001). Such
defluorination was observed for example in the case
of an antimalarial drug 5-fluoro-amodiaquine
(Harrison et al. 1992) or hormone
2-fluoroethynilestradiol (Morgan et al. 1992). In rare
instances, even the trifluoromethyl group may
undergo defluorination (Thompson et al. 2000).
 Fluorine in medicine
Fluorine-containing volatile anesthetics
The first inhalation anesthetic, methoxyfluran, was
widely used in clinical anesthesia until its
association with nephrotoxicity was reported
(Crandell et al. 1966). In some cases fatal renal
failure was described (Panner et al.1970). A high
urine output syndrome leading to dehydration was
related to the extensive metabolism of
methoxyflurane joined with high serum
concentrations of inorganic fluoride, since
methoxyflurane is metabolized to oxalic acid and
free fluoride. The increased intrarenal fluoride
concentration has been suggested as the most
important factor in methoxyflurane nephrotoxicity
(Kusume 1999).
Further volatile fluorine-containing anesthetics
such as halothane, isoflurane, sevoflurane, enflurane,
and desflurane were synthesized later. A concern
about the potential nephrotoxicity and/or
hepatotoxicity of new anesthetics have led to
numerous clinical studies during the last two
decades. The toxicity of these anesthetics might be
caused by their biotransformation to toxic
metabolites. Flurane anesthetics are metabolized to
hexa-fluoro-isopropanol and inorganic fluoride by
the human liver (Kharasch 1996). In vitro
investigations have identified a role for human
cytochrome P450 (CYP 2E1 and 2A6) in oxidation
and CYPs 2A6 and 3A4 in reduction. Kharash and
Thummel (1993) demonstrated that CYP2E1 is the
principal, if not sole human liver microsomal
enzyme catalyzing the defluorination of the
fluorinated ether anesthetics in vivo. The rank order
of anesthetic metabolism, assessed by fluoride
production at saturating substrate concentrations,
was methoxyflurane > sevoflurane > enflurane >
isoflurane > desflurane > 0. Until recently, inorganic
fluoride has been thought to be the main etiological
agent responsible for fluorinated anesthetic
nephrotoxicity, with a toxic concentration threshold
of 50 µmol/L in serum (Gentz and Malan 2001),
exceeded the reported basal values (about 3 µmol/L)
5–20 times. However, numerous studies including
hundreds of patients have not shown evidence of
their nephrotoxicity based on the biochemical
parameters for kidney functions examined after the
termination of anesthetic administration (Gentz and
Malan 2001, Conzen et al. 2002). It seems that the
human body has an efficient homeostatic mechanism
to respond to a short time peak in the serum fluoride
level.
However, the wide scale of variations in the
serum fluoride level and case reports of the
individual adverse effects indicate caution in using
flurane anesthetics particularly when prolonged
anesthesia and surgery are planned. It has been
reported that AlFx can affect the activity of many
145
ion channels and enzymes in the kidney (Strunecká
and Patočka 1999). When AlF3 or NaF at various
concentrations were given to rats in drinking water
for 45 weeks (Varner et al. 1998), pathological
changes were found in the kidneys of all groups.
The kidneys from rats drinking the NaF water
exhibited glomerular hypercellularity, renal
mesangial proliferation, and the deposition of
proteins in the renal tubules. Histological evidence
of glomerular distortions was present in both the
AlF3 and NaF groups.
Formation of nephrotoxic halogenated alkenes
during alkaline degradation in carbon dioxide
absorbers, such as 1-chloro-1,2-difluorovinyl
difluoromethyl ether or fluoromethyl-2,2-difluoro-1-
(trifluoromethyl)vinyl ether (compound A) were
suggested as an alternative mechanism for renal
toxicity (Orhan et al. 2001). The mechanism of
compound A renal toxicity is controversial, with the
debate focused on the role of the renal cysteine
conjugate β-lyase pathway in the biotransformation
of compound A.
Fluorine-containing antiviral and antibacterial
compounds
Some new fluorine containing substituted 3-thioxo-1,
2, 4-triazin-5-ones have been synthesized and many
of them have retained a significant antiviral activity
(Abdel-Rahman 1991). Also some fluorinated purine
nucleotides and nucleosides show significant
antiviral (anti-HIV) activity (Marquez et al. 1990).
Fluorine has been introduced into both the base and
the sugar residue. Fluorine-containing
antimetabolites are of interest in the development of
anti-HIV drugs, such as alovudine, the direct
fluorine analogue of zidovudine (3-azidothymidine,
AZT). Alovudine is phosphorylated in cells to the 5-
triphosphate, which is the active inhibitor of
HIV-associated reverse transcriptase (Matthes et al.
1988). Recently, emtricitabine [ (-)-beta-L-2',3'-
dideoxy-5-fluoro-3'-thiacytidine] has been approved
by the Food and Drug Administration for the
treatment of human immunodeficiency virus (HIV)
(Anonymous 2003).
5-fluorouracil is a major antimetabolite used in
the treatment of solid cancers. This compound is
converted into a pharmacologically active metabolite
5-fluoro-deoxyuridine monophosphate, which
inhibits the enzyme thymidylate synthetase, which
then results in diminished formation of one of DNA
wall stone – thymidine (Thomas and Zalcberg 1998,
Feng et al. 2004). Because 5-fluorouracil and its
metabolites are concentrated in cancer cells, the
enzymatic blockade inhibits tumor growth.
5-fluorouracil is also metabolised into the highly
 Strunecká et al.
toxic fluoroacetate, by scission of the pyrimidine
ring (Arellano et al. 1998). The toxicity of
fluoroacetate is evoked by its entry into the
tricarboxylic acid cycle in mammalian cells and its
conversion into fluorocitric acid (Patočka and Cabal
1999). In addition, a catabolite of 5-fluorouracil
after fluorinated pyrimidine degradation induces
cytotoxicity in tumors (Kubota 2003). Anthracycline
derivatives with fluorine atom in different position
of the molecules have also found use in modern
oncology.
The most known and very much used fluorine-
containing antibacterial compounds are
fluoroquinolone antibiotics. A fluorine substituent
strongly enhances the antibacterial potential of the
drug. Fluoroquinolones features a broad
antimicrobial spectrum. In general, fluoroquinolones
were considered to be remarkably safe.
Nevertheless, several side-effect were reported,
including hepatic reactions, neurotoxicity,
phototoxicity, cardiotoxicity, tendinopathy, and
chondrotoxicity (Stahlmann 2002). In premarketing
trials with 7000 patients, trovafloxacin was
associated with no cases of liver failure and about
2.5 million patients received Trovan®, up to
300,000 prescriptions per month. In July 1998, the
FDA advised revision of the package insert to
reflect hepatic toxicity. A public health advisor
reported 140 patients with serious hepatic events.
Fourteen patients developed acute hepatic failure:
5 received liver transplants (1 died), 5 patients died
without transplantation, and 4 others recovered.
Hepatotoxicity occurs after an unpredictable
trovafloxacin exposure time, ranging from 2 to
60 days. There appears to be increased risk with
greater than 14 days of use, and some cases
occurred after re-exposure. Six out of the first 40
reported patients had peripheral eosinophilia,
suggesting a hypersensitivity reaction (Rubinstein
2001). The use of trovafloxacin has been
significantly restricted due to substantial mortality
and morbidity associated with liver toxicity (Bertino
and Fish 2000).
The most common adverse events in clinical use
of fluoroquinolones are nausea, diarrhea, headache,
and dizziness. All fluoroquinolones have the
potential to cause photosensitivity (Chignell 1998).
Photosensitization can result when light interacts
with chemical agents in the skin and eyes. This
process can produce undesirable clinical
consequences, such as phototoxicity (i.e.
exaggerated sunburn), photoallergy or
photocarcinogenicity. People receiving
fluoroquinolones are warned on the product inserts
not to expose themselves to direct sunlight. The first
symptom is a developing rash on the exposed areas.
In order to suppress the toxic effect of fluorine in
chinolones, new compounds without the usual
146
6-fluorine substituent have been recently described
as potent antibacterial agents. A series of non-
fluorinated analogues of the antibacterial quinolone
levofloxacin were synthesized and tested (Gray et
al. 2003).
Moxifloxacin shares the quinolone-class
warnings and precautions regarding use in pediatric
populations, pregnant women, nursing women, and
patients with central nervous system disorders. The
class warnings regarding convulsions, increased
intra-cranial pressure, psychosis, central nervous
system stimulation, hypersensitivity reactions,
pseudomembranous colitis, and tendon ruptures are
also similar.
Since the introduction of fluoroquinolones on the
market in 1987 more than 200 cases of
rhabdomyolysis, tendinitis, tendon rupture etc. have
been reported in the literature (Ramanujam 2001).
In October 1994 the Japan Pharmaceutical Affairs
Burelu (JPAB) was the first to amend the product
information for fluoroquinolones to state that muscle
destruction – a condition known as rhabdomyolysis
may occur (JPAB 1994). For example ciprofloxacin,
which has been in use since 1987 for a variety of
other indications and was the most-widely used
fluoroquinolone in humans and animals worldwide,
was withdrawn because of strong adverse effects.
Fatal liver failure associated with ciprofloxacin was
reported by Fuchs et al. (1994). The most common
side-effects of ciprofloxacin are gastrointestinal in
nature such as nausea, diarrhea, vomiting, and
abdominal pain. In 2000 the FDA approved its use
in treatment for inhalational anthrax. As soon as the
first cases of anthrax resulting from suspicious mail
became known, ciprofloxacin was bought on a mass
scale. Ciprofloxacin administration results in
elevated serum fluoride levels. In a series of tests
evaluating the safety of ciprofloxacin in children,
serum fluoride levels increased after 12 hours in
79% of the children; on day 7 the 24-hour urinary
fluoride excretion was higher in 88.9% of children
observed (Pradhan et al. 1995). Ciprofloxacin has
been implicated in several cases of acute renal
failure (Zimpfer et al. 2004).
Fluorine-containing anti-inflammatory compounds
Anti-inflammatory drugs are medications which, as
well as having pain-relieving (analgesic) effects,
have the effect of reducing inflammation when used
over a period of time. Also in this group of drugs
there are quite a number of fluorinated derivatives.
The drugs vary in strength and side effects. There
are many other potential side effects, but these vary
according to the drug chosen and the individual
taking it. Fluorine-containing anti-inflammatory
drugs can be metabolized by defluorination, which
 Fluorine in medicine
favors formation of the stable and toxic fluoride ion
(Boiteau et al. 1979). An example of the toxic
action of the fluorinated anti-inflammatory drug,
niflumic acid, has been described in France. An
86 year-old man who for many years took 500 mg
of niflumic acid a day, suffered heavy osteofluorosis
and had severe renal insufficiency (Welsch et al.
1990). Similar health problems were suffered by a
61 year-old man who consumed 2.5 l a day of
Vichy St-Yorre (a mineral water containing 8 mg of
fluorine ions per liter) for 11 years. These two
observations serve as a reminder of the
indispensable precautions to be observed when
prescribing fluorine salts in the treatment of
osteoporosis and prescribing fluorine-containing
drugs generally.
Fluorine-containing psycho-pharmaceuticals
The introduction of fluorine into psycho-
pharmaceuticals escalates penetration of the drug
across membranes to the site of action – obviously
the central nervous system. Centrally acting drugs
must pass through the blood-brain barrier in
sufficient concentration to elicit their
pharmacological effect. For example some
neuroleptics that act by blocking dopamine receptors
in the CNS, such as butyrophenones,
diaylbutylamines or tricyclics contain either fluoro-
phenyl or trifluoromethyl group, which contribute to
the pharmacological activity of these drugs by
enhancing CNS penetration. The most widely used
butyrophenone is haloperidol. In the search for more
potent neuroleptics, it was found that a prostacyclin exhibits a half-life 150 times, and has
compoundwhich contains fluorophenyl groups was
longer acting than haloperidol (Park and
Kitteringham 1994). Also fluorine-containing
phenothiazines – fluphenazine, trifluoropromazine,
and trifluperazine, are more active than the mother
compound chlorpromazine (Resnati 1990).
The most often used fluorine-containing psycho-
pharmaceuticals are antidepressants and
antipsychotics. Particularly, fluoxetine (Prozac) and
citalopram are very favored. Prozac is widely used
for the treatment of depression, obsessive-
compulsive disorder, and bulimia nervosa.
Fluoxetine and citalopram can cause nausea,
headache, anxiety, insomnia, drowsiness, and loss of
appetite (Edwards and Anderson 1999).
Fluoxetine has been implicated in serious skin
rashes and vasculitis (Sannicandro et al. 2002).
Increased blood pressure can occur and should be
monitored. Seizures have been reported. Life-
threatening interactions can occur in combination
with MAO inhibitors. MAO inhibitors and
fluoxetine should not be taken together and a
waiting period of 14 days between taking these two
147
classes of medications is strongly advised (Sternbach
1988).
Other fluorine-containing drugs
It has been shown that fluorinated analogues of
naturally occurring biologically active compounds
including amino acids, often exhibit unique
physiological activity. Fluorination of natural
hormones can lead to molecules with new
pharmacokinetic and/or pharmacodynamic
properties. For example the introduction of fluorine
into corticosteroids has a dramatic effect on their
metabolism (Bush and Mahesh 1964). Because the
metabolism of steroid hormones is very important
for their physiological activities, the exchange of a
hydrogen atom under fluorine atom can be very
meaningful. Also other endogenous compounds
markedly exchange their biological properties, if one
or more fluorine atoms are installed into their
molecule. For example, the potent platelet
aggregating agent thromboxane A2 has a half-life in
vivo of only 32 seconds. Incorporation of two
fluorine atoms into the oxetane ring of thromboxane
A2 reduces the rate of carbonium ion formation and
acid hydrolysis, so that 7,7-difluoro-thromboxane A2
8
has a rate of hydrolysis 10 -fold slower than the
natural substance (Fried et al. 1984). Likewise
prostacyclin, which is an inhibitor of platelet
aggregation, has a very short biological half-life.
Fluorination improves the stability of the molecule
toward acid hydrolysis and the stability in
organisms. Thus 10,10-difluoro-13-dehydro-
equal potency to, the natural compound (Fried et al.
1980).
Cerivastatin, a fluorinated drug from the statin
class, which had caused deaths and serious adverse
health effects was withdrawn from the market in
2001 (Furberg and Pitt 2001). It had been linked to
at least 31 deaths. Cerivastatin also induced muscle
destruction (rhabdomyolysis) and displayed
compounded toxicity when used with other drugs.
CONCLUSION
The trend toward fluorinating pharmaceuticals
contributes to well-documented human fluoride
overload from the living environment (Bryson
2004). Of particular concern must be those who are
most vulnerable to fluoride’s toxic effects, which
include infants and children, high water consumers,
the elderly, those who are hypersensitive to fluoride,
those with poor health and kidney dysfunction.
Fluoride in the presence of trace amounts of
 Strunecká et al.
aluminum (which is present everywhere) can act as
the messenger of false information, activating
G proteins and evoking numerous pathological
changes. Moreover, fluoride in the form of
aluminofluoride complex might potentiate the
subclinical pathophysiological alterations. Serious
health problems can arise after application of
fluorinated hormones. No one can responsibly
predict what happens in a human body after
administration of fluorinated compounds. Large
groups of people, including neonates, infants,
children, and ill patients serve thus as the subjects
of pharmacological and clinical research.
Albert Gilman said in his Nobel prize lecture:
”The ultimate dream is to design drugs that will
prevent aberrant G protein action.” Fluoride plus
aluminum produce aberration of G proteins. How
many human subjects will applied biomedicine need,
to accept this knowledge? The awareness of the
health risks of an increasing load of fluoride and
aluminum ions would contribute significantly to the
decline of risks of many severe disorders in the
st
21 century.
ACKNOWLEDGEMENT
Preparation of the manuscript was supported by
Academia Medica Pragensis, Czech Republic.
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Ann. rheum. Dis. (1955), 14, 378.

COMPARISON OF RHEUMATOID (ANKYLOSING)

SPONDYLITIS AND CRIPPLING FLUOROSIS*t
BY

CHARLES LEROY STEINBERG

Rochester General Hospital
AND
DWIGHT E. GARDNER, FRANK A. SMITH, AND HAROLD C. HODGE
Division of Pharmacology and Toxicology
Department of Radiation Biology
University of Rochester School of Medicine and Dentistry
Rochester, New York
(RECEIVED FOR PUBLICATION JULY 5, 1955)
Crippling fluorosis and rheumatoid (ankylosing) characterized in their advanced stages by a "poker-
spondylitis present a confusing similarity; both are back" spine with calcification of the ligaments of the
* This paper is based in part on work performed under contract
spinal column (Fig. 1). Rheumatic pains of various
with the U.S. Atomic Energy Commission at the University of degree are common in the early stages of both
Rochester Atomic Energy Project, Rochester, New York. diseases.
t Presented but not read at the Annual General Meeting of the One of us (C.L.S.), noting the similarity between
American Rheumatism Association, 1955. See p. 443 of this issue.

Fig. 1.-"Poker Back", comparison of limitation of motion and characteristic stance in (A and B) rheumatoid spondylitis, and (C and D)
crippling fluorosis. C and D are reproduced with the permission of the publishers from Roholm (1937, opp. p. 145, Figs 33b and c).
378
 RHEUMATOID (ANKYLOSING) SPOND YLITIS AND CRIPPLING FLUOROSIS 379
these conditions, suggested the importance of formed. In some instances areas of osteoporosis
presenting a comparison of the two conditions.
Recent public health undertakings in the United
States, designed to reduce the incidence of dental
caries by adding fluoride to the communal water
supply, have increased the importance of this
investigation. It would be unfortunate if these
undertakings were erroneously accused of producing
serious bone changes through the inadvertent
diagnosis of rheumatoid (ankylosing) spondylitis as
crippling fluorosis.
Rheumatoid (Ankylosing) Spondylitis
This condition is usually considered by most
rheumatologists to be a variant of rheumatoid
arthritis. It usually affects males in contra-
distinction to the usual variety of rheumatoid
arthritis which generally affects females. It usually
begins in youth, is characterized by exacerbations
and remissions of back pain, and may or may not be
associated with the sciatic syndrome. As the disease
progresses a gradual stiffening of the back occurs,
eventually resulting in a "poker-back" spine.
Expansion of the chest on inspiration becomes
diminished and finally nil as ankylosis of the costo-
vertebral joint occurs. The radiographic picture is
pathognomonic. The first changes usually occur
in the sacro-iliac joints. The joint surface becomes
irregular; there is progressive increase in density in
the contiguous bone surfaces of this joint. Even-
tually the sacro-iliac joints may be completely
obliterated by bony ankylosis. At this particular
point the area in which the joint has been erased is
usually very dense; the surrounding bone area may
show a decrease in density. The trabeculae become
more prominent. Calcification occurs in the
anterior and longitudinal ligaments of the vertebral
column. However, there is no calcification in the
sacral tuberous and other ligaments of the pelvis,
nor are the fasciae involved. Primary fibrous and
subsequent bony ankyloses of the apophyseal joints
result in a rigid spinal column ("poker-back" spine).
Approximately 25 per cent. of these patients have
involvement of the peripheral joints with a clinical
pattern not unlike rheumatoid arthritis. The sedi-
mentation rate is elevated in a majority of the cases.
Crippling Fluorosis
Crippling fluorosis is a specific form of skeletal
disease which follows the absorption of excessive
amounts of fluoride for prolonged periods of time.
Osteosclerosis and exostoses are the outstanding
findings; mottled dental enamel may be seen if the
period of absorption includes the first 8 years of life
when the enamel of the permanent teeth is being
also are seen. As the disease progresses all bones
eventually become sclerotic; there seems to be a
predilection, however, for flat bones, such as those
of the pelvis and jaw, and especially the lumbar
vertebral system to show the first detectable changes
(Felson, 1955). In severe cases, exostoses become
evident on the long bones, and on the lower edges of
the vertebrae. Eventually the vertebrae fuse together,
the spinal ligaments become calcified at their points
of attachment, and the typical rigid spinal column
ensues (Figs 2, 3, and 4, overleaf). Crippling fluorosis
of industrial origin was fully described by Roholm
(1937) in his investigation of the disease in Danish
cryolite workers. The condition is also endemic in
various parts of the world, India, China, Argentina,
and South Africa, where water supplies contain
2-16 parts per million of fluoride. From data
presented by McClure (1943), fluoride doses probably
must be greater than 0 1 mg./kg./day during the
first 8 years of life to produce mottled enamel.
It has been estimated that the daily consumption of
0 3-1 0 mg. fluoride per kg. body weight for a
period of 10-20 years will result in crippling fluorosis
(Roholm, 1937; Hodge and Smith, 1954).
Present Investigation
To our knowledge no one has reported the fluoride
content in the skeletal tissues of an individual
suffering from rheumatoid spondylitis. It was our
unusual fortune recently to study such a case; this
man who had had the disease for a period of 10 years
died suddenly of a subarachnoid haemorrhage.
Case History
A white male aged 40 years, first seen on September 22,
1948, gave a 10-year history of low back pain with
progressive spinal stiffening, and increased pain and
stiffness of the hips. He had lived in Rochester, N.Y., all
his life, and never had left the area for any period longer
than a few days. The fluoride content of the tap water
by analyses in the period 1945 to 1952 was low, about
0-06 parts per million; presumably this is a reliable
estimate of the fluoride content of Rochester's water
supply during the man's life time.
The physical examination revealed no dental mottling.
He lacked 150 abduction in both shoulders; there was no
chest expansion on deep inspiration, which was thought
to be indicative of ankylosis of the costovertebral joints.
He was unable to abduct either hip, and a 450 flexion
deformity was present in both. His entire spine was
rigid.
Laboratory Findings.-September 22, 1948:
Antistreptolysin titre, 83 units; red blood cells,
4,530,000; haemoglobin, 12 g. per cent.; white blood
cells, 13,600.
380 ANNALS OF THE RHEUMATIC DISEASES

Fig. 2.-Moderately advanced crippling fluorosis in male, lumbo- Fig. 3-Advanced crippling fluorosis, lumbo-sacral area. Note
sacral area. Note increased bone density (sclerosis) and loss of complete loss of bone trabecular pattern and "marble" type bone
normal trabecular pattern. due to increased bone sclerosis. Moderate calcification of ligaments.

Differential Blood Count: stabs, 2 per unit; segmented

neutrophils, 78 per cent.; lymphocytes, 10 per cent.;
eosinophils, 3 per cent.; monocytes, 7 per unit; blood
uric acid, 1 '6; serum calcium, 10 4; serum phosphorus,
3 - 9 mg. per cent.; erythrocyte sedimentation rate, 35 mm./
hr (Wintrobe-Landsberg). Subsequent sedimentation
rates varied between 21 and 39 mm. Bone marrow fat
3, plasma 48, erythromyeloid layer 9, haematocrit 40 vol.
per cent. The marrow showed no abnormalities.
Radiographs (September 22, 1948).-Anterior-pos-
terior stereo and lateral films of the cervical spine (Fig. 5,
opposite) showed calcification in the anterior vertebral
ligaments. In addition there was evidence of bony
sclerosis or ligamentous calcification along the posterior
portion of the articular facet in the lower cervical region.
The cervical bodies and intervertebral spaces appeared
to be normal.
In the thoracic spine moderate scoliosis was seen with
a major curve at the lumbo-dorsal region with the
convexity on the left side. There was evidence of mild
osteoporosis involving the thoracic segments, but no
:s~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~.s
other definite changes.
The lumbar spine and pelvis (Figs 6 and 7, opposite)
Fig. 4.-Advanced crippling fluorosis, lumbo-sacral area. Advanced showed advanced ligamentous calcification along the
calcification of ligaments (arrows). Marked increase in bone sclerosis
appears to "obliterate" normal sacro-iliac joints. anterior borders of the lower lumbar vertebral bodies
 RHEUMATOID (ANKYLOSING) SPONDYLITIS AND CRIPPLING FLUOROSIS 381
Fig. 5.-Rheumatoid spondylitis, lateral view of cervical spine.
Note bony ankylosis of apophyseal joints.
*i 9 ,...
Fig. 6.-Rheumatoid spondylitis, lateral view of
lumbo-sacral area. Note calcification of anterior
spinal ligament.
and suspected calcification in the posterior ligaments.
There was no evidence of bony sclerosis in the sacro-iliac
region on either side, but there was evidence of destructive
arthritic change involving both hips with irregularity of
the femoral head and acetabulum. Ligamentous calci-
fication was seen inferiorly about both hip joints.
Treatment.-A left cup arthroplasty was done on
January 14, 1949. There was slight irregular new bone
formation in an area where the cartilage was denuded.
The periosteum was thickened irregularly.
A right cup arthroplasty was done on May 9, 1949.
The microscopic sections revealed a markedly prolifera-
tive synovial tissue with foci of inflammatory cells
beneath the mesothelium. The bone tissue was essen-
tially normal.
Death.-On May 13, 1952, the patient died suddenly
of a subarachnoid haemorrhage.
Autopsy.-Portions of the ribs, vertebrae, and sacrum
and ilium immediately adjacent to the sacro-iliac joint
were taken for fluoride analysis. The soft tissue adhering
to each of the specimens and marrow from the two rib
specimens were analysed separately. The vertebral
sample was separated into the spongy and dense portions,
(Fig. 8, overleaf). The soft tissues were analysed
according to the method described by Smith and Gardner
(1951) for blood fluoride. After ashing the hard tissues,
fluoride was separated by the perchloric acid distillation
of Willard and Winter (1933); fluoride in the distillate
was determined by salt-acid thorium titration (Smith and
Gardner, 1950). The data obtained are shown in Table I
(overleaf).
Fig. 7.-Rheumatoid spondylitis, anterior-posterior view of pelvis. Note
ankylosis of sacro-iliac joints and increased trabeculation of bone.
382 ANNALS OF THE RHEUMATIC DISEASES
There were no known opportunities for this
patient to have been exposed to excessive amounts
of fluoride. Nevertheless, the fluoride content of
bone samples, which are shown to be normal, con-
elusively rule out fluorosis as a factor in the disease.

Discussion
Fluoride is a normal trace constituent of bone, the
contents depending on the fluoride intake, the age of
the individual, and probably on other factors.
Rib and vertebral specimens from 40 to 50-year-old
male residents of the Rochester area contained 400 to
1,300 p.p.m. fluoride in the ash (Smith, Gardner, and
Hodge, 1955). Martin (1948) has
reported similar fluoride concen-
trations in dry defatted samples
from the crest of the ilium obtained
in Evanston, Illinois, prior to water

II
5j \ i fluoridation; using the data of
SgW~s8&3 i % r; Robinson ( 1952) for fat content,
C these adult bones were calculated
to contain 470 to 1,430 p.p.m.
fluoride in the ash.
t The data in Table I show that the

tissues of the patient

ribs of our

contained low but normal amounts

of fluoride, whereas the vertebra
Fig. 8.-Separation of vertebral sample from a case of rheumatoid contained slightly less fluoride than had been found
spondylitis for fluoride analysis: (a) spongy Iportion, 410 p.p.m.
fluoride in ash; (b) soft tissue, 17 p.p.m. fluoride fresh wt.; (c) dense
- in control patients of the same age (Smith, Gardner,
portion, 310 p.p.m. fluoride in aash. and Hodge, 1953). The ilium also contained
slightly less fluoride than Martin (1948) reported
TABLE I
for a series of nine samples of the iliac crest.
FLUORIDE CONCENTRATIONS 1IT 4 TISSUES Soft tissues contain normally only traces of
fluoride; the finding that fluoride concentrations in
Fluoride the soft tissues and marrow (9 to 17 p.p.m.) were
((pats p mIl)- much lower than those found for the hard tissues
Site of Tissue
in in Fresh
was expected. Concentrations found for com-
Ilium
Sacrum
-320
Ash

310
Tissue

parable tissues from five patients without rheumatoid

spondylitis, 14 to 86 years of age, averaged 9 to
Soft tissue between sacrum
26 p.p.m.
and ilium 9
The data obtained in this study indicate that the
Smaller rib including marrow 420
Smaller rib without marrow 440 increased osteosclerosis encountered in rheumatoid
Smaller rib marrow 17 spondylitis is not associated with increased skeletal
Rheumatoid Soft tissue around smaller rib
Spondylitis
Patient Larger rib including marrow 420
Larger rib without marrow 440 TABLE II
Larger rib marrow 10
Soft tissue around larger rib 9 FLUORIDE CONCENTRATIONS IN BONE
Vertebra, spongy portion 410
Soft tissue from vertebra 17
Vertebra, dense portion 310 Fluoride (parts per million)
Site
Rib 405-1,2155 Normal* Rheumatoid Crippling
Soft tissue around rib 9-21 Spondylitis Fluorosist
Controls* Rib marrow 26
Rib .. 405-1,215 420-440 9,900-11,200
Vertebra 440-1,320 Vertebra .. 440-1,320 310-410 9,300-13,100
lSoft tissue round vertebra 7-20
* Smith and others (1953).
* Smith, Gardner, and Hodge, 1955. t Roholm (1937), p. 193.
 RHEUMATOID (ANKYLOSING) SPONDYLITIS AND CRIPPLING FLUOROSIS 383
TABLE III
COMPARISON OF RHEUMATOID SPONDYLITIS, CRIPPLING FLUOROSIS, AND METASTATIC CARCINOMA

Condition Rheumatoid Spondylitis Crippling Fluorosis Metastatic Carcinoma

(Prostate and Breast)
(1) Increase in trabecular pattern upon Coarse and blurred trabeculae, Localized areas of increased bone
roentgenological examination diffuse increased density of bone density
on roentgenological examination
(2) Increased density of sacro-iliac Vertebral system and pelvis affect- Pelvic area and lumbar spine
joints and increased density of ed first and most severely; later affected first. Areas of increased
ilium and sacrum with progres- extended to ribs and extremities. bone density usually discrete,
sive disease All bones are affected, par- but occasionally diffuse. No
ticularly cancellous bones. Exo- cortical thickening
stoses on long bones
Ii-
(3) Universal occurrence Endemic where water supplies Universal occurrence
contain excessive amounts of
fluoride. Formerly seen in
workers handling fluoride-con-l
taining compounds
(4) Calcification of ligaments limited Excessive calcification of tendons, No ligamentous calcification
to anterior and lateral spinal ligaments, fasciae
column
(5) Peripheral joints swollen in 25 per Bones of extremities thickened No peripheral joint involvement
cent. of cases
(6) No mottled enamel Mottled enamel may be present No mottled enamel
if fluoride exposure excessive
during period of formation
of enamel of permanent teeth
(7)* No increased urinary fluoride Urinary excretion of fluoride No increase in urinary fluoride
excretion increased excretion
(8)t Skeletal fluoride concentration not Increase in skeletal fluoride con- No increase in skeletal fluoride
increased centration concentration
(9) No increase in serum phosphatase No increase in serum phosphatase Increase in serum alkaline, acid
phosphatase, or both

* When the fluoride concentration in the urine is consistently less than 5 mg./I., no roentgenographically demonstrable osteo-
sclerosis develops (Irwin, 1954).
t Normal concentration of fluoride in human bone (Smith,
Gardner, and Hodge, 1955, unpublished data): fluorosis, and metastatic carcinoma is presented in
Table III. The data on metastatic carcinoma are
Sex Site Age P.p.m. included because the increased x-ray density of
Rib 10 300 certain lumbar vertebrae has presented a problem
90 1,480 in differential diagnosis.
Male ..
Vertebrae 10 380
90 1,520 Summary
Rib 10 (1) Fluoride concentrations were determined for
Female
90 autopsy samples of rib, sacrum, ilium, vertebra,
Vertebrae 10 adhering soft tissue, and rib marrow from a patient
90 suffering from rheumatoid (ankylosing) spondylitis
of 10 years' duration. The fluoride concentrations
were not increased above normal levels. In this
deposition of fluoride. Indeed, the skeletal fluoride case, the increased bone density seen in this disease
concentrations were near or less than the normal was not the result of increased skeletal fluoride
limits previously established. Fluoride cannot be deposition.
held responsible for the bony changes in rheumatoid (2) A tabular comparison of rheumatoid spondyl-
spondylitis. Roholm (1937) has shown that the itis, crippling fluorosis, and metastatic carcinoma is
skeletal tissues of patients disabled with fluorosis presented.
contain relatively high concentrations of fluoride.
Representative data for rib and vertebra are shown Dr. Robert A. Robinson, formerly of the Division of
in Table II. Wolff and Bauer (1938) reported Orthopaedic Surgery, of the University of Rochester
School of Medicine and Dentistry, gave us a number of
greatly decreased fluoride concentrations in occipital, valuable suggestions and assisted in preparing the samples
parietal, and frontal bones in a series of six cases of of sacrum and ilium for analysis. The Department of
Paget's disease (osteitis deformans). Medical Photography, Rochester General Hospital,
A comparison of rheumatoid spondylitis, crippling prepared Figs 5-7. Mr. Leon Schwartz of the Photo-
384 ANNALS OF THE RHEUMATIC DISEASES
graphy Section, University of Rochester Atomic Energy
Project, prepared the diagram Fig. 8. Mr. Fred Brandlin,
formerly of the Industrial Hygiene Section, University of
Rochester Atomic Energy Project, prepared the x-ray
shown in Fig. 8.
REFERENCES
Felson, B. (1955). Personal communication.
Hodge, H. C.,and Smith, F. A. (1954). "Some Public Health Aspects
of Water Fluoridation", in "Fluoridation as a Public Health
Measure", ed. J. H. Shaw, p. 79. Amer. Assoc. Advance. Sci.,
Washington, D.C.
Irwin, D. (1954). Personal communication.
Martin, D. J. (1948). J. dent. Res., 27, 27.
McClure, F. J. (1943). Amer. J. Dis. Child., 66, 362.
Robinson, R. A. (1952). J. Bone Jt Surg., 34-A, 389.
Roholm, K. (1937). "Fluorine Intoxication", p. 121. Nyt Nordisk
Forlag, Busck, Copenhagen; Lewis, London.
Smith, F. A., and Gardner, D. E. (1950). Arch. Biochem., 29, 311.
(1951). J. dent. Res., 30, 182.
,and Hodge, H. C. (1953). Fed. Proc., 12, 368.
(1955). Unpublished observations.
Willard, H. H., and Winter, 0. B. (1933). Industr. Engng Chem.,
Anal. Ed., 5, 7.
Wolff, W. A., and Bauer, J. T. (1938). Bull. Ayer clin. Lab., 3, 209.
Comparaison de la spondylite rhumatismale et
de la fluorose mutilante
RESUME
(1) On a determine le taux de fluor dans les pieces
d'autopsie provenant des c6tes, du sacrum, de l'os
iliaque, des vertebres, des tissus
mous adherants et de la
moelle costale d'un sujet ayant suffert de spondylite
rhumatisante pendant dix ans. Le taux de fluor n'etait
pas au dessus de la normale. Dans ce cas donc la
condensation osseuse habituelle dans cette maladie ne
pouvait pas &re attribute a l'augmentation des dep6ts
fluores du systeme locomoteur.
(2) On presente des tableaux compares de spondylite
rhumatismale, de fluorose mutilante et de carcinoma
metastasique.
Comparacion de la espondilitis reumatoide y de la
fluorosis mutilante
SUMARIO
(1) Se determinaron las cifras de fluor en fragmentos
de autopsia de costillas, sacro, ili6n, vertebras, tejidos
blandos adyacentes y medula costal de un sujeto con
espondilitis reumatoide de 10 anos de duraci6n. Las
cifras de fluor no rebasaron las normales. En este caso
la condensaci6n 6sea que se suele encontrar en esta
enfermedad no fue debida al aumento de los dep6sitos
de fluor en los tejidos del sistema locomotor.
(2) Se present una comparaci6n tabulada de la
espondilitis reumatoide, de la fluorosis mutilante y del
carcinoma metastasico.
Food and Beverage Sources of Fluoride Exposure – Compiled by
Maureen Jones and David C Kennedy, DDS, Past President International Academy of Oral
Medicine and Toxicology. 3243 Madrid St., San Diego, CA 92110. (800) 728-3833.

Stannard JG et al. Fluoride levels and fluorides contamination of fruit juices. Journal of
Clinical Pediatric Dentistry; 16:38-40, 1991. Forty-three ready-to-drink fruit juices were examined
for fluoride ion concentration. The fluoride levels of the juices ranged from 0.15 to 6.80 (Gerber
White Grape juice). It was found that 42% of the samples had more than 1 ppm of fluoride. Given
that increasing numbers of people are consuming beverages instead of water, fluoride
supplementation should not be based solely upon the concentration of the drinking water, but
should also consider the amount of different beverages consumed and their fluoride content.

Kiritsy, MC et al. Assessing fluoride concentrations of juices and juice-flavored drinks. Journal
American Dental Association; 127: 895-901, 1996. In this study, the authors analyzed 532 juices
and juice drinks for fluoride. Fluoride ion concentration ranged from 0.02 to 2.80 parts per
million. Children’s ingestion of fluoride from juices and juice-flavored drinks can be substantial
and a factor in the development of fluorosis.

Heilman, JR el al. Fluoride concentrations of infant foods. Journal American Dental Association;
128: 857-63, 1997. In this study, the authors analyzed the fluoride concentration of 238
commercially available infant foods. Fluoride concentrations ranged from 0.01 to 8.38 micrograms
of fluoride per gram, (ppm) with the highest fluoride concentrations found in infant foods
containing chicken.

Heilman, JR el al. Assessing fluoride levels of carbonated soft drinks. Journal American Dental
Association; 130: 1593-99, 1999. The authors examined the fluoride concentrations of 332 soft
drinks. The fluoride levels of the products ranged from 0.02 to 1.28 ppm, with a mean level of
0.72. Fluoride levels exceeded 0.60 ppm for 71 percent of the products.

Burgstahler, AW et al. Fluoride in California wines and raisins. Fluoride; 30: 142-146, 1997.
The water-extractable F content of five brands of California raisins varied from 0.83 to 5.20 ppm
(mean 2.71 ppm). Elevated F levels in these wines and raisins appear to result from pesticide use of
cryolite (Na3AlF6) in the vineyards.

Sequoia Analytical, Redwood City, CA, May 1998.

Dole Pineapple juice .................... 0.78 ppm

Lucerne 2% milk ......................... 0.72
Snapple ......................................... 0.29
Coka Cola Classic ...................... 0.82
Hansens Soda ................................ 0.45
Minute Maid juice ........................ 1.20
Capri Sun juice............................... 0.37
Gerber Strawberry juice ................. 1.80
Horizon milk (organic ) .................. 0.22
Sunny Delight ................................ 0.31
Pepsi ............................................. 0.37
Knudson Recharge ......................... 0.28
Gerber White Grape ....................... 3.50
Expert Chemical Analysis, Inc., San Diego CA, June, 1998.

Gerber Graduates Berry Punch ................ 3.00 ppm

Coca Cola Classic .................................... 0.98
Minute Maid Premium Orange juice ........ 0.98
Kellogs Fruit Loops cereal ....................... 2.1 mg/kilogram

Jupiter Environmental Laboratories, Inc., Jupiter, Fl, June, 1998.

Gerber White Grape Juice .........................3.50 ppm

Gatorade Punch Concentrate ................... 0.44
Diet Coke ................................................. 1.12
Lipton Ice Tea ...........................................0.56
Sprite ........................................................0.73
Hawaiian Punch ........................................0.85
Publix Orange Juice ..................................0.79

Analytica Alaska Inc., Juneau, AK. September, 1998.

Welch’s White Grape Juice (conc.) ...........1.80 ppm

Coca Cola Classic .................................... 0.82

Northwest Testing Laboratories, Portland, OR, July 1960.

Post’s Grape Nuts cereal .......................... 6.40 ppm

Kellogg’s Shredded Wheat ........................9.40
General Mill’s Wheaties ......................... 10.10

Environmental Protection Agency (EPA) Pesticide Tolerance for residues of the insecticidal
fluorine compounds cryolite and/or synthetic cryolite (sodium aluminum fluoride). Effective
Dec. 5, 1997 to Nov. 21, 2001.

Potatoes, on or in....................................... 2.00 ppm

Processed potato waste for animal feed ... 22.00

Aug. 1997, proposed tolerances for residues of cryolite and/or synthetic cryolite:

Cabbage .................................................. 45.00 ppm

Citrus fruits ............................................. 95.00
Collards ................................................... 35.00
Eggplant ................................................. 30.00
Lettuce, head ........................................ 180.00
Lettuce, leaf ........................................... 40.00
Peaches .................................................... 10.00
Raisins ................................................... 55.00
Tomatoes ............................................... 30.00
Tomato paste .......................................... 45.00