Chemicals - Osho Ass 1

Diazinon
From Wikipedia, the free encyclopedia
This article needs additional citations for verification. Please

help improve this article by adding citations to reliable sources.
Unsourced material may be challenged and removed. (January 2013)
Diazinon
IUPAC name[hide]
O,O-Diethyl O-[4-methyl-6-(propan-2-yl)pyrimidin-2-yl]
phosphorothioate
Other names[hide]
Diethoxy-[(2-isopropyl-6-methyl-4-pyrimidinyl)oxy]thioxophosphorane
Identifiers
CAS number
333-41-5
PubChem
3017
ChemSpider
2909
UNII
YUS1M1Q929
KEGG
D07856
ChEBI
CHEBI:34682
ChEMBL
CHEMBL388560
ATCvet code
QP53AF03
Jmol-3D images
Image 1
SMILES
[show]
InChI
[show]
Properties
Molecular formula
C12H21N2O3PS
Molar mass
304.35 g mol1
Appearance
Colorless to dark brown

liquid
Density
1.116-1.118 g/cm3 at 20 C[1]
Solubility in water
40 mg/L[2]
log P
3.81 (octanol/water)[3]
Except where noted otherwise, data are given for materials in

their standard state (at 25 C (77 F), 100 kPa)
(verify) (what is:
?)
Infobox references
Diazinon (IUPAC name: O,O-Diethyl O-[4-methyl-6-(propan-2-yl)pyrimidin-2-yl]
phosphorothioate, INN -Dimpylate), a colorless to dark brown liquid, is a thiophosphoric acid ester
developed in 1952 by Ciba-Geigy, a Swiss chemical company (later Novartis and then Syngenta). It is a
nonsystemic organophosphate insecticide formerly used to control cockroaches, silverfish, ants,
and fleas in residential, non-food buildings. Diazinon was heavily used during the 1970s and early
1980s for general-purpose gardening use and indoor pest control. A bait form was used to control
scavenger wasps in the western U.S. Diazinon is used in flea collars for domestic pets in Australia and
New Zealand. Residential uses of diazinon were outlawed in the U.S. in 2004 but it is still approved for
[4]
agricultural uses. An emergency antidote is atropine.
Contents
[hide]
History[edit]
Diazinon was developed in 1952 by the Swiss company Ciba-Geigy as a replacement for the insecticide
DDT. Diazinon became available for mass use in 1955, as DDT production tapered. Prior to 1970
diazinon had issues with contaminants in the solution. However, by the 1970s, alternative purification
methods were utilized to reduce residual materials. After this, diazinon became an all-purpose indoor
and outdoor commercial pest control product. In 2004, U.S. residential use of diazinon was outlawed,
except for agricultural purposes and cattle ear tags .
Structure and reactivity[edit]

The structure of diazinon contains a thiophosphoric ester. The phosphorus center is the reactive site of
the chemical. However, no known mechanisms currently exist. A novel mechanism does exist, which
proposes that the sulfur is protonated in acidic medium via a hydronium ion which ultimately delivers a
hydroxide group to the phosphorus center and can react readily.
The form of diazinon varies widely as it can be in dusts, granules, liquids, concentrates,
microencapsulations, wettable powders, and seed dressings. Its appearance varies depending on
purity, ranging from a dark brown (industrial grade), to a colorless liquid (pure). Indicative of its
functionality of a thiophosphoric ester, the chemical has a pronounced smell similar to that of diethyl
ether.
Diazinon is relatively stable under standard ambient temperature and pressure but is susceptible to form
toxic phosphine gas upon heating. Furthermore, diazinon can oxidize into toxic phosphorus oxides if in
the presence of a strong oxidizing agent.
Synthesis[edit]
According to the German Patent bureau, the industrial synthesis of diazinon is as follows:
-isobutyrylaminocrotonic acid amine was cyclized with NaOR (R is either a hydrogen or
aliphatic chain of 1 to 8 carbons) in a mixture of 0 to 100% by weight of water and an alcohol
having 1 to 8 carbon atoms, above 90C (but below the boiling point of the mixture used).
Sodium pyrimidinolate was precipitated out in an inert solvent, such as benzene, with
simultaneous removal of the water formed. The potassium salt is then reacted with
diethylthiophosphoryl chloride by heating for several hours. When the reaction finished, the
potassium chloride formed was washed with water and the solvent was removed under
reduced pressure leaving diazinon.
Metabolism and mechanism of action[edit]

Diazinon functions as an acetylcholinesterase (AChE) inhibitor. This enzyme breaks down the
neurotransmitter acetylcholine (ACh) into [choline] and an acetate group. (1) The inhibition of the
AChE causes an abnormal accumulation of ACh in the synaptic cleft. When Diazinon enters the
body, it is oxidatively degenerated to diaxozon, an organophosphate compound that is much more
poisoning than diazinon and causes mainly the inhibition of AChE (6). The activation of diazinon
(Reaction 1) is located in the liver microsomal enzyme system and requires O 2 and NADPH.
Additionally it can also be degenerated via oxidation in the microsomal enzyme system (Reaction
2). Both reactions are possible, and likely are catalyzed nonspecifically by the same mixed function
oxidase. Once formed diazoxon is biotransformed again as it is degenerated. Diazoxon is
degenerated due to the very effective hydrolyases in the microsomal and other sub cellular factions
within the liver (Reaction 3). Mammalian specie degenerate diazoxon at a much slower rate though
(with a half-life of 2 to 6 weeks). Insects lack this hydrolysis step which allows for the toxic species
to accumulate rapidly. The detoxification of diazoxon is processed through the mircosomal mixed
function oxidase system. Although not fully known, it is believed that this is the cause for the
selectivity of diazinon against insects. After the hydrolysis or oxidation diazinon is further
degenerated (Reaction 4).
The mechanism, described above of the biotransformation of Diazinon

Toxicity and effects on animals: Diazinon is considered to be of relatively high toxicity for
vertebrates. The common method of administering diazinon is absorption although inhalation is
possible as well. The observed toxification symptoms conform to other acetylcholinesterase
inhibitors. Symptoms are as follows:
Colics
Diarrhea and/or Vomiting
Vertigo
Headaches
Miosis
Bradycardia
Sudden Drop in blood pressure
Convulsion
Apnea
Lethal Dose
LD50
Observations
214 mgkg1 (human, oral, TDLo) (2,3)

66 mgkg1 (rat, oral, LD50) (2,4)
17 mgkg1 (mouse, oral, LD50) (2,5)
Symptoms in humans[edit]
Intoxication of diazinon produces the following signs and symptoms:
Eyes, ears, nose, and throat

Small pupils (unreactive to light)
Tearing, increased
Cardiovascular
Low or high blood pressure

Slow or rapid heart rate
Respiratory
Breathing difficulty
Chest tightness
Nervous system
Anxiety
Convulsions
Coma
Dizziness
Excitability
Headache
Weakness
Tremor
Twitching
Skin
Irritation
Redness
Sweating
Gastrointestinal
Abdominal cramps
Diarrhea
Loss of appetite
Nausea
Vomiting
Typically treatments will vary depending on exposure and method of administration of the toxin.
Critical biomarkers such as urine samples, blood content and heart rates are measured while
detoxifying the patient. Common treatments for patients suffering from diazinon poisoning include:
Assisted Breathing
Intravenous fluids (IV)
Irrigation (washing of the skin and eyes)
[5]
Medicinal Treatments; including the antidotes atropine and oxime.
Gastric Lavage
Patients that continue to improve over the first 4 to 6 hours (after medical treatment) usually
recover unscathed. Prolonged treatment often is needed to reverse the poisoning, including
intensive care hospitalization and long-term therapy. Some toxicity may persist for weeks or
months, or even longer.
Efficacy and side effects[edit]

Diazinon is a contact insecticide which kills insects by altering normal neurotransmission within the
nervous system of the insect. As mentioned above, diazinon inhibits the enzyme
acetylcholinesterase (AChE), which hydrolyzes the neurotransmitter acetylcholine (ACh) in
cholinergic synapses and neuromuscular junctions. This results in abnormal accumulation of ACh
within the nervous system. Diazinon, although a thiophosphoric ester, shares a common
mechanism of toxicity with other organophosphate insecticides such as chlorpyrifos, malathion and
parathion, and is not very effective against the organophosphate-resistant insect populations.
Symptoms of acute diazinon exposure develop in minutes to hours following exposure, depending
of the exposure pathway. The initial symptoms of humans are nausea, dizziness, salivation,
headache, sweating, lacrimation, and rhinorrhea. The symptoms can progress to vomiting,
abdominal cramps, diarrhea, muscle twitching, weakness, tremor, a lack of coordination and
miosis. Furthermore, some studies have even reported some psychiatric side effects as well
including memory loss, confusion, and depression.
Because diazinon is fat soluble, there is potential for delayed toxicity if significant amounts of
diazinon are stored in fatty tissues. Intermediate syndrome generally occurs within 2496 hours
after exposure. Intermediate syndrome in humans is characterized by difficulty breathing and

muscular weakness, often in the face neck and proximal limb muscles. Cranial nerve palsies and
depressed tendon reflexes have also been reported.
Studies have suggested that exposure to some organophosphate pesticides can result in long-term
neurological problems including organophosphate-induced delayed neuropathy (weakness or
paralysis as well as paresthesia in the extremities); however, reports of these symptoms following
diazinon exposures are rare. Human poisoning victims have shown increased levels of serum
amylase and glucose as well as elevated urinary diastase levels accompanied by symptoms
considered to be indicative of acute pancreatitis.
Saccharin
(Redirected from Sodium saccharin)
Saccharin[1]
IUPAC name[hide]
2H-16,2-benzothiazol-1,1,3-trione
Other names[hide]
Benzoic sulfimide
Ortho sulphobenzamide
Identifiers
CAS number
81-07-2
PubChem
5143
ChemSpider
4959
UNII
FST467XS7D
KEGG
D01085
ChEBI
CHEBI:32111
ChEMBL
CHEMBL310671
Jmol-3D images
Image 1
SMILES
[show]
InChI
[show]
Properties
Molecular formula
C7H5NO3S
Molar mass
183.18 g mol1
Appearance
White crystalline solid
Density
0.828 g/cm3
Melting point
228.8-229.7 C
Solubility in water
1 g per 290 mL

(verify) (what is:
?)
Infobox references
[2]
Saccharin is an artificial sweetener with effectively no food energy which is approximately 300 times
as sweet as sucrose or table sugar, but has a bitter or metallic aftertaste, especially at high
concentrations. It is used to sweeten products such as drinks, candies, cookies, medicines, and
toothpaste.
Origins[edit]
Saccharin derives its name from the word "saccharine", meaning of, relating to, or resembling sugar.
Properties[edit]
[3]
Sodium salt of saccharin: A white powder

Saccharin is unstable when heated but it does not react chemically with other food ingredients. As such,
it stores well. Blends of saccharin with other sweeteners are often used to compensate for each
sweetener's weaknesses and faults. A 10:1cyclamate:saccharin blend is common in countries where
both these sweeteners are legal; in this blend, each sweetener masks the other's off-taste. Saccharin is
often used together with aspartame in diet carbonated soft drinks, so that some sweetness remains
should the fountain syrup be stored beyond aspartame's relatively short shelf-life. Saccharin is believed
to be an important discovery, especially for diabetics, as it goes directly through the human digestive
system without being digested. Although saccharin has no food energy, it may trigger the release
of insulin in humans and rats, presumably as a result of its taste, but this is not conclusive as the same
[4][5][6]
study states "No statistically significant changes in plasma insulin were found."
This is similar for
[7]
aspartame (another artificial sweetener).
In its acid form, saccharin is not water-soluble. The form used as an artificial sweetener is usually
its sodium salt. Thecalcium salt is also sometimes used, especially by people restricting their dietary
sodium intake. Both salts are highly water-soluble: 0.67 grams per milliliter water at room
[8][9]
temperature.
History[edit]
Saccharin, historical wrapping;Sugar Museum (Berlin)

Saccharin was produced first in 1878 by Constantin Fahlberg, a chemist working oncoal tar derivatives
in Ira Remsen's laboratory at the Johns Hopkins University. (As discussed below, the relative
contributions of Fahlberg and Remsen to the discovery were later contested, with no final resolution in
sight; the 1879 paper announcing the discovery lists both names as authors, with Fahlberg's name first.)
Fahlberg noticed a sweet taste on his hand one evening, and connected this with the compound that he
[10][11]
had been working on that day.
Fahlberg and Remsen published articles on benzoic sulfimide in
[8][12]
1879 and 1880.
In 1884, then working on his own in New York City, Fahlberg applied for patents in
[13]
several countries, describing methods of producing this substance that he named saccharin. Two
years later he began production of the substance in a factory in a suburb of Magdeburg, Germany.
Fahlberg would soon grow wealthy, while Remsen merely grew irritated, believing that he deserved
credit for substances produced in his laboratory. On the matter, Remsen commented, "Fahlberg is a
[14]
scoundrel. It nauseates me to hear my name mentioned in the same breath with him."
Although saccharin was commercialized not long after its discovery, it was not until sugar shortages
during World War I that its use became widespread. Its popularity further increased during the 1960s
and 1970s among dieters, since saccharin is a calorie-free sweetener. In the United States, saccharin is
often found in restaurants in pink packets; the most popular brand is "Sweet'n Low".
Government regulation[edit]
Starting in 1907, the USDA began investigating saccharin as a direct result of the Pure Food and Drug
Act. Harvey Wiley, then the director of the bureau of chemistry for the USDA, viewed it as an illegal
substitution of a valuable ingredient (sugar) by a less valuable ingredient. In a clash that had career
consequences, Wiley told President Theodore Roosevelt that "Everyone who ate that sweet corn was
deceived. He thought he was eating sugar, when in point of fact he was eating a coal tar product totally
devoid of food value and extremely injurious to health." But Roosevelt himself was a consumer of
saccharin, and, in a heated exchange, Roosevelt angrily answered Wiley by stating, "Anybody who says
[15]
saccharin is injurious to health is an idiot." The episode proved the undoing of Wiley's career.
In 1911, the Food Inspection Decision 135 stated that foods containing saccharin were adulterated.
However, in 1912, Food Inspection Decision 142 stated that saccharin was not harmful.
More controversy was stirred in 1969 with the discovery of files from the FDA's investigations of 1948
and 1949. These investigations, which had originally argued against saccharin use, were shown to
prove little about saccharin being harmful to human health. In 1972, the USDA made an attempt to
[16][full citation needed]
completely ban the substance.
However, this attempt was also unsuccessful, and the
sweetener continued to be widely used in the United States. It is now the most popular artificial
sweetener after sucralose and aspartame.
In the European Union, saccharin is also known by the E number (additive code) E954.
The current status of saccharin is that it is allowed in most countries, and countries like Canada are
[17]
considering lifting their previous ban of it as a food additive. The claims that it is associated with
[18]
bladder cancer were shown to be unfounded in experiments on primates. (It is, however, prohibited to
[19]
mail saccharin tablets or packets to France.)
Saccharin was formerly on California's list of chemicals known to the state to cause cancer for the
[20]
purposes of Proposition 65, but it was delisted in 2001.
Warning label addition and removal[edit]

In 1958, the United States Congress amended the Food, Drugs, and Cosmetic Act of 1938 with
the Delaney clause to mandate that the Food and Drug Administrationnot approve substances that
"induce cancer in man, or, after tests, [are] found to induce cancer in animals." Studies in laboratory rats
during the early 1970s linked saccharin with the development of bladder cancer in rodents. As a
consequence, all food containing saccharin was labeled with a warning meeting the requirement of
[21]
the Saccharin Study and Labeling Act of 1977.
However, in 2000, the warning labels were removed because scientists learned that rodents, unlike
humans, have a unique combination of high pH, high calcium phosphate, and high protein levels in their
[22][23]
urine.
One or more of the proteins that are more prevalent in male rats combine with calcium
phosphate and saccharin to produce microcrystals that damage the lining of the bladder. Over time, the
rat's bladder responds to this damage by over-producing cells to repair the damage, which leads to
tumor formation. Since this does not occur in humans, there is no elevated risk of bladder cancer.
The delisting of saccharin led to legislation, known as the Sweetness Act; which was signed into law on
[citation
December 21, 2000, repealing the warning label requirement for products containing saccharin.
needed]
In 2001, the U.S. Food and Drug Administration and the state of California reversed their positions
[24]
on saccharin, declaring it safe for consumption. The FDA's decision followed a 2000 determination by
the U.S. Department of Health and Human Services' National Toxicology Program to remove saccharin
from its list of carcinogens.
The EPA has officially removed saccharin and its salts from their list of hazardous constituents and
commercial chemical products. In a December 14, 2010 release, the EPA stated that saccharin is no
[25]
longer considered a potential hazard to human health.
Chemistry[edit]
[26]
Saccharin can be produced in various ways. The original route by Remsen & Fahlberg starts
[27]
with toluene; another route begins with o-chlorotoluene. Sulfonation by chlorosulfonic acid gives
the ortho and para substituted sulfonyl chlorides. The ortho isomer is separated and converted to
the sulfonamide with ammonia. Oxidation of the methyl substituent gives the carboxylic acid, which
[28]
cyclicizes to give saccharin free acid:
In 1950, an improved synthesis was developed at the Maumee Chemical Company of Toledo,
Ohio. In this synthesis, anthranilic acid successively reacts with nitrous acid (from sodium
[28]
nitrite and hydrochloric acid), sulfur dioxide, chlorine, and then ammonia to yield saccharin:
The free acid of saccharin has a low pKa of about 2 (the acidic hydrogen being that attached
[29][30]
to the nitrogen).
Saccharin can be used to prepare exclusively
[31]
disubstituted amines from alkyl halides via a nucleophilic substitution, followed by Gabriel
synthesis.
Aspartame
(Redirected from Aspertame)
Aspartame[1]
IUPAC name[hide]
N-(L--Aspartyl)-L-phenylalanine,
1-methyl ester
Identifiers
CAS number
22839-47-0
ChemSpider
118630
UNII
Z0H242BBR1
DrugBank
DB00168
KEGG
C11045
ChEBI
CHEBI:2877
ChEMBL
CHEMBL171679
Jmol-3D images
Image 1
SMILES
[show]
InChI
[show]
Properties
Molecular formula
C14H18N2O5
Molar mass
294.30 g mol1
Density
1.347 g/cm3
Melting point
246247 C
Boiling point
decomposes
Solubility in water
sparingly soluble
Solubility
slightly soluble in ethanol
Acidity (pKa)
4.56.0[2]
Hazards
NFPA 704
1
1
0

(verify) (what is:
?)
Infobox references
Aspartame (APM; /sprtem/ or /sprtem/) is an artificial, non-saccharide sweetener used as
a sugar substitute in some foods and beverages. In the European Union, it is codified as E951.
Aspartame is a methyl ester of the aspartic acid/phenylalanine dipeptide. It was first sold under the
brand name NutraSweet; It was first synthesized in 1965 and the patent expired in 1992.
The safety of aspartame has been the subject of several political and medical
[3][4][5]
controversies, congressional hearings and Internet hoaxes
since its initial approval for use in food
[6]:2
products by the U.S. Food and Drug Administration (FDA) in 1981.
The European Food Safety
Authority concluded in its 2013 re-evaluation that aspartame and its breakdown products are safe for
[7]
[8]
human consumption at current levels of exposure, corroborating other medical reviews. However,
because its breakdown products include phenylalanine, aspartame must be avoided by people with the
genetic condition phenylketonuria (PKU).
Chemistry[edit]
Aspartame is a methyl ester of the dipeptide of the natural amino acids L-aspartic acid and Lphenylalanine. Under strongly acidic or alkaline conditions, aspartame may
generate methanol by hydrolysis. Under more severe conditions, thepeptide bonds are also hydrolyzed,
[9]
resulting in the free amino acids.
[10]
While known aspects of synthesis are covered by patents, many details are proprietary. Two
approaches to synthesis are used commercially. In the chemical synthesis, the two carboxyl groups of
aspartic acid are joined into an anhydride, and the amino group is protected by a compound that will
prevent further reactions of that group. Phenylalanine is methylated and combined with the N-protected
aspartic anhydride, then the blocking group is removed from aspartic acid by acid hydrolysis. The
drawback of this technique is that a byproduct, the bitter tasting -form, is produced when the wrong
carboxyl group from aspartic acid links to phenylalanine. A process using an enzyme from Bacillus
thermoproteolyticus to catalyze the condensation of the chemically altered amino acids will produce high
yields without the -form byproduct. A variant of this method, which has not been used commercially,
uses unmodified aspartic acid, but produces low yields. Methods for directly producing aspartylphenylalanine by enzymatic means, followed by chemical methylation, have also been tried, but not
[11]
scaled for industrial production.
Properties and use[edit]
Beta-aspartame differs from aspartame based upon which carboxyl group of aspartate binds to the
nitrogen of phenylalanine.
Aspartame, an artificial sweetener, is approximately 200 times sweeter than sucrose, or table sugar.
Due to this property, even though aspartame produces four kilocalories of energy per gram when
metabolized, the quantity of aspartame needed to produce a sweet taste is so small that its caloric
[8]
contribution is negligible. The taste of aspartame and other artificial sweeteners differs from that of
table sugar in the times of onset and how long the sweetness lasts, though aspartame comes closest to
[10]
sugar's taste profile among approved artificial sweeteners. The sweetness of aspartame lasts longer
than sucrose, so it is often blended with other artificial sweeteners such as acesulfame potassium to
[12]
produce an overall taste more like sugar. Aspartame can be synthesized from its constituent amino
acids, L-phenylalanine andL-aspartate.
Like many other peptides, aspartame may hydrolyze (break down) into its constituent amino acids under
conditions of elevated temperature or high pH. This makes aspartame undesirable as a baking
sweetener, and prone to degradation in products hosting a high pH, as required for a long shelf life. The
stability of aspartame under heating can be improved to some extent by encasing it in fats or
in maltodextrin. The stability when dissolved in water depends markedly on pH. At room temperature, it
is most stable at pH 4.3, where its half-life is nearly 300 days. At pH 7, however, its half-life is only a few
days. Most soft-drinks have a pH between 3 and 5, where aspartame is reasonably stable. In products
that may require a longer shelf life, such as syrups for fountain beverages, aspartame is sometimes
[13]
blended with a more stable sweetener, such as saccharin.
Aspartame's major decomposition products are its cyclic dipeptide (in a 2,5-diketopiperazine, or DKP,
form), the de-esterified dipeptide (aspartyl-phenylalanine), and its constituent
[14]
[15]
[16]
components, phenylalanine, aspartic acid, and methanol. At 180 C, aspartame undergoes
[17]
decomposition to form a diketopiperazine derivative.
In products such as powdered beverages, the amine in aspartame can undergo a Maillard reaction with
the aldehyde groups present in certain aroma compounds. The ensuing loss of both flavor and
sweetness can be prevented by protecting the aldehyde as an acetal.
Descriptive analyses of solutions containing aspartame report a sweet aftertaste as well as bitter and
[18]
off-flavor aftertastes.
Discovery and approval[edit]

Aspartame was discovered in 1965 by James M. Schlatter, a chemist working for G.D. Searle &
Company. Schlatter had synthesized aspartame as an intermediate step in generating a tetrapeptide of
[19]
the hormone gastrin, for use in assessing an anti-ulcer drug candidate. He accidentally discovered its
sweet taste when he licked his finger, which had become contaminated with aspartame, to lift up a piece
[8][20][21]
of paper.
In 1975, prompted by issues regarding Flagyl and Aldactone, a U.S. FDA task force team reviewed 25
studies submitted by the manufacturer, including 11 on aspartame. The team reported "serious
[6]
deficiencies in Searle's operations and practices". The FDA sought to authenticate 15 of the submitted
studies against the supporting data. In 1979, the Center for Food Safety and Applied Nutrition (CFSAN)
concluded, since many problems with the aspartame studies were minor and did not affect the
[6]
conclusions, the studies could be used to assess aspartame's safety.
In 1980, the FDA convened a Public Board of Inquiry (PBOI) consisting of independent advisors
charged with examining the purported relationship between aspartame and brain cancer. The PBOI
concluded aspartame does not cause brain damage, but it recommended against approving aspartame
[6]:9496[22]
at that time, citing unanswered questions about cancer in laboratory rats.
[23]
Citing data from a Japanese study that had not been available to the members of the PBOI, and after
seeking advice from an expert panel that found fault with statistical analyses underlying the PBOI's
[6]:53
hesitation, yet argued against approval,
FDA commissioner Hayes approved aspartame for use in
[6]
dry goods. In 1983, the FDA further approved aspartame for use in carbonated beverages, and for use
in other beverages, baked goods, and confections in 1993. In 1996, the FDA removed all restrictions
from aspartame, allowing it to be used in all foods.
Several European Union countries approved aspartame in the 1980s, with EU-wide approval in 1994.
The European Commission Scientific Committee on Foodreviewed subsequent safety studies and
reaffirmed the approval in 2002. The European Food Safety Authority reported in 2006 that the
previously establishedAcceptable daily intake was appropriate, after reviewing yet another set of
[24]
studies.
Compendial status[edit]
[25]
British Pharmacopoeia
[26]
United States Pharmacopeia
Safety and approval controversies[edit]

Main article: Aspartame controversy
Aspartame has been found to be safe for human consumption by more than ninety countries
[27][28]
worldwide,
with FDA officials describing aspartame as "one of the most thoroughly tested and
[29]
studied food additives the agency has ever approved" and its safety as "clear cut", but has been the
[3]
[30]
subject of several controversies, hoaxes and health scares.
Initially aspartame was approved by the U.S. Food and Drug Administration (FDA) in 1974, however,
problems with Searle's safety testing program, including testing of aspartame, were discovered
subsequently. The approval was rescinded the following year, but after outside reviews of the
problematic tests and additional testing, final approval was granted in 1981. Because allegations
[6][31][32]
of conflicts of interest marred the FDA's approval of aspartame,
the U.S. Government
Accountability Office reviewed the actions of involved officials in 1986 and the approval process in 1987;
neither the allegations of conflict of interest nor problems in the final approval process were
[6][33]
substantiated.
In addition, the Centers for Disease Control investigated in 1984 and was unable to find any
[34]
significant epidemiological associations to serious risk or harm.
Since December 1998, a widely circulated email hoax cited aspartame as the cause of numerous
[35]
diseases.
The weight of existing scientific evidence indicates that aspartame is safe at current levels of
[8]
consumption as a non-nutritive sweetener. Reviews conducted by regulatory agencies decades after
[36]
aspartame was first approved have supported its continued availability. The consumer
advocacy group the Center for Science in the Public Interest continues to promote the position that
[37]
aspartame is not safe.
Safety and health effects[edit]

The safety of aspartame has been studied extensively since its discovery with research that includes
[38]
animal studies, clinical and epidemiological research, andpostmarketing surveillance, with aspartame
[39]
being one of the most rigorously tested food ingredients to date. Peer-reviewed comprehensive
review articles and independent reviews by governmental regulatory bodies have analyzed the
published research on the safety of aspartame and have found aspartame is safe for consumption at
[8][38][40][41]
current levels.
Aspartame has been deemed safe for human consumption by over one hundred
[41]
(100) regulatory agencies in their respective countries, including the UK Food Standards
[42]
[43]
[44]
Agency, the European Food Safety Authority (EFSA) and Health Canada.
Intake[edit]
The acceptable daily intake (ADI) value for aspartame, as well as other food additives studied, is
defined as the "amount of a food additive, expressed on a body weight basis, that can be ingested daily
[45]
over a lifetime without appreciable health risk." The Joint FAO/WHO Expert Committee on Food
Additives (JECFA) and theEuropean Commission's Scientific Committee on Food has determined this
[46]
value is 40 mg/kg of body weight for aspartame, while FDA has set its ADI for aspartame at
[47]
50 mg/kg.
The primary source for exposure to aspartame in the United States is diet soft drinks, though it can be
consumed in other products, such as pharmaceutical preparations, fruit drinks, and chewing gum
[8]
among others in smaller quantities. A 12 US fluid ounce (355 ml) can of diet soda contains 180
milligrams (0.0063 oz) of aspartame, and for a 75 kg (165 lb) adult, it takes approximately 21 cans of
diet soda daily to consume the 3,750 milligrams (0.132 oz) of aspartame that would surpass the FDA's
[47]
50 milligrams per kilogram of body weight ADI of aspartame from diet soda alone.
Reviews have analyzed studies which have looked at the consumption of aspartame in countries
worldwide, including the United States, countries in Europe and Australia, among others. These reviews
have found that the even high levels of intake of aspartame, studied across multiple countries and
different methods of measuring aspartame consumption, is well below the ADI for safe consumption of
[8][38][41][46]
aspartame.
Reviews have also found that populations that are believed to be especially high
consumers of aspartame such as children and diabetics are below the ADI for safe consumption, even
[8][38]
considering extreme worst-case scenario calculations of consumption.
In a report released on 10 December 2013, the EFSA said that, after an extensive examination of
evidence, it ruled out the "potential risk of aspartame causing damage to genes and inducing cancer,"
[48]
and deemed the amount found in diet sodas an amount safe to consume.
Metabolites[edit]
Aspartame is rapidly hydrolyzed in the small intestines. Even with ingestion of very high doses of
[8]
aspartame (over 200 mg/kg), no aspartame is found in the blood due to the rapid breakdown. These
metabolites have been studied in a wide range of populations including infants, children, adolescents,
and healthy adults. In healthy adults and children, even enormous doses of aspartame do not lead to
plasma levels of metabolites that are a concern for safety.
Upon ingestion, aspartame breaks down into residual components, including aspartic
[49]
[50]
acid, phenylalanine, methanol, in ratio of 4:5:1 by mass and further breakdown products
[51]
including formaldehyde and formic acid, accumulation of the latter being suspected as the major
cause of injury in methanol poisoning. Human studies show that formic acid is excreted faster than it is
formed after ingestion of aspartame. In some fruit juices, higher concentrations of methanol can be
[15]
found than the amount produced from aspartame in beverages.
Aspartate[edit]
Aspartic acid (aspartate) is one of the most common amino acids in the typical diet. As with methanol
and phenylalanine, intake of aspartic acid from aspartame is less than would be expected from other
dietary sources. At the 90th percentile of intake, aspartame provides only between 1% and 2% of the
[52][53]
daily intake of aspartic acid. There has been some speculation
that aspartame, in conjunction with
other amino acids like glutamate, may lead to excitotoxicity, inflicting damage on brain and nerve cells.
[8]
However, clinical studies have shown no signs of neurotoxic effects, and studies of metabolism
suggest it is not possible to ingest enough aspartic acid and glutamate through food and drink to levels
[41]
that would be expected to be toxic.
Methanol[edit]
The methanol produced by the metabolism of aspartame is absorbed and quickly converted
into formaldehyde and then completely oxidized to formic acid, which, due to its long half life, is
considered the primary mechanism of toxicity in methanol poisoning. The methanol from aspartame is
unlikely to be a safety concern for several reasons. The amount of methanol in aspartame is less than
that found in fruit juices and citrus fruits, and there are other dietary sources for methanol such
asfermented beverages. Therefore, the amount of methanol produced from aspartame is likely to be
less than that from natural sources. With regard to formaldehyde, it is rapidly converted in the body, and
the amounts of formaldehyde from the metabolism of aspartame are trivial when compared to the
amounts produced routinely by the human body and from other foods and drugs. At the highest
expected human doses of consumption of aspartame, there are no increased blood levels of methanol
[8]
or formic acid, and ingesting aspartame at the 90th percentile of intake would produce 25 times less
[41]
methanol than what would be considered toxic.
Phenylalanine and phenylketonuria[edit]

High levels of the naturally-occurring essential amino acid phenylalanine are a health hazard to those
born with phenylketonuria (PKU), a rare inherited disease that prevents phenylalanine from being
properly metabolized. Since individuals with PKU must consider aspartame as an additional source of
phenylalanine, foods containing aspartame sold in the United States must state "Phenylketonurics:
[54]
Contains Phenylalanine" on their product labels.
In the UK, foods that contain aspartame are legally required by the country's Food Standards Agency to
list the substance among the product's ingredients and carry the warning "Contains a source of
phenylalanine" this is usually at the foot of the list of ingredients. Manufacturers are also required to
print '"with sweetener(s)" on the label close to the main product name on foods that contain "sweeteners
such as aspartame" or "with sugar and sweetener(s)" on "foods that contain both sugar and
[55]
sweetener".
In Canada, foods that contain aspartame are legally required by the country to list the substance among
the product's ingredients and include a measure of the amount of aspartame per serving. As well, labels
must state that the product contains phenylalanine this is usually in the order of ingredients, contained
[56]
in brackets.
Phenylalanine is one of the essential amino acids and is required for normal growth and maintenance of
life. Concerns about the safety of phenylalanine from aspartame center largely on hypothetical changes
in neurotransmitter levels as well as ratios of neurotransmitters to each other in the blood and brain that
could lead to neurological symptoms. Reviews of the literature have found no consistent findings to
[41]
support such concerns, and while high doses of aspartame consumption may have some biochemical
effects, these effects are not seen in toxicity studies to suggest aspartame can adversely affect neuronal
[8]
function. Like methanol, the typical diet will lead to ingestion of significantly higher amounts of
[41]
phenylalanine than would be expected from aspartame consumption. People with the genetic
disorder phenylketonuria are advised to avoid aspartame as they have a decreased ability to metabolize
phenylalanine. Common foods such as milk, meat, and fruits provide far greater amounts of these
[41]
metabolites in a diet than does aspartame.
Lactation[edit]
In a study done in 1979, the effect of aspartame ingestion on blood and milk amino acid levels in
[57]
lactating women was tested. In this study, six women from the ages of 20 to 29 with established
lactation were studied after oral administration of aspartame or lactose (50 mg/kg body weight) in a
random order, with the intent to study the differences in breast milk between the two. The study resulted
with the conclusion that aspartame administration at 50 mg/kg body weight has a small effect upon the
milk aspartate levels and although a small increase in aspartate time-effect scores was noted over the
four-hour postabsorptive period, no significant difference was noted over the entire 24-hour watching
[57]
period.
Cancer[edit]
Reviews have found no association between aspartame and cancer. These reviews have looked at
numerous carcinogenicity studies in animals, epidemiologic studies in humans, as well as in
vitro genotoxicity studies. These studies have found no significant evidence that aspartame causes
cancer in animals, damages the genome, or causes cancer in humans at doses currently
[8][38][41]
[58]
used.
This position is supported by multiple regulatory agencies like the FDA and EFSA as well
[47]
as scientific bodies such as the National Cancer Institute.
Concern about possible carcinogenic properties of aspartame was originally raised and popularized in
the mainstream media by John Olney in the 1970s and again in 1996 by suggesting that aspartame may
be related to brain tumors. Reviews have found that these concerns were flawed, due to reliance on
[59]
the ecological fallacy and the purported mechanism of causing tumors being unlikely to actually cause
cancer. Independent agencies such as the FDA and National Cancer Institute have reanalyzed multiple
[41]
studies based on these worries and found no association between aspartame and brain cancer.
As discussed in the article on controversies around aspartame, the Cesare Maltoni Cancer Research
Center of the European Ramazzini Foundation of Oncology and Environmental Sciences released
several studies which claimed that aspartame can increase several malignancies in rodents, concluding
[60][61]
[62]
that aspartame is a potential carcinogen at normal dietary doses.
The EFSA and the
[58]
FDA discounted the study results and found no reason to revise their previously established
acceptable daily intake levels for aspartame.
Neurological and psychiatric symptoms[edit]

Numerous allegations have been made on the Internet and in consumer magazines purporting
neurotoxic effects of aspartame leading to neurological or psychiatric symptoms such
[8]
as seizures, headaches, and mood changes. Review of the biochemistry of aspartame has found no
[63]
evidence that the doses consumed would plausibly lead to neurotoxic effects. Comprehensive
[8][38][41]
reviews have not found any evidence for aspartame as a cause for these symptoms.
One review
did provide a theoretical biochemical background of neurotoxicity and suggested further
[64]
testing. However, a panel of EFSA experts noted that this review's conclusions were partially based
on Internet sources and therefore were not scientifically robust. These experts also concurred with a
critique that significant scientific errors were made in the critical review that led to unsubstantiated and
[38]
misleading interpretations. A review of the pediatric literature did not show any significant findings for
safety concerns with regard to neuropsychiatric conditions such as panic attacks, mood
[65]
changes, hallucinations or with ADHD or seizures.
Headaches[edit]
[8]
Headaches are the most common symptom reported by consumers. While one small review noted
aspartame is likely one of many dietary triggers of migraines, in a list that includes "cheese,
chocolate, citrus fruits, hot dogs, monosodium glutamate, aspartame, fatty foods, ice cream, caffeine
[66]
withdrawal, and alcoholic drinks, especially red wine and beer," other reviews have noted conflicting
[8][67]
studies about headaches
and still more reviews lack any evidence and references to support this
[38][41][65]
claim.
Weight change and hunger[edit]

Since the caloric contribution of aspartame is negligible, it has been used as a means for weight loss
through its role as a sugar substitute, with reviews finding that aspartame may aid in weight loss as part
of a multidisciplinary weight loss program. On its own, aspartame is not known by medical literature to
[8][41]
cause weight gain or weight loss.
Although researchers have theorized that aspartame contributes
[8][68]
to hunger or increases appetite psychologically,
broad reviews and regulators conclude that
[8][38]
aspartame has no appreciable effect on appetite.
Commercial uses[edit]
Under the trade names Equal, NutraSweet, and Canderel, aspartame is an ingredient in approximately
6,000 consumer foods and beverages sold worldwide, including (but not limited to) diet sodas and other
soft drinks, instant breakfasts, breath mints, cereals, sugar-free chewing gum, cocoa mixes, frozen
desserts, gelatin desserts, juices, laxatives, chewable vitamin supplements, milk drinks, pharmaceutical
drugs and supplements, shake mixes, tabletop sweeteners, teas, instant coffees, topping mixes, wine
coolers and yogurt. It is provided as a table condiment in some countries. Aspartame is less suitable
for baking than other sweeteners, because it breaks down when heated and loses much of its
sweetness.
NutraSweet Company[edit]
In 1985, Monsanto Company bought G.D. Searle, and the aspartame business became a separate
Monsanto subsidiary, the NutraSweet Company. In March 2000, Monsanto sold it to J.W. Childs Equity
[69]
[70]
Partners II L.P. European use patents on aspartame expired starting in 1987, and the U.S. patent
expired in 1992. Since then, the company has competed for market share with other manufacturers,
including Ajinomoto, Merisant and the Holland Sweetener Company.
Ajinomoto[edit]
[10]
Many aspects of industrial synthesis of aspartame were established by Ajinomoto. In 2004, the
market for aspartame, in which Ajinomoto, the world's largest aspartame manufacturer, had a 40
percent share, was 14,000 metric tons a year, and consumption of the product was rising by 2 percent a
[71]
[72]
year. Ajinomoto acquired its aspartame business in 2000 from Monsanto for $67M.
In 2008, Ajinomoto sued British supermarket chain Asda, part of Wal-Mart, for a malicious falsehood
action concerning its aspartame product when the substance was listed as excluded from the chain's
[73]
[74]
product line, along with other "nasties". In July 2009, a British court found in favour of Asda. In
June 2010, an appeals court reversed the decision, allowing Ajinomoto to pursue a case against Asda
[75]
to protect aspartame's reputation. Asda said that it would continue to use the term "no nasties" on its
[76]
own-label products, but the suit was settled in 2011 with ASDA choosing to remove references to
[77]
aspartame from its packaging.
In November 2009, Ajinomoto announced a new brand name for its aspartame sweetener
[78]
AminoSweet.
Holland Sweetener Company[edit]

A joint venture of DSM and Tosoh, the Holland Sweetener Company manufactured aspartame using the
[79]
enzymatic process developed by Toyo Soda (Tosoh) and sold as the brand Sanecta. Additionally,
[80]
they developed a combination aspartame-acesulfame salt under the brand name Twinsweet. They
left the sweetener industry in late 2006, because "global aspartame markets are facing structural
oversupply, which has caused worldwide strong price erosion over the last five years", making the
[81]
business "persistently unprofitable".
Competing products[edit]
Because sucralose, unlike aspartame, retains its sweetness after being heated, and has at least twice
[82]
the shelf life of aspartame, it has become more popular as an ingredient. This, along with differences
in marketing and changing consumer preferences, caused aspartame to lose market share to
[83][84]
sucralose.
In 2004, aspartame traded at about $30/kg and sucralose, which is roughly three times
[85]
sweeter by weight, at around $300/kg.
Dicalcium phosphate
Dicalcium phosphate
IUPAC name[hide]
Calcium hydrogen phosphate dihydrate
Other names[hide]
Calcium monohydrogen phosphate
Phosphoric acid, calcium salt (1:1)
Identifiers
CAS number
7757-93-9
7789-77-7
(dihydrate)
PubChem
104805
ChemSpider
10605753
UNII
L11K75P92J
Jmol-3D images
Image 1
SMILES
[show]
InChI
[show]
Properties
Molecular formula
CaHPO4
Molar mass
136.06 g/mol
Appearance
white powder
Density
2.929 g/cm3
Solubility in water
0.02 g/100 mL
Hazards
EU Index
Not listed
NFPA 704
0
1
0
Flash point
Non-flammable

(verify) (what is:
?)
Infobox references
Dicalcium phosphate, also known as dibasic calcium phosphate or calcium monohydrogen
phosphate, is a type ofcalcium phosphate that is dibasic. It is usually found as the dihydrate, with the
chemical formula of CaHPO42H2O, but it can be thermally converted to the anhydrous form, which has
[1]
been referred to by the abbreviation 'DPCA'. It is practically insoluble in water, with a solubility of 0.02
g per 100 mL at 25 C. It contains about 29.5 percent calcium in its anhydrous form. On contact with
water, it converts to hydroxyapatite, which is insoluble solid, and phosphoric acid
Preparation[edit]
Dicalcium phosphate is produced by the reaction of calcium chloride and phosphoric acid:
CaCl2 + H3PO4 + 2 NaOH CaHPO4 + 2 NaCl + 2 H2O
Calcium carbonate is also used in place of the calcium chloride and sodium hydroxide.
Uses[edit]
Dicalcium phosphate is mainly used as a dietary supplement in prepared breakfast cereals, dog
treats, enriched flour, and noodle products. It is also used as a tableting agent in some
pharmaceutical preparations, including some products meant to eliminate body odor. It is used in
poultry feed. It is also used in some toothpastes as a tartar control agent.
18% p205, 21% Calcium
Potassium chloride
This article is about the chemical compound. For other uses, see KCL.
Potassium chloride
Other names[hide]
Sylvite
Muriate of potash
Identifiers
CAS number
7447-40-7
PubChem
4873
ChemSpider
4707
UNII
660YQ98I10
DrugBank
DB00761
KEGG
D02060
ChEBI
CHEBI:32588
ChEMBL
CHEMBL1200731
RTECS number
TS8050000
ATC code
A12BA01,B05XA01
Jmol-3D images
Image 1
SMILES
[show]
InChI
[show]
Properties
Molecular formula
KCl
Molar mass
74.5513 gmol1
Appearance
white crystalline solid
Odor
odorless
Density
1.984 g/cm3
Melting point
770 C
Boiling point
1420 C
Solubility in water
281 g/L (0C)

344 g/L (20C)
567 g/L (100C)
Solubility
soluble in glycerol, alkalies

slightly soluble in alcohol, insoluble
in ether[1]
Acidity (pKa)
~7
Refractive index(nD)
1.4902 (589 nm)

Structure
Crystal structure
face centered cubic

Thermochemistry
Std molar
83 Jmol1K1[2]
entropy So298
Std enthalpy of
436 kJmol1[2]
formation fHo298
Hazards
MSDS
ICSC 1450
EU Index
Not listed
NFPA 704
0
1
0
Flash point
Non-flammable
LD50
2.6 g/kg (oral/rat), 0.142 g/kg

(intravenous/rat)[3]
Related compounds
Other anions
Potassium fluoride
Potassium bromide
Potassium iodide
Other cations
Lithium chloride
Sodium chloride
Rubidium chloride
Caesium chloride
Related compounds
Potassium chlorate
Potassium perchlorate

(verify) (what is:
?)
Infobox references
The chemical compound potassium chloride (KCl) is a metal halide salt composed
of potassium and chlorine. In its pure state, it is odorless and has a white
or colorless vitreous crystal appearance, with a crystal structure that cleaves easily in three directions.
Potassium chloride crystals are face-centered cubic. Potassium chloride was historically known as
"muriate of potash". This name is occasionally still encountered in association with its use as
a fertilizer. Potash varies in color from pink or red to white depending on the mining and recovery
process used. White potash, sometimes referred to as soluble potash, is usually higher in analysis and
is used primarily for making liquid starter fertilizers. KCl is used inmedicine, scientific applications,
and food processing. It occurs naturally as the mineral sylvite and in combination withsodium
chloride as sylvinite.
Chemical properties[edit]
Solubility of KCl in various solvents
(g KCl / 1 kg of solvent at 25C)[4]
H2O
360
Liquid ammonia
0.4
Liquid sulfur dioxide
0.41
Methanol
5.3
Formic acid
192
Sulfolane
0.04
Acetonitrile
0.024
Acetone
0.00091
Formamide
62
Acetamide
24.5
Dimethylformamide
0.170.5
In chemistry and physics, it is a very commonly used standard, for example as acalibration standard
solution in measuring electrical conductivity of (ionic) solutions, since carefully prepared KCl solutions
have well-reproducible and well-repeatable measurable properties.
Potassium chloride can react as a source of chloride ion. As with any othersoluble ionic chloride, it will
precipitate insoluble chloride salts when added to asolution of an appropriate metal ion:
KCl(aq) + AgNO3(aq) AgCl(s) + KNO3(aq)

Although potassium is more electropositive than sodium, KCl can be reduced to the metal by
reaction with metallic sodium at 850C because the potassium is removed by distillation (see Le
Chatelier's principle):
KCl(l) + Na(l) NaCl(l) + K(g)
This method is the main method for producing metallic potassium. Electrolysis(used for
sodium) fails because of the high solubility of potassium in molten KCl.
As with other compounds containing potassium, KCl in powdered form gives a lilac flame
test result.
Physical properties[edit]
Potassium chloride has a crystalline structure like many other salts. Its structure is facecentered cubic. Its lattice constant is roughly 6.3. Some other properties are
Transmission range: 210 nm to 20 m

Transmittivity = 92% at 450 nm and rises linearly to 94% at 16 m
Refractive index = 1.456 at 10 m
Reflection Loss = 6.8% at 10 m (two surfaces)
6
dN/dT (expansion coefficient)= 33.210 /C
6
dL/dT (refractive index gradient)= 4010 /C
Thermal conductivity = 0.036 W/(cmK)
2
2
Damage threshold (Newman & Novak): 4 GW/cm or 2 J/cm (0.5 or 1 ns pulse rate); 4.2
2
J/cm (1.7 ns pulse rate Kovalev & Faizullov)
Synthesis and production[edit]
Sylvite
Sylvinite
Potassium chloride occurs naturally as sylvite, carnallite, and potash, and it can be extracted
from these ores. It is also extracted from salt water and can be manufactured by crystallization
from solution, flotation or electrostatic separation from suitable minerals. It is a by-product of
the making of nitric acid from potassium nitrate and hydrochloric acid.
Synthesis[edit]
Potassium chloride is inexpensively available and is rarely prepared intentionally in the
laboratory. It can be generated by two routes that are of instructive but not practical value:
One way is to treat potassium hydroxide (KOH) with hydrochloric acid:
KOH + HCl KCl + H2O
This conversion is an acid-base neutralization reaction. The resulting salt can then be
purified by recrystallization. Another method would be to allow potassium to burn in the
presence of chlorine gas, also a very exothermic reaction:
2 K + Cl2 2 KCl
Uses[edit]
The majority of the potassium chloride produced is used for making fertilizer, since
the growth of many plants is limited by their potassium intake. As a
chemical feedstock, it is used for the manufacture of potassium
hydroxide and potassiummetal. It is also used in medicine, lethal
injections, scientific applications, food processing, and as a sodium-free substitute
for table salt (sodium chloride).
It is sometimes used in water as a completion fluid in petroleum and natural
gas operations, as well as being an alternative to sodium chloride in
household water softener units. KCl is useful as a beta radiation source
for calibration ofradiation monitoring equipment, because natural potassium contains
40
0.0118% of the isotope K. One kilogram of KCl yields
16350 becquerels of radiation consisting of 89.28% beta and 10.72% gamma with
1.46083 MeV. Potassium chloride is used in some deicing products that are
designed to be safer for pets and plants, though these are inferior in melting quality
to calcium chloride (lowest usable temperature 12 F (11 C) v. 25 F (32 C)). It
is also used in various brands of bottled water, as well as in bulk quantities for fossil
fuel drilling purposes.
Potassium chloride was once used as a fire extinguishing agent, used in portable
and wheeled fire extinguishers. Known as Super-K dry chemical, it was more
effective than sodium bicarbonate-based dry chemicals and was compatible
with protein foam. This agent fell out of favor with the introduction of potassium
bicarbonate (Purple-K) dry chemical in the late 1960s, which was much
less corrosive and more effective. It is rated for B and C fires.
Along with sodium chloride and lithium chloride, potassium chloride is used as
a flux for the gas welding of aluminium.
Potassium chloride is also an optical crystal with a wide transmission range from
210 nm to 20 m. While cheap, KCl crystal is hygroscopic. This limits its application
to protected environments or short term uses such as prototyping. Exposed to free
air, KCl optics will "rot". Whereas KCl components were formerly used for infrared
optics, it has been entirely replaced by much tougher crystals like zinc selenide.
Potassium chloride has also been used to create heat packs which
[5]
employ exothermic chemical reactions, but these are no longer being created due
to cheaper and more efficient methods, such as the oxidation of metals ('Hot Hands',
one time use products) or the crystallization of sodium acetate (multiple use
products).
Potassium chloride is used as a scotophor with designation P10 in dark-trace CRTs,
e.g. in the Skiatron.
Biological and medical properties[edit]

Potassium is vital in the human body, and oral potassium chloride is the common
means to replenish it, although it can also be diluted and given intravenously. It can
be used as a salt substitute for food, but due to its weak, bitter, unsalty flavor, it is
usually mixed with ordinary table salt (sodium chloride) for this purpose to improve
the taste. The addition of 1 ppm of thaumatin considerably reduces this
[6]
bitterness. Complaints of bitterness or a chemical or metallic taste are also
[7]
reported with potassium chloride used in food.
Medically, it is used in the treatment of hypokalemia and associated conditions as

[8]
an electrolyte replenisher. Brand names include K-Dur, Klor-Con, Micro-K, Slow-K,
Sando-K and Kaon Cl. Side effects can include gastrointestinal discomfort
including nausea and vomiting, diarrhea and bleeding of the digestive
tract. Overdosescause hyperkalemia, which can lead
to paresthesia, cardiac conduction blocks, fibrillation, arrhythmias,
[9]
and sclerosis. Prescription potassium citrate (the potassium naturally found in fruits
and vegetables) can be prescribed as an alternative to potassium chloride. Slow-K is
a 1950s development where the medicine is formulated to enter the bloodstream at
delayed intervals. It was first only prescribed to British military forces to balance their
[10]
diets while serving in Korea.
Some cardiac surgery procedures cannot be carried out on the beating heart. For
these procedures, the surgical team will bypass the heart with a heart-lung
machineand inject potassium chloride into the heart muscle to stop the heartbeat.
The lethal effects of potassium chloride overdoses have led to its use in lethal
injection, as the third of a three-drug combination. Additionally, KCl is used (albeit
rarely) in fetal intracardiac injections in second- and third-trimester induced
[11][12]
abortions.
Jack Kevorkian's thanatron machine injected a lethal dose of
potassium chloride into the patient, which caused the heart to stop functioning, after
[13]
a sodium thiopental-induced coma was achieved.
Precautions[edit]
Orally, potassium chloride is toxic in excess; the LD50 is around 2.5 g/kg (meaning
that a lethal dose for 50% of people weighing 75 kg (165 lb) is about 190 g
(6.7ounces)). However, this is not far from oral toxicity of sodium chloride (table salt),
of 3.75 g/kg, thus potassium chloride is harmless for alimentation (and even good for
health, see previous paragraph). But intravenously, without the step of digestive
[14]
absorption, this is reduced to just over 30 mg/kg. Most concerns are its severe
effects on the cardiac muscles: high doses can cause cardiac arrest and rapid death,
thus the aforementioned use as the third and final drug delivered in the lethal
injection process.
Ascorbic acid
This article is about the molecular aspects of ascorbic acid. For information about its role in nutrition,
see Vitamin C.
L-Ascorbic acid
IUPAC name[hide]
(5R)-[(1S)-1,2-dihydroxyethyl]-3,4-dihydroxyfuran-2(5H)-one
Other names[hide]
Vitamin C
Identifiers
CAS number
50-81-7
PubChem
5785
ChemSpider
10189562
UNII
PQ6CK8PD0R
EC number
200-066-2
KEGG
D00018
ChEBI
CHEBI:29073
ChEMBL
CHEMBL196
ATC code
A11GA01,G01AD03,S01XA15
Jmol-3D images
Image 1
Image 2
SMILES
[show]
InChI
[show]
Properties
Molecular formula
C6H8O6
Molar mass
176.12 g mol1
Appearance
White or light yellow solid
Density
1.65 g/cm3
Melting point
190 to 192 C (374 to 378 F; 463 to

465 K) decomposes
Solubility in water
330 g/L
Solubility inethanol
20 g/L
Solubility inglycerol
10 g/L
Solubility inpropylene
50 g/L
glycol
Solubility in other
insoluble in diethyl
solvents
ether,chloroform, benzene,petroleum
ether, oils, fats
Acidity (pKa)
4.10 (first), 11.6 (second)

Hazards
MSDS
JT Baker
Oxford University
NFPA 704
1
1
0
LD50
11.9 g/kg (oral, rat)[1]

(verify) (what is:
?)
Infobox references
Ascorbic acid is a naturally occurring organic compound with antioxidant properties. It is a white solid,
but impure samples can appear yellowish. It dissolves well in water to give mildly acidic solutions.
Ascorbic acid is one form ("vitamer") of vitamin C. It was originally called L-hexuronic acid, but, when it
was found to have vitamin C activity in animals ("vitamin C" being defined as a vitamin activity, not then
a specific substance), the suggestion was made to rename L-hexuronic acid. The new name for Lhexuronic acid is derived from a- (meaning "no") and scorbutus (scurvy), the disease caused by a
deficiency of vitamin C. Because it is derived from glucose, many animals are able to produce it, but
humans require it as part of their nutrition. Other vertebrates lacking the ability to produce ascorbic acid
include other primates, guinea pigs, teleost fishes, bats, and some birds, all of which require it as a
[2]
dietary micronutrient (that is, in vitamin form).
There exists a D-ascorbic acid, which does not occur in nature. It may be synthesized artificially. It has
identical antioxidant properties to L-ascorbic acid yet has far less vitamin C activity (although not quite
[3]
zero). This fact is taken as evidence that the antioxidant properties of ascorbic acid are only a small
part of its effective vitamin activity. To be specific, L-ascorbate is known to participate in many specific
enzyme reactions that require the correct epimer (L-ascorbate and not D-ascorbate). L-ascorbic acid
has a specific rotation of
[4]p. 35
History[edit]
From the middle of the 18th century, it was noted that lemon juice could help prevent sailors from
getting scurvy. At first, it was supposed that the acid properties were responsible for this benefit;
however, it soon became clear that other dietary acids, such as vinegar, had no such benefits. In 1907,
two Norwegian physicians reported an essential disease-preventing compound in foods that was distinct
from the one that prevented beriberi. These physicians were investigating dietary-deficiency diseases
using the new animal model of guinea pigs, which are susceptible to scurvy. The newly discovered foodfactor was eventually called vitamin C.
From 1928 to 1932, the Hungarian research team led by Albert Szent-Gyrgyi, as well as that of
the American researcherCharles Glen King, identified the antiscorbutic factor as a particular single
chemical substance. At the Mayo clinic, Szent-Gyrgyi had isolated the chemical hexuronic acid from
animal adrenal glands. He suspected it to be the antiscorbutic factor but could not prove it without a
biological assay. This assay was finally conducted at the University of Pittsburgh in the laboratory of
King, which had been working on the problem for years, using guinea pigs. In late 1931, King's lab
obtained adrenal hexuronic acid indirectly from Szent-Gyrgyi and, using their animal model, proved
that it is vitamin C, by early 1932.
This was the last of the compound from animal sources, but, later that year, Szent-Gyrgyi's group
discovered thatpaprika pepper, a common spice in the Hungarian diet, is a rich source of hexuronic
acid. He sent some of the now-more-available chemical to Walter Norman Haworth, a British sugar
[5]
chemist. In 1933, working with the then-Assistant Director of Research (later Sir) Edmund Hirst and
their research teams, Haworth deduced the correct structure and optical-isomeric nature of vitamin C,
[6]
and in 1934 reported the first synthesis of the vitamin. In honor of the compound's antiscorbutic
properties, Haworth and Szent-Gyrgyi now proposed the new name of "a-scorbic acid" for the
compound. It was named L-ascorbic acid by Haworth and Szent-Gyrgyi when its structure was finally
[7]
proven by synthesis.
In 1937, the Nobel Prize for chemistry was awarded to Haworth for his work in determining the structure
of ascorbic acid shared with Paul Karrer, who received his award for work on vitamins and the
prize for Physiology or Medicine that year went to Albert Szent-Gyrgyi for his studies of the biological
functions of L-ascorbic acid.
The American physician Fred R. Klenner, M.D. promoted vitamin C as a cure for many diseases in the
1950s by elevating the dosages greatly to as much as tens of grams vitamin C daily by injection. From
1967 on, Nobel prize winner Linus Pauling recommended high doses of ascorbic acid as a prevention
against cold and cancer; he took 18 grams daily. The results of Klenner have been controversial as yet,
[8]
since his investigations do not meet the modern methodologic standards.
Acidity[edit]
Canonical structures for the ascorbate anion

Ascorbic acid is classed as a reductone. The ascorbate anion is stabilized by electron
delocalization, as shown above in terms of resonance between two canonical forms. For this
reason, ascorbic acid is much more acidic than would be expected if the compound contained only
isolated hydroxyl groups.
Antioxidant mechanism[edit]
End-product of oxidation of ascorbic acid

The ascorbate ion is the predominant species at typical biological pH values. It is a mild reducing
agent and antioxidant. It is oxidized with loss of one electron to form a radical cation and then with
loss of a second electron to form dehydroascorbic acid. It typically reacts with oxidants of
the reactive oxygen species, such as the hydroxyl radical. Such radicals are damaging to animals
and plants at the molecular level due to their possible interaction with nucleic acids, proteins, and
lipids. Sometimes these radicals initiate chain reactions. Ascorbate can terminate these chain
radical reactions by electron transfer. Ascorbic acid is special because it can transfer a single
electron, owing to the resonance-stabilized nature of its own radical
ion called, semidehydroascorbate. The net reaction is:
RO + C6H7O6 ROH + C6H6O6
The oxidized forms of ascorbate are relatively unreactive and do not cause cellular damage.
However, being a good electron donor, excess ascorbate in the presence of free metal ions
can not only promote but also initiate free radical reactions, thus making it a potentially
dangerous pro-oxidative compound in certain metabolic contexts.
Reactions[edit]
Nucleophilic attack of ascorbic enol on proton to give 1,3-diketone
Food chemistry[edit]
Ascorbic acid and its sodium, potassium, and calcium salts are commonly used
as antioxidant food additives. These compounds are water-soluble and, thus, cannot
protect fats from oxidation: For this purpose, the fat-soluble esters of ascorbic acid with
long-chain fatty acids (ascorbyl palmitate or ascorbyl stearate) can be used as food
[9]
antioxidants. Eighty percent of the world's supply of ascorbic acid is produced in China.
The relevant European food additive E numbers are:
1.
2.
3.
4.
5.
E300 ascorbic acid (approved for use as a food additive in the

[10]
[11]
[12]
EU USA and Australia and New Zealand)
E301 sodium ascorbate (approved for use as a food additive in the
[10]
[13]
[12]
E302 calcium ascorbate (approved for use as a food additive in the
[10]
[11]
[12]
E303 potassium ascorbate
E304 fatty acid esters of ascorbic acid (i) ascorbyl palmitate (ii) ascorbyl
stearate.
[14]
It creates volatile compounds when mixed with glucose and amino acids in 90 C.
It is a cofactor in tyrosine oxidation.
[15]
Niche, non-food uses[edit]
Ascorbic acid is easily oxidized and so is used as a reductant in photographic

developer solutions (among others) and as a preservative.
In fluorescence microscopy and related fluorescence-based techniques, ascorbic
acid can be used as an antioxidant to increase fluorescent signal and chemically
[16]
retard dye photobleaching.
It is also commonly used to remove dissolved metal stains, such as iron, from
fiberglass swimming pool surfaces.
In plastic manufacturing, ascorbic acid can be used to assemble molecular chains
[17]
more quickly and with less waste than traditional synthesis methods.
Heroin users are known to use ascorbic acid as a means to convert heroin base to a
[18]
water-soluble salt so that it can be injected.
As justified by its reaction with iodine, it is used to negate the effects of iodine tablets
in water purification. It reacts with the sterilized water, removing the taste, color, and
smell of the iodine. This is why it is often sold as a second set of tablets in most
sporting goods stores as Portable Aqua-Neutralizing Tablets, along with the
potassium iodide tablets.
Intravenous high-dose ascorbate is being used as a chemotherapeutic and biological
[19]
[20]
response modifying agent. Currently it is still under clinical trials.
Biosynthesis[edit]
Main article: Vitamin C
Ascorbic acid is found in plants and animals where it is produced

[21]
from glucose. Animals must either produce it or digest it, otherwise a lack of vitamin C
may cause scurvy, which may eventually lead to death. Reptiles and older orders of birds
make ascorbic acid in their kidneys. Recent orders of birds and most mammals make
ascorbic acid in their liver where the enzyme L-gulonolactone oxidase is required to
[21]
convert glucose to ascorbic acid. Humans, other higher primates, guinea pigs and most
bats are not able to make L-gulonolactone oxidase because of a genetic mutation and
are, therefore, unable to make ascorbic acid. Synthesis and signalling properties are still
[22]
under investigation.
Animal ascorbic acid biosynthesis pathway[edit]

The biosynthesis of ascorbic acid starts with the formation of UDP-glucuronic acid. UDPglucuronic acid is formed when UDP-glucose undergoes two oxidations catalyzed by the
enzyme UDP-glucose 6-dehydrogenase. UDP-glucose 6-dehydrogenase uses the co+
factor NAD as the electron acceptor. The transferase UDP-glucuronate
pyrophosphorylase removes a UMP and glucuronokinase, with the cofactor ADP,
removes the final phosphate leading to D-glucuronic acid. The aldehyde group of this is
reduced to a primary alcohol using the enzyme glucuronate reductase and the cofactor
NADPH, yielding L-gulonic acid. This is followed by lactone formation with the
hydrolase gluconolactonase between the carbonyl on C1 and hydroxyl group on the C4.
L-gulonolactone then reacts with oxygen, catalyzed by the enzyme L-gulonolactone
oxidase (which is nonfunctional in humans and other primates) and the cofactor FAD+.
This reaction produces 2-oxogulonolactone, which spontaneously
[23]
undergoes enolization to form ascorbic acid.
Plant ascorbic acid biosynthesis pathway[edit]

There are many different biosynthesis pathways for ascorbic acid in plants. Most of these
pathways are derived from products found in glycolysis and other pathways. For example,
[22]
one pathway goes through the plant cell wall polymers. The Plant Ascorbic Acid
Biosynthesis Pathway most principal seems to be L-galactose. L-galactose reacts with
the enzyme L-galactose dehydrogenase, whereby the lactone ring opens and forms again
but with between the carbonyl on C1 and hydroxyl group on the C4, resulting in L[23]
galactonolactone. L-galactonolactone then reacts with the mitochondrial avoenzyme
[24]
[23]
L-galactonolactone dehydrogenase. to produce ascorbic acid. An interesting fact
about L-ascorbic acid is that it has shown to have a negative feedback on L-galactose
[25]
dehydrogenase in spinach. Ascorbic acid efflux by embryo of dicots plants is a well[26]
established mechanism of iron reduction, and an step obligatory for iron uptake.
Industrial preparation[edit]
Ascorbic acid is prepared in industry from glucose in a method based on the
historical Reichstein process. In the first of a five-step process, glucose is
catalyticallyhydrogenated to sorbitol, which is then oxidized by
the microorganism Acetobacter suboxydans to sorbose. Only one of the six hydroxy
groups is oxidized by this enzymatic reaction. From this point, two routes are available.
Treatment of the product with acetone in the presence of an acid catalyst converts four of
the remaininghydroxyl groups to acetals. The unprotected hydroxyl group is oxidized to
the carboxylic acid by reaction with the catalytic oxidant TEMPO (regenerated by sodium
hypochlorite bleaching solution). Historically, industrial preparation via the Reichstein
process used potassium permanganate as the bleaching solution. Acid-catalyzed
hydrolysis of this product performs the dual function of removing the two acetal groups
and ring-closing lactonization. This step yields ascorbic acid. Each of the five steps has a
[27]
yield larger than 90%.
A more biotechnological process, first developed in China in the 1960s, but further
developed in the 1990s, bypasses the use of acetone-protecting groups. A
secondgenetically-modified microbe species, such as mutant Erwinia, among others,
oxidises sorbose into 2-ketogluconic acid (2-KGA), which can then undergo ring-closing
lactonization via dehydration. This method is used in the predominant process used by
the ascorbic acid industry in China, which supplies 80% of world's ascorbic
[28]
acid. American and Chinese researchers are competing to engineer a mutant that can
carry out a one-pot fermentation directly from glucose to 2-KGA, bypassing both the need
[29]
for a second fermentation and the need to reduce glucose to sorbitol.
The outdated, but historically-important industrial synthesis of ascorbic acid from glucose
via the Reichstein process.
Determination[edit]
The traditional way to analyze the ascorbic acid content is the process of titrationwith
an oxidizing agent, and several procedures have been developed, mainly relying
on iodometry. Iodine is used in the presence of a starch indicator. Iodine is reduced by
ascorbic acid, and, when all the ascorbic acid has reacted, the iodine is then in excess,
forming a blue-black complex with the starch indicator. This indicates the end-point of the
titration. As an alternative, ascorbic acid can be treated with iodine in excess, followed by
[30]
back titration with sodium thiosulfate using starch as an indicator. The preceding
iodometric method has been revised to exploit reaction of ascorbic acid
with iodate and iodide in acid solution. Electrolyzing the solution of potassium iodide
produces iodine, which reacts with ascorbic acid. The end of process is determined
by potentiometric titration in a manner similar to Karl Fischer titration. The amount of
ascorbic acid can be calculated by Faraday's law.
An uncommon oxidising agent is N-bromosuccinimide, (NBS). In this titration, the NBS
oxidizes the ascorbic acid in the presence of potassium iodide and starch. When the NBS
is in excess (i.e., the reaction is complete), the NBS liberates the iodine from the
potassium iodide, which then forms the blue-black complex with starch, indicating the
end-point of the titration.
Potassium sorbate
Potassium sorbate[1][2]
IUPAC name[hide]
Potassium (2E,4E)-hexa-2,4-dienoate
Other names[hide]
E202
Sorbistat-K
Sorbistat potassium
Identifiers
CAS number
24634-61-5
PubChem
23676745
ChemSpider
4445644
KEGG
D02411
ChEBI
CHEBI:77868
Jmol-3D images
Image 1
SMILES
[show]
InChI
[show]
Properties
Molecular formula
C6H7KO2
Molar mass
150.22 g mol1
Appearance
White crystals
Odor
yes
Density
1.363 g/cm3
Melting point
270 C (decomp.)
Solubility in water
58.5 g/100 mL (100 C)
Solubility in other solvents
Soluble in ethanol,propylene glycol
Slightly soluble in acetone
Very slightly soluble

inchloroform, corn oil, ether
Insoluble in benzene
Hazards
NFPA 704
1
2
0
LD50
4920 mg/kg (rat, oral)

(verify) (what is:
Infobox references
?)
Potassium sorbate is the potassium salt of sorbic acid, chemical formula CH3CH=CH-CH=CH-CO2K. It
is a white salt that is very soluble in water (58.2% at 20 C). It is primarily used as a food preservative (E
[3]
number 202). Potassium sorbate is effective in a variety of applications including food, wine,
and personal care products. While sorbic acid is naturally occurring in some berries, virtually all of the
world's production of sorbic acid, from which potassium sorbate is derived, is manufactured
synthetically.
Production[edit]
Potassium sorbate is produced industrially by neutralizing sorbic acid with potassium hydroxide. The
precursor sorbic acid is produced in a two-step process via the condensation
[4][5][6]
of crotonaldehyde and ketene.
Uses[edit]
Potassium sorbate is used to inhibit molds and yeasts in many foods, such
[7]
as cheese, wine, yogurt, dried meats, apple cider, soft drinks and fruit drinks, and baked goods. It is
used in the preparation of items such as Sweet maple syrup and Milk shakes served by fast
[8] [9] [10]
food conglomerates such as Mc Donalds.
It can also be found in the ingredients list of
many dried fruit products. In addition, herbal dietary supplement products generally contain potassium
sorbate, which acts to prevent mold and microbes and to increase shelf life, and is used in quantities at
[11]
which there are no known adverse health effects, over short periods of time. Labeling of this
preservative on ingredient statements reads as "potassium sorbate" or "E202". Also, it is used in
many personal care products to inhibit the development ofmicroorganisms for shelf stability. Some
manufacturers are using this preservative as a replacement for parabens. Tube feeding of potassium
[12]
sorbate reduces gastric burden of pathogenic bacteria.
Also known as "wine stabilizer", potassium sorbate produces sorbic acid when added to wine. It serves
two purposes. When active fermentation has ceased and the wine is racked for the final time after
clearing, potassium sorbate will render any surviving yeast incapable of multiplying. Yeast living at that
moment can continue fermenting any residualsugar into CO2 and alcohol, but when they die no new
yeast will be present to cause future fermentation. When a wine is sweetened before bottling, potassium
sorbate is used to prevent refermentation when used in conjunction with potassium metabisulfite. It is
primarily used with sweet wines, sparkling wines, and some hard ciders but may be added to table
wines which exhibit difficulty in maintaining clarity after fining.
Some molds (notably some Trichoderma and Penicillium strains) and yeasts are able to detoxify
sorbates bydecarboxylation, producing piperylene (1,3-pentadiene). The pentadiene manifests as a
[13]
typical odor of kerosene orpetroleum.
Toxicology[edit]
[14]
Potassium sorbate is a skin, eye and respiratory irritant. Although some research implies it has a long
[15]
term safety record, in vitro studies have shown that it is both genotoxic and mutagenic to human
blood cells. Potassium sorbate is found to be toxic to human DNA in peripheral blood lymphocytes, and
[16]
hence found that it negatively affects immunity. It is often used with ascorbic acid and iron salts as
they increase its effectiveness but this tends to form mutagenic compounds that damage DNA
[17]
molecules.
Typical usage rates of potassium sorbate are 0.025% to 0.1% (see sorbic acid), which in a 100 g
serving yields intake of 25 mg to 100 mg. Acceptable daily intakes for human is 12.5 mg/kg, or 875 mg
daily for an average adult (70 kg), according to FAO/World Health Organization Expert Committee on
[11]
Food Additives.
Sulfonic acid
(Redirected from Sulphonic acid)
General structure of a sulfonic acid with the blue marked functional group
A sulfonic acid (or sulphonic acid) refers to a member of the class of organosulfur
compounds with the general formula RS(=O)2OH, where R is an
organic alkyl or aryl group and the S(=O)2OH group a sulfonyl hydroxide.[1] A sulfonic
acid can be thought of as sulfuric acid with one hydroxyl group replaced by an
organic substituent. The parent compound (with the organic substituent replaced by
hydrogen) is the hypothetical compound sulfurous acid. Salts or esters of sulfonic acids
are called sulfonates.
Preparation[edit]
Ball-and-stick model of methanesulfonic acid.
Sulfonic acid is produced by the process of sulfonation. Usually the sulfonating agent
is sulfur trioxide. A particularly large scale application of this method is the production of
alkylbenzenesulfonic acids:
RC6H5 + SO3 RC6H4SO3H
In this reaction, sulfur trioxide is an electrophile and
the arene undergoes electrophilic aromatic substitution.[1]
Thiols can be oxidized to sulfonic acids:
RSH + 3/2 O2 RSO3H
Certain sulfonic acids, such as perfluorooctanesulfonic acid are prepared
by electrophilic fluorination of preformed sulfonic acids. The net conversion can
be represented simplistically:
C8H17SO3H + 17 F2 C8F17SO3H + 17 HF
Properties[edit]
Sulfonic acids are much stronger acids than the
corresponding carboxylic acids. p-Toluenesulfonic acid, with a pKa of -2.8, is
about a million times stronger acid thanbenzoic acid, with a pKa of 4.2.
Similarly, methanesulfonic acid, pKa = -1.9, is also about one million times
stronger acid than acetic acid. Because of their polarity, sulfonic acids tend
to be crystalline solids. They are also usually colourless and nonoxidizing,
which is convenient. Because of their high acidity, sulfonic acids are often
soluble in water or exhibit detergent-like properties.
The structure of sulfonic acids is illustrated by the
prototype, methanesulfonic acid. The sulfonic acid group, RSO2OH features
a tetrahedral sulfur centre, meaning that sulfur is at the center of four atoms:
three oxygens and one carbon. The overall geometry of the sulfur centre is
reminiscent of the shape of sulfuric acid.
Representative sulfonic acids and derivatives.
Taurine, a bile acid, and one of the few naturally occurring sulfonic acids
(shown in uncommontautomer).
PFOS, a surfactant and a controversial pollutant.
Toluenesulfonic acid, a widely used reagent in organic synthesis.
Nafion, a polymeric sulfonic acid useful in fuel cells.
Sodium dodecylbenzenesulfonate, an alkylbenzenesulfonatesurfactant used

in laundry detergents.
Applications[edit]
Although both alkyl and aryl sulfonic acids are known, most of the
applications are associated with the aromatic derivatives.
Detergents and surfactants[edit]
Detergents and surfactants are molecules that combine highly nonpolar and
highly polar groups. Traditionally, soaps are the popular surfactants, being
derived fromfatty acids. Since the mid-20th century, the usage of sulfonic
acids has surpassed soap in advanced societies. For example, an estimated
2 billion kilograms ofalkylbenzenesulfonates are produced annually for
diverse purposes. Lignin sulfonates, produced by sulfonation of lignin are
components of drilling fluids and additives in certain kinds of concrete.[2]
Dyes[edit]
Many if not most of the anthroquinone dyes are produced or processed via
sulfonation.[3] Sulfonic acids tend to bind tightly
to proteins and carbohydrates. Most "washable" dyes are sulfonic acids (or
have the functional sulfonyl group in them) for this reason. pCresidinesulfonic acid is used to make food dyes.
Acid catalysts[edit]
Being strong acids, sulfonic acids are also used as catalysts. The simplest
examples are methanesulfonic acid, CH3SO2OH and p-toluenesulfonic acid,
which are regularly used in organic chemistry as acids that are lipophilic
(soluble in organic solvents). Polymeric sulfonic acids are also
useful. Dowex resin are sulfonic acid derivatives of polystyrene and is used
as catalysts and for ion exchange (water softening).Nafion, a fluorinated
polymeric sulfonic acid is a component of proton exchange membranes
in fuel cells.[4]
Drugs[edit]
Antibacterial drugs sulfa drugs are produced from sulfonic acids.
Flow Batteries[edit]
Methanesulfonic acid is used as the supporting electrolyte of the zinccerium and lead-acid (methanesulfonate) flow batteries.
Neem oil
Neem expeller oil
Neem oil is a vegetable oil pressed from the fruits and seeds of the neem (Azadirachta
indica), an evergreen tree which isendemic to the Indian subcontinent and has been
introduced to many other areas in the tropics. It is the most important of the commercially
available products of neem for organic farming and medicines.
Neem oil varies in color; it can be golden yellow, yellowish brown, reddish brown, dark
brown, greenish brown, or bright red. It has a rather strong odor that is said to combine
the odours of peanut and garlic. It is composed mainly of triglycerides and contains
many triterpenoid compounds, which are responsible for the bitter taste. It
is hydrophobic in nature; in order to emulsify it in water for application purposes, it must
be formulated with appropriate surfactants.
Azadirachtin is the most well known and studied triterpenoid in neem oil. The
azadirachtin content of neem oil varies from 300ppm to over 2500ppm depending on the
extraction technology and quality of the neem seeds crushed. Neem oil also
contains steroids(campesterol, beta-sitosterol, stigmasterol).
Average composition of neem oil fatty acids
Common Name
Acid Name
Composition range
Omega-6
Linoleic acid
6-16%
Omega-9
Oleic acid
25-54%
Palmitic acid
Hexadecanoic acid
16-33%
Stearic acid
Octadecanoic acid
9-24%
Omega-3
Alpha-linolenic acid
?%
Palmitoleic acid
9-Hexadecenoic acid
?%
Neem oil method[edit]

The method of processing is likely to affect the composition of the oil, since the methods
used, such as pressing (expelling) or solvent extraction are unlikely to remove exactly the
same mix of components in the same proportions. The neem oil yield that can be
obtained from neem seed kernels also varies widely in literature from 25% to 45%.
The oil can be obtained through pressing (crushing) of the seed kernel both through cold
pressing or through a process incorporating temperature controls 40 TO 50 C. Neem
seed oil can also be obtained by solvent extraction of the neem seed, fruit, oil, cake or
kernel. A large industry in India extracts the oil remaining in the seed cake using hexane.
This solvent-extracted oil is of a lower quality as compared to the cold pressed oil and is
mostly used for soap manufacturing. Neem cake is a by-product obtained in the solvent
extraction process for neem oil.
Uses[edit]
Neem oil is not used for cooking purposes. In India, it is used for
preparing cosmetics (soap, hair products, body hygiene creams, hand creams) and
in Ayurvedic,Unani and folklore traditional medicine, in the treatment of a wide range of
afflictions. The most frequently reported indications in ancient Ayurvedic writings are skin
diseases, inflammations and fevers, and more recently rheumatic disorders, insect
repellent and insecticide effects.[1]
Traditional Ayurvedic uses of neem include the treatment of acne, fever, leprosy, malaria,
ophthalmia and tuberculosis. Various folk remedies for neem include use as
an anthelmintic, antifeedant, antiseptic, diuretic, emmenagogue, contraceptive, febrifuge,
parasiticide, pediculocide and insecticide. It has been used in traditional medicine for the
treatment of tetanus, urticaria, eczema, scrofula and erysipelas. Traditional routes of
administration of neem extracts included oral, vaginal and topical use. Neem oil has an
extensive history of human use in India and surrounding regions for a variety of
therapeutic purposes. Puri (1999) has given an account of traditional uses and
therapeutic indications and pharmacological studies of this oil, in his book on neem.[2]
Formulations made of neem oil also find wide usage as a biopesticide for organic
farming, as it repels a wide variety of pests including the mealy bug, beet
armyworm,aphids, the cabbage worm, thrips, whiteflies, mites, fungus gnats, beetles,
moth larvae, mushroom flies, leafminers, caterpillars, locust, nematodes and
the Japanese beetle. Neem oil is not known to be harmful to mammals, birds,
earthworms or some beneficial insects such as
butterflies, honeybees and ladybirds (ladybugs in US English) if it is not concentrated
directly into their area of habitat or on their food source. It can be used as a household
pesticide for ant, bedbug, cockroach, housefly,sand
fly, snail, termite and mosquitoes both as repellent and larvicide.[2] Neem oil also
controls black spot, powdery mildew, anthracnose and rust fungi.
Neem seed oil has also been found to prevent implantation and may even have an
abortifacient effect similar to pennyroyal, juniper berries, wild ginger, myrrh andangelica.
The effects were seen as many as ten days after fertilization in rats though it was most
effective at no more than three days. (Sinha, et al., 1984)[not specific enough to verify]; (Lal et al.,
1985)[not specific enough to verify]. In a study on rats, neem oil was given orally eight to ten days
after implantation of the fetuson the uterine wall. In all cases, by day 15, the embryos
were all completely resorbed by the body. The animals regained fertility on the next cycle
showing no physical problems. Detailed study of the rats revealed increased levels
of gamma interferon in the uterus. The neem oil enhanced the local immune response in
the uterus.(Mukherjee, 1996)[3][not specific enough to verify] Post coital use of neem oil as birth
control does not appear to work by hormonal changes but produces changes in the
organs that make pregnancy no longer viable (Tewari, 1989)[not specific enough to
verify]
(Bardham, 1991)[not specific enough to verify].
Neem seed oil has also been used as a renewable source for the preparation of
polymeric coatings. It has been converted into various polymeric resins, including
polyesteramides and polyetheramides. These resins may be utilized further for
preparation of polyurethane coatings.[4][5] Ashok Chaudhari, Anil Kuwar, Pramod
Mahulikar, Dilip Hundiwale, Ravindra Kulkarni and Vikas Gite, RSC Advances, 2014, 4,
1786617872
Toxicity[edit]
Studies done when Azadirachtin (the primary active pesticidal ingredient in neem oil) was
approved as a pesticide showed that when neem leaves were fed to male albino rats for
11 weeks, 100% (reversible) infertility resulted.[6]
Neem oil and other neem products such as neem leaves and neem tea should not be
consumed by pregnant women, women trying to conceive, or children.[citation needed]
There is some evidence that internal medicinal use may be associated with liver damage
in children.[7]
Calcium propanoate
(Redirected from Calcium propionate)
Calcium propanoate[1]
IUPAC name[hide]
Calcium propanoate
Other names[hide]
Calcium propionate
Calcium dipropionate
Mycoban
Identifiers
CAS number
4075-81-4
PubChem
19999
ChemSpider
18840
EC number
223-795-8
Jmol-3D images
Image 1
SMILES
[show]
InChI
[show]
Properties
Molecular formula
C6H10CaO4
Molar mass
186.2192 g/mol
Appearance
White crystalline solid
Solubility in water
49 g/100 mL (0 C)
55.8 g/100 mL (100 C)
Solubility
slightly soluble
in methanol,ethanol
insoluble in acetone,benzene
Structure
Crystal structure
monoclinic
Hazards
NFPA 704
1
2
0
(verify) (what is:
?)
Infobox references
Calcium propanoate or calcium propionate has the formula Ca(C2H5COO)2. It is the calcium salt
of propanoic acid.
Uses[edit]
As a food additive, it is listed as E number 282 in the Codex Alimentarius. Calcium propanoate is used
as a preservative in a wide variety of products, including but not limited to bread, other baked goods,
[2]
processed meat, whey, and other dairy products. In agriculture, it is used, amongst other things, to
[3]
prevent milk fever in cows and as a feed supplement Propanoates prevent microbes from producing
the energy they need, like benzoates do. However, unlike benzoates, propanoates do not require an
[4]
acidic environment.
[5]
Calcium propanoate is used in bakery products as a mold inhibitor, typically at 0.1-0.4% (though
animal feed may contain up to 1%). Mold contamination is considered a serious problem amongst
[6]
bakers, and conditions commonly found in baking present near-optimal conditions for mold growth.
[7]
A few decades ago, Bacillus mesentericus (rope), was a serious problem, but today's improved
sanitary practices in the bakery, combined with rapid turnover of the finished product, have virtually
[citation needed]
eliminated this form of spoilage.
Calcium propanoate and sodium propanoate are effective
[8]
against both B. mesentericus rope and mold.
Metabolism of propanoate begins with its conversion to propionyl coenzyme A (propionyl-CoA), the
usual first step in the metabolism of carboxylic acids. Since propanoic acid has three carbons, propionylCoA can directly enter neither beta oxidation nor the citric acid cycles. In most vertebrates, propionylCoA is carboxylated to D-methylmalonyl-CoA, which is isomerised to L-methylmalonyl-CoA. A vitamin
B12-dependent enzyme catalyzes rearrangement of L-methylmalonyl-CoA to succinyl-CoA, which is an
intermediate of the citric acid cycle and can be readily incorporated there.
When propanoic acid is infused directly into rodents' brains, it produces reversible behavior changes
(e.g. hyperactivity, dystonia, social impairment, perseveration) and brain changes (e.g. innate
[9]
neuroinflammation, glutathione depletion) that may be used as a model of human autism in rats.
[10]
According to the Pesticide Action Network North America, calcium propionate is slightly toxic. This
rating is not uncommon for food products; vitamin C is also rated by the same standards as being
[11]
[12]
slightly toxic.
Calcium propanoate can be used as a fungicide on fruit.

Chemicals - Osho Ass 1

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Chemicals - Osho Ass 1

Uploaded by

Copyright:

Available Formats

Diazinon

From Wikipedia, the free encyclopedia

This article needs additional citations for verification. Please

Colorless to dark brown

1.116-1.118 g/cm3 at 20 C[1]

Except where noted otherwise, data are given for materials in

Structure and reactivity[edit]

Metabolism and mechanism of action[edit]

The mechanism, described above of the biotransformation of Diazinon

214 mgkg1 (human, oral, TDLo) (2,3)

Eyes, ears, nose, and throat

Low or high blood pressure

Efficacy and side effects[edit]

after exposure. Intermediate syndrome in humans is characterized by difficulty breathing and

(Redirected from Sodium saccharin)

White crystalline solid

Except where noted otherwise, data are given for materials in

Sodium salt of saccharin: A white powder

Saccharin, historical wrapping;Sugar Museum (Berlin)

Warning label addition and removal[edit]

slightly soluble in ethanol

their standard state (at 25 C (77 F), 100 kPa)

Properties and use[edit]

Discovery and approval[edit]

Safety and approval controversies[edit]

Safety and health effects[edit]

Phenylalanine and phenylketonuria[edit]

Neurological and psychiatric symptoms[edit]

Weight change and hunger[edit]

Holland Sweetener Company[edit]

Except where noted otherwise, data are given for materials in

18% p205, 21% Calcium

white crystalline solid

281 g/L (0C)

soluble in glycerol, alkalies

1.4902 (589 nm)

face centered cubic

2.6 g/kg (oral/rat), 0.142 g/kg

Except where noted otherwise, data are given for materials in

Liquid sulfur dioxide

KCl(aq) + AgNO3(aq) AgCl(s) + KNO3(aq)

Transmission range: 210 nm to 20 m

Synthesis and production[edit]

Biological and medical properties[edit]

Medically, it is used in the treatment of hypokalemia and associated conditions as

White or light yellow solid

190 to 192 C (374 to 378 F; 463 to

4.10 (first), 11.6 (second)

11.9 g/kg (oral, rat)[1]

Except where noted otherwise, data are given for materials in

their standard state (at 25 C (77 F), 100 kPa)

Canonical structures for the ascorbate anion

End-product of oxidation of ascorbic acid

RO + C6H7O6 ROH + C6H6O6

Nucleophilic attack of ascorbic enol on proton to give 1,3-diketone

E300 ascorbic acid (approved for use as a food additive in the

Niche, non-food uses[edit]

Ascorbic acid is easily oxidized and so is used as a reductant in photographic

Ascorbic acid is found in plants and animals where it is produced

Animal ascorbic acid biosynthesis pathway[edit]

Plant ascorbic acid biosynthesis pathway[edit]

58.5 g/100 mL (100 C)

Solubility in other solvents

Soluble in ethanol,propylene glycol