liveonearth (liveonearth) wrote,

Pepto Bismol

I had an upset stomach for most of last weekend and finally agreed to take the medicine that Suzanne offered. And it worked like a charm, nausea be gone! So I had to find out: what is this stuff?

Ingredients of pepto bismol:
benzoic acid
magnesium aluminum silicate
saccharin sodium
salycilic acid
sodium salicylate
sorbic acid

And then I googled benzoic acid and learned found which is from the INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY and is a CONCISE INTERNATIONAL CHEMICAL ASSESSMENT DOCUMENT NO. 26, the assessment being of BENZOIC ACID AND SODIUM BENZOATE. They don't mention pepto bismol. Wikipedia says the active ingredient in pepto is Bismuth subsalicylate, C7H5BiO4, a salt of salicylic acid. Bismuth salicylate displays anti-inflammatory action and also acts as an antacid and mild antibiotic. It can also cause a black tongue and black stools in some pepto users, when it combines with trace amounts of sulfur in their saliva and gastrointestinal tract. This discoloration is temporary and harmless. (I eat a lot of cilantro which is high in sulfur....but my poop didn't turn black.) Children should not take medication with bismuth subsalicylate while recovering from influenza or chicken pox, as epidemiologic evidence points to an association between the use of salicylate-containing medications during certain viral infections and the onset of Reye's syndrome. REYE'S SYNDROME! What's the connection, do you think?

Benzoic acid (CAS No. 65-85-0) is a white solid that is slightly
soluble in water. Sodium benzoate (CAS No. 532-32-1) is about 200
times more soluble in water. Benzoic acid is used as an intermediate
in the synthesis of different compounds, primarily phenol (>50% of
the amount produced worldwide) and caprolactam. Other end products
include sodium and other benzoates, benzoyl chloride, and diethylene
and dipropylene glycol dibenzoate plasticizers. Sodium benzoate is
primarily used as a preservative and corrosion inhibitor (e.g., in
technical systems as an additive to automotive engine antifreeze
coolants). Benzoic acid and sodium benzoate are used as food
preservatives and are most suitable for foods, fruit juices, and soft
drinks that are naturally in an acidic pH range. Their use as
preservatives in food, beverages, toothpastes, mouthwashes,
dentifrices, cosmetics, and pharmaceuticals is regulated. The
estimated global production capacity for benzoic acid is about
600 000 tonnes per year.
Worldwide sodium benzoate production in 1997
can be estimated at about 55 000-60 000 tonnes. Benzoic acid occurs
naturally in many plants and in animals. It is therefore a natural
constituent of many foods, including milk products. Anthropogenic
releases of benzoic acid and sodium benzoate into the environment are
primarily emissions into water and soil from their uses as
preservatives. Concentrations of naturally occurring benzoic acid in
several foods did not exceed average values of 40 mg/kg of food.
Maximum concentrations reported for benzoic acid or sodium benzoate
added to food for preservation purposes were in the range of 2000
mg/kg of food.

After oral uptake, benzoic acid and sodium benzoate are rapidly
absorbed from the gastrointestinal tract and metabolized in the liver
by conjugation with glycine, resulting in the formation of hippuric
acid, which is rapidly excreted via the urine. To a lesser extent,
benzoates applied dermally can penetrate through the skin. Owing to
rapid metabolism and excretion, an accumulation of the benzoates or
their metabolites is not to be expected.

In rodents, the acute oral toxicity of benzoic acid and sodium
benzoate is low (oral LD50 values of >1940 mg/kg body weight). In
cats, which seem to be more sensitive than rodents, toxic effects and
mortality were reported at much lower doses (about 450 mg/kg body

Benzoic acid is slightly irritating to the skin and irritating to
the eye, while sodium benzoate is not irritating to the skin and is
only a slight eye irritant. For benzoic acid, the available studies
gave no indication of a sensitizing effect; for sodium benzoate, no
data were identified in the literature.

In short-term studies with rats, disorders of the central nervous
system (benzoic acid/sodium benzoate) as well as histopathological
changes in the brain (benzoic acid) were seen after feeding high doses
(>1800 mg/kg body weight) over 5-10 days. Other effects included
reduced weight gain, changes in organ weights, changes in serum
parameters, or histopathological changes in the liver. The information
concerning long-term oral exposure of experimental animals to benzoic
acid is very limited, and there is no study available dealing
specifically with possible carcinogenic effects. From a limited
four-generation study, only a preliminary no-observed-(adverse-)effect
level (NO(A)EL) of about 500 mg/kg body weight per day can be derived.
With sodium benzoate, two long-term studies with rats and mice gave no
indication of a carcinogenic effect. However, the documentation of
effects is inadequate in most of these studies; therefore, no reliable
NO(A)EL values can be derived. Data on its precursors support the
notion that benzoic acid is unlikely to be carcinogenic.

Benzoic acid tested negative in several bacterial assays and in
tests with mammalian cells, while in vivo studies were not
identified. Sodium benzoate was also inactive in Ames tests, whereas
tests with mammalian cells gave consistently positive results. In one
in vivo study (dominant lethal assay with rats), a positive result
was obtained. At present, a genotoxic activity of sodium benzoate
cannot be ruled out entirely.

For benzoic acid, two limited studies gave no indication of
adverse reproductive or developmental effects. With sodium benzoate,
several studies on different species have been performed, and
embryotoxic and fetotoxic effects as well as malformations were seen
only at doses that induced severe maternal toxicity. In a dietary
study in rats, a NO(A)EL of about 1310 mg/kg body weight was
established. Data on its precursors support the notion that benzoic
acid is unlikely to have adverse reproductive effects at dose levels
not toxic to the mother.

In humans, the acute toxicity of benzoic acid and sodium benzoate
is low. However, both substances are known to cause non-immunological
contact reactions (pseudoallergy). This effect is scarce in healthy
subjects; in patients with frequent urticaria or asthma, symptoms or
exacerbation of symptoms was observed. A provisional tolerable intake
of 5 mg/kg body weight per day can be derived, although benzoates at
lower doses can cause non-immunological contact reactions
(pseudoallergy) in sensitive persons. As there are no adequate studies
available on inhalation exposure, a tolerable concentration for
exposure by inhalation cannot be calculated.

From their physical/chemical properties, benzoic acid and sodium
benzoate emitted to water and soil are not expected to volatilize to
the atmosphere or to adsorb to sediment or soil particles. From the
results of numerous removal experiments, the main elimination pathway
for both chemicals should be biotic mineralization. Data from
laboratory tests showed ready biodegradability for both substances
under aerobic conditions. Several isolated microorganisms (bacteria,
fungi) have been shown to utilize benzoic acid under aerobic or
anaerobic conditions. From the experimental data on bioconcentration,
a low to moderate potential for bioaccumulation is to be expected.

From valid test results available on the toxicity of benzoic acid
and sodium benzoate to various aquatic organisms, these compounds
appear to exhibit low to moderate toxicity in the aquatic compartment.
The lowest EC50 value of 9 mg/litre (cell multiplication inhibition)
reported in a chronic study was observed in the cyanobacterium
Anabaena inaequalis. EC50/LC50 values for the other aquatic
species tested were in the range of 60-1291 mg/litre. Immobilization
of Daphnia magna has been demonstrated to be pH dependent, with a
lower 24-h EC50 (102 mg/litre) at acidic pH. For the freshwater fish
golden ide (Leuciscus idus), a 48-h LC50 of 460 mg/litre has been
determined. Developmental effects have been found in frog (Xenopus)
embryos at a concentration of 433 mg/litre (96-h EC50 for
malformation). For sodium benzoate, exposure of juvenile stages of
aquatic organisms in a multispecies test (including Daphnia magna,
Gammarus fasciatus, Asellus intermedius, Dugesia tigrina,
Helisoma trivolvis, and Lumbriculus variegatus) resulted in 96-h
LC50 values of greater than100 mg/litre. A 96-h LC50 of 484
mg/litre has been determined in the freshwater fish fathead minnow
(Pimephales promelas). Owing to the limited available data on
exposure levels in water, a quantitative risk characterization with
respect to aquatic organisms in surface waters could not be performed.
Taking into account the rapid biodegradability, the low to moderate
bioaccumulation potential, the low toxicity to most aquatic species,
and the rapid metabolism of these substances, benzoic acid and sodium
benzoate will -- with the exception of accidental spills -- pose only
a minimal risk to aquatic organisms.

The few available data indicate that benzoic acid and sodium
benzoate have only a low toxicity potential in the terrestrial
environment. Except for the antimicrobial action of benzoic acid,
characterized by minimum microbiocidal concentrations ranging from 20
to 1200 mg/litre, no data on toxic effects of benzoic acid on
terrestrial organisms were available. For sodium benzoate, bacterial
and fungal growth were inhibited in a pH-dependent manner by
concentrations ranging from 100 to 60 000 mg/litre. Owing to the lack
of measured exposure levels, a sample risk characterization with
respect to terrestrial organisms could not be performed.
Tags: biochemistry, digestion, medicine, reyes syndrome

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