CHEMICAL AGENTS

Environmental and industrial contaminants

HEAVY METALS
 Mercury, lead, arsenic, cadmium (regulated 0.05 – 2mg/kg)
 Other regulated metals: copper, tin, zinc, antimony
 Emitted into the environment: fuel combustion, incineration, industrial
processes, occupation, industrial products, poor maintenance of toxic
waste
 Exposure to human: ingestion, inhalation, skin absorption
MERCURY
1) Mercury salt, 2) methyl mercury (CH3Hg)
 Formation of methyl mercury in food chain: -
Mercury methyl mercury plankton fish
anaerobic bacteria human
Characteristics of methyl mercury:
 Fat soluble (lipophilic)
 Persistent
 Bioaccumulation: increase in the concentration of a chemical in an
organism over time. This chemical which are taken up by the organism tend
to accumulate and stored faster than they are broken down (metabolized) or
excreted.
 Biomagnification: the incremental increase in concentration of contaminant
at each level of food chain.
Two types of mercury poisoning:
1. Acute: results from the ingestion of large amount of soluble mercury salts
(violently corrode mucous membranes).
2. Chronic: occurs through the regular absorption of small amounts of mercury
Toxicity:
 Affect development of the brain of infant (pregnant woman, nursing mothers)
 Neurological changes in adults (sensory impairment)
 LEAD
Sources of lead:
1) Lead based paint and lead-contaminated dust found in deteriorating buildings
2) Lead soldered cans
3) Lead glaze pottery and ceramic ware
4) Water storage tanks or piping lined with lead
5) Drink container made of crystals
 Bioaccumulative
 Absorption into body: inhalation and ingestion
 Storage site:
1. Blood, soft tissues (highest in liver, lung and kidney)
2. bones and teeth (lead phosphate)
Toxicity: Lead poisoning (plumbism >10ug/dl)
 As surface acting poison (low sperm count, low RBC, women: miscarriage and smaller
babies)
*Lead palsy of the
 Affect development of the brain
arm (Wrist drop)
 Neurological changes in adults (sensory impairment)
 Affect enzyme activity:-able to mimic other biologically important metals (calcium, iron and
zinc) which act as cofactors in many enzymatic reactions example it affects ferrochelatase
and ALAD (zinc binding protein) activity by decreasing RBC production
 ARSENIC
Two types:
1) Inorganic arsenic: combine with oxygen, chlorine or sulfur
2) Organic arsenic: in plant and animal tissues as methylated form
 Inorganic arsenic is more toxic than organic arsenic
 Soluble ingested arsenic is well absorbed (60% to 90% absorption) by gastrointestinal tract
 Upon absorption arsenic is initially accumulate in the liver, spleen, kidney, lungs, and
gastrointestinal tract, some accumulate in the bones and teeth but rapidly clear except from
hair (>7 ppm concern), nail and skin
Sources:
1. Contaminated food especially seaweed and marine food
2. Drinking water from contaminated area
3. Pesticides manufacturing (sodium arsenite, calcium arsenate, lead arsenate)
4. "Paris green" (cupric acetoarsenite) a wood preservative
5. Burning of fossil fuels
Toxicity of arsenic:
1. Bind to body tissues and cell:
Impact of binding to red blood cells:
Cause hemolysis of RBC, as a result this cause impairment of tissues
respiration, also induce spontaneous abortion and congenital malformation
Impact of binding to bone marrow:
Cause hemolysis of bone marrow, as result this will decrease RBC and WBC
production
2. Inhibit enzyme activity: arsenic binds with sulfhydryl groups and disrupts
sulfhydryl containing enzymes (proteases)

Symptoms:
1) Acute: gastrointestinal disturbance
2) Subacute: irritation to eyes, skin, respiratory tract, redness and
swelling of skin
3) Chronic: risk of cancer (skin, lung, liver, kidney and colon),
melanosis (hyperpigmentation), hyperkeratosis (thickening of
skin of palm and soles), whitish “Mee’s line” on nails
 CADMIUM
 Manufacturing of batteries (re-chargeable nickel–cadmium batteries),
metal soldering, welding

Sources of contamination:
1. Eating foods obtained from cadmium contaminated water, highest in
shellfish, liver, and kidney of fish.
2. Drinking contaminated water.

Toxicity by ingestion of contaminated food:

1) Acute: increases salivation, gastrointestinal disturbance
2) Chronic: kidney damage (build up of cadmium in the kidneys), fragile
bones, abdominal pain, high blood pressure, iron-poor blood, liver
disease, and nerve or brain damage.
 Polychlorinated biphenyls (PCBs)
 PCBs are chemicals formed by attaching one or more chlorine atoms to a pair of connected
benzene rings.

 Depending on the number and position of chlorine atoms attached to the biphenyl ring
structure, 209 different PCB congeners can be formed.
 Dioxin-like toxicologic effects.
 Used as plasticizers in paint and cement, coolant and insulating fluid, lubricating oil, water
proofing compound.
 Improper disposal of PCB waste, poorly maintained toxic waste sites, contaminated ground
water.
 Fish, milk and dairy products, vegetables, meat and animal fat.
Characteristics:
 Highly lipophilic: very readily absorbed; increase with increase in degree of chlorination
(tetra through hexachlorobiphenyls) and position of chlorine
 Persistent: 1) chemically stable 2) resistant to biodegradation; strongly absorb to soil
particles, low solubility in water and low volatility (depends on the degree of chlorination)
 Bioaccumulative
  Biomagnified
 LD50-values in rats : 0.4–11 g/k

Toxicity:
 Acute: rash, skin acne (chloracne)
 Most common sign of exposure to PCB: chloracne and elevation in liver
enzymes
 Chronic exposure:
1. Disrupt hormone balances
2. Reproductive failures
3. Liver and biliary tract cancer
4. Exposure of women to PCBs during pregnancy appears to have a long
term impact on the intellectual function of children, smaller babies
5. Mutagenic
FOOD ADDITIVES
 FOOD ADDITIVES
Toxicity of food additives: Allergic reaction, Psychological effect and Cancer
or tumor
TOXIC FOOD COLORS
1) Sudan dyes (red colors)
 Sudan I through IV, Sudan Orange G, Sudan Red B, Sudan Red G, and
Sudan Red 7B.
 Chili powders, spices, tomato sauces, pastas and sausages (EU rapid alert
system, 2003)
 Toxicity: carcinogen (amine), mutagen and teratogen
2) Orange II
 Golden yellow
 Chinese siu mei, lo mei, vegetarian food and bakery products
 Toxicity: may cause irritation of digestive tract
3) Rhodamine B
 Bright pinkish
 Chili powder, shrimp paste, Chinese red bun, pastries, Mi Ku, Siew Ku and Huat Kuih
 Toxicity:
 Acute: irritation to lungs, eyes, throat, nose, intestines
 Chronic: carcinogen
4) (dimethylamino) azobenzene (butter yellow) and para red
 Chilli powder and curry
 Toxicity: carcinogen and teratogen
5) Boric acid (E284) and sodium tetraborate (borax) (E285)
 Toxic component: boron
 Often used as an antiseptic, insecticide, herbicides and fungicide
 Yellow noodles (to control starch gelatinization, enhance colour, texture and flavor)
 Toxicity:
 Acute: gastrointestinal irritation; death :minimal lethal dose of ingested boric acid
was reported to be 2-3 g in infants, 5-6 g in children and 15-20 g in adults
(Locatelli et al. 1987; Wong et al. 1964).”
 Chronic: redness and peeling skin, seizures and kidney failure.
 POTASSIUM BROMATE (Flour treatment agent (E924)
 Oxidizing agent to strengthen bread dough, elastic
 Toxicity: carcinogen of kidney and thyroid gland

NON-NUTRITIVE SWEETENERS:
 Saccharin, cyclamate, aspartame, sucralose, acesulfame-k (potassium
acesulfame)
 Diet soft drinks and sugar free foods (candy, chewing gum, yogurt)

Toxicity of saccharin: Hermesetas™, Sweet N’ Low™; Sucaryl

 Have been shown to cause tumor in rats (urinary bladder, ovary,
uterine, forestomach, skin, thyroid, vascular and lung)

Toxicity of cyclamate: Sugar Twin™; Hermesetas™

 Known to cause migraine
 Have been shown to cause damage to testicles and embryos of rat
and mice
Toxicity of aspartame: Equal™ ; NutraSweet™
 Hydrolyze into aspartic acid, phenylalanine and methanol
 Affect phenylketonuria (PKU) person (inability to metabolise
phenylalanine); (accumulation of phenylalanine in the brain lead to
decrease level of serotonin); retard physical and intellectual
development, emotional disorder such as depression
 Excitotoxin (act as neurotransmitter, cause influx of calcium in
neuron cells of brain leading to death of brain cells. Brain related
symptoms such as tumor, induce seizure, ADD (attention deficit
disorder), memory loss

Toxicity of ACESULFAME-K (“ACE-K”): Sunett™ ; SweetOne™

 Possibly carcinogen: metabolite (acetoacetamide) cause thyroid
tumor in rats

Toxicity of sucralose: Splenda™

 May affect thymus gland
 MONOSODIUM GLUTAMATE (MSG)
 Sodium salt of glutamic acid (glutamate): amino acid
 Not required to list amount
 0.6% optimum addition (eat more and faster), obesity: increase appetite, increase insulin
secretion (insulin increase body cells to take up glucose, excess glucose convert into fat
(adipose tissue)
Mechanism of action:
 Excitotoxin: cause excitation (overstimulating) of glutamate receptor of the neuron in
the brain, kill or damage neuron with glutamate receptor
Symptoms:
1. “Chinese Restaurant Syndrome”: A collection of symptoms when eating Chinese food
heavily seasoned with MSG (numbness at back of the neck, feeling pressure in face
and upper chest muscles)
2. Infant and prenatal: learning disability and emotional
3. Adult: Headache, seizure, stroke, alzheimer and parkinson disease
AGRICULTURAL PRACTICES
 AGRICULTURAL PRACTICES
 Pesticides (insecticides, herbicides, fungicides) residues
 Characteristics of pesticides:
1. Selectivity to target species not well develop

ORGANOCHLORINE
 eg chlordane (lipophilic, 0.002 – 0.3mg/kg) Dichlorodiphenyltrichloroethane
(DDT), heptachlor (lipophilic, 0.006 – 0.2mg/kg) , kepone, lindane, mirex,
toxophane, aldrin (lipophilic, 0.006 – 0.1mg/kg), dieldrin, endrin, endosulfan,
hexachlorobenzene and pentachlorophenol
Characteristics:
 Neurotoxic
 Strongly lipid soluble (lipophilic: readily absorb to tissue and cells)
 Bioaccumulative
 Persistent in environment
Toxicity: on central nervous system (CNS)
1) Alters opening of porous channels on cell membrane (interfere with the
transport of sodium and calcium across CNS); calcium (neurotransmitter
function)
2) Inhibit neuronal ATPase
Other toxicity:
 Mimic or block the action of reproductive hormones
Symptoms:
 Respiratory depression, throat irritation, blurred vision, hepatotoxicity
 Reproductive functioning such as interfere with steroid metabolism,
reduce testicular size, reduce sperm count and mobility
ORGANOPHOSPHOROUS: parathion, chloropyrifos, malathion, diazinon (lipophilic:0.02-
2mg/kg)
CARBAMATE: aldicarb, carbaryl, carbofuran, methomyl
 Have been used to replace organochlorine pesticides
 Do not persist in environment and animal tissue
 But cause serious health risk if consumed in high concentrations
 Anti-acetylcholinesterase insecticides
Mechanism of action: inhibit acetylcholinesterase activity.
1) Organophosphorous: bind irreversibly with acetylcholinesterase
2) Carbamate: bind temporarily with acetylcholinesterase
Symptoms:
 Central nervous system related symptoms (eg increase in secretion (PSL syndrome=
perspiration, salivation and lacrimation), gastrointestinal cramp, mental confusion)
 Chronic exposure: flu like symptoms
 BIPYRIDILIUM: paraquat (0.01-10mg/kg in rice) and diquat (0.01-5mg/kg)
 Highly persistent in soil
Toxicity:
1) Acute: skin and eye irritation, lung congestion, respiratory failure
2) Chronic toxicity: lung problem, damages fingernails, reproductive effect,
mutagenic
GLYPHOSATE (0.1-0.5mg/kg): active ingredient in Roundup
Highly persistent
Toxicity:
1)Acute toxicity: sore throat, abdominal pain, erosion of pharynx, esophagus and stomach,
pneumonia
2)Chronic toxicity: cause salivary gland lesions, decrease sperm count, cancer of thyroid, liver
and pancreas
CHLOROPHENOXY COMPOUND (2,4-D and 2,4,5-T)
Toxicity: probable carcinogen, soft tissue sarcomas and non-Hodgkin lymphoma
 Veterinary Drug Residues
 Applied to animals through feed, water, implant, inject into blood

Major Classes of Drugs Used in Food Animals:

1)Antiseptics, bacteriocides, and fungicides

1)Ionophores: such as monensin, lasalocid, laidlomycin, salinomycin and narasin (antimicrobial

compound that increase the transport of ion across cell membrane, ↑permeability of membrane
to certain ions, killing susceptible bacteria): provide more efficient of bacterial conversion of feed
(↑ feed efficiency) in ruminant animal

1)Steroid growth promoters and peptide production enhancers (e.g. bovine somatotropin (BST)
hormone, insulin like growth factor, Diethylstilbestrol (DES)).

1)Non-steroidal anabolic and metabolism accelerator: Clenbuterol

1)Antiparasite drugs : Furazolidone and its metabolites (Nitrofurans, Nitroimadazoles)

1)Antibiotics : penicillin, oxytetracycline, sulphonamides, neomycin, gentamicin, streptomycin

(regulated)
 Antibiotics and Growth Enhancer
Antibiotics:
1. Can provoke strong allergic reaction in sensitive person
2. Encourage spread of antibiotic resistant bacteria
3. Disruption of normal human microflora in the intestine
Types of antibiotics: oxytetracycline, penicillin, sulfonamides, salbutamol,
neomycin, gentamicin

Toxicity of oxytetracycline (regulated):

 Occasionally associated with discolored teeth, allergic reactions, peripheral
blood changes, induce antibiotic resistance in coliforms in the human
intestine

Toxicity of penicillin (regulated):

 Can provoke strong allergic reaction in sensitive person, encourage spread
of antibiotic resistant bacteria
Toxicity of sulphonamides:
 Has been associated with thyroid hypothalamus, hypersensitivity reactions
(primarily skin rashes)
 Muscle, liver, fat, kidney, milk (regulated MFA & R)

Toxicity of salbutamol: A beta-agonist (banned)

 Heart-related diseases, headaches, dizziness
 Breathing difficulties and palpitations
 Other beta-agonists (bronchidilatory agents):
o Clenbuterol, cimaterol, isoxsuprine, ractopamine, ritodrine, salmeterol,
terbutaline and zilpaterol

Toxicity of neomycin and gentamicin:

 Regulated MFA & R
 Not readily metabolised and caused damage to kidney. Neomycin can also
cause deafness to susceptible person
 Antiparasitic drugs:
Nitrofurans (banned), Nitroimadazoles, Furazolidone as an
anti-protozoal
Has been shown to induce cancer in animals
Steroid growth hormone:
1) Bovine somatotropin (BST) hormone: to regulate growth and increase milk
production in cattle

2) Diethylstilbestrol (DES): a synthetic estrogen formerly used commercially as a

growth promoting agent in livestock
 Toxicity: cause cancer, reproductive and teratogenic effect

3) Trenbolone acetate and melengesterol acetate: synthetic hormone, used as

growth promoter only in sheep and cattle.

Non-steroidal anabolic and metabolic accelerator:

 Clenbuterol (beta agonist)
 Toxicity: increased heart rate
PROCESSING INDUCED TOXICANTS
 PROCESSING INDUCED TOXICANTS
 Toxic compounds formed during food processing
1. Lead:
i. Solded canned food
ii. Drinking water stored in lead lined storage tanks
iii. Leached out from inadequately glazed earthenware
potteries/ceramic wares
2. Food additives: food coloring
3. Benzoic acid, potassium bromate
4. Acrylamide :
5. Heterocyclic amines (HCAs)
6. Polycyclic aromatic hydrocarbons (PAHs)
7. Nitrosamines
 Nitrosamine
 In meat product cured with nitrite
 Nitrosopyrrolidine, n-nitrosdimethylamine (or dimethylnitrosoamine)
 Formed when amines in meat combine with nitrites which is added into
cured meat as preservative
 Heating at high temperature induce the formation of nitrosamine
Toxicity:
 Carcinogenic (esophageal and gastrointestinal cancer)
 Mutagenic
 Methemoglobinemia (hemoglobin loses its ability to carry oxygen)
Safety measures:
1. Inhibition of nitrosamine formation : addition of ascorbic acid (US: 550ppm in
cured meat) or erythorbic acid, alpha tocopherol (vitamin E)
2. Cooking methods, temperature, amount of nitrite, amount of amine
3. USDA regulation : sodium nitrite (200ppm; dry cured); (immersion or pumped;
120ppm)
 Acrylamide
 Byproduct of cooking food at high temperature
 Maillard reactions: non-enzymatic browning
 In foodstuffs that had been heated at high temperature (160°C) and increase
with the duration of heating especially starchy (high carbohydrate) food like
potato (fried, deep fried and oven baked) and cereal products
 Most acrylamide in food is formed when a natural amino acid called asparagine
reacts with certain naturally occurring sugars such as glucose, fructose etc or
with reactive carbonyls in starchy foods
 Dietary exposure 2011: potato chips and bread
Toxicity:
1) Mutagenic: damage DNA (glycidamide, metabolite of acrylamide bind with
DNA), chromosome aberration
2) Neurologic and reproductive effect at high dose
3) Potential carcinogen in human: Have been shown to cause tumors in rat

Safety measures: asparaginase, HACCP (CCP)

 Polycyclic aromatic hydrocarbons (PAHs)
 A group of over 100 different chemicals that are formed during the
incomplete burning of coal, oil, gas and garbage
 Example of PAHs are naphthalene, acenaphthylene, acenaphthene,
fluorene, phenanthrene, anthracene, fluoranthene, pyrene, chrysene,
benzo[a]pyrene, benzo[k]fluoranthene, benzo[b]fluoranthene
Sources:
1. Food grown in contaminated soil or air
2. Cooking meat or other foods at high temperature that results in
charring of the food increases the amount of PAHs in such foods
 Smoked, grilled (charcoal grilling), barbecued or burned foods
 Characteristics: lipophilic, stored mostly in kidney, liver and fat tissues
Toxicity:
1) Potential carcinogen
2) Mutagenic
 Heterocyclic amines (HAs)
 Chemicals formed in food cooked above 150°C (in pan, grilled,
overheated food, heavy charring grilled meat such as fish, beef, poultry)
 Frying, broiling, and barbecuing produce the largest amounts of has;
meat juice formed during cooking, commercial sauces and meat stock
(from beef extract)
 Formed when sugar, amino acid and creatine/creatinine in muscle react
at high cooking temperature
 Eg thermal degradation of tryptophan produce β-carbolines; other
amino acids (threonine, glycine, lysine, alanine and serine) producing
imidazo-quinoline or imidazo-quinoxalin-2-amine
Toxicity:
 Human carcinogen
 2-Amino-3-methylimidazo[4,5-f]quinoline (IQ) HCAs
 2-amino-3,4-dimethylimidazo[4,5-f ]quinoline (MeIQ)
 2-amino-3,8-dimethylimazo[4,5-f]quinoxaline (MeIQx)
 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)

 Mutagenic: chromosome aberration

 Aminoimidazoazaarenes
 Carbolines
NATURAL TOXICANTS IN FOODS (PLANT AND
ANIMAL)
 Natural toxicants in foods (plant and animal)
Natural toxicants in plant
1) Anti-nutritive substance
• Substance that cause nutritional deficiency by:
1. Interfere with the absorption and utilization of nutrient
2. Interfere with the function of nutrient
Three classes of anti-nutritive substances:
1. Enzyme inhibitor: substance that interfere with the normal function of
enzyme eg. anti-protease, anti-amylase, anti-cholinesterase
2. Anti-minerals: substance that interfere with the absorption or
utilization of minerals
3. Anti-vitamins: substance that inactivate or destroy vitamins
 Enzyme inhibitors
1) Anti-protease
 Source: most legume species especially soybean; other: potato,
eggplant
 Inhibit normal functioning of protease (trypsin and chymotrypsin)
Toxicity:
 Pancreatic hypertrophism (pancreatitis): inflammation of the pancreas
(activation of proteases causing destruction of pancreas)
 Growth retardation

2) Anti-amylase
 Source: wheat, kidney bean
 Inhibit conversion of starch and sugar
Toxicity:
 Result in energy deprivation of the body
3) Anti-cholinesterase
 Source: plant form solanum genus such as eggplant,
potato (sun green spot), tomato
 Toxin: solanine (a glycoalkaloid)
 Inhibit the normal functioning of cholinesterase
Toxicity:
 Neurological disorder such as respiratory difficulty,
abdominal cramp, hypertension
 ANTI-MINERALS
 Interfere with the absorption or utilization of minerals by:
1. Bind to the minerals (Zn, Fe, Co, Ca, Mg, Mn, Cu) and form insoluble
salts (phytate, oxalate) and render the minerals and micronutrients
unavailable

 Source of phytate: cereal grains and legume (wheat bran, oats, corn,
soybean).
 Source of oxalate: sugar beet, spinach, tea, celeries, cocoa (high amount);
tomato and cauliflower (low amount).

Toxicity:
 If bind to minerals (Zn, Fe, Co, Ca, Mg, Mn, Cu): cause mineral deficiency
and may lead to growth retardation, mild anemia, affect development of
bones and teeth.
2. Bind to iodine interfere with absorption of iodine by thyroid
gland
 Toxin: goitrogen
 Types of goitrogen: glucosinolate, thiocyanate, cheroline,
polyphenolic glucoside, hemagluttin
 Source: goitrogen containing food (especially from brassica family
such as brocolli, cauliflower, cabbage, turnip, brussel sprouts);
others soybean and peanuts
Toxicity:
 Goiter [enlargement of the thyroid gland, thyroid stimulating hormone
(TSH)]; TSH stimulates all aspects of thyroid hormone synthesis; it
also stimulates proliferation of follicle cells
 ANTI-VITAMIN
 Eg: anti-vitamin C, anti-vitamin B1 (thiamine), anti-biotin (vitamin
H)
 Substance that deactivate or destroy vitamins
Three classes of anti-vitamin compound:
1. Compound that have similar chemical structure with the
vitamin and compete with the vitamin in metabolism
2. Compound that change the structure of the vitamin and form
complex
3. Enzyme that attacks or destroys vitamin
1. Anti-vitamin C
 Causes: consumption of food containing ascorbic acid
oxidase (pumpkin and tomato especially outer layer of green
fruit).
 Ascorbic acid oxidase oxidize vitamin C into
dehydroascorbic acid then into diketogluconic acid, oxalic
acid and other oxidative products which will reduce the
vitamin C content.
Toxicity:
 Deficiency of vitamin C with symptom such as swollen gum
and tiredness
2. Anti-thiamine
 Causes:
1)Consumption of anti-thiamine food (tea, coffee)
2)Consumption of thiaminase rich food (bracken fern (Pteridium
aquilinum), raw fish (especially high in liver, egg, skin, head,
viscera)
 Thiaminase: enzyme that destroy thiamine (vitamin B1), interfere
with the function of thiamine
 Function of thiamine: metabolize CHO and fat (source : green
peas, spinach, unpolished rice)
Toxicity of thiaminase:
 Deficiency of thiamine lead to beri-beri (paralysis of limb), weight
loss, loss of appetite, slow heart beat (Shoshin beri-beri)
3. Anti-biotin
 Causes: consumption of large amount of food containing
avidin (in raw egg white)
 Avidin: bind to biotin (vitamin H or B7), prevent biotin
absorption and produce biotin deficiency
 Function of biotin: metabolize fat, CHO and protein
 Sources of food high in biotin: milk, egg yolk, liver, and peas
and beans
Toxicity:
 Infant: deficiency of biotin cause dermatitis such as dry scaly
scalp, shedding of hairs around eyes
 Adult: paralysis of legs
Cyanogenic glucoside: a bound form of cyanide
Sources:
 Apple, peach, pear, plum, bitter almond: amygladin
 Sorghum: dhurrin, high in unripe stage
 Cassava: isolinamarin, linamarin and lotoaustralin; high in
leaves, peel of root
 Lima bean: linamarin
 Legume: sambunigrin

Toxic form: hydrogen cyanide (HCN) and thiocyanate

 How is cyanide released from plant tissue:
Damage plant tissue cyanogenic glucoside (vacuoles) + β
glucosidase (cytosol) hydrogen cyanide (HCN) and thiocyanate
Toxicity:
1. Inhibit oxidative processes of cells (reacts with ferric iron in
cytochrome oxidase)
2. Probably cytotoxic: cause cell damage and malfunction
 Acute toxicity (mild dose): headache, tightness of throat, chest
and muscle weakness; fatal dose: respiratory arrest, collapse,
death
 Chronic toxicity: neurologic disorder

1)Phenolic acids: caffeic, ferullic, sinapic,

gallic acid and their derivatives; flavanoids,
lignin, tannin; ellagic acid and their
derivatives
Phenolic
Substances
1)Gossypol, phlorizin, myristicin, urushiols
and phenolic amines or cathecholamines
1. Gossypol
Yellow pigment present in pigment gland of leaves, stem, bark,
root and especially seed of cotton plant (Gossypium sp)
Source: cotton plant
Toxicity:
 Interfere with normal iron (Fe) utilization in hemoglobin synthesis
leads to anemia
 Bind with amino acid (eg lysine) leads to weight reduction, loss of
appetite, growth retardation, spastic paralysis
 Bind to protein eg enzyme cause enzyme inactivation thus
lowers protein digestibility or bind to tissue protein cause severe
damage to internal organ
2. Alkylated catechols
 Source: in mango, cashew, pistachio mango
 Mangifera caesia and M. Lagenfera (binjai and lanjut)
 Toxin: xanthones, mangiferin, isomangiferin, flavanoid, quercetin,
hydrolyzable tannins
 High in peel of green unripe mango fruit
 Toxicity: dermatitis, swelling of lips, cheek, chins, itching and
burning sensation

Cashew
• In the oil of cashew nut (shell)
• Toxin: salicyclic acid derivatives (anacardic acid) and resorcinol
derivatives (cardol)
• Toxicity: allergic skin rash and blistering of the mouth
3. Flavones
Source: in citrus fruits (tangerines, mandarin orange and oranges)
High in oil vesicles of the peel
Toxin: nobiletin, tangeritin
Toxicity: cytotoxic

4. Tannins
Source: mango, coffee, tea, cocoa, sorghum, grapes, banana, sapota
Abundant at unripe stage (astringent and bitter)
Toxicity:
1) Bind to protein
2) Potential carcinogen
3) Bind to iron (Fe) producing symptoms such as migraine and
suppress growth
5. Lectin protein
 Toxin: phytohemagglutinins
 Source: legume sp (red kidney beans, castor beans) especially
when eaten raw and not completely cooked
 Toxicity: agglutinate red blood cell

6. Lathyrogens
 Source: legume from genus Lathyrus especially chick peas (green part)
 Toxin: DBA (α-δ-diaminobutyric acid); ODBA (N- δ-oxalyl- α- δ-diaminobutyric
acid, ODPA (N-B-oxalyl- α-β-diaminopropionic acid and GAPN (δ-glutamyl-β-
aminopropionate)
Toxicity:
 Inhibit lysyl oxidase, an enzyme essential for interfibrillar crosslinking, this results in
defective collagen synthesis and interference of collagens and elastins crosslinking
 Neurotoxin attack motor neuron
Two types of lathyrism (paralysis of hind or lower limb):
1) Osteolathyrism : a severe skeletal deformitis
2) Neurolathyrism: paralysis related to motor neuron
6. Stimulant compounds
Toxin:
1) Caffeine: coffee, tea and cocoa
2) Theophylin : tea
3) Theobromine: cocoa
Toxicity:
 Stimulate synthesis and released of norepinephrine to brain tissue
 Induce release of epinephrine (adrenalin hormone) from adrenal
medulla (kidney)
 Potential mutagen
 7. Psychoactive compounds (myristicin, dioscarine, favic agents)

Myristicin
 Source: (nutmeg, black pepper, celery)
 Toxicity: similar to alcoholic intoxication, hallucination, depression
Dioscarine
 Source: yam (Dioscorea dumetorum, D. hirsuta, D. hispida)
 Toxicity: depression of central nervous system leading to paralysis,
speech disturbance, heat sensation
Favic agents
 Source: cooked or raw faba beans (Vicia faba) or inhalation of pollen
produce favism
 Toxin: vicin and convicine in the skin of the bean
 Toxicity: cause hemolytic reaction (lowering of erythrocytes, causing
hemolytic anemia, hemoglobinuria) dizziness
8. Vasoactive amines (tyramine and phenylethylamine)
1) Toxin: tyramine
 Source: banana pulp
Toxicity:
• Cause release of norepinephrine
• Cause constriction and dilation of blood vessel (affect blood pressure)
lead to hypertension, throbbing headache, and migraine

2) Toxin: phenylethylamine
 Source: chocolate, cheese, red wine
Toxicity:
• Cause dramatic change in blood flow through brain leading to headache
 Natural Toxicants In Animals (Seafood)
• Fish
Ciguatera fish poisoning
 Cause: consumption of carnivorous fish (large and older
fish more toxic)
 Source: barracuda, red snapper, grouper, sturgeon and
amberjack are usually the most commonly involved fish
(coral reef fish)
 Toxin: ciguatoxin (a neurotoxin) produced by dinoflagellate
Gambierdiscus toxicus.
 High concentration: liver, gonad, head and viscera of fish
 Health risk: above 0.1 ppb.
Characteristics of the toxin:
 Bio-accumulates
 Biomagnified through the food chain (larger and older fish are
more toxic)
 Heat stable
 Acid stable

Toxicity:
 Affect nervous system; gastrointestinal, neurologic and
cardiovascular symptoms such as abdominal cramp,
respiratory paralysis, salivation, neck stiffness
 “Reversal thermal sensation”
 Scombroid fish poisoning
 Cause: consumption of fish containing histamine
 Source: large dark meat fish (Scombroidea family) including tuna,
mackerel, bonito, skipjack, marlin
 Contaminated fish : peppery and bitter taste
 Toxin: histamine
 Formation of histamine:
Histidine in fish bacteria + histidine decarboxylase (cause
decarboxylation) histamine
 Bacteria: Proteus (Morganella) morganii, Klebsiella pneumoniae, Hafnia
alvei, Clostridium perfringens
Symptoms: rash, facial flushing, palpitation, headache, nausea, diarrhea,
loss of vision
 Puffer (balloon, blow, bubble, globe) fish poisoning

 Cause: consumption of puffer fish (Fugu oblungus, F. ocellatus

obsurus, F. ocellatus ocellatus, F. peoalonalus)
 Japanese: Tiger puffer fish (Takifugu rubripes).
 Toxin: tetradotoxin or fugutoxin
 Liver, ovaries, skin and testes of fish
 Mechanism of action: block movement of sodium ion in neuron
membrane of nervous system
 Symptoms: muscular paralysis, hypersalivation, hyperperspiration,
rapid pulse
 Mati makan telur ikan buntal

DUNGUN 15 Feb.2009 – Keseronokan lima nelayan menikmati makanan hasil tangkapan

mereka di laut bertukar menjadi tragedi apabila salah seorang daripada mereka mati
dipercayai selepas memakan telur ikan buntal. Nordin Sulong, 43, dari Kampung Teluk
Bidara, di sini meninggal dunia dalam bot kira-kira pukul 11.15 malam tadi ketika dibawa
pulang untuk mendapatkan rawatan. Empat lagi termasuk seorang anak mangsa, Ahmad
Hafiz, 18, dimasukkan ke wad Hospital Dungun kerana mengalami keracunan yang teruk.
Tiga nelayan yang dirawat selain Ahmad Hafiz ialah Khalid Jusoh, 52, Mohd. Azroy Mohd.
Ghani, 21 dan Zainuddin Jaafar, 43. Sementara itu, Ketua Polis Daerah Dungun,
Suprintendan Dahlan Mohd. Noor ketika dihubungi mengesahkan kejadian itu. Beliau
berkata, mangsa dipercayai mati akibat termakan makanan beracun. “Hasil soal
siasat ke atas nelayan yang memasak makanan tengah hari itu mendapati, dia
memasukkan beberapa biji telur ikan buntal ke dalam kari masakannya. “Ketika
memasukkan telur ikan tersebut mereka tidak menyedari racun dalam perut ikan itu
melalui hempedunya turut termasuk dalam telur ikan terbabit,” katanya. Beliau
berkata, jenazah mangsa dituntut oleh keluarganya dan dikebumikan di Kampung Teluk
Bidara, di sini.

Al Fatihah to the family members and friends.

 Shellfish poisoning

 Cause: consumption of bivalve mollusk containing toxic dinoflagellates

and diatoms
 Red tide: massive multiplication or bloom of toxic algae (pigmented
phytoplankton) causes ocean water to turn red or dark brown color.
 Species in the United States that release these harmful toxins include:
1. Alexandrium fundyense - found along the Atlantic coast from the
Canadian Maritimes to southern New England
2. Alexandrium catenella - found along the Pacific coast from
California to Alaska
3. Karenia brevis - found in the Gulf of Mexico along the west coast of
Florida
 Paralytic shellfish poisoning
 Source: shellfish contains dinoflagellate of Gonyaulas catenella and G.
tamarensis toxin
 Toxin: saxitoxin (heat and acid stable)
 Produced highest incidence of fatal cases of shellfish poisoning
 Mechanism of action: block sodium ion movement in nerve and muscle
cell membrane
 Symptoms: paresthesia of lip, tongue, gum, incoordination, difficulty of
breathing, swallowing and complete loss of speech

Neurologic shellfish poisoning

 Source: shellfish contains dinoflagellate of Ptychodiscus brevis
 Toxin: brevetoxin
 Mechanism of action: bind and stimulate sodium flux in sodium channel
of nerve and muscle cells
 Symptoms: paresthesia of the face, reversal of hot/cold sensation
 Diarrheal shellfish poisoning
• Source: shellfish contains dinoflagellate Dinophysis and
Prorocentrum
• Toxin: okadaic acid
• Toxicity: bind to intestinal epithelial cells and increase in
permeability of the intestinal wall
• Symptoms: diarrhea

Amnestic shellfish poisoning

• Source: shellfish contains diatoms Nitzschia pungens cf
multiseries
• Toxin: Domoic acid (excitotoxic neurotransmitter amino
acid)
• Toxicity: affect neuron functioning
• Symptoms: memory loss and confusion
TOXIC CHEMICALS IN PACKAGING MATERIALS
 Packaging materials: paper, fibreboard, glass, tinplate, aluminium and various
types of plastics.
 Plastic packaging resin: polystyrene (PS), polyethylene terephthalate (PET,
PETE), Polypropylene (PP), high-density polyethylene (HDPE), low-density
polyethylene (LDPE), polyvinyl chloride (PVC or vinyl)
 The Society of the plastics industry (SPI) resin identification code assigns each
of these resins a number from 1 to 6.
 Plasticizer: a polymer additive that serves to increase the polymer’s flexibility,
elongation or ease of processing
 Phthalate plasticizers [DEHP (Di-Ethylhexyl Phthalate) and DINP (Di-Isononyl
Phthalate)]: most commonly used plasticizers in PVC also used in food packaging.
 Migration of plasticizers increase at higher temperature
 DEHP (Di-Ethylhexyl Phthalate)

 Migrate out of the plastic as a vapor over 30° C

 In fatty foods, such as butter, cheese, and prepared meat
products packaged in PVC, significant amounts of DEHP or
DINP have been found in surface layers
 Highly soluble in fats and oils

Toxicity:
 Chronic: long term accumulation and high level may lead to liver
and kidney damage
 Affect the ability to reproduce
 DEHA [di(ethylhexyl) adepate]
 Commonly used as a plasticizer in polyvinyl chloride (PVC) film
wrap
 Ability to migrate into food at high temperatures
 Migration level increase in proportion:
1. To the time that the food was in contact with the PVC wrap
2. With the rise in cooking temperature
3. Fatty food (eg meat, chicken, bakery products)
4. With direct contact
Toxicity:
 Suspected carcinogen
 Styrene/polystyrene (styrofoam) (PS)
 Chemical name: ethylbenzene
 Polystyrene foam containers (coffee cups, fast food containers),
containers for microwaving foods)
 Migrate into food from polystyrene foam containers when food was
heated.
1) Eating fatty foods packaged and heated in polystyrene containers
2) Drinking contaminated water
3) Living near industrial facilities or hazardous waste sites
 At trace levels in food can give a “plastic” taste
 Vary directly with the fat content of the food : highest concentration in
fruit yogurt, sandwich cookies, margarine, butter and cake doughnuts
Toxicity:
 Induce skin tumor in animals
 CNS depression
 Polyethylene terephthalate (PET)
 Plastic resins used as packaging materials
 Contain acetyldehyde, ethylene glycol
 Widely used for food and beverages bottling such as packaging of soda, pourable
dressings, edible oils, peanut butter, cereal box liners, soda bottles, mineral water
bottles, boil-in-the-bag pouches, and microwave food trays
 Resistance (does not break easily), lightweight, transparency, flexible, recyclable,
low production cost
 As plastic film wrap provides a functional barrier to adhesive components
 It was demonstrated recently that the film allowed the migration of adhesive
components into foods when oils or foods were cooked in contact with it
Toxicity:
 Reduce mitosis
 Induce chromosome aberrations
 Growth retardation