Hexachlorobenzene
1. NAME
1.1 Substance
Hexachlorobenzene
1.2 Group
Organochlorine pesticide - fungicide
1.3 Synonyms
Benzene, hexachloro-
Esaclorobenzene (Italian)
HCB
Hexa CB
Hexachlorobenzol (German)
Julin's carbon chloride
Pentachlorophenyl chloride
Perchlorobenzene
Phenyl perchloryl (RTECS, 1994)
1.4 Identification Numbers
1.4.1 CAS number
118-74-1 (RTECS, 1994)
1.4.2 Other numbers
UN NUMBER: UN 2729 (RTECS, 1994)
RTECS NUMBER: DA 2975000 (RTECS, 1994)
OHM-TADS NUMBER: 8l00010 (HSDB, 1994)
1.5 Main brand names/main trade names
To be completed by each center.
1.5 Main manufacturers/main importers
To be completed by each center.
2. SUMMARY
2.1 Main risks and target organs
HCB has low acute toxicity. Most cases of poisoning are due to
subchronic or chronic ingestion.
Liver is the main target organ of HCB toxicity.
HCB interferes with porphyrin metabolism, it may cause acquired
porphyria cutanea tarda.
HCB crosses the placenta; it is excreted in breast milk and
nursing infants of mothers exposed to HCB are at risk of
intoxication.
HCB is a potential carcinogen in human.
2.2 Summary of clinical effects
Ingestion of very large amounts of HCB may result in CNS effects:
headache, dizziness, nausea, vomiting, numbness of hands and
arms, apprehension, partial paralysis of extremities, loss of
equilibrium and vibratory sense, coma and convulsions.
HCB may induce porphyria cutanea tarda characterized by
blistering and epidermoly-sis of the skin, hypersensitization to
sunlight and minor mechanical traumas, hyperpigmentation, scars,
hypertrichosis, permanent alopecia or corneal opacities.
Infection involves deeper tissues with suppurative arthritis and
osteomyelytis. Complications progress to weakness, convulsions
and death.
2.3 Diagnosis
History of exposure to HCB in occupational settings or by
ingestion of HCB-contaminated food or water.
Syndrome resembling porphyria cutanea tarda including a vesicular
and bullous disease is frequently associated with hepatomegaly,
porphyria and death.
Clinical variation may include hyperpigmentation, hypertrichosis,
alopecia or hirsutism, corneal opacities, deformation of the
exposed parts, loss of body weight, wasting of skeletal muscles.
The urine frequently shows a characteristic port wine color
associated with porphyria.
2.4 First aid measures and management principles
Monitor airway, breathing and circulation and restore vital
functions if necessary.
Remove all contaminated clothes.
Wash chemicals out of the eyes with clear water.
Wash chemicals off the skin with soap and water.
If HCB has been ingested, do not give any milk, fat, oil or lipid
by mouth.
If very large amount of HCB has been ingested, perform gastric
lavage.
Administer activated charcoal.
If necessary, control convulsions.
Symptomatic treatment.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
Synthetic. May be produced by chlorination of benzene;
isolation from by-product residues of tetrachloroethylene;
reaction of hexachlorocyclohexane with chlorine or sulfuryl
chloride. (HSDB, 1994)
3.2 Chemical structure
Chemical name: Hexachlorobenzene
Molecular weight: 284.80
Molecular formula: C6Cl6
3.3 Physical Properties
Normal state at room temperature: solid needle-like crystals
(SAN, 1989)
Colour: White (San, 1989)
Odour: Faint, not unpleasant (CHRIS, 1994)
Ph: No data available
Viscosity: No data available
Volatility: vapor pressure 1089 X 10-5 mm Hg at 20 °C (Budavari,
1989 -Hayes, 1991)
Solubility in water: practically insoluble (Hayes, 1991), 7.9
mg/L (Burton, 1987)
Solubility in alcohol: sparingly soluble in cold alcohol
(Budavari, 1989)
Solubility in ether: soluble (Budavari, 1989)
Flammability: HCB may burn but does not ignite readily (Dept.
Transportation, 1987)
Flash point: 468 °F. CC. (CHRIS, 1994)
Stability: Very stable, even to acids and bases (Hartley, 1983)
Reactivity with water: No reaction
Reactivity with dimethyl formamide: Reacts violently above 65 °C
(National Fire Prot. Ass., 1986)
3.4 Other characteristics
Hazardous combustion/products of combustion: When heated to
decomposition, emits toxic fumes of chlorides (Sax, 1989)
Environmental risks: HCB is formed as a waste product in the
manufacture of several chlorinated hydrocarbons and is a
contaminant in some pesticides. It may enter the environ-ment in
air emissions and waste water from manufacture and in flue gases
and fly ash from waste incineration. Non-point source dispersal
of HCB results from its presence as a conta-minant in pesticides.
HCB is a very persistent environmental chemical due to its
chemical stability and resistance to biodegradation. If released
in the atmosphere, HCB will exist primarily in the vapor phase
and degradation will be extremely slow (estimated half-life with
hydroxyl radicals is 2 years). Volatilization from the water is
rapid but strong adsorption to sediment can result in long period
of persistence. HCB will concentrate in fish and enter into the
food chain. (HSDB, 1994)
Disposal: At the time of the review, criteria for disposal
practices are subject to significant revision.
Possible contaminants: Polychlorinated dibenzo-p-dioxins and
dibenzofurans can be present; octa-chlorinated and hepta-
chlorinated congeners dominate at 0.35 - 58.3 ppm (HSDB, 1994)
Boiling point: 323 - 326 °C (Budavari, 1989)
Melting point: 231 °C (Budavari, 1989)
4. USES/CIRCUMSTANCES OF POISONING
4.1 Uses.
The major use in many countries has been as a fungicide applied
to seeds, particularly cereals grains. It also has been used as
a wood preservative, in pyrotechnic compositions and in the
manufacture of dyes, polyvinyl chloride and synthetic rubber.
Use of HCB as fungicide has almost ceased, but emissions from
industrial processes and its presence as a contaminant in other
pesticides still result in release to the environment. (Burton,
1987) High risk circumstance of poisoning.
Human poisonings will result from contaminated ambient air,
contaminated drinking water and food, and contact with
contaminated soil or in the workplace (HSDB, 1994).
HCB is particularly toxic to fetus. It is also excreted in
breast milk and breast-fed children may be most severely affected
by this toxin. (Ellenhorn, 1988, Klaassen, 1986)
4.3 Occupationally exposed populations.
Occupational exposure will occur at plants manufacturing
chlorinated solvents and some pesticides (Currier, 1980).
Workers in wood preservative industry are also exposed to HCB
both by cutaneous absorption and inhalation.
Farmers and pesticides sprayers will be exposed by handling and
applying pesticides in which it is a contaminant or by handling
contaminated soil. (Burns, 1974 -HSDB, 1994)
5. ROUTES OF ENTRY
5.1 Oral
Major route for human exposure is ingestion. (CHRIS, 1994)
5.2 Inhalation
HCB may be absorbed by dust inhalation. (CHRIS, 1994)
5.3 Dermal
Dermal absorption is not a major route of contamination but
animal studies have demonstrated cutaneous absorption in rats.
Dermal contamination can be source of absorption and personal
hygiene is likely to have a profound influence on the body burden
of HCB (Koizumi, 1991)
5.4 Eye
No data available.
5.5 Parenteral
No data available.
5.6 Others
No data available.
6. KINETICS
6.1 Absorbtion by route of exposure
HCB is readily absorbed via the gastrointestinal system (Burton,
1987). Absorption from the intestinal tract appears to depend on
the solvent vehicle. Thus, when HCB is administered in olive
oil, approximately 80% of the dose is absorbed; in aqueous
solution or in solid crystalline form, relatively little is
absorbed (< 20%). Intestinal absorption of HCB occurs primarily
through lymphatic channels with only a minor portion absorbed
into the portal circulation. (U.S. EPA, 1991)
6.2 Distribution by route of exposure
Following intestinal absorption, HCB, which is lipophilic,
distributes to tissues that are rich in lipid content. Adipose
tissue accumulates the greatest concentrations although bone
marrow and skin also accumulate HCB. The adrenal cortex
accumulates HCB at levels near those of fat. Other tissues
(liver, kidneys, lungs, heart, spleen and blood) usually contain
lower amounts of HCB (U.S. EPA, 1991 -U.S. EPA, 1984)
HCB crosses the placenta and is distributed in fetal tissues
(U.S. EPA, 1991 -U.S. EPA, 1984)
6.3 Biological half-life by route of exposure
The half-life for HCB in sheep, chickens and pigs is 10 - 18
weeks, 8 -14 weeks and 10 - 12 weeks respectively (Menzie, 1978).
In rats, the biological half-life was 4 to 5 months. (Clayton,
1981)
In dogs, the estimated biological half-life is 6 weeks to 3
years. (Sundlof, 1982 -Budavari, 1989)
6.4 Metabolism
HCB is metabolized slowly by the liver to pentachlorophenol,
pentachlorobenzene, tetrachlorobenzene and some unidentified
compounds. Some tetrachlorophenol and traces of trichlorophenol
were detected, partly in the form of glucuronides. (Hayes 1991)
A number of sulfur-containing metabolites have been identified
including tetra- and penta-chlorobenzenethiol,
methylthiopentachlorobenzene, 1,4-bis(methylthiol)-2,3,4,6-
tetrachlorobenzene, methylthiotetrachlorobenzenethiol,
tetrachlorobenzenethiol and N-acetyl-S-(pentachlorophenyl)-
cysteine. (Hayes, 1991)
6.5 Elimination by route of exposure
The excretion of HCB is slow and occurs mainly through the faeces
with relatively little being excreted in the urine. In rats,
about 7% of a single dose is eliminated in urine and 27% in
faeces as metabolites over a 4 weeks period. (Courtney, 1979).
Milk excretion has been shown to be a quantitatively important
route for elimination of HCB (Bleavins, 1982 -Courtney, 1979)
7. TOXICOLOGY
7.1 Mode of action
HCB causes porphyria by partially blocking haem biosynthesis,
leading to accumulation and excretion of uroporphyrin (Klaassen,
1986).
The involvement of reactive toxic metabolites like
pentachlorophenol has been suggested.
Two hypotheses on the mechanism of metabolic block of HCB have
been proposed: HCB may be metabolized to reactive derivatives
causing inactivation of uroporphyrinogen-decarboxylase by
covalent binding to the active center; or it may block indirectly
by stimulating production of peroxides and free radicals. (De
Matteis, 1985)
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
It was estimated that porphyria cutanea tarda occured in
individuals who had consumed 50 - 200 mg of
hexachlorobenzene/day for a "relatively long period of
time". (Courtney, 1979) Lowest reported acute toxicity for
man: 220 mg/-Kg. (Sax, 1989)
7.2.1.2 Children
2.6 to 4.1 mg/kg/day (Hayes, 1991)
7.2.2 Relevant animal data
Oral:
LD50 (Rat) : 10 g/kg
LD50 (Mouse) : 4 g/kg
LD50 (Rabbit) : 2600 mg/kg
LD50 (Guinea pig): > 3 g/kg
LD50 (Cat) : 1700 mg/kg
LD50 (Mammal) : 1047 mg/kg
LD50 (Quail) : >6400 mg/kg
Inhalation:
LC50 (Rat) : 3600 mg/m3
LC50 (Mouse) : 4 g/m3
LC50 (Rabbit) : 1800 mg/m3
LC50 (Cat) : 1600 mg/m3 (RTECS, 1994)
7.2.3 Relevant in vitro data
No data available.
7.2.4 Workplace standards
No occupational exposure limits have been published by
ACGIH. (Clayton, 1981)
Czechoslovakia: TWA: 1 mg/m3, STEL: 2 mg/m3, January 1993.
France: Carcinogen, January 1993
Russia: 0.9 mg/m3, Skin, January 1993 (RTECS, 1994 - U.S.
EPA, 1991)
7.2.5 Acceptable daily intake
In 1978, Joint FAO/WHO Food-Standards Programme Codes
Committee on Pesticide Residues proposed an acceptable daily
intake of hexachlorobenzene of 0.0006 mg/kg body weight but it
has now been withdrawn (WHO, 1984).
The U.S. EPA (1991) verified a reference dose (RFD) in May
1988 for HCB. The RFD is 8E-4 mg/kg/day. (U.S. EPA 1991)
The U.S. EPA determined that HCB is a suspected carcinogen and
since there is no recognized safe concentration for human
carcinogen, the recommended concentration of HCB in water for
maximum protection of human health is zero.
Drinking Water Unit Risk: 4.6E-5 per mg/L.
Drinking Water Concentrations at specified risk levels
(U.S. EPA, 1994)
Risk Level Concentration
---------------------------------------------------
E-4 (1 in 10,000) 2 mg/L
E-5 (1 in 100,000) 2E-1 mg/L
E-6 (1 in 1,000,000) 2E-2 mg/L
According to WHO, the guideline value recommended for HCB in
drinking water is 0.01 mg/L on the basis of the 10-5 risk
level (WHO, 1984).
7.3 Carcinogenicity
The International Agency for Research on Cancer (IARC) has
classified HCB under group 2B. Evidence for carcinogenicity to
humans is inadequate but there is sufficient evidence for
carcinogenicity in animals (IARC, 1979 - IARC, 1987).
No report of a direct association between HCB and human cancer is
available. Hepatocellular carcinoma has been associated with
porphyria. However, although abnormal porphyrin metabolism
persisted at least 20 years after an epidemic of porphyria
cutanea tarda in Turkey, caused by consumption of grain treated
with HCB, no excess in cancer occurrence has been reported in
this population even 25 years after the accident. (IARC, 1979 -
IARC, 1987)
The liver appears to be the primary target organ for HCB-induced
cancer in animals although neoplasms of the thyroid and kidney
have also been observed. (WHO, 1984)
HCB was tested in animals by oral and intra-peritoneal
administration. It produced hepatomas, liver
haemangioendotheliomas, thyroid adenomas and renal-cell adenomas.
(IARC, 1979 - IARC, 1987)
In a two-generation feeding study in rats with lower dose levels,
increased incidence of parathyroid adenomas and adrenal
pheochromocytomas were observed in animals of each sex and liver
neoplastic nodules in females of the F generation. After 90
weeks' feeding of HCB to rats, 100% of surviving females and only
16% of males had developed liver tumours. (Smith, 1985)
7.4 Teratogenicity
HCB has been shown to cross the placenta in a number of species
including humans. Treatment of pregnant rats and mice with HCB
produced an increased incidence of enlarged kidneys in the
offspring. Increased perinatal mortality and abnormal immune
system development have also been reported in mice offspring.
Negative teratology studies have been reported as well in mice
and rats. In these reports, abnormalities in the offspring were
not seen in the absence of maternal toxicity. Human
teratogenicity studies with HCB have not been reported.
(Scialli, 1994)
7.5 Mutagenicity
According to studies in animals, HCB does not appear to be a
potent mutagen (Clayton, 1981). No genotoxicity has been
onserved in Salmonella typhimurium (AMES test), E. Coli, and
human peripheral blood lymphocytes in vitro. (Siekel, 1991)
7.6 Interactions
A number of experiments have demonstrated that iron loading can
hasten the onset and increase the intensity of porphyria caused
by HCB in rats. Other factors known to influence the porphyria
produced by HCB include sex hormones, some other steroids,
alcohol and caloric intake. Ultraviolet light (sunlight)
enhances the development of dermal lesions. (Hayes, 1991).
8. TOXICOLOGICAL AND BIOMEDICAL INVESTIGATIONS
9. CLINICAL EFFECTS
9.1 Acute poisoning
9.1.1 Ingestion
Ingestion of large amounts of HCB may result in central
nervous system effects which may include headache, dizziness,
nausea, vomiting, numbness of hands and arms, apprehension,
partial paralysis of extremities, loss of equilibrium and
vibratory sense, coma and seizures. (Morgan, 1994)
9.1.2 Inhalation
Breathing HCB can irritate the nose, throat and lungs.
(Morgan, 1994)
9.1.3 Skin exposure
Extensive contact can cause skin irritation. (Morgan, 1994)
9.1.4 Eye contact
Contact can cause eye irritation. (Morgan, 1994)
9.1.5 Parenteral exposure
No data available.
9.1.6 Other
No data available.
9.2 Chronic poisoning
9.2.1 Ingestion
Chronic ingestion caused a vesicular and bullous disease
resembling porphyria cutanea tarda which was frequently
associated with hepatomegaly and death.
9.2.2 Inhalation
There was no evidence of porphyria cutanea tarda or other
adverse effects associated with inhalation of HCB. (Currier,
1980)
9.2.3 Skin exposure
No data available.
9.2.4 Eye exposure
No data available.
9.2.5 Parenteral exposure
No data available.
9.2.6 Other
No data available.
9.3 Course, prognosis, cause of death
Chronic ingestion of HCB causes a vesicular and bullous disease
resembling porphyria cutanea tarda and is frequently associated
with hepatomegaly and death.
In mild cases, lesions develops early with the vesicles and
bullae appearing particularly in skin areas exposed to sunlight.
In children, the initial lesions resembled comedones and milia,
while in adults, bullous lesions developed promptly. Frequently,
lesions become crusted and at times ulcerated.
There are many clinical variations which include
hyperpigmentation, hypertrichosis, alopecia (in some instances
permanent) or excessive growth of hair, corneal opacities,
deformation of the exposed parts, loss of body weight, wasting of
skeletal muscles and hepatomegaly.
Generally, recovery occurs following cessation of ingestion.
Symptoms of subacute or chronic HCB intoxication may involve
cutaneous, hepatic, arthritic, visceral, urinary and neurological
effects that may persist for 20 years and more.
HCB has been found in breast milk and nursing infants may develop
"pembe yara" or pink sore (see 11.1). The mortality rate in
affected children is 95%. It begins with diarrhea, fever and
pink or skin-colored papular on the back of the hands and
fingers, on the wrists and sometime on the feet and legs. Later,
the skin lesions form plaques and rings of different colour and
texture. X-ray examination reveal an infiltration of the lungs.
Subcutaneous abcesses develop in some cases. Infants lose weight
and become dehydrated. The liver is hypertrophied and there is
severe hypochromic anemia and leucocytosis. Resolution of the
skin lesions and improvement of general health often require 1 -
2 months. (Hayes, 1991)
9.4 Systematic description of clinical effects
9.4.1 Cardiovascular
No data available.
9.4.2 Respiratory
Irritation of respiratory tract may result from inhalation.
(Dreisbach, 1983)
9.4.3 Neurological
9.4.3.1 CNS
Acute: CNS effects including headache, dizziness, nausea,
vomiting, apprehension, loss of equilibrium and vibratory
sense, coma and convulsions may occur.
9.4.3.2 Peripheral nervous system.
Acute: Partial paralysis of extremities, numbness of hands
and arms may occur.
Chronic: Paresthesiae, cogwheeling.
9.4.3.3 Autonomic nervous system
No data available.
9.4.3.4 Skeletal and smooth muscle
No data available.
9.4.4 Gastrointestinal
Acute: When ingested, HCB can cause nausea and vomiting
especially when dissolved in petroleum distillates.
Chronic: Diarrhoea in infants has been reported.
9.4.5 Hepatic
Chronic: Hepatomegaly is common.
9.4.6 Urinary
9.4.6.1 Renal
No data available.
9.4.6.2 Others
Urine may appear port wine red or darker.
9.4.7 Endocrine and Reproductive Systems
Chronic: Enlarged thyroid.
9.4.8 Dermatological
Acute: Irritation
Chronic: Generalized hyperpigmentation, hypertrichosis,
scarring on the cheeks and hands, photosensitization.
9.4.9 Eye, ears, nose and throat, local effects
Acute: Irritation of nose and throat.
Chronic: Corneal opacities
9.4.10 Haematological
Chronic: HCB induces porphyria cutanea tarda.
9.4.11 Immunological
Immunotoxicity has been documented in experimental animals.
(Clayton, 1981)
9.4.12 Metabolic
9.4.12.1 Acid base disturbances
No data available.
9.4.12.2 Fluid and electrolyte disturbances
No data available
9.4.12.3 Others
Chronic: Fever in infants has been reported (CAM, 1960).
9.4.13 Allergic reactions
No data available.
9.4.14 Other clinical effects
No data available.
9.4.15 Special risks: Pregnancy
Pregnancy: HCB has been shown to cross the placenta and
accumulate in the fetus.
Breast-feeding: HCB has been found in breast milk and nursing
infants may absorb sufficient to cause symptoms, even in
asymptomatic mothers . (Hayes, 1991)
9.5 Others
Chronic: Weakness, suppurative arthritis, osteomyelitis, swelling
and spindling of fingers.
Osteoporosis restricted to the phalanges, the metacarpal and
carpal bones, and distal metaphysis and epiphysis of both ulna
and the radius and the corresponding bones of the lower
extremities.
Interphalangeal arthritis. (Hayes, 1991; U.S. EPA, 1991).
10. MANAGEMENT
10.1 General principles
Seizures, hypoxemia and resultant acidosis are the immediate
life-threatening emergencies.
Diazepam is the anticonvulsant of choice. Moderately to severely
poisoned patients should have intravenous lines and a cardiac
monitor. (Burns, 1974).
When ingestion is recent and in quantities sufficient to cause
poisoning, gastric lavage and catharsis are indicated.
If skin is contaminated, wash the area with soap and copious
amount of water.
Do not give milk, fat or oils by mouth because they may enhance
absorption.
Do not give adrenaline or other adrenergic amines because of the
enhanced myocardial irritability induced by chlorinated
hydrocarbons.
10.2 Relevant laboratory analyses and other investigations
10.3 Life supportive procedures and symptomatic treatment
Control convulsions with appropriate drug regimen.
10.4 Decontamination
Remove and discard contaminated clothing.
Irrigate exposed eyes with copious amount of water.
Wash skin with soap and copious amount of water.
Cholestyramine or activated charcoal may be administered.
10.5 Elimination
Dialysis, diuresis and hemoperfusion are ineffective.
10.6 Antidote treatment
No data available.
10.7 Management discussion
CaEDTA 0.5 to 1.5 g/day i.v. has been tried but there has been no
controlled trial of its effectiveness. (Hayes, 1991)
11. ILLUSTRATIVE CASES
11.1 Case reports from the literature
From 1955 through 1959, in southeastern Turkey, approximately 4
000 people developed porphyria following ingestion of wheat
intended as seed, not food. The wheat contained HCB. They
developed porphyria cutanea tarda characterized by photosensitive
skin lesions, hyperpigmentation, hirsutism, scarring of the hands
and face, pinched faces, fragile skin, enlarged liver, small
hands with sclerodermoid thickening and shortening of distal
phalange, painless arthritis and enlarged thyroid. (Cripps,
1980; Cripps, 1984; Hayes, 1991)
In the same areas, "pembe yara" occurred in at least one adult
but chiefly in children who had eaten contaminated bread. The
mortality rate of about 95% almost eliminated children between 2
and 5 years in many villages in the years between 1955-1960. HCB
was demonstrated in the milk of their mothers. It began with
diarrhea, fever and pink or skin-colored papules on hands and
fingers. Some infants were saved through removal from breast-
feeding and attention to supportive care. (Cripps, 1980; Cripps,
1984; Hayes, 1991)
A case that was typical in its clinical manifestations was
atypical in that the illness was attributed to the patient's work
as a farmer. HCB was found in substantial concentration in the
patient's blood. The source of HCB was said to be an insecticide
which also contained dieldrin and HCH. This suggests that the
patient had used HCB in an unconventional way and does not
indicate that he had eaten residues of the fungicides. (Hayes,
1991)
Measurement of HCB levels in adipose tissue and maternal milk is
a useful tool for monitoring body stores; these are clearly
higher in Spain than in other European or American countries.
Porphyria cutanea tarda is a relatively frequent disease in
Spain. More than 700 cases were observed in Madrid from 1964 to
1988. It seems that this high incidence of porphyria cutanea
tarda may be related to environmental contamination with HCB.
(Enriquez, 1990)
11.2 Internally extracted data on cases
To be completed by each center.
11.3 Internal cases
To be completed by each center.
12. ADDITIONAL INFORMATION.
12.1 Availability of antidotes
To be completed by each center.
12.2 Specific preventive measure
No data available.
12.3 Other
No data available.
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14. AUTHOR, REVIEWER, DATE, COMPLETE ADDRESS
Author: Nida BESBELLI
Address: Poison Center
Refik Saydam Hygiene Institute
Cemal Gursel Cad. No 18 Sihhiye
06100 Ankara/TURKEY
Tel: 90 4 1337001
Fax: 90 4 1337000
Telex: 2860-944830 POISON-TR
Co-author: Lyse LEFEBVRE
Pharmacienne
Address: Centre de Toxicologie du Québec
2705, boul. Laurier
Sainte-Foy (Québec)
G1V 4G2
Tel: (418) 654-2254
Fax: (418) 654-2754