1.1 Substance
   1.2 Group
   1.3 Synonyms
   1.4 Identification Numbers
      1.4.1 CAS number
      1.4.2 Other numbers
   1.5 Main brand names/main trade names
   1.5 Main manufacturers/main importers
   2.1 Main risks and target organs
   2.2 Summary of clinical effects
   2.3 Diagnosis
   2.4 First aid measures and management principles
   3.1 Origin of the substance
   3.2 Chemical structure
   3.3 Physical Properties
   3.4 Other characteristics
   4.1 Uses.
   4.3 Occupationally exposed populations.
   5.1 Oral
   5.2 Inhalation
   5.3 Dermal
   5.4 Eye
   5.5 Parenteral
   5.6 Others
   6.1 Absorbtion by route of exposure
   6.2 Distribution by route of exposure
   6.3 Biological half-life by route of exposure
   6.4 Metabolism
   6.5 Elimination by route of exposure
   7.1 Mode of action
   7.2 Toxicity
      7.2.1 Human data Adults Children
      7.2.2 Relevant animal data
      7.2.3 Relevant in vitro data
      7.2.4 Workplace standards
      7.2.5 Acceptable daily intake
   7.3 Carcinogenicity
   7.4 Teratogenicity
   7.5 Mutagenicity
   7.6 Interactions
   9.1 Acute poisoning
      9.1.1 Ingestion
      9.1.2 Inhalation
      9.1.3 Skin exposure
      9.1.4 Eye contact
      9.1.5 Parenteral exposure
      9.1.6 Other
   9.2 Chronic poisoning
      9.2.1 Ingestion
      9.2.2 Inhalation
      9.2.3 Skin exposure
      9.2.4 Eye exposure
      9.2.5 Parenteral exposure
      9.2.6 Other
   9.3 Course, prognosis, cause of death
   9.4 Systematic description of clinical effects
      9.4.1 Cardiovascular
      9.4.2 Respiratory
      9.4.3 Neurological CNS Peripheral nervous system. Autonomic nervous system Skeletal and smooth muscle
      9.4.4 Gastrointestinal
      9.4.5 Hepatic
      9.4.6 Urinary Renal Others
      9.4.7 Endocrine and Reproductive Systems
      9.4.8 Dermatological
      9.4.9 Eye, ears, nose and throat, local effects
      9.4.10 Haematological
      9.4.11 Immunological
      9.4.12 Metabolic Acid base disturbances Fluid and electrolyte disturbances Others
      9.4.13 Allergic reactions
      9.4.14 Other clinical effects
      9.4.15 Special risks: Pregnancy
   9.5 Others
   10.1 General principles
   10.2 Relevant laboratory analyses and other investigations
   10.3 Life supportive procedures and symptomatic treatment
   10.4 Decontamination
   10.5 Elimination
   10.6 Antidote treatment
   10.7 Management discussion
   11.1 Case reports from the literature
   11.2 Internally extracted data on cases
   11.3 Internal cases
   12.1 Availability of antidotes
   12.2 Specific preventive measure
   12.3 Other
    1. NAME

          1.1 Substance

          1.2 Group

          Organochlorine pesticide - fungicide

          1.3 Synonyms 

          Benzene, hexachloro-
          Esaclorobenzene (Italian)
          Hexa CB             
          Hexachlorobenzol (German)
          Julin's carbon chloride
          Pentachlorophenyl chloride
          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 

          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 
          Administer activated charcoal.
          If necessary, control convulsions.
          Symptomatic treatment.


          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)


          4.1 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) 


          5.1 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.


          6.1 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, 
          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) 

          7.1 Mode of action
          HCB causes porphyria by partially blocking haem biosynthesis, 
          leading to accumulation and excretion of uroporphyrin (Klaassen, 
          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


                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) 


                2.6 to 4.1 mg/kg/day (Hayes, 1991)

             7.2.2 Relevant animal data

               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

               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). 



          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, 

             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


                Acute: CNS effects including headache, dizziness, nausea, 
                vomiting, apprehension, loss of equilibrium and vibratory 
                sense, coma and convulsions may occur. 

       Peripheral nervous system.

                Acute: Partial paralysis of extremities, numbness of hands 
                and arms may occur. 

                Chronic: Paresthesiae, cogwheeling.

       Autonomic nervous system

                No data available.

       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


                      No data available.


                      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

       Acid base disturbances

                No data available.

       Fluid and electrolyte disturbances

                No data available

                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 
          Interphalangeal arthritis. (Hayes, 1991; U.S. EPA, 1991).


          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 
          Do not give adrenaline or other adrenergic amines because of the 
          enhanced myocardial irritability induced by chlorinated 

          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) 


          11.1 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, 
          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.


          12.1 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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    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
    Address:   Centre de Toxicologie du Québec
               2705, boul. Laurier
               Sainte-Foy (Québec)
               G1V 4G2
    Tel:       (418) 654-2254  
    Fax:       (418) 654-2754

    See Also:
       Toxicological Abbreviations
       Hexachlorobenzene (EHC 195, 1997)
       Hexachlorobenzene (HSG 107, 1998)
       Hexachlorobenzene (ICSC)
       Hexachlorobenzene (FAO/PL:1969/M/17/1)
       Hexachlorobenzene (WHO Pesticide Residues Series 4)
       Hexachlorobenzene  (IARC Summary & Evaluation, Supplement7, 1987)
       Hexachlorobenzene  (IARC Summary & Evaluation, Volume 20, 1979)
       Hexachlorobenzene  (IARC Summary & Evaluation, Volume 79, 2001)