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    Labour Organisation, or the World Health Organization.

    Published under the joint sponsorship of
    the United Nations Environment Programme,
    the International Labour Organisation,
    and the World Health Organization

    World Health Orgnization
    Geneva, 1984

         The International Programme on Chemical Safety (IPCS) is a
    joint venture of the United Nations Environment Programme, the
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    Organization. The main objective of the IPCS is to carry out and
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    1.1. Summary
         1.1.1. Identity, analytical methods, and
                 sources of exposure
         1.1.2. Environmental concentrations and
         1.1.3. Kinetics and metabolism
         1.1.4. Studies on experimental animals
         1.1.5. Effects on man
         1.1.6. Effects on the environment
    1.2. Recommendations


    2.1. Identity
    2.2. Properties and analytical methods
         2.2.1. Physical and chemical properties
         2.2.2. Analytical methods


    3.1. Uses
    3.2. Levels and exposure
    3.3. Transport and distribution
         3.3.1. Abiotic degradation and bioaccumulation


    4.1. Absorption
         4.1.1. Inhalation
         4.1.2. Gastrointestinal tract
         4.1.3. Dermal exposure
    4.2. Distribution and storage
    4.3. Biotransformation
    4.4. Elimination
         4.4.1. Human studies
         4.4.2. Animal studies


    5.1. Short-term studies
         5.1.1. Single dose
         5.1.2. Repeated dose
    5.2. Reproduction studies
    5.3. Mutagenicity
    5.4. Carcinogenicity



    7.1. Toxicity for aquatic organisms
    7.2. Toxicity for terrestrial organisms
         7.2.1. Plants
         7.2.2. Earthworms
         7.2.3. Bees
         7.2.4. Birds
    7.3. Toxicity for microorganism
    7.4. Bioaccumulation and biomagnification



    9.1. Evaluation of health risks for man
    9.2. Evaluation of overall environmental effects
    9.3. Conclusions



    While every effort has been made to present information in the 
criteria documents as accurately as possible without unduly 
delaying their publication, mistakes might have occurred and are 
likely to occur in the future.  In the interest of all users of the 
environmental health criteria documents, readers are kindly 
requested to communicate any errors found to the Manager of the 
International Programme on Chemical Safety, World Health 
Organization, Geneva, Switzerland, in order that they may be 
included in corrigenda, which will appear in subsequent volumes. 

    In addition, experts in any particular field dealt with in the 
criteria documents are kindly requested to make available to the 
WHO Secretariat any important published information that may have 
inadvertently been omitted and which may change the evaluation of 
health risks from exposure to the environmental agent under 
examination, so that the information may be considered in the event 
of updating and re-evaluation of the conclusions contained in the 
criteria documents. 

                          *   *   *

     A detailed data profile and a legal file can be obtained from
the International Register of Potentially Toxic Chemicals, Palais
des Nations, 1211 Geneva 10, Switzerland (Telephone no. 988400 -



Dr E. Astolfi, Faculty of Medicine of Buenos Aires, Buenos
   Aires, Argentina

Dr I. Desi, Department of Environmental Hygienic Toxicology,
   National Institute of Hygiene, Budapest, Hungary

Dr R. Drew, Department of Clinical Pharmacology, Flinders
   University of South Australia, Bedford Park, South

Dr S.K. Kashyap, National Institute of Occupational Health,
   Ahmedabad, India

Dr A.N. Mohammed, University of Calabar, Calabar, Nigeria

Dr O.E. Paynter, Office of Pesticide Programs, US
   Environmental Protection Agency, Washington DC, USA

Dr W.O. Phoon, Department of Social Medicine and Public
   Health, Faculty of Medicine, University of Singapore,
   Outram Hill, Singapore  (Chairman)

Dr D. Wassermann, Department of Occupational Health, The
   Hebrew University, Hadassah Medical School, Jerusalem,

 Representatives of Other Organizations

Dr H. Kaufmann, International Group of National Associations
   of Agrochemical Manufacturers (GIFAP)

Dr V.E.F. Solman, International Union for Conservation of
   Nature and Natural Resources (IUCN), Ottawa, Ontario,


Dr S. Dobson, Institute of Terrestrial Ecology, Monks Wood
   Experimental Station, Abbots Ripton, Huntingdon, United
   Kingdom (Temporary Adviser)

Dr M. Gilbert, International Register for Potentially Toxic
   Chemicals, United Nations Environment Programme, Geneva,

Dr K.W. Jager, Division of Environmental Health, International
   Programme on Chemical Safety, World Health Organization,
   Geneva, Switzerland  (Secretary)

Dr D.C. Villeneuve, Health Protection Branch, Department of
   National Health and Welfare, Tunney's Pasture, Ottawa,
   Ontario, Canada (Temporary Adviser)  (Rapporteur)

Mr J.D. Wilbourn, Unit of Carcinogen Identification and
   Evaluation, International Agency for Research on Cancer,
   Lyons, France


    Following the recommendations of the United Nations Conference 
on the Human Environment held in Stockholm in 1972, and in response 
to a number of World Health Resolutions (WHA23.60, WHA24.47, 
WHA25.58, WHA26.68), and the recommendation of the Governing 
Council of the United Nations Environment Programme, (UNEP/GC/10, 
3 July 1973), a programme on the integrated assessment of the 
health effects of environmental pollution was initiated in 1973.  
The programme, known as the WHO Environmental Health Criteria 
Programme, has been implemented with the support of the Environment 
Fund of the United Nations Environment Programme.  In 1980, the 
Environmental Health Criteria Programme was incorporated into the 
International Programme on Chemical Safety (IPCS).  The result of 
the Environmental Health Criteria Programme is a series of criteria 

    A WHO Task Group on Environmental Health Criteria for 
Organochlorine Pesticides other than DDT (Endosulfan, Quintozene, 
Tecnazene, Tetradifon) was held at the Health Protection Branch, 
Department of National Health and Welfare Ottawa from 28 May - 
1 June, 1984.  The meeting was opened by Dr E. Somers, Director-
General, Environmental Health Directorate, and Dr K.W. Jager 
welcomed the participants on behalf of the three co-sponsoring 
organizations of the IPCS (UNEP/ILO/WHO).  The Task Group reviewed 
and revised the draft criteria document and made an evaluation of 
the health risks of exposure to quintozene. 

    The drafts of this document were prepared by Dr D.C. Villeneuve 
of Canada and Dr S. Dobson of the United Kingdom. 

    The efforts of all who helped in the preparation and 
finalization of the document are gratefully acknowledged. 

                            * * *

    Partial financial support for the publication of this criteria 
document was kindly provided by the United States Department of 
Health and Human Services, through a contract from the National 
Institute of Environmental Health Sciences, Research Triangle Park, 
North Carolina, USA - a WHO Collaborating Centre for Environmental 
Health Effects. 


1.1.  Summary

1.1.1.  Identity, analytical methods, and sources of exposure

    Technical quintozene (pentachloronitrobenzene) is a white solid 
with a musty odour, that, is used in formulation as a soil 
fungicide and as a seed dressing.  Hexachlorobenzene is a possible 
major contaminant in technical quintozene. 

    Gas chromatography combined with electron capture detection is 
used for the analytical determination of quintozene. 

    Exposure of the general population is mainly via residues in 
the food. 

1.1.2.  Environmental concentrations and exposures

    Quintozene persists in soil with a half-life of approximately 
4 - 10 months.  Part of it is lost from the soil by volatilization.  
Biodegradation, mainly to pentachloroaniline is an important route 
of conversion.  Photodegradation is not important. 

1.1.3.  Kinetics and metabolism

    There are large animal species differences in the absorption of 
quintozene from the gastrointestinal tract.  There is no information 
on absorption via inhalation or via the skin.  After ingestion, 
faecal elimination of unchanged material is an important route of 
excretion. Pentachloroaniline and mercapturic acid conjugates are 
the major metabolites found in urine.  There is no tendency for 

1.1.4.  Studies on experimental animals

    Quintozene is practically non-toxic according to the scale of 
Hodge & Sterner (1956).  The oral LD50 for quintozene in the rat 
ranges from 1650 to more than 30 000 mg/kg body weight.  WHO (1984) 
classified quintozene in the category of technical products 
unlikely to present an acute hazard in normal use. 

    In long-term studies, no-observed-adverse-effect levels are 
1.25 mg/kg body weight and 0.75 mg/kg body weight for rats and 
dogs, respectively.  At higher dosages, there is liver hypertrophy 
with some histopathological changes.  In dogs, dose-related liver 
damage including fibrosis was induced. 

    Purified quintozene was not teratogenic at levels of up to 500 
mg/kg body weight in mice.  Positive results obtained with 
technical quintozene in mice (500 mg/kg body weight) implicate the 
involvement of hexachlorobenzene in the teratogenic response.  
Quintozene was not teratogenic in rats at levels up to 1563 mg/kg. 

    Quintozene is generally negative in short-term tests for 
genetic activity.  In carcinogenicity studies where rats and mice 
were fed quintozene at levels up to 1200 mg/kg diet, equivocal or 
negative findings have been reported.  Hexachlorobenzene, a possible 
impurity in technical quintozene, is carcinogenic to mice, rats, 
and hamsters. 

1.1.5.  Effects on man

    Quintozene is a weak skin sensitizer, but not an irritant. 

    Except for 1 case of conjunctivitis in an occupational setting, 
instances of accidental overexposure have not been reported. 

1.1.6.  Effects on the environment

    There are indications that quintozene applied at recommended 
rates as a soil fungicide could produce a significant adverse 
effect on earthworm survival. There is no evidence that quintozene 
represents a threat to other organisms tested.  Its bioaccumulation 
in fish is low. 

1.2.  Recommendations

    1.  Further data on absorption resulting from
        different routes of exposure to quintozene are

    2.  Levels of impurities, especially hexachloro-
        benzene, in quintozene should be kept to a minimum.

    3.  Adequate carcinogenicity studies are required on


2.1.  Identity

Chemical Structure

Molecular formula:            C6Cl5NO2

CAS chemical name:            pentachloronitrobenzene

Common trade names:           avicol, botrilex, brassicol, earthcide,
                              fartox, folosan, fomac 2, fungiclor,
                              GC 3944-3-4, kobu, kobutol, KP 2,
                              NCI-C00419, olpisan, PCNB, entagen,
                              pterraclor, terrafum, tilcarex,
                              tritisan.  A complete list of trade
                              names is available from IRPTC (1983).

CAS registry number:          82-68-8

Relative molecular mass:      295.36

2.2.  Properties and Analytical Methods

2.2.1.  Physical and chemical properties 

    Quintozene is a pale yellow-to-white (depending on the
purity) solid with a musty odour and has a melting point of 142 - 
146 C.  It is soluble in carbon disulfide, benzene, chloroform, 
ketones, and aromatic and chlorinated hydrocarbons but is 
practically insoluble in water (0.44 mg/litre at 20 C); in ethanol 
its solubility is 2% at 25 C (IARC, 1974).  It has a vapour 
pressure at 20 C of 10-8 x 667 kPa (Berkowitz et al., 1976).  
Hexaachlorobenzene is often found as a contaminant in quintozene 
and levels can range up to 3% (in the past, levels as high as 30% 
were found). 

    It is quite stable in soil but eventually degrades to
pentachloroaniline (PCA).

    Quintozene is primarily registered for use as a soil fungicide 
for use in agriculture and on field crops, selected vegetables, 
horticultural crops, and in greenhouses.  It is also used as a 
seed-treatment fungicide for crop seeds such as cotton, peanuts, 

soybeans, and grain.  It has been formulated as wettable powder, 
dust, emulsifiable concentrate, granules, and combination products.  
It has been sold under a variety of trade names. 

    The first laboratory synthesis was reported in 1868 (Berkowitz 
et al., 1976).  It was first introduced in Germany as a soil 
fungicide in the 1930s.  It has been produced in the USA since 1962 
(IARC, 1974). 

    Quintozene is produced by either the chlorination of 
nitrobenzene or the nitration of chlorinated benzenes.  In 1972, 
production levels in the USA were estimated to be 1.3 million kg, 
of which 30 - 40% was exported (Berkowitz et al., 1976). 

2.2.2.  Analytical methods

    Methods of cleanup and analysis for quintozene have been 
summarized by Berkowitz et al. (1976).  These include a 
colorimetric and a gas chromatographic method.  The latter is the 
most sensitive and can be used in combination with a 
microcoulometric (Burke & Holswade, 1964) or electron capture 
detector (Kuchar et al., 1969).  Cleanup of extracts can be 
accomplished by column chromatography using silicic acid (Methratta 
et al., 1967) or florisil (US DHEW, 1973). 


3.1.  Uses

    The major uses of quintozene are summarized in Table 1 and some 
information is provided on the quantities used. 

Table 1.  Usage data for quintozene in selected countriesa
Area            Quantity     Year      Uses                        
Colombia        12 305 kg    1982      fungicide recommended for   
                15 926 kg    1981      treatment of millet, corn,  
                23 965 kg    1980      and sorghum                 
Malaysia                               fungicide                   
Mexico          313 000 kg   1983      seed treatment              
Sweden          10 000 kg    1981      fungicide in various crops; 
                2000 kg      1981      Home and garden fungicide   
                                       on lawns                    
Tanzania        500 tonne    1981-82   applied to bananas,         
                                       cereals, beans, etc.        
United Kingdom  22.89 tonne  1975-79   fungicide used on non-      
                                       edible crops and turf; as   
                                       a dust applied to soil      
                                       before sowing or planting   
                                       edible crops; used on       
                                       onion seed; as a paste      
                                       applied to the stems of     
                                       cucumber plants             
USA             2043 - 2183  1982      fungicide                   
a  From:  IRPTC, personal communication, 1984.

3.2.  Levels and Exposures

    General population

    No data are available for the concentrations of quintozene in 
air or water. 

    It is persistant in soil, and is often present in crops grown 
on treated soil.  In a  market basket survey in the USA, residues 
ranged from 0.001 to 0.003 mg/kg in 6 out of 240 composites 
examined.  Three of the composites contained only trace amounts.  
It was most common in the fats and oils class.  Quintozene residues 
on lettuce in greenhouses sprayed at levels of 30 g/m2 in the open 

air declined from 60 g/g after 5 days to almost zero after 7 weeks 
(Dunsing & Windschild, 1976).  In a study by Heikes (1980), it was 
found that residues in 11 samples of peanut butter averaged 5.05 

    Infants and children

    In a market basket survey by the US FDA (Johnson et al., 1979), 
quintozene was found in 2 out of 10 samples of food composites for 
infants 6-months-old, and one of these had only a trace amount.  
The residue values ranged from trace to 0.03 mg/kg.  In the food 
composites for toddlers 2-years-old, PCNB was found in 4 out of 10 
samples, 1 containing a trace amount, and the residues in the other 
sample ranging from 0.004 to 0.016 mg/kg.  The residues occurred in 
the oils and fats class as in the adult survey. 

    PCNB does not appear to accumulate to any appreciable degree in 
cows' milk (Goursaud et al., 1972; Glofke, 1973). 

3.3.  Transport and Distribution

(a)  Air

    Contamination of the air is often due to volatilization from 
the soil.  Quintozene has a relatively high volatility (10-6 x 1775 
kPa at 25 C) and thus the principal mechanism of loss from the 
soil is volatilization (Lee, 1975).  It has an affinity for the 
air-water interface and thus moist air passing over the soil could 
account for a percentage of the loss by a "codistillation" 
process.  In a study done by Caseley, this amount was found to be 
62% (Berkowitz et al., 1976).  Such loss would be greater 
immediately after application and would depend on the adsorbent 
properties of the soil (Lee, 1975). 

(b)  Water

    Since quintozene is practically insoluble in water, it may be 
assumed that leaching is negligible (Leistra & Smelt, 1974).  
However, few data are available on residues in water bodies and 
drinking-water.  In one study, urban storm run-off was analysed and 
quintozene was found in only negligible amounts or not at all.  
However, this has not been correlated with use patterns in the area 
(Dappen, 1974). 

(c)  Soil

    The fate of quintozene in soil has been more extensively 
studied.  It persists in Californian soils and has a half-life of 
4.7 - 9.7 months (Wang & Broadbent, 1973).  Longer half-lives were 
associated with soils rich in organic matter.  In an analysis of 22 
samples collected from potato fields, treated for 11 years, 
residues averaged 7.06 mg/kg with a range of 0.06 - 25.25 mg/kg 
(Beck & Hansen, 1974).  In a study by Rautapaa et al. (1977), 
quintozene levels of 0.05 - 27.0 mg/kg were found in the soil of 
forest tree nurseries.  In one case, it was found that all the 

quintozene applied (20 - 40 kg/ha) was left in the soil.  No 
explanation was given for this phenomenon.  The authors found that, 
in general, residues in cereal and clover fields were less than 
those in forest-tree nurseries.  Residues in the soil of those 
cereal and clover fields were 0.4%.  Appreciable levels of the 
associated impurities and metabolites were also found. 

3.3.1.  Abiotic degradation and bioccumulation

    Studies on the photoreduction of quintozene have shown that 
ultraviolet irradiation results mainly in reductive dechlorination.  
Irradiation of solutions in hexane produces pentachlorobenzene, 
1,2,4,5-tetrachlorobenzene, and 2,3,4,6-and 2,3,4,5-tetra-
chloronitrobenzene (Crosby & Hamadmad, 1971).  However, this 
process is very slow and thus not likely to be important as a 
degradation route.  Biologically, soil microorganisms convert 
quintozene to pentachloroaniline (PCA) and methylthiopenta-
chlorobenzene (MTPCB) (Sijpensteijn et al., 1977). 

    Under aerobic growth conditions, fungi and actinomycetes have 
been shown to convert low concentrations of quintozene to PCA and 
MTPCB.  In a related study, Ko & Farley (1969) observed that 
microorganisms converted quintozene to PCA and that this process 
was greatest in submerged soil.  Although quintozene is taken up 
from the soil by plants, it does not accumulate to any important 
degree in animals (section 4.2) 


4.1.  Absorption

4.1.1.  Inhalation

    No information on the uptake of quintozene through inhalation 
is available. 

4.1.2.  Gastrointestinal tract

    There are no studies investigating the absorption of quintozene 
from the gastrointestinal tract.  However, studies relating to the 
faecal elimination of the parent material suggest that absorption 
by this route may be limited and species-dependent (section 4.4.2). 

4.1.3.  Dermal exposure

    No information on the uptake of quintozene through dermal 
exposure is available. 

4.2.  Distribution and Storage

    Human studies

    No data are available to indicate the extent of storage and 
distribution of quintozene in man. 

    Animal studies

    After feeding quintozene to dogs in the diet at levels of up to 
1080 mg/kg, for 2 years, none was found in the kidney, brain, 
skeletal muscle, liver, spleen, fat, bile, blood, urine, and faeces 
(Borzelleca et al., 1971).  Nor was quintozene detected in the 
skeletal muscle, liver, kidney, fat, or faeces of rats fed up to 
500 mg/kg diet for 33 weeks (Borzelleca et al., 1971).  Storage of 
quintozene did not occur in fat, skeletal muscle, liver, or kidney 
of cows administered an amount equivalent to 10 mg/kg diet for 12 
weeks (Borzelleca et al., 1971).  Only negligible amounts were 
detected in the milk of these cows.  Borzelleca et al. (1971) did, 
however, find tissue storage of hexachlorobenzene and penta-
chlorobenzene, contaminants of technical quintozene, in rats, dogs, 
and cows in degrees paralleling their contents in the quintozene.  
After sheep were dosed orally with quintozene (31 - 32 mg/kg body 
weight), quintozene was detected in the omental fat (0.5 mg/kg) for 
only 1 day (Avrahami & White, 1976).  Sixteen weeks of feeding 
chickens a diet containing 300 mg quintozene/kg resulted in fat 
levels of 0.85 mg/kg and levels in the egg yolk of approximately 
0.02 mg/kg (Simon et al., 1979).  Quintozene was not detected in 
the bile, gall bladder, liver, blood, or muscle of these animals. 

    In another study where pregnant rats were administered 
quintozene at levels of 50 - 200 mg/kg body weight, from day 6 to 
15 of gestation, residues were not detected in either maternal 
tissues (brain, liver, heart, spleen, kidney, adipose tissue) or in 

fetuses removed by Cesarean section (Villeneuve & Khera, 1975).  In 
mice, 4 daily doses of 500 mg/kg body weight led to the appearance 
of the metabolites, pentachloroanisole and pentachlorophenyl 
sulfide in the fatty tissue of pregnant mice and fetuses; these 
results indicated placental transfer of the metabolites (Courtney 
et al., 1976). 

    Analyses of tissue from 2 Rhesus monkeys sacrificed 24 and 48 h 
after being administered 2 mg/kg body weight orally showed that 
quintozene was eliminated quickly and had virtually no tendency to 
accumulate (Koegel et al., 1979). 

    In another study, where Rhesus monkeys were fed a diet
containing 14C-quintozene at 2 mg/kg for 550 days, a storage curve 
was constructed by subtracting the excreted from the administered 
radioactivity.  The storage curve reached a steady state plateau of 
2 - 3% of the administered dose after 30 - 40 days of treatment 
(Muller et al., 1978). 

4.3.  Biotransformation

    The proposed metabolic and excretory pathway for quintozene is 
shown in Fig. 1.  In animals, the major biotransformation products 
that appear in urine are pentachloroaniline (PCA), formed by 
reduction of the nitro group, and mercapturic acids formed after 
replacement of the nitro group with glutathione and subsequent 
further metabolism.  The relative contribution of each of these 
reactions to the overall biotransformation of quintozene is species 
dependent.  Rabbits dosed orally with 2 g quintozene excreted 14% 
in the urine as  N-acetyl- S-pentachlorophenyl-cysteine (PCC) 
and 12% as free and conjugated PCA.  The balance of the dose was 
excreted unchanged in the faeces (Betts et al., 1955) (section 
4.4.2).  In rhesus monkeys and sheep, PCA was identified as the 
major metabolite (Avrahami & White, 1976; Muller et al., 1978), 
whereas, in the rat, PCC is the major metabolite (O'Grodnick et 
al., 1981). 

    In addition to the above primary metabolites, a number of minor 
metabolites have been identified.  The nitro group can be replaced 
either with a methylthio group to form pentachlorothioanisole 
(PCTA) or with a hydroxyl group to form pentachlorophenol (PCP).  
PCTA has been shown to be formed in rats, dogs, chickens, and 
monkeys (Borzelleca et al., 1971; Muller et al., 1978; Dunn et al., 
1979) and PCP in rabbits, rats, and monkeys (Betts et al., 1955; 
Muller et al., 1978; O'Grodnick et al., 1981).  Following 
administration of quintozene pentachlorobenzene and tetrachloro-bis 
(methyl mercapto)-benzene were found in monkey urine (Muller et 
al., 1978) and pentachlorophenyl sulfide in rat urine (O'Grodnick 
et al., 1981). 

    Quintozene is converted by soil microorganisms and on plants to 
PCA and PCTA (Kuchar et al., 1969; Berkowitz et al., 1976; 
Sijpesteijn et al., 1977). 


4.4.  Elimination

4.4.1.  Human studies

    No information on the elimination of quintozene in man was 

4.4.2.  Animal studies

    The major routes of elimination of ingested quintozene are via 
the faeces as unchanged material or in the urine as metabolites 
(Fig. 1) 

    The amount of quintozene eliminated unchanged in the faeces is 
species-dependent.  Betts et al. (1955) administered 1,2, or 3 g of 
quintozene to rabbits by stomach tube and found an average of 46, 
62, and 59% of the dose was eliminated unchanged in the faeces over 
72 h.  The faecal elimination was also variable (range 27 - 82% of 
the dose).  In sheep dosed orally with 31 mg/kg body weight, 
approximately 80% of the dose was eliminated unchanged via the 
faeces (Avrahami & White, 1976).  In metabolic studies carried out 
on Rhesus monkeys (Koegel et al., 1979), only 7.4% of the 
administered oral dose (2 mg/kg body weight) was excreted as 
quintozene in the faeces.  After feeding rats with a diet 
containing 500 mg/kg diet, no detectable quintozene was found in 
the faeces, but unmetabolized quintozene was found in the faeces of 
dogs fed 1080 mg/kg diet for 2 years (Borzelleca et al., 1971). 

    Once absorbed, the elimination of quintozene is primarily as 
metabolites in the urine (section 4.3).  Although quintozene has 
been found in bile, the relative importance of this finding for the 
elimination or enterohepatic circulation of quintozene is unknown.  
Nevertheless, it would appear that elimination by this route is 
species-dependent, since quintozene has been identified in the bile 
of monkeys (Kogel et al., 1979) and mice (Courtney et al., 1976) 
but not in the bile of chickens (Kuchar et al., 1969; WHO 1975) or 
dogs (Borzelleca et al., 1971). 

    When a lactating cow was fed 5 mg/kg diet for 3 days, the 
parent compound was not detected in the milk using a method in 
which the sensitivity was 0.01 mg/kg (St. John et al., 1965). 
Traces of quintozene were found in milk from cows treated orally 
with the equivalent of 10 mg/kg diet for 8 weeks (Borzelleca et 
al., 1971).  It was also found in the milk of untreated cows and 
analyses of the feed showed quintozene levels of 0.002 - 0.006 

    Rhesus monkeys were fed diets containing quintozene at 2 mg/kg 
for 550 days.  A storage curve was constructed by subtracting the 
excreted from the administered radioactivity.  The storage curve 
levelled out after 30 - 40 days of treatment, resulting in a 
storage plateau of only 2 - 3% of the administered dose (Muller et 
al., 1978). 

    There was little accumulation of quintozene in fat tissue; 
slightly elevated concentrations are found in the liver and kidney 
as well as the thymus, lymph nodes, and bone marrow. 

    Residual levels in various tissues are given in Table 2. 

Table 2.  Tissue residue levels in Rhesus monkeys fed 2 mg/kg PCNB
in the diet for 550 daysa
Tissue      PCNB       Tissue                          PCNB
            (mg/kg)                                    (mg/kg)
Blood       0.07       adrenal cortex                  0.08
Muscle      0.01       thymus                          0.20
Brain       0.03       lymph nodes (large intestine)   0.12
Liver       0.19       bone marrow                     0.13
Kidney      0.14       omental fat                     0.21
a  From: Muller et al. (1978).

    As part of the same study, a Rhesus monkey dosed orally with 
radio-labelled quintozene at 2 mg/kg eliminated 92% of the 
radioactivity after 5 days, 91% of which was in the form of 
metabolites (Muller et al., 1978). 


    The toxicity and the residue data on quintozene have been 
reviewed several times by international bodies such as FAO/WHO 
(1970, 1974, 1976, 1978), IARC (1974), and CEC (1981).  For their 
conclusion, refer to section 8.  We refer to these reports, which 
contain more detailed information on the toxicity studies and 
residue data than the present report.  Moreover, several 
unpublished studies have been evaluated and reported there. 

5.1.  Short-Term Studies

5.1.1.  Single dose

    Data on the acute toxicity of quintozene are summarized in 
Table 3. 

Table 3.  Acute toxicity of quintozene
Animal    Route   LD50 (mg/kg body weight)        References        
rat (M)   oral    1710 (oil solution)             FAO/WHO (1970)    
rat (F)   oral    1650 (oil solution)             FAO/WHO (1970)    
rat       oral    > 30 000 (aqueous suspension)   FAO/WHO (1970)   
rat       ip      5000 (aqueous suspension)       FAO/WHO (1970)    
dog       oral    no deaths up to 2500 mg/kg      Berkowitz et al.   
rabbit    dermal  no deaths up to 4000 mg/kg      Berkowitz et al.   

    Rabbits were dosed dermally once, with quintozene as a 30% 
solution in dimethyl phthalate at 2 dose levels (10 and 13.3 ml/kg) 
and observed for 14 days (Borzelleca et al., 1971). There was no 
evidence of toxicity or skin irritation. 


    Quintozene, dissolved in corn oil, administered orally to cats 
once at a level of 1600 mg/kg, caused a significant elevation in 
methaemoglobin levels and an approximately 8-fold increase in the 
number of erythrocytes containing Heinz bodies (Schumann & 
Borzelleca, 1978).  This latter finding, together with the fact 
that a greater percentage of erythrocytes failed to stain properly 
in the course of time, suggested that a functional impairment of 
the erythrocyte had occurred. 

5.1.2.  Repeated dose


    Five groups of 7 male and 7 female albino rats of weaning age 
were fed diets containing technical quintozene at 0, 63.5, 635, 
1250, 2500, or 5000 mg/kg for 3 months.  Growth and survival were 

adversely affected at 5000 mg/kg in both sexes and also in males at 
2500 mg/kg.  Liver hypertrophy was observed at all levels except in 
females fed 63.5 mg/kg.  No haematological changes were seen and 
histological alterations were limited to fine vacuolization of 
liver cell cytoplasm at 5000 mg/kg (Finnegan et al., 1958).  An 
unspecified number of young rats were fed diets containing 0 or 
2000 mg quintozene/kg for 10 weeks (Wit et al., 1957).  No gross 
effects other than decreased growth rate in the males were noted.  
Groups of 10 male and 10 female rats were fed diets containing 0, 
1000, 5000, or 10 000 mg quintozene/kg for 90 days.  The animals 
showed a slight growth depression at 5000 mg/kg and marked growth 
depression at 10 000 mg/kg (Hoechst, unpublished data, 1964). 

    Groups of 10 male and 10 female rats were fed diets containing 
technical quintozene at concentrations of 0, 25, 100, 300, 1000, or 
2500 mg/kg diet for 2 years.  No changes in blood haematology were 
found.  In females, growth depression was observed at doses of 100 
mg/kg diet and above (Finnegan et al., 1958). 


    Groups of 3 mongrel dogs were fed diets containing 25, 200, or 
1000 mg quintozene/kg for 1 year.  No adverse effects were noted on 
body weight or survival.  No haematological changes were seen and 
histopathological changes were restricted to liver cell enlarge-
ment, which was not dose-dependent (Finnegan et al., 1958).  In a 
2-year study, groups of 3 male and 3 female dogs were fed diets 
containing 0, 500, 1000, or 5000 mg quintozene/kg.  Liver changes 
occurred in all groups in a dose-related manner.  The 5000 mg/kg 
level produced severe liver damage including fibrosis, narrowing of 
hepatic cell cords, increased size of the periportal areas, and 
leukocyte infiltration.  At 1000 and 500 mg/kg, the changes were 
similar but less pronounced. Reduced haematopoiesis and atrophy of 
bone marrow were observed in animals receiving the highest dose 
(FAO/WHO, 1970).  Purebred beagles (4 per sex per dose) were fed 
diets containing quintozene at levels ranging from 5 to 1080 mg/kg 
for 2 years.  Haematocrit values were depressed at 18 months in 
males receiving 30 and 180 mg/kg, but not in animals receiving 1080 
mg/kg.  No dose-related effects were observed on urine analysis, 
blood chemistry, mortality, body weight, food consumption, or 
estrous cycle.  Organ weight data revealed higher values for livers 
in dogs fed 1080 mg quintozene/kg.  Histologically, dogs sacrificed 
at 2 years after receiving 180 or 1080 mg/kg showed hepatic and 
renal effects deemed reversible by the authors (Borzelleca et al., 


    Two male and two female rhesus monkeys were fed 2 mg 
quintozene/kg for 70 days.  The haematological variables 
(haemoglobin, haematocrit, RBC, WBC), and the histopathological 
examination of the liver, stomach, small and large intestine, 
spleen, kidneys, heart, lung, thymus, cerebrum, cerebellum, pons, 
medulla, spinal cord, and bone marrow were carried out in 1 male 
and female monkey 

after 70 days.  The histopathology, clinical chemistry, and serum 
cortisol levels remained within normal limits (Muller et al., 

5.2.  Reproduction Studies

    Reproduction studies were carried out on rats fed a diet 
containing 0, 5, 50, or 500 mg quintozene/kg until the F/3b litters 
were weaned.  Quintozene had no effect on fertility 
(pregnancies/mating), gestation (litters cast/pregnancies), 
viability (live at 4 days/live at birth), or lactation (weaned/live 
minus discards) indices.  No dose-related histopathological 
abnormalities were recorded in any of the F3b pups.  It was not 
teratogenic to rats at dosages up to 1563 mg/kg body weight (Jordan & 
Borzelleca, 1973; Khera & Villeneuve, 1975; Courtney et al., 1976).  
Levels of 500 mg/kg body weight of technical quintozene (87% pure) 
administered from day 7 to 11 of gestation produced renal agenesis 
in C57B1/6 mice, but none were produced with purified material 
(99%) (Courtney et al., 1976).  Hexachlorobenzene, a major 
contaminant in the technical material, was implicated in the 
teratogenic response.  Quintozene did not produce any teratogenic 
response in AKR mice when administered at levels up to 500 mg/kg 
diet (Berkowitz et al., 1976). 

5.3.  Mutagenicity

    Quintozene was reported to give a positive mutagenic
response in a host cell reactivation deficient strain of 
 E. coli (Clarke, 1971).  It was not mutagenic when studied in an 
Ames test system consisting of several bacterial strains using 
Aroclor 1254 activation (Mohn, 1971).  It was reported to be 
negative in a reverse mutation assay using 5 tester strains of 
 Salmonella typhimurium and  E. coli (Moriya et al., 1983).  It was 
shown to be negative in a dominant lethal test in mice where the 
chemical was administered for 7 weeks in the diet (no 
concentrations specified) (Van Logten, 1977).  It produced no 
significant increase in mutation rates in  Salmonella typhimurium  
and  Serratia marcescens; it also gave negative results in spot 
tests against the same strains of  Salmonella typhimurium and 
 Serratia marcescens (Buselmaier et al., 1973).  Both FAO/WHO 
(1978) and CEC (1981) concluded that there were no indications for 
mutagenic activity. 

5.4.  Carcinogenicity

    The carcinogenicity of quintozene was evaluated by IARC in
1973 (IARC, 1974).  Studies evaluated at that time as well as
additional studies are summarized below.

    In a large screening study, 18 male and 18 female (C57BL/6
x C3H/Anf)F1 mice and similar numbers of (C57BL/6 x AKR)F1
mice were given single doses of 464 mg quintozene/kg body
weight (unspecified purity) by stomach tube, when the animals
were 7 days of age, and this same absolute dose was then given
daily until the animals were 28 days of age.  This was followed by 

a diet containing 1206 mg/kg diet, which was administered up to 78 
weeks.  Hepatomas were the only tumours found in excess over the 
controls; 2/18 male and 4/18 female (C57BL/6 x C3H/Anf)F1 mice 
developed hepatomas compared with 8/79 and 0/87 in controls.  Of 
the (C57BL/6/ x AKR)F1 mice, 10/17 males and 1/17 females developed 
hepatomas compared with 5/90 and 1/82 in controls.  The incidence 
of other tumours was similar in treated and control animals (Innes 
et al., 1969). 

    Ten stock albino mice of each sex were painted twice weekly 
with 0.2 ml of a 0.3% solution of quintozene in acetone for 12 
weeks.  This was followed by twice-weekly paintings with a 0.5% 
solution of croton-oil in acetone for 20 weeks followed by 
observation for 40 weeks.  In a control group, acetone alone was 
given followed by treatment with croton oil.  The total number of 
skin tumours at the end of croton-oil treatment was 12 in 9 
surviving controls and 50 in 13 survivors in the quintozene group.  
One tumour in the quintozene group had progressed to a squamous-
cell carcinoma.  An infiltrating squamous-cell carcinoma was also 
observed in 1 control mouse killed 31 weeks from the start of the 
croton-oil treatment (Searle, 1966). 

    Two unpublished studies on the carcinogenicity of quintozene 
(containing 2.7% hexachlorobenzene) were reviewed by the FAO/WHO 
Joint Meeting on Pesticide Residues in 1975.  Groups of 100 male 
and 100 female Swiss mice and 50 male and 50 female Wistar rats 
were administered levels of 0, 100, 400, or 1200 mg/kg diet.  In 
mice, a non-dose-related increase in the incidence of liver 
hyperplastic nodules was observed in males and an increased 
incidence of subcutaneous fibrosarcomas was observed in females at 
the highest dose level.  No increased tumour incidence was reported 
in rats (FAO/WHO, 1976).  No further details of this study are 

    Groups of 50 male and 50 females Osborne-Mendel rats and
B6C3F1 mice were given technical grade quintozene (purity 97%
with 12 impurities) in their diet for 78 weeks.  In rats, the
average dietary concentrations were 10 064 and 5417 mg/kg of
diet for males and 14 635 and 7875 for females; in mice,
average dietary concentrations were 5213 and 2606 for males
and 8187 and 4093 for females.  Observation continued for 33 -
35 additional weeks in rats and for 14 - 15 additional weeks
in mice.  Adequate numbers of animals survived long enough to
permit the detection of late developing tumours.  No
statistically-significant increase in the incidence of
neoplasms was seen in either species.  It was concluded that
quintozene was not carcinogenic under the conditions of this
bioassay (NCI, 1978).

    Hexachlorobenzene, a potential impurity in quintozene, is
carcinogenic in mice, rats, and hamsters producing tumours of
the liver (IARC, 1979; Smith & Cabral, 1980).


    In patch tests, a quarter-inch square of cotton cloth was
moistened with water, dipped in a 75% quintozene wettable powder 
(Olin formulation), and then placed on the volar surface of the 
right forearms of 50 human volunteers.  The patches were then 
covered with a 1-inch square of aluminum foil held in place by a 2-
inch square of adhesive tape.  After 48 h, the patches were 
removed.  No evidence of irritation was seen in any of the 
subjects.  Two weeks later, the same test was repeated on the left 
arm of the same subjects.  After 48 h, 46 of the 50 subjects showed 
no signs or irritation.  In 3 of the 4 reported reactions, a 1-inch 
square area showed erythema, oedema, and small vesicle formation 
with marked itching; the 4th subject had only erythema and itching.  
Of the 46 subjects who were negative when the second patch was 
removed, 9 developed a delayed reaction.  Time of onset varied from 
approximately 8 h to several days.  In 2 of these persons, the 
reaction included erythema, oedema, small vesicle formation, and 
itching.  The skin reaction reached a peak during the first few 
days of symptoms and subsided with time, with some scaling of the 
skin (Finnegan et al., 1958).  One instance of keratoconjunctivitis 
has been reported in the literature (Fujita et al., 1976) and 
resulted from the application of the pesticide.  Remission of the 
condition took a month. 


7.1.  Toxicity for Aquatic Organims

    Quintozene is of low toxicity for aquatic organisms.  The only 
data on the toxicity of quintozene for aquatic organisms is from 
Nishiuchi & Yoshida (1972) who quote a 48-h LC50 value of 10 000 
g/litre for carp and a 3-h LC50 value for  Daphnia of 40 000 

7.2.  Toxicity for Terrestrial Organisms

7.2.1.  Plants

    Vishunavat & Shukla (1981) examined the effects of quintozene 
on seed germination, plant stand, and yield of lentils.  There were 
no significant effects.  Brown et al. (1982) did not find any 
effects on the germination of orchids when 99% pure quintozene was 
applied at concentrations of 25 and 50 mg/litre.  At 100 mg/litre, 
 Cattleya elongata did not germinate, but germination of  Laelia  
was unaffected and  Vanda tricolor showed improved germination.  
Quintozene eliminated growth of excised shoot tips in orchids of 
the Cymbidium family. 

7.2.2.  Earthworms

    Roark & Dale (1979) reared earthworms  Eisenia foetida in
soil pre-mixed with quintozene at a dose of 0.679 g/4719 cm3
of soil, corresponding to 226.8 g over 929 cm2 of turf.  The
dose was calculated as the total of 3 applications of the 
recommended dosage for turf.  The worms did not reproduce in 
treated soil.  Survival of worms was not significantly reduced 
within the first 10 days, but fell to zero within 29 days of 
treatment with quintozene. 

7.2.3.  Bees

    No information is available on toxicity of quintozene for bees.  
However, since the main uses of quintozene are on soil or as a seed 
dressing, it is unlikely that bees would be exposed. 

7.2.4.  Birds

    Dunn et al. (1979a) fed white leghorns with concentrations
of 0, 10, 50, 100, or 1000 mg quintozene/kg diet and examined
egg production and hatchability.  None of these concentrations
caused obvious toxic effects, death, or histopathological changes 
in either control or treated groups.  Egg production during the 
25th to the 35th week was not significantly affected.  However, at 
a higher dose level of 1000 mg/kg diet, onset of egg production was 
delayed for 1 month, and the number of chicks hatched from fertile 
eggs significantly decreased from 91% in the controls to 69% in 
treated birds.  Shell strength of the eggs was not significantly 
altered (Dunn et al., 1979a).  In another study (Dunn et al., 
1979b), the authors reported that bioaccumulation of PCNB or its 

metabolites only occurred in trace concentrations; body weight 
gains were significantly lower in hens fed 1000 mg quintozene/kg 

7.3.  Toxicity for Microorganisms

    Tu (1980) reported that quintozene at doses up to 5000 mg/litre 
did not induce any effects on 3 strains of the bacterium  Rhizobium 
 japonicum in culture.  Quintozene also did not show any effects 
on 25 strains of  Rhizobium bacteria, isolated from root nodules of 
red clover, at doses up to 1000 mg/litre in the culture medium 
(Heinonen-Tanski et al., 1982).  Smiley & Craven (1979) applied 
quintozene 9 times annually for 3 years, at weekly intervals during 
July and August, to a turf of Kentucky blue grass.  There were no 
significant effects on the populations of bacteria, actinomycetes, 
or fungi.  The effects of quintozene on carbon dioxide evolution 
and on the enzyme activities in organisms in soil were observed by 
Mitterer et al. (1981).  The recommended soil dosage of the 
fungicide caused an increase in carbon dioxide evolution from soil 
cultures.  After a second and third application, this initial 
increase was followed by a decrease in carbon dioxide release to 
below the value for untreated control soil.  Quintozene showed a 
severe and continuous inhibition of xylanase activity, in marked 
contrast to other fungicides tested. 

7.4.  Bioaccumulation and Biomagnification

    Ogiso & Tanabe (1982) measured residues in different tissues of 
crop plants.  High concentrations of quintozene in plant tissues 
relative to soil levels were only found in the outer layers of 
roots and tubers directly in contact with soil.  There is little 
evidence of systemic uptake. 

    Kanazawa (1981) reported a bioconcentration factor for 
quintozene by top mouth gudgeon  Pseudorasbora parva  of 238.  The 
flow-through system maintained water concentrations of between 5 
and 20 g quintozene/litre. 


    The Joint Meeting on Pesticide Residues (JMPR) reviewed 
residues and toxicity data on quintozene in 1969, 1973, 1975, and 
1977 (FAO/WHO, 1970, 1974, 1976, 1978).  The conclusion in 1977 was 
that 25 mg/kg diet, equivalent to 1.25 mg/kg body weight was a no-
observed-effect-level in the rat and 30 mg/kg diet, equivalent to 
0.75 mg/kg body weight in the dog.  On the basis of this, the 
estimate of an acceptable daily intake (ADI) for man was 0 - 0.007 
mg/kg body weight. 

    IARC (1974) did not come to a conclusion on the carcinogenicity 
of quintozene because of lack of data at the time.  FAO/WHO (1978) 
concluded that there were no indications that administration of 
quintozene resulted in carcinogenic activity. 

    CEC (1981) concluded that there was a need to set limits on the 
impurities present in technical quintozene. 

    WHO, in its "Guidelines to the Use of the WHO Recommended 
Classification of Pesticides by Hazard" (WHO, 1984), classified 
quintozene in the category of technical products unlikely to 
present an acute hazard in normal use. 

    Regulatory standards established by national bodies in 12 
different countries (Argentina, Brazil, Czechoslovakia, the Federal 
Republic of Germany, India, Japan, Kenya, Mexico, Sweden, the 
United Kingdom, the USA, and the USSR) and the EEC can be found in 
the IRPTC (International Register of Potentially Toxic Chemicals) 
legal file (IRPTC, 1983). 


9.1.  Evaluation of Health Risks for Man

    Quintozene toxicity

    Quintozene is practically non-toxic according to the scale of 
Hodge & Sterner (1956).  The oral LD50 in rats was 1650 to more 
than 30 000 mg/kg body weight.  WHO (1984) classified quintozene in 
the category of technical products unlikely to present an acute 
hazard in normal use. 

    No-observed-adverse-effect levels in long-term studies on the 
rat and the dog were 1.25 and 0.75 mg/kg body weight (25 and 30 
mg/kg diet), respectively.  In long-term studies with rats and at 
higher dosages (63 mg/kg diet), quintozene can give rise to liver 
hypertrophy with some histopathological changes and in dogs to more 
severe liver damage with fibrosis (5000 mg/kg diet).  In short-term 
studies on female rats, quintozene caused induction of mixed-
function oxidases. 
    Quintozene is both metabolised and excreted unchanged and
does not accumulate in tissues.

    Quintozene is not considered to be teratogenic.

    Quintozene is generally negative in short-term tests for 
genetic activity.  In carcinogenicity studies on rats and 
mice, equivocal or negative findings have been reported.  
Hexachlorobenzene, a possible impurity in technical quintozene 
is carcinogenic for mice, rats, and hamsters. 

    Except for 1 case of conjunctivitis in an occupational setting, 
no other cases of poisoning or adverse effects have been reported 
in man. 

    Exposure to quintozene

    The general population can be exposed via residues in food, 
especially in oils and fats.  Information on exposure from other 
sources is lacking.  No cases of accidental or occupational 
overexposure have been reported. 

    Hazard assessment

    With the exception of some data on residues in food, no human 
exposure data are available for quintozene.  It is therefore 
difficult to evaluate the hazard for man of present exposure to 
this substance.  Nevertheless, in view of its low toxicity in 
short-term and long-term animal studies, the data available on 
quintozene would indicate a low degree of concern in relation to 
human health effects. 

9.2.  Evaluation of Overall Environmental Effects

    The only significant adverse effect reported for quintozene is 
on earthworms.  According to laboratory tests, quintozene applied 
at recommended doses as a soil fungicide appears to have long-term 
toxic effects on the earthworm.  Unfortunately, no observations of 
the effects on earthworms of quintozene alone, during field use, 
are available. 

    There is no evidence that quintozene represents a threat to 
non-target organisms.  It has a very low acute toxicity for fish 
and  Daphnia.  

    Its bioaccumulation by fish is low, and no effects have been 
reported on terrestrial plants, birds, or microorganisms. 

9.3.  Conclusions

    1.  The general population does not appear to be at
        risk from residues of quintozene in food.

    2.  Exposure of the general population via air and
        drinking-water could not be evaluated because of lack
        of data.

    3.  Occupational exposure has not been reported to
        cause any adverse effects.

    4.  There is limited information on the effects of
        quintozene in the general environment.  It has been
        shown to be toxic to earthworms, in laboratory
        tests.  Data on other organisms suggest that
        quintozene is not a problem in the general

    5.  Quintozene does not biomagnify.

    6.  The major toxicological concern with quintozene
        is the presence of hexachlorobenzene as an impurity.


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    See Also:
       Toxicological Abbreviations
       Quintozene (HSG 23, 1989)
       Quintozene (ICSC)
       Quintozene (FAO/PL:1969/M/17/1)
       Quintozene (WHO Pesticide Residues Series 3)
       Quintozene (WHO Pesticide Residues Series 4)
       Quintozene (WHO Pesticide Residues Series 5)
       Quintozene (Pesticide residues in food: 1977 evaluations)
       Quintozene (Pesticide residues in food: 1995 evaluations Part II Toxicological & Environmental)