Toxicology 3 Branches

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Toxicology 3 Branches Powered By Docstoc
					3 Branches of Toxicology:                                    • Biomagnifications–magnification of contaminant
   • Occupational Toxicology – deals w/                            concentration 100x or 1000x after passing
     chemicals found in the workplace                              thru a food chain e.g. Polychlorinated biphenyls
    - Emphasis:                                           (PCBs)
      ~ Identify the agents of concern                           i.e. residues waste bodies of water
      ~Define the conditions leading to their                         phytoplankton fish => 50,000 fold animals
          safe use                                                    man
       ~Prevent absorption of harmful amounts             • Hazard – ability of a chemical agent to cause
        i.e. safe air concentration is maintained by         injury in a given situation or setting
          the establishment of threshold limit values        - Primary considerations: conditions of use
           (TVs)                                                                     : exposure
• Environmental Toxicology- deals w/the impact               - To assess hazard – one must know:
      of chemicals present as pollutants on living                 * inherent toxicity of a substance
      organisms                                                    * amount to w/c individual are liable to be
    - Environment include:                                          exposed
      ~air – industrialization, technologic dev.                i.e. toxic subs.=safe to use if conditions
             including urbanization                                     minimizing absorption are established &
      ~soil – human=>use of pesticides                                  respected
              persist as residues or ingredients         • Risk – expected frequency of the occurrence
                in food product                                of an undesirable effect arising from
    ~To prevent over exposure:                                 exposure to a chemical or physical gent
       FAO/WHO - adopted Acceptable                         - Estimation of risk:
                   Daily Intake (ADI)                          * Use of dose-response data
          - denotes daily intake of                            * Extrapolation from the observed
            chemical that imposes/causes                           relationship to the expected responses
            no appreciable risks during                            occurring in actual exposure situations
            the entire lifetime                             - Limiting factors in the estimation:
 • Ecotoxicology                                               * Quality         of biologic data used in
   – concerned with the toxic                                  * Suitability the estimation
      effects of chemical and physical agents               • Route of Exposure – entry for chemicals
      on pop’n & communities of living                           to the body
      organisms w/in defined ecosystem                         * Major Routes Of Entry:
   - includes:                                                    ** Industrial setting
      * transfer pathways of the agents                               – inhalation
      * their interaction w/ the environment                          - transdermal
   Traditional toxicology = concerned w/                              - oral = relatively minor
        toxic effects on individual organisms                     ** Atmospheric pollutants:
   i.e. an environmental event that affects                            - air = inhalation
          an individual organism may not                               - water & soil = oral
          have an impact on pop’n or an                   •Duration Exposure:
          ecosystem                                         * Acute – single or multiple exposure over
   hence: Environmental Toxicology ≠                                    1 or 2 days
          interchangeable w/ Ecotoxicology                  * Chronic – multiple exposures continuing
Important Toxicological Terms:                                           over a longer period of time
   • Bioaccumulation – intake of contaminants by an            i.e. occupational setting:
        organism exceeds its ability to metabolize or               > acute => e.g. accidental discharge
        excrete the substance, the chemical accumulates             > chronic exposure => repetitive
        w/in the tissues of the organism                                  handling of chemicals
           =>pollutants in ground water- environment         of the body
• Environmental Considerations:                           * COHb interferes w/ the dissociation of O2
   * Degradability                                            from the remaining OHb  reducing the
      ~ mobility – through air, water and soil                the transfer of O2 to tissues
      ~ bioaccumulation – occur or will not occur         * CO has also a direct damaging effect on the
      ~ transport and biomagnifications through               body cells
         food chain                                      ~ Brain and heart are the most sensitive
    - poor degradation=biotic or abiotic pathways            organs on CO effects
  * Persistence – persistent chemicals tend to           ~ Normal nonsmoking adults COHb level <1%
                 accumulate                                 saturation (1% of total Hb is in the form of
       e.g. Lipophilic subs.=>tend to accumulate            COHb)
           to body fat resulting tissue residues         ~ 1% saturaton=> endogenous formation of
Different Toxicological Concerns:                            CO from heme catabolism
  - Air pollutants                                        ~ Smokers = 5-10% saturation (depending on
  - Solvents                                                 their smoking habits)
  - Insecticides                                          ~ Individual breathing 0.1% CO (1000ppm)
  - Herbicides                                                ≈ COHb level of about 50%
  - Environmental Pollutants                           Clinical Effects of CO Exposure:
  - Heavy Metals                                         * Principal S x S:
                                                           ~ Hypoxia w/c progress into:
AIR POLLUTANTS                                               > psychomotor impairment
                                                             > headache and tightness in the temporal
5 Major Air Pollutants:                                        area
  - CO = 52%              NO = 14%                           > confusion and loss of visual acuity
  - SO = 14%                                                 > tachycardia, tachypnia, syncope
  - Hydrocarbons = 14%                                       > deep coma, convulsions, shock and
  - Particulate matter = 4%                                     respiratory failure
                                                       * Other s x s of CO poisoning:
Sources:                                                 ~ Delayed neuropsychiatric impairment
  - Transportation              - space heating          ~ Slow resolution of behavioral consequences
  - Industry                  - refuse disposal        * Variability of individual responses to
  - Generation of electric power                          different COHb levels:
CARBON MONOXIDE:                                          ~ <15% -rarely produce symptom
    > Colorless, tasteless, odorless, and non-            ~ around 40% collapse and syncope
      irritating gas                                      ~ >60% - death may ensue
   > by-product of incomplete combustion               * Aggravating Factors for CO Clinical Effects:
   > ave. conc. in atmosphere = 0.1 ppm                   ~ Heavy labor
               heavy traffic >100.0 ppm                   ~ High altituddes
   > TLV-TWA = 25.0 ppm                                   ~ High ambient temperature
      TLV-TWA = conc. for a normal 8hr.workday or 40    ~ presence of cardiovascular diseases –
          workwk to w/c workers may be repeatedly           increase ris k w/ CO exposure
exposed w/o                                              ~ pregnancy-fetus=>susceptible to CO effects
          adverse effects                                ~ smoking – CO poisoning= chronic among
Mechanism of action how CO exert its toxic                 cigarette smokers
  effect: CO + Hb           COHb                            e.g. of effect: atherosclerotic coronary
     CO has 220x affinity to Hb compare to O2                   disease
 therefore:                                            Treatment of Carbon Monoxide Poisoning:
   * O2 cannot be transported to the whole part        * Acute intoxication-
  > Removal of the individual from the                         - no specific treatment
      exposure source                                          - depends on therapeutic maneuvers
  > Maintainance of respiration                                    used in respiratory tract irritation
     i.e. adm. Of O2–specific antagonist to CO                       NITROGEN OXIDES
       o Elimination of Halftime of CO:                  * NO2 – brownish irritant gas associated w/
          -- room air at 1 atm. =320 mins.                         fires
          -- w/ 100% O2 = 80 mins.                               - formed from fresh silage
          -- w/ hyperbaric O2 at 2-3 atm.= 20                    - common exposures of farmers
             minutes                                             - can lead to silo-filler’s disease
SULFUR DIOXIDE                                                   - TLV-TWA = 3ppm; TLV-STEL =5ppm
     •      Colorless                                      ** Mech. Of Action: NO2 is a deep lung
     •      Irritant gas                                         irritant producing pulmonary edema
     •      TLV-TWA = 2ppm; TLV-STEL= 5 ppm             Effects on Exposure to NO2:
   ** TLV-STEL = Threshold Limit Value-Short               > 25ppm – irritating to some individuals
        Term Exposure Limit                                > 50ppm – moderately irritating to the eyes
          = max. conc. that should not be                               and nose
            exceeded at anytime during a 15 min.           > 1hr to 50ppm – pulmonary edema and
           exposure period                                      perhaps subacute or chronic pulmonary
     • Commonly Affected:                                       lesions
  > elderly                                                > 100ppm – pulmonary edema to death
  >w/ preexisting cardiac or respiratory disease           > On acute exposure type I cells are affected
     • Mechanism of Action How SO2 Exerts its Effect:   Clinical Effects of NO2 Exposure:
 - On contact with moist membranes, SO2 forms             o Acute
   sulfurous acid w/c is responsible for its                 - Irritation of eyes and nose
   severe irritant effects on the eyes, mucous               - Cough
   membranes and skin                                        - Mucoid or frothy sputum
     •      Absorption of SO2:                               - Dyspnea and chest pain
 - Absorbed thru the upper respiratory tract                 - Pulmonary edema w/in 1-2hrs.
 - 90% of the inhaled is absorbed                            - s x s may subside in about 2 wks.
   Effects of SO2 Inhalation:                           Clinical Treatment for NO2 Intoxication:
    - Bronchial constriction                             * No specific treatment employed for NO2 acute
    - parasympathetic reflexes                              poisoning
    - altered smooth muscle tone                         * Therapeutic measures are those for:
   Effects on Exposure to Different Concentration:           - management of deep lung irritation
   * 5-10 ppm = severe bronchospasm                          - noncardiogenic pulmonary edema
   * Lower concentration= 10-20% healthy young             > included are:
        adult pop’n. can be reactive                           -- Maintenance of gas exchange w/
   * Asthmatic individuals  more sensitive to                   adequate oxygenation and alveolar
                 SO2 exposure                                    ventilation
 Clinical Effects of SO2 Poisoning:                        -- Drug Therapy for NO2 Intoxication:
   * irritation of the eyes, nose and throat                     Bronchodilators
   * reflex bronchoconstriction                                  Sedatives
   * delayed onset of pulmonary edema –                          Antibiotics
         severe exposure                                OZONE
   * chronic exposure= associated w/                    O3 – bluish irritant gas
         aggravation of chronic                             - normally occurs in the atmosphere
        cardiopulmonary disease                             - it is an imptortant absorbent of UV light
Treatment for SO2 Poisoning:                                - source in a workplace:
        * High-voltage electrical equipment              * Animals –
        * Ozone-producing devices use for air and           > CNS depressant
           water purification                               > injury of liver, kidney and heart
        * urban-polluted air                                > carcinogenicity – due to CCl4, CCl3,
        * TLV-TWA = 0.05; TLV-STEL = NA                       trichloethylene and tetrachloroethylene
Clinical Effects of Ozone:                             * Human – CNS depressant
 * Mild exposure =upper respiratory tract irritation         . CCl3 – most potent
 * Severe exposure = deep lung irritation w/                        - widely used as anesthetic agent
      pulmonary edema                                        . Tetrachloethylene – chronic exposure
 *SXS:                                                                 - impaired memory
    ~ formation of reactive free radicals                              - peripheral neuropathy
    ~ gas causes: shallow rapid breathing                    . 1,1,1 trichloroethane – depressing agent
        : decrease in pulmonary compliance                   . CCl4 –most potent hepatotoxic agent
    ~ enhanced sensitivity of the lungs to                   . CCl4, CCl3 & trichloroethylene
       bronchoconstrictors                                             - nephrotoxicity
  ~ exposure to 0.1ppm for 10-30 mins.=>                 o Carcinogenicity – effects of low-level long
       irritation and dryness of the throat                   term exposure
  ~ >0.1ppm. = changes in visual acuity                    -Trichloroethylene– environmental exposure
  ~ substernal pain                                        - CCl3 – household exposure            very
  ~ dyspnea                                                         large margin of safety for human
  ~ >0.8ppm= pulmonary function is impaired            Treatment for Acute Intoxication of Halogenated
  ~ human = airway hyper responsiveness                  Aliphatic H-C:
             = airway inflammation                       o No specific treatment
Clinical Treatment of Ozone Toxicity:                    o Management depends on the organ system
   - no specific treatment for acute O3
         intoxication                                  AROMATIC HYDROCARBONS
   - Management depends on therapeutic                 * Benzene
     measures utilized for:                               o Uses :
        * deep lung irritation                              -- as solvent
        * noncardiogenic pulmonary edema                    -- intermediate in the synthesis of other
SOLVENTS                                                    -- TLV-TWA = 0.5ppm; TLV-STEL = 2.5ppm
                                                          o Acute Toxic Effect of Benzene:
HALOGENATED ALIPHATIC HYDROCARBONS                          -- Depression of the CNS
  • Uses                                               * Exposure to 7500ppm for 30 mins. = fatal
   * Industrial solvents
   * Degreasing agents                                 * >3000ppm – causes:
   * Cleaning agent                                         ~ Euphoria
                                                            ~ Nausea
• Included w/ these Hydrocarbons:                           ~ Locomotor problems
    * CCl4 –TLV-TWA = 5ppm; TLV-STEL = 10ppm                ~ Coma
    * CCl3 -         = 10ppm;         = NA               > 250 – 500ppm. =vertigo, drowsiness, head
    * Trichloroethylene = 50ppm;          = 100ppm             ache and nausea
    * Tetrachloroethylene (perchloroethylene) –        o Chronic Exposure to Benzene:
       TLV-TWA = 25ppm; TLV-STEL = 100ppm                 -- insidious to unpredictable injury of the
    * 1,1,1 trichloroethane (Methylchloroform) –             bone marrow
       TLV-TWA = 350ppm; TLV-STEL =450ppm                 -- aplastic anemia
Toxicity Effects of Halogenated Aliphatic H-C:            -- leukopenia
   -- pancytopenia                                    * persistent chemicals
   -- thrombocytopenia                                * degradationis quite slow
   -- leukemia                                        * bioaccumulate particularlyin aquatic eco-
   ** Bone marrow cells in early dev.stage =             systems
       most sensitive to benzene                      * mobility in soil
  ** Early symptoms of benzene intoxication:            ** presence of organic matter – favors
    -- headache                                             adsorption onto the soil
    -- fatigue                                          ** sandy soils – adsorption is poor
    -- loss of appetite                                     - once adsorbed – do not readily desorbed
o Treatment for acute benzene intoxication- no
    specific treatment recommended                   Organophosphorus Insecticide
* Toluene - Methylbenzene                                 • Dangerous to human and highly effective as
 ~ CNS depressant                                       insecticide
 ~ Difference from that of benzene                        •     Biotransformation = rapid
  >No myelotoxic properties as that of benzene            • Less stable than carbamates when dissolved
  > Not associated with leukemia                         in water thus have limited half-life in the
 ~ TLV-TWA = 50ppm.; TLV-STEL = NA                       environment compared to halogenated
 ~ Acute Exposure Effect:                                hydrocarbons
  > 800ppm =severe fatigue and ataxia                Absorption of Organophosphorus Except
  > 10,000ppm. = rapid loss of consciousness           Echothiophate:
                                                      * Skin               * Conjunctiva
INSECTICIDES                                          * Respiratory tract * CNS
                                                      * GIT
Organochlorine Insecticides                          Human Toxicology of Orgonophosphorus:
     •    Include the ff:                             * Mechanism of action – inhibition of acetyl-
   > DDT (Chlorophenothane) and analogs –                 cholinesterase through phosphorylation of
       poorly absorbed in the skin                        the esteratic site- known to be
   > Benzene hexachlorides –                              cholinesterase inhibitors
   > Cyclodienes – e.g. dielderin very efficiently   S X S for acute intoxication of
       absorbed in the skin                            Organophosphorus:
   > Toxaphenes                                        > accumulation of acetylcholine
Mechanism Action of Organochlorine:                    > some of the agents possess direct
       > Organochlorine interfere w/ inactivation         cholinergic activity
  of the sodium channel in excitable membranes         > altered neurologic and cognitive function
  and cause rapid repetitive firing in most            > psychological symptoms        caused by
  neurons -- Calcium ion transport is inhibited                     exposure to high concentration
  -- affect repolarization and enhance the            > Organophosphorus ester-induced delayed
  excitability of neurons - major effect =                polyneuropathy (OPIDP – particularly
  CNS stimulation                                          sensitive are hens
S X S of Organochlorine intoxication:                > Human : neurotoxicity –particularly
     • W/ DDT = tremor                                      observed w/ the used of triortho-cresyl
         = Convulsions                                      phosphate such as:
     • W/ other compounds                                   ** dichlorvos        ** mipalox
    convulsion =first sign of intoxication                  ** trichlorfon       ** leptophos
Treatment of Organochlorine Intoxication:                   ** methamidophos ** trichloronat
 - No specific treatment had yet been establish        - Thiophosphates are quite lipid-soluble
    for acute organochlorine poisoning                 - Absorbed by all routes
Environmental Toxicology of Organochlorine:            - Activated in the body by conversion to the
      oxygen analogs- occurs both in insects and                 since acute effects of cholinesterase
      vertebrate                                                 agents may last for 24 – 48 hrs. or
    -- Malathion and a few other                                 longer
       organophosphate insecticides – rapidly              ** 1 gm. Of atropine/day can be given
       metbolized by other pathways to inactive          for as long as 1 mo. to fully control
       products in birds and mammals but not             muscarinic x’s
       insects                                                •     Cholinesterase regenerator cpds. – involves the
      -- safe enough for sale in gen. public               regeneration of active enzyme from the
    - not detoxified by fish                                oranophosphorus-cholinesterase complex
-- Parathion- not detoxified effectively in                 to form oxime agents
              vertebrates                                 ** Pralidoxime (PAM) – most studied in human
            - more dangerous than malathion to                  - only available for clinical use in U.S.A.
              human and livestocks and is not                   - most effective in regenerating the
              available for public use                    associated w/ skeletal muscle neuromuscular
Organoprshosphates are cholinesterase inhibitors          junctions
  - initial signs of acute intoxication manifest          - ineffective in reversing the central effect of
    those of muscarinic excess                              organophosphate poisoning
    o miosis            o salivation                        i.e. because its positive charge prevents entry
    o sweating          o bronchial constriction                 into the CNS
    o vomiting           o diarrhea                       - administered by I.V. , 1-2gms. given over
                                                            15-30 mins.
      CNS involvement accompanied by                      - Excessive doses of PAM can induce the ff.:
   peripheral nicotinic effect especially                   > neuromuscular weakness
   depolarizing neuromuscular blockade                      > other adverse effects observed
Therapy of Organophosphate Acute Intoxication:                • Diacetylmonoxime (DAM) – crosses the blood-
    • Maintenance of vital signs – respiraion in           brain barrier
     particular may be impaired                           - in animals – have been to
    • Decontamination – to prevenrt further                    regenerate some of the CNS cholinesterase
  absorption                                                  •     Pretreatment w/ reversible enzyme inhibitors –
  > remove all clothing                                      to prevent binding of irreversible
  > washing of the skin in cases of exposure                 organophosphate inhibitor
     to dust and sprays                                      e.g. pyridostigmine, pysostigmine
    • Atropine –parenterally administered in large        => reserved only wherein lethal poisoning is
 dose given as often as required to control signs              anticipated e.g chemical warfare
 of muscarinic excess                                     => simultaneous use of atropine is required to
                                                                control muscarinic excess
Treatment for Severe Organophosphate
 Poisoning:                                             Carbamate Insecticides:
    •    Tertiary amine e.g atropine must be used not    - inhibit acetylcholinesterase by carbamoylation
   amine – treats both the CNS and peripheral               of the esteratic site
          effects                                        - non-persistent pesticides => small impact on
    o dose -                                                the environment
       * Parathion & chemical warfare nerve=             - Clinical effects:
  1 – 2 mg. of atropine sulfate; administered               > similar to organophosphate but of shorter
   intrvenously every 5 – 15 mins. Until signs                 duration
  of effects such as dry mouth, reversal of                 > the range between doses causing
  meiosis, etc. appear                                         intoxication and lethality is larger in
  ** Atropine adm. – repeated many times                       carbamates than w/ organophosphates
                                                      •      Highly toxic to mamma
   > compared to organophosphate reactivation         •      Major site of toxic action = CNS
      of cholinesterase is more rapid after           •      Absorption = ingestion, inhalation and skin –not
      inhibition by carbamates                                                   significant
    >Carbamates are referred to as reversible          • Toxic Effects of Pyrethrum Insecticides:
        cholinesterase inhibitors                    > Excitation          > contact dermatitis
      Organophosphates – irreversible                > Tetanus paralysis >cutaneous paresthesias
        cholinesterase inhibitors                    > Convulsions
 - Treatment of Carbamate Poisoning:                   •     Targets of Pyrethrum:
    > Similar to that of organophosphate             > Voltage gated sodium channel
      poisoning but PAM is not recommended           > Voltage gated calcium channel
                                                     > Voltage gated chloride channel
BOTANICALNSECTICIDES                                 > Peripheral–type benzodiazepine receptor
    •   Derived from natural sources                   • Treatment for Pyrethrum Intoxication:
    •   It includes the ff.:                         > symptomatic treatment is employed
  * Nicotine – from Nicotiana tabacum                > anticonvulsants = not consistently effective
                 N rustica                           > chloride channel agonist:
  * Rotenone                                             * ivermectin
  * Pyrethrum                                            * pentobarbital
                                                         * mephenesin
   •    Absorption:                                HERBICIDES
 > Free alkaloid but not the salt – readily            1. Chlorophenoxy Herbicides –
     absorbed from the skin                          > 2,4 Dichlorophenoxyacetic acid (2,4-D)
   •    Mechanism of action:                            * toxicity rating=4
  > Nicotine reacts w/ acetylcholine receptor of        * human lethal dose = 50 – 500 mg/kg BW
   the postsynaptic membrane i.e. sympathetic        > 2,4,5 Trichlorophenoxyacetic acid (2,4,5-T)
   and parasympathetic ganglia, neuromuscular          * toxicity rating = 3
   junction--->resulting in depolarization of          * human lethal dose =500– 5000mg/kg BW
   the mucous membrane                              > Salts and esters of 2,4-D & 2,4,5-T
   --->Toxic doses cause stimulation rapidly       Human Toxicity Effects:
       followed by blockade of transmission          > 2,4-D
   •    Treatment:                                        coma
  > Maintenance of vital sign                             muscle hypotonia
  > Supression of convulsion                         > 2,4,5-T
                                                         coma
ROTENONE                                                 muscular dysfunction
    •    Effects of oral ingestion:                      occupational exposure=> associated
  > GIT irritation       > Pharyngitis                      w/ increased risk of Non-Hodgkin’s
  > Conjunctivitis       > Rhinitis                         lymphoma
    •    Treatment:                                 Soft tissue sarcoma = equivocally suspected
  > symptomatic
 PYRETHRUM                                         Pls. note:
    •    Includes:                                   - Care in establishing toxicological profile
  > Pyrithrin I       > Cinerin II                     especially 2,4,5-T => intoxication can be
  > Pyrethrin II      > Jasmolin I                     caused by contaminants most important of
  > Cinerin I         > Jasmolin II                    w/c is Tetrachlorodibenzo-p-dioxin (TCDD)
    •    Esters are extensively biotransformed     2. Bipyridyl Herbicides
    * Paraquat – most important agent of                     **TCDDs effect in lab animals:
         bipyridyl herbicides                                  - wasting syndrome - carcinogenicity
       o Mechanism of action:                                  - thymic atrophy
          > Involves single electron reduction of              - epidermal changes
              the herbicide to free radical species            - hepatotoxicity
       o Toxicity rating = 4                                   - effects on reproduction and development
          Human lethal dose = 50- 500 mg/kg                    - teratogenicity
     • Toxicity Effects of Paraquat:                         > effects observed in animals are not
  - Accumulates slowly in the lungs by an active                 observed in human
     process causing:                                        > workers involved in manufacturing:
       > lung edema                                             .. 2,4,5-T perhaps exposed to TCDD
       > alveoliits                                                - contact dermatitis
       > progressive fibrosis                                      - chloracne
  - S X S in human:                                             .. Severely TCDD-intoxicated patients =
       > after oral ingestion                                         discrete chloracne
          .. GIT irritation=> hematemesis, bloody             > presence of TCDD in 2,4,5-T =
                               stool                             responsible for other human toxicities
> Delayed Toxicity:                                     2. Endocrine Disruptors:
    .. Respiratory distress                                 - chemicals that mimic or enhance or inhibit
    .. Congestive hemorrhagic pulmonary edema                  a hormonal action
    .. Cellular proliferation                               - included are:
    .. Hepatic, renal or cardiac involvement                   o plant constituents – phytoestrogen
    .. Death – several weeks after ingestion                   o mycoestrogens
     •       Treatment of Paraquat Intoxication:               o persistent organochlorine- DDT, PCBs
  > Prompt removal of paraquat from GIT by:                    o brominated flame returdants
      .. Use of gastric lavage                              - Properties: bioaccumulation
      .. Use of cathartics> Delayed Toxicity:                  o potent toxicant
    .. Respiratory distress                                    o increasing contaminatrion of the
    .. Congestive hemorrhagic pulmonary edema                    environment
    .. Cellular proliferation
    .. Hepatic, renal or cardiac involvement
    .. Death – several weeks after ingestion
     •       Treatment of Paraquat Intoxication:
  > Prompt removal of paraquat from GIT by:
      .. Use of gastric lavage
      .. Use of cathartics
Polychlorinated dibenzo-p-dioxin(PCDDs) or
  dioxins= group of congeners of PCBs
 * 2,3,7,8-tetrachlorodibenzo-p-dioxins(TCDD) =
      most important congener
 * Polychlorinated dibenzofurans(PCDFs)
 * Coplanar biphenyls               dioxin-like cpds.
   ** TCDDs and PCDFs:
        - like PCBs = very stable
                    = highly lipophilic
                = poorly metabolized
                = very resistant to environmental

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