toxicology · goals for prevention protection the public health protection the workers health...
TRANSCRIPT
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TOXICOLOGY
FOR ENGLISH SPEAKING STUDENTS
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DEFINITION
THE STUDY ABOUT THE NATURE AND MECHANISMS OF CHEMICALS´ EFFECTS ON LIVING ORGANISMUS AND OTHER BIOLOGIC SYSTEMS
QUANTITATIVE ASSESSMENT OF THE SEVERITY AND FREQUENCY OF SUCH EFFECTS
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GOALS FOR PREVENTION
PROTECTION THE PUBLIC HEALTH
PROTECTION THE WORKERS
HEALTH PROMOTION
DEVELOPMENT OF SAFER CHEMICALS USED AS DRUGS, FOOD ADDITIVES, PESTICIDES, INDUSTRIAL CHEMICALS
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THE MAIN PREVENTIVE TASK
TO ESTABLISH:
THE ACCEPTABLE DAILY INTAKE = safe level for life-long exposure to the sum of chemicals
THE SAFE LIMITS (HIGHEST TOLERABLE CONCENTRATIONS)
IN WATER, AIR (ambient, indoor), FOODS
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SORTS OF TOXICOLOGY
ANALYTICAL
CLINICAL
FORENSIC
OCCUPATIONAL
ENVIRONMENTAL
REGULATORY
CONVENTIONAL, …
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SCOPES OF TOXICOLOGY
MEDICINE: diagnosis, prevention, treatment
FOOD INDUSTRY: additives
AGRICULTURE: pesticides, growth regulators, animal food additives, veterinary drugs
INDUSTRY
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EPIDEMIES OF POISONING
POMPEII – VESUVE, DUST, SO2,
SMOG REDUCTIVE (dust, CO, PAH): Donora, London
SMOG OXIDATIVE (O3, NOx, CO2 hydrocarbons): Los Angeles
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EPIDEMIES - continue
MINAMATA, NIIGATA, IRAQ, USA - METHYLMERCURY
ITAI-ITAI - CADMIUM
YUSHO, YUCHENG - PCBs
MITCHIGAN – PBBs
SEVESO – PCDD (TCDD)
BHOPALE - METHYLISOCYANATE
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September 11, 2001 - NY
DISSEMINATION OF CHEMICALS as:
ASBEST, PAH
HEAVY METALS (Cd, Pb, Hg, Cr, …)
CHLORINATED HYDROCARBONS (PCB, PCDD, PCDF…)
ORGANIC SOLVENTS
OTHERS (HCN, CS2 , H2S,…)
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ROUTES OF INTAKE
GASTROINTESTINAL TRACT
RESPIRATORY TRACT
SKIN
VAGINA, RECTUM, EAR, EYES
PARENTERAL APPLICATION
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TYPES OF UPTAKE
PASSIVE DIFUSSION
FILTRATION
CARRIER-MEDIATED TRANSPORT
ENGULFING BY THE CELLS (pinocytosis)
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BARRIERS
MUCOCILLIAL CLEARANCE
SKIN „FILM“ (ACID and FATTY)
RATE OF ABSORPTION
PLACENTAL (fetus protection)
CEREBROVASCULAR (brain protection)
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BIOTRANSFORMATION
The main influencing factor:
WATER / LIPO – SOLUBILITY
WATER – SOLUBILE => EXCRETION WITHOUT METABOLISATION
POLARIC = > AFTER CONJUGATION
LIPO-SOLUBILE => 2 STEPS METABOLISM
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Ist STEP /PHASE
OXIDATION, REDUCTION, HYDROLYSIS
CATALYTIC MICROSOMAL ENZYMES
METABOLITES DEVELOPED BY OXIDATION ARE BOTH LESS AND MORE ACTIVE THAN THE MATERNAL COMPOUND
DUE TO OXYGEN / FREE RADICALS
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OXIDATIVE BIOTRANSFORMATION
MICROSOMAL ENZYMES – COMPLEX of
CYTOCHROM P450
GENETIC DIFFERENCES IN GENOTYPE – GENETIC POLYMORPHISM
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CYTOCHROM P450
ENVIRONMENTAL INFLUENCE ON FENOTYPE:
SOME DRUGS, DDT, PCBs, PCDDs, chemicals in VEGETABLES
CAN INDUCE THE RELEASE OF OXIDATIVE ENZYMES P450
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CYTOCHROM P 450 – exampl.
CYP 1A1: lungs, placenta
PAH
CYP 1A2: liver
AFLATOXINS, NITROSAMINES
CYP 2A6: lungs, liver, …
NITROSAMINES, NICOTINE
CYP 1B1, 2C9,2C19, 2D6, 2E1, 3A…
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2nd STEP / PHASE
CONJUGATION:
GLUCURONIDES FORMATION: the most important and common way,
Catalyzing enzymes:
UDP- GLUCURONYL TRANSPHERASEs:
Aliphatic and aromatic alcohols, amines, sulfhydryl compounds, …
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2 nd STEP /PHASE
GLUTATHIONE FORMATION
Enzymes GLUTATHION-S-TRANSPHERASEs:
Polycyclic aromatic hydrocarbons
ACETYLATION: enzymes N-ACETYL TRANSPHERASEs: SLOW/FAST ACETYLATORS
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2nd STEP /PHASE
SULPHATES FORMATION – enzymes SULPHOTRANSPHERASES
METHYLATION
GENETIC POLYMORPHISM:
„HAPPY“ / „UNHAPPY“ PEOPLE
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POLYMORPHISM IN PRACTICE
VULNERABILITY TO:
- INDUSTRIAL CHEMICALS,
- DRUGS
- DEPENDENCE (nicotine)
ETHICAL PROBLEMS
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EXCRETION OF CHEMICALS
URINARY, BILIARY
EXPIRATED AIR
SALIVA
EVAPORATION
SKIN ADNEXES (HAIR, NAILS)
MOTHER´S MILK, FOLLICULAR FLUID, EJACULATE
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DEPOTS
TARGET ORGANS
FATTY TISUE
BONE
TEETH
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TESTs OF EXPOSURE
LEVELS OF THE SUBSTANCE or IT´S SPECIFIC METABOLITE: CO in the expirated air, cotinine, BaP DNA adducts
LEVELS OF NON-SPECIFIC METABOLITES: urinary glucuronides, thioethers
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TESTs OF EXPOSURE
ASSESSMENT OF THE ORGANISM´S RESPONSE: anemia in the Pb chronic exposure, Chromosomal aberations in the exposure to mutagens
ASSESSMENT OF THE INDIVIDUAL VULNERABILITY: genetic polymorphism in induction of microsomal enzymes, sexual /ethnic /age differences
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SPECTRUM OF EFFECTS
LOCAL x SYSTEMIC
REVERSIBLE x IRREVERSIBLE
IMMEDIATE x DELAYED
MORPHOLOGIC x FUNCTIONAL x BIOCHEMICAL
ALLERGIC x IDIOSYNCRATIC
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SPECTRUM OF EFFECTS
IRRITATION, INFLAMATION
TOXICITY (according to the target organ): hemato-, hepato-, neuro-, nephro-, cardio-, …
EMBRYOTOXICITY
TERRATOGENICITY
MUTAGENICITY
CARCINOGENICITY
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EPIGENETIC EFFECTS
NON-MUTAGENIC CHANGES OF PHENOTYPE
ON MOLECULAR BASIS INVOLVES:
DNA-methylation,
ALTERATION OF miRNAs, piwiRNAs, longRNAs
MODIFICATION OF HISTONE
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MECHANISMS of ACTION:
CELLs PROLIFERATION,
ANTI-APOPTOSIS
REVASCULARISATION of TUMOROUS TISSUE and METASTASES
LOWER CELLs ADHERENCE
HORMONAL DYSRUPTORS
PROMOTION of P450 ENZYMEs RELEASE
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DIFFICULTIES IN RESEARCH
EXTRAPOLATION from the ANIMAL EXPERIMENTS to the HUMAN REALITY
DOSE – RESPONSE RELATIONSHIP
THE (upper) LIMITS FOR THE PHYSIOLOGIC RESPONSE
INTERACTION OF CHEMICALS IN MIXTURES
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ANTI-CHEMICAL DEFENSE
CONTINUAL EXCHANGE/REPLACEMENT OF DAMAGED CELLS IN GATES
INDUCTION OF DETOXIFYING BIOTRANSFORMATION
ACTIVE EXCRETION OF HYDRO-SOLUBLE SUBSTANCES
DNA REPAIR
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IS THE NATURE SAFE?
DEFENSE HAS DEVELOPED IN THE EVOLUTION DUE TO EXPOSURE TO NATURAL CHEMICAL COMPOUNDS
ALL SURVIVE PLANTS HAVE DEVELOPED THEIR PROTECTION
AGAINST THEIR NATURAL ENEMIES = NATURAL PESTICIDES
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NATURAL PESTICIDES
ARE CHEMICALY SIMILAR TO THOSE PRODUCED BY INDUSTRY
SOME OF THEM ARE STRONG TOXINS AND CARCINOGENS (botulotoxine, aflatoxine)
PLANTS CAN CHANGE both the CONCENTRATIONS and the SORT
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TOO MANY RHODENT CARCINOGENS
There were tested more than
1000 INDUSTRIAL CHEMICALS and
50 NATURAL CHEMICALS
In both groups, about
50% are RHODENT CARCINOGENS
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EXPERIMENTAL TESTS
The MAXIMAL TOLERATED DOSES, and their fractions (1/2 ¼) ARE USED
WHICH MATHEMATIC MODEL OF EXTRAPOLATION FOR HUMAN EXPOSURE IS THE BEST?
LINEAR? EXPONENTIAL?
DOES THE SAFE TRESHOLD EXISTS?
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EPIDEMIOLOGIC/CLINIC STUDIES
ARE ONLY ACCEPTABLE FOR HUMAN RISK ASSESSMENT = >
CHEMICAL ACCIDENTS and DISASTERS ARE ASSESSED IN LONGITUDINAL PROSPECTIVE STUDIES
Also PROFESSIONAL EXPOSURES are the sources of IMPORTANT DATA
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CARCINOGENS´ CLASSIFICATION
CATEGORIES HUMAN / ANIMAL DATA
HUMAN C. 1A suffic. suffic./limited
PROBABLE 2A limited sufficient
POSSIBLE 2B inadeq. suffic/limited
NO-CLASSIF. 3 absent inadeq/absen
NOT CARCIN.4 absent negative in 2
species
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CARCINOGENIC EFFECTS
OF CHEMICAL SUBSTANCES RISE THE MAJOR CONCERN OF RESEARCHES:
GENOTOXIC THEORY OF CARCINOGENESIS: INITIATION of DNA MUTAGENIC CHANGES – REPLICATION – PROMOTION – MANIFESTATION
EPIGENETIC (non-mutagenic) THEORY
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WHAT DO WE KNOW?
WE CAN MEASURE THE MUTAGENICITY (Ames´s test) AND RESPONSE (Chromosomal abberations, sister chromatide exchanges, DNA adducts…)
THERE ARE RELATIONSHIPS BETWEEN SHORT-TERM MARKERS and CANCER INCIDENCE
CELLs PROLIFERATION IS IMPORTANT
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WHAT WE DON´T KNOW?
WHICH MODEL FOR EXTRAPOLATION
IS THE MOST PRECIOUS ?
WHICH IS THE ROLE OF NATURAL CHEMICALS and CONDITIONS ?
WHICH SIGNALS OF RESPONSE ON EXPOSURE ARE IMPORTANT FOR USE THEM TO ESTABLISH THE ACCEPTABLE LIMITS ?
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POLITICAL POINT OF VIEW:
TO KEEP LIMITS IN MORE DIFFICULT THAN TO ESTABLISH THEM
HOW MANY VULNERABLE PEOPLE WE WILL PROTECT BY THE LIMITS
CAN WE ACCEPT SOME SPECIFIC PROTECTION OF VULNERABLE PART OF POPULATION
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ENVIRONMENTAL HYSTERY
VERY OFTEN ENHANCES THE PUBLIC INTEREST ABOUT LOW-RISK FACTORS (sacharin, DDT, PBCs, Alar, …)
AND
OBSCURES / UNDERESTIMATES THE REAL RISKS (nutrition, smoking, poor hygiene, …)
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ALL CANCER MORTALITY:
ATTRIBUTIVE RISK IN LIFE STYLE
NUTRITION …………………… 35%
SMOKING ……………………… 30%
INFECTIOUS AGENTS …….. 10%
SEXUAL BEHAVIOUR ………. 7%
ALCOHOL ………………………. 4%
TOGETHER ……………………. 87%
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ALL CANCER MORTALITY
ATTRIBUTIVE RISK IN ENVIRONMENT
OCCUPATION …………………… 4%
MEDICAL TREATMENT ………. 3%
GEOPHYSICAL FACTORS ……. 3%
POLLUTED AIR, WATER …….. 2%
FOOD ADDITIVES/CONTAM. . <1%
TOGETHER ………………………. 13%
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CONCLUSSIONS
TOXICOLOGY IS DYNAMIC, EXCITATING SCIENCE
TOXICOLOGY CAN DISCOVER MANY MYSTERIOUS THINGS IN LIFE
TOXICOLOGY CAN REDUCE HUMAN CHEMOPHOBIA