acronyms

ELD

environmental liability directive

RA

risk assesment

toxicity

ability to harm organism

dose

amount of substance that is absorbed

exposure

contact with a substance

effect

response to exposure

LD (DL)

lethal dose

dosis lethalis

TCDD

tetra-chloro-di-benzo-di-oxine

4-Cl+2-CH+2-O

HPC

highest permissible concentration

Hb

hemoglobin (blood)

ppm

parts per million

hm

heavy metal

Hg mercury

Pb lead

As arsenic

Cd cadmium

ADP adenosin trophosphate

ADP

adenosine triphosphate

POP

persistent organic pollutant

PCB

polychloro bifenyl

NOEL

non observeable effect

OC

OW

n factor

exponent

ERA

environmental risk assesment

stressor is defined by?

NOAEL

no observable adverse effect level

LOAEL

lowest observable adverse effect level

ADME

adsorption distribution metabolism excretion

(how organism processes substance)

ABP

absorption, biodegradatoin, photolysis …

(how environment deals with substandes

D=kct

relationship of how the inhibitors bin with the substances

**n exponents**

n

U=fc

LNAPL

light non aqueous phase liquid (floats on water)

DNAPL

dense non aqueous phase liquid (stays under water)

logKow

concentration of chemical in n-octanol / concentration in water

logKoc

conc in soul / conc in water

high logKow substances

are lipophilic, high polarity, fast sorption in OM

OM

organic matter

high logKoc substances

sorb heavily into soil

ADsorption

accumulation of molecules on surface

ABsorption

penetration of molecules

when concentration of LogKoc is low ?

mobile, releases easily into other components

half life

time where half of molecules decompose

which is more dangerous: persistent substances or rapidly decomposing substances

persistent

POP

persistent organic pollutant (banned)

fate of xenobiotics in organisms

ADME

ADME

adsorption, distribution (in body), metabolic transformation, excretion (from body)

what affects distribution in body?

affinity to fat, chemical andphysical properties of substance

what system is well protected from xenobiotics

CNS

CNS

central nervous system

biotransformation phases (2)

oxidation, merging

products of metabolism

waterphilic, soluable in water, less toxic

basal substances are better extreted in acidic/basic pH?

acidic pH

PEC

predicted environmental concentration

PNEC

predicted non-effect environmental concentration

MVOC

microbial volatile organic compounds (stuff bacteria and fungi produce)

TU

toxic unit

acute effect

after 1 exposure

chronic effect

after repeated exposure

solvay process

manufacture NaCl in 6 steps

LeBlanc process

manufacture NaCl in 3 steps

Silent spring

book from 1957 talking about DDT and stuff that helped to form USA pesticide policy

ECHA

european chemicals agency

BASF

badisch + anilin soda fabrik

what does the effect of toxin depend on

maturity of organism, vulnerability

acute toxicity levels

strongly toxic, toxic, harmful

values for strongly toxic

values for toxic

25-200mg/kg

values for harmful

200-2000mg/kg

threshold

dosage where effects are observable

what substances don’t have a threshold

TCDD (carcinogenic substances)

how can xenobiotics have different effect?

depends on how they enter the body and where to they get distributed in the body

how do toxins work in body?

directly toxic, biotoxicity, immunotoxic, carcinogenic, mutagenic, teratogenic, organ specific

direct toxicity

critical location in body

biochemical toxicity

affects vital biochemical reactions in body

competitive inhibition

inhibitor binds to active enzyme site **slowing down** reaction

non competitive inhibition

inhibitor binds to enzyme altering it and reaction stops

immunotoxicity

response to toxin by changes in immune system (allergy, immuno surpression)

how does allergy work

immune system produces antibodies despite substance not being toxic

carcinogenic toxicity

mutates DNA, excites mutated tissue

\-vinyl chlorid *for sure*

\-DDT *most likely*

\-polyethylene *maybe*

HPC

highest permissible concentration

LC

lethal concentration