PART 5_2 Chemical contaminants and ecotoxicology

Environmental Chemistry 

Part 5 Biospheric Chemistry 

5.2 Chemical contaminants 

and ecotoxicology

Ecotoxicology 

• Ecotoxicological study is a multi-step 

process, involving: 

– The entry, distribution and fate of 

pollutants within the environment; 

– The entry and fate of pollutants in living 

(biota) organisms within an ecosystem; 

and 

– The harmful effects of the chemical 

pollutants on the constituents (biotic & 

abiotic) of ecosystems (which include 

man).

Beyond our toxin trail 

Is the grave deeper than we thought 

Transport 

and fate 

Ingested 

Metabolized 

and/or stored 

Toxin 

emitted 

Ecosystem 

effects 

Contacts 

human 

Reaches 

an organ 

Community 

effects 

Population 

effects 

Physiological 

chain of events

Toxicology and Ecotoxicology are 

similar but not identical 

Toxicology 

• Absorption 

• Distribution 

• Metabolism 

• Elimination 

Ecotoxicology 

Release into environment 

Fate and disposition 

Metabolism 

No counterpart

There are also differences. 

Toxicology 

• Host defense 

mechanisms 

• Individual 

susceptibility states 

• Single effects 

• Cumulative 

exposure 

Ecotoxicology 

• Bioaccumulation 

• Bioconcentration 

(in water) 

• Biomagnification 

• Never single 

effects 

• Movement 

between media (air, 

water)

Ecological bases of Ecotoxicology 

• The basis for determining the effects of 

contaminants on ecosystem is at 

organism level 

• At organism level, response can be: 

– Acute toxicity causing mortality 

– Chronically accumulating damage ultimately 

causing death 

– Sublethal impairment of various aspects of 

physiology and morphology 

– Sublethal behavioral effects 

– Measurable biochemical changes

•At population level, response can be: 

–Size and dynamics (based on birth rates, death 

rates, gains, from immigration and losses from 

emigration) 

–Cause a reduction or an increase in the natural 

flowchart of numbers, in the biomass, sex ratio, etc. 

•At community level, response can be: 

–species diversity 

–predator prey relationship, etc 

•Change in ecosystem 

–nutrient cycling rates, patterns of nutrient flow, 

–physical-chemical conditions etc.

Understanding ecotoxicology

Assessment of Structural Changes 

changes in species / population structure 

- appearance/disappearance of an 

indicator species 

- number of individuals of a species 

- biomass of a species 

- presence or absence of a species 

Biomass-a quantitative estimate of the total mass of 

living plant or animal materials

changes in community/ecosystem structure 

- biomass 

- abundance 

- biotic indices (e.g. trophic types) 

- species richness / diversity 

- dominance 

- food chain length/complexity

Chemicals of Ecotoxicological 

interest 

• They are toxic and in many cases their 

metabolites are also harmful e.g. DDT & DDE 

(metabolite of DDT) 

• They are very stable both chemically and 

environmentally 

• Their stability has lead to their persistence and 

ubiquitous nature in the environment 

• Almost all chemicals of ecotoxicologigal interest 

are bioavailable and in most cases undergo 

bioaccumluation and biomagnification (food 

chain)

Chemical behavior and Bioavailability 

Bioconcentration (from external 

environment) 

Bioaccumulation (from external 

environment/food ) 

Biomagnification (at higher tropic level)

Bioavailabiltiy The fraction of a chemical 

that is in an available form to an organism 

e.g. fish: food, absorption from water 

Bioconcentration - where the chemical 

concentration in an organism exceeds the 

concentration in the surrounding media (i.e. 

aquatic environment) as a result of exposure 

through the respiratory surfaces (i.e. gills/dermal 

surfaces) - not food! 

Bioconcentration Factor = conc. in organism 

conc. in ambient medium (usually water)

Bioaccumulation - where the chemical 

concentration in an organism achieves a level 

that exceeds that in the water/media as a result 

of chemical uptake through all routes of 

exposure. 

Bioaccumulation factor = Conc. in organism 

Conc. in food 

(or ingested water) 

•Bio-accumulation of Cd is higher than most 

metals as it is assimilated rapidly and 

excreted slowly 

•depends on the rate of excretion

Biomagnification - where the chemical 

concentration in an organism achieves a 

level that exceeds that in the organism’s diet 

due to dietary absorption. i.e. higher trophic 

levels accumulate more chemical 

Biomagnification Factor = 

Conc. in predator 

Conc. in prey

Factors that influence bioaccumulation 

•Environmental persistence 

•Lipophilicity 

•Biotransformation

ECOSYSTEMS: Fate of Metals 

• The ultimate compartment is the whole 

planet but compartment can be 

– individual organism or 

– as small as single cells 

– Or even organelles within a cell 

• Metals are non-biodegradable 

• However there is the formation and 

degradation of organometallic 

compounds e.g. MeHg,

Fate of Metals 

• Certain metals are assimilated by 

organisms to a greater extent than others 

• Bio-accumulation of Cd is higher than most 

metals as it is assimilated rapidly and 

excreted slowly 

• Bio-availability is another reason for a high 

bio-concentration factor in that the 

chemical in question may be more bioavailable

Fate of Metals 

• pH is very important when it comes 

to metal bio-availability 

• Some metals e.g. Al is insoluble at 

normal to slightly acidic pH but 

below pH 4.5 its solubility increases 

dramatically and becomes most 

important responsible for fish kills 

in acidified lakes

ECOSYSTEMS: Terrestrial 

• Soils are contaminated 

– by metals and radioactive isotopes 

resulting from 

• industrial, mining or other activity or 

deposition from agricultural practices such 

as application of 

– metal-containing pesticides or 

– metal-contaminated sewage sludge 

– or wet or dry deposition from smelting 

activity, lead-containing car exhaust, 

atmospheric nuclear weapon testing or 

accidents such as Chernobyl.


• Mobility of metals in soils is dictated 

largely by 

– clay content 

– amount of organic matter 

– pH 

• In general the higher the clay and/or 

organic matter content and pH, the more 

firmly bound are the metals and the longer 

is their residence time in soil 

• Acid rain helps in leaching nutrient 

(magnesium in European soil) from top to 

lower soil (inaccessible to root system)


• Contamination of soils by radioactive 

materials is largely due to nuclear 

weapon testing (Australian and 

Nevada deserts) 

• Accident has also contributed to that 

e.g. Chernobyl fallout outside the 

former Soviet Union. 

• When soils are contaminated 

organisms living in soils are affected

ECOSYSTEMS: Aquatic 

• The ultimate “sink” for metal is the ocean 

but difficult to estimate effect on biota due 

to massive dilution 

• Effect of metals on biota is much felt in 

estuaries especially those receiving water 

from contaminated sites 

• In estuaries the flow rate diminishes, 

suspended sediments settled and dissolved 

metals precipitated 

• Contaminated water affect organisms living 

in it

Biomarkers 

A xenobiotically induced alteration in 

cellular or biochemical components or 

processes, structures, or functions that is 

measurable in a biological system or 

sample. 

Types of Biomarkers 

Biomarkers of exposure 

Biomarkers of effect 

Biomarkers of susceptibility

1. Biomarkers of exposure 

Biomarkers of exposure include exogenous 

chemicals, metabolites, or products of 

interactions between environmental toxicants 

and target molecules or cells that are measured 

in a compartment within an organism (Travis, 

1993).

Internal dosimeters- 

1. measure the amount of a toxicant or its metabolite 

present in cells, tissues, or body fluids. Ex. 

urinary nitrophenol concentration used as a 

marker for methyl parathion exposure. 

2. account for individual differences in absorption 

and bioaccumulation of the xenobiotic and are 

relatively easy to measure. 

The biologically effective dose is the amount of the 

internal dose necessary to elicit a response or 

health effect.

2. Biomarkers of Effect 

Biomarkers of effect are measurable alterations 

of an organism that can indicate a potential or 

established health impairment or disease (Travis, 

1993). These can include an alteration in a tissue or 

organ, an early event in a biologic process that is 

predictive of disease, a health impairment or clinical 

disease, or a response parallel to the disease 

process, but correlated with it, and able to predict 

health impairment. Ex. the change in blood 

cholinesterase activity after exposure to anticholinesterase 

organophosphorous pesticides.

hypersensitivity) 

Nonspecific 

The induction of mixed function oxidase 

The formation of DNA adducts 

Sister chromatid exchange 

Strand breakage 

Porphyrin profile alteration 

Induction of vitellogenin in oviparous vertebrates 

Immunochanges (immunosupression,

Biomarkers in order of decreasing specificity 

Source: Walker et al. Principles of Ecotoxicology (2001) 2nd Edition [DUHS-P]

3. Biomarkers of Susceptibility 

Biomarkers of susceptibility indicate individual factors 

that can affect response to an environmental toxicant 

(Bearer, 1998). They are indicators of inherent or 

acquired properties of an organism that may lead to an 

increase or decrease in the internal dose of the 

xenobiotic or an increased or decreased level of the 

response resulting from the exposure. 

Genetic polymorphisms fall into this category of 

biomarkers. 

P450 1A1 induction 

Decreases in conjugated enzymes 

Inhibit the activity of immune system

Biomarker interpretation 

• Species different-ex.P450 induction 

• to integrate multiple chemical exposure across 

an area with a variety of chemical contaminants 

•Relationship between biomarker and disease 

pathology 

•To predict disease 

•To predict environmental and genetic risk

Toxic Effects 

• The biochemical (molecular in nature) or 

physiological (observed at organ and whole 

organism levels) changes which adversely 

affect individual organisms’ birth, growth 

or mortality rates. 

• Both biochemical and physiological 

changes could lead to behavioral (whole 

organism level) changes

Example 

• The pollutant binding to a receptor 

• Followed by biochemical response at 

both cellular and organ levels 

• Leading to physiological responses 

• Finally, behavioral changes on the 

individual leading to effects on the 

population, community and the 

ecosystem.

BEHAVIORAL EFFECTS: 

– Migration, 

– intraspecific attraction, 

– aggregation, 

– aggression, 

– predation, 

– vulnerability, 

– mating

• Binding: 

– Reversible vs. Irreversible binding 

• Irreversible binding (covalent) causes harmful 

effects. 

• Types of bonding: 

– Covalent > ionic > Hydrogen binding > Vanderwaals > 

hydrophilic 

• Biochemical responses: 

– Biochemical response could be protective or nonprotective 

(may or may not cause harmful effect). 

• Non-protective biochemical responses have 

Carcinogenic, Mutagenic, Teratogenic and 

Neurotoxic potentials.

• Protective biochemical responses: 

– Monoxygenase (OCs and PAHs) 

– Induction and binding to metalothionein (Cu, 

Cd, Zn and Hg) 

– Binding to blood plasma, bones and hair 

(Metals and xenobiotics) 

– Dissolving in fat (organics- e.g. OCs) 

– Mineralization ( e.g. MeHg to Hg 2+) 

– Demineralization (As to MeAs)

Protective biochemical response 

• Heavy metals for example can be stored and 

detoxified by organisms either by binding to 

specific proteins e.g. metallothioneins (-SH 

proteins) 

• In some cases it is mineralized to inorganic 

form, which is less toxic: e.g. Hg bound to Se 

is a mineralized Hg (detoxified Hg: MeHg to 

Hg). On the other hand, the inorganic form, 

which is more toxic can be methylated to a 

less toxic form e.g. As.

Protective biochemical response 

PHASE 1 REACTION. 

• Organic pollutants could also be metabolized and 

detoxified by Cytochrome P450 enzymes 

(Microsomal Monoxygenase; MMO). 

PHASE 2 REACTION 

• The metabolites undergo conjugation with 

endogenous molecules e.g. GSH. 

• For some chemicals the metabolites/conjugated 

form are more toxic than the parent compound and 

can lead to cancer formation.

Non-protective response 

– Binding to DNA (DNA adduct) 

– DNA Structural damage (strands break) 

induced by genotoxic compounds 

– Binding to SH-Protein (Protein adduct); 

enzymes and proteins 

– Nerotoxicity: prolongation of K and Na flow 

and inhibition of AChE activity in the brain


– Mitochondrial Poison (lost of proton 

gradient) 

– Inhibition of vitamin K cycle (competition 

with vit K binding site) 

– Inhibition of Thyroxine (competition with 

thyrosine binding site) 

– Inhibition of ATPase (enzymes for 

transport of ions e.g. K, Na, Ca)


• Environmental Estrogens (eg DDT) and 

androgens (tributhyl Tin) 

• Endocrine disrupters (binding to endocrine 

receptors) 

• Photosystems of Plants (interruption of 

electron flow) 

• Plant growth regulation

Physiological changes 

Non-protective biochemical responses lead to 

Physiological changes which could be 

observed at organ and organism levels 

• Organ level: 

– accumulation of Cd in kidney, which could cause 

cell death (cytotoxicity), resulting in dysfunction of 

the kidney 

– PAHs and Lung cancer 

• Organism level: 

– decrease in production (growth and reproduction) 

– changes in gene frequency 

– decrease in resources acquisition and uptake

Behavioral Changes 

– Either or both physiological and biochemical 

effects could lead to behavioral effects at 

organism level- 

– e.g. caring for young ones and avoidance of 

predator. 

Biochemical, Physiological and Behavioral 

effects on the individual organism culminate 

effects observed at the Population, 

Community and Ecosystem levels.

Population Changes 

• Changes in population may come about as a 

result of direct changes in numbers of 

individual organism and gene frequency 

(resistance) 

• By indirect means (decrease in 

population of predators due to toxic 

chemicals could lead to increase in 

numbers of its prey).

Diclofenac residues as the cause of 

vulture population decline in Pakistan. 

Nature. 2004 Feb 12;427(6975):630-3. 

• Diclofenac 

causes kidney 

damage, 

increased serum 

uric acid 

concentrations, 

visceral gout, and 

death.

• Changes in community structure 

– change in pyhtoplankton assemblage due to 

eutrophication 

– acid rain affecting microorganisms in the soil, 

aquatic life 

• Changes in Ecosystem level (earth as 

an ecosystem) 

– carbon dioxide increase 

– ozone depletion

Some General effects of pollution on an 

Ecosystem 

• Decrease in the suitability of the abiotic 

component as a habitat for the biotic 

components of the ecosystem, which have 

been naturally established and adapted to 

that ecosystem 

• Detrimental impact on part of the biotic 

component (vulnerable species) as related to 

the intensity and type of pollution 

• Alteration to the community structure and in 

most cases, there is a declined in the number 

of species present

Some General effects of pollution 

on an Ecosystem 

• Matter and Energy flow within the 

ecosystem changes 

• Removal of larger organisms with longer 

life spans 

• The appearance of opportunistic species 

with short life spans exhibiting large 

population fluctuations in time and 

space

What is an Endocrine 

Disruptor 

“An exogenous agent that interferes 

with the synthesis, secretion, 

transport, binding, action, or 

elimination of natural hormones in 

the body that are responsible for the 

maintenance of homeostasis, 

reproduction, development and/or 

behavior. “

Mechanisms of endocrine disrupting 

compounds 

1) Binding and activating the estrogen receptor 

2) Binding but not activating the estrogen 

receptor (therefore acting as an anti-estrogen) 

3) Binding other receptors 

4) Modifying the metabolism of natural 

hormones 

5) Modifying the number of hormone receptors 

in a cell 

6) Modifying the production of natural hormones

Hormone regulation and feedback control 

Estrogen levels depend on 

Estrodiol serum-binding proteins 

α-fetoprotein (AFP) 

Testosterone-estradiol binding globulin 

Xenoestrogens (ex. DES) 

100-fold lower affinity than E2 to these binding 

protein 

Bioavailability increased

Non-genomic mechanisms of ED 

action 

• Compounds of the azole type, such as 

ketoconazole and the fungicide fenarimol, 

inhibit these CYP isoforms and 

consequently can also affect steroid 

synthesis while the now-banned anti-fouling 

agent tributyltin and its metabolites, which 

have strong ED potential, are thought to act 

by the same mechanism, probably by 

inhibition of aromatase.

Genomic mechanisms of ED action 

• bind to oestrogen receptors and so act as 

pseudoestrogens in vivo, giving feminising effects 

• tamoxifen and diethylstilbestrol) and industrial 

chemicals (e.g. octylphenol and bisphenol-A 

• fungicide vinclozolin binds competitively to the 

androgen receptor (Shono et al., 2004), blocking 

the cellular actions of testosterone on androgendependent 

tissue growth and behaviour patterns 

• chlordecone, inhibit binding to the oestrogen and 

progesterone receptors (Guzelia, 1982), whereas 

bisphenol-A can block ligand binding to the thyroid 

receptor

Timing, duration, and amount of exposure. 

Organization vs. activation 

Timing, duration, and amount of exposure are each 

important determinants of the outcome. There are 

windows of vulnerability during fetal development in 

which small exposures to endocrine disruptors may 

have profound effects not observed in adults. 

Studies of the intrauterine position of mice during 

fetal development show that slight fluctuations of 

steroid hormone levels influence genital morphology, 

timing of puberty, sexual attractiveness, sexual 

behavior, aggressiveness, and activity level of 

offspring.

Various Classes of EDCs 

Flame Retardants 

Fungicides 

Herbicides 

Insecticides 

Metals 

Pharmaceuticals 

Phenols 

Plasticizers 

Polyaromatic 

Hydrocarbons 

Soy Products 

Surfactants 

Polybrominated diphenyl ether 

Vinclozolin 

Atrazine 

Methoxychlor 

Tributyltin 

Ethynyl Estradiol 

Bisphenol A 

Phthalates 

PCBs, dioxins 

Genistein 

Alkylphenol 

Ethoxylates

PBDEs( 多溴二苯基醚 ) 

• Polybrominated diphenyl ethers (PBDEs) 

are a class of recalcitrant and 

bioaccumulative halogenated 

compounds that have emerged as a 

major environmental pollutant. PBDEs 

are used as a flame-retardant and are 

found in consumer goods such as 

electrical equipment, construction 

materials, coatings, textiles and 

polyurethane foam (furniture padding).

Bioavailability of PBDEs 

‣Found in animals 

‣Increase in fish 

‣Increase in whales 

‣Sewage sludge 

‣PCBs Found in Lake Washington 

Fish (PBDEs next) 

‣Found in human (breast milk)

PBDEs Breast Milk - Sweden 

(Norén and Mieronyté, 1998)

Health Effects of PBDEs 

‣Similar to PCBs (Polychlorinated biphenyls) 

‣PBT (Persistent Bioaccumulative Toxicant) 

‣No human data 

‣Animals studies indicate 

‣Effects thyroid hormone levels 

‣Neurobehavioral toxicity 

‣Effects development - alters Behavior 

‣Impairs memory and learning 

‣Delays sexual development

Vinclozolin 

• Vinclozolin is a fungicide that has been 

shown to cause Leydig cell tumors and 

atrophy of the accessory sex glands in 

adult rodents. In addition, exposure of 

rats during pregnancy causes a pattern 

of malformations in the male urogenital 

tract . 

• Androgen receptor antagonist

Atrazine 

• A chlorotriazine herbicide, is used to control 

annual grasses and broadleaf weeds. 

• suppression of the luteinizing hormone surge 

during the estrus cycle by atrazine leads to the 

maintenance of elevated blood levels of 17betaestradiol 

(E2) and prolactin. 

• The mechanism for tumor development may 

include one or more of the following: the induction 

of aromatase (CYP19) and/or other P450 

oxygenases, an antagonist action at the estrogen 

feedback receptor in the hypothalamus, an 

agonist action at the mammary gland estrogen 

receptor or an effect on adrenergic neurons in the 

hypothalamic-pituitary pathway.

双酚 A 

Bisphenol-A 

BPA is used in the manufacture of 

polycarbonate plastics and epoxy resins from 

which food and beverage containers and dental 

materials are made. Perinatal exposure to 

environmentally relevant BPA doses results in 

morphological and functional alterations of the 

male and female genital tract and mammary 

glands that may predispose the tissue to earlier 

onset of disease, reduced fertility and mammary 

and prostate cancer

聚氯乙烯 (PVC) 

让长牙的婴儿咬玩得固齿器、洗澡玩得软性玩具、价格不贵的流 

行卡通玩具常常是 PVC 制品 , 在使用中可能释放出邻苯二甲酸 

(phthalates) 这类有致癌性的环境荷尔蒙。 

【安全替代品】仔细查看成分标示 , 凡是婴幼儿可能放在口中把 

玩的玩具一定选择 PE( 聚乙烯 ) 制品。 

苯乙烯 alkylphenol ( 烷基酚 ) 

摊贩、自助餐店、速食店的热饮杯 ( 装汤、茶、咖啡 )、方便 

面的面碗及面杯绝大多数都是使用聚苯乙烯 (polystyren) 的塑 

胶容器 , 简称 PS。其原料单体叫苯乙烯 , 是已知致癌物。并且 

制造过程所添加的增塑剂 alkylphenol( 烷基酚 ) 也是会干扰内 

分泌的环境荷尔蒙 , 二者在使用过程中很容易溶出到食物中。

化妆品中的环境荷尔蒙 

多数的化妆品、卸妆用清洁用品含有几类的环境 

荷尔蒙 : 

• 壬基苯酚乙烯 ( 一种非离子表面活性剂 ) 

• 邻苯二甲酸 (phthalates) 

• 烷基酚 (alkylphenol)

Tributyltin (TBT) 

三丁基锡是一种有机锡化合物 , 

常被添加于船舶油漆中 , 以防止贝类 

及藻类附着于船身 , 由于具有杀菌效 

果 , 所以也可以作为杀菌剂使用。

收到三丁基锡或三苯基锡污染的雌岩螺 , 因生殖孔阻塞受 

精卵无法排出 , 堆积在生殖管道内变红变黑形成坏死组织 , 

此时长出阴茎的雌化作用也同时引发。

许多生物对有机锡的代谢能力低 , 在低浓 

度长时间的污染下 , 负面效果即能呈现 , 有机 

锡累积在食物链顶端的鲸豚肝脏也普遍存在 

(up to 10 mg/kg)。鉴于有机锡污染对海域生 

态的威胁 , 全世界将禁止三丁基锡作为油漆添 

加物。 

此外 , 有机锡还有致畸胎作用。

Phthalates 邻苯二甲酸酯 

• 软化剂 , 广泛存在于化妆品、儿童玩具 

和食品包装袋中 

• 聚氯乙烯 PVC 制品在使用中可释放出邻 

苯二甲酸酯 

• male infertility 

• Interfere with cholesterol uptake and 

androgen biosynthesis

Alkylphenol( 烷基酚 ) 

• 聚苯乙烯制品制造过程中所添加的增塑剂 

alkylphenol( 烷基酚 ) 也是会干扰内分泌的环 

境荷尔蒙 disrupted reproduction in pikeperch 

• In juvenile fish a decrease in the percentage 

of males and an increase of intersex fish was 

observed in relation to dose of NP and time of 

exposure to this alkylphenol. 

• Exposure of adult males to the NP led to the 

reduction in fecundity, milt quality and fertility.

EDSTAC Tier 1 Assays 

Concerned with detecting 

• Receptor binding assays (ER and AhR) 

• Uterotrophic 

• Hershberger 

• Pubertal female 

• Steroidogenesis 

• Frog metamorphosis 

• Fish reproductive screen

EDSTAC Tier 2 

dose-response relationship 

• Mammal development and 

reproduction 

• Bird development and reproduction 

• Mysid shrimp life cycle 

• Fish reproduction and development 

• Amphibian development and 

reproduction

Species-dependent sex determination 

Mammal XY/XX 

synthesis of testosterone/functional androgen receptors 

estrogen receptor in the brain 

Birds WZ/WW 

The ability to synthesize and recognize 17β-estradiol is 

necessary for female CNS and gonadal sexual 

development to occur 

Reptile 

temperature-dependent sex determination (aromatase 

related)

Temperature-dependent sex determination 

thermosensitive period (TSP)

Temperature 

determines their 

sex. A nest 

temperature of 

73.5 degrees 

would develop 

males. If it heats 

up to 83.5, 

hormones would 

trigger changes 

causing the 

embryonic cells 

to differentiate 

as females.

III. Field studies 

Manipulative 

Observational (biomonitoring) 

This sections looks briefly at the field of microcosm 

and mesocosm toxicity testing. 

Microcosms - laboratory systems that are 

intended to physically simulate an ecosystem or a 

major subsystem of an ecosystem. They are an 

attempt to create systems that display ecosystem 

properties while permitting control of conditions and 

replication of treatments at reasonable cost.

There are two types of microcosms, assembled and 

excised. 

One of the more common assembled type is the aqutic 

microcosm developed by Taub (see Suter, 1993). This 

system consists of ten species of algae, five 

zooplankters (cladoceran, amphipod, ostracod, 

protozoan, and rotifer), and a bacterium in a defined 

aqueous medium with serile sand sediment all contained 

in gallon jar under fluorescent lights. The advantage of 

the system is that it is standardized, similar results can 

be achieved from different labs, researchers can 

compare results with different chemicals, and the limited 

and constant array of species makes it more likely that 

the cause of observed responses can be determined 

making it possible to model the ecosystem level 

interactions for extrapolation to the field. However, they 

are very much oversimplified.

Excised microcosms are segments of ecosystems that 

have been removed from the environment as a unit or a 

few units and placed in containers in the laboratory. 

They contain natural assemblages of biota, natural 

median and are more realistic. The are also less 

amenable to quality control and to comparisons. 

Examples include: 

•Mixed flask culture - mixed culture of microbes and 

microinvertebrates derived from one or more natural 

communities and held in the lab. 

•Pond microcosm - water, sediment, macrophytes, and 

associated biota obtained from a shallow pond or the 

littoral zone of a lake or slow-moving river 

•Site-specific aquatic microcosm - large tank of 

ambient water, a sediment core suspended in the water, 

and associated biota

Mesocosms - outdoor experimental systems that are 

delimited and to some extent enclosed. 

These systems offer more realism than microcosms due 

to their larger size and more natural physical conditions 

but can still provide replication, control of chemical 

exposure, and some control of biotic components. 

Mesocosm studies are currently a requirement for 

pesticide registration in the U.S. Mesocosms are also 

either assembled such as artificial ponds and streams or 

delimited such as limnocorrals and other enclosures of 

portions of an ecosystem.

Biomonitoring

生物監測 (Biomonitoring) 在歐洲國家於 20 世紀 

初首先使用藻類腐水指標系統監測水質 , 其後陸續 

建立底棲生物及魚類指標監測方法。一般河川水質 

監測只有分析水中理化參數 , 而忽略水中生物之存 

在與否。Loeb 及 Spacie(1994) 指出 , 水中生物 

因長期生活棲息之水中環境 , 任何外來物質刺激 

(Stress), 他們首當其衝 , 故他們才是最佳環境 

監測器。他們身體健康情況或存在與否 , 即是反映 

水質好壞。 

河川生物監測 

藻類評估水質使用之方法為藻屬指數 

底棲水生昆蟲使用之方法為科級生物指標及快速生 

物評估法 

魚類評估方法有魚類生物整合性指標法及魚類指標 

法

An Index of Biotic Integrity (IBI) is a tool (index) which 

we use to determine the health (integrity) of the fish 

community (biotic) in a given river. Webster's defines 

an index as "a ratio or other number derived from a 

series of observations and used as an indicator or 

measure". Biotic is defined as "of or relating to 

life". And integrity is defined as "the quality or state of 

completeness". 

The IBI examines three components of the fish 

community to determine its health. By knowing the 

abundance (total number of fish), the diversity 

(number of different species), and trophic (food chain) 

interactions, we get an idea of how healthy the fish 

community is in a given area.

Indicator species 

A species whose status provides information 

on the overall condition of the ecosystem and 

of other species in that ecosystem. 

Particular tolerant or sensitive to 

environmental contamination. 

Ex. Ephemeroptera, Plecoptera, and 

Trichoptera 

Biomarker responses to specific chemical 

are well characterized 

Accumulated environmental contaminants

Example 1 

• What will happen When Raw Domestic 

Sewage from a Sewered Community of 

40,000 people flows into a stream

Ecological Risk Assessment 

has three primary phases 

Problem formulation 

Analysis 

Risk characterization

•Data required to conduct an ecological risk 

assessment include the following: 

•Toxicity to wildlife, aquatic organisms, plants, an 

nontarget insects 

•Environmental fate 

•Environmental transport 

•Estimated environmental concentrations 

•Where and how the pesticide will be used 

•What animals and plants will be exposed 

•Climatologic, meterologic, and soil information

PART 5_2 Chemical contaminants and ecotoxicology

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