The observed in vivo effects thus always start at molecular level (molecular
initiating event, MIE, within the frame of an AOP concept), which may be either
specific (key-lock principle) through binding the toxicant to a specific place on
DNA or a protein (e.g., activation of estrogenic receptor by endocrine disruptive
compounds) or—more commonly—nonspecific, when the chemical does not have a
specific target and broadly interacts with diverse molecules in a biological system.
Key examples include accumulation of lipophilic molecules in the cell membranes
(narcotic or basal toxicity), which is inherited to all organic compounds including,
e.g., PAHs, BTEX, aliphatic hydrocarbons, or damage to biological molecules—
proteins, nucleic acids, phospholipids—caused by (pro)oxidative conditions.
It should also be understood that—depending on the actual situation—one
chemical may activate several different modes of actions, which could be of both
“specific” or “non-specific” nature. These events can occur and propagate in parallel
causing synergistic or antagonistic effects. For example, chromium(VI) may cause
direct damage to DNA (leading potentially to mutation and eventually tumor
development) but the same toxicant also activates intracellular repair systems,
which remove the potential risk of developing cancer by controlled death—apoptosis—of the affected cell. Similarly, simultaneous presence of zinc in the soil leads to
a decreased uptake of toxic cadmium to biota lowering thus its potential toxic effects
and hazards (Murtaza et al. 2017).
The outlined complexity increases when addressing the effects of complex
samples (chemical mixtures) such as contaminated water or soil, wastes, effluents,
etc. (Carvalho et al. 2014). In the exposed biota, many diverse and hardly predictable
events may occur simultaneously and are likely to be modulated by various components present within the sample. For example, the effects of pesticide
chloroacetanilide on earthworms highly differ depending on levels of H
+ (pH),
concentrations of ions, salts, or non-toxic metals; fragments of naturally present
dead organic matter (e.g., humic acids); and many small organic molecules like
peptides, aminoacids, nucleotides, phospholipids, DNA or RNA, etc. All the components—mentioned as an example—affect both bioavailability and effects of the
chemical on the studied organism (Hofman et al. 2014).
27.3 Principles of Ecotoxicity Testing
Despite the years of research, it is still difficult to reach the ultimate goal of
ecotoxicology, i.e., thorough understanding as well as predicting and protecting
populations in communities from the effects of environmental pollutants.
Researchers continue studying the complex systems and developing advanced
approaches such as mechanistic high-throughput chemical screenings in vivo, utilization of “omic” responses and biomarkers, computational in silico ecotoxicology,
or higher tier modelling of populations, communities, and ecosystems (Cao et al.
2017; Fernandez et al. 2011; Groth et al. 2016). However, such approaches are still
not ready to be used in practice. Therefore regulators, risk assessors, and
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L. Bláha and J. Hofman
initiating event, MIE, within the frame of an AOP concept), which may be either
specific (key-lock principle) through binding the toxicant to a specific place on
DNA or a protein (e.g., activation of estrogenic receptor by endocrine disruptive
compounds) or—more commonly—nonspecific, when the chemical does not have a
specific target and broadly interacts with diverse molecules in a biological system.
Key examples include accumulation of lipophilic molecules in the cell membranes
(narcotic or basal toxicity), which is inherited to all organic compounds including,
e.g., PAHs, BTEX, aliphatic hydrocarbons, or damage to biological molecules—
proteins, nucleic acids, phospholipids—caused by (pro)oxidative conditions.
It should also be understood that—depending on the actual situation—one
chemical may activate several different modes of actions, which could be of both
“specific” or “non-specific” nature. These events can occur and propagate in parallel
causing synergistic or antagonistic effects. For example, chromium(VI) may cause
direct damage to DNA (leading potentially to mutation and eventually tumor
development) but the same toxicant also activates intracellular repair systems,
which remove the potential risk of developing cancer by controlled death—apoptosis—of the affected cell. Similarly, simultaneous presence of zinc in the soil leads to
a decreased uptake of toxic cadmium to biota lowering thus its potential toxic effects
and hazards (Murtaza et al. 2017).
The outlined complexity increases when addressing the effects of complex
samples (chemical mixtures) such as contaminated water or soil, wastes, effluents,
etc. (Carvalho et al. 2014). In the exposed biota, many diverse and hardly predictable
events may occur simultaneously and are likely to be modulated by various components present within the sample. For example, the effects of pesticide
chloroacetanilide on earthworms highly differ depending on levels of H
+ (pH),
concentrations of ions, salts, or non-toxic metals; fragments of naturally present
dead organic matter (e.g., humic acids); and many small organic molecules like
peptides, aminoacids, nucleotides, phospholipids, DNA or RNA, etc. All the components—mentioned as an example—affect both bioavailability and effects of the
chemical on the studied organism (Hofman et al. 2014).
27.3 Principles of Ecotoxicity Testing
Despite the years of research, it is still difficult to reach the ultimate goal of
ecotoxicology, i.e., thorough understanding as well as predicting and protecting
populations in communities from the effects of environmental pollutants.
Researchers continue studying the complex systems and developing advanced
approaches such as mechanistic high-throughput chemical screenings in vivo, utilization of “omic” responses and biomarkers, computational in silico ecotoxicology,
or higher tier modelling of populations, communities, and ecosystems (Cao et al.
2017; Fernandez et al. 2011; Groth et al. 2016). However, such approaches are still
not ready to be used in practice. Therefore regulators, risk assessors, and
552
L. Bláha and J. Hofman