Multiple stressors

what is a stressor?

• stressor → it is anything that causes stress - a physiological or ecological disruption - to an organism, population, or an ecosystem

• examples of stressors:

  • temperature change

  • pollution

  • hypoxia

  • acidification

  • pathogens

  • fishing/predation risk

• organisms try to maintain homeostasis to combat against these stressors

• however stressors push organisms away from homeostasis causing a physiological cost

performance curve

• every organism has na optimal range where performance is highest (growth, survival reproduction). Outside this range, both low and high extremes cause stress

• drivers → a chemical or biological agent, environmental condition, external stimulus, or an event seen as causing a positive or negative change to an organism.

  • environmental factor that pushes organism toward optimal range

• stressor → a chemical or biological agent, environmental condition, external stimulus, or an event seen as causing stress to an organism

  • factor that pushes organism away from optimal range

• example: temperature

  • too low = stressor

  • moderate = driver

  • too high = stressor

stressors in marine systems

• marine organisms face many stressors simultaneously

• abiotic stressors:

  • temperature stress

  • heatwaves

  • salinity changes

  • acidification

  • hypoxia

  • nutrient loads

  • contaminants

  • microplastics

  • storms

  • browning (light reduction)

• biotic stressors:

  • predators

  • viruses

  • parasites

  • bacteria

  • invasive species

  • fishing pressure

• multiple stressors = abiotic + biotic combined

why multiple stressors matter

• stressor interactions produce different outcomes

• additive →

  • A + B = expected sum

  • if individually reduce performance by 20% and 10%, together it is 30%

• synergistic →

  • A + B = more than expected

  • 20% + 10% = 50% loss

  • bad news - most common in marine ecosystems

• antagonistic →

  • A + B = less than expected

  • a strong stressor overshadows the weaker one

  • sometimes caused by wrong null model (one can only die once)

the role of mechanism of action

• if stressors act on similar pathways → likely additive

• if stressors act on different pathways but linked pathways → likely synergistic

• if one stressor dominates → antagonistic

• stressors may interact at physiological, behavioural, and life history level

null models and expectations 

• a null model is a statistical prediction of what combined stressors should do if they don’t interact

• these models matter because

  • wrong null model → wrong conclusion

  • antagonism may be misclassified if organism already near max stress

bliss independence model

• this is used when stressors act independently

• it predicts combined effects using the formula

  • pAB = pA + pB - (pA x pB)

• this tells us if the observed effect is

  • additive (equal to observed value)

  • synergistic (lower than observed value)

  • antagonistic (higher than observed value)

cross tolerance

• cross tolerance → exposure to one stressor makes organism more resistant to another stressor

• some examples

  • heat shock → produces heat-shock proteins

  • these proteins also protect against osmotic shock (salinity)

• timing matter; needs recovery period

• mechanism must overlap; shared pathways

summary of interactive stressor effects

• interactions between stressors can be additive, antagonistic, and synergistic

• stressors acting through similar mechanisms may be additive, while those acting through alternative but dependent pathways may be synergistic

• sometimes it is difficult to detemrine what your expected null model is

• different assumptions can lead to different interaction categories

• one can only die oncce

• hardly / no cases where one actually gets better from being exposed to more stressors

timing of stressors 

• timing is critical

• if stressors act:

  • sequentially → effects can differ

  • simultaneously → effects combine

  • during sensitive windows (embryos, larvae) → stronger effect

levels of biological organisation

• stressor effects differ depending on the level:

  • individual level:

    • physiology

    • behaviour

    • reproduction

    • survival

  • population level:

    • growth rates

    • abundance

    • evolutionary tolerance

  • community level

    • species interactions food webs

    • competition predator prey dynamics

  • ecosystem level:

    • biodiversity

    • habitat strucutre

    • regime shifts

    • recovery dynamics

real ecosystem examples

• coral reefs: bleaching driven by temperature + light + acidification

• plankton: warming + nutrient changes alter food webs

• metals + predation risk → increased toxicity

• contaminats bioamplify differently across trophic levels

studying multiple stressors

• experiments

• mesocosms

• process based models

• data driven models

final summary

• stressors interact in complex, nonlinear pathways

• interactions depend on mechanisms, timing, scaling

• stressors can be classified into

  • abiotic and biotic

  • physical and chemical

  • natural and anthropogenic stressors

• stressors can directly or indirectly interact

• you can only die once → null model assumption matters

• real ecosystems = many stressors at once, not isolated

• lab experiments struggle to replicate natural complexity

• most often the stressors have antagonistic or synergistic effects

the papers

paper 1 - gunderson et al. (2016)

• organisms in the ocean are rarely exposed to a single stressor, instead they are exposed to multiple, co-occuring stressors such as

  • warming, hypoxia, acidification

  • salinity change

  • pollution

  • food availability

  • predators

• the paper argues that because stressors overlap, their combined effects cannot be predicted by single stressor studies

• stress and homeostasis

  • organisms try to maintain homeostasis (internal stability)

  • stressors push them away from homeostasis causing physical strain

• perfomance curves

  • every organism has →

    • an optimal range where performance is best

    • lower/higher extremes where performance drops (stress)

    • lethal limits (death)

  • this explains why different levels of the same stressor can help or harm them

• there are three types of stressor interactions

  • additive →

    • this is where the different stressor effects add up

    • this is the simplest, but least common

  • synergistic → 

    • there is a combined effect that is greater than expected

    • this is the most common effect and dangerous one because the effects multiply rather than add

  • antagonistic →

    • the combined effect is less than expected because one stressor dominates; organisms are already near their tolerance limit (one can only die once); or stressors interfere with each other

• if stressors act through the same physiological pathways, interactions are often additive

• if stressors act on different but connected pathways, interactions are often synergistic

• if one stressor overwhelms another, antagonism occurs

• interactions can occur at the physiological level, behavioural level, and/or life history level

• challenges identified in the paper:

  • lab studies usally test one stressor at a time, which does not reflect real-life conditions

  • stressors in nature vary over space and time

  • organisms may acclimate or adapt to timing, order intensity, and duration matter

  • null models (what you expect) determines how you classify an interaction

  • real ecosystems have many stressors, not just two

• multiple stressors iteract in complex, often unpredictable ways, and synergistic effects are common, which can amplify marine ecosystem impacts far beyond expectation

• prediction requires understanding mechanisms,timing, and biology, not just measuring stressors separately

paper 2 - przeslawski et al. (2015)

• the authors reviewd multiple stressor experiments and perfomred a meta analysis to test

  • how different stressor combination affect early life stages

  • which combinations are most harmful

  • which taxa are most vulnerable

• findings:

  • syngeristic effects were more common, meaning early life stages often respond much worse to combined stressors than predicted by single stressor studies

  • early life stages are extremely vulnerable. This is because they have/consist of/are:

    • undeveloped immune systems

    • limited energy reserves

    • poor acid-base regulation

    • thin or absent protective structures (shells, exoskeleton)

    • limited mobility, so they cant escape stress

    • this makes them bottlenecks for population survival

  • certain stressors are more harmful in combination. The strongest negative interactions were:

    • temperature x acidification

    • temperature x hypoxia

    • temperature x salinity changes

    • temperature seemed to always be involved as a synergistic amplifier

  • different taxa respond differently to stressors

    • the most sensitive ones were molluscs, and echinoderms (calcifiers) because calcification suffers under low pH

    • the most tolerant ones were crustacenas as they had a better acid-base and osmoregulatory control

  • the stressor intensity and timing affected the outcome. Small changes in the timing or intensity can completely change the interaction type

• overall, multistressor impacts on embryos and larvae are mostly synergistic, and common stressor combinations (warming + acidification + hypoxia) threaten early life stages and therefore entire marine populations and food webs

ASK JAN ABOUT THE BLISS MODEL INTERACTIONS