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Keywords:

  • Intermittent exposure;
  • Pulse;
  • Variable concentration

Abstract

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. APPROACHES FOR DETERMINING THE BIOLOGICAL EFFECTS OF EPISODIC STRESSOR EXPOSURE
  5. QUALITY AND QUANTITY OF EPISODIC TOXICITY DATA AVAILABLE IN THE SCIENTIFIC LITERATURE
  6. SUMMARY OF COLLATED INFORMATION BY EXPOSURE CHARACTERISTIC
  7. CHALLENGES TO INCLUDING EPISODIC TOXICITY DATA IN ENVIRONMENTAL WATER QUALITY MANAGEMENT
  8. SUMMARY
  9. Acknowledgements
  10. REFERENCES

Water quality monitoring tools that rely on data from stress-response tests with continuous exposure at constant concentrations are not always appropriately protective when stressor exposure in the field is episodic in nature. The present study identifies various approaches that have attempted to account for episodic stressor exposure, describes the development of a toxicological effects database of episodic stressor exposure collated from published scientific literature, and discusses whether any discernible trends are evident when these data are reviewed. The episodic stressor exposure literature indicated that few generalizations can be made regarding associated biological responses. Instead, when attempting to characterize the hazard of a certain episodic pollution event, the following situation-specific information is required: the specific species affected and its age, the specific stressor and its concentration, the number of exposures to the stressor, the duration of exposure to the stressor, and the recovery time after each exposure. The present study identifies four main challenges to the inclusion of episodic toxicity data in environmental water quality management: varying stressor concentration profiles, defining episodic stressor concentration levels, variation resulting from routes of exposure and modes of action, and species-specific responses to episodic stressor exposure. The database, available at http://iwr.ru.ac.za/iwr/download, could be particularly useful for site-specific risk assessments related to episodic exposures. Environ. Toxicol. Chem. 2012; 31: 1169–1174. © 2012 SETAC


INTRODUCTION

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. APPROACHES FOR DETERMINING THE BIOLOGICAL EFFECTS OF EPISODIC STRESSOR EXPOSURE
  5. QUALITY AND QUANTITY OF EPISODIC TOXICITY DATA AVAILABLE IN THE SCIENTIFIC LITERATURE
  6. SUMMARY OF COLLATED INFORMATION BY EXPOSURE CHARACTERISTIC
  7. CHALLENGES TO INCLUDING EPISODIC TOXICITY DATA IN ENVIRONMENTAL WATER QUALITY MANAGEMENT
  8. SUMMARY
  9. Acknowledgements
  10. REFERENCES

There are many circumstances in the aquatic environment in which toxicologically relevant temporal variation in physicochemical stress occurs at a scale less than the life span of the organism. Several terms have been used to describe fluctuating stressor exposure including: episodic, intermittent, pulse, plug, and spike. The present study uses the term episodic as a synonym for these different terms.

Aquatic biota experience two major types of episodic stress, one is excessive natural variation in water quality variables and the other is from anthropogenic pollutants. Examples of natural variation include fluctuations in physicochemical water quality (temperature, dissolved oxygen, pH, electrical conductivity, etc.) with season, rainfall, and time of day 1, 2. Episodic stressor exposure originating from anthropogenic activities can be because of accidental or deliberate releases of pollutants from the following four main sources: urban stormwater runoff, agricultural activities, sewage treatment works, and industrial activities 1. The concentration of pollutants in water resources will fluctuate depending on the quantity released in to the environment as well as the dilution rate and the potential degradation of the pollutant within the environment 3. The nature of the episodic stress is also dependent on whether the pollutant's entry in to the environment is from a point source or is diffuse in origin. The resultant episodic pollution is thus sometimes composed of a single stressor (e.g., a pesticide chemical), but most often it is a combination of various stressors (e.g., an effluent).

The application of traditional water quality monitoring and regulatory tools, which are most often derived from the results of controlled laboratory tests in which the test organisms are continuously exposed to constant stressor concentrations for a specified time span, have in certain circumstances 4–6 been shown not to be appropriately protective when stressor exposure in the field is episodic. The present study identifies the various approaches that have attempted to account for episodic exposure, describes the development of a toxicological effects database of episodic stressor exposure from data published in the literature, and discusses whether any discernible trends are evident when the collated episodic data are reviewed. Although the biological effects of episodic stressor exposure are also influenced by ecological factors (e.g., resilience rates of organisms within a community influencing ecosystem recovery 7), only toxicological factors are considered in the present study.

APPROACHES FOR DETERMINING THE BIOLOGICAL EFFECTS OF EPISODIC STRESSOR EXPOSURE

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. APPROACHES FOR DETERMINING THE BIOLOGICAL EFFECTS OF EPISODIC STRESSOR EXPOSURE
  5. QUALITY AND QUANTITY OF EPISODIC TOXICITY DATA AVAILABLE IN THE SCIENTIFIC LITERATURE
  6. SUMMARY OF COLLATED INFORMATION BY EXPOSURE CHARACTERISTIC
  7. CHALLENGES TO INCLUDING EPISODIC TOXICITY DATA IN ENVIRONMENTAL WATER QUALITY MANAGEMENT
  8. SUMMARY
  9. Acknowledgements
  10. REFERENCES

Defining an exposure is done in terms of its magnitude (the severity of the stress, e.g., stressor concentration), frequency (the number of exposure events), and duration (the time of the exposure event). The combination of these three factors makes the prediction of the effects of episodic toxicity exposure on organisms very difficult 8. An attempt to address episodic toxicant exposures utilizing data from traditional toxicity test methods was first proposed by the U.S. Environmental Protection Agency (U.S. EPA) 9 and was termed the two-number criteria system. The first criterion, derived from chronic toxicity data, was not to be exceeded as a 24-h average. The second criterion was a maximum or peak permissible concentration, derived from acute toxicity data, and could only be maintained for a duration, such that the 24-h average was not exceeded. Several studies designed to test the validity of the two-number criteria concept in Daphnia sp. and fish demonstrated that it did not consistently protect aquatic life 10. The two-number criteria approach has not been widely adopted owing to the lack of a sound basis for selecting the averaging period and the high frequency of monitoring required 10. Subsequent efforts to address episodic toxicant exposure have focused on two main approaches.

Experimental approaches

The first approach is the development of alternative toxicity test endpoints that attempt to incorporate the episodic nature of exposure to pollutants. For example, mortality can be compared with chemical accumulation in specific tissues of the test organism. This approach relies on the assumption that the contamination of the body tissue measured is the ultimate cause of death. However, fish have been shown to rapidly accumulate toxins after death 11, therefore, the time of death is an important consideration for correctly determining tissue residue data.

For the second approach, Handy 4 proposed the use of biochemical and physiological responses as alternatives with which to compare mortality data. However, the normal range of these types of responses is often very large, leading to uncertainty with regard to whether the measured responses are because of toxicity exposure or just natural variation and whether the response is an indicator of impairment or is just part of a homeostatic response indicating that the organism is successfully dealing with the exposure 12, 13.

Predictive model approaches

Predictive models use traditional constant exposure data to predict toxicity under episodic exposure conditions. Methods that integrate the fluctuating levels of a toxicant's concentration (such as deriving median lethal concentration [LC50]) have been shown to inadequately interpret the biological effects observed during these episodic exposures 3, 14. Consequently, much effort has been directed toward models that are capable of adequately representing the actual exposure concentration of the episodic event. Mancini 15 and Breck 16 created models using toxicokinetic equations to predict toxicant concentration at the site of action within the organism as a function of ambient or nominal concentration and uptake/clearance rates. Under varying ambient concentrations, body tissue residue levels of toxicants (controlled by the rates of toxicant accumulation and depuration or repair by exposed organisms) have shown the potential to adequately predict the levels of biological response 10, 15. These simple toxicokinetic models use data from classical bioassay tests obtained using constant toxicant exposures together with information regarding the accumulated dose of the toxicant in the organism to estimate probable effects of time-varying exposures to the toxicant. Butcher et al. 3 made adaptations by using the time history of response (hourly adjustments in mortality using numerical integration) instead of end-of-test net response (e.g., LC50) as an input to the model. In addition, they made use of variable kinetic response inputs (e.g., uptake and depuration rates varied with exposure concentration).

At present, the models do not show a good enough fit with observed biological effects to allow for use in a regulatory setting 17. For example, the kinetic model developed by Diamond et al. 17 described only 50 to 60% of the variability observed in the survival of fathead minnow Pimephales promelas exposed separately to copper and zinc, and Daphnia magna exposed to copper. Increasing the quantity of experimental data fed into the models may aid in reducing unexplained variability 3. Thus, at present, addressing episodic stressor exposure can be undertaken only in a site- or situation-specific manner by using a risk assessment type of approach 18. The success of this type of approach would depend on access to relevant episodic toxicity data, hence, the episodic toxicity database was developed.

QUALITY AND QUANTITY OF EPISODIC TOXICITY DATA AVAILABLE IN THE SCIENTIFIC LITERATURE

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. APPROACHES FOR DETERMINING THE BIOLOGICAL EFFECTS OF EPISODIC STRESSOR EXPOSURE
  5. QUALITY AND QUANTITY OF EPISODIC TOXICITY DATA AVAILABLE IN THE SCIENTIFIC LITERATURE
  6. SUMMARY OF COLLATED INFORMATION BY EXPOSURE CHARACTERISTIC
  7. CHALLENGES TO INCLUDING EPISODIC TOXICITY DATA IN ENVIRONMENTAL WATER QUALITY MANAGEMENT
  8. SUMMARY
  9. Acknowledgements
  10. REFERENCES

The database of toxicological responses to episodic stressors was developed to provide an accessible reference for water resource managers and scientists seeking to identify and manage the hazards of particular episodic stressors. The information could have applications in the ongoing refinement of predictive toxicokinetic models, ecological risk assessments, and development of water quality guidelines. The development of a database required the collection, assessment, and collation of applicable information.

Data collection

The search for available literature was undertaken between July and September, 2009, by searching the online scientific reference databases ScienceDirect, EBSCOhost, and SpringerLink using the keywords “episodic or pulse* OR periodic OR intermittent AND exposure” within the life sciences subject area, producing 8,952 hits. The archives of specific toxicology related journals were searched independently (Environmental Toxicology and Chemistry, Australasian Journal of Ecotoxicology, etc.) resulting in over 200 additional hits. The citations were downloaded to RefWorks database manager and titles were assessed for applicability, yielding 435 references with potential aquatic episodic toxicity information. The files of these references were downloaded, and after further assessment 112 were found to provide relevant episodic toxicity data.

Assessment of literature

Suitable references were assessed for the quality of the aquatic toxicity data by using the method refined by Hobbs et al. 19 for the Australian and New Zealand water quality guidelines. This method was used because it is the most recently developed data quality assessment scheme, is clearly described, and is objective and easily applied. Although not directly applicable to episodic toxicity data, the method does give an indication of the scientific rigor or the standards used to generate the data. All references included in the database were found to be of acceptable quality.

Database format

The database was designed to record as much pertinent information from the episodic references as possible. Information recorded included the type of stressor and whether it was tested singly or in combination with another stressor (e.g., a chemical concentration tested varying pH levels). The genus, species, common name, and age of the test organism were noted. Other information recorded included the following: exposure scenario (e.g., the stressor's concentration, pulse duration and frequency, interpulse period, postexposure recovery time, and stressor concentration profile); toxicity test location; experimental medium used and its water chemistry (e.g., pH, water hardness); any inferred chemical information that might affect the bioavailability of the toxicant (e.g., amount of ammonia in the water produced by the test organisms as a result of stocking density); the biological endpoint tested (e.g., mortality or reproduction); and the effect measured (no-observed-effect concentration [NOEC] or LC50, etc.). Finally, the results and any other pertinent information such as body burden information or toxicant mode of action, if stated, were summarized. The database is available from http://iwr.ru.ac.za/iwr/download/. Once downloaded, searches for specific information are possible (type of stressor, particular organism, etc).

SUMMARY OF COLLATED INFORMATION BY EXPOSURE CHARACTERISTIC

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. APPROACHES FOR DETERMINING THE BIOLOGICAL EFFECTS OF EPISODIC STRESSOR EXPOSURE
  5. QUALITY AND QUANTITY OF EPISODIC TOXICITY DATA AVAILABLE IN THE SCIENTIFIC LITERATURE
  6. SUMMARY OF COLLATED INFORMATION BY EXPOSURE CHARACTERISTIC
  7. CHALLENGES TO INCLUDING EPISODIC TOXICITY DATA IN ENVIRONMENTAL WATER QUALITY MANAGEMENT
  8. SUMMARY
  9. Acknowledgements
  10. REFERENCES

Characteristics of the episodic toxicity of six metals, 44 pesticides, four physical water parameters, and 27 other assorted stressors (Table 1) are summarized in the database. It is not possible to provide a summary of biological responses to each stressor here; however, an overview of discernible responses to particular characteristics of episodic stressor exposure is provided. Generally, increased harm to the organism was observed when the number of pulse exposures and the length of each pulse exposure were increased and when a decrease in the recovery time between pulses occurred. However, there were exceptions, most often caused by differences in the sensitivity of exposed organisms, probably as a consequence of morphological differences 20, that is, significant species- and age-related differences in the uptake and depuration rates of specific chemicals.

Table 1. List of stressors included in the online toxicity databasea
StressorNumber of references in databaseStressorNumber of references in database
PesticideMetal
  • a

    Some stressors were tested in combination, and this is indicated in the database.

Atradex (atrazine)2Aluminium3
Carbaryl3Arsenic1
Cartap1Cadmium8
Chloramine-T1Copper12
Chlorpyrifos7Selenium2
Creosote1Zinc6
Cyanazine1Physiochemical
Cypermethrin2Light1
DDT1Oxygen5
Diazinon2pH9
Dimethoate1Sediment3
Dinoseb1Others
Diquat117ß-Estradiol (E2)1
Diuron24-Nonylphenol (4-NP)1
Endosulfan1Ammonia4
Endrin1Chlorine (free residual)1
Esfenvalerate6Cyanide1
Fenitrothion1Discharged offshore oil and gas production water1
Fenoxycarb1Drought disturbance1
Fenvalerate8Estradiol (female sex hormone)1
Glyphosphate1Fluoxetine (antidepressant medication)1
Imazamox1Hydroquinone1
Imidacloprid2Monochloramine (disinfectant)1
Isoproturon2Nitric acid1
Lambda-cyhalothrin1Nitrite1
Malathion1N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)2
Methoxychlor4N-nitrosodiethylamine (DENA)1
Metsulfuran-methy1N-nitroso-N-methylurea (MNU)1
Paraoxon-methyl3p-Aminophenol1
Pendimethalin1p-Chlorophenol1
Pentachlorophenol (PCP)3p-Cyanophenol1
Permethrin2Phenol3
p-Hydroxyacetophenone1p-Nitrophenol1
p-Hhydroxybenzoic acid1Pretreated sewage water1
p-Hydroxybenzyl alcohol1Romet-30 (antibacterial drug)1
Pirimicarb1Salinity1
Propyzamide1Sodium chloride1
Simazine1Sodium pentachlorophenol (NaPCP)1
S-metolachlor1Thiocyanate (SCN-) (As KSCN)2
Terbuthylazine1  
Thiacloprid1  
Triclopyr butoxyethyl ester (TBEE)1  
Tripphenyltin hydroxide (TPTH)1  
Velpar L1  

Naturally, the magnitude of stress (concentration of the stressor) is the primary determinant of toxic effect. At low concentrations (below the threshold of effect level), recovery from exposure to the stressor was observed regardless of the number of pulses and the length of exposure. However, at higher concentrations, the complexity of episodic exposures (the relationship between the length of exposure and the number of pulses) became apparent. In the text that follows, time durations of 24 h or less are expressed in hours and durations greater than 24 h in days.

Effect of repeated pulse exposures

Increasing the number of pulsed exposures to a toxicant generally resulted in increased toxicant effects on the organism, probably because of a threshold tissue burden being exceeded. For example, Pynnonen 21 showed that repeated pulse exposures reduced the ability of freshwater clams (Anodonta anatina and Unio pictorum) to eliminate aluminium.

With exposure concentration kept constant, Diamond et al. 22 determined that the survival of P. promelas was significantly lowered when the number of copper pulses increased from one to two. In addition, the biomass of P. promelas was negatively correlated with the number of pulses 22. Although Bearr et al. 23 reported that P. promelas survival was not significantly different between the single- and the double-pulse treatments to copper (with 4 d of recovery time between), the addition of a third pulse (4 d after the second pulse) did result in a significant decrease in fish survival. A similar response was observed when Andersen et al. 24 exposed D. magna to dimethoate, an organosphosphate insecticide. After the first exposure pulse, recovery from immobility was seen for all pulse durations. However, after the second pulse, mortality occurred and increased significantly during the recovery period for pulse durations greater than 2 h.

Even if no mortalities occur as a result of increasing the number of pulse exposures, sublethal effects are sometimes significant. For example, in an experiment testing the effects of the exposure frequency of ammonia (eight or 24 pulses of 0.2–0.4 mg/L over a 53-d period) on brown trout (Salmo trutta), Milne et al. 25 recorded no mortalities. However, lower fish weights were recorded in some instances, and growth, gill condition, organ weights, and hematocrit were all significantly affected by repeated exposures, particularly at the higher exposure frequency 25.

Effect of the duration of the pulse exposure

Increasing the length of exposure to a cadmium pulse was found by Gama-Flores et al. 26 to reduce the population growth rate of cladocerans (Moina macrocopa) and rotifers (Brachionus calyciflorus). A similar response was observed for P. promelas biomass, which was negatively correlated with the length of copper pulse exposure 22. However, the relationship between exposure duration and biological effect can be complicated. Bearr et al. 23 report that P. promelas fry exposed to two copper pulses of 3, 6, or 24 h had significantly lower mortality than fry exposed to two pulses of 12 h in length, regardless of the recovery time between pulses. Bearr et al. 23 suggest that the 3- and 6-h exposure durations might have been too brief to elicit adverse effects on survival, whereas the 24-h exposure initiated acclimation of sorts in surviving organisms.

For D. magna, Hoang and Klaine 27 found that daphnids exposed to a single 4- to 24-h pulse of between 800 and 2,000 µg/L selenium showed no mortality during exposure but latent mortality postexposure, with mortality increasing with pulse exposure duration and exposure concentration. In the case of zinc, daphnids were more sensitive to 24-h pulses of 250 to 1,000 µg/L (with continued mortality even postexposure), whereas 3- to 6-h pulses at high concentrations resulted in no effects on daphnid survival or reproduction 8.

Effect of recovery time between pulse exposures

The literature indicated that longer recovery times between multiple exposure pulses led to greater survival in D. magna8 and amphipod (Hyalella azteca) 6 exposed to copper, and D. magna exposed to selenium 27 and zinc 8. A recovery period of at least 3 d between pulses of the organophosphate insecticide chlorpyrifos was necessary for daphnids to recover from a 0.5-µg/L pulse, while a longer recovery period of 4 d was necessary for a 1.0-µg/L pulse 28. Milne et al. 25 report that rainbow trout (Oncorhynchus mykiss) and S. trutta juveniles exposed to repeated pulses of potentially lethal ammonia concentrations were able to survive if enough time for recovery was allowed. However, it appears that if the length of exposure exceeds a certain duration or the stressor concentration exceeds a certain threshold, recovery time between pulses becomes irrelevant. For example, Naddy et al. 28 show that when daphnids were exposed to two 12-h pulses of 0.5 µg/L chlorpyrifos, >85% mortality was observed, regardless of the interval between pulse exposures, which was 0, 3, 7, or 14 d.

Bearr et al. 23 reported a more complex relationship between postexposure mortality and length of recovery between pulses. Pimephales promelas exposed to 24-h copper pulses of 30 to 40 µg/L had significantly higher mortality when pulses were spaced farther apart in time (to a threshold) than when pulses of the same magnitude were spaced more closely, that is, exposures having a 2- to 4-d recovery time between pulses resulted in less mortality than did treatments with shorter (12–24 h) or longer (5–6 d) recovery times 23. Diamond et al. 8 report on an experiment in which P. promelas's biochemical defense system was activated by copper exposure for approximately 2 to 4 d, after which it ceased if copper was removed from the media, leaving the fish susceptible to a new pulse.

Effect of organism age on toxicity of a pulse exposure

Hoang and Klaine 29 investigated the effects of a 12-h pulse of either arsenic, copper, selenium, or zinc on D. magna of various ages (3 h to 10 d old) and monitored the effects after 20.5 d of recovery. They found that the 21-d mortality increased with organism age from 3 h to 2 d and then decreased with age from 2 to 10 d for arsenic and selenium. For copper and zinc however, the 21-d mortality increased with organism age from 3 h to 4 d old and then decreased with age from 4 to 10 d. No difference in the 21-d growth was detected by the study for the metals tested. Reproduction was affected, however, with 21 d cumulative reproduction for arsenic decreasing with age from 3 h to 3 d old and then increasing with age from 3 h to 3 d. For copper and zinc, the 21-d cumulative reproduction decreased with age from 3 h to 4 d and then increased with age from 4 to 10 d, and for selenium, the 21-d cumulative reproduction decreased with age from 3 h to 2 d and then increased with age from 2 to 10 d. Hoang and Klaine 29 concluded that D. magna are particularly susceptible to these four metals at the time of first moulting and for a short period thereafter.

However, Andersen et al. 24 exposed D. magna aged <24 h and 3 d to a single pulse of dimethoate, an organophosphate insecticide, and found no significant difference in recovery based on age. In addition, Hosmer et al. 30 exposed D. magna of varying ages (<24 h, 4–6 d, 8 d, 11 d) to varying concentrations of the insecticide fenoxycarb and monitored effects for 21 d. There were no significant effects on survival or time to first brood of first- and second-generation daphnids in any age group at any exposure concentration.

Australian crimson-spotted rainbowfish (Melanotaenia fluviatilis) larvae were exposed by Reid et al. 31 to a 2-h cyanazine pulse at concentrations between 1.9 and 43.2 mg/L, and recovery was monitored for a further 94 h. Five age groups were exposed (0, 3, 6, 9, and 12 d posthatch). Toxicity was found to decrease with larval age. There was a considerable reduction in cyanazine toxicity between 0 and 3 d posthatch, with no further reduction in toxicity for 6-, 9-, and 12-d-old fish. The authors proposed this as evidence of hepatic xenobiotic metabolism, suggesting that the liver of larval rainbowfish becomes increasingly more functional with age. However, results could also be influenced by the greater respiration rates and small body surface area of smaller larvae 31.

Finally, Parker and McKeown 32 exposed eggs and alevin of Kokanee or Sockeye salmon (Oncorhynchus nerka) to a 24-h pulse of pH 4 and reported variation in sensitivity by developmental stage, the most sensitive stage being early embryonic development and newly hatched alevins. The most significant effect on survival and median hatching time was noted when the eggs were episodically exposed during early development, and exposure at later stages had no apparent effect on egg survival 32.

Consequently, when attempting to determine the hazard of an episodic pollution event, the specific situation must be investigated, that is, the specific affected species involved and its developmental stage, the specific chemical stressor (not just chemical grouping) and its concentration, and naturally, the number of pulses, length of pulse exposure, and recovery time between pulses.

CHALLENGES TO INCLUDING EPISODIC TOXICITY DATA IN ENVIRONMENTAL WATER QUALITY MANAGEMENT

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. APPROACHES FOR DETERMINING THE BIOLOGICAL EFFECTS OF EPISODIC STRESSOR EXPOSURE
  5. QUALITY AND QUANTITY OF EPISODIC TOXICITY DATA AVAILABLE IN THE SCIENTIFIC LITERATURE
  6. SUMMARY OF COLLATED INFORMATION BY EXPOSURE CHARACTERISTIC
  7. CHALLENGES TO INCLUDING EPISODIC TOXICITY DATA IN ENVIRONMENTAL WATER QUALITY MANAGEMENT
  8. SUMMARY
  9. Acknowledgements
  10. REFERENCES

A review of the literature detailed in the episodic toxicity database 33 indicated four main challenges to the inclusion of episodic toxicity data in environmental water quality management.

Varying exposure profiles

Temporal variation in toxicant concentration can be square, sinusoidal, or skewed 4, and these different profiles can elicit varying responses from exposed organisms 4 and greatly affect the method used to define the toxicants exposure concentration.

Defining episodic toxicant concentration levels

There is no standardized approach; some approaches that have been used include the mean test concentration, the mean exposure concentration, and the peak concentration 4. In addition, Morton et al. 18 describe a risk assessment approach that uses the area under the curve of the continuously fluctuating toxicant exposure to derive toxic exposure equivalents (akin to the hazard quotients regularly used in toxicology).

Routes of exposure and modes of action vary in chemicals

The responses of organisms to a toxicant are dependent on the characteristics of the chemical. As an example, a short (24-h) exposure to high concentrations of copper or ammonia to the water flea D. magna and P. promelas resulted in mortality during the pulse, but a cessation of mortality during the recovery period. However, the same short exposure of the same species to zinc resulted in continued latent mortality for 4 d of the recovery period 8.

Variable responses of organisms to episodic exposure

Physiological differences in response mechanisms to toxicant stress vary among organisms. For example, Diamond et al. 8 reported that D. magna survival was improved with increased recovery times between copper pulses, whereas P. promelas survival was significantly lower with copper pulses in excess of 4 d apart. These results are attributed to D. magna's control of copper toxicity by using the outer integument, which has limited ability to regulate the internal concentration of contaminants. As a result, the more closely spaced the pulses, the more likely the internal chemical accumulation will exceed the threshold level, resulting in mortality. For P. promelas, however, it is postulated that physiological response mechanisms to the copper exposure occur in the gills (e.g., induction of metallothioneins) and that the observed resistance of P. promelas to the copper exposure was activated for only 2 to 4 d, after which it was removed when the copper was removed from the media, leaving the fish susceptible to a new pulse of copper 8.

SUMMARY

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. APPROACHES FOR DETERMINING THE BIOLOGICAL EFFECTS OF EPISODIC STRESSOR EXPOSURE
  5. QUALITY AND QUANTITY OF EPISODIC TOXICITY DATA AVAILABLE IN THE SCIENTIFIC LITERATURE
  6. SUMMARY OF COLLATED INFORMATION BY EXPOSURE CHARACTERISTIC
  7. CHALLENGES TO INCLUDING EPISODIC TOXICITY DATA IN ENVIRONMENTAL WATER QUALITY MANAGEMENT
  8. SUMMARY
  9. Acknowledgements
  10. REFERENCES

The present study briefly reviews the various approaches used to account for toxicological effects of episodic stressor exposure, describes the development of a biological effects database of episodic stressor exposure data, and discusses broad discernible trends evident from the review of collated episodic data. A summary of the episodic toxicity data available in the literature for each of the stressors in Table 1 has been provided by Gordon et al. 33. The present study concludes with an identification of four main challenges to the inclusion of episodic toxicity data in environmental water quality management. The database may be particularly useful for site-specific risk assessments related to episodic pollution exposure.

Acknowledgements

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. APPROACHES FOR DETERMINING THE BIOLOGICAL EFFECTS OF EPISODIC STRESSOR EXPOSURE
  5. QUALITY AND QUANTITY OF EPISODIC TOXICITY DATA AVAILABLE IN THE SCIENTIFIC LITERATURE
  6. SUMMARY OF COLLATED INFORMATION BY EXPOSURE CHARACTERISTIC
  7. CHALLENGES TO INCLUDING EPISODIC TOXICITY DATA IN ENVIRONMENTAL WATER QUALITY MANAGEMENT
  8. SUMMARY
  9. Acknowledgements
  10. REFERENCES

Input from workshop attendees (P. Gola, N. Griffin, A. Holland, P. Mensah, N. Odume, A. Slaughter) is acknowledged, and contributions from the Department of Water Affairs and Resource Quality Services scientists S. Jooste and G. Cilliers are especially appreciated. Funding was provided by the Water Research Commission of South Africa.

REFERENCES

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. APPROACHES FOR DETERMINING THE BIOLOGICAL EFFECTS OF EPISODIC STRESSOR EXPOSURE
  5. QUALITY AND QUANTITY OF EPISODIC TOXICITY DATA AVAILABLE IN THE SCIENTIFIC LITERATURE
  6. SUMMARY OF COLLATED INFORMATION BY EXPOSURE CHARACTERISTIC
  7. CHALLENGES TO INCLUDING EPISODIC TOXICITY DATA IN ENVIRONMENTAL WATER QUALITY MANAGEMENT
  8. SUMMARY
  9. Acknowledgements
  10. REFERENCES
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