Temporal Patterns Of Risk Research Articles

Temporal variability, threat sensitivity and conflicting information about the nature of risk: understanding the dynamics of tadpole antipredator behaviour

The importance of temporal variability in predation risk has recently come to the forefront of research examining the behavioural ecology of predator–prey relationships. Temporal variability has been known to drive patterns of behavioural responses associated with foraging, reproduction and territorial defence of prey animals. We investigated whether larval woodfrog, Rana sylvatica, tadpoles learn to adjust the intensity of their antipredator responses to match (1) the temporal patterns of risk they experience throughout the day and (2) the risk level of a predator. We also examined how tadpoles incorporate temporally conflicting information on the risk posed by the predators. Our results indicate that tadpoles show dynamic adjustments in their behaviour, adjusting their response to predators according to the level of threat associated with the predator and the time of day at which the predator represents the most significant threat. Moreover, tadpoles responded to conflicting information by adjusting their response intensity depending on the nature of the change in vulnerability (whether the risk increased or decreased) and the time that the conflicting information was experienced (whether it was recent or old information). We discuss our results within the context of predator predictability in natural systems and game theory approaches to the behavioural response race between predator and prey.

Temporal patterns of predation risk affect antipredator behaviour allocationby Iberian rock lizards

Prey experience a broad range of temporal patterns of predation risk and may face different problems when assessing risk level and deciding how to allocate costly antipredator behaviour across time. We simulated in the laboratory repeated predatory attacks of different intensity (low versus high risk) to Iberian rock lizards, Iberolacerta cyreni, with similar numbers of low- and high-risk attacks across a trial, but with different temporal patterns of presentation (i.e. a series of low-risk and then a series of high risk, or vice versa, or successive attacks where risk changed randomly). We measured activity levels, time hidden in refuges after each predatory attack, and propensity to hide in refuges when the predator is close but not actually attacking (‘false alarm’ flights). Antipredator responses were of higher intensity when risk was high, but responses also depended on temporal patterns of risk. When previous attacks were of low-risk or when risk was random, prey activity did not change between risk levels. False alarm flights in the low-risk situation were more frequent when risk was random or immediately after a series of high-risk attacks. When successive attacks were of similar risk level, lizards seemed able to predict risk level in the next attack and modified their antipredator behaviour accurately. However, when risk level was random, lizards did not seem able to predict risk level and adopted a conservative strategy, overestimating risk even though costs of the antipredator responses increased.

Larval amphibians learn to match antipredator response intensity to temporal patterns of risk

The importance of temporal variability in risk has recently come to the forefront of research examining the behavioral ecology of predator–prey relationships. Temporal variability has been known to drive patterns of behavioral responses associated with foraging, reproduction, and territorial defense of prey animals. However, it is unknown if such behavioral responses are a result of selective depredation, which leads to innate temporal patterns of behavior, or, alternatively, are a result of learning by the prey. Here, we investigated whether larval wood frog (Rana sylvatica) tadpoles can learn to adjust the intensity of their antipredator responses to match the temporal patterns of risk they experience. Tadpoles were exposed to the odor of a predatory salamander paired with injured conspecific cues (salamander present and feeding) during the morning and received the salamander odor alone in the evening (salamander present but not feeding—morning risk treatment), whereas another group received the opposite treatments (evening risk treatment). The 2 groups were treated for 9 days. When subsequently exposed to salamander alone in the evenings, the tadpoles from the evening risk treatment responded with greater antipredator response intensity than the tadpoles from the morning risk treatment. This indicates that tadpoles have the ability to learn the change in predation risk they experience throughout the day and respond to such threats with an intensity reflecting their vulnerability to the predators.

BREEDING BEHAVIOR UNDER TEMPORAL RISK OF PREDATION IN MALE ROOT VOLES (MICROTUS OECONOMUS)

We examined breeding behavior responses of male root voles (Microtus oeconomus) to temporal risk of predation by using acute and chronic exposure to predator odor. The 2 series of exposure experiments provided 2 types of temporal patterns of risk: continuous safety with a brief period of risk and sustained risk with a brief period of safety. Male root voles that were acutely exposed to predator odor for 1 h suppressed their breeding behavior, but bred immediately after exposure to control odor for 1 h. Those chronically exposed to predator odor for 20 days maintained behavioral suppression during the 1-h period of exposure to control odor. Acutely exposed males did not change their physiological patterns of breeding, but those chronically exposed to predator odor had reduced testosterone concentration and epididymis index. Our results indicate that breeding behavior in a given situation depends on the overall patterns of risk experienced by male root voles, and the acute and chronic stress responses that affect reproduction are responsible for different behavioral responses to the 2 types of temporal patterns of risk. We also discuss the reasons for conflicting results about breeding suppression of voles between previous studies in the laboratory and the field.

Multistage models and the incidence of cancer in the cohort of atomic bomb survivors.

The analyses in this paper show that a number of biologically based models describe cancer incidence among the A-bomb survivors equally well. However, these different models can predict very different temporal patterns of risk after irradiation. No evidence was found to support the previous claim of Pierce and Mendelsohn that excess cancer risks for the solid tumors depend only upon attained age and not on age at exposure or time since exposure. Although the A-bomb survivor cohort is the largest epidemiological data set for the study of radiation and cancer, it is not large enough to discriminate among various possible carcinogenic mechanisms. Unfortunately for hypothesis generation, the data appear to be consistent with a number of different mechanistic interpretations of the role of radiation in carcinogenesis.

Ionizing radiation and cancer risk: evidence from epidemiology.

Ron, E. Ionizing Radiation and Cancer Risk: Evidence from Epidemiology. Radiat. Res. 150 (Suppl.), S30-S41 (1998). Epidemiological studies provide the primary data on the carcinogenic effects of radiation in humans. Much of what is known has come from studies of the atomic bomb survivors, and to a lesser extent from patients receiving radiotherapy. These studies demonstrate that exposure to moderate to high doses of radiation increases the risk of cancer in most organs. For all solid cancers combined, cancers of the thyroid, breast and lung, and leukemia, risk estimates are fairly precise, and associations have been found at relatively low doses (<0.2 Gy). Associations between radiation and cancers of the salivary glands, stomach, colon, bladder, ovary, central nervous system and skin have also been reported, but the relationships are not as well quantified. Associations between radiation and cancers of the liver and esophagus, and to a lesser extent multiple myeloma and nonHodgkin's lymphoma, have been reported in a few studies, but results are inconsistent. Chronic lymphocytic leukemia, Hodgkin's disease, and cancers of the pancreas, prostate, testis and cervix have rarely been linked to radiation exposure. A linear no-threshold model adequately describes the dose-response relationship for solid cancers, although at extremely high doses the risk appears to flatten out. Because few populations have been followed until the end of life, the temporal patterns of risk are not completely known. An increased risk, however, does continue for several decades. In contrast, radiation-related leukemias begin to occur shortly (2-3 years) after exposure and, at least in the A-bomb survivors, a linear-quadratic dose response seems to fit the data better than a pure linear model. Radiation does not act entirely in isolation. It can interact with other carcinogens, e.g. tobacco or chemotherapeutic agents, and with host factors such as age at exposure, gender or reproductive history. Interactions with medical interventions or with certain heritable mutations have also been suggested. While the studies of high-dose exposures are essential for understanding the overall biological consequences of radiation exposure, the public is more concerned about the long-term health effects from protracted exposures at low doses. Unfortunately, the inherent limitations of epidemiology make it extremely difficult to directly quantify health risks from these exposures. While most epidemiological data are compatible with linear extrapolations from exposures at high doses or high dose rates, they cannot entirely exclude other possibilities. As the field of epidemiology advances, understanding more about the health effects of prolonged and low-dose exposures will be the next

Prey responses to pulses of risk and safety: testing the risk allocation hypothesis

The risk allocation hypothesis predicts that prey responses to predation risk should depend on the temporal pattern of risk. In systems where activity is dangerous, predicted activity levels should be ranked as follows: activity during a pulse of safety>activity during continual safety>activity during continual risk>activity during a pulse of risk. We conducted the first experimental test of the basic predictions of the risk allocation hypothesis by examining responses of freshwater physid snails, Physa gyrina, to chemical cues associated with predation on snails by predatory crayfish,Orconectes juvenilis . As predicted, the snails' pattern of activity, microhabitat use and response to risk depended on the temporal pattern of risk. Snails held in continual risk had very low activity levels, but showed an immediate, large increase in activity during a brief period of safety. In contrast, snails held in continual safety showed moderate levels of activity, but surprisingly, only a weak reduction in activity when exposed to a pulse of danger. Further studies are needed to identify general patterns for how temporal variation in risk influences antipredator behaviour.

Does Risk of Nest Failure or Adult Predation Influence Hatching Patterns of the Green-Rumped Parrotlet?

Abstract Parent birds may adjust the onset of incubation to minimize periods of high risk of nest failure due to predation (the Nest Failure Hypothesis) or of mortality to adult birds (the Adult Predation Hypothesis). We examine temporal patterns of risk of nest failure and predation on adult females in a population of Green-rumped Parrotlets (Forpus passerinus) to determine whether those patterns explain observed patterns of incubation. Over one-third of nests (38.6%) failed completely, and an additional 2.2% failed after fledging one or more young. Most nests failed due to predation and infanticide. Because parrotlets begin incubation on the first egg, we examined a range of hypothetical failure rates for the period prior to the onset of incubation. Daily survival probabilities for nests were higher during the nestling stage than during incubation or fledging. Survival of adult females varied little through the nesting cycle, but was highest while attending nestlings. Model predictions were highly dependent on assumptions made about survival rates during the pre-incubation period. When empirically based values were used for this period, maximum productivity was achieved with first-egg incubation, consistent with observed patterns. Models were most sensitive to those parameters most difficult to estimate. This study represents the first test of the Nest Failure model with a nonpasserine or tropical species, and the first assessment of the Adult Predation model using field data.

DOES RISK OF NEST FAILURE OR ADULT PREDATION INFLUENCE HATCHING PATTERNS OF THE GREEN-RUMPED PARROTLET?1

Abstract Parent birds may adjust the onset of incubation to minimize periods of high risk of nest failure due to predation (the Nest Failure Hypothesis) or of mortality to adult birds (the Adult Predation Hypothesis). We examine temporal patterns of risk of nest failure and predation on adult females in a population of Green-rumped Parrotlets (Forpus passerinus) to determine whether those patterns explain observed patterns of incubation. Over one-third of nests (38.6%) failed completely, and an additional 2.2% failed after fledging one or more young. Most nests failed due to predation and infanticide. Because parrotlets begin incubation on the first egg, we examined a range of hypothetical failure rates for the period prior to the onset of incubation. Daily survival probabilities for nests were higher during the nestling stage than during incubation or fledging. Survival of adult females varied little through the nesting cycle, but was highest while attending nestlings. Model predictions were highly depen...

Leukemia after exposure to benzene: temporal trends and implications for standards.

Benzene is a human leukemogen. Risk assessment, and the setting of occupational and environmental standards, has assumed that risk is constant in time after a unit of exposure. Leukemia risk is known to vary with time after exposure to ionizing radiation. A matched case-control study of leukemia risk in relation to the temporal pattern of benzene exposures was performed using data from the National Institute of Occupational Safety and Health. Leukemia risk following exposure to benzene varied with time in a manner similar to that following exposure to ionizing radiation. More recent exposures were more strongly associated with risk than were more distant ones. There was no significant relation between leukemia death and benzene exposures incurred more than 20 years previously. Recent analyses of specific occupational and environmental carcinogens, including benzene and radon, have indicated that cancer risk tends to decline as the time from exposure increases. This suggests that standards for the control of occupational or public risk must be selected to control exposures over a narrower time frame than the usual lifetime one. In the case of benzene, it would appear that risk is attributable primarily to exposures incurred during the previous 10 to 20 years, with exposures in the most recent 10 years being the most potent. To limit risk, exposures must be controlled during that interval. It is important that epidemiologists explore the temporal pattern of risk in their studies to facilitate the risk assessment of other carcinogens.

The timing of academic difficulties among maltreated and nonmaltreated children

Objective: In this study we examined the relationship between child maltreatment and the timing of academic difficulties. Method: This study uses survival analysis to investigate the timing of risk of experiencing an academic difficulty for the first time. Three types of academic difficulties were examined—grade repetitions, poor English grades, and poor math grades. The sample included approximately 300 maltreated and 300 nonmaltreated children aged 5–18. Results: Maltreated children displayed greater risk than nonmaltreated children of repeating a grade and receiving a poor English and mathematics grade for the first time across most elementary years. Maltreated and nonmaltreated children share the same peaks in risk: first grade for their first grade repetitions and kindergarten for their first poor English and math grade. The best-fitting discrete time hazards models suggested underlying temporal patterns of risk vary according to the type of academic difficulty. For instance, maltreated children were at substantially higher risk than nonmaltreated children of repeating kindergarten and first grade. From second through sixth grade, maltreated and nonmaltreated children were indistinguishable in their risk of repeating a grade for the first time. In contrast, discrete-time hazards modeling showed that while the absolute risk of receiving a poor English or mathematics grade changes across the elementary years, the relative risk by maltreatment status does not. Conclusions: While maltreated and nonmaltreated children share the same peaks in risk, the relative risk changes across time for grade repetitions but not for the first occurrence of a poor English or mathematics grade. In summary, this study highlights the importance of time in understanding the relationship between child maltreatment and academic difficulties.

Ionizing Radiation and Cancer Risk: Evidence from Epidemiology

Epidemiological studies provide the primary data on the carcinogenic effects of radiation in humans. Much of what is known has come from studies of the atomic bomb survivors, and to a lesser extent from patients receiving radiotherapy. These studies demonstrate that exposure to moderate to high doses of radiation increases the risk of cancer in most organs. For all solid cancers combined, cancers of the thyroid, breast and lung, and leukemia, risk estimates are fairly precise, and associations have been found at relatively low doses (<0.2 Gy). Associations between radiation and cancers of the salivary glands, stomach, colon, bladder, ovary, central nervous system and skin have also been reported, but the relationships are not as well quantified. Associations between radiation and cancers of the liver and esophagus, and to a lesser extent multiple myeloma and non-Hodgkin's lymphoma, have been reported in a few studies, but results are inconsistent. Chronic lymphocytic leukemia, Hodgkin's disease, and cancers of the pancreas, prostate, testis and cervix have rarely been linked to radiation exposure. A linear no-threshold model adequately describes the dose-response relationship for solid cancers, although at extremely high doses the risk appears to flatten out. Because few populations have been followed until the end of life, the temporal patterns of risk are not completely known. An increased risk, however, does continue for several decades. In contrast, radiation-related leukemias begin to occur shortly (2-3 years) after exposure and, at least in the A-bomb survivors, a linear-quadratic dose response seems to fit the data better than a pure linear model. Radiation does not act entirely in isolation. It can interact with other carcinogens, e.g. tobacco or chemotherapeutic agents, and with host factors such as age at exposure, gender or reproductive history. Interactions with medical interventions or with certain heritable mutations have also been suggested. While the studies of high-dose exposures are essential for understanding the overall biological consequences of radiation exposure, the public is more concerned about the long-term health effects from protracted exposures at low doses. Unfortunately, the inherent limitations of epidemiology make it extremely difficult to directly quantify health risks from these exposures. While most epidemiological data are compatible with linear extrapolations from exposures at high doses or high dose rates, they cannot entirely exclude other possibilities. As the field of epidemiology advances, understanding more about the health effects of prolonged and low-dose exposures will be the next challenge.

Repeat victimization among adolescents and young adults

Prior research has shown that victimization incidents are disproportionately concentrated among relatively few victims and that prior victimization is a consistent predictor of future risk. This paper expands existing knowledge on victimization by describing temporal patterns of risk and by developing and testing alternative explanatory models of the link between past and future risk. Analyses based on panel data from the National Youth Survey support both state dependence and heterogeneity interpretations of the correlation in risk over time. In other words, prior victimization predicts future risk in part because it alters something about the individual, and because it indicates an unmeasured propensity for victimization that persists over time. The theoretical implications of these findings, including the feasibility of a victim labeling perspective, are discussed.

Cancer Incidence in Atomic Bomb Survivors. Part III: Leukemia, Lymphoma and Multiple Myeloma, 1950-1987

This paper presents an analysis of data on the incidence of leukemia, lymphoma and myeloma in the Life Span Study cohort of atomic bomb survivors during the period from late 1950 through the end of 1987 (93,696 survivors accounting for 2,778,000 person-years). These analyses add 9 additional years of follow-up for leukemia and 12 for myeloma to that in the last comprehensive reports on these diseases. This is the first analysis of the lymphoma incidence data in the cohort. Using both the Leukemia Registry and the Hiroshima and Nagasaki tumor registries, a total of 290 leukemia, 229 lymphoma and 73 myeloma cases were identified. The primary analyses were restricted to first primary tumors diagnosed among residents of the cities or surrounding areas with Dosimetry System 1986 dose estimates between 0 and 4 Gy kerma (231 leukemias, 208 lymphomas and 62 myelomas). Analyses focused on time-dependent models for the excess absolute risk. Separate analyses were carried out for acute lymphocytic leukemia (ALL), acute myelogenous leukemia (AML), chronic myelocytic leukemia (CML) and adult T-cell leukemia (ATL). There were few cases of chronic lymphocytic leukemia in this population. There was strong evidence of radiation-induced risks for all subtypes except ATL, and there were significant subtype differences with respect to the effects of age at exposure and sex and in the temporal pattern of risk. The AML dose-response function was nonlinear, whereas there was no evidence against linearity for the other subtypes. When averaged over the follow-up period, the excess absolute risk (EAR) estimates (in cases per 10(4) PY Sv) for the leukemia subtypes were 0.6, 1.1 and 0.9 for ALL, AML and CML, respectively. The corresponding estimated average excess relative risks at 1 Sv are 9.1, 3.3 and 6.2 respectively. There was some evidence of an increased risk of lymphoma in males (EAR = 0.6 cases per 10(4) PY Sv) but no evidence of any excess in females. There was no evidence of an excess risk for multiple myeloma in our standard analyses.

Estimation of temporal effects in treatment-induced second cancer.

Cancer chemotherapy has been remarkably successful in the treatment of several types of malignancies, but has also been demonstrated to cause leukaemia and perhaps other cancer in long-term survivors. Radiotherapy also carries a carcinogenic risk. A large case-control study of second cancer has been carried out, with the aim of quantifying the risk due to chemotherapy and radiotherapy. One of the most important goals of this study is the estimation of the temporal pattern of risk following chemotherapy. Methods are presented for modelling risk as a function of type of treatment and the interval since treatment. The methods are applications of generally available linear regression programs for epidemiological data, and could be equally well applied to studies of occupationally induced cancer.