Stresses for Trainee Counselling Psychologists | Review

Stresses for Trainee Counselling Psychologists | Review Title: A critical commentary on the following research paper: Kumary, A Martyn, B. (2008) Stresses reported by UK trainee counselling psychologists. Counselling Psychology Quarterly, March; 21:19-28 The prospect of entering any postgraduate training program can often be intimidating. Not only due to the academic commitment required, but because of the emotional demands and potential financial stranglehold placed on a student. These issues alone can leave trainees in both counselling and related psychological professions vulnerable to stress, which can not only damage the well-being of the student, but lower the overall quality of care experienced by patients when trainees are on placement (Cushway Tyler 1996; Kumary Baker 2008). Kumary Martyns make the simple argument, based loosely around Crushways (1992) study of UK clinical psychology trainees, that there are key aspects of training that impact on self-reported stress levels. These included poor supervision, financial costs, childcare, personal therapy and extra supervision. Some of these stressors identified cannot be thought of as essential or necessary aspects of training but this in itself is an area of key debate. (Kumary et al 2008). Other research has also highlighted the same key issues within counselling (Szymanska 2002), but has only looked at one issue in isolation and with this in mind, the present study was an investigation of UK counselling psychology trainees self-reports of their experiences of stress when training. One might go as far to question the rational of any study examining potential stress within such professions considering that having gone through an undergraduate degree already, students are already accustomed to a moderate l evel of stress and it simply goes with the territory (Cooper Quick 2003). On the other hand, such a study has never been conducted and may produce compelling results. Subjects were easy to identify and obtain although only UK counselling trainees who were studying for Part 1 of the BPS diploma were recruited. Are we to assume that this is when stress levels are at an optimal level? Questionnaires were sent out to all institutions. While the general characteristics of the sample are well represented, there was only a 41% return rate. This is good, but not outstanding in comparison to research conducted in similar domains, despite numerous follow-up e-mails and telephone calls (Robertson Sundstorm 1990). A financial incentive might have improved this return rate, but pre-paid return envelops were provided. However this data was collected in 2003, but not submitted for publication until 2007. Ethically, this delay in analysis and publication produces results that are already four years out of date in an education system that is constantly evolving (Hadley et al 1995). While such a simple methodology may initially seem sound, on closer inspection, the differences between the training programs of clinical and counselling are only glossed over and there is some evidence to suggest that the disparity between the two hinder a repetition of a seemingly straightforward approach last consulted in 1992 by Cushway. Aside from the time lapse, it is therefore important to consider the other issues surrounding the modification of a methodology previously used to investigate stress in clinical trainees. Firstly, counselling psychologist training tends to be less scientifically orientated than its clinical counterpart and most NHS posts are only open to Clinical Psychologists (Mayne, Norcross Sayette 2000). For example, it is generally accepted that counselling psychologists focus more on the therapeutic alliance with clients having to complete 450 hours of contact by the end of 3rd year training (Hadley et al 1995). While there are considerable similarities between the two disciplines, Norcorss (2000) documents many salient differences including professional activities, theoretical orientations, employment and training settings, graduate admissions and research areas. The question what are the differences in training clinical and counselling psychologists? -does not lend itself to an easy answer because psychology can be applied in so many ways. Traditionally, the main difference is in their training and perspective (Mayne et al 2000). It would appear to be an oversight on Kumary et als (2008) part to use a similar, modified methodology, previously applied to clinical trainees when the stress causing factors may be quite different. With these differences outlined in more detail, the old methodology would appear to require a more radical modification or adaptation from that used previously. Two main instruments were used to examine stress within the sample. The Counselling Psychology Trainee Stress Survey (CPTSS) and The General Health Questionnaire (GHQ12) (Wemeke, Goldberg Yalcin 2000). The CPTSS was developed from Cushways (1992) stress survey for clinical psychology trainees with four categories (academic stressors, placement stressors, organizational stressors and personal stressors). What is concerning is the lack of both research confirming the validity of the measure and the small brainstorm session using five trainees under those headings. Furthermore, from their discussion the CPTSS, constructed from 36 items, was only piloted on a further six trainees. This did lead to some changes being made with the authors settling on four descriptive categories slightly different from Cushways; academic demands, lack of support systems, placement stressors and personal and professional development. This displays neither convergent or discriminant validity. Finally, despi te other more valid forms of questionnaires available measuring stress (for example the Psychological Stress Measure (PMS), this study chose one which was quickly devised from a brief investigation and remains untested in the general population (Lemyre Tessier 2003; Trovato et al 2006). The General Health Questionnaire (GHQ12) on the other hand has been specifically validated for use in non-psychotic populations (Wemeke et al 2000). Because it is a shortened, 12-item version of the GHQ, it allows for quick completion, is likely to increase participant response, is quick to code and statistical mistakes also become less likely. For the purposes of this study, it appears to be the ideal choice and has been used to great effect in a large body of pervious work (Winefield, Goldney, Winefield, Tiggemann 1989; Vaglum Falkum 1999; Quek, Low, Razack, Loh 2001). A recent review by Jackson (2007) however, pointed out that the 28 item is usually used because the GHQ28 has been more widely used in other working populations, which allows for better comparisons, but the reliability coefficients have ranged from 0.78 to 0.95 in numerous studies and Jackson concludes (2007, p. 57) that: ‘In using this tool with postgraduate students conducting research in many areas of occupational health, the GHQ rarely fails to provide reliable and effective measures of well-being that usually correlate very highly with other measures of working environments or organizations Regardless of how carefully survey data is collected and analyzed, the value of the final result depends on the truthfulness of the respondents answers to the questions asked. Over the last twenty years, researchers have debated extensively about the truthfulness of peoples self-reports, and no clear cut conclusion has emerged (Zechmeister, Zechmesiter, Shaughnessy 2001). If someone is asked whether or not they enjoyed their bath, there is generally no need to question whether this accurately reflects their real feelings. However, in everyday life there are some situations in which researchers should have reason to be suspect. Survey research involves reactive measurement because respondents know that their responses are being recorded. Pressures may be strong for people to respond as they think they should rather than what they actually feel or believe (Zechmeister et al 2001). The term used to describe theses pressures is social desirability and in Kumary Martyns study (2008) the se issues are present in their entirety (Zechmeister et al 2001). For example, a trainee counselling psychologists attitudes towards their own stress and health levels, may be a far cry from their actual stressful behavioural responses. Both the questioners administered rely solely on self report and this gives rise to some further criticism. The approach is straightforward, but there is a trade-off between allowing for a simple analysis and the complex use of questionnaires in any survey based study. It is a fine balance that is difficult to maintain. Self-report questionnaires are all answered at different times and in different locations by each subject. As a result, the measures are vulnerable to inaccuracies caused by confounding variables. For example, a trainee filling in a stress based measure might have just had a particularly stressful day or experience that will effect their score. They could even have exams in a few weeks. Alternatively, reporting the issue of time-management and stress may be meaningless when the respondent evidently has time to sit down and take part in such a study anyway. The results from any self report also lack directness. While there is no ideal direct measure of stress, it is possible to get a better indication by measuring some of the physiological effects in the body. For example, stress might be better measured via heart rate, blood pressure, breathing rate, brain waves, muscle tension, skin conductance or temperature (Lemyre et al 2003). While more costly, such a study could be replicated using skin conductance monitors, worn by trainee counselling psychologists and correlate daily activities with any changes. This might produce results documenting what aspects of the course give rise to more stress and allow for re-development and changes to be applied where necessary. A more elementary approach might be to use an electronic pager device which asks every hour, how stressed are you now and what are your currently doing? In summary, researchers and clinicians must be careful when adapting clinical tools and methodologies to assess stress. They were designed for pathological disorders and validated using clinical populations and so the statistical distributions are not normal (Trovato et al 2006). As Lemyre et al (2003, p. 1159) state: The concept of stress refers to a set of affective, cognitive, somatic and behavioral manifestations within the range of functional integrity Despite this, thirteen items from the CPTSS were identified as being the most stressful issues in the sample population (none came from lack of support), which were split into two groups. The first included practical issues of finding time, funds and suitable placements. One item was also linked with negotiating these three key areas and could have a subsequent impact on their social life. A second group comprised of more general postgraduate issues: academic pressure and professional socialization. In order to determine a basis for the four groupings within the 37 single items of the CPTSS they were employed as four sub-scales (academic, placement, PPD and lack of support). These also gave acceptable levels of reliability. (Kumary et al 2008). The authors also found some good evidence for demographic variants in stress, with significantly higher stress ratings reported by younger participants and lower for those who were older. The GHQ12 results were in two scoring forms casesness and extend of distress with 54 participants identified as cases had significantly higher CPTSS scores than the 39 non-cases. Key findings from Kumary et al (2008, p. 24) included: The higher the stress rated for an aspect of counselling psychology training, the clearer the indicators of psychiatric distress became older participants had lower CPTSS ratings especially on placement issues men reported lower CPTSS ratings, most notably on academic items The support items attracted less attribution in comparison to academic, placement and PPD issues, despite pilot discussions (Kumary et al 2008), suggesting again that the methodology behind this study was flawed from the start. This does to some extent mirror Cushways (1992) data in that support was viewed by participants as a resource to ease training-induced stress, and participants viewed it as a resource to be used rather than a cause of stress because it was insufficiently provided. Again, with this knowledge available at the outset, why was the same methodology used? At this point, one might mention the issue of correlation and how this does not imply causation, but no profile of a stressed student was possible because most of the results were not significant. The authors admit themselves that the data collected is nothing to be proud of (2008, p. 25). It is difficult to believe that Krumary et al (2008) did not clearly see the unsophisticated and non-standardized status of the CPTSS as a serious issue before conducting such a study particularly when compared with more experimental research methods (Lemyre et al 2003). It is possible that the measures used were not sensitive enough to pick up on individual stress differences between participants. The fact remains however, that the fundamental assumptions were wrong and the question remains, do trainees in professions such as clinical and counselling psychology experience more stress than those within the normal population and if so are such emotional demands a critical part of training? Should t rainees be exposed to unacceptable stress levels and their apparent resilience used as an assessment criterion of professional suitability? (Hadley Mitchell 1995) The basis of this study is not sound enough to warrant any overall generalizations within the target population. The approach was oversimplified at the expense of generalized, poor-quality results. In this sense, the study has contributed little to our knowledge into how trainee counselling psychologists experience stress. The lack of an original approach is a reminder of how academic journals vary in the quality of the research they publish. It is nevertheless important that it was published to illustrate a methodology that clearly failed and thus prevents further repetition. This is the constant winding road of modern applied psychological research. References Cooper, L. C., Quick, C. J. (2003). The stress and loneliness of success. Counselling Psychology Quarterly, 16, 1-7 Cushway, D. (1992). Stress in clinical psychology trainees. British Journal of Clinical Psychology, 31, 169-179 Cushway, D., Tyler, P. (1996). Stress in clinical psychologists. British Journal of Clinical Psychologists, 31, 169-179 Goldberg DP, et al. (1978) Manual of the General Health Questionnaire (NFER Publishing, Windsor, England). Hadley Mitchell (1995). Counselling Research and Program Evaluation. London: Brooks/Cole Publishing Company Jackson, C. (2007). The General Health Questionnaire. Occupational Medicine, 57, 79 Kumary, A Martyn, B. (2008). Stresses reported by UK trainee counselling psychologists. Counselling Psychology Quarterly, 21,19-28 Lemyre, L., Tessier, R. (2003). Measuring psychological stress concept, model and measurement instrument in primary care research. Canadian Family Physician, 49, 1159-1160 Mayne, T. J., Norcross, J. C., Sayette, M. A. (2000). Insiders guide to graduate programs in clinical and counseling psychology (2000-2001 ed). New York: Guilford. Norcross C. J. (2000) Clinical Versus Counselling Psychology: Whats the Diff? Eye on Psi Chi, 5 (1), 20-22 Quek, F. K, Low, Y. W., Razack, H. A., Loh, S. C. (2001). Reliability and validity of the General Health Questionnaire (GHQ-12) among urological patents: A Malaysian study. Psychiatry and Clinical Neurosciences, 55 (5), 509-513 Robertson, M. T., Sundstrom, E. (1990). Questionnaire design, return rates, and response favorableness in an employee attitude questionnaire. Journal of Applied Psychology, 75 (3), 354-357 Szymanska, K. (2002). Trainee expectations in counselling psychology as compared to the reality of the training experience. Counselling Psychology Review, 17, 22-27 Trovato, M. G., Catalano, D., Martines, G. F., Spadaro, D., DI Corrado, D., Crispi, V., Garufi, G., Nuovo, S. (2006). Psychological stress measure in type 2 diabetes. European Review for Medical and Pharmacological Sciences, 10, 69-74 Vaglum, P., Falkum, E. (1999). Self-criticism, dependency and depressive symptoms in a nationwide sample of Norwegian physicians. Journal of Affective Disorders, 52 (1-3), 153-159 Wemeke, U., Goldberg, D., Yalcin, I. (2000). The stability of the factor structure of the General Health Questionaire. Psychological Medicine, 30, 823-829 Winefield, R. H., Goldney, D. R., Winefield, H. A., Tiggemann, M. (1989) The General Health Questionnaire: Reliability and Validity For Australian Youth. Australian and New Zealand Journal of Psychiatry, 23 (1), 53-58 Zechmeister, S. J., Zechmesiter, B. E., Shaughnessy, J. J. (2001). Essentials of Research Methods in Psychology, McGraw-Hill Higher Education Schizophrenia: the biological and psychological effect Schizophrenia: the biological and psychological effect The study of psychosis has been much published within the literature. Investigations into the biological, psychological and clinical aspects of the disorder have been greatly seen. An approach which views schizophrenia as a disturbance of information processing appears promising as a way of linking all of the aspects of the disorder. A review of the research in this area led to the suggestion that the basic disturbance in schizophrenia is a weakening of the influences of stored memories of regularities of previous input on current perception. It is argued that the link between information processing disturbances and biological abnormalities may be facilitated by the use of paradigms derived from animal learning theory (latent inhibition and Kamins blocking effect). In a number of animal model studies and indeed human subject studies, on an individuals pattern of performance in acute schizophrenics, the information gained is consistent with the cognitive model. The ways in which such an information-processing disturbance may lead to schizophrenic symptomatology will thus be outlined, with particular reference to the formation and maintenance of delusional beliefs. The core cognitive abnormality may result from a disturbance in any of the brain structures involved in the prediction of subsequent sensory input. The proposed circuit implicates in particular the hippocampus and related areas and is consistent with studies of brain pathology in schizophrenia. Thus, this paper will aim to provide an insight into the biological and psychological effects of schizophrenia and will give an insight into the current treatments available and their effects on the individual and their biological status. Introduction Understanding the varied presentation of the many types of psychotic disorders is still a major challenge within todays scientific capacity. The approaches utilized to clarify their complex nature of such disorders of the neurological system present an ongoing challenge, due to the complexity of the interaction between both biological entities (the brain) and the psychological effects. Thus, the aim of this paper is to review the evolution of our understanding of schizophrenia in terms of the biological and psychological effects of the disorder, based upon a review of the literature findings. Studies, which have been conducted regarding the life-long evolution of mental illnesses, especially schizophrenia, have been publicized for decades and this has managed to initiate the early standing of schizophrenia and of the nature of its chronic states. These experiences have further contributed to the views we hold today regarding the illness, leading in a third phase to the development of a biological-psychosocial model of its evolution which has proved useful for both theoretical and practical purposes. Finally, an understanding of therapeutic experiences and theoretical explorations based on the biological and psychological has helped to minimize the effects of the disease within the patient population. Biological basis of schizophrenia Across the findings within the literature, the question of whether schizophrenia is associated with structural or functional abnormalities of the nervous system, or both, appears to have become the principal focus in many of the biological studies of schizophrenia. A number of different methods of investigation of this system have been conducted including computed tomography studies, which have been able to reveal ventricular enlargement and cortical atrophy in a subgroup of schizophrenic patients. When such enlargement is found within the brain of the majority of patients in the early stages of the illness, they appear to be most severe in patients with negative symptoms and poor outcome. Quantitative neuropathological studies have tentatively demonstrated decreased volume of specific brain areas, neuronal loss, and other changes in the limbic system, basal ganglia, and frontal cortex. Dopamine (DA) remains the neurotransmitter most likely to be involved in schizophrenia, although t here is also evidence for disturbances of serotonin and norepinephrine. Post-mortem and positron emission tomographic studies suggest an increased number of D2 DA receptors in some schizophrenics. Neuroendocrine studies reinforce the role of DA in schizophrenics. Viral infections and autoimmune disturbances may be responsible for some types of schizophrenia, but there is no firm experimental evidence to support either hypothesis. The possibility that mixtures of structural abnormalities and functional changes involving DA occur in the same patients rather than independently as part of two syndromes (Type I, II) seems attractive. The symptoms of schizophrenia patients appear to be diverse, with different elements of the disease having different impacts on different individuals. Since Bleulers (1950) conception of the schizophrenias as a heterogenous disease composed of symptomaticlly different subgroups, attempts have been made to identify biological correlates of specific behavioral dysfunction. Diagnosis of the illness could be seen to have been fraught with difficulties. The initial lack of differentiation between the manic episodes of bipolar affective disorder and schizophrenia still presents as being greatly problematic within studies published within the literature, and subsequent attempts to differentiate between subgroups of schizophrenics have yielded no discrete classification system. The search for an etiology has also been bedeviled by this lack of distinct classification. Nevertheless, the publication of and the conduction of a number of biological theories have contributed to an understanding o f schizophrenia by identifying specific dysfunctional neural areas in determining biochemical changes associated with symptomatology and in formulating new etiological hypotheses. Neurological correlation between neurological studies and the effects of schizophrenia have been examined by research conducted through the use of magnetic resonance imaging, computed and positron emission tomography, and, also postmortem morphological changes (Koning et al, 2010). Studies of cognitive function in association with metabolic and cerebrovascular activity have contributed to the identification of discrete neural dysfunction. In addition, development of the dopamine theory and its relationship to positive symptoms has assisted in diagnostic differentiation, while recent studies on the modulatory role of neuropeptides on neurotransmitters have expanded the scope of the dopamine theory. Several biological theories have been proposed for an etiology of schizophrenia. (Krabbendam et al, 2004) Perinatal complications and viral infection have been suggested either in isolation or in conjunction with genetic factors. Low birth weight has also been proposed as a predisposing or associated factor in the subsequent development of schizophrenia. The viral hypothesis has received impetus from recent research into retroviruses capable of genetic transmission and causing latent disease onset. It is also recognized that factors other than biological, in particular, Psychosocial influences may play an etiological role in schizophrenia. Discussion of these factors, however, will not be discussed in great detail in this paper due to time restrictions. The difficulty of diagnosis As etiological studies rely to a large extent on accurate diagnosis, it is important initially to identify diagnostic problems because this aids an understanding between the interplay between biological and psychological effects, which can be noted in schizophrenics. It has long been recognized that the term schizophrenia incorporates a heterogeneous collection of subgroups, possibly with different etiologies, disease processes, and outcomes. The subsequent categorization of such patients into meaningful groups therefore relies upon differences in symptomatology and long term outcome, and fall broadly into three categories- paranoid versus nonparanoid, negative versus positive, and chronic versus acute (Goldstein Tsuang, 1988) The literature proposes that paranoid groups show a better premorbid adjustment, cognitive performance, and prognosis than the nonparanoid group (Kumra and Schulz, 2008), it has been suggested that this represents a measurement artifact and depends on whether absolute or relative measures of paranoia are used. Studies using absolute predominance measures to the exclusion of other symptoms reject many subjects displaying both sets of symptoms. Many nonpredominance studies show no differences between the groups of an increase in negative outcome as paranoid symptoms increase. Other researchers have proposed that schizophrenics could be categorized into two types placed into their category upon the basis of positive or negative symptom preponderence. Type I, or the positive symptom group, display some of the Schneiderian first rank symptoms of hallucinations and delusions, while Type 2, or the negative symptom group, show affective loss or extinction, speech content poverty, psychomotor deficits, and a general loss of drive or will. One of the problems with this categorization is that many schizophrenics display both sets of symptoms and that schizophrenics with primary positive symptoms often develop negative symptoms over time (Phillips and Silverstein, 2003). This would mean that studies using young subjects showing predominantly Positive symptoms may not be adequately differentiating between groups. Recent refinements of the positive/negative dichotomy have led to a redefinition of negative symptoms congruent with familial genetic factors, developmental dys- function, and the development of psychometric scales to measure relative symptomatology (Pickett-Schnenk et al, 2006). However, the influence of neuroleptic drugs on attentional and extrapyramidal functioning could also contribute to the development of differential symptoms. Furthermore, the effects of early environmental factors, such as perinatal trauma and familial environment, and of concurrent disorders, such as depression, are not adequately taken into account in such studies. Thus, this highlights the difficulties, which can be seen when trying to relate the biological and psychological effects of schizophrenia to a certain pathological aspect of brain development. Within the Diagnostic and Statistical Manual of Mental Disorders (DSM-III-R; APA, 1987) chronicity is defined as persistence of disturbance for more than two years with further residual diagnosis if subsequent symptoms are primarily negative. It is assumed to be associated with negative symptoms within Crows typography (Crow, 1980). This classification is the most common in the literature because of its basis in psychiatric diagnosis and its relationship to poor prognosis and to biological and cognitive deficits. For the purpose of biological research, the argument appears to be somewhat circular however because, for example, research attempts to find biological correlates of subgroups that are often operationally defined by their biological correlates. Moreover, there is significant overlap between the two groups in that many initially acute schizophrenics subsequently become chronic (by definition). While researchers across the literature publications acknowledge the heterogeneity of the disease, they continue to rely operationally on a dichotomous diagnosis. Multiple research strategies on the same subgroup would assist in isolating behavioural and biological attributions and in refining diagnostic criteria. Biochemical research and the impact on our understanding of the effects of schizophrenia Disruptions of neural biochemical processes have been extrapolated both from the effects of psychomimetic drugs and from the actions of symptom-reducing neuroleptic drugs. Drugs such as amphetamine and L-dopa, which cause psychotic conditions (e.g., hallucinations and paranoia), are known to involve excesses of dopamine release (Goodwin, 1972). Although different classes of neuroleptics are known to block acetylcholine, noradrenaline, or serotinin transmission, all of them block dopamine, and symptom reduction is thought to emanate from the latter (Millar et al, 2001). Within the dopamine theory two models of dysfunction have been proposed: autoreceptor excess, and postsynaptic receptor mechanism deficit. Different classes of neuroleptics vary in whether action is pre- or postsynaptic, but an inhibition of dopamine transmission is effected by all classes. Two classes of dopamine receptors have been identified-D1 and DP as previously mentioned, and it is believed that they are related to schizophrenia and neuroleptic effects. Distinctions between the two are based upon their actions on adenylate cyclase: stimulatory for Dl and distinct or inhibitory for D2 (Murray et al, 2008). Dl neurons, which project from the substantia nigra to the corpus striatum, are implicated in Parkinsons disease. Inhibition of Dl receptors is believed to be the origin of neuroleptic side effects, such as tardive dyskinesia and parkinsonianism. D2 receptors are associated with the antipsychotic effects of neuroleptic drugs and form the mesolimbic dopamine system which projects to the frontal cortex and some limbic forebrain structures (Tseng et al, 2008). The proposition that schizophrenic symptoms are caused by an excess of D2 receptors was initially difficult to substantiate due to drug effects and disease process. In most postmortem studies showing higher densities of dopamine receptors, previous antipsychotic drug use is also implicated (Seeman, 1986). However, in several studies subjects had never been treated with neuroleptics and still evinced increased dopamine receptor density (Trower et al, 2004). The role of dopamine receptor anomalies has also been studied using differential effects of classes of neuroleptics on dopamine receptors. In vivo Positron Emission Tomography (PET) research using the ligand [Cl raclopride has indicated that diverse classes of neuroleptic drugs administered in clinically effective doses block D2 dopamine receptors in the putamen. suggesting increased D2 dopamine density in schizophrenic subjects (Thompson et al, 2001). Research on the role of the atypical neuroleptic, clozapine, on dopamine receptors has however yielded inconsistent results. It is thought that the relative absence of extrapyramidal side effects with clozapine administration is due to a selective effect on D2 dopamine activity in the ventral tegmental area and nucleus accumbens but not in the substantia nigra or striatum. Haloperidol, on the other hand, reduces dopamine activity in both areas. The effects of both drug classes have been observed in rats using in vivo extracellular sing le-unit recordings (Tseng et al, 2009). However, clozapine also acts antagonistically on cholinergic, a-adrenergic, his- tamine, and serotonin receptors and, in addition, the combination of haloperidol with the a-noradrenergic antagonist, prazosin, produces similar effects to clozapine administration, namely, reduced basal dopamine release in the striatum but not in the nucleus accumbens (Thimm et al, 2010). Studies on cerebrospinal fluid (CSF) levels of prolactin following clozapine administration have also yielded inconsistent reslults. Prolactin release is inhibited by dopamine and increased by conventional neuroleptics. However, in at least one study it has been found that administration of clozapine to human schizophrenic subjects produced no significant increase in prolactin levels 11 hours after administration, despite moderate to marked therapeutic effects (Meltzer, Goode, Schyve, Young, Fang, 1979). Several recent studies have also implicated Dl receptor blocks in the therapeutic effects of clozapine. A further obstacle to the initial acceptance of the dopamine theory has been the time discrepancy between drug administration and antipsychotic symptomatic effects. PET studies have shown immediate binding to dopamine receptor sites, yet their clinical effect is often delayed for several weeks (Tarrier et al, 1999). There have been suggestions that receptors blocks produce an initial overactivity of dopamine release to compensate for inhibition. Further evidence for the dopamine theory has come from measurements of CSF, and plasma levels of the dopamine metabolite, homovanillic acid (HVA). Although findings in unmedicated patients have not yielded consistent differences in HVA levels between schizophrenics and controls, neuroleptic treatment increases HVA levels (Abubaker et al, 2008). In unmedicated patients, a correlation between low HVA levels and cortical atrophy and ventricular enlargement has been found in at least one study. This has led to the suggestion that dopamine excess is related to Type 1 schizophrenia, an interpretation which is supported by a good response to neuroleptic drugs in this group (Crow, 1985). In addition, Allen et al (2008) has suggested a possible deficiency of dopamine in Type 2 schizophrenics. However, the Type l-Type 2 typography has not been fully supported, and there is evidence that neuroleptic drugs elicit response in negative symptom sufferers (Allen et al, 2008). From the evidence there is little doubt of the biological role of dopamine within some forms of schizophrenia. The influence of serotonin in schizophrenia was suggested by the antagonistic activity of the psychomimetic drug, D-lysergic acid diethylamide (LSD), on serotonin transmission (Addinton and Addington, 1993). This has been studied in CSF by measuring levels of the serotonin precuresor, tryptophan, and the metabolite 5- hydroxyindole acetic acid (5-HIAA). At least one study has found reduced levels of 5-HIAA in schizophrenics and no difference between those on and off neuroleptics, but the latter group had only been drug free for a short time (three weeks). Therefore residual effects cannot be discounted. It was not stated whether subjects were also suffering from depression, which is known to decrease serotonin levels (Akbarian and Huang, 2009). Neither increasing nor decreasing serotonin levels have had a beneficial effect on schizophrenic symptoms (Akbarian and Huang, 2009). Monoamine oxidase (MAO) metabolizes dopamine, serotonin, and noradrenaline, as well as endogenous stimulants or hallucinogens such as phenylethylamine and diethltryptamine. It has therefore been hypothesized that decreased MAO activity could be contributory to schizophrenia. Studies have been conducted into platelet MAO activity in schizophrenics with varying results. Meltzer and Arora (1980) found that decreased MAO platelet activity was positively correlated with paraniod and positive symptoms. Other studies have found no un- usual MAO platelet activity in paranoid or hallucinating schizophrenics (Arts et al, 2008) Recent research has also considered the role of neuro-peptides in modulating CNS functions and the possible implications for schizophrenic symptomatology. Endorphins have been the subject of the most intensive study because of their association to proposed neural deficit areas both in biochemical and neuropathlogical research. The B, y, and (Y endorphins originate in the basal hypothalamus and modulate neurotransmitter activity in several structures of the limbic system and brain stem. Of all the biochemical theories of schizophrenia, the dopamine hypothesis has been the most consistently substantiated in research. The implication of other neurotransmitters, however, suggests a possible diffuse dysfunction with dopamine eliciting the most severe disruption. Efforts have been made to control for medication, but residual drug effects cannot be discounted. Many studies now use chlorpromazine equivalents to control for the effects of varying medication levels. The problem with this method is that, although different classes of neuroleptics all reduce dopamine levels either pre- or postsynaptically, they do not have equivalent effects on serotonin, MAO, or noradrenalin. Further problems are encountered when attempts are made to ascribe an etiological function to neurotransmitter activity. It is equally probable that any such changes are caused by the disease process rather than their being causal. Structual brain abnormalities The neuropathology of schizophrenia has received considerable recent interest in the light of positron emmission tomography (PET), postmortem, cognitive function and cerebral blood flow (CBF) research. While PET scans and postmortem investigation have concentrated on structural measurements, cognitive studies have provided tacit support for such structural changes. It has been hypothosized that neuropathological abnormalities identified in subgroups of schizophrenics could be in vitro developmental disorders either genetically transmitted or resulting from prenatal trauma (Ashburner et al, 2008). The most consistent findings across the publications within the literature have been differences in ventricular size, in some sections of the temporal limbic and nigrostriatal systems and basal ganglia, and in the prefrontal cortex. Measurements of ventricular size have however, shown considerable inconsistency, with some studies finding no significant difference between subjects and non-schizophrenic controls (Bles et al, 2010), and some reporting significant differences between chronic paranoid and hebephrenic subjects and normal controls (Bales et al, 2010). Evidence to date suggests that ventricular enlargement is only salient for a small subgroup of schizophrenics subject to chronicity or other, as yet unidentified, factors. Inconsistency in the results could be due to deviations in subject samples. It has been proposed that atrophy of specific neural areas could account for some schizophrenic symptoms. While some evidence has come directly from postmortem studies. Abnormalities have also been inferred from the results of PET and CAT scans and CBF measurements performed in conjunction with cognitive tasks designed to activate specific neural areas. Postmortem studies have identified significant cortical atrophy in the lateral nigro-striatal area (Birchwood et al, 2004) and in the limbic portions of the temporal lobe, specifically the amygdala, hippocampus, and parahippocampal gyrus (Birchwood et al, 2004). Psychotherapies and social treatments The psychological effects and impacts of schizophrenia must be emphasized. Due to the impact of the different, aforementioned parts of the brain and the CNS in schizophrenia, the psychological impact of the disease is obviously one, which takes great effect as previously mentioned. Psychotherapies are thought to be important within the current treatment lines in schizophrenia and although antipsychotic medications are the mainstay of treatment for schizophrenia, pharmacotherapy alone produces only limited improvement in negative symptoms, cognitive function, social functioning and quality of life. Additionally, it has been found that a great number of patients continue to suffer from persistent positive symptoms and relapses particularly when they fail to adhere to prescribed medications. This underlines the need for multi-modal care including psychosocial therapies as adjuncts to antipsychotic medications to help alleviate symptoms and to improve adherence, social functioning and qu ality of life (Patterson and Leeuwenkamp, 20008). A short review of the evidence that has accumulated on the efficacy of the major modalities of psychosocial treatment highlights that treatments involving social skills training, psychoeducation and cognitive behavioural therapies (CBTs) can all have a role in the treatment of individuals with schizophrenia. The reasoning behind the success of each treatment can give guidance into the psychological effects of the disease. For example, Psychoeducational interventions provide information about the disorder and its treatment to patients and their family members, and additionally inform the patients and family members about strategies to cope with schizophrenic illness. From the literature findings, it is evident that an extensive body of literature has accumulated regarding the efficacy of these interventions. Meta-analyses suggest that these interventions reduce high expressed emotion among relatives, and decrease relapse and rehospita lization rates (Pitschel et al, 2002; Giron et al, 2010). In general, interventions that include family members are found to have a much greater level of success (Pharaoh et al, 2006). Multi-family psychoeducation group approaches, which provide family psychoeducation and additionally offer an expanded social network, are found to reduce rates of relapse as are peer-to-peer education programs for families and patients (Chien et al, 2006). Cognitive Behavior Therapy (CBT) About a third of patients with schizophrenia continue to suffer from persistent psychotic symptoms despite adequate pharmacotherapy. Cognitive Behavior Therapy (CBT) has therefore been presented as a system of treatment which has emerged to address this need, and is based on the hypothesis that psychotic symptoms such as delusions and hallucinations stem from misinterpretations and irrational attributions caused by self-monitoring deficits. CBT seeks to help patients rationally appraise their experience of disease symptoms and how they respond to them, thereby reducing symptoms and preventing relapse (Turkington et al, 2008). Meta-analytic evaluations of this data have found CBT to be effective in ameliorating positive symptoms (Rector and Beck, 2001) although effect sizes of CBT have been noted to be inconsistent across studies and a recent meta-analysis of six blinded studies (Lynch et al, 2010) found CBT to be ineffective in reducing any symptoms of schizophrenia or in preventing relapse; the fairness of this analysis has been questioned (Kingdon et al, 2010). CBT is reported to be ineffective in targeting negative symptoms and its effects on other treatment domains are not well studied. Although CBT is recommended as a standard of care for persons with schizophrenia (NICE, 2009) the results are thought to give the best outcomes in patients who are willing to comply with treatment. Cognitive remediation A substantive proportion of schizophrenia patients have impaired cognition, particularly in the domains of psychomotor speed, attention, working memory and executive function, verbal learning and social cognition. These deficits are robust and persist during the illness, and serve as rate limiting factors for functional recovery (Tandon et al, 2009). Several cognitive remediation approaches have been developed over the past two decades which involve compensation strategies to organize information, use of environmental aids such as reminders and prompts, and a range of techniques designed to enhance executive function and social cognition (Eack et al, 2010). Earlier reviews and meta-analyses which have been presented and published within the literature findings have suggested that cognitive remediation leads to modest improvements in performance on neuropsychological tests but has limited generalization to functional outcomes (Pilling et al, 2002) One large meta-analysis published by McGurk et al, (2007), however, found that cognitive remediation was associated with significant improvements in cognitive performance and symptoms, as well as psychosocial functioning in schizophrenia. Cognitive remediation has been found to be more effective in studies that provided adjunctive psychiatric rehabilitation in addition to cognitive remediation. Thus, it appears to be the case that the durability of benefits of cognitive remediation are not yet set in stone. Social skills training (SST) Schizophrenia patients manifest deficits in social competence and these contribute to poor outcome. The goal of SST is to improve day-to-day living skills by focusing on components of social competence such as self-care, basic conversation, vocational skills, and recreation. These skills are practiced mostly in group settings using techniques based on operant and social learning theory. Historically, token economy was the first such intervention that sought to improve the social behavior of patients with psychiatric illness. While effective, the results did not generalize beyond the therapeutic setting. A recent meta-analysis of randomized controlled trials of social skills training in schizophrenia showed a large effect size for improvement in skills, a moderate effect size for performance-based social and community skills and for community functioning, and a small effect size for symptoms and relapse (Kurts and Mueser, 2008) Conclusions Thus, in conclusion, and in review of the findings published within the literature, it si clear that the impact of both biological aspects of the disease and psychological impacts are prevalent within the schizophrenic population. In summary, research on psychosocial approaches to treatment of schizophrenia has yielded incremental evidence of efficacy of CBT, SST, family psychoeducation, ACT and supported employment. Relatively few rigorously conducted trials of psychosocial interventions have been reported in the early course of schizophrenia, a phase of the illness when effective interventions may yield long-term outcome benefits . More hypothesis-driven research is needed to examine active ingredients of the therapeutic modalities that work, to identify the synergistic effects of combinations of interventions, and to use the knowledge which we have gained from the biological impact of the disease and the understandings of the neurological circuitry and its implications in schizoph renia to aid the development of new methods of reducing the effects of schizophrenia on the patient population.

The English Peasant Uprising Essay -- British History

The English Peasant Uprising was motivated by a growing contempt with the government and clergy following the Black Death which was finally set off by a series of immediate social and economic causes. A shortage of workers followed the Black Death with an estimated forty-five per cent of the population dying in England . As entire towns were either deserted or left devoid of life, rural peasants increased their mobility into major cities. This shortage of rural workers led to famine as fields were left to go fallow, placing further economic pressure on the peasant classes who survived as the price of food increased. Due to the lack of labourers, the labourers who survived demanded greater wages as they now had increased leverage over employers. This ultimately led to economic inflation due to the increased labour cost to the upper classes. This was met with resistance from King Edward III and parliament, who issued the Ordinance of Labourers 1349 and the Statute of Labourers 1351 in an attempt to fix workers’ rates to that of before the Black Death and prohibit an increase in wages beyond pre-established limits . This put great stress on the peasantry as they were forced to work throughout famine for greater hours for limited pay under inflated prices and seeded an antipathy for the government. The general attitude towards the Church as an institution was also responsible for the English Peasant Uprising. At this time, the Church was still a major landowner with almost 60% of English land held by the Church . However, 40% of priests and monks died to the Black Death and the shortage of ecumenical authorities lead to good wages offered for people to step into the clergy . This lead many people unsuited to the roles of religious... ...ts Revolt of 1381. Bath: Pitman. pp. 373. Joint action against `Bad' lordship: The peasants' revolt in Essex and Norfolk. Russell, Josiah Cox (1948). British Medieval Population. Albuquerque: University of New Mexico Press. Henderson, Ernest F. (__) Select Historical Documents of the Middle Ages The Great Revolt of 1381 Anonimalle Chronicle: The English Peasants' Revolt of 1381 Charles Oman, The Great Revolt of 1381 , (Oxford: Clarendon Press, 1906), pp. 200-203, 205 England in the Aftermath of the Black Death GOOGLE BOOKS The English Rising of 1381 'The Peasants Revolt', in The Medieval Reader, edited by Norman Cantor (New York: Harper Collins, 1994), 284-93. E.B. Fryde, The Great Revolt of 1381, London: The Historical Association, 1981, 5-33 Peasant road to capitalism Peasant Politics and Class Consciousness: The Norfolk Rebellions of 1381 The English Peasant Uprising Essay -- British History The English Peasant Uprising was motivated by a growing contempt with the government and clergy following the Black Death which was finally set off by a series of immediate social and economic causes. A shortage of workers followed the Black Death with an estimated forty-five per cent of the population dying in England . As entire towns were either deserted or left devoid of life, rural peasants increased their mobility into major cities. This shortage of rural workers led to famine as fields were left to go fallow, placing further economic pressure on the peasant classes who survived as the price of food increased. Due to the lack of labourers, the labourers who survived demanded greater wages as they now had increased leverage over employers. This ultimately led to economic inflation due to the increased labour cost to the upper classes. This was met with resistance from King Edward III and parliament, who issued the Ordinance of Labourers 1349 and the Statute of Labourers 1351 in an attempt to fix workers’ rates to that of before the Black Death and prohibit an increase in wages beyond pre-established limits . This put great stress on the peasantry as they were forced to work throughout famine for greater hours for limited pay under inflated prices and seeded an antipathy for the government. The general attitude towards the Church as an institution was also responsible for the English Peasant Uprising. At this time, the Church was still a major landowner with almost 60% of English land held by the Church . However, 40% of priests and monks died to the Black Death and the shortage of ecumenical authorities lead to good wages offered for people to step into the clergy . This lead many people unsuited to the roles of religious... ...ts Revolt of 1381. Bath: Pitman. pp. 373. Joint action against `Bad' lordship: The peasants' revolt in Essex and Norfolk. Russell, Josiah Cox (1948). British Medieval Population. Albuquerque: University of New Mexico Press. Henderson, Ernest F. (__) Select Historical Documents of the Middle Ages The Great Revolt of 1381 Anonimalle Chronicle: The English Peasants' Revolt of 1381 Charles Oman, The Great Revolt of 1381 , (Oxford: Clarendon Press, 1906), pp. 200-203, 205 England in the Aftermath of the Black Death GOOGLE BOOKS The English Rising of 1381 'The Peasants Revolt', in The Medieval Reader, edited by Norman Cantor (New York: Harper Collins, 1994), 284-93. E.B. Fryde, The Great Revolt of 1381, London: The Historical Association, 1981, 5-33 Peasant road to capitalism Peasant Politics and Class Consciousness: The Norfolk Rebellions of 1381

Environmental Toxicology

Introduction to Environmental Toxicology A lecture by Dr Rick Leah (Long version of Notes prepared by Dr R T Leah, Biological Sciences, University of Liverpool but including material summarized and adapted from various locations on the www*) Aims The impact of toxic chemicals on wildlife and humans has been of great concern for the last fifty years. Unfortunately this is a very large, complex subject area which can only be covered superficially within the time available.However, this lecture is intended to give an introduction to fundamental aspects of how some pollutants interact with living organisms to cause deleterious effects. The complexity will be explained and simplified where possible. You should understand at least a little about the biology of key organisms and how pollutants cause damage at a physiological level. You should be aware of how pollutants can induce change in organisms which can be used as a ‘biomarker’ of the presence and action of the pollutants (although this will form the subject of a later lecture in this course).Thus as the main outcome of this lecture you should have an appreciation of the wide range of contemporary issues that are caused by toxic chemicals in the environment and what regulatory authorities are doing to monitor and control them. You should understand the main hazards that toxic chemicals pose and how risk to humans and wildlife is controlled. You should be aware of the main groups of pollutants of contemporary concern.The material covered will be useful for the consideration of two case studies on the impact of toxic chemicals in the Great Lakes of North America and the Baltic Sea in later lectures. [pic] Environmental Toxicology or Ecotoxicology? [pic] Introduction It was after World War II that increasing concern about the impact of toxic chemicals on the environment led Toxicology to expand from the study of toxic impacts of chemicals on man to that of toxic impacts on the environment. This subject became known as Environmental Toxicology.Ecotoxicology is a relatively new discipline and was first defined by Rene Truhaut in 1969. It attempts to combine two very different subjects: ecology (â€Å"the scientific study of interactions that determine the distribution and abundance of organisms† Krebs 1985) and toxicology (â€Å"the study of injurious effects of substances on living organisms†, usually man). In toxicology the organisms sets the limit of the investigation whereas Ecotoxicology aspires to assess the impact of chemicals not only on individuals but also on populations and whole ecosystems.During the early years, the major tools of Environmental Toxicology were: detection of toxic residues in the environment or in individual organisms and testing for the toxicity of chemicals on animals other than man. It was however, a very big jump in understanding from an experimental animal to a complex, multivariate environment and the subject of ECOTOXICOLOGY develop ed from the need to measure and predict the impact of pollutants on populations, communities and whole ecosystems rather than on individuals.There is an on-going debate as to the exact scope and definition of ecotoxicology. The simplest definition found to date is that ecotoxicology is â€Å"the study of the harmful effects of chemicals upon ecosystems† (Walker et al, 1996). A more complete definition of Ecotoxicology comes from Forbes & Forbes 1994 â€Å"the field of study which integrates the ecological and toxicological effects of chemical pollutants on populations, communities and ecosystems with the fate (Transport, transformation and breakdown) of such pollutants in the environment†. nd several books have been written recently which discuss this in some depth, these include: Cairns, J Jr & Niederlehner B R (1994) Ecological Toxicity Testing. CRC Press Inc: Boca Raton Forbes, V E & Forbes T L (1994) Ecotoxicology in Theory and Practice. Chapman & Hall Ecotoxicolog y Series 2: London. Walker C H, Hopkin S P, Sibly R M & Peakall, D B (1996) Principles of Ecotoxicology. Taylor & Francis: London There are three main objectives in ecotoxicology (Forbes & Forbes 1994): †¢ obtaining data for risk assessment and environmental management. meeting the legal requirements for the development and release of new chemicals into the environment. †¢ developing empirical or theoretical principles to improve knowledge of the behaviour and effects of chemicals in living systems. (More information about the highlighted terms used below can be found in the Definitions section. ) In order to achieve these objectives, the main areas of study are: The distribution of POLLUTANTS in the environment, their entry, movement, storage and transformation within the environment.The effects of pollutants on living organisms. At an individual level, TOXICANTS may disrupt the biochemical, molecular and physiological structure and function which will in turn have conseq uences for the structure and function of communities and ecosystems. At the population level it may be possible to detect changes in the numbers of individuals, in gene frequency (as in resistance of insects to insecticides) or changes in ecosystem function (e. g. soil nitrification) which are attributable to pollution.It may be possible to use BIOMARKERS to establish that a natural population has been exposed to pollution and these can provide a valuable guide to whether or not a natural population is at risk or in need of further investigation. For the purposes of the Regulation and Registration of chemicals the toxicity of individual chemicals is principally investigated via TOXICITY TESTING, the main tool of which is the Standard Toxicity Test (STT) which usually tests the DOSE or CONCENTRATION of a particular chemical that is toxic to under controlled, laboratory conditions.Toxicity tests are mainly carried out using individual animals although there has been a move towards the use of more complex systems known as MESOCOSMS. In some situations, particularly in the case of pesticides, it may be possible to carry out FIELD TRIALS to assess toxicity. Toxicity data are used to make assessments of the HAZARD and the RISK posed by a particular chemical. [pic] Significant Issues with Chemicals that have driven the development of Ecotoxicology [pic] 1. DDT – around the world 2. Cadmium in Japan 3. Mercury in Japan 4. PCBs in Japan and Taiwan 5.Dioxins – various 6. The contamination of pristine environments (eg Arctic) by atmospheric transport of organohalogens Most workers in the field of ecotoxicology refer to the publication of Rachel Carson’s Silent Spring (1962) as a landmark in the public’s awareness of potential damage to human and environmental health from man-made toxic substances. According to Rodricks (1992), Carson’s book â€Å"almost single-handedly created modern society’s fears about synthetic chemicals in the environment and, among other things, fostered renewed interest in the science of toxicology†.Certainly the consolidation of academic and related pursuits into the study of toxic substances in the environment dates from about the same time as the publication of Silent Spring. Prior to the 1960s, there were no coordinated programmes in research, in education or in regulation that systematically addressed toxic substances in the environment. Considerable progress has been made in all these areas during the past four decades. Fate of chemicals in the environment and within organisms As ecotoxicologists we are concerned with the movement and fate of toxic chemicals at both the organism level and that of the whole ecosystem.The relevant issues are: †¢ the source, †¢ transport, †¢ modification and †¢ final fate of the pollutants. At the organism level we need to be concerned with †¢ Uptake †¢ Excretion †¢ Sites of action, metabolism or storage T oxicity testing and the regulation and release of toxic chemicals As ecotoxicology largely arose from toxicology and the need to regulate the introduction of potentially toxic chemicals into the environment, toxicity testing remains central to the subject today. Most toxicity testing for pollutants is still based on tests on individual organisms in artificial test situations (see list of examples in next section).These tests are cheap, reliable and easy to perform but there is much debate about the relevance of many standard toxicity tests to ‘real life'. Initially in the early days of environmental toxicology the concept of the ‘most sensitive species' was used to relate the results of toxicity tests to the ‘real world'. Certain species in a particular community were assessed as being ‘most sensitive' to pollutants. The logic was that if a pollutant was non-toxic to the ‘most sensitive' species then it would be safe for the rest of the community.Essent ially, this logic remains today – the results of tests on single species, in artificial situations are extrapolated to predict the effects of pollutants on whole communities or ecosystems. It is assumed that if you have enough information about the effects of a pollutant on the parts of an ecosystem, then you can assemble the effects on the whole. There is however, some question about the usefulness of extrapolating from simple, highly artificial, single-species toxicity tests to complex, multi-variate ecosystems.Forbes & Forbes (1994) argue that â€Å"understanding and predicting the consequences of pollutant-induced effects on ecosystems requires that the effects be examined at the level of interest† i. e. the population, community or ecosystem. This debate has been the source of much division in ecotoxicology, between the Applied, often Industrial, Ecotoxicologists concerned with the practicalities of chemical registration and testing and the Pure or Academic Ecotox icologists who regard many toxicity testing regimes as inappropriate or at worst useless.Unfortunately, never the twain shall meet and the level of communication between the two camps has not been great. A fictional exchange makes the point well (from Forbes & Forbes 1994): â€Å"Academic Ecotoxicologist: Single species acute toxicity tests are too simplistic and have no connection with what is really going on out in nature. These standard tests are not only irrelevant and a waste of time, they may in fact do more harm than good if they lead us to believe that we can use them to adequately protect the environment when in fact we cannot.Industrial Ecotoxicologist: These tests may be oversimplified, but they are also cost-efficient, easy to perform, the procedures have been worked out, and the fact is they are required by government. We have absolutely no incentive to do more than is required by law, and, frankly, you have given us little hard evidence that current test procedures do fail to protect the environment adequately. Government Ecotoxicologist: Do you have any idea of the number of new chemicals that we have to assess each year?We can't tell industry to stop producing new chemicals and we can't wait until we understand the whole system before we try to protect it. If you think current procedures fail, then come up with some better tests – which must of course be simple, cheap and fast. Academic Ecotoxicologist: (Pause) †¦ Well, it's very complex, and of course I'll need much more data before I can give you an answer. But those single-species acute tests are oversimplified and have no connection with what is really going on out in the field †¦ Government Ecotoxicologist: We need tests! Give us tests! â€Å"The way forward for Ecotoxicology must be to integrate its two halves much more fully. Toxicity testing, using single species, do provide useful information and will almost certainly remain central to the regulation and registration of toxic chemicals but much can be done to expand the scope of toxicity testing, to add tests that apply to higher levels of organisation and so increase their relevance to the communities and ecosystems that are being protected. Testing methodologies An extensive range of ecotoxicological and biodegradation tests are required for the chemical, agrochemical and pharmaceutical industries.The tests often used include: †¢ Bacterial toxicity tests †¢ Algal Growth tests with a variety of species †¢ Acute toxicity tests with Lemna minor †¢ Acute and Reproduction tests in Daphnia magna †¢ Acute toxicity tests with the marine copepod Acartia tonsa †¢ Oyster embryo larval toxicity test †¢ Acute toxicity test with the marine invertebrate Mysidopsis bahia †¢ Earthworm toxicity tests †¢ Toxicity Tests with sediment dwelling organisms such as Chironomus or Lumbriculus †¢ Acute toxicity tests with freshwater and marine fish †¢ Bioaccumulatio n in fish †¢ Fish growth tests Early Life Cycle tests with fish Algal tests Several freshwater species are routinely tested. The most commonly used are Scenedesmus subspicatus and Pseudokirchneriella subcapitata. Other species used include Navicula Pelliculosa. Skeletonema costatum is the marine species preferred by most regulatory bodies. Electronic particle counters and size distribution analysers are used to monitor the growth of algae in the studies. Lemna is a useful substitute for higher plants. Invertebrate Tests Acute and reproduction studies are routinely conducted with Daphnia magna.Acute tests with other species are also available including the marine copepod Acartia tonsa, the freshwater sediment dwelling species Chironomus riparius or Lumbirculus variegatus and the amphipod Gammarus pulex. Fish Acute tests are conducted under static, semi-static or flow-through conditions. The choice of test regime is dependent upon the chemical properties. Tests using species comm only encountered wild in the UK are rare as most tests are conducted using species adapted for life in the laboratory including: The species used include: †¢ Rainbow trout †¢ Common carp Golden orfe †¢ Bluegill sunfish †¢ Fathead minnow †¢ Japanese killifish †¢ Zebra fish Studies can also be conducted using marine species such as Turbot and Sheepshead minnow. Definitions used in Ecotoxicology Some of the terms used in ecotoxicology, such as LD50, have simple, widely accepted definitions and hence can be defined here with some confidence. Others however vary quite widely in their interpretation from one text to another. I have tried to indicate these below and can only suggest that the reader refer carefully to the introduction of the text they are using.Where there is likely to be some contradiction I have listed the reference for the definitions given. [pic] ECOTOXICOLOGY †¢ is concerned with the toxic effects of chemical and physical agents on li ving organisms, especially on populations and communities within defined ecosystems: it includes the transfer pathways of those agents and their interactions with the environment. Butler, 1978. †¢ investigates the effects of substances on organisms. The hazard to animal and plant populations can be determined by using survey data (retrospective) or by performing specific tests (prospective).Rudolph & Boje, 1986. †¢ the science that seeks to predict the impacts of chemicals on ecosystems. Levin et al 1989. †¢ the study of harmful effects of chemicals upon ecosystems. Walker et al 1996. [pic] POLLUTANT or CONTAMINANT, XENOBIOTIC or ENVIRONMENTAL CHEMICAL? Variations of use of these terms are commonplace. â€Å"Environmental chemical† may be used to describe simply any chemical that occurs in the environment (Walker et al 1996) or substances which enter the environment as a result of human activity or occur in higher concentrations than they would in nature (Rombk e & Moltmann 1995).The terms contaminant and pollutant can be described separately but are often used as synonyms. Both words are used to describe chemicals that are found at levels judged to be above those that would normally be expected. â€Å"Pollutants† carries the connotation of the potential to cause harm, whereas contaminants are not by definition harmful. This is however, not an easy distinction to make. Whether or not a contaminant is a pollutant may depend on its level in the environment and the organism or system being considered, thus one particular substance may be a contaminant relative to one species but pollutant relative to another.Finally, in practice it is often difficult to demonstrate that harm is not being caused so that in effect pollutant and contaminant become synonymous. (Walker et al 1996). Xenobiotic is used to describe compounds that are ‘foreign' to a particular organism, that is they do not play a part in their normal biochemistry. A chemi cal that is normal to one organism may be foreign to another and so xenobiotics may be naturally occurring as well as man-made compounds (Walker et al 1996). The term Xenobiotic is sometimes also used in a more general sense to describe â€Å"foreign substances† in the environment (Rombke & Moltmann 1995). [pic]HARM or DAMAGE? Biological systems are resilient to harm caused by adverse factors in the environment since they are able to adapt to some insults. There is a fundamental difference in viewpoint between these two words, one defines harm as an effect regardless of any biological compensation that the population might make, the other defines damage as occurring only if there is an effect subsequent to any compensation. harm: biochemical or physical changes which adversely affect individual organisms' birth, growth or mortality rates. Such changes would necessarily produce population declines were it not that other processes may compensate. Walker et al 1996). damage: â⠂¬Å"the interaction between a substance and a biological system. The substance's potential to cause damage is weighed against the protective potential inherent in the biological system (e. g. excretion or metabolic reactions, adaptation or regeneration)† (Rombke & Moltmann 1995). [pic] ENDPOINTS, DOSE and CONCENTRATION There are many different ways in which toxicity can be measured but they are usually assessed relative to a particular outcome or END POINT. Initially, most Toxicity Tests measured the number of organisms killed by a particular DOSE or CONCENTRATION of the chemical being tested.With terrestrial animals the DOSE of chemical (taken orally, applied to the skin or injected) administered is usually recorded. DOSE is usually used where the dietary dose of a test chemical can be accurately determined. For aquatic organisms or where the test chemical is dosed into the surrounding medium, the tests usually measure the CONCENTRATION of chemical in the surrounding water/me dium. The following measures, known as a group as EDs or ECs (Effective Doses or Effective Concentrations) are frequently used to describe data from toxicity tests: LD50Median lethal dose, that is the dose that kills 50% of the population LC50 Median lethal concentration. ED50/EC50 Median effect dose/concentration, that is the dose that produced a defined effect to 50% of the population. NOED/NOEC No Observed Effect Dose (or Concentration) NOEL No Observed Effect Level. Sometimes this more general term is used to describe either of the above. It can be defined as the highest level (that is dose or concentration) of the test chemical that does not cause a statistically significant difference from the control. LOED/LOE Lowest Observed Effect Dose (or Concentration)There has been a move away from the use of lethal end points in toxicity testing towards the measurement of EFFECTS rather than death. Examples of EFFECTS which can be used include changes in: reproduction (eg. number of egg s laid or young hatched); growth (e. g. biomass or body length) and biochemical or physiological effects (e. g. enzyme synthesis or respiration). [pic] HAZARD AND RISK Toxicity data is used to make assessments of the HAZARD and the RISK posed by a particular chemical. Where: HAZARD is the potential to cause harm RISK is the probability that harm will be caused.Defining HAZARD involves answering two questions, ‘how much damage are we prepared to tolerate' and ‘how much proof is enough'. The first is a question for society, alleviating/avoiding/repairing damage involves costs, how much are we prepared to pay? The second is largely a scientific problem of providing sufficient evidence that damage is due to pollution. HAZARD is not necessarily directly related to toxicity, it is a product of exposure and toxicity, a compound with moderate toxicity but very high exposure may cause more damage that a very toxic chemical with very low exposure.RISK is usually defined using the predicted environmental concentration (PEC) and the predicted environmental no effect concentration (PNEC). Information on the movement and behaviour of pollutants in the environment are used to calculate the PEC whereas data from Toxicity Testing must be extrapolated to calculate the PNEC. The making of these calculations is not a precise art, apart from doubts about the extrapolation of Toxicity data from the lab to the field it can be very difficult to estimate the degree of exposure, particularly for mobile taxa such as birds and mammals. [pic]BIOMARKERS A Biomarker can be defined as a â€Å"biological response to a chemical or chemicals that gives a measure of exposure and sometimes, also, of toxic effect† (Walker et al 1996), they can be divided into biomarkers of exposure and of toxic effect. Examples of biomarkers range from the inhibition of AChE (acetylcholinesterase) in the nervous system of animals to the thinning of eggshells in birds. Biomarkers can help to brid ge the gap between the laboratory and the field by giving direct evidence of whether or not a particular animal, plant or ecosystem is being affected by pollution.They will often provide more reliable evidence of exposure than measurements of the pollutants themselves in the environment, the latter are often short-lived and difficult to detect, whereas their effects (detectable via biomarkers) may be much longer-term. [pic] A QUESTION OF SCALE AND ACCURACY The difficulty in extrapolating from simple, highly artificial, single-species toxicity tests to complex, multi-variate ecosystems has led to attempts to develop more complex systems which can be used in toxicity tests.Such systems are usually termed microcosms, mesocosms or macrocosms, that is small, medium or large multispecies systems. It must be possible to control conditions in these systems to such an extent that they can provide meaningful, reproducible (that is, the system could be accurately copied elsewhere), replicable (that is, two replicates of the same experiment would produce the same results) data in toxicity tests. Simply because they are more complex systems it is seldom possible to produce tests that are as precise and controlled as those carried out in single species STTs.However, despite their limitations these larger-scale tests can provide important insights into the effect of pollutants on whole systems rather than on single species. [pic] MIXTURES OF CHEMICALS, ADDITION OR MULTIPLICATION? In natural systems, organisms are often (usually) exposed to more than one pollutant at the same time. However, regulatory authorities usually assume – unless there is evidence to the contrary – that the toxicity of combinations of chemicals is roughly additive.Fortunately in many cases this is quite correct but in some cases, toxicity is more than additive in that is there is POTENTIATION of toxicity. One particular type of potentiation called SYNERGISM occurs where the effect of two or more chemicals combine to have greater impact than expected from their individual concentrations. [pic] Ecotoxicology – Pesticide Definitions [pic] What is a pesticide? A literal definition of a pesticide would be â€Å"a killer of pests†. In practice pesticides are no longer aimed exclusively at killing the pests they are used to control and the term has acquired a rather wider meaning uch as â€Å"the chemical tools used to manage all kinds of pests† or in the US it's more official definition is â€Å"any substance used for controlling, preventing destroying, repelling or mitigating any pest† (all definitions from Ware 1991). Hence pesticides include not only those chemicals which kill the pest they are used against but also those such as insect chemosterilants or plant and insect growth regulators which control pest populations without necessarily, physically, killing the pests they come into contact with.Pesticides have been divided into many diffe rent classes. Firstly, according to the target organism that they control, so insect-icides kill (or control) insects, rodent-icides control rodents etc. The -icide suffix has been widely used in the past, as shown in Table 1, but relatively few of these terms are in common use today. Secondly, pesticides can be classified according to their mode of action, that is the way in which they act on the pest population, e. g. attractants, repellents, chemosterilants etc.Finally, the definition of a pesticide has been widened once again to: â€Å"pesticides are used by man as intentional additions to his environment in order to improve environmental quality for himself, his animals or his plants† (Ware 1991). This definition allows the inclusion of 2 new classes of treatment. Firstly those such as plant growth regulators, which are not only used as herbicides to control weeds, but also to control directly the growth of the crop and hence improve its success.For instance, they are us ed to reduce the growth of cereals so that they do not become too tall and prone to ‘lodging' before harvest. Secondly, microbial pesticides which are not based on a chemical but on bacteria, fungi, nematodes and viruses which attack the pest. [pic] Table 1 Classes of pesticide according to : A. the target organism and B. pesticide mode of action. After Ware (1991). |CLASS |FUNCTION | |A.By Target Organism   | |acaricide |kills/controls mites | |algicide |kills/controls algae | |avicide |kills/controls or repels birds | |bactericide |kills/controls bacteria | |fungicide |kills/controls fungi | |herbicide |kills/controls plants | |insecticide |kills/controls insects | |larvicide |kills/controls larvae (usually mosquitoes) | |miticide |kills/controls mites | |molluscicide |kills/controls snails & slugs.May include oysters, clams, & mussels | |nematicide |kills/controls nematodes | |ovicide |kills/controls eggs | |pediculicide |kills/controls lice | |piscicide |kills/c ontrols fish | |predicide |kills/controls predators (usually such as coyotes) | |rodenticide |kills/controls rodents | |silvicide |kills/controls trees & brush | |slimicide |kills/controls slime | termiticide |kills/controls termites | |B. By Mode of Action – by affect on pest   | |attractants/pheromones |Attract animals, especially insects usually into traps. Often sexual pheromones. | |chemosterilants |Sterilise insects or vertebrates (birds, rodents). Usually sterilise males. | |defoliants |Remove leaves. | |desiccants |Speed drying of plants. Used not only to kill weeds but also as pre-harvest desiccants to make harvesting | | |easier. |disinfectants |Kill or inactivate harmful micro-organisms | |feeding stimulants |Cause insects to feed more vigorously | |growth regulators |Stimulate or retard plant or insect growth. Natural or artificial hormones used not only to kill weed species | | |but also to protect crops such as cereals from lodging. | |repellents |Repel insects, mites, ticks or pest vertebrates (dogs, rabbits, deer, birds). | |B. By Mode of Action – by timing of application | |curative (fungicides) |applied to the plant after initial infection. |eradicant (fungicides) |applied when disease symptoms have already become visible, often to prevent the spread of disease. | |protectant (fungicides) |applied to the plant surface before infection. | |pre-plant or pre-sowing |applied before crop is sown or planted | |(herbicides) | | |pre-emergence (herbicides) |applied before the crop has germinated | |post-emergence(herbicides) |applied after the crop has germinated | |B.By Mode of Action – by selectivity | |the degree to which a pesticide discriminates between target and non-target organisms. | |selective |A selective pesticide effects a very narrow range of species other than the target pest or may be. The chemical | | |itself may be selective in that it does not affect non-target species or it may be used selectively in such a | | |way that non-target species do not come into contact with it. | |non-selective |a non-selective pesticide kills a very wide range of plants, insects, fungi etc. | |B.By Mode of Action – by site of interaction with pest | |systemic |the pesticide is absorbed by the pest and moves around within the pest system to reach parts of the pest remote | | |from the point of application | |contact |contact pesticides directly affect the parts of the plant, insect, fungus etc to which they are applied. They | | |cause localised damage to the plant or animal tissue on contact. | References Barlow, F (1985) Chemistry and formulation. In: Pesticide Application: Principles and Practice. Ed: P T Haskell. Oxford Science Publications: Oxford. pp 1-34. Dent, D R (1995) Integrated Pest Management.Chapman & Hall: London, Glasgow, Weinheim, New York, Todyo, Melbourne, Madras. Rombke, J & J M Moltmann (1995) Applied Ecotoxicology. Lewis Publishers: Boca Raton, New York, London, Tokyo. Wa re, G W (1991) Fundamentals of Pesticides. A self-instruction guide. Thomson Publications: Fresno USA. [pic] Ecotoxicology – Pesticide Classification – Insecticides [pic] While pesticides can be divided into many classes by target organism, mode of action etc for most purposes chemical pesticides are divided into three major groups according to their target organism, that is: insecticides, herbicides and fungicides. These groups are then subdivided into chemical groups such as organophosphates, organochlorines, carbamates etc.This simplified classification effectively groups acaricides, nematicides and molluscicides in with insecticides as many chemicals that have acaricidal, nematocidal or molluscicidal properties are also insecticidal. The current proliferation of chemical insecticides dates from World War II, until this time the insecticides available were based on: arsenicals, petroleum oils, sulphur, hydrogen cyanide gas, cryolite and on extracts from plants such as pyrethrum, nicotine and rotenone. Table 2: Classification of Insecticides gives a summary of the main chemical classes of insecticide and the main chemicals in each class. The characteristics of the main classes of insecticide: the organochlorines, organophosphates, carbamates and pyrethroids are summarised below. Organochlorines Also called: chlorinated hydrocarbonsA large and varied group that has a particularly high public profile because of the environmental problems they have caused. They were mostly discovered in 1942-56 and were very important in the early success of synthetic insecticides. They are mostly Insecticides with a very wide range of actions, they can be divided into three main groups: DDT and related compounds including rhothane (DDD) and methoxychlor. Widely used during World War II for control of disease vectors (such as mosquitoes) and subsequently much used on agricultural pests such as ectoparasites of farm animals and insect disease vectors and also widel y used against insects in domestic and industrial premises. chlorinated cyclodiene insecticides such as aldrin, dieldrin and heptachlor. ost widely used as seed dressings and soil insecticides. hexachlorocyclohexanes (HCHs), such as lindane used against pests and parasites of farm animals, also in insecticidal seed dressings. Organochlorine insecticides are very stable solids with: limited vapour pressure, very low water solubility and high lipophilicity. They may be very persistent in their original form or as stable metabolites. They tend to be stored in body fats and are particularly hazardous because they are so stable and tend to accumulate in successive organisms in the food chain. DDT and the HCHs a regarded as only moderately toxic to mammals while the chlorinated cyclodienes are highly toxic.Action: all organochlorine insecticides are nerve poisons but DDT has a different action to the chlorinated cyclodienes and HCHs. DDT acts on the sodium channels in the nervous system s o that the passage of an ‘action potential' along the nerve is disrupted. It causes uncontrolled repetitive spontaneous discharges along the nerve. Uncoordinated muscle tremors and twitches are characteristic symptoms. The chlorinated cyclodienes and HCHs act on the GABA receptors which function as a channel for Cl – ions through the nerve membranes. They bind to the GABA receptors and reduce the flow of Cl – ions. Typical symptoms include convulsions. Organophosphates Also called: organic esters of phosphorus acid.Such as bromophos, chlorpyrifos, diazinon, dichlorvos, fenitrothion, malathion, parathion and phorate. The same basic constituents are combined with many additional chemicals to give a wide range of products with very different properties. Organophosphates were developed during the second world war and have two main uses: as insecticides and as nerve gases (chemical warfare agents). They are mostly liquids, liphophilic, with some volatility and a few a re solids. Generally, they are less stable and more readily broken down than organochlorines and are relatively short-lived in the environment, hence most of their hazard is associated with short-term (acute) toxicity.The water solubility of the various organophosphate compounds is very variable and they are prepared in numerous formulations: as emulsifiable concentrates for spraying and to control ectoparasites of farm animals (particularly sheep dips) and sometimes internal parasites (such as ox warble fly); as seed dressings and as granular formulations particularly used for the most toxic organophosphates (e. g. disyston and phorate) as the active ingredient is effectively ‘locked up' in the granule and is safer to handle and only slowly released into the environment. Organophosphates are also used to control vertebrate pests such as Quelea in Africa. Action: like organochlorines, organophosphates also act as a neurotoxin. They combine with the enzyme acetylcholinesterase and prevent conduction of nerve impulses at junctions in the nervous system where acetylcholine is the natural transmitter.As a result, acetylcholine builds up in the nerve synapse and eventually leads to synaptic block when the acetylcholine can no longer relay signals across the synapse. In neuro-muscle junctions this leads to tetanus, the muscle is in a fixed state, unable to contract or relax in response to nerve stimulation. Carbamates e. g. aldicarb, carbaryl, carbofuran, methiocarb, methomyl, pirimicarb and propoxur Carbamates are a more recent development than organochlorines or organophosphates, they are all derivatives of carbamic acid. The basic carbamate group is combined with different chemicals to produce insecticides with a wide range of properties (in particular they vary greatly in their water solubility) and actions.Carbamates are not only used as insecticides but also molluscicides and nematicides. Carbamates are also used as herbicides and fungicides but these ha ve a different mode of action and are described elsewhere. Carbamates are mainly used to control insect pests in agriculture and horticulture, they have abroad spectrum of activity and usually act by contact or stomach action although a few possess systemic activity (aldicarb, carbofuran). Action: basically the same as organophosphates, inhibiting the action of acetylcholine at the nerve synapses. Doses of carbamates are not accumulative and carbamate poisoning is more easy to reverse than that caused by organophosphates.They are generally regarded as representing a short-term hazard. Pyrethroids Such as cypermethrin, deltamethrin, permethrin, phenothrin, resmethrin. Pyrethrin insecticides were developed from naturally occurring chemicals found in the flower heads of Chrysanthenum sp. and these provided the model for the production of synthetic pyrethroid insecticides. Pyrethroids are generally more stables than natural pyrethrins. The development of pyrethroids can be traced over 4 main phases (Ware 1991). The first generation allethrin was a synthetic duplicate of a natural pyrethrum, cinerin I. The second generation included bioallethrin, phenothrin, resmethrin and bioresmethrin.These were marginally more effective than natural pyrethrums but were neither effective enough nor photostable enough to be used extensively in agriculture. However, they are still used in pest control formulations for the home. The third generation of pyrethroids included fenvalerate and permethrin which were stable in sunlight and only slightly volatile and could be used successfully in agriculture. Finally, the fourth and current generation of pyrethroids can be used at much lower concentrations (one-fifth to one-tenth) that those in generation 3 and are all photostable. Overall, most pyrethroids are not sufficiently soluble in water to be used a systemic insecticides. They are mainly formulated as emulsifiable concentrates for spraying.They control a wide range of agricultural a nd horticultural insect pests and are used extensively to control insect vectors of disease (e. g. tsetse fly in Africa) Action: pyrethroids are generally solids with very low water solubility and they act as neruotoxins in a very similar way to DDT. They are readily biodegradable but can bind to particles in soils and sediments and can be persistent in these locations. They are particularly toxic to insects as opposed to mammals and birds and the main environmental concerns are over their effects on fish and non-target invertebrates. Table 2: Classification of Insecticides Data from: Whitehead, R (1995) The UK Pesticide Guide. CAB International & BCPC. Chemical group |Compound |Action |Notes | |AMIDINES | | | | |   |amitraz |   |also ACARICIDE | |BOTANICAL | | | | |   |azadirachtin |insect growth regulator |extracted from Neem | |   |nicotine |contact, non-persistent general |extracted from tobacco | | | |purpose, | | |   |pyrethrin |contact, non-persistent |extracted from Pyrethrum | |   |rotenone |contact |extracted from Derris and Lonchocarpus | |CARBAMATES | | | |   |aldicarb |systemic |also NEMATICIDE | |   |bendiocarb |contact & ingested |   | |   |carbaryl |contact |also WORM KILLER, FRUIT THINNER | |   |carbofuran |systemic |also NEMATICIDE | |   |methiocarb |stomach acting |also MOLLUSCICIDE | |   |methomyl |fly bait |   | |   |pirimicarb |contact & fumigant aphids only |   | |   |propoxur |fumigant, maimainly in |   | | | |glasshouses | | |   |thiocarb |pelleted bait |also MOLLUSCICIDE | |ORGANOCHLORINES | | | | |diphenyl aliphatic derivatives |DDT |   |   | |   |rhothane (DDD) |   |   | |benzene derivatives |lindane ? amma HCH |contact, ingested & fumigant |   | |cyclodiene derivatives |aldrin |persistent |UK revoked 1989 | |   |dieldrin |persistent |UK revoked 1989 | |   |endosulfan |contact & ingested |also ACARICIDE | |ORGANOPHOSPHATES | | | | |aliphatic derivatives |dichlorvos |contact , fumigant    | |   |dimethoate |contact, systemic |also ACARICIDE | |   |disulfoton |systemic, granules |   | |   |malathion |contact |also ACARICIDE | |   |phorate |systemic |   | |phenyl derivatives |fenitrothion |contact, broad spectrum |   | |   |parathion |   |   | |heterocyclic derivatives |chlorpyrifos |contact & ingested |also ACARICIDE | |   |diazinon |contact |   | |ORGANOTINS | | | | |   |fenbutatin-oxide |   |ONLY ACARICIDE | |PYRETHROIDS | | | | |generation 1 |allethrin |   |   | |generation 2 |bioresmethrin |contact, residual |also ACARICIDE | |   |phenothrin |contact & ingested |   | |   |resmethrin |contact |   | |   |tetramethrin |contact |   | |generation 3 |fenvalerate |contact |   | |   |permethrin |contact & ingested, broad |   | | | spectrum | | |generation 4 |bifenthrin |contact, residual |also ACARICIDE | |   |cypermethrin |contact & ingested |   | |   |cyfluthrin |   |   | |   |fenpropathrin |contact & ingested |also ACARICIDE | [pic] Ecotoxicology – Pesticide Classification – Herbicides [pic] It is really only in the last 50 years that use of chemical weedkillers or herbicides has become widespread. Prior to this, the control of weeds in crops was carried out largely by manual weeding, crop rotation, ploughing and various ways of stopping weed seeds being dispersed in crop seed. Today, the heavy use of herbicides is confined to those countries that practice highly intensive, mechanised farming.In 1971 it was estimated that more energy was expended on weeding crops than on any other single human task (Brain 1971 ). Herbicides are also used extensively in non-crop and amenity situations such as industrial sites, roadsides, ditch banks, recreational areas etc. Herbicides can be classified in a number of different ways. The main classification used is often according to chemical class but they can also be classified according to their selectivity, the way th at they affect the plant, the timing of application and the area covered by an application. Herbicides are classed as selective if they kill some plant species but not others, for instance they may kill the weeds but not the crop and as non-selective if they kill all vegetation.Herbicides may be intrinsically selective in that they are active against some species of weed but not others but they may also be used selectively, that is in such a way that they only come into contact with the weeds and not the crop. There are two main ways in which herbicides affect the plants they are applied to: contact herbicides kill parts of the plant that they come into contact with. These are generally used against annual weeds and if they are to be effective need complete coverage of the target weed with the chemical. Systemic or translocated herbicides are absorbed either by the roots or foliage of the plant and then move within the plants system to areas remote from the site of application.Trans located herbicides tend to be slower acting than contact ones and while they can be used against annual weeds they are more commonly aimed at perennial weeds. With translocated herbicides a uniform, although not necessarily complete, coverage of the target weeds is necessary. Finally, herbicides can be classified according to the timing of application in relation to the crop they are being used in. Pre-plant, or pre-sowing herbicides must be applied to an area before the crop is planted. Pre-emergence herbicides are applied before the crop has emerged, this may allow an added level of selectivity as a herbicide can be applied to growing weeds while the crop itself is still protected by the oil. Finally, post-emergence herbicides are applied after the crop has emerged from the soil.Again, a level of selectivity may be introduced by applying a germination inhibitor to prevent further germination of weed seeds – after the crop itself has germinated. Phenoxy Herbicides e. g. 2,4- D, MCPA, 2,4,5-T All derivatives of phenoxyalkane carboxylic acids that act as plant growth regulator herbicides. Phenoxy herbicides were the first safe, selective herbicides discovered and they are still used in huge quantities. They act by simulating the action of natural hormones and produce uncoordinated plant growth. Their action is selective as they are toxic to dicotyledonous but not monocotyledonous plants. Hence they can be used to control ‘dicot' weeds (broad leaved weeds) in ‘monocot' crops (e. g. cereals, grass). Their physical properties vary greatly according to formulation.For instance, as alkali salts they are highly water soluble (can be formulated as aqueous solutions) whereas when as simple esters they have low water solubility and are lipophilic (generally formulated as emulsifiable concentrates). The main hazard they present is mainly posed by unwanted spray drift but they have also sometimes been contaminated with the highly toxic compound TCDD (or dioxin). Other related compounds, also with plant growth regulating properties include phenoxypropionic acids (e. g. CMPP) and phenoxybutyric acids (e. g. 2,4DB). Table 3: Classification of Herbicides Data from: Whitehead, R (1995) The UK Pesticide Guide. CAB International & BCPC. Chemical group |Compound |Uptake/action |Persistence |Timing/site of |Other uses | | | | | |application | | |ACETANILIDES | | | | | | |   |alachlor |via roots, |residual |pre/post-emergence |   | | | |translocated | | | | |AMIDES or substituted amides | | | | | | |   |napropamide |   |   |pre-emergence |   | |   |propachlor |   |   |pre-emergence | |BENZOICS or arylaliphatic acids | | | | | | |   |dicamba |translocated |   |soil/foliar |   | |BENZONITRILES or substituted nitriles| | | | | | |   |dichlobenil |   |residual |soil |   | |DIAZINONES | | | | | | |   |bentazone |contact |   |post-emergence |   | |BIPYRIDYLIUMS | | | | | | |   |diquat |contact |non-residual |f oliar |pre-harvest, CROP | | | | | | |DESICCANT | |   |paraquat |contact |non-residual |   |   | |CARBAMATES or carbanilates | | | | | | |   |asulam |translocated |   |foliar |   | |   |chlorpropham |   |residual |soiltubers |POTATO SPROUT SUPPRESSANT| |   |phenmedipham |contact |   |foliar |   | |CHLOROALKANOIC ACIDS or chlorinated | | | | | | |aliphatic acids | | | | | | |   |dalapon |   |persistent |soil? | |DINITROANILINES or nitroanilines | | | | | | |   |pendimethalin |   |residual |pre-emergence, soil|   | |   |trifluralin |   |   |soil-incorporated |   | |HBNs | | | | | | |   |bromoxynil |contact |   |post-emergence |   | |   |ioxynil |contact |   |post-emergence |   | |IMIDAZOLINONES or imidazoles | | | | | | |   |imazapyr |translocated |residual |foliar, soil |   | |   |imazaquin |   |   |   |   | |OXIMES or cyclohexenones | | | | | | |   |cycloxydim |translocated |   |post-emergence |   | |   |setho xydim |   |   |post-emergence |   | |PHENOXYACETIC ACIDS | | | | | | |   |MCPA |translocated |   |post-emergence |   | |PHENOXYBUTYRIC ACIDS | | | | | | |   |MCPB |translocated |   |post-emergence |   | |PHENOXYPROPRIONIC ACIDS | | | | | |   |diclofop-methyl |translocated |   |post-emergence |   | |   |fenoxaprop-P-ethyl |   |   |post-emergence |   | |   |fluazifop-P-butyl |   |   |post-emergence |   | |   |mecoprop |translocated |   |   |   | |   |mecoprop-P |translocated |   |post-emergence |   | |PHOSPONIC ACIDS or phosphona amino | | | | | | |acids or phosphates | | | | | | |   |glufosinate-ammonium |contact |non-residual |foliar |   | |   |glyphosate |translocated |non-residual |foliar |   | |PICOLINIC ACIDS | | | | | | |   |picloram |translocated |persistent |foliar, soil |   | |PYRIDINOXY ACIDS | | | | | | |   |fluroxypur |   |   |post-emergence |   | |   |triclopyr |   |   |foliar |   | |QUATER NARY AMMONIUM | | | | | | |   |difenzoquat |   |   |post-emergence |   | |SULFONYLUREAS | | | | | |   |metsulfuron-methyl |contact |residual |post-emergence |   | |   |triasulfuron |   |   |post-emergence |   | |THIOCARBAMATES | | | | | | |   |tri-allate |   |   |soil-acting, |   | | | | | |pre-emergence | | |TRIAZINES | | | | | | |   |atrazine |   |residual |pre/post emergence |   | |   |cyanazine |contact |residual |pre-emergence |   | |   |metribuzin |contact |residual |pre-/post-emergence|   | |   |simazine |root uptake |   |soil