Case studing (nursing science) Study Example | Topics and Well Written Essays - 750 words

Studing (nursing science) - Case Study Example His heart rate is increasing as well as his breathe per minutes. At his age, excitement is very much increased and is there for increasing also the cardiovascular activity. The cardiovascular system helps transport oxygen and nutrients to tissues, transport carbon dioxide and other metabolites to the lungs and kidneys, and distribute hormones throughout the body. The cardiovascular system also assists with thermoregulation. The runner's sympathetic nervous system is activated (central command), and catecholamines are released from the adrenal medulla. This is the reason in cardiac acceleration, increased myocardial contractility, increased cardiac output, peripheral vasoconstriction, and an increase in blood pressure. As the race started the following factors in the cardiovascular system are considered: the heart rate, peripheral resistance, skin blood flow, cardiac output, and blood flow distribution. Cardiovascular changes at the start of the game include the compression of the blood vessels in the contracting muscle leading to a reduction in the blood flow. Heart rate continues to increase during the race, until the rate reaches a plateau of about 180 beats/min at maximum effort. Peripheral resistance decreases because of relaxation of arterioles in active muscle and skin (as body temperature rises). Skin blood flow increases, which aids in heat loss. Blood flow to inactive muscle, kidney, and gastrointestinal tract is reduced. Because BP is a major determinant of afterload, the left ventricular wall stress, and thus the cardiac workload, is significantly higher. As the intensity of the race increases the BP is also increasing from 120 mmHg to approximately 200 mmHg. Maximum oxygen uptake leve l (VO2max) is reached during this state. Cardiac output increases during the race until 40% of VO2max (maximum oxygen uptake level) is reached. Cardiac output rises from approximately 80 mL/beat to approximately 120 mL/beat. HR increases with intensity until VO2max is reached. HR rises from approximately 70 beats per minute to approximately 200 beats per minute. Cardiac output increases with intensity until VO2max is reached. Cardiac output rises from approximately 5 L/min to approximately 25-30 L/min. (Suleman, 2006). The race is almost over the athletes are chasing to cross the finish line first. There is an increase in PaCO2 in the Kenyan athlete. PACO2 represents the amount of CO2 in solution. When there is an increase in blood PACO2, there is an increase in ventilation. During this stage more oxygen is needed and more CO2 and metabolic acid are produced. There is an increased cardiac output because the tissues need more oxygen supplied to them. This is also caused due to an increase of lung ventilation to support gas tensions in arterial blood, which experiences faster blood flow. When an individual is on the move, the venous blood shows signs of decreased O2 levels, increased CO2 levels, and an increase in H+ levels. During the race the blood flow to the leg muscles increases because of the local factors, which includes: the release of vasodilator metabolites (e.g. adenosine); the increase in muscle temperature; and the local decreased in pH (increased CO2 and lactic acid). The arterioles dilate and more capillaries open (capillary recruitment). Venous return is facilitated in running by the following: sympathetic-mediated contraction of capacitance vessels ; muscle compression of the leg veins with one-way

Collaboration and Consultation in Education Research Paper

Collaboration and Consultation in Education - Research Paper Example According to the research findings, it can, therefore, be said that collaborative learning is accomplished through the use of active engagement activities designed to exploit knowledge and to facilitate the sharing of the workload. In this method, learners can generate their individual parts of a larger assignment and then the parts are compiled as a group work. Collaboration is also a style employed by professionals in order to achieve a common and a shared goal. There are several terminologies that may be used interchangeably when discussing cooperation strategies. These terms include consultation, teamwork, collaborative work and collaborative consultation. However, the collaboration will be employed in this paper as the umbrella concept for the various collaborative strategies. Furthermore, there are different forms in which collaboration techniques are created. These are the student collaboration, teacher-student collaboration, teacher-parent collaboration, and student-parent co llaboration. All these forms of cooperation are primarily meant to help enhance the learning process of a student and to ensure they achieve the best in education. Collaboration is both advantageous in teaching and learning when it happens on various levels. Collective prioritizing of education by the students, teachers, members of a family, and the community as a whole is beneficial to teaching and learning process. The benefits will be more felt when all the stakeholders engage in activities that promote learning institutions, educators, and students. Additionally, the advantage of collaboration becomes more evident when teachers collaborate with other teachers to support innovative classroom practices. And aim at the high level of expectations for themselves and students as well. Further, the benefits of collaboration can be achieved more when students are granted the chance to work together for common academic goals in manners that improve learning.

Predicting Effects of Environmental Contaminants

Predicting Effects of Environmental Contaminants 1.1. Debunking some chemical myths†¦ In October 2008, the Royal Society of Chemistry announced they were offering  £1 million to the first member of the public that could bring a 100% chemical free material. This attempt to reclaim the word ‘chemical from the advertising and marketing industries that use it as a synonym for poison was a reaction to a decision of the Advertising Standards Authority to defend an advert perpetuating the myths that natural products were chemical free (Edwards 2008). Indeed, no material regardless of its origin is chemical free. A related common misconception is that chemicals made by nature are intrinsically good and, conversely, those manufactured by man are bad (Ottoboni 1991). There are many examples of toxic compounds produced by algae or other micro-organisms, venomous animals and plants, or even examples of environmental harm resulting from the presence of relatively benign natural compounds either in unexpected places or in unexpected quantities. It is therefore of prime impo rtance to define what is meant by ‘chemical when referring to chemical hazards in this chapter and the rest of this book. The correct term to describe a chemical compound an organism may be exposed to, whether of natural or synthetic origins, is xenobiotic, i.e. a substance foreign to an organism (the term has also been used for transplants). A xenobiotic can be defined as a chemical which is found in an organism but which is not normally produced or expected to be present in it. It can also cover substances which are present in much higher concentrations than are usual. A grasp of some of the fundamental principles of the scientific disciplines that underlie the characterisation of effects associated with exposure to a xenobiotic is required in order to understand the potential consequences of the presence of pollutants in the environment and critically appraise the scientific evidence. This chapter will attempt to briefly summarise some important concepts of basic toxicology and environmental epidemiology relevant in this context. 1.2. Concepts of Fundamental Toxicology Toxicology is the science of poisons. A poison is commonly defined as ‘any substance that can cause an adverse effect as a result of a physicochemical interaction with living tissue'(Duffus 2006). The use of poisons is as old as the human race, as a method of hunting or warfare as well as murder, suicide or execution. The evolution of this scientific discipline cannot be separated from the evolution of pharmacology, or the science of cures. Theophrastus Phillippus Aureolus Bombastus von Hohenheim, more commonly known as Paracelsus (1493-1541), a physician contemporary of Copernicus, Martin Luther and da Vinci, is widely considered as the father of toxicology. He challenged the ancient concepts of medicine based on the balance of the four humours (blood, phlegm, yellow and black bile) associated with the four elements and believed illness occurred when an organ failed and poisons accumulated. This use of chemistry and chemical analogies was particularly offensive to his contempo rary medical establishment. He is famously credited the following quote that still underlies present-day toxicology. In other words, all substances are potential poisons since all can cause injury or death following excessive exposure. Conversely, this statement implies that all chemicals can be used safely if handled with appropriate precautions and exposure is kept below a defined limit, at which risk is considered tolerable (Duffus 2006). The concepts both of tolerable risk and adverse effect illustrate the value judgements embedded in an otherwise scientific discipline relying on observable, measurable empirical evidence. What is considered abnormal or undesirable is dictated by society rather than science. Any change from the normal state is not necessarily an adverse effect even if statistically significant. An effect may be considered harmful if it causes damage, irreversible change or increased susceptibility to other stresses, including infectious disease. The stage of development or state of health of the organism may also have an influence on the degree of harm. 1.2.1. Routes of exposure Toxicity will vary depending on the route of exposure. There are three routes via which exposure to environmental contaminants may occur; Ingestion Inhalation Skin adsorption Direct injection may be used in environmental toxicity testing. Toxic and pharmaceutical agents generally produce the most rapid response and greatest effect when given intravenously, directly into the bloodstream. A descending order of effectiveness for environmental exposure routes would be inhalation, ingestion and skin adsorption. Oral toxicity is most relevant for substances that might be ingested with food or drinks. Whilst it could be argued that this is generally under an individuals control, there are complex issues regarding information both about the occurrence of substances in food or water and the current state-of-knowledge about associated harmful effects. Gases, vapours and dusts or other airborne particles are inhaled involuntarily (with the infamous exception of smoking). The inhalation of solid particles depends upon their size and shape. In general, the smaller the particle, the further into the respiratory tract it can go. A large proportion of airborne particles breathed through the mouth or cleared by the cilia of the lungs can enter the gut. Dermal exposure generally requires direct and prolonged contact with the skin. The skin acts as a very effective barrier against many external toxicants, but because of its great surface area (1.5-2 m2), some of the many diverse substances it comes in contact with may still elicit topical or systemic effects (Williams and Roberts 2000). If dermal exposure is often most relevant in occupational settings, it may nonetheless be pertinent in relation to bathing waters (ingestion is an important route of exposure in this context). Voluntary dermal exposure related to the use of cosmetics raises the same questions regarding the adequate communication of current knowledge about potential effects as those related to food. 1.2.2. Duration of exposure The toxic response will also depend on the duration and frequency of exposure. The effect of a single dose of a chemical may be severe effects whilst the same dose total dose given at several intervals may have little if any effect. An example would be to compare the effects of drinking four beers in one evening to those of drinking four beers in four days. Exposure duration is generally divided into four broad categories; acute, sub-acute, sub-chronic and chronic. Acute exposure to a chemical usually refers to a single exposure event or repeated exposures over a duration of less than 24 hours. Sub-acute exposure to a chemical refers to repeated exposures for 1 month or less, sub-chronic exposure to continuous or repeated exposures for 1 to 3 months or approximately 10% of an experimental species life time and chronic exposure for more than 3 months, usually 6 months to 2 years in rodents (Eaton and Klaassen 2001). Chronic exposure studies are designed to assess the cumulative toxici ty of chemicals with potential lifetime exposure in humans. In real exposure situations, it is generally very difficult to ascertain with any certainty the frequency and duration of exposure but the same terms are used. For acute effects, the time component of the dose is not important as a high dose is responsible for these effects. However if acute exposure to agents that are rapidly absorbed is likely to induce immediate toxic effects, it does not rule out the possibility of delayed effects that are not necessarily similar to those associated with chronic exposure, e.g. latency between the onset of certain cancers and exposure to a carcinogenic substance. It may be worth here mentioning the fact that the effect of exposure to a toxic agent may be entirely dependent on the timing of exposure, in other words long-term effects as a result of exposure to a toxic agent during a critically sensitive stage of development may differ widely to those seen if an adult organism is exposed to the same substance. Acute effects are almost always the result of accidents. Otherwise, they may result from criminal poisoning or self-poisoning (suicide). Conversely, whilst chronic exposure to a toxic agent is general ly associated with long-term low-level chronic effects, this does not preclude the possibility of some immediate (acute) effects after each administration. These concepts are closely related to the mechanisms of metabolic degradation and excretion of ingested substances and are best illustrated by 1.1. Line A. chemical with very slow elimination. Line B. chemical with a rate of elimination equal to frequency of dosing. Line C. Rate of elimination faster than the dosing frequency. Blue-shaded area is representative of the concentration at the target site necessary to elicit a toxic response. 1.2.3. Mechanisms of toxicity The interaction of a foreign compound with a biological system is two-fold: there is the effect of the organism on the compound (toxicokinetics) and the effect of the compound on the organism (toxicodynamics). Toxicokinetics relate to the delivery of the compound to its site of action, including absorption (transfer from the site of administration into the general circulation), distribution (via the general circulation into and out of the tissues), and elimination (from general circulation by metabolism or excretion). The target tissue refers to the tissue where a toxicant exerts its effect, and is not necessarily where the concentration of a toxic substance is higher. Many halogenated compounds such as polychlorinated biphenyls (PCBs) or flame retardants such as polybrominated diphenyl ethers (PBDEs) are known to bioaccumulate in body fat stores. Whether such sequestration processes are actually protective to the individual organisms, i.e. by lowering the concentration of the toxicant at the site of action is not clear (OFlaherty 2000). In an ecological context however, such bioaccumulation may serve as an indirect route of exposure for organisms at higher trophic levels, thereby potentia lly contributing to biomagnification through the food chain. Absorption of any compound that has not been directed intravenously injected will entail transfer across membrane barriers before it reaches the systemic circulation, and the efficiency of absorption processes is highly dependent on the route of exposure. It is also important to note that distribution and elimination, although often considered separately, take place simultaneously. Elimination itself comprises of two kinds of processes, excretion and biotransformation, that are also taking place simultaneously. Elimination and distribution are not independent of each other as effective elimination of a compounds will prevent its distribution in peripheral tissues, whilst conversely, wide distribution of a compound will impede its excretion (OFlaherty 2000). Kinetic models attempt to predict the concentration of a toxicant at the target site from the administered dose. If often the ultimate toxicant, i.e. the chemical species that induces structural or functional alterations resulting in toxicity, is the compound administered (parent compound), it can also be a metabolite of the parent compound generated by biotransformation processes, i.e. toxication rather than detoxication (Timbrell 2000; Gregus and Klaassen 2001). The liver and kid neys are the most important excretory organs for non-volatile substances, whilst the lungs are active in the excretion of volatile compounds and gases. Other routes of excretion include the skin, hair, sweat, nails and milk. Milk may be a major route of excretion for lipophilic chemicals due to its high fat content (OFlaherty 2000). Toxicodynamics is the study of toxic response at the site of action, including the reactions with and binding to cell constituents, and the biochemical and physiological consequences of these actions. Such consequences may therefore be manifested and observed at the molecular or cellular levels, at the target organ or on the whole organism. Therefore, although toxic responses have a biochemical basis, the study of toxic response is generally subdivided either depending on the organ on which toxicity is observed, including hepatotoxicity (liver), nephrotoxicity (kidney), neurotoxicity (nervous system), pulmonotoxicity (lung) or depending on the type of toxic response, including teratogenicity (abnormalities of physiological development), immunotoxicity (immune system impairment), mutagenicity (damage of genetic material), carcinogenicity (cancer causation or promotion). The choice of the toxicity endpoint to observe in experimental toxicity testing is therefore of critical importance. In recent years, rapid advances of biochemical sciences and technology have resulted in the development of bioassay techniques that can contribute invaluable information regarding toxicity mechanisms at the cellular and molecular level. However, the extrapolation of such information to predict effects in an intact organism for the purpose of risk assessment is still in its infancy (Gundert -Remy et al. 2005). 1.2.4. Dose-response relationships 83A7DC81The theory of dose-response relationships is based on the assumptions that the activity of a substance is not an inherent quality but depends on the dose an organism is exposed to, i.e. all substances are inactive below a certain threshold and active over that threshold, and that dose-response relationships are monotonic, the response rises with the dose. Toxicity may be detected either as all-or-nothing phenomenon such as the death of the organism or as a graded response such as the hypertrophy of a specific organ. The dose-response relationship involves correlating the severity of the response with exposure (the dose). Dose-response relationships for all-or-nothing (quantal) responses are typically S-shaped and this reflects the fact that sensitivity of individuals in a population generally exhibits a normal or Gaussian distribution. Biological variation in susceptibility, with fewer individuals being either hypersusceptible or resistant at both end of the curve and the maj ority responding between these two extremes, gives rise to a bell-shaped normal frequency distribution. When plotted as a cumulative frequency distribution, a sigmoid dose-response curve is observed ( 1.2). Studying dose response, and developing dose response models, is central to determining safe and hazardous levels. The simplest measure of toxicity is lethality and determination of the median lethal dose, the LD50 is usually the first toxicological test performed with new substances. The LD50 is the dose at which a substance is expected to cause the death of half of the experimental animals and it is derived statistically from dose-response curves (Eaton and Klaassen 2001). LD50 values are the standard for comparison of acute toxicity between chemical compounds and between species. Some values are given in Table 1.1. It is important to note that the higher the LD50, the less toxic the compound. Similarly, the EC50, the median effective dose, is the quantity of the chemical that is estimated to have an effect in 50% of the organisms. However, median doses alone are not very informative, as they do not convey any information on the shape of the dose-response curve. This is best illustrated by 1.3. While toxicant A appears (always) more toxic than toxicant B on the basis of its lower LD50, toxicant B will start affecting organisms at lower doses (lower threshold) while the steeper slope for the dose-response curve for toxicant A means that once individuals become overexposed (exceed the threshold dose), the increase in response occurs over much smaller increments in dose. Low dose responses The classical paradigm for extrapolating dose-response relationships at low doses is based on the concept of threshold for non-carcinogens, whereas it assumes that there is no threshold for carcinogenic responses and a linear relationship is hypothesised (s 1.4 and 1.5). The NOAEL (No Observed Adverse Effect Level) is the exposure level at which there is no statistically or biologically significant increase in the frequency or severity of adverse effects between exposed population and its appropriate control. The NOEL for the most sensitive test species and the most sensitive indicator of toxicity is usually employed for regulatory purposes. The LOAEL (Lowest Observed Adverse Effect Level) is the lowest exposure level at which there is a statistically or biologically significant increase in the frequency or severity of adverse effects between exposed population and its appropriate control. The main criticism of NOAEL and LOAEL is that there are dependent on study design, i.e. the dose groups selected and the number of individuals in each group. Statistical methods of deriving the concentration that produces a specific effect ECx, or a benchmark dose (BMD), the statistical lower confidence limit on the dose that produces a defined response (the benchm ark response or BMR), are increasingly preferred. To understand the risk that environmental contaminants pose to human health requires the extrapolation of limited data from animal experimental studies to the low doses critically encountered in the environment. Such extrapolation of dose-response relationships at low doses is the source of much controversy. Recent advances in the statistical analysis of very large populations exposed to ambient concentrations of environmental pollutants have however not observed thresholds for cancer or non-cancer outcomes (White et al. 2009). The actions of chemical agents are triggered by complex molecular and cellular events that may lead to cancer and non-cancer outcomes in an organism. These processes may be linear or non-linear at an individual level. A thorough understanding of critical steps in a toxic process may help refine current assumptions about thresholds (Boobis et al. 2009). The dose-response curve however describes the response or variation in sensitivity of a population. Biologica l and statistical attributes such as population variability, additivity to pre-existing conditions or diseases induced at background exposure will tend to smooth and linearise the dose-response relationship, obscuring individual thresholds. Hormesis Dose-response relationships for substances that are essential for normal physiological function and survival are actually U-shaped. At very low doses, adverse effects are observed due to a deficiency. As the dose of such an essential nutrient is increased, the adverse effect is no longer detected and the organism can function normally in a state of homeostasis. Abnormally high doses however, can give rise to a toxic response. This response may be qualitatively different and the toxic endpoint measured at very low and very high doses is not necessarily the same. There is evidence that nonessential substances may also impart an effect at very low doses ( 1.6). Some authors have argued that hormesis ought to be the default assumption in the risk assessment of toxic substances (Calabrese and Baldwin 2003). Whether such low dose effects should be considered stimulatory or beneficial is controversial. Further, potential implications of the concept of hormesis for the risk management of the combinations of the wide variety of environmental contaminants present at low doses that individuals with variable sensitivity may be exposed to are at best unclear. 1.2.5. Chemical interactions In regulatory hazard assessment, chemical hazard are typically considered on a compound by compound basis, the possibility of chemical interactions being accounted for by the use of safety or uncertainty factors. Mixture effects still represent a challenge for the risk management of chemicals in the environment, as the presence of one chemical may alter the response to another chemical. The simplest interaction is additivity: the effect of two or more chemicals acting together is equivalent to the sum of the effects of each chemical in the mixture when acting independently. Synergism is more complex and describes a situation when the presence of both chemicals causes an effect that is greater than the sum of their effects when acting alone. In potentiation, a substance that does not produce specific toxicity on its own increases the toxicity of another substance when both are present. Antagonism is the principle upon which antidotes are based whereby a chemical can reduce the harm ca used by a toxicant (James et al. 2000; Duffus 2006). Mathematical illustrations and examples of known chemical interactions are given in Table 1.2. Table 1.2. Mathematical representations of chemical interactions (reproduced from James et al., 2000) Effect Hypothetical mathematical illustration Example Additive 2 + 3 = 5 Organophosphate pesticides Synergistic 2 + 3 = 20 Cigarette smoking + asbestos Potentiation 2 + 0 = 10 Alcohol + carbon tetrachloride Antagonism 6 + 6 = 8 or 5 + (-5) = 0 or 10 + 0 = 2 Toluene + benzene Caffeine + alcohol Dimercaprol + mercury There are four main ways in which chemicals may interact (James et al. 2000); 1. Functional: both chemicals have an effect on the same physiological function. 2. Chemical: a chemical reaction between the two compounds affects the toxicity of one or both compounds. 3. Dispositional: the absorption, metabolism, distribution or excretion of one substance is increased or decreased by the presence of the other. 4. Receptor-mediated: when two chemicals have differing affinity and activity for the same receptor, competition for the receptor will modify the overall effect. 1.2.6. Relevance of animal models A further complication in the extrapolation of the results of toxicological experimental studies to humans, or indeed other untested species, is related to the anatomical, physiological and biochemical differences between species. This paradoxically requires some previous knowledge of the mechanism of toxicity of a chemical and comparative physiology of different test species. When adverse effects are detected in screening tests, these should be interpreted with the relevance of the animal model chosen in mind. For the derivation of safe levels, safety or uncertainty factors are again usually applied to account for the uncertainty surrounding inter-species differences (James et al. 2000; Sullivan 2006). 1.2.7. A few words about doses When discussing dose-response, it is also important to understand which dose is being referred to and differentiate between concentrations measured in environmental media and the concentration that will illicit an adverse effect at the target organ or tissue. The exposure dose in a toxicological testing setting is generally known or can be readily derived or measured from concentrations in media and average consumption (of food or water for example) ( 1.7.). Whilst toxicokinetics help to develop an understanding of the relationship between the internal dose and a known exposure dose, relating concentrations in environmental media to the actual exposure dose, often via multiple pathways, is in the realm of exposure assessment. 1.2.8. Other hazard characterisation criteria Before continuing further, it is important to clarify the difference between hazard and risk. Hazard is defined as the potential to produce harm, it is therefore an inherent qualitative attribute of a given chemical substance. Risk on the other hand is a quantitative measure of the magnitude of the hazard and the probability of it being realised. Hazard assessment is therefore the first step of risk assessment, followed by exposure assessment and finally risk characterization. Toxicity is not the sole criterion evaluated for hazard characterisation purposes. Some chemicals have been found in the tissues of animals in the arctic for example, where these substances of concern have never been used or produced. This realization that some pollutants were able to travel far distances across national borders because of their persistence, and bioaccumulate through the food web, led to the consideration of such inherent properties of organic compounds alongside their toxicity for the purpose of hazard characterisation. Persistence is the result of resistance to environmental degradation mechanisms such as hydrolysis, photodegradation and biodegradation. Hydrolysis only occurs in the presence of water, photodegradation in the presence of UV light and biodegradation is primarily carried out by micro-organisms. Degradation is related to water solubility, itself inversely related to lipid solubility, therefore persistence tends to be correlated to lipid solubility (Francis 1994). The persistence of inorganic substances has proven more difficult to define as they cannot be degraded to carbon and water. Chemicals may accumulate in environmental compartments and constitute environmental sinks that could be re-mobilised and lead to effects. Further, whilst substances may accumulate in one species without adverse effects, it may be toxic to its predator(s). Bioconcentration refers to accumulation of a chemical from its surrounding environment rather than specifically through food uptake. Conversely, biomagnification refers to uptake from food without consideration for uptake through the body surface. Bioaccumulation integrates both paths, surrounding medium and food. Ecological magnification refers to an increase in concentration through the food web from lower to higher trophic levels. Again, accumulation of organic compounds generally involves transfer from a hydrophilic to a hydrophobic phase and correlates well with the n-octanol/water partition coefficient (Herrchen 2006). Persistence and bioaccumulation of a substance is evaluated by standardised OECD tests. Criteria for the identification of persistent, bioaccumulative, and toxic substances (PBT), and very persistent and very bioaccumulative substances (vPvB) as defined in Annex XIII of the European Directive on the Registration, Evaluation, Authorisation and Restriction of Chemicals (REACH) (Union 2006) are given in table 1.3. To be classified as a PBT or vPvB substance, a given compound must fulfil all criteria. Table 1.3. REACH criteria for identifying PBT and vPvB chemicals Criterion PBT criteria vPvB criteria Persistence Either: Half-life > 60 days in marine water Half-life > 60 days in fresh or estuarine water Half-life > 180 days in marine sediment Half-life > 120 days in fresh or estuarine sediment Half-life > 120 days in soil Either: Half-life > 60 days in marine, fresh or estuarine water Half-life > 180 days in marine, fresh or estuarine sediment Half-life > 180 days in soil Bioaccumulation Bioconcentration factor (BCF) > 2000 Bioconcentration factor (BCF) > 2000 Toxicity Either: Chronic no-observed effect concentration (NOEC) substance is classified as carcinogenic (category 1 or 2), mutagenic (category 1 or 2), or toxic for reproduction (category 1, 2 or 3) there is other evidence of endocrine disrupting effects 1.3. Some notions of Environmental Epidemiology A complementary, observational approach to the study of scientific evidence of associations between environment and disease is epidemiology. Epidemiology can be defined as â€Å"the study of how often diseases occur and why, based on the measurement of disease outcome in a study sample in relation to a population at risk.† (Coggon et al. 2003). Environmental epidemiology refers to the study of patterns and disease and health related to exposures that are exogenous and involuntary. Such exposures generally occur in the air, water, diet, or soil and include physical, chemical and biologic agents. The extent to which environmental epidemiology is considered to include social, political, cultural, and engineering or architectural factors affecting human contact with such agents varies according to authors. In some contexts, the environment can refer to all non-genetic factors, although dietary habits are generally excluded, despite the facts that some deficiency diseases are envir onmentally determined and nutritional status may also modify the impact of an environmental exposure (Steenland and Savitz 1997; Hertz-Picciotto 1998). Most of environmental epidemiology is concerned with endemics, in other words acute or chronic disease occurring at relatively low frequency in the general population due partly to a common and often unsuspected exposure, rather than epidemics, or acute outbreaks of disease affecting a limited population shortly after the introduction of an unusual known or unknown agent. Measuring such low level exposure to the general public may be difficult when not impossible, particularly when seeking historical estimates of exposure to predict future disease. Estimating very small changes in the incidence of health effects of low-level common multiple exposure on common diseases with multifactorial etiologies is particularly difficult because often greater variability may be expected for other reasons, and environmental epidemiology has to rely on natural experiments that unlike controlled experiment are subject to confounding to other, often unknown, risk factors. However, it may still be of i mportance from a public health perspective as small effects in a large population can have large attributable risks if the disease is common (Steenland and Savitz 1997; Coggon et al. 2003). 1.3.1. Definitions What is a case? The definition of a case generally requires a dichotomy, i.e. for a given condition, people can be divided into two discrete classes the affected and the non-affected. It increasingly appears that diseases exist in a continuum of severity within a population rather than an all or nothing phenomenon. For practical reasons, a cut-off point to divide the diagnostic continuum into ‘cases and ‘non-cases is therefore required. This can be done on a statistical, clinical, prognostic or operational basis. On a statistical basis, the ‘norm is often defined as within two standard deviations of the age-specific mean, thereby arbitrarily fixing the frequency of abnormal values at around 5% in every population. Moreover, it should be noted that what is usual is not necessarily good. A clinical case may be defined by the level of a variable above which symptoms and complications have been found to become more frequent. On a prognostic basis, some clinical findings may carry an a dverse prognosis, yet be symptomless. When none of the other approaches is satisfactory, an operational threshold will need to be defined, e.g. based on a threshold for treatment (Coggon et al. 2003). Incidence, prevalence and mortality The incidence of a disease is the rate at which new cases occur in a population during a specified period or frequency of incidents. Incidence = The prevalence of a disease is the proportion of the population that are cases at a given point in time. This measure is appropriate only in relatively stable conditions and is unsuitable for acute disorders. Even in a chronic disease, the manifestations are often intermittent and a point prevalence will tend to underestimate the frequency of the condition. A better measure when possible is the period prevalence defined as the proportion of a population that are cases at any time within a stated pe

The Chrysanthemums :: essays research papers

1. The Chrysanthemums On Henry Allen's ranch east of Salinas Elisa plants yellow chrysanthemums as Henry is selling thirty head of cattle to agents of the Western Meat Company. After he and Scotty go to round up the cattle, a tinker shows up. He asks for work which Elisa says she hasn't. He asks for seeds for a lady on his route. Elisa gives him seedlings with instructions, and then she finds work for him which he does professionally. To celebrate the sale Henry drives her to Salinas for dinner at the Cominos Hotel and a movie; they drive past the tinker on the road and she privately weeps. 2. The White Quail Mary has her garden designed before its lot is bought, before she's married. She picks Harry because she thinks the garden will like him. After the house is built and the garden established Harry finds her perfect though untouchable. She doesn't care for his occupation (making loans for cars); it's unfair. She routinely locks him from her tiny bedroom on the garden. He tries the lock and leaves quietly. She refuses to let him have a setter pup since it might damage her garden. After a white quail visits the cement pond she fears a cat will come and asks Harry to put out poison fish. He refuses but will try to hit such a cat with his new air rifle. Next morning he shoots the white quail then tells Mary it was the cat he buried. 3. Flight Mama Torres makes Emilo and Rosy fish when they can. Pepà ©, who is beautiful but lazy, is sent to Monterey for medicine and salt. At Mrs. Rodriguez's he kills a man with his father's black switchblade knife. He returns before dawn, then rides into the high hills as his family bids him, now a man, adios. After a day's riding he sleeps and is awakened by a horse down the trail. He rides another day before his horse is shot out from under him. He exchanges shots and receives a granite splinter wound in his right hand. He runs on for several days and is finally shot dead. 4. The Snake Young marine biologist Dr. Phillips brings a sack of starfish from the tide pool to his laboratory on the cannery street in Monterey. The lab: rattlesnakes, rats, cats; killing a cat. Arrival of a tall, lean woman just as he begins timed work making a starfish embryo series. While she waits he begins embalming the cat. She wants to buy the male rattlesnake which she wants to keep in the lab. Her snakish behavior during the feeding annoys Phillips. The starfish series is ruined. She never comes back. 5. Breakfast A cold pre-dawn, by a country road, I see a tent with a lit campstove.

Plastic Water Bottles Essay

Specific Purpose: To persuade the audience to stop using plastic bottles because of the health concerns and its harmful effects on the environment. Introduction: How many people know that in the Pacific Ocean there’s a huge island consisting of plastic bags, bottles, and even toys that’s estimated to be twice the size of Texas? For those you didn’t know now you do, environmentalists refer to this island as the Great Plastic Vortex. As plastic use increases, the vortex will only grow more and more. In 2007 8. billion tons of bottled waters were sold, so the number of plastic water bottles is only increasing and ends up accumulating to the great plastic vortex. We can start helping the environment by stopping the usage of plastic water bottles. Thesis statement: Plastic water bottles are being questioned about their safety to both our health and our environment as well. Preview: Today, we will discuss the problems that come about with plastic water bottles and the causes and solutions to help our health and our environment as well. Body: I. There are multiple problems with plastic water bottles, which include danger to people’s health and the harmful effects to our environment. A. Plastic bottles contain a toxin called BPA, which can be a danger to our health. 1. According to Kate Barrett from ABC News, retrieved on April 15, 2008, a report found that exposure to this toxin could have effects on young children and infants by causing changes in the brain development. 2. As we are being exposed to this toxin at younger ages, we stand a higher risk of diseases and health problems. B. There are several ways in which plastic bottles are harmful to the environment. In an article on October 29, 2007 issue of Blast Magazine, Jack Bell says and I quote plastic generates toxic emissions and pollutants that contribute to global warming. 2. As a result of this, promoting the usage of plastic bottles will only create more chaos to our environment. Transition: The problems of the BPA’s potential to harm people combined with the dangerous effects of plastic water bottles on the environment can be associated with two main causes, which we will now go into. I. The two specific causes can be identified as: consumer’s ignorance and the producers lack of responsibility. A.  Consumers have certain habits that don’t even faze them; it is in fact second nature to them. 1. Plastic water bottles are meant for one time use only, yet tons of people reuse them. Most of us think using the same bottle again helps the environment as well as saves us money, but it may be costing us our health. 2. According to the â€Å"Time Magazine†, Lisa Cullen says, plastic bottles are meant for disposable and for one time use only. Reusing them causes bacteria to build up, spreading it throughout the mouth. B. The food and drug administration has deemed BPA safe, but studies and research doubt their decision. 1.  According to the â€Å"Time Magazine†, Bryan Walsh states this toxin might be linked to a variety of diseases, such as cancer and reproductive problems. 2. Even though the FDA has been unintentionally endorsing the use of this chemical, they have been effectively exposing people. Transition: Now that we have explored the causes, we examine the solutions we can do ourselves personally. II. Most of the solutions have to do with a little bit of self -effort. A. One solution is to write to the members of congress, the FDA, and/or the governor to urge for stricter regulations for bottled water labeling, public disclosure, and safety. .The Natural Resources Defense Council (NRDC) recommends writing to producers to display information about whether it has been approved by the Environmental Protection Agency. 2. According to the natural resources defense council there approach will be to write about setting strict limits about contamination and bacteria. B. Another solution is to try to use a non-plastic water bottle. It is recommended that people try to change to either stainless steel or aluminum water bottles. Conclusion: I. Conclusively, now you are aware of the dangers of plastic, more importantly plastic water bottles. With a better understanding of what is causing these problems-consumers ignorance as well as the producers lack of responsibility- we can concentrate on solving this threat. II. As more and more water bottles are disposed, they are only adding to the already giant land fields of plastic bottles. As more and more people drink from water bottles, it is only causing a higher risk for health problems. III. We can take from this as a realization- we need to start doing our part to help save our environment as well as our health.

President of the Academy of Finland

Alvar Aalto is considered a modern architect, yet his work exhibits a carefully crafted balance of intricate and complex forms, spaces, and elements, and reveals traditionalism rooted in the cultural heritage and physical environment of Finland. He was born Hugo Alvar Henrik Aalto in the Ostro-Bothnian village of Kourtane, Finland in 1898. He graduated with honors from Helsinki Polytechnic in 1921 after which he opened his own practice. He held the position of Professor of Architecture at MIT 1946 to 1948, and was President of the Academy of Finland 1963-68.Aalto was a religious man and a practicing Christian. Although his early work borrowed from the neoclassic movement, he eventually adapted the symbolism and functionalism of the Modern Movement to generate his plans and forms. It allowed him to create a series of functional and yet non-reductionist buildings. Even though he borrowed from the International style, his use of color, texture, and structure was creative and new in its own right. He refined the modern European architecture and molded it to develop and define a new Finnish architecture.His designs were always contextual as they were responsive to site, material and form unlike most of the other modernist architects who designed in isolation. Aalto produced a lot of work in countries like Germany, America and Sweden. A lot of his projects under construction at the same time have overlapping ideas and details. Moreover, Aalto was of the few architects who designed to the last detail and was aware and receptive to the needs of the people and the environment. Aalto was a master of form and planning.His buildings have provided renewed inspiration in the face of widespread disillusionment with high modernism on one hand, and post-modernism on the other. Aalto's mature work embodies a unique functionalist/expressionist and humane style, successfully applied to libraries, civic centers, churches, housing, etc. In their scale, mastery of light and distincti ve palettes, Aalto’s buildings were characterized with a robust humanism. During the mid-1930s Alvar Aalto's work began to embody a more tactile, romantic, and picturesque posture, becoming less machinelike in imagery.The presence of these characteristics in his work, coupled with a seemingly rekindled interest in Finnish vernacular building traditions and a concern for the alienated individual within modern mass society, signals a movement away from the functionalist tenets that formed his architecture in the early 1930s. In renouncing industrialized production as a compositional and formal ordering sensibility, Alvar Aalto moved toward a more personal style which solidified over the next decade, a direction achieving maturity in his work executed after World War II.Aalto’s Saynatsalo Town Hall, built between 1942- 1952, in Saynatsalo, Finland, was one of the civic projects he undertook. The building had a pioneering effort in using brick. Never before had red bricks been used in civic buildings in Finland as they common concept on them not being too formal existed. However, bricks were warm with reference to color and not as formidable looking as stone, so they fit right into context in the cold harsh climate of Finland. Aalto had strong political opinions and wanted to make the town governments strong enough to be able to stand up to central governments.He had individual freedom in mind while designing the Saynatsalo Town Hall. He changed the program brief to increase the footprint and the mass of the building. He introduced a courtyard in the centre with single loaded corridors to ensure well-lit offices and corridors. He utilized the principal idea of the Greek agora when designing the town hall. The building followed the contours of site and the courtyard level defined the spatial datum. The use of exposed timber trusses was there as well as a double height council chamber to give it that hierarchy.Similarly, the Baker House Dormitory, at t he MIT campus in USA was designed and built between 1946- 1949. In this building, Aalto comes up with a slightly different approach which he later carries on in his other projects such as the Church of the 3 crosses in Vuokesenniska. He uses the concept of duality and carries it out in detail throughout the project in the sinuous serpentine wall. It’s a large brick building with repetitive elements. The duality exists in the background vs. foreground relationship of the building, in the repetitive vs.the unique, the curvy vs. the rectilinear, the planar vs. the volumetric, the large vs. the small and the brick vs. the marble. The unique staircase projects out of the buildings and becomes the diagonal element. It gives a certain degree of dynamism to the project. Like the Baker House Dormitory, Aalto juxtaposes the rectilinear against the curvilinear in a lot of his other projects. He breaks away from the idea of symmetry and uses asymmetry to his advantage and for functional reasons.Aalto’s later work had a lot to do with acoustics as he attempted at making acoustically sound buildings such as the Finlandia hall or the Church of the 3 crosses. Before totally moving towards architecture ad designing buildings, Aalto designed products and furniture. So in 1935, with the assistance of Maire Gullichsen and with Nils Gustav Hahl as director, the firm of Artek was formed, which produced and marketed Alvar Aalto's furniture, fabric, and glassware designs. Amongst some of his most famous product designs is the Savoy vase which was an organic form.Aalto’s vases had a fluid sinuous shape in varying colors that let the users decide the use. They are being manufactured to this day. Aalto’s furniture was mainly bent wood light furniture which followed the principles of clean functional design. He made the Paimio Chair for the sanitorium in 1931-32. It was inspired by the tubular steel Marcel Breuer chairs in his own home and was devised to ease the breathing of tuberculosis patients in a combination of molded wood and plywood which, Aalto believed, would be warmer and more comfortable than metal.Alvar Aalto died in 1976 in Helsinki. Over the course of his 50-year career, Aalto, unlike a number of his contemporaries, did not rely on modernism's fondness for industrialized processes as a compositional technique, but forged an architecture influenced by a broad spectrum of concerns. Alvar Aalto's architecture manifests an understanding of the psychological needs of modern society, the particular qualities of the Finnish environment, and the historical, technical, and cultural traditions of Scandinavian architecture.Bibliography : †¢ Gardner’s Art through the Ages †¢ Alvar Aalto (Archipocket) by Alvar Aalto and Aurora Cuito †¢ Alvar Aalto by Richard Weston †¢ www. wikipedia. org/wiki/Alvar_Aalto †¢ www. scandinaviandesign. com/Alvar_Aalto †¢ www. designmuseum. org †¢ http://virtual. fi nland. fi/netcomm/news/showarticle. asp? intNWSAID=26966 †¢ http://architect. architecture. sk/alvar-aalto-architect/alvar-aalto-architect. php †¢ Finnish Architecture and the Modernist Tradition by Malco Quantrill †¢ www. artek. fi

Effects of ww1 essays

Effects of ww1 essays In my opinion, the outcome of World War I harmed the domestic policies and systems of the United States. From the result of the war, there were changes dealing with politics, economics, and public opinions in the United States. Relating to politics, Wilsons goal of the United States becoming part of the League of Nations was an overall negative effect on Wilsons reputation. The constant nagging of Wilson to get the United States to join hurt his reputation by the people and the government. Although the United States did not join, the League of Nations was created but did not live up to the countries expectations. The Treaty of Versailles also a benefactor in contributing negative outcomes from the war. Wilsons struggle to get the Senate to approve the Treaty of Versailles also harmed his relations with the government. Under this agreement, the allies forced Germany to pay a huge war debt. The treaty led to growing resentment and desperation in Germany toward both the allie s and America. This sentiment eventually would lead into World War II. Relating to changes in economics dealt with money. European countries were printing more and more money to pay back their debts. Because of this increase in money production, the countries were brought into periods of inflation. This hurt the economy of the United States because the United States could not perform affairs with the allied countries because of their debts. During the war, the United States spent a lot of money because of the necessity of new weapons and machinery in fighting. Since the major industries that were needed during the war were now insufficient, many Americans were now put of jobs. These debts and unemployment rates brought about the stock market crash of 1929. After the war, disillusionment towards the government spread throughout the world. Towards the end of the war, people had developed a mistrustful opi ...