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Q. What is the role of school nurse?A."Professional responsibilities have not changed overall," said Carolyn Duff, president of the National Association of School Nurses. "What has changed is the increasing number of students with chronic health conditions, including asthma, diabetes and severe allergies. All of these conditions have the potential for life-threatening emergencies. What this means for school nurses is an increasing need to train and maintain a competent team of unlicensed school personnel to prevent, recognize and respond to emergencies.”School nurses' duties expand with changing timesMaria SonnenbergBeyond sniffles and sneezes, they must manage complex conditions and chronic illnesses.(Photo: Tim Shortt, Florida Today)STORY HIGHLIGHTSSome nurses are assigned to several schools during a workweekNational Association of School Nurses recommends a 1-to-750 ratio of nurses to well studentsSchool nurses also go beyond the traditional boundaries of kindergarten to high school students to provide Head Start screenings and physicalsThe Boy Scout motto of "be prepared" equally applies to today's school nurses, who not only deal with the typical bruises and tummy aches that have always been part of school life, but must now contend with a student population that is increasingly more medically fragile.As school systems face budget cuts, nurses must also adapt to a "migrant" lifestyle as they are assigned to several schools during a workweek."There have been a lot of changes in the last 20 years," said Pamelia Hamilton, community health nurse consultant and school health coordinator for the Brevard Department of Health, which supervises the 160 nurses and health technicians who serve public schools in Brevard County.According to the National Association of School Nurses, a third of all school districts reduced nursing staff in the past year because of the recession, and a quarter of all school districts in the nation don't have nurses. In these districts, medical emergencies are typically handled by a school's front office staff, the way they were in Brevard until the late 1980s, when nurses were first introduced to local schools.Brevard's ratio of nurse to students — about 1 per 450 — is exemplary, when considering that Florida, with a nurse-to-student ratio of 1 to 2,537, is at the bottom of the list in the number of nurses in schools. Only Utah, North Dakota and Michigan are worse off in numbers. Vermont, on the other hand, has a ratio of 1 nurse per 396 students.The National Association of School Nurses recommends a 1-to-750 ratio for well students and 1 to 125 in student populations with complex health care needs."People who live here think our nursing program is the norm everywhere, but when they move out, they are in for a shock," Hamilton said."What we do is so extraordinary that we've been recognized with several awards."The health department hires, trains and pays the school district's nurses. In turn, the district reimburses the health department for most costs incurred in running the program.New responsibilitiesThe foremost duty of a school nurse is to keep kids learning as long as possible. These days, that can take the form of fixing an accidentally stapled finger or a nasty cold, as it did years ago, but it can also entail helping a pregnant teen stay in school and teaching them to become a good mother. Brevard's Teen Parent Program, for example, assists about 250 pregnant girls at Palm Bay, Eau Gallie, Titusville and Cocoa high schools.Nursing supervisor Travia Williams Torey McGhee in the Head Start classroom in Cocoa High School in Brevard County, Fla. (Photo: Tim Shortt, Florida Today)"We explain to them what is happening to their bodies and train them to care for their babies," Hamilton said.School nurses today also go beyond the traditional boundaries of kindergarten to high school students. Nurse Travia Williams and her team of technicians travel through the county's Head Start program sites to provide the screening, physicals and related services necessary for the little ones to be better prepared when their school days start.Other nurses are devoted to one-on-one care with medically needy students who otherwise would not be able to attend school.School nurses are also tasked with managing children's increasingly complex medical conditions and chronic illnesses. A child may have a tracheotomy or require nasal gastric tube feeds by an experienced nurse. Nurses may be required to monitor students' insulin pumps and keep track of inhalers and EpiPens. In some instances, Medicaid pays for a private duty nurse to be with the student one-on-one throughout the school day."Professional responsibilities have not changed overall," said Carolyn Duff, president of the National Association of School Nurses. "What has changed is the increasing number of students with chronic health conditions, including asthma, diabetes and severe allergies. All of these conditions have the potential for life-threatening emergencies. What this means for school nurses is an increasing need to train and maintain a competent team of unlicensed school personnel to prevent, recognize and respond to emergencies."Another change is a welcome change," Duff said. "There is now a greater emphasis on prevention and wellness in health care.""School nurses are identifying students at risk for both health and learning problems at an early age and are able to initiate early referrals for intervention and treatment."The National Association of School Nurses lists data that underscores why school nurses' duties are so varied these days. Among students ages 12 to 19, pre-diabetes and diabetes has increased from 9 percent in 1999 to 23 percent in 2008, and 32 percent of children ages 2 to 19 are obese. More than 10 million children suffer from asthma. The prevalence of food allergies among children younger than 18 increased 19 percent from 1997 to 2007.Mental health issues among students are on the rise. School nurses estimate they spent about a third of their time providing mental health services.Overall, 15 percent to 18 percent of children and adolescents have a chronic health condition, nearly half of whom could be considered disabling.ACA's impactThe enactment of the Affordable Care Act could provide an opportunity to strengthen a nurse program that serves the nation's 52 million school-age children. For many of these students, the school nurse is the sole provider of access to health care.Health care reform's emphasis on wellness dovetails with the goals of school nurses, who provide continuity of care and promote healthy lifestyles for students during their most critical developmental years. They perform early intervention services such as periodic assessments for vision, hearing and dental problems with the goal of removing barriers to learning.States are testing different health care models for high value rather than high cost and high volume. School nurses are included in the plan."Health care reform will lead to greater opportunity for school nurses to successfully connect students from low-income families to medical homes, because more students will be insured," Duff said."More widespread access to medical homes will provide greater opportunity for school health services to focus on prevention and wellness and tighter management of students with chronic disease."National Association of School NursesThe Roles & Responsibilities of School Health Nursingby Beth GreenwoodWhen the first school nurse was hired in New York City in 1902, her primary goal, according to the National Association of School Nurses, was to reduce student absences from communicable diseases. In the years since Lina Rogers first implemented the practice of school nursing, the role has expanded, but the goal has not changed. School nurses continue to perform valuable services to schools, individual students and the community.Children's Health NeedsThe rationale for placing nurses in school is based on the concept that a child with unmet health needs will have difficulty learning. School nurses are ideally placed to assess physical, emotional, mental and social health needs of the school children for whom they care. Chronic medical conditions such as asthma, epilepsy, Type I diabetes and mental health problems can increase absenteeism and affect learning. The school nurse can help manage the medical care of students who have chronic diseases, and promote education from the primary to the high school level.Health Education and ManagementThe National Association of School Nurses sees the school nurse as taking a lead role in the school community to oversee school health policies and programs. In addition to providing direct services, the school nurse is ideally placed to promote health education and to integrate health-care solutions into the school setting. As the number of children with increasingly complex medical problems has risen, school nurses have taken the primary role in issues such as the management of medical equipment and complicated treatments while the child is at school.Screening and ReferralsA school nurse may perform a wide variety of direct care tasks such as screening students for scoliosis, vision or hearing problems. When a problem is identified, the nurse will make referrals to the appropriate specialist or work with the primary care doctor to assure the child’s needs are met. The school nurse collaborates with parents or other family members and serves as the liaison between school personnel, family, health-care providers and the community at large.Emergency and Public Health FunctionsAs a nursing professional, prepared at the baccalaureate level, the school nurse often practices independently. In addition to routine care such as medication management and screenings, she may act as the first responder in health emergencies for both students and school staffers. School nurses also perform public health functions such as disease surveillance, to increase the opportunity to recognize a communicable disease outbreak and intervene early. A school nurse also helps to assure immunization compliance and promotes overall student health.Performance ExpectationsThe National Association of School Nurses has a number of expectations for school nurse performance. These include such responsibilities as facilitating normal development, providing leadership in the promotion of health and safety, acting as a case manager and intervening in both actual and potential health problems. The school nurse is an essential component of school educational teams such as committees for special education or individual educational plan teams, which must take health issues into account in their decision-making processes.

I could not understand if you are looking for syllabus of M.Sc in Environmental Course for your coursework or for preparation of entrance exam. If you are looking for coursework in Jawaharlal Nehru University, New Delhi; here you go.The M. Sc. programme is spread over four semesters. It carries 64 credits and comprises of four different components viz: I) Teaching II) Lab Work III) Field Work and IV) Dissertation.Distribution of credits for M. Sc. Programme is:Total Credits for M. Sc. Degree Programme = 64 credits I) Teaching = 50 creditsII) Lab work, Field work and Dissertation = 14 creditsDistribution of credits for teaching (Total 50 credits)i) Core courses = 26 credits ii) Optional courses = 24 creditsDistribution of credits for Lab work, Field work and Dissertation (Total 14 credits)a) Lab work = 6 credits (Lab Work I =3 credits; Lab Work II =3 credits)b) Field work = 3 creditsc) Dissertation = 5 creditsI) Teaching (50 credits)Teaching is a major component of the programme. It shares 50 credits out of total 64. The remaining three components i.e. Lab work, field work and dissertation share remaining 14 creditsVarious courses offered under M. Sc. programme are categorized as:A) Core courses B) Non Credit courses and C) Optional courses.Altogether there are 46 courses: 13 as core, 2 non credit courses and 31 optional courses. All core courses are offered in I and II semesters and all optional courses are offered in III and IV semester of the M. Sc programme.All Core Courses are of 2 credits each and compulsory for all the students. Non credit courses do not carry any credits, however, as per the JNU ordinance, completion of such courses by every student is a mandatory requirement for the award of the degree. Optional courses are of 3 credits each and cover all specialized courses across different sub disciplines of environmental sciences namely; Mathematics, Physics, Statistics, Geology, Chemistry and Biology. There is a running list of 31 optional courses, out of which students will have to choose any 8 optional courses (four in each semester) to obtain 24 credits.II) Lab work, Field work and Dissertation (14 credits)a) Lab work (6 credits)The lab work component is spread over first two semesters and is called as Lab work I and Lab work II to be completed in I and II semesters respectively. Under Lab Work I and II, sets of experiments specially designed for M. Sc. students by faculty members of the school are carried out in M. Sc. lab or in the lab of the concerned faculty member during the period of five working days in the afternoon.b) Field work (3 credits)To strengthen the field work component and to have a wider exposure of the field conditions, students will undergo extensive field work which will help them in developing the understanding of different aspects of environmental sciences. Field work is completed in second semester. Each student will submit his/her field work report for evaluation.c) Dissertation (5 credits)Each student will work for M. Sc. Project under the supervision of formally assigned supervisor in the school. Assigning of supervisor will be based on academic interest shown by the student in research specialization of the concerned faculty member followed by the consent given by the faculty member to supervise the project work of that particular student. Student shall complete the process of academic interaction to obtain teachers consent to supervise his/her project work by the end of second semester. The work on research project will start in 3rd semester under the supervision of concerned faculty member in his /her lab and will be completed by 4th semester with writing and submission of dissertation. Dissertation will be evaluated by a 3 member expert committee. Students will have to present their work and defend it in an open viva- voce.LIST OF COURSESA) Core Courses (Compulsory for all)(Total courses 13, Total credits: 13 x 2 =26)Remedial Mathematics ES-101ORRemedial Biology ES-102Environmental Chemistry ES-103Earth processes ES-104Ecology ES-105Statistics ES-106Environmental Pollution ES-107Natural hazards and disaster management ES-108Environmental Impact Assessment ES-109Energy and Environment ES-110Remote sensing and Geoinformatics ES-111Environmental Biochemistry and Toxicology ES-112Marine environment ES 113Soil Science ES-114B) Non- Credit Courses (Compulsory for all)Current Environmental Issues ES-11516. Scientific Writings and Ethics ES-116C) Optional Courses – (Total courses- 31 of 3 credits each; Students will have tochoose any 8 courses to obtain total 24 credits)1. Environmental Modeling ES-2012. Climatology ES-2023. Meteorology ES-2034. Noise Pollution ES-2045. Environmental Physics ES-2056. Environmental instrumentation and techniques ES-2067. Geochemistry ES-2078. Groundwater Hydrology ES-2089. Oceanography ES-20910. Natural resource Management ES-21011. Glaciology ES-21112. Biogeochemistry ES-21213. Environmental Geology ES-21314. Water Resources ES-21415. Air Pollution Chemistry ES-21516. Water Pollution Chemistry ES-21617. Soil Pollution Chemistry ES-21718. Solid and Hazardous Wastes Management ES-21819. Metrology ES-21920. Pollution Biology ES-22021. Biodiversity and conservation ES-22122. Forest ecology ES-22223. Microbial Ecology ES-22324. Ecosystem Dynamics ES-22425. Environmental Biophysics ES-22526. Ecology and sustainable development ES-22627. Environmental Xenobiotics and human health ES-22728. Fundamentals of Molecular Biology and Biotechnology ES-22829. Applied biotechnology and Bioremediation ES-22930. Eco-toxicology ES-23031. Environmental and Occupational health ES-231D) Lab Work1. Lab work I (3 credits) ES-2322. Lab work II (3 credits) ES-233E) Field Work (3 credits) ES-234F) Project Work (5 credits) ES-235-----------------------------------------------------------------------------------COURSE CONTENTA) Core CoursesRemedial Mathematics ES-101 (for Non- Mathematics students)Functions- polynomial, logarithmic, exponential, absolute value, trigonometric. Limits, Indeterminate forms, Continuity. Derivability. Differentiation of simple mathematical functions- product rule, quotient rule and chain rule. Integration- by parts, substitution and by partial fractions. Linear differential equations and their solution. Introduction to Matrices and Determinants. Introduction to Vectors- addition, subtraction, multiplication of vectors. Equation of Straight Line and Solving Linear System of Equations.OR2. Remedial Biology ES-102 (for Non- Biology students)History and scope of ecology, Evolution of biosphere, Diversity of life forms. Biological communities, species interaction, Communities properties, succession. Plant diversity and nomenclature with major classes of plants; Phytogeographical regions; Rare and threatened plants and exploration of plant wealth. Animal diversity and categories of animals; Rare and threatened species of mammals, aves, reptiles, pisces etc.; Exploration and conservation of faunal wealth. Microbial diversity, bacteria, fungi, actinomycetes; Microbial diversity in man-made ecosystems and natural ecosystems. Importance of flora and fauna in nutrient cycling, its effect, degradation and metabolism.3. Environmental chemistry ES-103Fundamental Chemistry: Elements, Chemical bonding, chemical reactions and equations, Organic functional groups, classes of organic compounds. Free radical reactions, catalytic processes.Elemental cycles (C, N, S, O) and their environmental significance.Fossil fuels: their types, properties, combustion and environmental implications.Atmospheric constituents, Green house gases and climatic changes. Chlorofluorocarbons and their substitutes. Photochemical smog. Water quality and wastewater treatment. Role of soaps, detergents and phosphorus fertilizers in eutrophication. Persistent organic pollutants: pesticides usage, toxicity and their environmental degradation. Earth crust and weathering mechanism; Soil formation and chemical characteristics. Chemical classes of Hazardous waste, their effects on the environment. Chemical treatment of hazardous wastes.4. Earth Processes ES-104Evolution of various branches of Geology. Origin of the earth. Primary differentiation and formation of core, mantle, crust, atmosphere and hydrosphere. Magma generation and formation of igneous and metamorphic rocks. Concept of Minerals and Rocks. Weathering, erosion, transportation and deposition of earth’s materials by running water, wind and glaciers. Formation of land forms and sedimentary rocks. Plate tectonics- sea floor spreading, mountain building, evolution of continents and structural deformation. Thermal, magnetic and gravitational fields of the earth. Concepts of engineering and urban geology.5. Ecology ES-105History and scope of ecology, autecoloty, synecology, population, community, biome, tolerance range and limiting factors. Distinguishing characters of forests grasslands, arid lands and wetlands; community organization- concept of habitat, functional role and niche, key stone species, dominant species, ecotone, edge effect. Analytical characters, synthetic characters like forms, species diversity and measurement of diversity. Population dynamics, models for single and interacting population, stable points, stable cycles, chaos competition, prey predation, etc. Ecological succession, primary and secondary processes in successions, models of successions, climax community and types of climax. Vegetation of India. Fundamentals of Microbial ecology. Microbial metabolism and microbial interaction. Biochemistry of biological nitrogen fixation and other microbial Pathways in terms of enzymology.6. Statistics ES-106Measures of central tendency. Measures of dispersion. Measures of skewness and kurtosis. Probability- definition, addition and multiplication laws,concept of random variable. Probability distributions- binomial, poisson and normal. Sampling theory- hypothesis testing and interval estimation for large samples. Chi-square test, t-test and F-test of significance. Correlation and regression. analysis. One way analysis of variance.7. Environmental Pollution ES-107Linkage between energy, environment and development. Human population issues. Definition of pollution. Different types of pollution- Air, Water and soil and their local, regional and global aspects. Air: Sources of air pollutants, their behavior in the atmosphere. Effects of air pollutants on humans, animals, plants and properties. Control approaches. Water: Sources, effects, water pollution treatment. Soil: Sources and nature of soil pollution and its harmful effects. Solid waste: generation, collection, environmental effects and safe disposal practices. Environmental problems associated with noise pollution, oil pollution and radioactive pollution.8. Natural hazards and disaster management ES-108Introduction to Hazards- Hazard classification-types of hazards ;Natural Hazards: causes, (continental drift, plate tectonics, sea floor spreading, isostacy, etc.,) distribution pattern, consequences and mitigation: Earthquake, Tsunami, Volcanoes, Cyclone, Flood, Drought, Landslide, cold and heat hazards, forest fire, etc.,- causes, types, distribution adverse effects, etc.,- Disaster introduction- disaster Management Capability-Vulnerability- risk- preparedness and mitigation- Disaster management cycle- community planning education and Engineered structure /structural strengthening techniques- Hazard zonation and mapping- Risk Reduction Measures.9. Environmental Impact Assessment ES-109Linkage between development and environment; global commons: carrying capacity: origin and development of EIA: relationship of EIA to sustainable development: EIA in project planning and implementation: EIA process: evaluation of proposed actions, scoping and base line study, identification and prediction of impacts, mitigation measures. Comparison of alternatives, review and decision making, public participation and compensatory actions: green belts: National Environmental Policies and guidelines in India. Conditions and approach for EIS review. Case studies: river valley projects: thermal power plants: mining projects: oil refineries and petrochemicals.10. Energy and Environment ES-110Energy resources and their exploitation, Sun as source of energy- nature of its radiation, Conventional energy sources: coal, oil, biomass and nature gas, non-conventional energy sources: hydroelectric power, tidal, wind, geothermal energy, solar collectors, photovoltaics, solar ponds, nuclear-fission and fusion, magneto-hydrodynamic power (MHD), Energy use pattern in different parts of the world and its impact on the environment. CO2 emission in atmosphere. Mechanism of radiation action on living systems- Stochastic and Non-stochastic effects; delayed effects, radioactivity from nuclear reactors, fuel processing and radioactive waste, hazards related to power plants, terrestrial and non terrestrial radiation, dose from environment and nuclear radiations, ultraviolet radiations, pathways analysis and dose assessment, radiologic age dating, radioactivity risk assessment, criterion for safe exposure.11. Remote sensing and Geo- informatics ES-111Introduction to Remote sensing & GIS. Principles of remote sensing & GIS. Spectra of Environmental Components. Terrestrial and Extra terrestrial satellites in Remote sensing and GIS. Remote sensing & GIS applications on Ocean, Atmosphere, Land, Geology, Water Resources (Ground water and Surface water). Cryosphere, Disaster, Defence studies. Use of softwares in Remote sensing and GIS to solve Environmental problems including Groundwater Exploration, Rainwater Harvesting, Biomass analysis and its relationship with Georesource evaluation. Use of Remote sensing and GIS in development of Early warning system to monitor Agriculture. Identification of Genetically modified crops in correlation with water quality and soil moisture by using Remote sensing & GIS. Applications of Remote sensing and GIS in early warning of Tsunami, Earthquake, Snowfall, Global warming, Forest fire, Landslide, Landsubsidance. Use of LANDSAT, SPOT, IRS ERS, RADARSAT and Extra terrestrial satellite data by using ERDAS, ARCGIS, ERMAPPER, IDRISI ENVI and S+ software for solving the Environmental problems. Sun-earth cosmic connection to understand environment of the Earth.12. Environmental Biochemistry and Toxicology ES-112Environmental physiology with considerations of intermediary metabolism- approaches for studying energy metabolism and body temperature changes; Thermo regulation and adaptation. Oxygen uptake from the environment, respiration and metabolism. Electron transport system and oxidative phosphorylation. Photosynthesis: C1, C3, C4 pathways and their regulation. Photorespiration. Biochemistry of altered membrane permeability, free radical formation, lipid peroxidation, lysosomal degradation, superoxide dismutase. Environmental pollutants and their effects on living system. Biochemical approaches to the detoxification of xenobiotics through cellular metabolism.13. Marine Environment ES-113Introduction-Classification- open ocean- shallow marine and deep sea environment- marine resources- marine ecology- marine organisms-productivity- coastal environment-coastal water movement- beaches- coastal dunes- barrier islands- cliffed coast- deltas-coast line- estuaries-mangroves- lagoons- salt marshes- coral reefs- classification of marine sediments- clay minerals- biogenic silica- evaporites- nutrient in oceans- carbon and global climate change- marine pollution- law of the sea.14. Soil Science ES-114Soil forming rocks and minerals- Classification- Weathering of rocks and minerals- Processes of weathering and factors affecting them. Soil formation- Factors of soil formation- Soil forming processes- Profile development- Definition of soil- Soil composition. Soil physical properties- Soil separates and particle size distribution- Soil texture and structure- Bulk density, particle density, pore space, soil air, soil temperature, soil water, soil consistence - Significance of physical properties to plant growth. Soil chemical properties- Soil colloids- Inorganic colloids- Clay minerals- amorphous- Ion exchange reactions- Organic colloids- Soil organic matter- Decomposition- Humus formation- Significance on soil fertility, Soil reaction- Biological properties of soil- nutrient availability.B) Non Credit Courses (Compulsory for all )1. Current Environmental Issues ES-115Contemporary and emerging environmental issues of local, regional and global significance. Broadly the topics will be pertaining to: i) Linkage between population, development and environment ii) climate change ii) stratospheric Ozone depletion iii) water resources iv) environmental toxicants and human health v) biodiversity conservation and vi) environmental episodic events, etc.2. Scientific Writings and Ethics ES-116Overview of Moral and Ethical questions in Scientific writing. Overall outline and structure of the article/manuscript. Description, value, and development of points/outlines before writing. Screening of Material for inclusion within the structure of the manuscript.Importance of Authors and their sequence, importance of clear title, abstract or summary. Introduction, Methods, Results, and Discussion. Numbers and statistics, Tables and Figures, Discussion. Writing Style: Active or passive, Punctuation, use of commas, apostrophe, semicolon and colon. Avoiding duplication and repetition. Importance of revisions and references.Plagiarism, paraphrasing and copy write violation. Consequences of plagiarism. Why not to fudge, tinker, fabricate or falsify data. Examples.C) Optional Courses1. Environmental Modeling ES - 201Role of Modeling in Environmental Science. Model Classification- Deterministic Models, Stochastic Models, Dynamic Models, Steady State Models. General Steps Involved in Modeling, Mass Balancing, Energy Balancing, Microbial Growth Kinetics- Exponential Growth Model, Logistic Growth Model, Monod Equation, Two Species Population Growth Model of Competition. Lotka-Volterra Prey-Predator Model, Oxygen Sag Model, Gaussian Plume Model.2. Climatology ES - 202Elements of climate, climate controls, Earth's radiation balance, latitudinal and seasonal variation of insolation, temperature, pressure, wind belts, humidity, cloud formation and precipitation, water balance, spatial and temporal patterns of climate parameters, Air masses and fronts, SW and NE monsoon, jet stream, tropical and extratropical cyclone, ENSO, QBO. Classification of climate- Koppen's and Thornthwaite' scheme. Climate change3. Meteorology ES - 203Meteorology fundamentals- Thermal structure of the atmosphere and its composition, Pressure, temperature, wind, humidity, moisture variables, virtual temperature, radiation, radiation from sun, solar constant, surface and planetary albedo, emission and absorption of terrestrial radiation, radiation windows, greenhouse effect, net radiation budget, atmospheric stability diagrams, turbulence, diffusion, dry and moist air parcel, thermodynamic diagrams, T-phigram and mixing height, thermodynamics of dry and moist air, specific gas constant, adiabatic and isoentropic processes, entropy and enthalpy, adiabatic processes of moist air4. Noise Pollution ES - 204Basic properties of sound waves, sound propagation, Definition of Noise, Health Effects of Noise, Concept of sound pressure level (SPL), decibel scale, addition of decibels, Frequency Response of Human Ear, Equal Loudness Contours, Weighting Networks, Octave Bands, Measurement and analysis of sound. Percentile Indices of Noise, Equivalent sound pressure level (Leq), Noise pollution level (NPL), Sound exposure level (SEL), Traffic noise index (TNI), Day-Night level (DNL), noise criteria curves; Noise sources; Industrial Noise and Traffic Noise, Noise control and abatement measures; absorbing materials, barrier materials and damping materials. Acoustic silencers and mufflers.5. Environmental Physics ES - 205Concept and scope of environmental Physics with respect to human environment; built environment; urban environment; global environment. Laws of thermodynamics, irreversible thermodynamics and entropy. Wind chill, Hypothermia. Heat balance (steady and transient), Electromagnetic Radiation, Thermal regulation in buildings- Thermal insulation, Thermal conduction effects, Convection effects, Radiation effects, U-values, Energy use and efficiency in buildings. Energy losses, calculation of energy losses, energy gains.Air regulation in buildings, heat pumps, condensation. Buildings of the future. Nano materials: their properties and influence on human health, environment, communication sector and energy. Method of preparation and Applications of nano materials.6.Environmental Instrumentation and Techniques ES - 206Physics of Dielectrophoresis and its environmental applications, Basics of NMR instrumentations, significance of relaxation time, Raman effect and experimental measurement, Raman Spectroscopy, LASER based techniques, LIDAR based methods and techniques, SODAR Radiofrequency measurement and techniques.7. Geochemistry ES - 207Atomic properties of elements, the periodic, table and geochemical classification of elements; abundance of elements in the bulk earth, crust, hydrosphere, atmosphere and biosphere; introduction to mineral structures and compositions; thermodynamic classification of elements into essential, structural, major and trace elements and their partitioning during mineral formation; chemical reactions involving proton and electron transfers, mineral stability diagrams and controls on the chemistry of natural waters; geochemical cycling-concepts with an example; radioactivity, decay of parent and growth of daughter nuclides and methods of radiometric dating; stable isotopes, their fractionation and application to geothermometry and paleoclimates. Interpretation of XRD and XRF data for Environmental components. Geochemical sample preparation. X-Ray Fluorescence. X-Ray Diffraction. Ion Chromatography, AAS and its interpretation.8. Groundwater Hydrology ES - 208Definition and concept of hydrology and hydrogeology. Distribution of water in the earth’s crust. Hydrological cycle. Genetic types of groundwater and residence time of groundwater, Geological control of groundwater, Vertical distribution of groundwater, Types of aquifers, springs and their classification, Classification of rocks with reference to their water bearing properties. Mode of occurrence of groundwater in different geological terrains of India. Darcy’s law and its validity, Determination of hydraulic conductivity, groundwater tracers. Environmental factors on Groundwater level fluctuations and Land subsidence due to changes in subsurface moisture. Effects of excessive use of groundwater resources. Sources of salinity, Chemical analysis of groundwater, Quality criteria for different uses, Groundwater quality in different provinces of India, pollution of groundwater resources. Ghyben-Herzberg relationship between fresh-saline water. Groundwater exploration. Construction and design of different types of wells. Well completion and development. Groundwater development and management: Groundwater development in urban areas and rainwater harvesting, artificial recharge methods. Management of groundwater and groundwater legislation.9.Oceanography ES - 209Introduction- historical, current and future- Earths structure- Physiography of oceans- origin and evolution of ocean basins (Continental and oceanic basins)- Continental drift, sea floor spreading, plate tectonics- shelf and deep sea sedimentation- physical, chemical and biological aspects of sea water- Ocean current (circulation)- Waves properties and motion- tidal currents and characteristics- air-water interface/ exchange, gas solubility and circulation models.10. Natural resource Management ES - 210Definition- land, water, soil, plants and animals: quality of life: renewable and non-renewable resources: Mineral occurrences, prospects: Mineral resources: Mineral reserves, ore minerals, coal, petroleum, oil and natural gas: water- hydropower, including tidal power; ocean surface waves used for wave power, wind- wind power, geothermal heat- geothermal power and radiant energy- solar power: sustainable development, Urban planning Environmental management, Understanding the resource ecology and life-supporting capacity of resources-Economic models: Green building concept- green technology concept.11. Glaciology ES - 211Glacier systems- Structure and morphology of glaciers- Glacial erosion; Landscape evolution under glaciers, glacial landforms- Mass balance- Glacier dynamics, Englacial and subglacial process and fluctuations- Glacier hydrology- Snow and melt water chemistry of- Approaches to Glaciology- Glacier modeling- Glacier and climate change impact- Glaciers- Glacier and water resources- Recent advances in Glaciology- Spatial Data Acquisition Glacier Hazards- Glaciers as tool for palaeo climate studies.12. Biogeochemistry ES - 212Introduction- Biogeochemical provinces- Atmosphere- Lithosphere: weathering process, soil biogeochemistry- Terrestrial systems: photosynthesis respiration- Wetlands: vegetation adaptations- Freshwater and Marine Biogeochemistry: Lakes, ponds, rivers, mangroves, salt marsh and estuaries- Oceans: productivity and limiting nutrient role, carbon chemistry- Global biogeochemical cycles: Nutrient cycles-Advances in biogeochemistry- Sediment biogeochemistry, stable Isotopes in Biogeochemistry and their application to various environmental problems. Nutrient dynamic in the atmosphere, hydrosphere, and Lithosphere. Nutrient budgeting and modeling13. Environmental Geology ES - 213Interior of the earth- minerals and rocks- earth processes- plate tectonics- sea floor spreading, mountain building, rock deformation- evolution of continents and earth quakes, volcanoes, landslides, subsidence, rivers and floods and coastal process- interactions between humans and the geological processes, Environmental Hazards-Pollution of the Environment- Waste Disposal, Natural Resources, and Energy Sources and their exploitation. Past, present and future environmental issues and their affect on the earth and our society.14. Water Resources ES - 214Hydrological cycle- Hydrometeorology and climate- hydrometric networks and catchment morphology- precipitation- evaporation and evapotranspiration- soil moisture-river flow-River, Lakes and Ground water- Occurrence of surface water and groundwater. Movement of water on the surface and below the surface. Springs and Hydrothermal phenomena. Ungauged river basin flow- River bank infiltration and recharge-precipitation analysis- evaporation calculation-river flow analysis- Time variation of stream flow levels- rainfall- runoff relationships- Ecohydrology- urban hydrology- Integrated Water Resource Management (IWRM), Urbanization effect on Water resources. Earthquake, Land subsidence and Water resources. Physical, chemical and biological characteristics of Water resources and water quality data processing and interpretation. Sea water intrusion in aquifer system-structural geological approach. Influence of Sun-Earth cosmic connection on Water resources.15. Air Pollution Chemistry ES - 215Chemical composition of atmosphere, Sources of air pollution. Types of air pollutants, organic and inorganic pollutants, their behavior and fate on local, regional and global scale, monitoring of criteria and non-criteria pollutants. Effects of air pollutants on human health, plants, animals and materials. Pollutants and health effects. Air pollution meteorology: Mixing heights, Wind roses, Inversion conditions, Stability of the atmosphere. Long range transport, plume behavior, Air pollution dispersion. Land-atmosphere-ocean interactions of air pollutants. Photochemistry of troposphere, Inorganic reaction in the atmosphere. Reactions involving organic pollutants, Gas to particle conversion. Ozone depletion, Acid rain, Greenhouse effect, Formation of photochemical smog, CFC, their nomenclature, sources and effect, Atmospheric Brown Cloud. Air pollution control technologies: Concept of clean environment, Green technologies, Carbon sequestration, Chemical methods, Electrostatic precipitators.16. Water Pollution Chemistry ES - 216Physicochemical properties of water, Water use- classifications and water quality standard. Basic principles of contaminant behavior in the environment. Hydrologic cycle. Types and sources of water pollution, Major Water Quality (physicochemical and bacteriological) Parameters and their Applications, Basics of water sampling. Water quality objectives and the major chemical, physical and biological processes necessary for designing and managing modern drinking water and wastewater treatment plants, Principles of coagulation, flocculation, sedimentation, chemical precipitation, porous media filtration, disinfection, ion exchange, adsorption, membrane Processes, advanced oxidation processes, air-stripping and other advanced treatment processes, Major contaminant groups and natural pathways for their removal from water.17. Soil Pollution Chemistry ES - 217Physical Chemistry of Soil: Soil Solution Phase, The Soil/Solution Interface, Surface exchange reactions, Soil acidity, Electrochemistry and the Soil, chemistry of waterlogged soil. Soil Pollution: Inorganic and Organic-Definition of pollution and contamination, sources of soil pollution, Effects of chemical residues on soil, (pesticides, fertilizers, heavy metals etc., Soil salinity and alkalinity, Soil pollution from nitrogen, phosphorus, sulfur, micronutrients or trace elements and radionuclide, land degradation, soil erosion. Soil pollution and climate change: Greenhouse gases production, emission, mitigation, carbon sequestration, soil quality.18. Solid and Hazardous Waste Management ES - 218Solid wastes: Definition, types, sources, characteristics, and impact on environmental health. Waste generation rates. Concepts of waste reduction, recycling and reuse. Collection, segregation and transport of solid wastes Handling and segregation of wastes at source. Collection and storage of municipal solid wastes. Solid waste processing technologies. Mechanical and thermal volume reduction. Biological and chemical techniques for energy and other resource recovery. Composting, Vermicomposting, Incineration of solid wastes. Disposal in landfills: site selection, design, and operation of sanitary landfills; secure landfills and landfill bioreactors; leachate and landfill gas management; landfill closure and post-closure environmental monitoring; landfill remediation.Hazardous wastes: Definition, sources and characteristics: Hazardous waste categorization, generation, collection, transport, treatment and disposal. Legislation on management and handling of municipal solid wastes and hazardous wastes19. Metrology ES - 219Fundamentals of metrology, Chemical metrology, Defining uncertainty of measurements, traceability of standards, validation of method, calibration of method, accuracy and precision of results, selectivity, sensitivity, detection limit, limit of determination, specificity, linearity, analytical error, Accreditation systems, Metrology in environment, QA/QC parameters in environmental studies, use of CRMs (Certified reference materials), inter-laboratory comparison exercise, participation in National and International round Robin tests. Representativeness of sampling site, selection of analytical method, selection of appropriate analytical technique, proper storage of samples with suitable preservative, sample blank, field blank, solvent blank, efficiency of extraction, efficiency of sampling, determination of uncertainty in flow, sample preparation.20. Pollution Biology ES - 220Concepts: Pollutants vs. resources; cycling of materials, tolerance ranges, carrying capacity, bioaccumulation. Air Pollution: Responses of plants and animals, monitoring (e.g. lichens) and control of air pollution by plants. Water pollution: Responses of plants and animals to changes in physico-chemical characteristics; distribution of plants in relation to pollution (microphytes; Phytoplankton, periphyton and moorophytes); Biological monitoring and control of pollution in water. Soil pollution: Responses of plants to soil pollution; changes in soil characteristics by waste disposal, sanitary land fills, mining wastes and human activities, and effects on plants and animals.21. Biodiversity and Conservation ES - 221Biodiversity concepts and patterns, Microbial diversity, Plant diversity, Agrobiodiversity, Soil biodiversity, Economic value of biodiversity, biodiversity losses. Biodiversity hotspots and their characteristic flora and fauna, threatened plants and animals of India, ecosystem people and traditional conservation mechanisms, Biodiversity Convention and Biodiversity Act, IPRs, national and international programmes for biodiversity conservation. Wildlife values and eco-tourism, wildlife distribution in India, problem in wildlife protection, role of WWF, WCU, CITES, TRAFFIC, Wildlife Protection Act 1972. In-situ conservation: sanctuaries, biospheres reserves, national parks, nature reserves, preservation plots. Ex-situ conservation: botanical gardens, zoos, aquaria, homestead garden; herbarium; In-vitro Conservation: germplasm and gene Bank; tissue culture: pollen and spore back, DNA bank.22. Forest Ecology ES - 222Forest and forest environment: Structure of forest ecosystem, major forest types of the world, forest types and forest cover of India, regeneration ecology of forest trees. Forest ecosystem function: Primary productivity of forest ecosystems, litter production and decomposition, nutrient cycling and nutrient conservation strategies, plant water relations. Forest ecosystem management: Forest management systems, joint forest management, forest hydrology, forest fire, application of remote sensing technique in forest ecology, deforestation and sustainable forestry, forest laws, non timber forest products. Role of Biology in management and habitat management techniques. Wildlife farming: Objectives, management design, wildlife products, disease control, breeding. Behavioral, ecology and evaluation.23. Microbial Ecology ES - 223An overview of microbial life and its importance in the environment, Microbial structure and function with special emphasis on Bacteria and Archaea, Evolution and microbial phylogenetic diversity, Microbial nutrition and metabolism with emphasis on microbial metabolic diversity, Environmental factors affecting microbial growth and microbial adaptations to extreme environments (like arctic regions and hot springs), Methods in microbial ecology including introduction to microbial genomics, Microbial habitats (air, soil, subsurface, freshwater, marine and the deep sea), Introduction to geomicrobiology, Natural microbial communities with emphasis on biofilms, Microbial biogeochemical processes of nutrient cycling and biodegradation, Microbial interactions: microbe-microbe interactions, plants as microbial habitats, animals as microbial habitats and human microbiome, Applying microbes in wastewater treatment and solid waste management, Industrial applications of microbes including products for health-pharmaceutical, food and beverage industry and biofuels, Molecular biotechnological applications including genetic engineering for the production of vaccines, diagnostics, biopesticides and transgenic plants, Microbial disease ecology and public health, Transmission of microbial diseases through the environment.24. Ecosystem Dynamics ES - 224The ecosystem concept, abiotic and biotic components. Energy input in ecosystem, standing crop, biomass, primary and secondary production, gross and net production, concept of food chain food web, ten percent law, net community production, methods of measuring productivity, pattern of primary production and biomass in the major ecosystem of the world, Energy flow, Feed back and control. Biogeochemical cycles, gaseous and sedimentary turnover rate and turnover item. Hydrological cycle, carbon cycle, nitrogen cycle, sulphur cycle, phosphorus cycle, nutrient budget, man’s impact on nutrient cycles. Population dynamics.25. Environmental Biophysics ES - 225Cellular function of cell, membrane structure and transport origin and conduction of impulses in nerve cell muscles, methods in bioelectric measurements. Radiation and molecular response, elementary aspects of atomic and molecular excitation, biointeractions with environment, fundamental and applied aspects of extremely low frequency, radio and microwave fields, bioacoustics, biomedical aspects of laser. Magnetic environments and geomagnetic fields, behavioural changes, therapeutic and diagnostic possibilities.26. Ecology and Sustainable Development ES - 226Ecosystem concept in space and time; Ecosystem level processes and landscape level processes; the concept of sustainable development temporal and spatial dimensions; Currencies for evaluations of sustainable development- Biophysical measurements; Environmental degradations and conservation issues; Global change and sustainability issues: Climate change, biological invasion, bio-diversity concerns; Ecosystem and social processes in: (a) Rehabilitation of degraded rural landscape, (b) Rehabilitation of unbalanced soils, (c) Rehabilitation of specialized habitats, e.g. water bodies, mangroves; (d) Mined area rehabilitation participatory research and education environmental decision making with people initiates.27. Environmental Xenobiotics and human health ES - 227Interaction of pollutants with biological systems at different levels, e.g., organism, organs, and cell organelles. Biochemical degradation of pollutants inside the cell as well as cellular interactions with the pollutants. Toxins of plant origin. Stress response in living systems. Toxicogenomics: Human population issues and population genetics. Pharmacogenomics; Epidemiology. Cellular interaction and metabolism of xenobiotics; metabolic disorders. Bioconversion of pollutants: active vs. inactive process; enzymic degradation by monooxygenases; Role of cytochrome P 450 and its multiple forms. Immunology: Immune cell responses, Immunity and Immunodeficiency. Allergy and hypersensitive reactions and disorders of immune responses. Carcinogens and Carcinogenesis. Metal toxicity: chemical form, metal biomacromolecule interaction, teratogenecity.28. Fundamentals of Molecular Biology and Biotechnology ES - 228Basic concepts of molecular biology needed for understanding biotechnology. DNA structure and organization into chromosomes. DNA replication. Repetitive DNA; coding and noncoding sequences in genomes. Gene structure and expression. Mechanics of transcription, translation and their regulation in both prokaryotes and eukaryotes. Key discoveries (restriction enzymes, bacterial plasmids, modifying enzymes) leading to recombinant DNA technology. Overview of basic techniques in genetic engineering: Introduction of cloned genes into new hosts using plasmid and phage vector systems. Expression cloning, affinity purification of expressed proteins. Nucleic acid hybridization and polymerase chain reaction as sensitive detection methods. DNA sequencing. Analysis of genomes and proteomes by bioinformatics tools. Genome-wide analysis using microarrays.29. Applied Biotechnology and Bioremediations ES - 229Practical aspects of genetic engineering with microorganisms from extreme environment: Use of extremophilic microorganisms in waste treatment and methane production from agro industrial wastes; Production of enzymes like cellulase, proteases, amylases; alcohol and acetic acid production; Biocomposting: Microbial process involvement, vermin composting, biofertilizer, biopesticides production. Biomining: Microbial leaching of low grade mineral ores, molecular probes for organisms in mines and mine tailings, Petroleum pollutant biodegradation. Alternate fuels: Source and mechanism of various biofuel production. Bioremediation: Concept, role of bioremediation in controlling various pollution problems e.g. solid water, sewage water, industrial effluents, heavy metals, radioactive substances, oil spillage. Phytoremediation: Abatement of different types of pollution using plants, types of phytoremediation, mechanism involved with case studies. Waste water treatment strategies: Domestic and Industrial waste-water, application of microbiology waste treatment. Metagenomics: Environmental Genomics, ecogenomics or community genomics, the study of genetic material recovered directly from environmental samples and future applications in bioremediation.30. Eco-Toxicology ES - 230Principles in toxicology; Definition of Xenobiotics. Animal management in toxicological evaluation; Animal toxicity tests; Statistical concepts of LD50; Dose-effect and dose response relationship; Frequency response and cumulative response; Biological and chemical factors that influence toxicity; Bio-transformation and bio-accumulation. Influence of ecological factors on the effects of toxicity; Concept of green chemistry. Pollution of the ecosphere by industries; Global dispersion of toxic substance; Dispersion and circulating mechanisms of pollutants; degradable and non-degradable toxic substances; food chain. Eco-system influence on the fate and transport of toxicants. Aquatic toxicity tests; Statistical tests; Response of planktons to toxicants; EC49; Photosynthetic bacteria; Bio-absorption of heavy metals. Information management system in eco-toxicology.31. Environmental and Occupational Health ES - 231Basic principle of environmental health. Physiological responses of man to relevant stresses in the environment. Cases and effects of pollution. Industrial Toxicology: Study of environmental dose effect relationships. Evaluation of toxicity and threshold limits. Principles and methods of occupational health. The relationship of occupation of hygiene and safety and disease. Health maintenance: Survey, analysis and recommendations regarding health and safety problems in the working and living environment. Biostatistics, epidemiology: Application of statistical methods to medical records in the study of health problems of human population in a given environment. Treatment of variation, with demographic, vital statistics and epidemiological data. Hazard evaluation in polluted environment with specific emphasis on radiological health. Industrial hygiene technology-laboratory remains illustrating the principles, methods of recognizing evaluating and controlling environmental hazards like air pollution, etc.I would suggest you to visit the link School of Environmental Sciences for further information.

Yes, as the American Urological Association is the authoritative source for the treatment of all urological conditions including Prostate cancer - Mayo Clinic .The consensus of urological expert doctors agree that the PSA test is the most critical component is the early detection of prostate cancer.AUA HP Brief "AUA Applauds New Jersey for Legislation Supporting PSA Test and for approving an act that opposes the U.S. Preventive Services Task Force (USPSTF) draft recommendations on the use of the prostate-specific antigen (PSA) test."AUA RESPONDS TO NEW RECOMMENDATIONS ON PROSTATE CANCER SCREENING"Association urges men to speak with their physicians about the value of prostate cancer testingLINTHICUM, Md., Oct. 7, 2011 /PRNewswire-USNewswire/ -- The American Urological Association (AUA) today released the following statement in response to the U.S. Preventive Services Task Force draft recommendations on the use of the prostate-specific antigen (PSA) test. The statement is attributed to AUA President Sushil S. Lacy, MD:The American Urological Association (AUA) applauds the U.S. Preventive Services Task Force for its interest in reviewing the use of the prostate-specific antigen (PSA) test. However, we are concerned that the Task Force's recommendations will ultimately do more harm than good to the many men at risk for prostate cancer both here in the United States and around the world. The AUA's current clinical recommendations support the use of the PSA test, and it is our feeling that, when interpreted appropriately, the PSA test provides important information in the diagnosis, pre-treatment staging or risk assessment and monitoring of prostate cancer patients.Not all prostate cancers require active treatment and not all prostate cancers are life threatening. The decision to proceed to active treatment is one that men should discuss in detail with their urologists to determine whether active treatment is necessary, or whether surveillance may be an option for their prostate cancer.The AUA is currently preparing a new clinical guideline on this topic, and has convened a panel of experts to review not only the use of the PSA test, but also early detection of prostate cancer overall, taking into account the new tests and diagnostics that are becoming available. Until there is a better widespread test for this potentially devastating disease, the USPSTF – by disparaging the test – is doing a great disservice to the men worldwide who may benefit from the PSA test.For more information about the AUA's position on the early detection of prostate cancer, or to arrange an interview with an expert urologist, please contact the AUA Communications Office at 410-689-3932."Detection of Prostate CancerAUA EARLY DETECTION OF PROSTATE CANCER: AUA GUIDELINEPanel Members:H. Ballentine Carter, Peter C. Albertsen, Michael J. Barry, Ruth Etzioni, Stephen J. Freedland, Kirsten Lynn Greene, Lars Holmberg, Philip Kantoff, Badrinath R. Konety, Mohammad Hassan Murad, David F. Penson and Anthony L. ZietmanPurposeThis guideline addresses prostate cancer early detection for the purpose of reducing prostate cancer mortality with the intended user as the urologist. This document does not make a distinction between early detection and screening for prostate cancer. Early detection and screening both imply detection of disease at an early, pre-symptomatic stage when a man would have no reason to seek medical care –an intervention referred to as secondary prevention. This document does not address detection of prostate cancer in symptomatic men, where symptoms imply those that could be related to locally advanced or metastatic prostate cancer (e.g. new onset bone pain and/or neurological symptoms involving the lower extremities, etc.).MethodologyThe AUA commissioned an independent group to conduct a systematic review and meta-analysis of the published literature on prostate cancer detection and screening. The protocol of the systematic review was developed a priori by the expert panel. The search strategy was developed and executed by reference librarians and methodologists and spanned across multiple databases. This search covered articles in English published between 1995 and 2013. These publications were used to inform the statements presented in the guideline as Standards, Recommendations or Options. When sufficient evidence existed, the body of evidence for a particular intervention was assigned a strength rating of A (high), B (moderate) or C (low).GUIDELINE STATEMENTSGuideline Statement 1: The Panel recommends against PSA screening in men under age 40 years. (Recommendation; Evidence Strength Grade C)In this age group there is a low prevalence of clinically detectable prostate cancer, no evidence demonstrating benefit of screening and likely the same harms of screening as in other age groups.Guideline Statement 2: The Panel does not recommend routine screening in men between ages 40 to 54 years at average risk. (Recommendation; Evidence Strength Grade C)For men younger than age 55 years at higher risk (e.g. positive family history or African American race), decisions regarding prostate cancer screening should be individualized.Guideline Statement 3: For men ages 55 to 69 years the Panel recognizes that the decision to undergo PSA screening involves weighing the benefits of preventing prostate cancer mortality in 1 man for every 1,000 men screened over a decade against the known potential harms associated with screening and treatment. For this reason, the Panel strongly recommends shared decision-making for men age 55 to 69 years that are considering PSA screening, and proceeding based on a man's values and preferences. (Standard; Evidence Strength Grade B)The greatest benefit of screening appears to be in men ages 55 to 69 years.Guideline Statement 4: To reduce the harms of screening, a routine screening interval of two years or more may be preferred over annual screening in those men who have participated in shared decision-making and decided on screening. As compared to annual screening, it is expected that screening intervals of two years preserve the majority of the benefits and reduce overdiagnosis and false positives. (Option; Evidence Strength Grade C)Additionally, intervals for rescreening can be individualized by a baseline PSA level.Guideline Statement 5: The Panel does not recommend routine PSA screening in men age 70+ years or any man with less than a 10 to 15 year life expectancy. (Recommendation; Evidence Strength Grade C)Some men age 70+ years who are in excellent health may benefit from prostate cancer screening.PurposeThis guideline addresses prostate cancer early detection for the purpose of reducing prostate cancer mortality with the intended user as the urologist. This document does not make a distinction between early detection and screening for prostate cancer. Early detection and screening both imply detection of disease at an early, pre-symptomatic stage when a man would have no reason to seek medical care –an intervention referred to as secondary prevention.In the US, early detection is driven by prostate specific antigen (PSA)-based screening followed by prostate biopsy for diagnostic confirmation. While the benefits of PSA-based prostate cancer screening have been evaluated in randomized-controlled trials, the literature supporting the efficacy of DRE, PSA derivatives and isoforms (e.g. free PSA, -2proPSA, prostate health index, hK2, PSA velocity or PSA doubling time) and novel urinary markers and biomarkers (e.g. PCA3) for screening with the goal of reducing prostate cancer mortality provide limited evidence to draw conclusions. While some data suggest use of these secondary screening tools may reduce unnecessary biopsies (i.e. reduce harms) while maintaining the ability to detect aggressive prostate cancer (i.e. maintain the benefits of PSA screening), more research is needed to confirm this. However, the likelihood of a future population-level screening study using these secondary screening approaches is highly unlikely at least in the near future. Therefore, this document focuses only on the efficacy of PSA screening for the early detection of prostate cancer with the specific intent to reduce prostate cancer mortality and not secondary tests often used after screening to determine the need for a prostate biopsy or a repeat prostate biopsy (e.g., PSA isoforms, PCA3, imaging).The framework for this guideline follows that of the Institute of Medicine (IOM) recommendations for guideline development, including a systematic review of the evidence by a multidisciplinary panel.While the evidence that guideline panels evaluate may be the same, the weighting of the evidence and the Panel's perspective can be very different (e.g., public health versus individual perspectives) leading to differing interpretations of evidence and policy implications (Figure 1). It is important to note that the guideline statements listed in this document target men at average risk, defined as a man without risk factors, such as a family history of prostate cancer in multiple generations and/or family history of early onset below age 55 years, or African American race. Because the harm-benefit profile of PSA-based prostate cancer screening is highly age dependent, guideline statements included in this document target four index patients; these age ranges were chosen to correspond to age ranges tested in randomized trials and data from population and simulation studies.Four Index PatientsMen <40 years of ageMen age 40-54 yearsMen age 55-69 yearsMen age 70+ yearsFigure 1: Influence of evidence and interpretation on policy creationMethodologyConsistent with AUA published guideline methodology,the process started by conducting a comprehensive systematic review. The AUA commissioned an independent group to conduct a systematic review and meta-analysis of the published literature on prostate cancer detection and screening. The protocol of the systematic review was developed a priori by the expert panel. The search strategy was developed and executed by reference librarians and methodologists and spanned across multiple databases including Ovid Medline In-Process & Other Non-Indexed Citations, Ovid MEDLINE, Ovid EMBASE, Ovid Cochrane Database of Systematic Reviews, Ovid Cochrane Central Register of Controlled Trials and Scopus. Controlled vocabulary supplemented with keywords was used to search for the relevant concepts of prostate cancer, screening and detection. The search focused on DRE, serum biomarkers (PSA, PSA Isoforms, PSA kinetics, free PSA, complexed PSA, proPSA, prostate health index, PSA velocity, PSA doubling time), urine biomarkers (PCA3, TMPRSS2:ERG fusion), imaging (TRUS, MRI, MRS, MR-TRUS fusion), genetics (SNPs), shared-decision making and prostate biopsy. The expert panel manually identified additional references that met the same search criteria to supplement the electronic search.The outcomes of interest were also a priori determined by the Panel and included prostate cancer incidence, mortality, quality of life, the diagnostic performance of each of the tests and the harms of testing (premature death and complications from testing and biopsy). Modeling studies were included when original studies were limited by follow-up time and screening protocols. The methodology team independently rated the methodological quality of the studies and provided an overall judgment of the whole body of evidence based on their confidence in the available estimates of effect.The framework for rating the quality of evidence is an adaptation and modificationof the GRADE framework (Grading of Recommendations, Assessment, Development and Evaluation).In this adaptation, the AUA rates the quality of evidence as high, moderate or low (A, B or C). The strength of a statement was rated according to AUA guideline methodology as further described below. The confidence in the estimates of effect (quality of the evidence) was determined based on study quality, imprecision, indirectness, inconsistency and the likelihood of reporting and publication bias.The methodology team summarized the data with an explicit description of study characteristics, methodological quality, main findings and the quality of the evidence (confidence in the estimates). The methodology team attended panel meetings and facilitated incorporation of the evidence into the guideline.AUA Nomenclature: Linking Statement Type to Evidence Strength. The AUA nomenclature system explicitly links statement type to body of evidence strength and the Panel's judgment regarding the balance between benefits and risks/burdens (see Table 1).Standards are directive statements that an action should (benefits outweigh risks/burdens) or should not (risks/burdens outweigh benefits) be undertaken based on Grade A or Grade B evidence. Recommendations are directive statements that an action should (benefits outweigh risks/burdens) or should not (risks/burdens outweigh benefits) be undertaken based on Grade C evidence. Options are non-directive statements that leave the decision to take an action up to the individual clinician and patient because the balance between benefits and risks/burdens appears relatively equal or appears unclear; Options may be supported by Grade A, B or C evidence.For some clinical issues, little or no evidence may exist from which evidence-based statements can be constructed. In such instances, the Panel may provide guidance in the form of Clinical Principles or Expert Opinions with consensus achieved using a modified Delphi technique if differences of opinion exist among Panel members.A Clinical Principle is a statement about a component of clinical care that is widely agreed upon by urologists or other clinicians for which there may or may not be evidence in the medical literature. Expert Opinion refers to a statement, achieved by consensus of the Panel, that is based on members' clinical training, experience, knowledge and judgment and for which there is no evidence. In the case of this guideline, such statement types were not included. The completed evidence report may be requested through the AUA by emailing [email protected] 1: AUA NomenclatureLinking Statement Type to Evidence StrengthStandard: Directive statement that an action should (benefits outweigh risks/burdens) or should not (risks/burdens outweigh benefits) be taken based on Grade A or B evidenceRecommendation: Directive statement that an action should (benefits outweigh risks/burdens) or should not (risks/burdens outweigh benefits) be taken based on Grade C evidenceOption: Non-directive statement that leaves the decision regarding an action up to the individual clinician and patient because the balance between benefits and risks/burdens appears equal or appears uncertain based on Grade A, B or C evidenceClinical Principle: a statement about a component of clinical care that is widely agreed upon by urologists or other clinicians for which there may or may not be evidence in the medical literatureExpert Opinion: a statement, achieved by consensus of the Panel, that is based on members' clinical training, experience, knowledge, and judgment for which there is no evidenceQuality of Individual Studies and Determination of Evidence Strength. The systematic review included over 300 eligible studies that addressed the questions of interest. In brief, six well known randomized trials addressed the question of mortality benefit of prostate cancer screening. Considering various methodological limitations and biases, the estimate for the effect of screening (versus no screening) on prostate cancer-specific mortality was obtained from the European Randomized Study of screening for Prostate Cancer (ERSPC).The quality of the evidence was moderate for benefits and high for harms in men aged 55 to 69 (see later discussion of RCTs). Follow-up was quite limited, and quality of evidence was low on screening benefits in men outside of this age range, population subgroups with greater than average risk of the disease and screening protocols different from those used in the ERSPC.Modeling studies were considered by the Panel to address these issues. A modeling study considers disease progression as a process of clinical or prognostic states and aims to estimate the rates of progression through these states in the absence of screening. Given the rate estimates, different screening protocols can be superimposed and their tradeoffs projected via computer simulation. To validate the models, specific screening protocols used in published studies can be considered and the model-projected incidence patterns compared with those observed in these studies. The primary model considered by the Panelhas been validated against prostate cancer incidence trends in the US population before and after the advent of screeningand against prostate cancer diagnosis patterns in the Prostate, Lung, Colorectal, and Ovarian (PLCO) trial.Modeling studies are increasingly being used to guide screening policies. The US Preventive Services Task Force (USPSTF) used modeling in developing its most recent breastand colorectal cancerscreening recommendations.The evidence concerning harms and adverse effects of screening was high quality, and fairly robust estimates of the incidence of these complications were obtained from randomized and non-randomized studies.Ample evidence was available to support the use of various shared-decision making processes that increased men's knowledge scores, reduced their decisional conflict and promoted greater involvement in decision making.Unfortunately, the literature supporting the efficacy of DRE and biomarkers other than PSA for screening average risk men provided minimal evidence to draw conclusions. For the most part, this evidence had low to moderate quality and was more relevant to cancer detection in higher risk men than true average risk population screening. The outcomes of these studies were often reported as diagnostic accuracy estimates rather than patient important outcomes such as mortality or quality of life.Limitations of the Literature. The systematic review and guideline process identified clear gaps in the available evidence base. Data are needed to clarify the harm/benefit balance of screening in men younger and older than those enrolled in the available randomized trials. Even for the age groups enrolled, critical outcomes, such as overdiagnosis and the additional number needed to treat, are not easily estimated from empirical trial data. Data on the harm-benefit balance are needed in men with varying spectra of family history of prostate cancer and men from various ethnicities and with other known risk factors of developing the disease. Outcomes of newer screening tests used in combination with PSA need to be determined. Men contemplating screening will need outcome data based on follow-up that exceeds the 10 year horizon currently available in the literature.Extrapolating results from one population to another must be done cautiously since the benefits of screening are dependent on the baseline incidence of and mortality from cancer without screening, the specific screening protocol, biopsy referral criteria and compliance with biopsy recommendations. The mortality from prostate cancer in the absence of screening is higher in the Netherlands and Sweden as compared to the USand these were the only two countries of the seven participating in the ERSPC trial where a mortality benefit was observed. Thus, the benefits of PSA-based screening seen in these two countries may not be generalizable to the US population. Further, the screening protocol, criteria for biopsy referral and compliance with biopsy recommendations differed considerably in the US population and ERSPC trial settings.The available evidence base permitted the Panel to recommend screening with limited confidence in the target group age 55 to 69 years. This age range represents the group with the highest quality evidence of benefit. However, the Panel recognizes the potential for harm, and for this reason recommends shared decision making prior to screening decisions.Panel Selection and Peer Review Process. The Panel was created by the American Urological Association Education and Research, Inc. (AUA). The Practice Guidelines Committee (PGC) of the AUA selected the Panel Chair and Vice Chair who in turn appointed a multidisciplinary panel with expertise in the guideline subject. All panel members were subject to and remain subject to the AUA conflict of interest disclosure criteria for guideline panel members and chairs. Panel members were predominantly urologists, and the target users of the guideline are urologists.The AUA conducted an extensive peer review process. The initial draft of this Guideline was distributed to 52 peer reviewers; 25 responded with comments. The Panel reviewed and discussed all submitted comments and revised the draft as needed. Once finalized, the Guideline was submitted for approval to the PGC. It was then submitted to the AUA Board of Directors for final approval. Funding of the Panel was provided by the AUA. Panel members received no remuneration for their work.BackgroundEvidence BaseRCT'sCharacteristics of trialsTrials. Previous meta-analysesand the AUA panel literature search identified six trials: Stockholm, Norrkoping, Quebec, ERSPC, Goteborg and PLCO. The first three trials provided limited evidence since, among other design problems, the Stockholm trial screened with only one test and a high cut-off of PSA for biopsy; the Stockholm, Norrkoping and Quebec trials lacked allocation concealment; and the Quebec trial did not report according to intention to screen. The Goteborg study is part of the ERSPC, but was independently designed, initiated and reported separately from ERSPC. Sixty percent of participants were included in ERSPC.Age groups. The trials included men age 45 to 80 years, but only the Quebec trial informs about men below age 50 and above age 74 years. Evidence from studies with little bias comes only from the PLCO trial for men age 55 to 74 yearsand only from the Goteborg trial for men age 50 to 55 years.The ERSPC main reportfocuses on men age 55 to 69 years. Thus the bulk of evidence is for men age 55 to 69 years included in the ERSPC, Goteborg and PLCO trials.None of the studies has power to analyze by ethnicity.Screening algorithms. The trials with least risk of bias used different screening algorithms, varying between annual PSA screening and DRE with a biopsy threshold of PSA 4.0 ng/mL (PLCO) to a range of algorithms in the ERSPC with threshold as high as 10.0 ng/mL in one center and a four year interval (in six of seven centers) to a two year interval with a threshold of 3.0 ng/mL in Goteborg.Contamination/Bias. The ERSPC and the PLCO trials have reported the extent of contamination in detail.The contamination was 20-25% in the ERSPC trial,and 77% with a PSA screen after five years in the PLCO trialwith a high exposure to PSA screening and DRE also at inclusion into the trial (prescreening). This likely contributed to the lower-than-expected number of deaths on both arms in the trial. Also, in PLCO there was a lack of adherence to diagnostic biopsies.There was a potential treatment bias in ERSPC; as compared with men in the control arm, men in the screened arm were more likely to be treated at a university center and more likely to receive aggressive treatment for localized cancers.However, differences in treatment received were not significant after adjustment for differences in disease stage and other patient/clinical characteristics in the screening and treatment arms.ResultsMortality. None of the studies were designed to estimate if PSA screening influences overall mortality. Meta-analyses of the trialsdo not show any statistically significant prostate cancer mortality reductions (risk ratios (RR) varying between 0.88 and 0.95). The estimates are not impacted by the inclusion or exclusion of studies with high risk of bias (Stockholm, Norrkoping, Quebec) or how the Goteborg study is handled in relation to ERSPC. The results of ERSPC and PLCO differ: the studies show an RR for prostate cancer mortality (with 95% confidence interval) of 0.79 (0.68-0.91) and 1.09 (0.87-1.36) respectively with a corresponding estimate in the Goteborg study of 0.56 (0.39-0.82). The effect size in PLCO was reduced by contamination, prescreening, and lack of adherence with diagnostic biopsies.The evidence profile for mortality outcomes can be found in Table 2.Numbers needed to screen and to diagnose. Numbers needed to invite to screen and additional number needed to diagnose to avoid one prostate cancer death in the ERSPC (11 years of follow-up) and the Goteborg (14 years of follow-up) studies are as follows: 1,055 to invite and 37 to diagnose, 293 to invite and 12 to diagnose, respectively. However, these estimates are extremely sensitive to follow-up duration and are likely to be much lower over the long term; for example, it has been estimated that the additional number to diagnose is less than 10 over the long term.Incidence of cancer and overdiagnosis. The occurrence of prostate cancer has been higher in the group invited to be screened in studies that estimated incidence (Norrkoping, ERSPC, Goteborg, PLCO: pooled estimate of RR=1.46), but with heterogeneity between studies.The RR was highest in the ERSPC and Goteborg studies. Modeling shows a range of estimates of lead times, and overdiagnosis estimates corresponding to US incidence lie between 23% and 42%,but are as high as 66% in data from the Rotterdam section of the ERSPC and increase with age.Overdiagnosis is defined in this document as the detection of a prostate cancer that would have remained undetected during life in the absence of screening.Other outcomes. Side effects of screening other than overdiagnosis have not been reported in a form that allows for summary estimates in meta-analyses. Fatal complications of biopsies are very rare,but the positive predictive value following an elevated PSA is low, reported to be less than 30%and complications requiring hospitalization within 30 days after biopsy occur in approximately 4% of cases, of which three in four are for infections.Reports hitherto report low levels of anxiety following screening,but studies assessing long-term effects of radical prostatectomy indicate that side effects of radical treatment are prevalent and long lasting.The evidence profile for additional harm outcomes can be found in Table 3.Table 2. Evidence profile for mortality outcomes*The quality of evidence regarding prostate cancer-specific mortality derived from PLCO is low due to methodological limitations relating to the degree of contamination in the control arm. Therefore, PLCO does not provide a direct comparison of screening v. not screening. Rates of screening in the control group increased from 40% in the first year to 52% in the sixth year for PSA testing and ranged from 41% to 46% for DRE.± After a median follow-up of 11 years in the core age group, relative risk reduction 21% (RR, 0.79; 0.68 to 0.91), and 29% after adjustment for contamination and noncompliance. Absolute risk reduction 1.07/ 1000 screened.Table 3. Harm OutcomesThe core age group, 136,689 screening tests were performed (average, 2.27 per subject). Of these tests, 16.6% were positive, and 85.9% of the men with positive tests underwent prostate biopsy.*The quality of evidence means how much confidence we have in the reported quantitative estimate. It does not mean the methodological quality of the study(s) although the latter is one factor that affects confidence in the estimate.Population dataIt is noteworthy that the introduction of PSA-based prostate cancer screening was followed by subsequent dramatic reductions in prostate cancer mortality. For example, in the US following the introduction of widespread PSA screening in the late 1980's, there ensued a ~70% increase in prostate cancer incidence.Despite steadily rising prostate cancer mortality throughout the 1970s and 1980s, several years after the introduction of PSA screening, mortality rates began to decline. By 2008, mortality rates had fallen nearly 40% relative to their highs in the early 1990s.Outside the US, similar patterns have been noted. In an analysis of prostate cancer incidence and mortality rates across the world, Center et al.noted that incidence rates have been rising steadily in the past 10 years. However, over this same time period, prostate cancer mortality rates have been falling.It is helpful to compare and contrast two different populations that had very different uptakes of prostate cancer screening: the US and the UK.In the US PSA screening became widespread in the late 1980s and early 1990s. In contrast, PSA screening was rarely performed in the UK and to this day remains lower than 10% of the population.Prostate cancer death rates in the US began to decline in the early 1990s and by 2009 had dropped by more than 40% since their peak in the early 1990s.The peak in incidence in the US was followed by a decline (36%) in mortality starting several years later. Though mortality rates also declined in the UK, the decline was much more modest (only 12%). Indeed, since 1994 prostate cancer mortality rates have declined four times faster in the US compared to the UK.However, other ecological studies within the US fail to support the relationship between PSA screening and prostate cancer mortality reductions,and the differences in the UK and US may be partly due to more aggressive treatment after diagnosis in the US when compared to the UK and differences in attribution of cause of death.Modeling StudiesModeling studies are used to supplement observed data on cancer outcomes by filling in the latent process of disease progression based on observed data on disease incidence under screening. By virtue of the fact that models address the latent process of disease progression they can provide information on unobservable aspects of the process. Thus, for example, models have provided estimates of the time by which screening advances prostate cancer diagnosis and of the frequency of overdiagnosis associated with PSA screening.Models have also been used to quantify the role of PSA screening in explaining population declines in prostate cancer mortalitythereby providing indirect evidence about screening benefit that is complementary to that obtained from randomized trials. Finally, models have been used to interrogate the vast array of potential PSA-based screening policies to identify those that are most likely to preserve benefit while reducing adverse outcomes and costs.First, models of prostate cancer natural history and progression have been used to estimate the lead time, which is the time by which screening advances diagnosis. The lead time is not directly observable because once a case has been detected by screening, the time at which a patient would have presented clinically is unknown. However, the distribution of the lead time can be deduced from data on disease incidence before and after the adoption of screening via appropriate models. Three modelshave been used to estimate the average lead time corresponding to US incidence trends based on data from the Surveillance, Epidemiology and End Results (SEER) registryfrom 1985 to 2000. The average lead time estimates range from 5.4 to 6.9 years across the models. The same models have also been used to estimate the frequency of overdiagnosis among men age 50 to 84 years during this same calendar interval.Estimates of the fraction of screen-detected cases that are overdiagnosed range from 23% to 42%. The estimate of 23% is the same as the estimate obtained in a different studythat used a very different model, but the same SEER incidence data to estimate the frequency of overdiagnosis in the US. The estimate of 42% is based on a modelinitially derived using data from the Rotterdam section of ERSPC. In that study, the frequency of overdiagnosis among screen-detected cases was 50%, but the likelihood that a screen-detected case has been overdiagnosed can vary from less than 5% to more than 75% depending on the age at diagnosis, the PSA level and the grade of the prostate biopsy.The second use of models has been to interpret trends in prostate cancer mortality under screening. Prostate cancer death rates in the US began to decline in the early 1990s and by 2009 had dropped by more than 40% since their peak in the early 1990s.Since PSA screening disseminated into population practice before trials of screening efficacy were mature, these evolving trends in population death rates provided a natural experiment for interrogating PSA screening benefit. However, it has been difficult to disentangle the effects of screening from the effects of changes in primary treatment that have occurred since the mid-1980s. These changes have primarily included increased use of radical prostatectomy for clinically localized disease, the ability to deliver greater doses of radiation to the prostate and the advent of neoadjuvant and adjuvant hormonal therapies.The third use of models has been as decision analysis tools,to determine the relative benefits and harms of competing screening policies in order to facilitate decisions by policy makers and clinicians about how best to use the PSA test in practice. The development of these decision analysis models began even as the two large screening trials in the US and Europe got under way. In the absence of observed results concerning PSA screening efficacy, the models typically relied on plausible mechanisms of screening benefit, most commonly a version of the stage-shift assumption. A recent article found this assumption to yield benefits consistent with that observed in the ERSPC trial.The models have generally produced consistent findings indicating that screening every other year provides benefit that is similar to annual screening while reducing costs, false positive tests and overdiagnosis. Screening men between age 40 and 50 years provides small increments in lives saved with little cost in terms of overdiagnosis but with high numbers of tests required. Screening men age 70+ years results in a high frequency of overdiagnosis and potential overtreatment but this can be mitigated by more conservative biopsy-referral criteria, less frequent screening of men whose PSA levels are low, or referral of low-risk cases to active surveillance.In conclusion, modeling studies have yielded the following inferences that are particularly pertinent for screening policy development. First, PSA screening yields survival benefits that have contributed, to some extent, to the dramatic and sustained drop in prostate cancer death rates in this country. Second, PSA screening advances prostate cancer diagnosis by five to six years on average. Approximately one in four screen-detected cases reflects overdiagnosis. Strategies that screen less frequently than every year, and even less frequently for men with low PSA levels, are likely to be of value in reducing costs and harms while preserving most of the potential benefit of PSA-based screening.Interpretation of the EvidenceThe AUA guideline panel interpretation of the evidence differs from that of a public health perspective. The AUA guideline panel interpreted the evidence from the perspective of the individual with emphasis on the information –both benefit and harm- that an asymptomatic man would need to make an informed decision about prostate cancer screening. The Panel evaluated the best evidence from randomized trials of screening, but did not assume that all trials were of equal relevance. For example, the PLCO and ERSPC randomized trials ultimately addressed different questions (see section on RCT's) screening versus no or little screening in ERSPC as compared to annual screening versus usual care in the PLCO trial. By the time the PLCO trial began, usual care was opportunistic screening in the US and was –on average- every other year. Furthermore, the Panel utilized population data as supporting evidence for a beneficial effect of screening, and used modeling studies to fill gaps in knowledge. This use of modeling was felt to be important given the short time horizon of a decade provided by current randomized trial results, and the paucity of data regarding the benefits of screening outside the age range of 55 to 69 years. The evidence reviewed by the Panel clearly shows that the current practice of prostate cancer screening in asymptomatic men with comorbidities that limit life expectancy, and treatment of virtually all men after diagnosis –even those with non-aggressive features and limited life expectancy- results in substantial harm. Thus, the Panel focused on both shared decision making in the face of uncertaintyand approaches to early detection of prostate cancer that would reduce harms while maintaining the benefits.A major difference in interpretation of the evidence is whether or not the ERSPC and PLCO should be considered equally relevant with respect to the benefits of screening. The trials tested two different hypotheses as noted above; screening versus no or little screening in the ERSPC and organized versus opportunistic screening in the PLCO. The latter interpretation of the PLCO trial is in line with statements in the PLCO publications.A modest effect of PSA screening versus none implies that a substantially larger study than PLCO is needed to meaningfully test more versus less frequent screening. Thus the PLCO was underpowered to address the question of organized versus opportunistic screening. The Panel interprets the randomized evidence to indicate that the ERSPC trial reflects the effect of PSA screening in a situation with low background screening.The bulk of the information comes from screening men age 55 to 69 years. The evidence from screening men under age 50 or over 69 years is very scarce; additionally, there is no evidence concerning the benefits of screening men of differing ethnicity. There is no data from head to head comparisons of the effect of screening interval length. The main evidence is from the ERSPC four-year interval and the Goteborg two-year interval, but these are not really comparable. There is substantial evidence for overdiagnosis of prostate cancer following PSA screening, but it is likely that this has been overestimated by the trials. If overdiagnosis also is followed by active treatment, both the psychological burden of cancer diagnosis and the risk of serious side effects that compromise quality of life ensue also in a group of men with no benefit. A further dilemma is that conservative approaches to management such as active surveillance have not yet been tested in randomized trials to establish treatment protocols and/or safety.Benefits of PSA screeningThe benefits of PSA screening merit careful consideration while developing an approach to prostate cancer screening. It is also important to emphasize that the benefits (or lack thereof) of PSA based screening for prostate cancer may not be representative of prostate cancer screening in general. While there are several potential tests that could be applied in screening for prostate cancer, almost all currently available data pertain to the use of PSA with or without DRE. As a primary screening test, there is no evidence that DRE is beneficial, but DRE in men referred for an elevated PSA may be a useful secondary test.Almost all of the randomized studies that have evaluated PSA based screening for prostate cancer have demonstrated a benefit in terms of lower stage and grade of cancer at diagnosis.Several studies have also revealed a significant reduction in prostate cancer specific mortality rates attributable to PSA based screening for prostate cancer.At least two of the older studies have been criticized for methodological issues and are not considered as robust.53,54 ERSPC and PLCO Cancer Screening trials are more recent and accepted as more well conducted studies; albeit addressing different questions as noted elsewhere (see section Interpretation of the Evidence). These studies have been the focus of much of the analysis and interpretations. In the ERSPC study, which to-date includes the largest randomized cohort of >182,000 men, prostate cancer specific mortality was significantly lower in men who underwent screening compared to unscreened men.The difference in mortality rates between screened and unscreened men also increased with time and when accounting for compliance.However in the PLCO study that was conducted in the US and enrolled over 76,000 men, there was no significant difference in the prostate cancer specific or overall mortality between the screened and the unscreened men.There have been well documented criticisms of the PLCO study mainly relating to the high rates of screening in the control group (3 in 4 men underwent at least one test) as well as the level of PSA screening prior to trial enrollment (up to 40%).These factors could have led to the null result of the trial even in the presence of a screening benefit.The rates of biopsy in men with an abnormal PSA at baseline or at subsequent screening were also lower in the PLCO study at 64% and 50% respectively.This can be compared to the nearly 86% rate of biopsy compliance in the ERSPC study.Prostate cancer specific mortality was the primary endpoint for both the ERSPC and the PLCO trials. However one cannot ignore the benefits of earlier detection through screening in decreasing the risk of metastatic disease.The incidence of metastatic disease at presentation has declined by approximately three-fourths in the US since the advent of PSA screening. Further, in data from the ERSPC, the cumulative risk of metastatic disease at 9 to 11 years of follow-up was 31% to 33% lower in the screened arm compared to the control arm.The Goteborg arm of the trial demonstrated a 56% reduction in risk of metastatic disease.Most of this reduction in metastatic disease was seen in cancers detected at the time of diagnosis in the screened arm and not following diagnosis.An alternative data source to randomized controlled trials is population level data. While population level data are considered a lower level of evidence, this does not mean they are without merit. Indeed, key strengths include large sample sizes and the use of "real world" data as opposed to an "idealized world" that occurs within a clinical trial setting.Since the advent of PSA screening, the incidence of patients presenting with advanced prostate cancer has declined remarkably and death rates from prostate cancer as reported in the National Cancer Database have declined at the rate of 1% per year since 1990.Other data indicate similar declines in prostate cancer related mortality in the US. The degree to which this is attributable to PSA screening is highly controversial even though it is temporally linked with the introduction of PSA-based screening.As previously discussed, in addition to seeing a decline in mortality, there is also an increase in disease incidence. This could reflect either greater screening practices or greater prevalence of true risk factors for prostate cancer in the population (e.g. changing dietary habits, increasing obesity rates, environmental toxins, etc.) or the advent of extended biopsy protocols that sample twice or more the number of cores that were being sampled in the early to mid- 1990's. Given the paradox of rising incidence but falling mortality, it is highly unlikely that the rising prevalence of a factor that truly increases prostate cancer risk could account for these findings.We recognize that population level data cannot establish causality. That being said, there is ecological data that provides supporting evidence that the introduction of PSA-based screening is generally followed by a decline in rates of advanced disease and – in some cases – by a fall in prostate cancer mortality. The degree to which the mortality decline is attributable to PSA-based screening is unclear and ultimately unknowable from empirical observation. Modeling studies have been employed to link declines in mortality to changes in prostate cancer screening and treatment. They have concluded that primary treatment explains up to one third of the mortality decline leaving two thirds to be explained by other factors, primarily PSA.Similar modeling studies have been conducted to partition declines in breast cancer mortality into those plausibly due to mammography screening and advances in adjuvant chemotherapy.The benefits of prostate cancer screening may extend beyond improving survival and could accrue from limiting disease morbidity arising from bladder outlet obstruction, hematuria, bone pain etc. Benefits from screening will also need to be considered from the man's viewpoint. Relevant endpoints considered in clinical trials and advantages in survival or lack thereof may not be valued similarly by every man.The time horizon that is optimal to detect a benefit from PSA based prostate cancer screening has also not been defined. Data from the ERSPC suggest that the benefit of screening increases with time.Time horizons that are important to individual men will obviously vary according to age. A younger male will have a longer time horizon and may be more likely to risk the potential harms of screening in order to gain the potential benefits; but will have to live with harms, if they occur, for a longer period. The tradeoff may not be as attractive for an older man with a shorter time horizon. Currently available data do not allow us to extrapolate in an empirical way beyond 10 to 14 years, which make it hard to forecast outcomes beyond that time frame. These studies will continue to accrue follow-up data, which may indicate a greater benefit with time.Models of primary treatment changes in the population have been combined with projections of treatment impact on disease-specific survival based on published trials and comparative effectiveness studies. Results indicate that less than half of the drop in disease-specific deaths can be explained by treatment changes alone.While this does not prove that screening is efficacious, it is highly suggestive that screening has played some role in the mortality decline. A previous modeling studytranslated the decline in the incidence of distant stage disease into deaths prevented each year through 1999 and concluded that a substantial fraction of the drop in deaths could be attributed to the shift in disease stage with screening followed by earlier treatment. This finding is consistent with another study that modeled the impact of population screening on disease-specific deaths in the US under a similar assumption, namely that cases that would have been diagnosed with distant-stage disease in the absence of screening but that were detected at an earlier stage by screening receive a corresponding disease-specific survival benefit.In summary, an approach to PSA based prostate cancer screening has to take into account the controversies surrounding available data and the fact that over a decade the benefits are modest in terms of prostate cancer deaths averted; 1 death per 1,000 men screened in the ERSPC.However the relative benefit (20% reduction in disease-specific deaths) could be very meaningful at the population level. The potential benefits of screening could extend beyond survival as a primary outcome, and will depend on the relevant time horizon for an individual. Further, disconnecting screening from automatic treatment will significantly impact the risk benefit ratio.HarmsProstate cancer screening itself is associated with a number of potential harms, both psychological and physical. The transrectal or transperineal prostate biopsy has risks of hematuria, hematochezia, hematospermia, dysuria and retention, pain and infection.Hematuria and hematospermia are the most frequently observed side effects with wide variation in observed rates. Hematospermia after biopsy occurs in 10% to 70% of patients while hematuria is seen 14% to 50% of the time.While the risk of hospitalization due to bleeding complications remains low, infectious complications are increasing steadily over time, possibly due to fluoroquinolone resistance.62,63 The 30 day risk of hospitalization after biopsy for any cause has been estimated to be approximately 4%, of which three in four are for infections.The use of routine fecal culture and sensitivity tailored antibiotic prophylaxis may be one approach to reduce infection rates.The American Urological Association has published a white paper to provide some guidance regarding periprocedural prophylaxis.The harms inherent to the biopsy process were used as one justification for the US Preventative Service Task Force's recommendation against prostate cancer screening. Since prostate biopsies are also an important part of some active surveillance programs, understanding these risks and communicating them to patients is not only integral to informed consent for prostate cancer screening but also for consideration of treatment options.Once diagnosed with prostate cancer, a man is faced with the risk of overtreatment of indolent disease due to the assumption that diagnosis with a malignancy must necessarily result in treatment of this malignancy. Estimates of overdiagnosis vary widely from less than 5% to more than 75%depending upon the population used with lead times of 5 to 15 years.In general, overdiagnosis estimates are not portable across geographic settings because they depend not only on the screening and biopsy protocol, and compliance with biopsy referral under screening, but also on practice patterns and disease incidence in the absence of screening. Our best estimatesfor the fraction of screen-detected cases overdiagnosed in the US in the 1990's is approximately one in four, but the likelihood of overdiagnosis is highly age dependent. Subsequent analyses taking nonattendance and contamination into account have lowered these numbers closer to that seen with breast and colon cancer screening,but the risk of overtreatment remains a valid concern due to the impact of treatment on quality of life.Although prostate cancer specific mortality and the need for related palliative care is decreased by screening, quality of life may be impaired as a result due to lasting impairment in urinary, bowel and sexual function.Thus, personal preferences should play a large role in both a decision to screen and in prostate cancer management if diagnosed.Lastly, the psychological impact of prostate cancer screening must be considered and viewed as a potential harm. There is considerable distress involved in the decision making process, the biopsy and deciding among treatment options. Along with the stress due to PSA screening and unnecessary biopsies, the diagnosis of prostate cancer alone may incite severe psychological stress with one study showing an increased rate of suicide and cardiovascular events in newly diagnosed men.Even when men select active surveillance rather than curative therapy, anxiety may continue and trigger intervention in men who would never have needed treatment in their lifetime;although it would appear that anxiety remains low for most men on surveillance in the short term. All of these potential harms must be carefully discussed with a man prior to embarking on a screening program and at each step of screening- whether this is the decision to have a PSA blood test or biopsy- the man should be given the information and the option of stopping based on his individual quality of life and longevity goals.Policy ImplicationsWhen medical interventions have both possible benefits and risks, then expected net benefit of the intervention for an individual will depend on how a man (in the PSA context) values the possible outcomes. For one man, the benefits may outweigh the risks, but for another, even with the same outcome probabilities, the risks may outweigh the benefits. In these "close call" situations, a shared decision making approach can be used to make the best possible decision about the intervention at the individual level.Shared decision making. Shared decision making between clinicians and men is a strategy for making health care decisions when there is more than one medically reasonable option. Each choice has different patterns of outcomes, and the values a man places on those outcomes need to be considered in order to make an optimal decision. Such decisions are said to be "preference sensitive."The characteristics of a shared decision making process include involvement, at minimum, of a clinician and man in the decision making process (although others may be invited in by either party), bilateral sharing of information, joint participation in the decision-making process and then reaching agreement on a management strategy to implement.Men should be able to invite others, such as a spouse, friend or family member into the process; however, it should not simply be assumed the man wants anyone else to participate. The bilateral information sharing involves the clinician helping the man understand their options and the risks and benefits of each option, while the man helps the clinician understand what matters to them in the context of the decision. From the clinicians' perspective, understanding a man's values and preferences can be seen as a diagnostic task,as important as the diagnosis of disease in a man presenting with symptoms. Shared decision making contrasts with a more paternalistic style of decision-making, where clinicians tell men what they should do, often based on their own values and preferences. A number of authors have proposed steps for shared decision-making in the office setting.Shared decision making can be facilitated with patient decision aids (PDAs). A number of guideline groups have recommended a shared decision-making process for helping individual men decide whether or not to have a PSA test for prostate cancer screening.(http://www.asco.org/sites/www.asco.org/files/psa_pco_decision_aid_71612.pdf). According to the International Patient Decision Aids Standards Collaboration, PDAs are, "...designed to help people participate in decision making about health care options. They provide information on the options and help patients clarify and communicate the personal value they associate with different features of the options."Patient decision aids are not shared decision making in and of themselves; rather, they are tools to make shared decision making practical in the busy world of medical practice.The most recent Cochrane Collaboration systematic review of randomized trials of PDAs for preference sensitive conditions identified 86 trials published through 2009 involving over 20,000 participants and addressing 35 different decisions.A meta-analysis of these trials showed that using decision aids compared to usual care resulted in greater patient knowledge, more accurate risk perceptions (when decision aids included probabilities), decisions more consistent with values (when explicit values clarification was included), lower decision conflict related to feeling uninformed and unclear about personal values, fewer people who were passive in decision making, and fewer people who remained undecided. Thus, there is strong evidence that a shared decision making process facilitated by PDAs improves the quality of preference-sensitive medical decisions.In the Cochrane review, 11 trials addressing PSA screening found a significant 15% reduction in PSA screening among men exposed to a PSA decision aid compared to usual care.However, these trials used decision aids that were produced before the evidence from the two large PSA screening trials became available. More information is needed on how men will decide about PSA screening when presented with the most recent evidence, but most likely some fully informed men will want to be screened, while others won't.The AUA systematic review summarized the evidence supporting decision making. High quality evidence indicated that shared decision making increased men's knowledge scores, reduced decisional conflict and promoted greater involvement in decision making. The comparative evidence regarding the best delivery method of shared decision making was considered to be of low quality.Information elements presented to men across the summarized shared decision making studies included the following:More commonly described:Putative mortality benefit of screening in absolute termsDescription of options after abnormal PSA is detectedThe likelihood of false-positive and false-negative resultsDescription of subsequent tests needed for follow up on abnormal screening resultsHarms of screening (additional procedures, hospitalization, sepsis)Less commonly described:Information about prostate gland anatomy and functionProstate cancer incidence and mortalityTreatment options for early and late prostate cancerComplications of treatment options for early and late prostate cancerThe Panel concluded that PSA-based screening should not be performed in the absence of shared-decision making. Thus, we recommend against organized screening in settings where shared-decision making is not part of routine practice (e.g., health fairs, health system promotions, community organizations).What a man needs to know prior to making a decision about testing. Men considering a screening test for prostate cancer should be aware of several facts that may influence their decision whether to obtain a PSA test or not. First, they should be aware that their risk of dying of prostate cancer is about 3% over a lifetime on average. Although many men may be diagnosed with prostate cancer, only a minority will ever progress to advanced disease and even fewer will have a fatal prostate cancer. From 1977 to 2005 the life time risk of being diagnosed with prostate cancer rose 2.3 fold from 7.3% to 17%. During this same period the life time risk of death from this disease decreased by 20% from 3% to 2.4%.Men should consider the threat posed by prostate cancer and weigh this against other potential life-threatening conditions.Second, no screening test is perfect. Some tests like the DRE are not very sensitive and will miss many early prostate cancers. Other tests, like the PSA test can generate a significant number of false positive results due to low specificity. The performance of a screening test is determined in part by the cut point utilized. This is the value that separates positive tests from negative tests and therefore predicts whether a cancer is present or absent. For PSA, a cut point of 4.0 ng/mL has been the historic threshold.When lower cut points such as 2.5 – 4.0 ng/mL are utilized approximately 80% of PSA tests will yield false positive results.Estimates from ERSPC (using a cutpoint of 3.0ng/mL) suggest that PSA screening will correctly predict the presence of prostate cancer in about one of every four biopsies.Fourth, prostate biopsies and treatments targeting localized prostate cancer carry risks. For every 1,000 men tested, approximately 100 to 120 will have an elevated PSA value.Most of these men will undergo a prostate biopsy, and approximately one third will experience some type of mild to severe symptom including pain, fever, bleeding, infection or problems urinating. Approximately 4% will be hospitalized within 30 days after biopsy.Among those men who are diagnosed with prostate cancer approximately 90% will undergo treatment,although over treatment rates may decrease with greater acceptance of active surveillance in the US. Treated men will experience one of three outcomes: 1) recurrent cancer that will progress despite their treatment, 2) no evidence of disease recurrence, but no benefit from treatment either because their cancer was never destined to progress and 3) no evidence of disease recurrence because their cancer was cured. While only some men benefit from treatment, all who are treated are exposed to the complications of treatment. For every 1,000 men screened, two will develop serious cardiovascular events, one will develop deep venous thrombosis or pulmonary embolus, 29 will develop erectile dysfunction, 18 will develop incontinence and less than 1% will die from treatment.The reader is reminded that these are estimates for men deciding on screening, not men deciding on treatment after diagnosis.Unfortunately, no data are available that provide estimates extending to 15 to 25 years. Data from randomized trials allow us to estimate how many men might benefit from PSA screening over a time horizon of about 10 years. Estimates from the ERSPC trial suggest that approximately 60 men of every 1000 between the ages of 55 to 69 years will develop clinical evidence of prostate cancer within 10 to 14 years if they choose NOT to be screened; while approximately 96 of every 1000 men will be diagnosed with prostate cancer if they choose to be screened.Of the 1,000 men who choose NOT to have screening, five will die of their disease within 10 to 14 years. Of the 1000 men who choose screening, four will die of their disease within 10 to 14 years. This amounts to one life saved by screening for every 1000 men screened; however, models have projected that over a man's lifetime, the number of lives saved by screening could be as many as 6 per 1,000 men screened.Increasing the ratio of benefit to harmScreening for cancer in asymptomatic individuals, including prostate cancer, involves a tradeoff of benefit and harm. Through a decade, the absolute benefits of prostate cancer screening are modest for men age 55 to 69 years, and the harms are substantial.Over a lifetime horizon the benefits increase but so do the harms. The ratio of benefit to harm can be improved by taking into account the age and health state of the individual,and a man's personal preferences. Furthermore, baseline PSA results can be used to guide alternative screening strategies that screen less frequently than every year; and using more conservative criteria (e.g. higher PSA thresholds) to refer older men to biopsy, may lead to reductions in false positive tests and overdiagnosis.The Panel encourages the use of tools that account for age and health state to estimate life expectancy for older men.Target PopulationThe strongest evidence of benefit for PSA screening for early diagnosis of prostate cancer is in the age group 55 to 69 yearssince this is the group studied in randomized trials. Thus, targeting of men age 55 to 69 years, after a risk benefit discussion, represents one approach to screening that is based on best evidence.For men below age 40 years, the Panel recommends against PSA-based screening. The low prevalence of disease in men below age 40 years means that even in the best case of screening benefit in this age group, the incremental number of lives save by screening this age group is likely to be very small.Men age 40 to 54 years often undergo PSA-based screening. However, as compared to initiating screening at age 50 years, it was estimated that screening beginning at age 40 years would result in the prevention of fewer than 1 prostate cancer death per 1,000 men.Given that 99% of deaths from prostate cancer occur above age 54 years, the Panel believes that screening average risk men below age 55 years should not be routine. For men younger than age 55 years at higher risk (e.g. positive family history or African American race), decisions regarding prostate cancer screening should be individualized based on personal preferences and an informed discussion regarding the uncertainty of benefit and the associated harms of screening. The reader is reminded that the likelihood of prostate cancer in an individual with a family history of the disease increases directly with the number of affected first degree relatives, and is higher if the disease occurred in multiple generations and/or was diagnosed at an early age (below age 55 years) as compared to a diagnosis in a single generation at an older age.Men age 70+ years have a high prevalence of prostate cancer but also have a greater risk of competing diseases and overdiagnosis when compared to younger men.In the ERSPC randomized trial of screening, there was no indication for a mortality reduction among men age 70 years or older;however, the trial was not powered to detect a benefit in this age group. In addition, there is strong evidence for a lack of treatment benefit for men in this age group, especially those with a life expectancy below 10-15 years.Therefore, given the lack of direct evidence for a benefit of screening beyond age 70 years, and especially beyond age 74 years, the Panel discourages routine screening in this age group.Some men with high risk aggressive prostate cancers with a life expectancy less than a decade, may benefit from the diagnosis and treatment of their disease.Thus, the goal should be to identify these men while avoiding the associated overdiagnosis and over treatment of those with lower risk disease that occurs with opportunistic screening.Several approaches, including higher PSA thresholds to recommend prostate biopsies for older men and discontinuing PSA testing among older men with lower PSA levels, could help achieve the goal of reducing overdiagnosis. In the PIVOT trial where the mean age at enrollment was 67 years,those with a PSA above 10ng/mL had a significant reduction in all-cause mortality after a decade following surgery when compared to observation; surgery provided no reduction in mortality among those with a PSA of 10ng/mL or below. In an observational study of men who had a PSA below 3ng/mL at age 70 to 75 years, the probability of death from prostate cancer during the remaining years of life was similar to the lifetime probability of death from prostate cancer in the general population (1% to 3%), and continued to decline with age. For those men with a PSA of 3.0ng/mL or more, their life time probability of prostate cancer death was approximately 7% and continued to increase with age.Thus, the Panel encourages several considerations for older men who choose to be tested beyond age 70 years that could increase the ratio of benefit to harm. First, increasing the trigger for a prostate biopsy (e.g. to 10ng/mL) based on the evidence that these men have the most to gain from a diagnosis and treatment of prostate cancer over a decade.Second, discontinuing PSA screening among older men age 70 to 75 years who have PSA levels below 3ng/mL.Testing FrequencyThere is evidence to suggest that annual screening is not likely to produce significant incremental benefits when compared with an inter-screening interval of two years. The PLCO trial compared annual screening with opportunistic screening in the US population, which corresponded to screening on average every two years.Prostate cancer mortality rates were similar in the two groups through 13 years of follow-up.Modeling studies have projected that screening intervals of two years will preserve most of the benefits of screening and reduce the harms (i.e., false positive tests and overdiagnosis)8 when compared with screening every year.Intervals for rescreening can be individualized by a baseline PSA level that is predictive of the risk of prostate cancer detection and the risk of development of an aggressive prostate cancer.A number of studies suggest that screening intervals of two to four years are unlikely to miss a curable prostate cancer.For example, in a population based screening study (Goteborg) with seven-year follow-up and a PSA biopsy prompt of 3ng/ml, only 3 cancers (detection rate 0.07%) were detected within three years among those men with a baseline PSA below 1.5ng/ml. Furthermore, in a study of men age 60 years whose serum was stored and later assayed for PSA, there was a 0.5% risk of developing metastatic disease and a 0.2% risk of prostate cancer death at 25 years after a baseline PSA level of 1.0ng/ml.Based on these data, the Panel believes that annual PSA screening as a routine should be discouraged for those who choose to be screened, that two year PSA intervals are a reasonable approach and will be unlikely to miss a curable prostate cancer in most men, and that for men over 60 with PSA levels below 1.0ng/ml, longer PSA screening intervals (e.g., of four years) could be considered. The reader is reminded that for men with a PSA below 3ng/mL at age 70 to 75 years, PSA screening could be safely discontinued if a man at this age is still being screened.Biopsy TriggerThere is no PSA level below which a man can be informed that prostate cancer does not exist. Rather, the risk of prostate cancer, and that of high grade disease, is continuous as PSA increases.In the intervention (screened) arm of the ERSPC randomized screening trial, a PSA trigger of 3ng/mL was associated with a reduction in prostate cancer mortality for men age 55 to 69 years when compared to the control arm (not screened).However, the Panel believes that the urologist should consider factors that lead to an increased PSA including prostate volume, age, and inflammation rather than using an absolute level to determine the need for a prostate biopsy –keeping in mind that PSA is not a dichotomous test but rather a test that indicates the risk of a harmful cancer over a continuum. The Panel believes that postponing and/or avoiding a prostate biopsy 1) in a man with a large prostate, 2) in the older male especially if in less than excellent health, and 3) in the setting of a suspicion of prostatic inflammation, would be acceptable even at PSA levels exceeding 3-4ng/mL. We could find no evidence to support the use of antibiotics to reduce PSA levels in otherwise asymptomatic men, and this practice could lead to an increased risk of post biopsy sepsis.Additionally, for those men over age 70 years and especially above age 74 years where there is no direct evidence for a benefit of screening, if screening is chosen, a higher PSA trigger could reduce the harms of screening by subjecting only those men to biopsy who are more likely to harbor a lethal phenotype and benefit most from treatment.Much effort has been invested in the discovery of methods for improving the ability of PSA to predict the presence of prostate cancer. At this point, the use of DRE, PSA derivatives (PSA density and age specific reference ranges) and PSA kinetics (velocity and doubling time), PSA molecular forms (percent free PSA and proPSA), novel urinary markers (PCA3), and prostate imaging should be considered secondary tests (not primary screening tests) with potential utility for determining the need for a prostate biopsy, but with unproven benefit as primary screening tests. The Panel recognizes that these tests can be used as adjuncts for informing decisions about the need for a prostate biopsy –or repeat biopsy- after PSA screening, but emphasizes the lack of evidence that these tests will increase the ratio of benefit to harm. Further, risk calculators that include multiple variables (in addition to PSA) as an aid to predicting the risk of prostate cancer have not been proven to increase the benefit to harm ratio, and their value in predicting cancer on biopsy is not necessarily generalizable to a population that differs from that in which the tool was developed.Downstream Consequences of TestingAs outlined previously, PSA screening can lead to psychological harm and biopsy related complications. However, the greatest harm associated with prostate cancer screening is the detection of cancers that would otherwise have remained undetected without screening (overdiagnosis), subsequent treatment of these cancers (over treatment) and the associated side effects from a treatment that does not improve survival. For screening to be an acceptable population intervention, these harms must be reduced. Thus the Panel discourages the use of PSA screening for early diagnosis of prostate cancer in older men, especially those that have associated comorbidities that limit life expectancy to 10 to 15 years or less for whom diagnosis and treatment is unlikely to improve health outcomes.STATEMENTS/DISCUSSIONAge ±40 yearsGuideline Statement 1: The Panel recommends against PSA screening in men under age 40 years. (Recommendation; Evidence Strength Grade C)Discussion. The prevalence of prostate cancer in men under age 40 years is extremely low. Population based studies reveal the prevalence of prostate cancer in men below age 40 years to be about 0.1% with numbers as low as 700 cases being reported to the SEER registry between 2001 and 2007.Prior autopsy studies have been able to identify clinically undetected cases of prostate cancer in men as young as 20 years of age but the prevalence has been low even in these retrospective studies of small cohorts of men.US studies reveal a higher prevalence of 2% to 29% of undiagnosed cancer at autopsy even in men under age 40 years, particularly African-Americans, compared to studies from Europe and Asia.The prevalence among European men in their 20's is ±5% while it rises to 5% to 10% in men in their 30's.Even in men under age 40 years who are found to have prostate cancer at autopsy, the disease tends to be of low volume and low Gleason grade.None of the prospective randomized studies evaluating the benefits of PSA based screening for prostate cancer included men under age 40 years. Hence there are no data available to estimate the benefit of prostate cancer screening in this population. However, the harms that can accrue from screening, which include the side effects of diagnostic biopsies and perhaps subsequent treatment will certainly apply to men in this age group who would be subject to screening. Therefore, due to the relatively low prevalence of clinically detectable prostate cancer in men below age 40 years, the absence of any evidence demonstrating benefits of screening and the known harms, screening is discouraged for men under age 40 years of age.Age 40 to 54Guideline Statement 2: The Panel does not recommend routine screening in men between ages 40 to 54 years at average risk. (Recommendation; Evidence Strength Grade C)Discussion. The Panel recommends that screening, as routine practice, not be encouraged in men age 40 to 54 years who are not at increased risk for the disease based on family history and race, for example. There is no high-quality evidence to support this practice in the general population. Specifically, the two large randomized clinical trials (PLCOand ERSPC) did not include men under age 55 years and, therefore, do not inform the decision. While there is some lower-quality evidence (quality rating=c) that an absolute reduction in prostate-cancer mortality rate may be associated with population-wide screening of men in their 40's at average risk, the benefit is relatively small. Howard et al.noted that annual PSA screening of men in their 40's is associated with a 10-year prostate cancer-specific mortality rate of 0.037 deaths/1000 men compared to 0.041 deaths/1000 men if no screening was performed. While the evidence of benefit of screening of men age 40 to 55 years indicates that the effect size is marginal at best, at least in terms of prostate-cancer specific mortality, the weight and quality of the evidence demonstrating the harms of screening remains high. Effectively, the Panel concluded that the harms of screening in this population were at least equal to the benefits, if not higher and, to this end, recommends that screening should not be routine practice.In making this recommendation, the Panel recognizes that there may be other benefits associated with screening that we either did not consider or have not been demonstrated by the current literature. Effectively, we acknowledge that the "absence of evidence does not constitute evidence of absence" and, as such, we are not explicitly stating that screening should be actively discouraged in this group of men. The literature in this area is quite dynamic and future studies may document additional benefits in this younger population. For example, Lilja et al.have documented in a large study of 21,277 men from Malmo, Sweden, that a single PSA measurement taken between age 33 to 50 years is highly predictive of subsequent prostate cancer diagnosis and advanced stage at diagnosis. Whether or not this information would lead to a decrease in morbidity or mortality from the disease is uncertain, however, and to this end, the benefit of this risk stratification is uncertain.The Panel recognizes that certain subgroups of men age 40 to 54 years may realize added benefit from earlier screening. For example, men at increased risk for prostate cancer, such as those with a strong family history or those of African-American race, may benefit from earlier detection, given their higher incidence of disease.These men should be informed of both the known harms and the potential benefits of screening at an earlier age and shared decision making should ensue with an understanding that there are no comparative data to demonstrate that men at higher than average risk for prostate cancer will benefit more from screening when compared to those at average risk. In the future it is possible that individuals at high risk of developing a lethal prostate cancer phenotype may be identifiable at an early age through genetic testing and/or new biomarkers. These individuals could then be targeted for more intense screening even at a young age.In summary, given the Panel's interpretation of the evidence concerning the benefits and harms of annual screening in men age 40 to 55 years who are not at an increased risk for prostate cancer and the rarity of fatal prostate cancers arising in this age group, the Panel does not recommend this practice as a routine. The reader is advised to remember that this does not imply that there is absolutely no benefit to screening this age group, rather that there are significant enough harms associated with screening that the benefits likely are not great enough to outweigh the harms.Age 55 to 69Guideline Statement 3: For men ages 55 to 69 years the Panel recognizes that the decision to undergo PSA screening involves weighing the benefits of preventing prostate cancer mortality in one man for every 1,000 men screened over a decade against the known potential harms associated with screening and treatment. For this reason, the Panel strongly recommends shared decision-making for men age 55 to 69 years that are considering PSA screening, and proceeding based on men's values and preferences. (Standard; Evidence Strength Grade B)Discussion. Although there are considerable harms associated with screening and the quality of evidence supporting this statement is high (A), the Panel felt that in men age 55 to 69 years, there was sufficient certainty that the benefits of screening could outweigh the harms that a recommendation of shared decision-making in this age group was justified. The Panel believes that the test should not be offered in a setting where this is not practical, for example community-based screening by health systems or other organizations.Evidence for screening benefit in this setting is moderate and is derived from large RCTs. Specifically, results from ERSPC document a relative risk reduction of prostate cancer-specific death of 21% at a median follow-up of 11 yearsWhile the absolute reduction in prostate cancer-specific mortality was relatively small (0.10 deaths per 1,000 person-years or 1.07 deaths per 1,000 men randomized), this may represent an underestimate of benefit given the length of follow-up of the study and the degree of non-compliance in the intervention arm. The Panel acknowledges that the prostate component of PLCO failed to show a benefit to screening with a median follow-up of 13 years,but attributes this finding to high rates of screening in the control arm biasing the study to the null.Any discussion of the benefits and harms of prostate cancer screening in men age 55 to 69 years should consider the man's individual life expectancy. Prior studies have documented that men with less than a 10 to 15 year life expectancy are unlikely to realize a benefit from aggressive treatment for localized prostate cancerand as such, it follows that the earlier disease detection associated with screening in these men likely will be less beneficial, if beneficial at all. To this end, shared decision making should include a discussion of the man's baseline mortality risk from other co-morbid conditions, their individual risk for prostate cancer, given their race/ethnicity and family history, and the degree to which screening might influence their overall life expectancy and chance of experiencing morbidity from prostate cancer or its treatment.Guideline Statement 4: To reduce the harms of screening, a routine screening interval of two years or more may be preferred over annual screening in those men who have participated in shared decision-making and decided on screening. As compared to annual screening, it is expected that screening intervals of two years preserve the majority of the benefits and reduce overdiagnosis and false positives. (Option; Evidence Strength Grade C)Discussion. While RCT's have used both two- and four-year screening intervals, there is no direct evidence supporting a specific screening interval. The available evidence is mostly based on modeling, and some evidence may be gleaned from randomized trials, although none of these trials actually randomized men to different intervals as a primary objective. Modeling studies8, 45 have projected that screening men every two years preserves the majority (at least 80%)of lives saved compared with annual screening while materially reducing the number of tests, the chance of a false positive test and overdiagnosis.The two largest screening trials have provided some indirect evidence about the likely benefits of more versus less frequent screening. In the ERSPC, a comparison between the Rotterdam section (interscreening interval four years) and the Swedish section (interscreening interval two years) suggested that a two year screening interval significantly reduced the incidence of advanced disease.Evidence on the comparison of a two-year screening interval with annual screening was provided by the PLCO trial. This trial compared annual screening with a control group that had screening rates similar to those in the US population which corresponded to screening on average every two years.Prostate cancer mortality rates were similar in the two groups through 13 years of follow-up, suggesting little benefit from screening more frequently than every two years. In addition, data from a randomized trial (Goteborg) and a case-control study suggest that a rescreening interval of four years is not likely to miss a curable prostate cancer among men with a PSA below 1.0ng/ml.Age 70+Guideline Statement 5: The Panel does not recommend routine PSA screening in men age 70+ years or any man with less than a 10 to 15 year life expectancy. (Recommendation; Evidence Strength Grade C)Discussion. The Panel recognizes that men age 70+ years can have a life-expectancy over 10 to 15 years , and that a small subgroup of men age 70+ years who are in excellent health may benefit from PSA screening, but evidence to support the magnitude of benefit in this age group is extremely limited. Men in this age group who choose to be screened should recognize that there is strong evidence that the ratio of harm to benefit increases with age and that the likelihood of overdiagnosis is extremely high particularly among men with low-risk disease.Evidence for screening benefit in this setting is unclear and indirect. An absolute reduction in mortality is possible but likely small with a quality rating of C. The quality of the evidence for harm remains high or at least higher than benefit (A). The certainty in the balance of harm and benefit is moderate justifying a recommendation against routine PSA-based screening.The rationale for this recommendation is based on the absence of evidence of a screening benefit in this population with clear evidence of harms. In the ERSPC randomized trial of screening, there was no reduction in mortality among men age 70 years or older.Although men in this age group have a higher prevalence of prostate cancer and a higher incidence of fatal tumors, they also have increased competing mortality compared to younger men,and no compelling evidence of a treatment benefit, especially in men with a limited life expectancy below 10 to 15 years.Therefore, given the lack of direct evidence for benefit of screening beyond age 70 years, and especially beyond age 74 years, as well as higher quality data regarding harms, the Panel discourages routine screening in this age group.Men age 70+ years who wish to be screened should do so after an understanding that the ratio of benefit to harm declines with age, although there is evidence that men with high risk disease in this age range may benefit from early diagnosis and treatment over a decade or less.In order to identify the older man more likely to benefit from treatment if screening takes place, the Panel recommends two approaches. First, increasing the prostate biopsy threshold based on evidence that men with a PSA level above 10ng/ml are more likely to benefit from treatment of prostate cancer when compared to those with a PSA below 10ng/ml.Second, discontinuation of PSA screening among men with a PSA below 3ng/ml, given evidence that these men have a significantly lower likelihood of being diagnosed with a lethal prostate cancer during the remaining years of life when compared to men with a PSA above 3ng/ml.The likelihood of overdiagnosis increases as men age, and is particularly high for older men with low-risk disease. Modeling studies of overdiagnosis in the US population have estimated that among men aged 70 to 79 years, half or more of cases detected by PSA screening with PSA less than 10 and Gleason score 6 or below are overdiagnosed. Among men over age 80 years, three-fourths or more of cases detected by PSA screening with PSA less than 10 and Gleason score 6 or below are overdiagnosed.Because of the harms of biopsy, overtreatment, and overdiagnosis in this population, shared decision making and consideration of individual values, preferences, and quality of life goals are paramount.Research Needs and Future DirectionsFrom a public health perspective, the current strategy of PSA based prostate cancer screening is not acceptable due to the high rates of overdiagnosis and over treatment. Estimates suggest that 1 in 4 US men diagnosed with prostate cancer harbor indolent diseaseand that 90 percent of all men diagnosed with prostate cancer are treated. However, a recommendation against use of PSA screening for the early detection of prostate cancer ignores the proven benefits that accrue with time for some of the men who are screenedand does not account for an individual man's preferences, age and family history. Thus, the Panel recognizes the limitations of the current literature to inform men regarding the balance of benefit and harm of prostate cancer screening, and the need for further research in this area.Knowledge Gaps. To be successful, the benefits of prostate cancer screening must outweigh the harms. Reductions in prostate cancer mortality and the burden of advanced disease must exceed any loss of quality of life associated with screening and treatment. The Panel identified four major areas where knowledge gaps prevented a precise assessment of the magnitude of screening benefits and the harms. First, the outcomes from randomized trials of prostate cancer screening are limited to one decade. Any benefits accruing beyond this point have yet to be assessed. Public health advocates have highlighted the substantial quality of life decrements that are immediate and prolonged that are associated with the treatment of prostate cancer,however these harms may be balanced by future reductions in prostate cancer mortality. Second, the absence of evidence for any benefit of screening outside the age range of 55 to 69 years does not necessarily mean that there is no benefit. This does, however, preclude recommendations for the starting age for PSA screening and the age at which PSA screening should be discontinued. While recommendations for screening men age 40 to 50 years are often made under the assumption that these men have the most to gain because of a longer life expectancy; a low prevalence of disease, longer lead times, and a prolonged time living with the side effects of treatment, make assessments of benefits and harms difficult. Competing causes of death reduce the benefits of screening older men age 70+ years. Thus, the Panel was unable to recommend routine PSA screening for the average risk man for whom direct evidence of benefit for screening is absent (i.e., men below age 55 years and above age 70 years). Third, the ideal approach to serial PSA screening once initiated is unknown. There is no evidence that annual screening will improve the ratio of benefit to harm when compared to testing at intervals of two to four years –intervals that have been associated with a reduction in prostate cancer specific death for men between the age of 55 to 69 years.There have been no direct comparisons of various screening intervals or comparative studies that base screening intervals on baseline PSA levels. Fourth, direct evidence for any additional benefit of using DRE, PSA derivatives (PSA density, PSA kinetics, age adjusted PSA levels), PSA molecular forms (proPSA, freePSA, complexed PSA), novel urinary biomarkers (PCA3), or imaging as primary screening tests is absent. Although DRE has been considered a mainstay of screening together with PSA, the Panel could find no evidence to support the continued use of DRE as a first line screening test. For men who have undergone PSA based screening and present for evaluation, the interventions above including DRE and risk assessment tools using the results of multiple tests, could be useful in determining the need for a prostate biopsy, or the chance that cancer has been missed on a prior biopsy.Communicating these uncertainties to men, identifying the men most likely to benefit from screening, and identifying the men once diagnosed who are more likely to benefit from treatment, are research priorities.Communication. Unlike many interventions in which the ratio of benefit to harm is high and the choice clear cut, prostate cancer screening is a preference sensitive intervention for which there are reasonable choices to screen or not. For this reason, the Panel emphasized the importance of shared decision making as a prerequisite to screening. Shared decision making implies that physicians and men have informative data regarding benefit and harm prior to a decision. Decision support tools that help provide this information have been developed, but optimal methods (pictograms, text, computerized) that best communicate uncertainty to men and that allows individualized decisions regarding screening are needed. Further, improved tools for estimating life expectancy would help identify those more likely to benefit from screening.Clinical Research. The lack of comparative effectiveness studies of screening and no screening with follow-up beyond a decade was problematic in developing a guideline for PSA based prostate cancer screening. The absolute benefits of PSA based prostate cancer screening relative to the rates of overdiagnosis and overtreatment of disease among different populations is an important area for future research. Further, evaluation of the optimal management of screen detected cancers and the cost effectiveness of these options will be important to understand before making broad policy decisions regarding prostate cancer screening.The ERSPC investigators continue to follow men in the intervention and control arms of the largest screening trial reported to date.Longer follow up will provide further evidence to help assess the benefits and harms of screening.In addition, longer follow-up in ERSPC will provide insights into the optimal approaches to screening in terms of testing intervals and age cut points to discontinue screening. Because men age 40 to 50 years have not been enrolled in randomized trials of screening, modeled outcomes will be an important research priority to help inform decisions in this age group, and clarify optimal screening strategies.In addition, the ProtecT trial,an intervention trial comparing active surveillance, radiation, and prostatectomy among men in a large PSA based screening study will further define the benefits of screening among men age 50 to 69 years, and the most appropriate management options after diagnosis.Basic Research. Identification of those men at greatest risk for prostate cancer development and progression would provide a means of targeted screening, thereby reducing unnecessary testing, false positive tests, and the burden of overdiagnosis and over treatment. Current collaborative efforts using germ line DNA to identify risk alleles are ongoing.An improved understanding of the interaction between inherited risk alleles and the environment (lifestyle choices) could provide a potential means of prevention. Future studies of the genetic and epigenetic basis of disease development and progression may provide biomarkers and/or panels of biomarkers with improved specificity when compared to PSA. When available, risk assessment tools combining multiple predictors will need to be evaluated in carefully designed trials to be generalizable to the population in which they would be used.ReferencesGordis L: The Epidemiologic Approach to Evaluating Screening Programs. Epidemiology (4th edition). Saunders 2009; 311.Institute of Medicine: Clinical practice guidelines we can trust. 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