MRS JONES A-LEVEL BIOLOGY - Home



Extended HomeworkSmoking pages 178-185 Answer sheet.TASK ARead pages 178- 9: Describe the effects of smoking on the mammalian gas exchange system, with reference to the symptoms of chronic bronchitis, emphysema (chronic obstructive lung disease) and lung cancerWhat is the mammalian exchange system (3) Trachea, bronchi, bronchioles, alveoli, goblet cells, mucus, ciliaName the 3 main substances in cigarette smoke that can be harmful (3) Tar, carbon monoxide, nicotineSummarise the short term and long term effects of tar on the mammalian gas exchange system (12)TAR: short term effect: accumulates on lining of lungs and increases diffusion pathway of oxygen into blood, so blood is less oxygenated. (1) Chemicals in tar can cause an allergic reaction which causes smooth muscle to contract and so restrict air flow to alveoli (1) Tar paralyses/destroys cilia on surface of airways so they cannot remove mucus (1) Stimulates goblet cells to secrete more mucus which collects and blocks airways (1) Bacteria/viruses become trapped in mucus and multiply, leading to increased infections. (1) Such as influenza/pneumonia (1)TAR: long term effect: Smokers cough due to irritation in airways ( trying to clear excess mucus) (1) This constant cough causes the lining of airways/alveoli to become damaged (1) This produces scar tissue which is thicker and less flexible(1) Smooth muscle layer thickens (1) This reduces the size of the lumen in the airways and so permanently restricts the flow of air (1) Frequent infections inflames the lining of the airways: epithelium (1) White blood cells accumulate to fight pathogenic microorganisms, need to move from blood to airways and release enzymes to digest the linings of the lungs (1) Enzyme is elastase which damages the elastic tissue in the lining of the lungs (1)this affects small bronchioles and alveoli, loss of elastic tissue reduces the elastic recoil in exhalation so trapping air (1) This can cause alveoli to burst (1)For the following diseases: Chronic bronchitis (2), Emphysema (4) COPD (2) and lung cancer (6) describe the symptoms and how smoking causes these.LUNG CANCER: Symptoms: coughing/ shortness of breath (1), pain in chest (1) coughing up blood in sputum (1) Carcinogens in cigarette smoke, accumulate in the tar on lung surface (1) Benzopyrene most harmful (1) Carcinogens enter the nuclei of cells of the lung tissue and can lead to genetic mutations (1) can affect the genes that control cell division, which can lead to uncontrolled cell division, cancer (1) These cancers often occur where tar accumulates at the entrance to bronchi, can take 20-30 years to develop. (1)CHRONIC BRONCHITIS: Symptom: continual coughing (1), coughing up mucus (1) inflammation of the lining of the airways (1) damaged cilia, over production of mucus leads to irritation, coughing, infection (1)EMPHYSEMA: Loss of elasticity in alveoli , which causes alveoli to burst (1) This gives a reduced surface area for gas exchange (1) Symptoms : Short of breath, hard to exhale as elastic recoil lost (1) breathing shallow and rapid, so blood is less well oxygenated= fatigue (1)COPD: combination of diseases (1) chronic bronchitis, emphysema and asthma (1) All symptoms above!Complete the exam questions below:Describe how smoking could cause changes in alveoli, such as those shown in the figure above. 6 marksIn your answer you should make the links between the changes and their causes clear.named component of cigarette smoke(correctly linked to a stated problem); tar, hydrogen cyanide, carbon monoxide (but NOT in context ofHb), ammonia, sulphur dioxidedestroy / paralyse, cilia; mucus not removed;tarover-active goblet cells / extra mucus produced; (accumulation of mucus) leads to, infections / bronchitis;e.g.‘tar destroys cilia’ = 2(1 for this mark, linking the component with a statedproblem, and also the mark for destroying cilia)DO NOT CREDIT tar more than onceIGNORE nicotine neutrophils / phagocytes / macrophages / monocytes (invade);secrete, enzyme / elastase;elastin / elastic fibres, digested / destroyed;low(er) level of, elastase inhibitor / α antitrypsinase;alveoli fail to recoil;constriction of (terminal) bronchioles;(so) coughing / forced expiration, causes alveoli to burst;reduced surface area;ALLOW white blood cells, DO NOT CREDIT lymphocytes, CREDIT formation of scar tissue / fibrosis5 maxQWC; Award if at least 1 mark has been given from each of themark scheme sections for this question. Use the QWC symbol and add to the content mark(s). 1 markDescribe two signs or symptoms of emphysema. 2 marksshortness of breath / shallow breathing /strained breathing / hard to breathe out / wheezing; barrel chest; fatigue / extreme tiredness / cannot exert themselves;pulmonary hypertension / high blood pressure to lungs; enlargement of right side of heart; heart failure / congestive cardiac failure / fluid build up in lungs;cyanosis / skin with blue tinge;DO NOT CREDIT difficulty in breathing / heavy breathing /hard to breathe in e.g. cannot walk farDO NOT CREDIT heart attack / MI / CHD / COPD ALLOW grey / ashenDO NOT CREDIT pale unqualified 2 maxEmphysema is described as a chronic disease, suggest the meaning of the word chronic (2 marks)long term / lifelong / persistent; slow onset / takes time for the symptoms to show;(usually) degenerative / gets (progressively) worse; ALLOW no cure / irreversible IGNORE ref to death 2 max One of the symptoms of smoking is the development of a smoker’s cough. Explain how smoking causes a smoker’s cough and how the cough can lead to further problems in the lungs over a period of time In your answer you should clearly distinguish between the development of the cough and the effects of prolonged coughing (7) (1 mark QWC for the causes tar ;2 (cigarette smoke) destroys / damages / paralyses, cilia / ciliated epithelium ; 2 ALLOW in response to any component of cigarette smoke 2 DO NOT CREDIT ‘kills cilia’ / ‘cilia die’ 2 IGNORE ‘cilia stick together’3 (cigarette smoke stimulates) goblet cells to release more mucus ; 3 ALLOW in response to any component of cigarette smoke Must contain the idea of more mucus than normal4 mucus ( in airways) , builds up / cannot be removed / AW ;5 more, pathogens / bacteria / viruses / microbes, collect / trapped / accumulate (in mucus) ;5 IGNORE ‘pathogens’ alone must have idea of increasingnumber of pathogens e.g. ACCEPT ‘breeding’ ‘multiplying’ /AW 5 ACCEPT ‘higher number of pathogens present’ 5 ACCEPT ‘infections more likely’6 idea that cough is an attempt to , increase air flow / remove microbes , by removing mucus ;effects6 There must be a reason for removing the mucus 6 ACCEPT ‘to clear the throat by removing mucus’ 6 ACCEPT ‘to reduce infections by removing mucus’7 (frequent coughing) damages / inflames, (named) airway / alveoli / elastic fibres ; 7 IGNORE damage to lungs7 IGNORE damage as a result of elastase / emphysema8 formation of scar tissue ; 8 CREDIT in any part of lung9 airway / bronchi / bronchiole, walls thicken ; 9 IGNORE ‘trachea’9 CREDIT ‘smooth muscle (in wall) thickens’10 lumen of , airway / bronchi / bronchiole , narrows ; 10 IGNORE ‘trachea’11 flow of air restricted ; 11 ‘airflow restricted due to extra smooth muscle’ = 2 marks, mp9 and 1112 (damage to alveoli causes) reduced surface area for gas exchange / oxygen diffusion ;6 maxQWC – One cause of cough and one effect of cough 1 Award if at least 1 mark has been given from eachDescribe how smoking contributes to the development of lung cancerIn your answer you should make the links between smoking and the development of lung cancer (6 marks; 1 =QWC)tar/cigarette smoke contains carcinogens / is carcinogenic ; (IGNORE cigaretees)benzopyrene / formaldehyde / other e.g. ; enters , lung / epithelial , cells ; idea that destroyed cilia prevent removal of , carcinogens / tar , which then have greater contact time with epithelial cells ; enters nucleus / in contact with DNA ; (needs to be stated not implied!)causes mutation ; (ignore description)proto-oncogenes to oncogenes ; accept switching on of oncogenesuncontrollable , cell division / mitosis ; (accept cell multiplication) IGNORE: growth/ref to speed of cell divisionformation of , tumour / mass of cells ; (accept lump of cells)no , programmed cell death / apoptosis ; 5 MAXQWC: showing link between smoking and lung cancer : 1 mark awareded from mps 1-5 and 1 mark awarded from mps 6-10Name 3 other diseases associated with smoking (3 marks)mouth / tongue / throat / oesophageal , cancer ; Accept secondary cancerschronic bronchitis / COPD ; DO not credit smoker’s coughemphysema / COPD ; credit COPD once onlyatherosclerosis ; thrombosis ; ignore thrombuscoronary heart disease / CHD / angina / heart attack / myocardial infarction / MI ; IGNORE CVD, hypertension/chronic heart disease.stroke ; peripheral vascular disease / arteriosclerosis ; Smoking increases the risk of lung infections. Explain how the mucus and the cilia in the air passages reduce the chance of developing lung infections. (2)mucus traps, bacteria / microbes / pathogens / microorganisms / viruses / spores ; ( IGNORE reference to dirt/dust}cilia, sweep / move / waft, mucus / bacteria / pathogens / microorganisms / viruses / spore, upwards / AW ; (accept suggestion of movement to mouth/swallowed etc)TASK B: Read pages 180-3 Describe the effect of nicotine and carbon monoxide in tobacco smoke on the cardiovascular system with reference to the course of events that lead to atherosclerosis, coronary heart disease and stroke What is the cardiovascular system? (1)Blood, heart, arteries, veins and capillaries.Describe the effect of nicotine on the human body (5)Causes addictionMimics action of transmitter substances at synapses, makes ns more sensitive, smoker more alertCauses release of adrenaline: increases HR, BR, constricts arterioles= raised BPConstriction of arterioles to body extremities= reduced blood flow/oxygen/amputationMakes platelets more sticky= increases the risk Describe the effects of carbon monoxide on the cardiovascular system (5)Enters rbc +haemoglobin (1)Carboxyhaemoglobin= stable molecule (1)Reduces oxygen carrying capacity of blood (1)Causes HR to rise (1)Can damage lining of arteries (1)What is CHD? (2)Coronary heart disease (1)Multifactorial disease (1)Disease caused by a number of risk factorsDescribe the course of events in a flow diagram leading to: atherosclerosis (10)Carbon monoxide damages the endothelium of the arteriesIf a person has HBP/other risk factors this increases the damage to the artery liningPhagocytes repair the damageThey encourage growth of smooth muscle and deposition of fatty substancesDeposits include cholesterol from ld lipoproteins that transport cholesterol around body in bloodHBP also increases cholesterol depositsThese deposits are called atheroma’s: can include fibres, dead blood cells, plateletsThis process is called atherosclerosisAtheroma’s occur under endothelium but can grow and break through endotheliumThis atheroma then forms a plaque which protrudes into artery lumenArtery wall is rough and less flexibleReduces the lumen size=reduced blood flowDescribe the course of events in a flow diagram leading to: thrombosis (6)Blood flowing past plaque cannot flow smoothly, increases chance of a blood clotStickiness of platelets (caused by nicotine) further increases chance of a clotIf the membrane covering plaque is damaged, rbc stick to exposed fatty depositsThis blood clot is called a thrombusClot in an artery can stop blood flow in that arteryPieces of clot may break off and travel until it reaches a smaller artery and block thatDescribe the course of events in a flow diagram leading to: CHD (coronary heart disease) (6)Arteries supplying blood to the heart are the coronary arteriesThey branch off from aorta close to heart= blood under high pressure: more susceptible to damage/atherosclerosisLumen of coronay artery reduced/narrowed by plaques, reduces blood flow to heart muscleLess oxygen for respirationLead to CHD: 3 forms: angina; severe pain in chest/down left arm/up to neckHeart attack/myocardial infarction: deat of part of heart muscle, usually by clot in coronary arteryHeart failure: heart cannot pump, by a major clot in coronary arteryDescribe the course of events in a flow diagram leading to: A stroke (4)A stroke is the death of brain tissueCaused by loss of blood flow to the brainCaused by a blood clot( thrombus) floating around in blood which blocks a small artery leading to the brainAn artery to the brain bursts: haemorrhage. What are cardiovascular diseases? (5)Diseases that affect the heart/circulatory systemAtherosclerosisCHDStrokearteriosclerosisDistinguish between CVD and CHD (2)CVD: diseases that affect the heart or the circulatory systemsCHD a CVD that is a disease of the HEART caused by a malfunction of the coronary arteries supplying blood to the heartDistinguish between atherosclerosis and arteriosclerosis (2)Atherosclerosis is deposition of fatty substances (cholesterol) in the walls of arteries, under the endotheliumArteriosclerosis is hardening of artery walls by deposition of minerals such as calcium in the atheroma’s.What are the symptoms of cardiovascular disease and explain why? (3)High blood pressure and hypertension: results from narrow lumens caused by atheroma’s, Narrow lumen increases friction between blood and artery wall; Heart pups against friction = raised BPAtheroma makes the artery walls less elastic; artery walls cannot dilate as much, or recoil easilyArterosclerosis: hardening of artery walls, makes elastic recoil worse, makes walls less flexibleWhat are the symptoms of CHD and explain why? (5)More difficult to exercise, out of breath: due to atherosclerosis in coronary arteriesReduced blood flow to cardiac muscle: atheroma blocks coronary artery lumenHeart muscle does not receive enough oxygen for respiration and is put under strain to pump more bloodCardiac muscle has less blood=pumping less stronglyLess blood flowing to body, muscles and lungsDescribe the symptoms of a stroke (5)Sudden: brain/part brain receives less oxygenNumbness/weakness of face, arm, leg, especially one side of bodyConfusion/difficulty speaking/understandingDifficulty seeing in one/both eyesTrouble with walking/dizziness/loss of balance/coordinationSevere sudden headache with no other cause.Make a table showing each of the factors that increase the risk of CHD and explain how each contributes to a person developing the disease (14)Risk factorHow they contribute to the risk of CHDAgeRisk increases as you get older as have more fatty deposits in arteries, blood vessels narrow and are less elastic.SexMen are more likely under the age of 50 to die of CHD (woman =oestrogen protects before menopause)Cigarette smokingIncreases deposition of fatty substances in coronary artery walls, increases BP, and increases likelihood of blood clotsObesityPlaces more stress on the heartHypertension: high BPIncreases deposition in coronary artery walls/artery wallsHigh blood cholesterol concentrationIncreases depositionPhysical inactivityAllows circulatory system to loose efficiency. Increases BPDiet high in saturated animal fatIncreases cholesterol= atheromasHigh salt intakeIncreases BP as kidneys retain water (blood)Absence of polyunsaturated fats Less good lipoproteins to transport cholesterolAbsence of antioxidants such as vitamin A, C, EAntioxidants, such as vitamins C and E and carotenoids help protect healthy cells from damage caused by free radicalGenetic factors/family history of CVDPredisposition to the condition.DiabetesOther risk factors: hypertension, obesity, saturated fat, cholesterol levels etc.Stress Continual stress = raised BPWhy is CHD less of a problem in less economically advanced counties? (5)Lifestyle differences/ lower life expectancyDie of other diseases such as malaria/HIV?AIDS before they have lived longenough to develop CHDMore active lifestyleDiet is more healthy therefore less obeseEconomic situation: less likely to be heavy smokersAnswer the following exam questions:Smoking is a contributing factor in 19% of all cases of CHD. The table below list a number of effects of cigarette smoke. (4 marks)effectnicotinecarbonmonoxideincreases heart rate;constricts arterioles;damages the lining of arteries;reduces the ability of haemoglobin to carry oxygen;makes platelets sticky;Describe the effects of these three components of cigarette smoke on the body.8 marks (1 QWC)max 3 for each named componentcarbon monoxide (no mark)c1binds to haemoglobin / forms carboxyhaemoglobin;c2irreversibly / permanently; A greater affinity than for oxygenc3less effective oxygenation of haemoglobin; R oxidationc4shortage of breath;c5damages lining of arteries;c6AVP;max 3 nicotine (no mark)n1addictive;n2adrenaline released;n3increases heart rate;n4reduced circulation to extremities / vasoconstriction;R contract A narrow lumenn5sticky platelets;n6cause blood clotting / thrombosis;n7AVP; e.g. ref to effect on synapse / brain functionmax 3 tar (no mark)t1coats the (internal) surfaces of breathing system; A lungst2reducing efficiency of exchange;t3irritation of mucous membranes;t4goblet cells stimulated / over secretion of mucus;t5inactivation of, cilia / ciliated epithelium;A destroys / damages R killst6mucus not moved;t7coughing;t8carcinogenic / cancer-causing / causes mutations;t9causes emphysema / described; R ref to elastin damage alonet10AVP; e.g. ref to more infections / increased risk of chronicbronchitismax 3 may be awarded anywhereAVP; strain on heart / heart diseaseAVP; raised blood pressure / hypertension8 marksc) The smoke produced by burning tobacco leaves contains over 4000 different chemical compounds. Whilst some of these compounds may be harmless, others are addictive or may cause an increased risk of certain diseases.(a)Name one compound in tobacco smoke that is addictive. [1]: nicotine;1(b)Name two other harmful substances found in tobacco smoke. For each substance describe briefly the nature of the damage caused to the gaseous exchange system. [5]any two fromcarbon monoxide / CO;binds to haemoglobin / forms carboxyhamoglobin;Hb has greater affinity for CO / CO binds more strongly than oxygen;A irreversibly reduces oxygen carrying ability / amount of oxygenthat can be carried; (3 max)tar;accumulates, in lung / on alveolar surface;increases, diffusion barrier / thickness of barrier between air andblood / AW;reduces rate of diffusion / gaseous exchange more difficult / AW;causes cancer / carcinogenic;paralyses / damages cilia; R kills ciliaincreases mucus production / AW;increases chance of infection;production of scar tissue;reduces elasticity of the airway / (oxidants) increase activity of, elastase (emphysema); (3 max)carcinogen;causes cancer;changes DNA / mutation;uncontrolled mitosis / no programmed cell death / no apoptosis;tumour; (3 max)AVPs (2 × 3 max)e.g.arsenic;interferes with cytochromes in respiratory chain;prevents ATP production;replaces phosphate group in ATP;benzpyrene;adheres to surfaces;cancer-causing;A nicotine if not given in (a)5 maxName the two medical conditions described in the passage. [2 marks] (chronic) bronchitis; emphysema, COPD Max 2Describe how changes in the walls of coronary arteries make it likely that a blood clot will develop. 3 marksdamage to, artery wall / lining / endothelium;A scarring R damage to artery / damage in arteryinvasion by phagocytes;cholesterol / fat / LDLs, deposited / accumulates, in artery wall;growth / proliferation of, smooth muscle / fibrous tissue;wall thickens / lumen becomes narrow / reduces blood flow;rougher surface / AW; A ‘stickier’ / more frictionplatelets secrete clotting factor(s);endothelial cells secrete less, anti-clotting factor(s) / prostaglandins;AVP; e.g.atheroma, breaks open / bursts through wall loss of elasticity/ ‘walls do not stretch as much’max 3Outline how nicotine and carbon monoxide in cigarette smoke may increase the risks of atherosclerosis and blood clotting. [3]nicotineincreases, heart rate / blood pressure (possibly leading to damage toartery walls);A ref to hypertensionA for CO as well – but only once in answerdecreases width of arteries / lumen smaller / reduces blood flow;increases number of platelets / makes platelets more ‘sticky’;decreases antioxidants;COdamages walls of arteries;reduces oxygen carrying capacity of blood / binds with haemoglobin /forms carboxyhaemoglobin;bothincrease development of, plaque / atheroma;stimulate production of, fibrinogen / clotting factors;reduces production of enzymes that remove clots;increase blood cholesterol (concentration);AVP; e.g. ref to nicotine and adrenalinmax 3TASK CRead pages 184-5 Evaluate the epidemiological and experimental evidence linking cigarette smoking to disease and early deathWhat is epidemiology? (2)Is the study of the distribution of a disease in a population (1) and the factors that influence its spread.(1)What information does an epidemiological study provide? (4)Provides: which countries may be at greater riskWhich age range may be at greater riskWhich sex may be at greater riskWhich lifestyle factors may increase/decrease the riskInfo used for:What can the information gained be used for? (6)Help countries/organsiations target future spendingTarget research at risk factors to find a cureTarget screening to find those at early riskTarget advice/education to parts of population at most riskPredict where a disease may become more prevalent in futureTaret geographical areas at risk to use preventative medicines/measures to stop disease spreadingCheck how well campaigns/preventative measures are working.What is the evidence linking increased cigarette smoking to the risk of early death? (3)Regular smoker x3 likely to die prematurely than a non-smoker50% smokers die of smoking related diseaseThe more cigarettes a person smokes the more likely they will die prematurely/youngerWhat is the evidence linking increased cigarette smoking to lung cancer? (4)A smoker is 18x more likely than a non-smoker to develop lung cancer25% smokers die of lung cancerA heavy smoker (25+) is 25x more likely than a non-smoker to die of lung cancerThe chance of developing lung cancer reduces as soon as a person stops smokingWhat is the evidence linking increased cigarette smoking to other lung diseases? (3)COPD rare in non-smokers98% of people with emphysema are smokers20% of smokers have emphysemaWhy is it difficult to prove a link between smoking and CHD? (2)Because there are so many risk factors contributing to CVDSubstance’s in cigarette smoke can influence the circulatory system in a way that is likely to increase atherosclerosis and other circulatory diseases.What is the experimental evidence using animals in experiments? (5)Dogs breathing unfiltered smoke developed changes in lungs similar to COPDand developed early stages of lung cancerDogs breathing filtered smoke were healthier but cells were developing changes that could lead to cancerShowed that filtering removed some harmful substances in cigarette smokeChemical analysis of tar revealed carcinogens such as benzopyreneAnother study put tar on bare skin of mice= cancer in skin cellsWhat is the current information on the levels of smoking? (3)Western world adult smoking decliningOpposite true in younger peopleLEDC people are smoking moreEffects of smoking on health can take up to 20 years to developAnswer the following data questions: What do you need to remember when answering data type questions?An investigation was conducted into the effect of smoking on lung function. One measure of lung function is peak flow rate. The peak flow rate is the maximum volume of air expelled from the lungs in one minute (dm3 min–1).Describe the data shown in the figure above. 4 marksrises in both, initially / until age 15;(always) lower in smoker / higher in non smoker;gap / difference, increases with age;in non smoker, plateaus / flattens / increase slows,after 17 / at 18 or 19;in smoker falls after, 15 / 16;in smoker, trough / fall then rise / minimum / anomaly, at 17;figs to compare;Two sets of x and y figures with units for peak flow rateat least once – must compareeither peak flow of smoker and non-smoker at samestated ageor peak flow at two different stated ages for same personCould be in the same place or in different parts of theanswer 4 maxExplain the results obtained for the smoker. 2 marksinitial increase as) lungs grow with age;loss of, elastin / elastic fibres, in alveoli; reduced / no, recoil;decreased diameter of / thicker smooth muscle in / scar tissue in / inflammation of / blockage due to mucus of, (named) airways;increase in resistance to air flow;suitable explanation for, low / anomalous, reading at 17;e.g. infection / unreliable (procedure) / asthmaIGNORE ref to increased smoking 2 maxSuggest three ways of improving the reliability of this investigation. 3 marksmore individuals (male) should be used;replicates / repeat measurements (at one time);calculate, mean / average;identify / deal with, anomalous results;take measurements at more frequent intervals;controlled variable;e.g. every 6 monthsSuitable examples include but are not limited tomake sure that …?same number of cigarettes smoked?same type of cigarette?similar level of fitness?similar, build / body size?exclude individuals with other respiratory problems(e.g. asthma / bronchitis)?same exposure to,passive smoking / environmental pollutionDO NOT CREDIT ref to females / (general) health /occupation unqualified / lifestyle11.3% correct answwr =2 marks evn if no working out(2.75-2.44) divided by 2.75 x 100(0.31 divided by 2.75) x 100Allow 1 mark for an unrounded answerA correct answer rounded to wrong decimal placeA rounded answer to wrong rounding e,g 11.2Describe the trends shown by the results in figure 5.1 (4 marks)590550000Radiation is one factor……………. Using the data in the table,Calculate by how much smoking increases the risk of developing lung cancer; [1](X) 10 / 900% (increase);NOT 10% increaseignore 1000% increaseComment on the risks of radon and smoking on the development of lung cancer. [2]candidates may use information from the passagee.g.typical [NOT average] = 20 unitsthreshold = 200 unitsno increase, between 0 and 20 units / at low levels / well below threshold, of radon;radon increasing, from 20 to 200 units / towards threshold, increases risk;by 10X / 900%;high radon and smoking gives greatest risk;other suitable quantitative risk statement;;consequence / relevant effect on cell 2 maxThe diagram below shows the results of a study into the effects of smoking patterns in different socio-economic groups in the UK.With reference to the diagram above, describe the relationship between socio-economic group and the percentage of heavy smokers. [2]% heavy smokers rises from, professional / gp 1, to, unskilledmanual workers / gp 6 / AW; A statements comparing groups 1 and 6ref to figures used as a comparison;What evidence is there for or against this view? [2]as % heavy smokers increases so does number of people sufferinglong-standing illness;the relative increase in smoking is far greater than the relative increasein long-standing illness / not a proportional increase / AW;use of figures to illustrate;e.g.smoking increases more than 6 fold while long-standing illnessincreases less than 2 foldsmoking increases from 3% to 19% while long-standing illnessincreases from 290 to 420 (per 1000)AVP; e.g. ref to anomalous point2 maxSuggest two other factors that may contribute to the higher rates of long-term illness found in the groups of manual workers as compared to non-manual workers. [2]qualified ref tomedical services;working environment;living conditions;income;education (about diet / possible relief from long-term illness);diet;work-related injury;alcohol intake;(work related) stress;(aerobic) exercise;2 max ................
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