Occupational Disease Manual

Transcription

1 Occupationa Disease Manua

2 Foreword Occupationa disease and work reated disease caims present practitioners with new and different chaenges to those arising from an accident or other singe event. Over the past decade disease caims have generated a significant amount of case aw. New disease and work reated conditions have been the subject of caims. Practitioners need a means of capturing and retaining the weath of disease reated data which crosses their desk amost on a daiy basis. Kennedys Occupationa Disease Unit has therefore produced a pocket-sized manua or reference guide which provides information on a number of occupationay induced conditions and which wi hopefuy be a usefu aide memoire of the reevant case aw. I sincerey hope that the manua wi prove to be a very usefu and portabe too. Kennedys offer a nationa occupationa disease service from the offices in Birmingham, Chemsford, London, Manchester, Taunton and Sheffied. Kieron West Partner and Head of Occupationa Disease Unit k.west@kennedys-aw.com

3 Contents Topic Page Number 1. Asbestos Reated Iness 2 2. Hand/Arm Vibration Syndrome (HAVS) 7 3. Industria Asthma Industria Deafness Carbon Monoxide (CO) Poisoning Contact Dermatitis Stress At Work Work Reated Upper Limb Disorders (WRULDs) Other Disorders: 32 Siicosis 32 Leptospirosis/Wei s Disease 33 Fibrotic Hypersensitivity Pneumonitis 35 Q Fever 36 1

4 Asbestos Reated Iness Asbestos is a naturay occurring fibrous siicate minera with we known fire resistant properties. Its fibrous structure aows it be spun and woven into coth. Besides its fire resistance, asbestos is an efficient heat and sound insuator. When mixed with cement and water, asbestos cement can be mouded to make pipes, boards and ties. It can be appied by hand to ag heating pipes and boiers. Certain types of asbestos fibre can even be sprayed. Sprayed asbestos insuation known as Limpet spray was used iberay inside ships and power stations. TYPES OF ASBESTOS FIBRE The main types of asbestos fibres are: Crocidoite bue asbestos Amosite brown asbestos Chrysotie white asbestos Crocidoite and Amosite beonged to a category of asbestos fibres known as amphiboes. Such fibres are short and rigid and once ingested, are difficut for the ungs to expe. Chrysotie (white asbestos) has onger but soft, cury fibres known as serpentine fibres. These fibres are more easiy ceared from the ungs by the act of coughing. Because they are more difficut for the body to expe, amphiboe fibres have a greater propensity to cause asbestos induced inesses, particuary asbestos induced cancers. Crocidoite is 500 times more toxic in the causation of mesotheioma than is chrysotie. Amosite is 100 times more toxic than chrysotie in causing mesotheioma. Fortunatey, 95% of a of the asbestos which was imported into the UK comprised chrysotie. In 1930, the Merewether and Price report highighted the incidence of asbestosis inside asbestos manufacturing workshops. Subsequenty, their recommendations were given statutory force by the introduction of the Asbestos Industry Reguations Dr Richard Do made the first association between asbestos exposure and the incidence of ung cancer in He noted a significant increase in bronchia tumours amongst asbestotics. Then in June 1960 a paper was pubished by an epidemioogist, Dr Christopher Wagner et a identifying a new form of peura cancer amongst persons who were iving cose to a crocidoite mine in the North West Cape. This paper was the first paper to be written about mesotheioma 2

5 and its pubication proved to be quite controversia amongst epidemioogists and oncoogists. However in 1965 Newhouse & Thompson produced their semina paper in which they pubished their findings reative to persons iving in cose proximity to an asbestos factory in the East End of London. Their study estabished that reativey ow-eve exposure to crocidoite coud cause mesotheioma in persons who have had no occupationa exposure to asbestos. This ead to the introduction of the Asbestos Reguations These Reguations not ony superseded the 1931 Reguations but appied across the board. They were not restricted to the asbestos manufacturing industry. Now, anyone using asbestos in any process was required to adhere to stringent rues of industria hygiene. NON MALIGNANT CONDITIONS 1. Diffuse interstitia pumonary fibrosis a.k.a. asbestosis This condition is caused by very significant, usuay proonged exposure to asbestos dust and fibres. The ung tissue becomes cogged with asbestos fibres causing the tissue to fibrose (become scarred). The scarring restricts the ungs abiity to expand and so respiratory capacity is reduced. Asbestosis is dose reated and progressive. The condition is incurabe and sometimes fata. An asbestotic is at an increased risk of contracting ung cancer. 2. Diffuse peura thickening This condition is aso caused by significant exposure to asbestos. The peura or ining of the ung thickens, thus restricting respiratory function. Peura thickening is aso dose reated and progressive. 3. Circumscribed peura thickening a.k.a. peura paques. This is a benign, asymptomatic condition, which is ony detectabe radioogicay. The House of Lords rued in the case of Rothwe and Others v Chemica and Insuating Company Limited that asymptomatic peura paques do not constitute an actionabe injury. This area remains a hotbed for poitica debate. On 8 January 2010 the Court of Session in Scotand rejected the appication made by a number of major insurance companies for judicia review of the Damages (Asbestosreated Conditions) (Scotand) Act 2009, which effectivey overturns Rothwe as far as caims in Scotand are concerned and the insurers further appea has since aso been rejected [ ]. On 25 February 2010, the MoJ confirmed that the decision in Rothwe is not to be overturned and peura paques wi remain non-compensatabe (unti such time as further medica evidence/ research becomes avaiabe). However, the Government accepted that individuas who had made an understandabe caim for peura paques prior to the House of Lords ruing in October

6 and whose caims were effectivey on hod, woud be eigibe for a newy created fixed payment scheme of 5,000. A series of further announcements were made and can be read in greater detai via the MoJ website MALIGNANT CONDITIONS 1. Lung cancer Whist it is cear that many asbestotics go on to contract ung cancer, the most informed medica opinion now seems to be that where there has been significant exposure to asbestos, then ung cancer shoud be considered to be asbestos attributabe. In a case where there is asbestosis and the victim is or has been a heavy smoker, the combined effects of asbestos exposure and smoking significanty increase the risk of ung cancer. 2. Mesotheioma This is a rare cancer that is amost aways associated with previous asbestos exposure. This cancer usuay occurs in the peura (i.e. the ining of the ung) but can aso occur in the peritoneum (the ining of the abdomina cavity) and more rarey in other parts of the body. Mesotheioma is a atent condition and rarey occurs ess than 20 years after first exposure. The mean atency period of a mesotheioma is between 30 and 40 years after first exposure. The condition is incurabe and ife expectancy is usuay between 6 months and 2 years from the manifestation of first physica symptoms. First symptoms usuay consist of chest or shouder pain accompanied by breathessness because the peura cavity has accumuated a significant quantity of a straw cooured fuid. This accumuation of peura fuid known as an effusion can be aspirated or drained resuting in a short-term improvement. Theoreticay, chrysotie cannot cause mesotheioma. However, much of the chrysotie used commerciay over the years has been contaminated by tremoite, another type of amphiboe fibre. Whist mesotheioma is dose reated, it can be caused by reativey ow eves of exposure. QUANTUM The ninth edition of the Judicia Studies Board (JSB) Guideines provides tabuar information as to the appropriate bracket these caims fa into. In more recent years we have seen an increase in the higher eves of compensation paid out towards the upper end of the bracket. One such exampe is Mayfied v Adeaide Engineering [2009] in which the 68 year od Caimant was 4

7 awarded 80,000 having undergone surgery and chemotherapy and who was expected to suffer worsening pain eading up to his death. (C) Asbestos-reated Disease (a) Mesotheioma 35,000 to 83,750 (b) Lung cancer 51,500 to 66,000 (c) Asbestosis 31,500 to 69,500 (d) Peura thickening 25,250 to 51,500 (e) Provisiona awards for the east serious cases within (d) where the provisiona award excudes any risk of the deveopment of mesotheioma, ung or other cancer or asbestosis. 4,350 to 7,250 USEFUL CASE LAW In the foowing ist of cases you wi note we have referred to cases which dea with the issue of causation, apportionment of damages and knowedge. Sabin v BRB [2010] whether the deceased had asbestosis or usua interstitia fibrosis (UIP) unreated to asbestos exposure found in favour of the caimant Feet v Feet [2009] EWHC measure of damages; mesotheioma; death from mesotheioma Revenue and Customs v Sicock [2009] EWHC mesotheioma; show cause; aegations of negigent exposure to asbestos at work; burden of proof at show cause hearings Horsey v Cascade Insuation Services Ltd [2009] EWHC asbestosis; contributory negigence; discounts; future oss; genera damages; measure of damages; smoking Sienkiewicz v Greif (UK) Ltd; Wimore v Knowsey Metropoitan Borough Counci [2011] SC duty of care, mesotheioma, proof, correct test for determining causation; occupationa and environmenta exposure Abraham v G Ireson & Son (Properties) Ltd [2009] EWHC extent of asbestos exposure; causation; foreseeabiity; knowedge Durham v BAI (Run Off) Ltd [2010] CA EL Poicy Trigger Litigation: causation; empoyers iabiity insurance; interpreting determination of event triggering insurer s iabiity 5

8 Brett v Reading University [2007] CA breach of duty of care; evidence required of breach of duty; empoyers iabiity Barker v Corus (UK) Ltd [2006] HL causation; severa iabiity; apportionment of iabiity according to share of responsibiity for creating materia risk of mesotheioma Boton MBC v Municipa Mutua Insurance Company Ltd and Another [2006] CA poicy wording, oca authorities; accidenta bodiy injury or iness occurring during currency of poicy Bone v Ministry of Defence [2006] quantum; award to widow for death of husband from ung cancer foowing exposure to asbestos dust at work ( ) Pinder v Cape Pc [2006] EWHC duty of care to pubic to dispose of hazardous waste appropriatey; foreseeabiity of harm Badger v Ministry of Defence [2005] EWHC contributory negigence; ung cancer caused by smoking and exposure to asbestos; reduction in damages attributabe to smoking Maguire v Harand & Woff Pc and Another [2005] CA foreseeabiity; wife exposed to asbestos from husband s cothing; iabiity for mesotheioma caused by exposure Rothwe v Chemica and Insuating Limited [2005] HL (formery known as Grieves and Others v F T Everard and Sons and Others [2006]) causes of action; asbestos; peura paques; risk of future disease and consequent anxiety; actionabe damage Fairchid v Genhaven Funera Services and Others [2002] HL mesotheioma; empoyers iabiity; exposure to asbestos whie working for more than one empoyer; causation Baantine v Newas Insuation Co Limited [2000] CA measure of damages; industria diseases; benefits to be deducted in fu from persona injury damages award Hotby v Brigham and Cowan (Hu) Ltd [2000] CA joint tortfeasors; asbestosis; exposure to asbestos by more than one empoyer; caimant to prove causation; apportionment of responsibiity on time exposure basis Margereson and Hancock v J W Roberts Limited [1996] CA iabiity of factory owner; reasonabe foreseeabiity of risk of harm estabished from state of contemporary knowedge 6

9 Hand/Arm Vibration Syndrome (HAVS) HAVS is the coective name for injuries to bood vesses, nerves and musces caused by hand transmitted vibration. The typica symptoms are tinging, numbness, cod induced whiteness of the fingers and weakness of grip. HAVS can be defined as a disease with three separate components: 1. Circuatory disturbances aso sometimes referred to as a vasospasm, finger banching ( white finger ) or vascuar injury; 2. Sensory and motor disturbances aso sometimes referred to as neuroogica injuries; and 3. Muscuar skeeta symptoms (athough these are sometimes strain reated rather than vibration induced). The diagnosis of HAVS is based on: a) The history of the symptoms provided by the patient, b) The history of reevant and significant vibration exposure, and c) No evidence of an underying cause to account for the symptoms. Note that Raynaud s Phenomenon (which is a descriptive term for cod induced episodic whiteness affecting the fingers which is the principa vascuar symptom of HAVS) may be caused by Raynaud s disease that is a constitutiona condition. It can aso be caused by connective tissue disease, arteria disease, toxins/drugs as we as having traumatic causes that incude but are not imited to hand transmitted vibration. The eve of symptomoogy is cassified according to the Stockhom Workshop Scae that assesses both neuroogica and vascuar symptoms. 7

10 Tabe 1 The Stockhom Workshop Scae for the cassification of Cod-Induced Raynaud s Phenomena in the Hand/Arm Vibration Syndrome STAGE GRADE DESCRIPTION 0 No attacks. 1 Mid Occasiona attacks affecting ony the tips of one or more fingers. 2 Moderate Occasiona attacks affecting dista and midde (rarey aso proxima) phaanges of one or more fingers. 3 Severe Frequent attacks affecting a phaanges of most fingers. 4 Very Severe As in Stage 3, with trophic skin changes in the fingertips. Note that the staging is made separatey for each hand. In the evauation of the subject the grade of the disorder is indicated by the stages of both hands and the number of affected fingers on each hand e.g. 2L(2)/1R(1). Tabe 2 Sensorineura Stages of the Hand/Arm Vibration Syndrome STAGE SYMPTOMS 0 SN Exposed to vibration but not symptoms. 1 SN Intermittent numbness with or without tinging. 2 SN Intermittent or persistent numbness, reduced sensory perception. 3 SN Intermittent or persistent numbness, reduced tactie discrimination and/manipuative dexterity. FORESEEABILITY/DATE OF KNOWLEDGE This is the date when any individua empoyer ought first to have recognised that work with vibratory equipment gave rise to a foreseeabe risk of injury is often referred to as being the date of knowedge however it is important to consider whether this is in fact appropriate for each individua case since the date of knowedge in HAVS cases varies between industries and many cases draw a distinction between the date when the empoyer shoud have been aware of the risk and the date by when it shoud have instituted precautions to reduce or eiminate that risk. 8

11 Exampes of various dates of knowedge are: Rai Industry knowedge of risk ought to have arisen by 1973 and by the end of 1973 a system of issuing warnings to work as ought to have been in pace and by the end of the foowing year periodica medica surveiance ought to have been introduced to a empoyers exposed to the use of hand hed vibratory equipment [Aen v British Rai Engineering Ltd [1998]. Coa Industry date of knowedge 1973 with an obigation to take precautionary steps by issuing warnings and undertaking medica surveiance by 1975, a duty to undertake job rotation by 1976 and a duty to adapt toos to minimise vibration at some unspecified point thereafter [Armstrong v British Coa Corporation 31 Juy [1998]. Woodworking Industry date of knowedge by which point empoyers shoud have been monitoring their empoyee s heath with respect to vibration injuries (Doherty v Rugby Joinery [2004] EWCA Civ147). BREACH OF DUTY Vibration Leves For a caimant to estabish breach of duty he must first show that the defendant exposed him to excessive vibration (i.e. vibration which exposed him to a foreseeabe risk of injury) and secondy that he faied to take appropriate and necessary precautionary/preventative measures to reduce the risk of injury to an appropriate eve. The key standards that had been pubished addressing vibration eves are: Draft Deveopment Standard pubished by the British Standards Institution in 1975 DD43. This stated vibration magnitudes of beow 1.0 ms 2 were acceptabe vibration magnitudes and magnitudes above 10ms 2 were unacceptabe vibration magnitudes. This upper imit appy to exposure durations of 2 1 /2 hours and ess per day. The ower boundary of 1 ms 2 appied to exposure durations of 400 ms 2 per day roughy up to 2 1 /2 hours it shoud be 150 minutes. Heath and Safety Executive Guidance Document HS(G)88. This guidance was pubished in 1994 but is based upon the British Standard BS 6842 first pubished in HS(G)88 prescribes an action eve of 2.8 ms 2 A(8). The A(8) is a reference to an assumed or norma hours working day of 8 hours. Therefore 2.8 ms 2 A(8) is a measure of the average vibration eve over the course of the 8-hour working day. 9

12 The action eve of 2.8 ms 2 A(8) is not a safe eve of vibration which if it is compied with it is ikey to avoid a injury. The action eve is based upon statistica data demonstrating that a vibration dose equivaent to the action of 2.8 ms 2 A(8) woud resut in 10% of the exposed popuation deveoping symptoms of HAVS within 8 years. The Contro of Vibration at Work Reguations These came into force on 6 Juy 2005 and define exposure imits as 5 ms 2 A(8) and daiy exposure actions vaue as 2.5 ms 2 A(8). Note that these measurements differ from those set out in the earier Standard and Guidance due to the way in which the vibration eve is now measured. As such the eves are not directy comparabe. The empoyer is required not to expose empoyees or others who may be affected by his work to vibration eves above the exposure imit. Where it is not reasonaby practicabe to eiminate the risk from exposure to vibration at source and the exposure action imit is ikey to be reached or exceed the empoyer is required to reduce exposure eves to the owest eve reasonaby practicabe. Liabiity at Common Law The empoyers common aw duty of care is not an absoute one but rather one of reasonabe care in a the circumstances incuding any known susceptibiity or vunerabiity of the empoyee. Not every exposure to vibration wi suffice potentiay to found iabiity. The exposure wi need to be significant and such as to give rise to a foreseeabe risk of injury. Tortious exposure wi amost aways be in excess of A8 of 1.0 ms. An empoyer wi need to show that he has taken reasonabe steps to contro exposure to vibration if he is to avoid iabiity at common aw. These incude: Pre-empoyment screening for HAVS symptoms; Providing training and information to empoyees on the nature of the risk from vibration and what signs or symptoms they shoud ook out for and report; Providing routine heath surveiance; Controing vibration eves by, where possibe, engineering out processes which expose the empoyee to vibration and where not using toos designed for ow vibration and propery maintaining these; 10

13 Controing how the empoyees work so as to imit exposure times (e.g. by way of breaks and job rotation); and Ensuring toos are handed in such a way so as to imit vibration being transmitted into the hand e.g. by training empoyees not to grasp toos tighty. Liabiity under Statute The Contro of Vibration at Work Reguations 2005 set out obigations to: Eimination or contro of exposure to vibration at the workpace; Assess of the risk to heath created by vibration at the workpace; Provide heath surveiance where the is a risk to heath from vibration or the exposure action imit is ikey to be reached or exceeded; and Provide information, instruction and training where the is a risk to heath from vibration or the exposure action imit is ikey to be reached or exceeded. Quantum (i) Most Serious 20,750 to 25,250 (ii) Serious 11,000 to 20,750 (iii) Moderate 5,700 to 11,000 (iv)minor 2,000 to 5,700 Apportionment HAVS is a divisibe, dose reated condition the causation of which is capabe of apportionment between those who have exposed the caimant to vibration in ine with the principes of Hotby v Brigham & Cowan (Hu) Ltd [2000] i.e. the defendant shoud ony be iabe for those symptoms which his breach of duty has caused. However the position is often compicated since, unike the inear deveopment of NIHL, there wi usuay be a atent period where exposure may have been negigent but there are no symptoms. Caimants are often described as having a vibration reservoir which is graduay fied by exposure to vibration but where they do not deveop symptoms. When that reservoir is fu the caimant goes on to deveop symptoms. 11

14 There are often mutipe empoyers and therefore defendants in these cases. Often the caimant has not deveoped symptoms unti a ater period of empoyment. This coud give rise to the argument that in the absence of any injury the caimant has no right of action against a defendant who has exposed the caimant to vibration but where there is no tempora connection with the deveopment of symptoms. There is no definitive case aw on this issue yet. In practise, defendants and insurers often take a pragmatic approach by apportioning quantum on a time exposed basis in the absence of specific evidence on eves of exposure during the exposure period even where symptoms may not have deveoped unti a ater period of empoyment. However in the case of Brookes v South Yorkshire Passenger Transport Executive (1) and Mainine Group Ltd (2) [2005] the Court of Appea addressed a facet of this issue when ooking at whether an empoyee s damages shoud be discounted for pre-date of knowedge (and therefore innocent) exposure. The caimant in that case had not deveoped symptoms unti some years after the negigent exposure of one of the defendants had begun. The Court rued that there shoud be no discount, as without the negigent exposure the caimant woud have never deveoped symptoms. Some defendants and insurers are seeking to rey upon this case to support the proposition that a of the iabiity for damages shoud fa to the defendant who was the caimant s empoyer when symptoms arose. There is some force in this but there is no direct case aw on the point. 12

15 Industria Asthma This is a disease process caused by the narrowing or infammation of the ung passageways making breathing difficut. Symptoms incude wheezing, tightness in the chest and difficuty exhaing air. Most peope with asthma have sudden attacks or periods of more severe symptoms interspersed with periods of mid or no symptoms at a. When a person with asthma is exposed to one of the triggers persona to that individua, the airways begin to swe and narrow, making it difficut to exhae. Asthma cannot be cured but can be controed by medication. The earier the diagnosis, the better the prospects for greater contro and avoidance of permanent ung infammation and airway hypersensitivity. WHAT IS OCCUPATIONAL ASTHMA? A respiratory disease caused by exposure to a trigger in the workpace, usuay inhaed. Potentia triggers are wide ranging and can be found in amost any workpace, incuding offices, factories, shops and hospitas. The ist of industries and jobs where there may be exposure to triggers incude pastics, rubber, chemicas, texties, eectronics, baking, food processing, ceaning, spray painting, sodering and weding. It must be remembered that constitutiona asthma is very commony triggered by exposure to a wide range of common irritants such as poen, perfume, anima fur, house dust mites and tobacco smoke. Occupationa asthma can thus occur as: an aggravation of a pre-existing condition caused by reguar exposure to a new trigger causing hypersensitivity to the trigger and resutant attacks, or an irritant asthma caused by exposure to certain substances or conditions in the workpace irritating the airways with immediate symptoms. Risk factors for occupationa asthma incude: Frequent exposure to the triggers; Aergies; Famiy history; and Smoking. 13

16 Occupationa asthma requires a history of exposure to a sensitising agent. The atency period depends on the substance but can range from a matter of weeks to years. Medica causation is particuary difficut because of the prevaence of the condition to the genera pubic. Issues to be considered incude: Tempora reationship between exposure to a workpace trigger and the onset of symptoms; Variabiity of airfow obstruction measured by peak expiratory fow rates and spirometry; Patch testing as evidence of the sensitivity to the aeged trigger; and Persona/famiy history. Data reeased by the HSE indicates that the incidence has faen as a resut of better contro but occupationa asthma remains a major concern. APPLICABLE LAW The most significant egisation is the Contro of Substances Hazardous to Heath Reguations [1998] [COSHH] as amended in 2002 and 2004 and specific guidance notes reeased by the HSE. COSHH requires an empoyer to contro substances that are hazardous to heath. The standard is a very high one. The aim of the reguatory regime is to provide a uniform code of the contro of any substance that may be harmfu to heath. The HSE aso pubish a ist of Occupationa Exposure Limits [OEL] for over 700 substances incuding short term [15 minutes] and ong term [eight hours] exposure imits. The definition of a substance hazardous to heath is extremey wide. It incudes substances with specified occupationa exposure imits, bioogica agents, infectious bacteria and viruses, dust of any kind in substantia concentrations in air or any other substance which because of its chemica or toxicoogica properties creates a risk of injury to heath. Date of knowedge under common aw is unikey to provide grounds for defence in occupationa asthma cases. In Dugmore v Swansea NHS Trust [2002] the Court of Appea hed that a date of knowedge defence was not reevant when appying Reguation 7 of COSSH. The case concerned the risk of wearing atex goves causing sensitisation. The Court of Appea hed that the question of knowedge of the risk was irreevant as: Every empoyer sha ensure that exposure of his empoyees to substances hazardous to heath is either prevented or where this is not reasonaby practicabe, be adequatey controed. 14

17 The Dugmore decision means that foreseeabiity is not an issue to be considered under COSHH. Reguation 7, sub-section 1 uses the anguage of strict iabiity and providing that an empoyer sha ensure that exposure is either prevented or adequatey controed. The primary duty is to prevent exposure atogether uness this is not reasonaby practicabe nowhere is there any reference to the reasonabe foreseeabiity of risk. Nor is the duty dependent upon what a risk assessment woud have reveaed. In these circumstances, where a causative connection is estabished between the substance and the asthmatic condition, it wi be virtuay impossibe for any empoyer to escape iabiity. QUANTUM (D) Asthma (a) Severe and permanent disabing asthma 28,250 to 43,000 (b) Chronic asthma 17,250 to 28,250 (c) Bronchitis and wheezing 12,600 to 17,250 (d) Reativey mid asthma-ike symptoms 7,000 to 12,600 (e) Mid asthma, bronchitis, cods and chest probems Up to 3,400 15

18 Industria Deafness Traditionay those at particuar risk of hearing damage were those in heavy industry such as shipbuiding, meta work, driing and quarrying or where the use of noisy machinery is utiised such as engineering, woodworking, texties and printing. Many heavy industries have disappeared or been scaed down and new pant and methods of working introduced with consequent reduction in noise eves. Nevertheess in spite of this and the increased awareness of the risk and contros over noise eves, noise induced deafness sti occurs during the course of empoyment and insurers continue to receive a steady stream of deafness caims. The main difference from the thousands of caims of the seventies and eighties is that present day caims concern, in the greater part, ower eves of hearing oss. HOW IS NOISE DEAFNESS CAUSED? The cochea, a spira cavity in the inner ear, is fied with fuid and ined by ces with very fine hairs. For reasons that are not entirey cear, some of these ces are more sensitive than others to unwanted sound or noise and are damaged as a resut of exposure. Over time hearing acuity can be compromised by exposure to such noise. The first symptom of noise induced hearing oss is usuay difficuty hearing a conversation against a noisy background such as in a busy restaurant. Sometimes this hearing oss is accompanied with intermittent high-pitched ringing in the ears caed tinnitus. Typicay, by the time the symptoms have become sufficient to prompt medica consutation and to be measured by audiometry, the damage wi be severe and with every further session of noise exposure progressive. Sound can measured scientificay in terms of intensity but aso be reated to particuar frequency bands. Pitch or frequency is measured in hertz [Hz]. The higher the pitch wi sound, the higher the frequency of it. Sound intensity is measured in decibes [dba]. Noise induced hearing oss wi begin to affect the hearing of certain frequencies. This can be noted with a dip on an audiogram usuay at the 4 5 KHz s range. With continued exposure to noise, the oss of sound perception progresses both in severity and into ower frequency ranges as we. NIHL CLAIMS During the 1970s and eary 1980s thousands of deafness caims were itigated many on behaf of shipyard workers who had been exposed to decades of noise. In the ead case of Thompson v Smiths ShipRepairers [1984] it was decided that from 1963 empoyers exposing empoyees to 16

19 eves of noise in excess of 90 db[a] were in breach of duty unti such time as adequate ear protection was provided. Caimants were thus ony abe to recover for damage suffered between those dates. The many who had been exposed to noise prior to 1963 were thus ony compensated for the proportion of their hearing oss attributabe to the negigent exposure post The decision was based on a detaied review of the medica and other information avaiabe to an empoyer about the need to protect empoyees against noise. On the key question of date of knowedge it was decided that unti the eary sixties, the need to protect empoyees was not generay known and so negigence was not estabished in respect of prior empoyment. As a resut of the Thompson decision as we as various agreements reached between Insurers and certain Unions for payment of scaed compensation, there was comparativey itte industria deafness itigation unti the ate nineties when attention was directed to the potentia for damage at eves of noise ess than the 90 db[a] threshod. In Baker v Quantum Cothing, Meridian Limited and Pretty Poy Limited [2011] the Supreme Court considered the aeged hearing oss suffered by textie workers, prior to the introduction of the Noise at Work Reguations 1989 on 1 January 1990, where the noise exposure had been between eves of 85 to 90dB[A]. At first instance it was hed that at common aw, the acceptabe standard for the average empoyer to adhere to was 90dB[A], as per the 1972 Code of Practice pubished by the Department of Empoyment. The second European draft Directive, which utimatey became the Noise at Work Reguations 1989, was pubished in From that date, average empoyers shoud have been aware as to the risks of noise exposure between 85 and 90dB[A]. A period of two years was aowed for empoyers to impement protective measures, meaning that the average empoyer had no common aw iabiity before 1 January 1990 (athough this precise date was not made cear, but has since been carified by the Supreme Court). A distinction was made for empoyers with greater than average knowedge who were hed to have a date of knowedge from The same two year impementation period was appied and they were therefore in breach from Section 29(1) of the Factories Act 1961, which stated that every pace at which any person has at any time to work sha, so far as is reasonaby practicabe, be made and kept safe for any person working there, did not add materiay to the common aw duty. However, on appea to the Court of Appea, whist the common aw position was agreed, the impementation period for protective measures was restricted to six to nine months and, as such, iabiity arose from January 1988 and ate 1983 respectivey. The fundamenta difference in the Court of Appea judgment reated to Lady Justice Smith s interpretation of Section 29. It was hed 17