For non-life threatening allergies the following are recommended: Avoid contact with NRL gloves or products \200 Avoid areas where there is a risk of inhal ation of powder from NRL gloves worn by others Substitute to other glove materials where appropriate, e.g. nitrile, PVC, or neoprene. If use of NRL gloves is necessary they should be single use disposable gloves and be low-protein (<50 g/g) and powder-free. Relevant legislation Employers and employees need to comply with the COSHH Regulations 2002 (as amended) (see b p. 532, Control of Substances Hazardous to Health). This includes asse ssing and reducing risks and providing health surveillance in appropriate cases (see b p. 4 26, Skin surveillance and b p. 428, Respiratory health surveillance). Further information a nd guidance HSE Latex allergy . Available at: M http://www.hse.gov.uk/skin/employ/latex.htm NHS. Latex allergy: occupational aspects of management. Available at: M http://www.nhsplus .nhs. uk/providers/images/library/ \201 les/guidelines/Latex_allergy_guidelines.pdf HSE (1998). Medical aspects of occupational skin disease, MS24. HSE, Sudbury. 07_Smedley_Chap07.indd 203 12/31/2012 8:52:23 PM CHAPTER 7 Respiratory and cardiovascular disorders 204 Byssinosis Epidemiology and pathogenesis This disease has been associated historically with exposure to cotton dust. It is thought that the disease is caused by an endotoxin, which i s pro- duced by bacteria within raw cotton, but the precise pathology is unclear. Byssinosi s is rare, having largely been eliminated by good exposure con- trols in the textile indust ry. In the UK, the disease was most common in Lancashire and Northern Ireland; both are are as that have local textile mills. The condition is more prevalent in developing countries w ith large textile industries (e.g. India and China) where poor control of exposure may resu lt in extremely high exposures, in some cases >100mg/m 3 . Clinical features \200 Wheezing and chest tightness \200 Typically worse after a break from work (Mondays), improving with return to exposure (better towards the end of the worki ng week) \200 Temporal relationship can be obscured after prolonged exposure. Causal exposures/industries \200 Raw cotton, \202 ax, or hemp \200 Development of bys sinosis within 10yrs of exposure is rare; usually symptoms are associated with >20yrs of exposure Textile and rope-making industry. Individual susceptibility Cigarette smokers develop more severe disease. Clinical assessment and treatment \200 Lung function: cross-shift decline in FEV 1 \200 There are no speci \201 c radiological abnormalities associated with byssinosis Treatment is with bronchodilators and antihistamines. Prevention Exposure controls include enclosure of carding operations and steaming of raw co tton to reduce particle formation. Compensation Byssinosis is a prescribed disease (D2) for Industrial Injuries Disablement Be ne \201 t in those who work with raw cotton or \202 ax. Relevant legislation Byssinosis is reportable under RIDDOR. 07_Smedley_Chap07.indd 204 12/31/2012 8:52:23 PM ORGANIC DUST TOXIC SYNDROME 205 Organic dust toxic syndrome The syndrome known as organic dust toxic syndrome (ODTS) is an acute in \202 ammatory disorder of the lower respiratory system. Precise pathology is uncl ear, but is thought to be caused by a toxic reaction to organic dusts. It occurs in the abs ence of immunological sensitization. Epidemiology ODTS is primarily a disorder of agricultural workers. It does not feature in r outinely collected statistics, but surveys of farming populations suggest a prevalence of a round 6%. Clinical features \200 Fever, chills, malaise, dry cough, dyspnoea \200 Acute onset 4 \200\2236h after exposure \200 Brief duration (<36h) \200 Transient decrease in lung fu nction (FEV 1 , FVC, and peak expiratory \202 ow (PEF)). Causal exposures/industries \200 Moldy grain and vegetable material \200 Agricultural w orkers \200 Clusters of cases are typically associated with very heavy exposures (e.g. emptying silos). Differential diagnosis and clinical assessment ODTS shares many features with acute hyperse nsitivity pneumonitis (farmer \200\231s lung (farmer \200\231s hypersensitivity pneumonitis , FHP)), including exposure, a similar clinical presentation, and the presence of neutrophi ls in alveolar lavage \202 uid. However, the prognosis and treatment are different, and d ifferentiation is important. ODTS is distinguished from FHP by: \200 Short duration of sy mptoms \200 Benign natural history, with absence of progressive lung damage \200 Absenc e of immunological hypersensitivity \200 Absence of lung in \201 ltrates on CXR \200 A bsence of hypoxaemia. Treatment and prognosis \200 Self-limiting \200 No speci \201 c medical intervention r equired. Prevention \200 Reduction of exposure to moldy organic material (see b p. 114, Organic dusts and mists). PPE for high exposure activities \200 Because of the link to heavy exposures, education o f farm workers is particularly important. 07_Smedley_Chap07.indd 205 12/31/2012 8:52:23 PM CHAPTER 7 Respiratory and cardiovascular disorders 206 Hypersensitivity pneumonitis Also known as extrinsic allergic alveolitis (EAA), this in \202 ammatory disorder of the lower respiratory system results from an immunological reacti on to speci \201 c allergens (particularly thermophilic Actinomycetes and Aspergillus spp. ) in moldy organic material. The classical pathological feature is lym- phocytic interstiti al pneumonitis. Pathogenesis is not fully understood, but it is likely to result from a typ e III (immune complex) or type IV (cell-mediated) reaction. It is not an IgE-mediated (type I) allergic condition. Epidemiology \200 In the UK, an average of 47 cases of allergic alveolitis per year (2006 \200\2232010) were reported to the Surveillance of Work-related and Occupational Resp iratory Disease (SWORD) reporting scheme by respiratory and occupational physicians. There have been fewer than 5 cases per year assessed for Industrial Injuries Disablement Bene \201 t over the same period. These \201 gures are likely to be an underestimate of the nu mber of new cases Data from death certi \201 cates in the UK shows attribution of death to occupational allergic alveolitis of <10 cases per year The most prevalent form is farmer \200\231s hypersensitivity pneumonitis (FHP) or farmer \200\231s lung, but a number of other forms are recognized, each with a speci \201 c causa l antigen (Table 7.2). Up to 5% of farmers report symptoms. HSE has reported a recent incre ase of cases related to metal working and wash \202 uids in the engineering sector. There is some evidence of EAA in association with exposure to hard metals (nickel). Table 7.2 Forms of EAA, causal antigens, and source Disorder Antigen Antigen source Moldy hay, grain, straw Farmer \200\231s lung (FHP) Thermophyllic actinomycetes including Saccharopolyspora rectivergula Aspergillus species. Bird fanciers lung Avian proteins Bird excreta and bloom Mushroom workers lung Aspergillus fumigatus, Aspergillus umbrosis Mushroom compost Bagassosis Thermoactinomyces sacchari Bagasse ( \201 brous residue of sugar cane) Malt workers lung Aspergillus clavatus Moldy barley in whisky distilling Ventilation pneumonitis Thermophilic actinomycetes species Water reservoirs in air-conditioning systems This list is not intended to be exhaustive. 07_Smedley_Chap07.indd 206 12/31/2012 8:52:23 PM HYPERSENSITIVITY PNEUMONITIS 207 Clinical features Acute form \200 Fever, chills, cough, dyspnoea, myalgia, headache \200 Onset 4 \200\2238h after exposure to antigen \200 Resolution after 1 \200\2233 days. Su bacute/chronic form \200 Gradual onset of dyspnoea over months or years \200 Recurrent acute attacks may be distinguished in some cases \200 Chronic productive cough. Causal exposures/industries \200 Agricultural workers \200 Forestry workers \200 Mush room workers \200 Bird handlers \200 Sugar cane processors \200 Distillery workers. Clinical assessment \200 i Erythrocyte sedimentation rate (ESR) and neutrophil count (peripheral blood eosinophilia does not occur) Lung function (d FEV 1 , FVC, typically with restrictive pattern, although mild obstructive changes may occur) Impaired gas transfer (d transfer factor for carbon monoxide); hypoxia may occur Chest X-ray (CXR) shows diffuse pulmonary in \201 ltrates (acute) or upper and mid-zone in terstitial \201 brosis (chronic); 20% of CXRs in acute cases are normal Serum precipitins to causal allergens. Treatment and prognosis \200 Low-dose oral steroids \200 Avoidance of exposure \200 P rognosis is highly variable. Can be progressive, with lung \201 brosis. If \201 brosis develops, the main functional consequences for work are reduced stamina and physical capabi lity. Prevention \200 Reduction of exposure to moldy organic material (see b p. 114, Organic dust and mists) PPE for high exposure activities. Compensation EAA is prescribed for Industrial Injuries Disablement Bene \201 t (B6) in tho se who are exposed to molds, fungal spores, or heterologous proteins. Relevant legislation EAA is reportable under RIDDOR 1995. 07_Smedley_Chap07.indd 207 12/31/2012 8:52:23 PM CHAPTER 7 Respiratory and cardiovascular disorders 208 Humidi \201 er fever Humidi \201 er fever is a self-limiting illness that is associated w ith exposure to humidi \201 ed air from air-conditioning systems. The pathophysiology is i ncompletely understood. However, the disorder is distinct from hyper- sensitivity pneumonit is (ventilation pneumonitis), which can result from the same exposure. It is currently thou ght that humidi \201 er fever is caused by either a direct effect of organisms in contamin ated humidi \201 er reser- voirs, or a product of such organisms (e.g. endotoxin). Epidemiology Because of the self-limiting nature of this condition, prevalence estimates ar e neither readily available nor likely to be accurate. Clinical features \200 Usually non-speci \201 c: fever, chills, myalgia \200 Dyspnoea and wheezing can occur \200 Onset 6 \200\2238h after exposure \200 Rapid and complete r ecovery \200 Usually occurs after a break from work (e.g. on Mondays). Differential diagnosis \200 Can develop mild hypoxia, d gas transfer, and audible crackle s at the lung bases. Distinguished from hypersensitivity pneumonitis (HP) by an invariably normal CXR. Serum precipitins to organisms that are present in humidi \201 er \202 uid are often pos itive. However, these do not bear any relation to disease activity, and are only useful as a marker of exposure. The presence of serum precipitins cannot help to distinguish from HP, as they are positive in both disorders. Treatment and prognosis Self-limiting; medical intervention is not indicated. Causal exposures \200 Recirculated air from air-conditioning units, particularly where th e aim is to achieve high humidity Long list of possible causative organisms in humidi \201 er \202 uid include many species of bacteria, fungi, and protozoa \200 Ubiquitous exposure in many of \201 c e environments \200 Highest risk in textile industry where high humidity is desirable as this makes \201 bres pliable and easier to work. Prevention Guidance on the selection, maintenance, and cleaning of humidi \201 ers and air -conditioning systems to minimize the risk of humidi \201 er fever and other disorders is available from HSE. 07_Smedley_Chap07.indd 208 12/31/2012 8:52:23 PM This page intentionally left blank CHAPTER 7 Respiratory and cardiovascular disorders 210 Metal fume fever This benign disease results from deposition of \201 ne metal particulate s in the alveoli. The precise pathological mechanism is unknown. No epide- miological infor mation is available, as the mild symptoms are often over- looked and tolerated by metal wor kers. Causal exposures and industries \200 Primarily caused by zinc oxide fume generated by cut ting, welding, or brazing galvanized steel Similar effects can be caused by other metal fumes. However, although these metals have been implicated, there is little evidence in the literature. Mor eover, the nature of work activities is such that exposure is often to a mixture of metal o xides: \200 iron \200 copper \200 aluminum \200 tin \200 magnesium Found in a wide range of jobs involving metal working: welders \200 oxy-fuel gas cutters Typically in heavy engineering industries: shipbuilding \200 foundries \200 scrap metal industry \200 demolition \200 motor ve hicle repair. Factors affecting exposure Exposure is increased by: \200 increasing thickness of metal i n cutting operations \200 speed of metal cutting and arcing (welding) time \200 automat ed cutting \200 poor ventilation. Clinical features \200 In \202 uenza-like illness with fever, chills, headache, and myal gia \200 Dyspnoea and cough \200 Metallic taste in the mouth \200 Tolerance over the working week, with recurrence after break from exposure ( \200\230Monday fever \200\231) \200 Onset 4 \200\22312h after exposure \200 Benign illness, self-limiting after 1 \200\2232 days. (cid:2) Must not be confused with exp osure to cadmium fume, which can cause a severe toxic reaction in lungs and kidneys. Prevention \200 It is dif \201 cult to avoid metal cutting completely in demolition and shipbuilding 07_Smedley_Chap07.indd 210 12/31/2012 8:52:23 PM METAL FUME FEVER 211 Alternative cutting methods (thermal and non-thermal) are available. However, they are not suitable for all purposes, and all have associated hazards to health. Specialized advice on use of cutting tools is required Using the correct nozzle for cutting \200 Turning off the torch during pauses in activity \200 Fume capture methods including local exhaust ventilation \200 Use of appropriate respiratory protective equipment \200 Training and information, including advice on hygie ne (hand washing and avoiding eating or smoking in the work area) and other risk controls. Further information HSE Oxy-fuel cutting: control of fume, gasses and noise , HSE 668/30. A vailable at: M http://www.hse. gov.uk/fod/infodocs/668_30.pdf#search=%22metal%20fume%20%22 07_Smedley_Chap07.indd 211 12/31/2012 8:52:24 PM CHAPTER 7 Respiratory and cardiovascular disorders 212 Chronic obstructive pulmonary disease This is a group of chronic lung disorders comprising chronic bronchitis and emphysema. They are characterized by irreversible air \202 ow limit ation, with impairment of lung function and debility in severe cases. Epidemiology \200 The main risk factor is smoking \200 Population studies have estimate d the burden of COPD that is attributable to occupational causes, with a population attributable risk percent of 15% (me dian). 1 This equates to around 4000 deaths per year 145 cases of chronic bronchitis and emphysema were prescribed for Industrial Injuries Disablement Bene \201 t during 2010. Clinical features \200 Exertional dyspnoea \200 Wheeze \200 Chronic productive cough for >3mths of the year. Causal exposures/industries An increased risk of COPD has been associated with the followin g: \200 Mineral dusts: \200 coal mining \200 manmade vitreous \201 bres \200 oil mists \200 cement (construction) \200 silica \200 Organic dusts: Farming \200\224animal con \201 nement (especially pigs), grain dust \200 \202 our mi ll work and baking \200 cotton textile work \200 wood (paper milling) Chemicals: cadmium \200 welding fumes \200 vanadium \200 polycyclic aromatic hydrocarbons \200 isocyanates. Clinical assessment \200 Lung function declines progressively: FEV 1 <80% of predicted va lues, FEV 1 /FVC <70% (obstructive pattern). The pattern of lung function in occupational c ases can be complicated by dual pathology (e.g. pneumoconiosis), and restrictive patterns m ay be seen in coal miners and silica-exposed workers CXR is not necessary for diagnosis. 1 HSE (2011). Chronic Obstructive Pulmonary Disease (COPD): COPD in Great Britain . Availab le at: M http://www.hse.gov.uk/statistics/causdis/copd/copd.pdf 07_Smedley_Chap07.indd 212 12/31/2012 8:52:24 PM CHRONIC OBSTRUCTIVE PULMONARY DISEASE 213 Treatment and prognosis \200 Removal from occupational exposure \200 Advise smoking ces sation \200 Inhaled bronchodilators \200 Inhaled corticosteroids \200 Oral corticoste roids and antibiotics for acute infective exacerbations \200 Supportive treatment for adv anced disease \200 Prognosis is variable; severe disease can result in respiratory failur e. Prevention See ( b p. 114, Organic dust and mists, b p. 218, Coal worker \200\231s pneumo- coniosis) for preventive measures and exposure control. Compensation \200 Chronic bronchitis and emphysema have recently been added to the list o f prescribed diseases for Industrial Injuries Disablement Bene \201 t (IIDB) (D1), but onl y for coal miners who have spent >20yrs working underground. FEV 1 must be reduced by 1L to qualify for bene \201 t \200 Emphysema is prescribed for IIDB (C18) for those exposed t o cadmium fumes for a cumulative period of (cid:3) 20yrs. Relevant legislation and further information See b p. 218, Coal worker \200\231s pneumoconi osis for legislation and guidance relevant to dust control in the mining industry. 07_Smedley_Chap07.indd 213 12/31/2012 8:52:24 PM CHAPTER 7 Respiratory and cardiovascular disorders 214 Asbestos-related diseases A number of medical conditions are related to asbestos exposure: \200 Asbestosis \200 Pleural disorders: \200 mesothelioma \200 diffuse pleural thic kening \200 benign pleural effusion \200 pleural plaques Lung cancer \200 Laryngeal cancer. Details of epidemiology, clinical features and managem ent are covered under each condition (Asbestosis, Lung cancer, Pleural disorders, and Laryn geal cancer). Aspects that are common to all asbestos-related dis- ease (exposure, preventi on, compensation and legislation) are covered here. Causal exposures/industries \200 Historically, asbestos has been widely used for \201 r e protection and insulation. In the past (before the danger of asbestos was recognized) controls were poor, and exposures in some industries were very high. \200 dockyards \200\224 shipbuilders, sh ip breakers, and \201 tters \200 railroad engineering \200 asbestos textile industry \200 construction \200 plumbing \200 pipe lagging and thermal insulation/pipe \201 tters \200 asbestos mining and distribution \200 engineering (brake linings and clutch faces) Currently, exposure mainly occurs during the demolition or renovation of old buildings (asbestos insulation, lagging, and roof tiles). Prevention \200 Mainly by elimination (replacement of asbestos with other materials) \200 UK legislation: prohibits import, supply, and use of most asbestos products \200 de \201 nes exposure li mits for asbestos \200 controls the identi \201 cation and removal of asbestos in buildi ngs. Health surveillance \200 Employees who are currently exposed to asbestos above a de \201 ned action level must undergo regular health surveillance (2-yearly lung function) by a do ctor who has been appointed by HSE CXRs are not required as part of health surveillance. Individuals who have been exposed previously need not undergo surveillance. However, it is important to : \200 Document previous exposure carefully, in cluding historical hygiene measurements where available. It is appropriate to inform the GP with the individual \200\231s consent, so that the exposure is noted in the event of futur e asbestos-related disease. 07_Smedley_Chap07.indd 214 12/31/2012 8:52:24 PM ASBESTOS-RELATED DISEASES 215 Counsel the individual about the risk of asbestos-related disease and the availability of compensation 2 Counsel the individual about smoking cessation, as the risk of lung cancer from smoking and asbestos is multiplicative. Compensation It can be dif \201 cult to clarify the source and extent of exposure after >2 0yrs latency. It is essential to take an exhaustive occupational history to ensure that aff ected patients have appropriate access to bene \201 ts. Industrial injuries disablement bene \201 t Some asbestos-related disorders are prescribed : \200 Asbestosis (D1) \200 Mesothelioma (D3) \200 Primary carcinoma of the lung a ccompanying evidence of asbestosis (D8, D8A) Diffuse pleural thickening (D9). Speci \201 c details of prescription according to exposur e activities are out- lined in the List of Prescribed Diseases. 1 Surviving next of kin can claim up to 6mths posthumously. War Pensions Scheme Those who develop asbestos-related disease as a result of exposure whil st working in HM Forces may be eligible for compensation. Civil compensation If an employee can prove negligence on the part of his/her employer, he/ she may be successful in seeking compensation through the civil courts. Claims must be dec lared within 3yrs of the diagnosis of asbestos-related disease, including pleural plaques. Relevant legislation \200 Asbestosis is reportable under RIDDOR 1995 \200 Control of As bestos Regulations 2006 \200 Asbestos (Licensing) Regulations 1983 \200 Asbestos (Prohi bitions) Regulations 1992. Further information HSE Asbestos health and safety . Available a t: M http://www.hse.gov.uk/ asbestos/index.htm 1 DWP. Appendix 1: List of diseases covered by Industrial Injuries Disablement Bene \201 t . Available at: M http://www.dwp.gov.uk/advisers/db1/appendix/appendix1.asp 07_Smedley_Chap07.indd 215 12/31/2012 8:52:24 PM CHAPTER 7 Respiratory and cardiovascular disorders 216 The pneumoconioses Pneumoconioses are a group of chronic lung diseases caused by long-term exposure to respirable particles ( < 5 m diameter) of mineral dust (see Table 7.3). Epidemiology In the UK, an average of 167 cases of pneumoconiosis per year (2005 \200\223 2 010) were reported to the SWORD reporting scheme by respiratory and occupational physicians . This is likely to be an underestimate of the number of new cases. Pathophysiology The classical features of pneumoconiosis are as follows: \200 Deposition of mineral dust in the alveoli \200 Mineral particles are phagocytosed by alveolar macrop hages \200 Localized in \202 ammatory reaction leads to long-term changes in the histology of the lung: \200 \201 brotic reaction in the surrounding lung parenchyma, wi th reticulin formation and collagen deposition necrosis and cavitation of the \201 brotic nodules can occur in the later stages of the disease progressive disease leads to coalescence of \201 brotic areas into large parenchymal masses (progressive massive \201 brosis (PMF)) Gas diffusion is affected, leading to d transfer factor \200 Lung volumes are d (FEV 1 an d FVC), classically a restrictive pattern. Table 7.3 The pneumoconiosis Disease Exposure Cross reference b p. 218, Coal worker \200\231s pneumoconiosis b p. 220, Asbestosis b p. 22 2, Silicosis Coal worker \200\231s pneumoconiosis Coal dust Asbestosis Asbestos \201 bres Silicosis Quartz (crystalline silica) b p. 225, Kaolin pneumoconiosis b p. 224, Berylliosis b p. 226, The \200\230simple \200 \231 pneumoconosis b p. 226, The \200\230simple \200\231 pneumoconosis b p. 226, The \200 \230simple \200\231 pneumoconosis Kaolin pneumoconiosis Kaolin (china clay) Berylliosis Beryllium Stannosis Tin ore Siderosis Iron oxide Baritosis Barium sulfate Bauxite worker \200\231s lung, Shaver \200\231s disease Aluminum 07_Smedley_Chap07.indd 216 12/31/2012 8:52:24 PM THE PNEUMOCONIOSES 217 Radiological features CXR shows small nodular opacities in the lung parenchyma. Distributio n depends on the speci \201 c disease, but tends to affect the upper lobes \201 rst. \200 PMF is associated with large areas of con \202 uent shadowing, usually starting in the upper zones The International Labor Organization (ILO) has devised a classi \201 cation system for the CXR features of all pneumoconioses. 1 This classi \201 cation is used to determine severity of disease for compensation purposes, and is based on the size, shape, and distribution of the opacities: \200 size \200\224small round opacit ies p (up to 1.5mm), q (1.5 \200\2233mm), or r (3 \200\22310mm). Irregular small opacities are classi \201 ed by width as s , t , or u (s ame sizes as for small rounded opacities) profusion (frequency) of small opacities is classi \201 ed on a four-point major category scale (0 \200\2233), with each major category divided into three, giving a 12-point scale b etween 0/ \200\223 and 3/+ large opacities are de \201 ned as any opacity >1cm that is present in a \201 lm. Large opacities are classi \201 ed as category A (for one or more large op acities not exceeding a combined diameter of 5cm), category B (large opacities with combine d diameter >5cm, but not exceeding the equivalent of the right upper zone), or category C ( larger than B). Natural history Natural history, clinical features, and radiological appearance vary accord - ing to the speci \201 c mineral exposure. Some conditions always follow a benign course (stannosis, siderosis), others are often aggressive (asbesto- sis), and CWP can follow eith er a benign or a progressive pattern. Management There is usually no speci \201 c treatment. Management is to remove from exposu re, and treatment of advanced disease is supportive. Compensation Pneumoconiosis is prescribed for Industrial Injuries Bene \201 t (D1) in thos e who have been exposed to the appropriate mineral at work. In general, pneumoconiosis woul d have to be at least ILO category 2 on CXR for an employee to be eligible for bene \201 t s. Relevant legislation Pneumoconiosis is reportable under RIDDOR 1995 if it complies with cat egories 1, 2, 3 on the ILO classi \201 cation, whether simple or with PMF categories A, B and C. There is no requirement to report a case that is assigned to category 0. 1 International Labor Of \201 ce (ILO) (2011). Guidelines for the use of the ILO Internati onal Classi \201 cation of radiographs of pneumoconioses , rev edn. M http://www.ilo.org/s afework/info/publi- cations/WCMS_168260/lang \200\223 en/index.htm 07_Smedley_Chap07.indd 217 12/31/2012 8:52:24 PM CHAPTER 7 Respiratory and cardiovascular disorders 218 Coal worker \200\231s pneumoconiosis Coal worker \200\231s pneumoconiosis (CWP) is a form o f pneumoconiosis caused by exposure to coal dust, characterized pathologically by collec- t ions of coal-laden macrophages in the lung parenchyma, surrounded by \201 brosis and loca lized emphysema. Epidemiology The onset of CWP lags behind exposure by > 10yrs, and so incidence and mortality re \202 ect past exposures and working conditions Mortality is declining in developed countries: new cases are uncommon in the UK because of improved dust control and the decline in coal mining cases are still common in China and there is a low, but signi \201 cant incidence in India. In the UK: more than 65% of new cases occur in those who have reached retirement age ( > 65yrs), although in the past miners would develop symptoms in their thir ties and forties published incidence data are based on claims for Industrial Injuries Bene \201 t. Compensation is well established in the industry. An average of 251 cases/yr prescribed for IIDB 2005 \200\2232010. Clinical features Severity of disease varies according to local conditions, including compo si- tion of the coal (proportional content of silica and other minerals) and its surroundin g strata. It is also related to total cumulative respirable dust exposure. Simple CWP \200 Often asymptomatic \200 Minor impairment in ventilatory capacity is dif \201 cult to distinguish from the effects of cigarette smoking. Complicated CWP \200 Progressive massive \201 brosis (PMF): development of large or con \202 uent solid \201 brotic nodules in the lung parenchyma. Cavitation and necrosis can occur in la rger lesions, leading to expectoration of tarry black sputum (melanoptysis). Local emphysem a can develop Dyspnoea and productive cough. Comorbidity It is accepted that COPD develops in parallel with \201 brosis in coal miners . They are also at risk of silicosis. It can be dif \201 cult to distinguish silicosis oth er than at autopsy, as the radiological features are similar. Causal exposures/industries \200 Coal mining: the dustiest jobs give rise to the highest risk (face work, roof bolting, drilling holes for shot placement) Coal trimming and transportation. 07_Smedley_Chap07.indd 218 12/31/2012 8:52:24 PM COAL WORKER \200\231S PNEUMOCONIOSIS 219 Individual susceptibility A rare complication of CWP is described in miners who are rheumat oid factor +ve. Large cavitating parenchymal nodules develop at relatively low dust exposur e levels (Caplan \200\231s syndrome). Diagnosis \200 History of chronic exposure to coal dust \200 Lung function: Simple CWP \200\224normal FEV 1 and FVC, but transfer factor can be reduced PMF \200\224 dFEV 1 and FVC with restrictive pattern, or obstruction if widespread emphysema has developed; transfer factor d \200 X-ray \201 ndings: nodular o pacities, predominantly in the upper zones (see b p. 216, The pneumoconiosis for ILO classi \201 cation of radiographic changes). Prognosis \200 Simple CWP is benign in most cases \200 Prognosis in complicated CWP is variable. Severe disease can be debilitating. Life expectancy can be normal, but some devel op life-limiting cor pulmonale There is no increased risk of lung cancer or emphysema with CWP \200 The effect of exposu re to cigarette smoke is additive. Prevention Exposure controls in the mining industry including ventilation, dust reduc- tion measures, and use of PPE. Health surveillance Miners must undergo regular CXRs at 4-yearly intervals. Those in whom e arly signs of CWP are detected should be removed from exposure. Compensation CWP is prescribed (D1) for Industrial Injuries Disablement Bene \201 t (see b p. 218, Coal worker \200\231s pneumoconiosis) in those who have been exposed chronically t o coal dust in mining or above ground. Relevant legislation \200 CWP is reportable to HSE as a pneumoconiosis under RIDDOR 1995. \200 The Coal Mines (Control of Inhalable Dust) Regulations 2007. Available at: M http://www.legislation.gov.uk/uksi/2007/1894/contents/ 07_Smedley_Chap07.indd 219 12/31/2012 8:52:24 PM CHAPTER 7 Respiratory and cardiovascular disorders 220 Asbestosis This disease is characterized by chronic pulmonary interstitial \201 brosis, r esulting from exposure to asbestos (in particular amphibole \201 bres). Epidemiology \200 The disease develops after a long latent period of 25 \200\22340yrs fol lowing exposure There is a clear dose \200\223response relationship, and asbestosis tends to occur in those who have been exposed heavily In Great Britain: although exposures have improved, the incidence is still increasing due to historical exposure. Claims for Industrial Injuries Disablement Bene \201 t (IIDB) rose from 405 in 1999 to 1015 in 2010 industries most commonly cited in IIDB claims are construction, extraction, energy, and wat er supply industry, and manufacturing 189 deaths due to asbestosis were recorded in 2009. 1 Clinical features \200 Gradual onset of dyspnoea and cough \200 Basal crepitations on a uscultation \200 Finger clubbing in 40% of cases. Individual susceptibility Smoking is associated with i severity and rate of deterioration o f asbestosis. Clinical assessment and diagnosis \200 Lung function typically shows d FEV 1 and FVC with a restrictive pattern, although obstructive or mixed patterns can occur d Transfer factor \200 Radiographic investigations: CXR shows \201 ne nodular shadowing predominantly in the lower zones. Other hallmarks of asbestos exposure (pleural plaques) may be present because CXR is relatively insensitive for early disease, high- resolution CT scanning is often used to con \201 rm the diagnosis. \200 Lung biopsy is t he gold standard for diagnosis, showing interstitial \201 brosis and asbestos bodies. Treatment and prognosis \200 No speci \201 c intervention can halt the disease \200 Pa tients should be advised to stop smoking \200 Treatment is supportive in the later stages \200 Up to 40% of patients progress after removal from exposure \200 The correlation b etween CXR \201 ndings, lung function, and clinical progression is poor The risk of lung cancer is increased. 1 Based on death certi \201 cates, where asbestosis was the main cause of death. 07_Smedley_Chap07.indd 220 12/31/2012 8:52:24 PM ASBESTOSIS 221 Other aspects For causal exposures/industries, prevention, compensation, legislation, and f urther sources of information see b p. 214, Asbestos-related diseases. Further information Further information on the epidemiology of asbestosis can be found on t he HSE statistics website. See HSE (2011). Asbestosis: asbestosis mortality in Great Britai n 1978 \200\2232009 . Available at: M http://www.hse.gov.uk/statistics/causdis/asbestosis/a sbestosis.pdf 07_Smedley_Chap07.indd 221 12/31/2012 8:52:24 PM CHAPTER 7 Respiratory and cardiovascular disorders 222 Silicosis This is a pneumoconiosis associated with exposure to respirable crystal- line sil ica. Silica is encountered mainly as crystalline quartz, a component of igneous rocks. Epidemiology \200 There is a long latent period between exposure to silica and onset of disease The risk of disease varies according to level of exposure \200 Silicosis is now rare beca use of substitution and controls in mining. Clinical features There are three recognized types of silicosis: \200 Acute: early onset of dyspnoea and dry cough within a few months of heavy exposure to \201 ne dusts (e.g. sa nd-blasting). CXR shows patchy small airway consolidation (appearance similar to pulmonary oedema). Progression over 1 \200\2232yrs, with respiratory failure Subacute: gradual onset of dyspnoea and dry cough over years after moderate exposure. CXR s hows upper- and mid-zone nodular \201 brosis, with classical feature of \200\230egg-shel l \200\231 calci \201 cation of the hilar lymph nodes. PMF can occur, with coalescence of the \201 brotic nodules. Restrictive pattern of impaired lung function Chronic: slow development of nodules on CXR over many years after low level exposure. Silicosis is associated with larger nodules on CXR and more rapid pro- gression than coal w orker \200\231s pneumoconiosis with which it may co-exist. However, with the exception of e gg shell calci \201 cation, silicosis can be dif- \201 cult to distinguish from CWP clin ically and radiologically in dual exposed cases. i Risk of infection with tuberculosis (TB) (thought to be due to impair- ment of phagocytosis in the lung). Characterized by cavitati on on CXR. Causal exposures/industries \200 Mining: silica is often contained in surrounding strata in coal and other mineral mines. Tunnel drillers/blasters, roof bolters, transportation cre w are at highest risk (although face workers and others are also exposed) Quarries: workers who blast, cut, and transportation stone \200 Stone-working: stone-masonry (granite dressing and grinding) \200 \202 int-knapping Heavy engineering and manufacture: shot blasting \200 preparation and use of grinding wheels/stones (historically, cutlers) \200 use of compressed airlines to clean off silica-containing material 07_Smedley_Chap07.indd 222 12/31/2012 8:52:24 PM SILICOSIS 223 Foundries: sand-molding \200 shot-blasting \200 compressed air cleaning of molded items \200 fet tling Ceramics and pottery making \200 Brick-making. Prognosis and treatment \200 No speci \201 c intervention halts progression \200 Remov e from further exposure \200 Regular examination of sputum for tubercle bacilli; con \201 rmed infection is treated with standard anti-tuberculous chemotherapy 10 \200\22330% of silicosis cases progress after removal from exposure. Health surveillance Health surveillance (respiratory questionnaire, lung function tests, an d CXR) is required for those who are exposed above a de \201 ned threshold exposure (despi te control measures). See b p. 223, Further information, for sources of speci \201 c guida nce from HSE. Prevention Control of exposure is through substitution with low-silica sand for mold- ing a nd shot-blasting, dust control measures (ventilation, suppression), and use of RPE. See b p . 40 for workplace exposure limit (WEL). Compensation Silicosis is prescribed (D1) for Industrial Injuries Disablement Bene \201 t (see b p. 216, The pneumoconiosis) in those who have been mining, quarry- ing, or working w ith silica rock or dust (sand). Relevant legislation Silicosis is reportable to HSE as a pneumoconiosis under RIDDOR 1995. Further information HSE (2004). Silica , Construction Information Sheet No 36 Revision 1. M http://www.hse.gov.uk/ pubns/cis36.pdf HSE (2002). Control of exposure to silica dust in small potteries . M http://www.hse.gov.uk /pubns/ ceis2.pdf 07_Smedley_Chap07.indd 223 12/31/2012 8:52:24 PM CHAPTER 7 Respiratory and cardiovascular disorders 224 Berylliosis Beryl is a hard crystalline ore (aluminum beryllium silicate), found in the str ata of mines dug for other purposes. Beryllium is an extremely hard metal, producing useful alloys when mixed with copper and other metals. The metal, oxide, and soluble salts are al l extremely toxic. Epidemiology Berylliosis is extremely rare (because of elimination from industrial use). Causal exposures/industries \200 Because of its extreme toxicity, the previous widespread use in \202 uorescent light tubes and the ceramic industry has been eliminated However, it is still used: in the nuclear industry \200 in the production of X-ray tubes. Clinical features There are two main forms of disease. Acute \200 Follows inhalational exposure to high levels of the dust of soluble beryllium compounds Severe bronchoalveolitis with tissue necrosis \200 High fatality rate within a few days \200 Progression to subacute phase, with tissue scarring, in the survivors. Subacute/chron ic \200 Only a proportion of those exposed (<5%) develop the disease \200 Florid non-ca seating granulomata heal by \201 brosis, with disruption of the normal lung architecture Progression to diffuse interstitial \201 brosis, leading to respiratory failure, is usual CXR shows \201 ne nodular shadowing and hilar lymphadenopathy \200 Lung function tests show a restrictive de \201 cit \200 d Transfer factor. Differential diagnosis is from sa rcoidosis, which has similar clinical and CXR features. Treatment and prognosis Treatment is with high-dose oral corticosteroids. Treatment can be tailed off, but needs to be prolonged for many months in chronic cases. Relapse can follow early cessation of therapy. Prevention Prevention is by elimination, or by containment, ventilation (with \201 lterin g of discharged air), and fastidious use of PPE. Compensation Chronic beryllium disease is prescribed for Industrial Injuries Disablement Be ne \201 t (C17) in those who are exposed to beryllium and its compounds. 07_Smedley_Chap07.indd 224 12/31/2012 8:52:25 PM KAOLIN PNEUMOCONIOSIS 225