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 Kaolin pneumoconiosis Kaolin (china clay) is a multilayered particulate containing aluminum hydroxide and silicon oxide. Formed from the action of water on granite, and commonly cont aminated by silica-containing compounds. Epidemiology \200 Historically, this was variable in different kaolin mining regions beca use of differing levels of contamination and extraction methods Generally low incidence in the exposed populations gave rise to a belief that contaminating silica was responsible for lung disease in kaolin workers It is now accepted that kaolin itself can cause pneumoconiosis. Clinical features \200 Asymptomatic, or mild exertional dyspnoea \200 Mild d FVC \200 CXR shows small nodular opacities consistent with interstitial \201 brosis \200 Progre ssive massive \201 brosis can occur \200 No speci \201 c treatment. Causal exposures/industries China clay mining. Prevention Prevention is by dust abatement measures. 07_Smedley_Chap07.indd 225 12/31/2012 8:52:25 PM CHAPTER 7 Respiratory and cardiovascular disorders 226 The \200\230simple \200\231 pneumoconioses These disorders are all relatively uncommon. Exposures \200 Siderosis: exposure to iron ore (haematite) \200 iron ore mining \200 welding (mild steel) \200 classic \201 nding of red lungs at autopsy Stannosis: exposure to tin ore \200 Fuller \200\231s earth pneumoconiosis: occurs in workers who extract clay material \200 traditional use of fuller \200\231s eart h to clean wool \200 results from exposure to a mixture of silicates of sodium, potassium, aluminum, and magnesium. Baritosis: exposure to barites in mining, processing, or handling \200 Gypsum pneumoconio sis: exposure in open-cast or deep mining, and production of plasterboard. Clinical features \200 Asymptomatic \200 Benign course \200 Normal lung function \200 Small rounded opacities on CXR (appearance similar to coal worker \200\231s pneumoconiosis). Prevention Prevention is by dust suppression and ventilation, and use of PPE. 07_Smedley_Chap07.indd 226 12/31/2012 8:52:25 PM This page intentionally left blank CHAPTER 7 Respiratory and cardiovascular disorders 228 Lung cancer Epidemiology \200 90% of lung cancers are related to smoking \200 The propo rtion of lung cancer that can be attributed to occupation (based on 2004/05 data) is 14.5%, but (like most other occupational cancers) is higher in men than women: \200 attributabl e fraction men 21.2% \200 attributable fraction women 5.3% 4749 lung cancer deaths were attributable to occupation in 2005 \200 150 new cases of lun g cancer were associated with applications for Industrial Injuries Disablement Bene \201 t in 2010 The interaction between smoking and both asbestos and nickel are multiplicative (or between additive and multiplicative). Clinical features Clinical presentation is very variable, and some patients present with me t- astatic features rather than the effects of local disease. The most common features are: \200 Weight loss \200 Cough with haemoptysis \200 Dyspnoea \200 Chest pain \200 Unresolving pneumonia. Causal exposures/industries \200 Crystalline silica: \200 mining \200 quarrying \200 stone masonry \200 glass manufacture \200 foundries \200 shot-blasting and grinding \200 ceramic and pottery manufacture Asbestos \201 bres: shipbuilding and \201 tting \200 mining \200 asbestos textile industry \200 constru ction \200 engineering (particularly railroad works) Radon daughters : tin mining \200 Arsenic \200 Nickel (nickel re \201 ning) \200 Bis -chloromethyl ether (BCME) \200 Polycyclic aromatic hydrocarbons aluminum smelting \200 coke production Chromates (zinc, calcium, strontium) \200 Passive smoking, e.g. in the entertainment and catering industry. 07_Smedley_Chap07.indd 228 12/31/2012 8:52:25 PM LUNG CANCER 229 Clinical management and prognosis \200 De \201 nitive investigation is with CXR or CT, b ronchoscopy, and biopsy \200 Surgical resection \200 Chemotherapy \200 Radiotherapy \200 Prognosis is variable, and depends on the stage at diagnosis. Prevention Prevention is mainly through exposure control. Compensation Primary carcinoma of the lung is prescribed for Industrial Injuries Disablemen t Bene \201 t in those who have: \200 Worked underground in a tin mine \200 Been expos ed to BCME, or zinc, calcium, or strontium chromates (D10) Worked with asbestos in de \201 ned circumstances (D8) \200 Been exposed to crystalline silica in de \201 ned industries (D11) \200 Worked before 1950 in the re \201 ning of n ickel (C22(b)) \200 Been exposed to fumes, dust, or vapor of arsenic or arsenic-containing compounds (C4). Relevant legislation Asbestos-related lung cancer is reportable to HSE under RIDDOR 1995. Further information HSE Index of data tables. Available at: M http://www.hse.gov.uk/statist ics/tables/index.htm 07_Smedley_Chap07.indd 229 12/31/2012 8:52:25 PM CHAPTER 7 Respiratory and cardiovascular disorders 230 Pleural disorders Benign pleural disorders Pleural plaques These are the most common sequel ae of asbestos exposure, occurring in up to 50% of an exposed population: \200 Can occur after low-level exposure \200 Discrete areas of pleural thickening calci \201 cation \200 Latent period of 20 \200\22330yrs after exposure \200 No evidence that the plaque lesions are pre-malignant \200 Usually asymptomatic; rarely mild dyspnoea if suf \201 ci ently extensive to restrict expansion of the underlying lung Lung function usually normal. Diffuse pleural thickening \200 Dose-related, usually after heavier exposures \200 Extensive poorly circumscribed areas of adhesion in the parietal pleura and \201 brosis in the visceral pleura Often symptomatic (chest pain and exertional dyspnoea), and can be associated with restrictive lung function tests CXR shows extensive shadowing (>25% of chest wall affected) obliteration of the costophrenic angles Surgical treatment is dif \201 cult, and the results are often unsatisfactory \200 Impor tant differential diagnosis is mesothelioma; investigation (biopsy) is required in an attempt to exclude malignancy. Benign pleural effusion \200 Dose-related, usually after heavier exposures \200 Usually develops within 10yrs of exposure \200 Typically asymptomatic \200 Pleural aspiration and biopsy to exclude malignancy \200 No evidence of progression to mesothelioma. Mesothelioma Mesothelioma is a diffuse malignant tumor that arises in the pleural, peri- to neal, or (rarely) pericardial lining. Epidemiology \200 Asbestos exposure is the single major cause (>90% mesotheliomas) \200 Any asbestos type can cause the disease, but the risk is highest with amphibole \201 bres Long latency between exposure and disease of 15 \200\22360 (mean 40) years. 2 Unlike asbest osis, there is no dose \200\223response relationship. There is no threshold below which the re is no risk, but the risk is very small at low exposure levels. Mesothelioma has occurred in workers \200\231 spouses who have washed contaminated work clothes. In Great Britain \200 Applications for Industrial Injuries Disablement Bene \201 t have risen steadily in the past 10yrs (640 in 1996 to 1895 in 2010) and continue to rise 07_Smedley_Chap07.indd 230 12/31/2012 8:52:25 PM PLEURAL DISORDERS 231 Deaths due to mesothelioma have i steadily from 153 in 1968 to 2321 in the year 2009. 1 It has been estimated that annual deaths will peak in the year 2016, with 2100 per annum. The highest mortality occurs in geographical areas where shipbuilding or railroad engineering w ere common (Dumbartonshire and Clyde, Tyne and Wear, Portsmouth, Southampton, and Plymouth, and Eastleigh, Doncaster, and Crewe, respectively). Clinical features \200 Usually presents with pleural effusion \200 Chest wall pain and dyspnoea \200 Rarely presents with ascites, pericardial effusion, or encasement syndromes CXR (or CT) shows: \200 pleural effusion \200 pleural mass or thickening free \202 uid \200 local invasion of chest wall, heart, or mediastinum \200 concomitant pleural plaques or pulmonary \201 brosis (minority). Treatment and prognosis \200 Surgical intervention (pleurectomy) is offered in some cases \200 Palliative treatment: drain effusions, pleurodesis \200 Typically fatal over 1 \200\2232yrs. Other aspects Causal exposures/industries, prevention, compensation, legislation, and furth er sources of information are covered in b p. 214, Asbestos-related diseases. 1 Mesothelioma age standardized death rates per million by region, time period, and sex. 07_Smedley_Chap07.indd 231 12/31/2012 8:52:25 PM CHAPTER 7 Respiratory and cardiovascular disorders 232 Nasal disorders Nasal cancer Cancer of the nasal passages has been noted to have an occupat ional asso- ciation since early descriptions in nickel workers in the 1920s, furniture make rs in the 1960s, and workers in the boot and shoe manufacturing industry in the 1970s. Epidemiology \200 The proportion of sinonasal cancer attributable to occupation in 2004 was: \200 46% in men \200 20% in women In the years 2005 and 2004, respectively, occupational sinonasal cancer gave rise to 39 deaths and 133 cancer registrations Approximately 5 cases per year are awarded Industrial Injuries Disablement bene \201 t due to cancer of the nasal cavity Adenocarcinoma of the ethmoids and middle turbinates are the most common tumors (although still very rare). Clinical features \200 Blood-stained nasal discharge \200 Unilateral nasal stuf \201 n ess/obstruction \200 Facial pain \200 Facial numbness. Causal exposures/industries \200 Leather and wood dust in: boot and shoe manufacture \200 furniture and cabinet making \200 Isopropyl alcohol manu facture \200 Nickel and nickel compounds. Compensation Primary cancer of the nose or para nasal sinuses is prescribed for Industrial Injuries Disablement Bene \201 t: \200 In tho se who worked before 1950 in the re \201 ning of nickel (exposure to oxides, sulfides, or water-soluble compounds of nickel) (C22 (a)) \200 In those working in the repair and manu facture of wooden goods or footwear (D6). Other nasal disorders \200 Chronic hypertrophic rhinitis, nasal mucosal atrophy, and nasa l polyps have been associated with woodworking Nasal septal ulceration associated with long-term exposure to chromates (work with dyes, tanning agents and chromium plating tanks). 07_Smedley_Chap07.indd 232 12/31/2012 8:52:25 PM NASAL DISORDERS 233 Prevention Prevention is through exposure control: \200 enclosure with exhaust ventilatio n \200 portable tools with dust extraction \200 use of respiratory PPE. Further information HSE (2007). COSHH and the woodworking industries . Available at: M http ://www.hse.gov.uk/pubns/ wis6.pdf HSE (1997). Wood dust: hazards and precautions , Woodworking sheet No. 1, revised. Availabl e at: M http://www.hse.gov.uk/pubns/wis1.pdf 07_Smedley_Chap07.indd 233 12/31/2012 8:52:25 PM CHAPTER 7 Respiratory and cardiovascular disorders 234 Laryngeal cancer Laryngeal cancer has been associated with a number of carcinogens that are used in occupational settings. The disease is rare. \200 2.6% of laryngeal cancer cases are attributable to occupation \200 20 deaths were attributable to occupation in 2005 Causal exposures/industries \200 Asbestos (see b p. 214, Asbestos-related diseases for li st of industries) \200 Mustard gas (also carcinoma of the pharynx) \200 Nickel and nick el compounds (nickel re \201 ning) \200 Strong inorganic acid mists (e.g. sulphuric acid ) (these are used widely in industry). Clinical features and management \200 Hoarse voice, dysphagia \200 Surgical treatment, but prognosis poor. Prevention Generic exposure control measures. Relevant legislation \200 See b p. 214, Asbestos-related diseases. 07_Smedley_Chap07.indd 234 12/31/2012 8:52:25 PM This page intentionally left blank CHAPTER 7 Respiratory and cardiovascular disorders 236 Occupational voice loss Epidemiology \200 US statistics suggest that 25% of employees cri tically rely on their voice for their work. There are no comparable UK statistics available Voice disorders are common in the general population, with prevalence rates of: 13.5% of men and 21.5% of women having a \200\230dry throat \200\231 \200 15.1% of men a nd 18.6% of women reporting a \200\230sore throat \200\231 \200 In some occupations havi ng common respiratory symptoms can impair ability to undertake the task requirements of the job, but does not mean that the job causes the voice disorder. Clinical features Voice disorders, whether caused or impacting on occupation, produce the s ame symptoms, i.e. hoarseness, dry throat, repeated clearing of the throat, weak voice, and a lack of vocal projection. Occupational causes The following general features of work increase the risk of voice disor ders: \200 Excessive voice use, e.g. frequently shouting \200 Poor upper body posture \200 Work in contaminated environments (such as those involving exposure to dusts, vapors and fumes). The literature contains many studies linking voice disorders to speci \201 c occupations, but most are cross-sectional and do not prove causation. Teachers are over-represented in o utpatient attendances for voice disorders. 3 This is not evidence that voice disorders are caused by teaching as it may indicate that if there is a voice condition then the job of te aching is more dif \201 cult and prompts access for medical advice. Prevention Prevention involves: \200 Work design : e.g. ensuring shorter scripts for call center workers \200 Workplace design: reduce ambient noise to prevent the need to talk-over colleagues in of \201 ces classroom design \200 adequate humidity and ventilation Education and information: individuals who rely on their voice for their job need to be provided with advice on prevention: \200 avoid shouting and highly charged explosive speech \200 ensure adequate hydration \200 use aids such as microphones. 07_Smedley_Chap07.indd 236 12/31/2012 8:52:25 PM OCCUPATIONAL VOICE LOSS 237 Clinical assessment and diagnosis An individual who has had a hoarse voice for longer than 2 \200\2233wks should be referred to a multi-disciplinary service to primarily exclude mali gnancy. Usually an ENT specialist will carry out an initial assessment, but once malignancy is excluded, follow up is with a speech therapist. The corner- stone of management is educ ation about: Vocal hygiene \200 Exercises \200 Advice on breathing. Compensation/legal aspects Civil litigation has been pursued and been successful in some jo bs, e.g. call center workers, but a review by the Industrial Injuries Advisory Committee (I IAC) found insuf \201 cient evidence for inclusion as an industrial injury. Further information Williams N, Carding P (2005) Occupational voice loss . Taylor & Francis , Boca Raton. 07_Smedley_Chap07.indd 237 12/31/2012 8:52:25 PM CHAPTER 7 Respiratory and cardiovascular disorders 238 Coronary heart disease Ischaemic heart disease (IHD) is one of the most common causes of de ath in industrialized nations. Interest in occupational risk factors for coronary heart dis ease has grown with increasing research into the role of job strain as a risk factor for hy pertension, acute coronary syndromes, and sudden death. Research suggests that workers in j obs with low decision latitude and high psychological demands are at increased risk of card iovascular disease. Epidemiology \200 Shift work is associated with 40% i risk of heart disease. However, con founding by social class has been suggested as an explanation for this \201 nding Major organizational downsizing (>18% of staff laid off) doubled the risk of cardiovascular deaths among workers in one prospective Finnish study. Individual susceptibility \200 It was once thought that type A behavior was a risk factor for coronary vascular disease. Type A behavior is characterized by excessive competitivene ss, impatience and anger/hostility. However, the evidence of i risk of IHD is stronger for one component of type A behavior, namely hostility, than type A behavior overall Depression and anxiety are associated with an increased risk of coronary vascular disease a nd a poorer prognosis. The i risk attributable to psychosocial factors such as depression i s of a similar scale to risk factors such as smoking, i cholesterol, and hypertension. Clinical assessment The investigation of coronary heart disease is the same whether occupa- tional risk factors are suspected or not. However, where chemical expo- sures are implicat ed, an exposure history is indicated. Possible causal exposures/industries \200 Solvents: dichloromethane (methylene chloride, CH 2 Cl 2 ) \200 carbon disulphide (CS 2 ) Job strain (low job control and high workload) \200 Shift work \200 Long working hours \200 Low organizational justice: unfair inconsistent treatment of workers \200 Effort/r eward imbalance. Historically, workers in the viscose rayon industry were heavily exposed t o CS 2 and may have had an increased risk of IHD. Painters may be exposed to CH 2 Cl 2 in c on \201 ned spaces. Metabolism of CH 2 Cl 2 leads to production of carbon monoxide and thu s angina. Health surveillance No health surveillance is currently recommended in the UK for workers e xposed to job strain or shift work. 07_Smedley_Chap07.indd 238 12/31/2012 8:52:25 PM CORONARY HEART DISEASE 239 Prevention \200 Some organizations offer their senior executives periodic health checks w hich often include screening for cardiac risk factors. The inverse care law, which states t hat those least in need are most likely to receive care, appears to operate here National workplace health promotion initiatives (e.g. Healthy Working Lives) seek to addres s such health inequalities by addressing lifestyle risk factors, such as smoking, obesity, and lack of exercise. 07_Smedley_Chap07.indd 239 12/31/2012 8:52:26 PM This page intentionally left blank 241 Chapter 8 Skin disorders Dermatitis 1 242 Dermatitis 2: management 244 Contact urticaria 246 Skin cancers 247 Skin p igmentation disorders 248 Folliculitis and acne 249 Photodermatitis 250 Scleroderma 251 Occ upational skin infections 252 08_Smedley_Chap08.indd 241 12/31/2012 8:54:03 PM CHAPTER 8 Skin disorders 242 Dermatitis 1 Epidemiology Prevalence data 1 suggest that 20 000 people in the UK have skin problems that are caused or made worse by work. Occupational dermatitis (OD) makes up the g reatest proportion of these. Data come from two main sources: \200 Voluntary reporting sc hemes for occupational physicians and dermatologists: the incidence of OD is falling steadily. 2 Of 2055 new cases of occupationa l skin disease reported in 2010, 1497 (73%) were due to dermatitis. However, this is likely to be an underestimate as mild cases might not present to a dermatologist and many workpla ces do not have access to OH services Industrial Injuries Disablement Bene \201 t: 55 awards in Great Britain in 2009/10, but th ese are a small proportion of the most severe OD. Classi \201 cation Endogenous eczema An inherited disorder often associated with other ato pic conditions, such as rhinitis. Not primarily caused by work that may be exacerbated by e xposures at work. Acquired occupational contact dermatitis \200 Irritant contact dermatitis (IrCD): skin ir ritation from direct contact with irritant agents, e.g. chemicals or plants. Reversible imp airment of the barrier properties and local in \202 ammation of skin is dose related for m ild (chronic) irritants Allergic contact dermatitis (ACD): has an immune-mediated mechanism due to a type IV (cell-mediated) reaction. Sensitization can occur within 7 \200\22310 days of exposure; usually develops after months or years. Once sensitized, the individual can r eact to very low level exposures. Clinical features The clinical appearance of dermatitis derives from oedema of the epider- mis and in \202 ammatory in \201 ltration in the dermis. Typically, onset is slow and >24 h after exposure. There may be a temporal relationship to work, with improvement during hol idays. IrCD is classically con \201 ned to areas of contact, usually the face and hands. W ith ACD, involvement of eyelids and spread to secondary sites, not directly exposed, is com mon. See HSE website for color pictures of dermatitis is available at: M http://www.hse. go v.uk/skin/imagelibrary.htm Acute features \200 Redness \200 Pruritis \200 Vesiculation, exudation, and crusting \200 Dryness, cracking, and \201 ssuring. Chronic features \200 Cracking \200 Liche ni \201 cation. 08_Smedley_Chap08.indd 242 12/31/2012 8:54:04 PM DERMATITIS 1 243 Complications 2 bacterial infection. Causal exposures/industries Exposures 3 Causal exposures often occur in combination \200 Chemicals or biological agents: irritants (common examples include weak acids and alkalis, soaps and detergents, oxidizing and reducing agents, solvents) sensitizing agents Frequent hand washing (wet work) \200 Gloves and other PPE \200 Mechanical trauma \200 Radiation and UV light. Jobs Dermatitis can occur in any job, but is particularly common in: \200 Health care work \200 Cleaning \200 Engineering (cutting oils) \200 Hairdr essing \200 Catering \200 Printing \200 Agriculture \200 Chemical manufacture. Individual susceptibility \200 The response of normal skin to physical and mechanical dam age and to irritant agents varies widely in the population The risk of sensitization i if the barrier integrity of skin is impaired, e.g. pre-existing skin conditions which lead to i antigen presentation \200 Risk of irritation and sensitization i in those with a history of atopy. Compensation Non-infective dermatitis is prescribed for Industrial Injuries Disablement Ben e \201 t (D5) in workers whose skin is exposed to irritants. Dermatitis and skin ulceratio n (C30) is prescribed in those exposed to chromic acid, chromates, or dichromates. Relevant legislation and further information \200 Occupational dermatitis is reportable u nder RIDDOR. A list of agents for which associated dermatitis would be reportable is given in the guidance document (see b Appendix 3), but exposure to any known irritant or sensitiz ing agent would qualify HSE (2011). Statistics on work-related skin disease. Available at: M http://www.hse.gov.uk/statistics/causdis/dermatitis/skin.pdf 1 Self-reported work-related illness survey 2010 \200\22311. 2 The Health and Occupation Reporting Network (THOR) scheme (see b p. 692, Routine health s tatistics). 08_Smedley_Chap08.indd 243 12/31/2012 8:54:04 PM CHAPTER 8 Skin disorders 244 Dermatitis 2: management Clinical investigation and treatment Differential diagnosis It can be dif \201 cult to distinguish IrCD and ACD from history and exami- nation alone. Clues include exposure to a known irritant or sensitizing agent. However, always consider whether a previously unknown sensi- tizer might be responsible. Careful enquiry into exposures at home and work is important, but it can be dif \201 cult to identify the cause. A history o f childhood eczema indicates endogenous dermatitis, but exacerbation by irritants or sensit izers at work should still be considered. 3 Skin patch testing is crucial in making a diagn osis. This should include common allergens, medicaments, and agents that are present at wor k. Patch testing is a specialized procedure. It should be carried out by an experienced der matologist, particularly when investigating rare or pos- sible new sensitizers, as standard ized skin patch test reagents may not be available commercially. Care is needed in the stan dardization of tests in this context, and the interpretation of results. The occupational h ealth team has an important role in: \200 Providing dermatologist with a list of possible workplace exposures \200 Ensuring that samples of products, excipients, and other potent ial causative agents are supplied to the investigating clinic. Treatment The treatment of occupational dermatitis is the same as for endogenous eczema. To pical emollients and topical steroids. Occupational health input Advise the employer about primary prevention \200 Substitution of known sensitizing agents with suitable alternatives \200 Engineering controls (e.g. en close computerized cutting operations to reduce contact between cutting oils and the skin of operators) \200 Use of PPE (gloves). (cid:2) Some components of gloves (typically carbamates and thiurams used as preservatives and accelerants) can themselves cause sensiti zation Education about the risks and good hand care (see Box 8.1). Manage individual cases \200 Facilitate careful clinical investigation and diagnosis \200 Reinforce education about go od hand care (see Box 8.1) \200 Advise about adjustments to work to reduce direct skin co ntact with irritants or allergens. Epidemiological surveys Sometimes it can be dif \201 cult to determine if a single case of dermatitis is occupational. It is useful to ascertain whether there is a higher incidence of dermatitis among the population of employees who have similar dermal exposures. Surveys are also useful for investigating unexplained clusters of cases. It is important to underta ke epidemiological investigations ethically, and to involve the employees \200\231 represen tatives. 08_Smedley_Chap08.indd 244 12/31/2012 8:54:04 PM DERMATITIS 2: MANAGEMENT 245 Box 8.1 Good hand care: measures to d risk of irritant dermatitis \200 Ensure hands are n ot wet for >2h/day or >20 times each day. For potent irritants d these exposure limits Avoid wearing gloves for >4h/day \200 Use tools that avoid wet-work or contact with irrit ants \200 Wash hands in warm (not cold or hot) water and dry thoroughly \200 Use protec tive gloves from the start of wet-work \200 Minimize glove use \200\224induces dermatitis by occluding skin surface \200 If protective gloves used for >10min wear cotton gloves u nderneath \200 Keep gloves intact and dry inside \200 Avoid introducing irritants into the gloves \200 Do not wear rings at work \200\224they trap water and contaminants \200 Use lipid-rich moisturizing creams at and after work. Health surveillance Skin surveillance is required under the COSHH Regulations where there i s a signi \201 cant risk of dermatitis. The detail of skin surveillance programs is covere d on b p. 426, Skin surveillance. OH has a role in: \200 Advising employers about the nee d for and format of surveillance \200 Training competent persons \200 Follow-up of case s identi \201 ed by routine surveillance. Prognosis \200 Because irritant contact dermatitis is dose related, it is usually possibl e to manage by attention to exposure controls outlined here Allergic contact dermatitis can be much more dif \201 cult to manage: once an individual is sensitized, he/she reacts to very low levels of exposure; elimination of the allergen is not always possible redeployment is sometimes required as a last resort if symptoms cannot be controlled by oth er means, but the risks of dermatitis need to be weighed carefully against the (often great er) health risks of losing employment completely if the allergen is common in the environment outside work, symptom control is more dif \201 cult to achieve. Further information and guidance HSE (2004). Medical aspects of occupational skin disease , guidance note MS24, 2nd edn. Available at: M http://hse.gov.uk/pubns/ms24.pdf HSE Skin at work . Available at: M http://www.hse.gov.uk/skin/index.htm Concise guidance to good practice: diagnosis, management, and prevention of occupational contact dermatitis . Available at: M http://www.nhsplus.nhs.uk/providers/images/library/ \201 les/guidelines/ D ermatitis_concise_guideline.pdf Dermatitis: occupational aspects of management \200\224a national guideline . (Full guideli ne and associated lea \202 ets). Available at: M http://www.nhsplus.nhs.uk/providers/clini caleffectiveness-guidelines-e videncebased.asp BOHRF (2012). Occupational contact dermatitis: evidence review . Avaialble at: M http://www .bohrf. org.uk/projects/dermatitis.html 08_Smedley_Chap08.indd 245 12/31/2012 8:54:04 PM CHAPTER 8 Skin disorders 246 Contact urticaria Epidemiology Data from the specialist physicians reporting schemes 1 show that the annual incidence of reported new cases of occupational contact urticaria is decli ning; 56 cases were reported in 2010. Clinical features \200 Wheal and \202 are: \200\230nettle rash \200\231, itchy skin lu mps with erythema: rapid onset within 20min of exposure \200 subsides within hours of exposure \200 see HS E website for color pictures of urticarial. Available at: M http://www.hse.gov.uk/skin/imagelibrary.htm Associated with systemic features: asthma, GI symptoms, anaphylaxis. Non-allergic contact urticaria Tends not to have systemic features and is probably due to l ocal release of histamines and bradykinins in response to direct stimulus. Causal exposures \200 Certain arthropods, jelly \201 sh, algae \200 Nettles and certai n seaweeds \200 Benzoic acid, ascorbic acid. Allergic contact urticaria This is a classical type I (IgE-mediated) hypersensitivity react ion. It occurs when an individual who has been previously sensitized to an allergen is re-e xposed. Causal exposures/industries \200 Exposures: latex (see b p. 202, Latex allergy) \200 protein allergens, e.g. animal products \200 f oods, spices, herbs, food additives (benzoic acid, cinamic acid) \200 resins \200 disin fectants Industries: health care \200 rubber manufacture \200 veterinary practitioners \200 food handlers \200 horticulture. Investigation \200 Skin-prick testing \200 Total and speci \201 c IgE. Management Alle rgen avoidance. 1 Under The Health and Occupation Reporting Network, (THOR) scheme (see b p. 692, Routine h ealth statistics). 08_Smedley_Chap08.indd 246 12/31/2012 8:54:04 PM SKIN CANCERS 247 Skin cancers Epidemiology \200 Skin neoplasia is the second most commonly reported form o f occupational skin disease, comprising 20% of all reported cases 1 Data from the specialist physicians reporting schemes 2 show that 390 new cases of occupati onal skin neoplasia were reported in 2010. Types \200 Squamous cell carcinoma \200 Basal cell carcinoma \200 Melanoma. Causal exposures/industries \200 UVA and UVB radiation: any occupation where work is pred ominantly outdoors, e.g. agricultural and construction workers Ionizing radiation \200 PAHs: historically an important cause of skin cancer, but now rar e because of good hygiene controls Arsenic and arsenicals. Clinical features and management \200 Skin nodule; itching or color change in existing na evi \200 Surgical excision. Prevention \200 Education and protection against the sun for outside workers \200 Reduc ing exposure to tar, pitch, and mineral oils through substitution and engineering controls Control of ionizing radiation (see b p. 20, Ionizing radiation 3: exposure control). Compensation Primary carcinoma of the skin is prescribed for Industrial Injuries Disablemen t Bene \201 t (C21) in those who are exposed to arsenic or arsenic compounds, tar, pitch, bitumen, mineral oil (including paraf \201 n), or soot. Relevant legislation \200 Skin cancer that is attributable to occupational exposure is re portable under RIDDOR The EU directive on optical radiation requires health surveillance fo r workers who are exposed to optical radiation and are likely to have health effects.