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. 1 Self-reported Work-related Illness Survey 2010 \200\2232011. 2 Under The Health and Occup ation Reporting Network (THOR) scheme (see b p. 692, Routine health statistics). 08_Smedley_Chap08.indd 247 12/31/2012 8:54:04 PM CHAPTER 8 Skin disorders 248 Skin pigmentation disorders Altered skin color Causal exposures \200 Silver and silver sa lts produces blue-gray skin pigmentation: argyria \200 Trinitrotoluene (TNT) causes orang e staining of skin \200 A number of other chemicals can cause skin staining: potassium permanganate \200 \202 uorescein, etc. Hyperpigmentation Causal exposures \200 Pitch, tars; associated with photosensitivity \200 Mercury compounds \200 Arsenic and arsenicals. Hypopigmentation (vitiligo) Can be localized or generalized, and is indistinguishable from naturally occurring vitiligo. Causal exposures \200 Hydroquinones \200 Phenols \200 Catechols. Screening Using a Wo ods lamp, loss of melanin can be detected before it is apparent in white skin. This method is useful for detection of occupational vitiligo in exposed workers. Compensation Vitiligo is prescribed for Industrial Injuries Disablement Bene \201 t (C25) in those exposed to paratertiarybutylphenol, paratertiarybutylcatechol, para-amylphenol, hy droquinone, monobenzyl ether of hydroquinone, or monobutyl ether of hydroquinone. 08_Smedley_Chap08.indd 248 12/31/2012 8:54:04 PM FOLLICULITIS AND ACNE 249 Folliculitis and acne Epidemiology Data from the specialist physicians reporting schemes 1 show that reported new cases of occupational folliculitis and acne are declining. Three cas es were reported in 2009 and no cases in 2010. Clinical features Oil folliculitis \200 Papules and pustular lesions \200 Discoloration of the hair follicles \200 Comedone formation with marked in \202 ammatory component \200 Typically occurs on thighs and forearms, where prolonged contact with oil saturates clothing. Chloracne \200 Pale comedones and cysts (unlike the in \202 amed lesions of oil acne) \200 Typically on the face: cheeks, forehead, and neck \200 Less commonly on the trunk, limbs, and genitalia \200 Larger in \202 ammatory lesions in chronic cases. Coal tar acn e \200 Comedone formation \200 Photosensitivity \200 Skin pigmentation. Causal exposures Oil folliculitis \200 Cutting oils \200 Lubricants. Chloracne \200 C hlorinated naphthalenes (used as a synthetic insulating wax) \200 Polychlorinated bipheny ls (PCBs), e.g. chlorinated dibenzodioxins and dibenzofurans (used as heat insulator in ele ctric transformers and capacitors). Coal tar acne Coal tar and products (used in roo \201 ng and civil engineering). Prevention The incidence of oil acne has reduced drastically because of exposure controls, particularly the decrease in use of cutting oils, use of safer prod- ucts, and better hygie ne. The use of PCBs has been greatly restricted in the UK. Compensation Oil folliculitis and acne are prescribed for Industrial Injuries Disablement B ene \201 t under D5 (non-infective dermatitis). 1 Under The Health and Occupation Reporting Network (THOR) scheme (see b p. 692, Routine he alth statistics). 08_Smedley_Chap08.indd 249 12/31/2012 8:54:04 PM CHAPTER 8 Skin disorders 250 Photodermatitis Some occupational exposures can give rise to skin damage through inter- act ion with UV light. Polycyclic aromatic hydrocarbons \200 Coal tar \200 Pitch \200 Creosote \200 Indust ries: gas production \200 coke oven work \200 roo \201 ng \200 production of graphite from pitch. Plants Many plants cause dermatitis that is triggered by sunlight. \200 Compositae \200 Umbelliferae: giant hogweed \200 celery, etc. \200 Some lichens \200 Gardeners and grounds men are at risk when handling plants, but particularly when using lawn strimmers to cut verges, etc. Others Methylene blue causes dermatitis through a phototoxic reaction. 08_Smedley_Chap08.indd 250 12/31/2012 8:54:04 PM SCLERODERMA 251 Scleroderma Occupational scleroderma is rare. Causal exposures Inhalation of vinyl chloride monomer (VCM) Scleroderma-like changes have b een reported in association with expo- sure to the following: \200 Pesticides \200 Epox y resins \200 Perchlorethylene and trichloroethylene \200 Silica. Clinical features Thickened shiny skin on the \201 ngers. VCM disease Occurs as part of a syndrome which includes the following: \200 Acro-osteolys is: resorption of the terminal phalanges on X-ray \200 Raynaud \200\231s phenomenon: digi tal vascular spasm giving rise to blanching in cold conditions Associated features of VCM exposure include: hepatic \201 brosis \200 angiosarcoma of the liver. Prevention VCM disease has been virtually eliminated by good hygiene controls (enclosure) i n the PVC manufacturing industry. Compensation Sclerodermatous thickening of the skin of the hands is prescribed for Industri al Injuries Disablement Bene \201 t (C24b (iii)) in those who are exposed to vinyl chlorid e monomer in the manufacture of PVC. 08_Smedley_Chap08.indd 251 12/31/2012 8:54:04 PM CHAPTER 8 Skin disorders 252 Occupational skin infections Occupation can be a risk factor for skin infection because of either asso- ciation with environmental conditions that favor microbial overgrowth or expos ure to speci \201 c organisms. Epidemiology Data from the specialist physicians reporting schemes 1 show that new cases of infective skin disease due to occupation have been declining over the past decade \200\224 26 cases were reported in 2010. Saturation diving Divers who live for prolonged periods in dive chambers are susceptible to infections of the skin and ear because of the persistently warm humid conditions. Pseudomo nas species are a particular problem. Prevention of otitis externa requires meticulous aura l toilet. Zoonotic skin infections These are a hazard for agricultural workers, veterinary practition ers, abbatoir, and \201 sh-processing workers. They include Orf, Herpes Simplex, Anthrax, Scabies, Lyme Disease. Multi-resistant Staphylococcus aureus Persistent carriage of MRSA h as been described in HCWs. This has mainly been described as nasal colonization on repeated swabbing, and is mostly asymptomatic. It usually clears with topical antibiotic treatment for the nose and chlorhexidine body washes. However, true infections (e.g. of skin lesions) are potentially serious and dif \201 cult to treat. Those who are at increased risk of mu lti-resistant Staphylococcus aureus (MRSA) carriage include HCWs with hand eczema or persis tent respiratory tract infection (e.g. sinusitis or bronchiectasis). (cid:2) There is no de \201 nitive guidance on exclusion of HCWs who are at risk of MRSA colonization or infecti on, or those who are chronically colonized. Decisions to restrict from work where there is a high risk of acquiring MRSA, or transmitting infection to patients (e.g. care of surgical wounds) should be made on an individual basis. There is little hard evidence to guide such decisions, and the risk of legal challenge in the event of loss of employment is signi \201 cant. Compensation Certain occupational zoonoses that affect skin are prescribed for Industrial I njuries Disablement Bene \201 t. \200 Cutaneous anthrax (B1) \200 Glanders (B2) \200 Orf (B12). Relevant legislation Any infection that is clearly attributable to occupation is reportable under RIDDOR. 1 Under The Health and Occupation Reporting Network (THOR) scheme (see b p. 692, Routine he alth statistics). 08_Smedley_Chap08.indd 252 12/31/2012 8:54:04 PM 253 Chapter 9 Musculoskeletal disorders Low back pain 254 Work-related upper limb disorders 1 256 Work-related upper limb disorders 2 258 Osteoarthritis of the hip 260 Bursitis 262 09_Smedley_Chap09.indd 253 12/31/2012 8:56:41 PM CHAPTER 9 Musculoskeletal disorders 254 Low back pain Epidemiology \200 LBP has a lifetime prevalence of 60 \200\22380%, point pr evalence of 15 \200\22340%, and annual incidence of 5%. It is: \200 the second most common cause of work-related ill health (prevalence 207 000, annual incidence 51 000) 1 the second most common cause of absence from work (7.6 million days/year lost) 1 the second most common reason for claiming incapacity bene \201 t \200 There has been a reduction in the prevalence and incidence of work-related back pain since 2001/02. Causal exposures/industries \200 Exposures: physical (lifting, bending, twisting, whole-body vibration) \200 psychosocial (high deman d, low control, low job satisfaction) \200 Industries: exposures are ubiquitous, but LBP most common in: transportation and logistics \200 construction \200 agriculture \200 clinical health care. Features and investigation \200 Pain radiating to the thigh is common (740% of cases) \200 In most cases, pathology is not de \201 ned (non-speci \201 c or mechanical LBP) \200 <10% of cases have identi \201 able pathology, e.g. nerve root compression \200 X- rays and MRI are not useful in most cases of mechanical back pain. \200 Investigations ai m to distinguish cases of serious spinal pathology. This is mainly done on the basis of cli nical markers (red \202 ags, see Box 9.1) \200 Conceptual models of LBP recognize the i mportance of psychological and social factors (biopsychosocial theme). Prevention Ergonomic risk controls (covered on b p. 8, Vibration 1: whole body vibration, b p. 120, Lifting and handling, b p. 124, Posture). Prognosis \200 Natural history: most episodes of mechanical LBP are self-limiting. more than 50% of episodes resolve completely within 4 weeks, but up to 20% have some symptoms for a year there is a marked tendency to recurrence, 70% of those with back pain go on to experience three or more attacks \200 20% of those with LBP develop chronic symptoms Probability of return to work d with i duration of sickness absence \200 Clinical examina tion and investigations are poor predictors of disability \200 Outcome is strongly in \202 uenced by individual psychological, workplace and cultural factors (see Box 9.1; b p. 256, Work-related upper limb disorders 1). 1 2010/11 Labor Force Survey. 09_Smedley_Chap09.indd 254 12/31/2012 8:56:42 PM LOW BACK PAIN 255 Box 9.1 Red \202 ags indicate possible of serious spinal pathology Thoracic pain, fever, weight loss, bladder or bowel dysfunction, carci- noma, other illness, progressive neurolog ical de \201 cit, disturbed gait, sad- dle anesthesia, age <20yrs or >55yrs, structural de formity, systemic steroid therapy Yellow, blue and black \202 ags are risk factors for chronicity and disability Yellow \202 ags are psychological and behavioral \200 A \200\223ve attitude that back pain is h armful or severely disabling \200 Fear avoidance behavior and reduced activity levels \200 Expectation that passive, rather than active, treatment will be bene \201 cial A tendency to depression, low morale, and social withdrawal \200 Social or \201 nancial problems. Blue \202 ags are occupational psychological factors \200 Poor job satisfact ion \200 Blaming working conditions \200 Adverse job characteristics (heavy work, poor relationships). Black \202 ags are organizational and social factors \200 Health bene \201 ts or insurance \200 Litigation \200 Sickness policies. Management \200 Refer those with red \202 ags for urgent clinical assessment \200 Reh abilitation comprises: encouragement to stay active; early physical therapy; reassurance \200 advise early retur n to work, d risk by adjustments and job redesign \200 rarely, restriction from work or r edeployment Early rehabilitation and job redesign d employment costs and litigation. Relevant legislation HSE (2009). The Manual Handling Operations Regulations 1992 (amended). Available at: M http:// www.hse.gov.uk/pubns/priced/l23.pdf HSE (2009). Work with display screen equipment: Health and Safety (Display Screen Equipment ) Regulations 1992 as amended by the Health and Safety (Miscellaneous Amendments) Regulatio ns 2002 . Available at: M http://www.hse.gov.uk/pubns/priced/l26.pdf Further information and guidance Waddell, G, Burton, AK (2000). Occupational Health Guideli nes for the management of low back pain. Evidence review and recommendations . Faculty of O ccupational Medicine, London. Available at: M http://www.fom.ac.uk/publications-policy-guid ance-and-consultations/publications/faculty- publications NICE (2009). Low back pain: early management of persistent non-speci \201 c back pain , NI CE clinical guideline 88. Available at: M http://www.nice.org.uk/nicemedia/pdf/CG88NICEGuid eline.pdf HSE Back pain . Available at: M http://hse.gov.uk/msd/backpain/index.htm 09_Smedley_Chap09.indd 255 12/31/2012 8:56:42 PM CHAPTER 9 Musculoskeletal disorders 256 Work-related upper limb disorders 1 Epidemiology \200 Upper limb and neck pain are common . In some surveys, up to 17 \200\22320% of people complain of neck \200\223shoulder pain an d 20% of hand \200\223wrist pain during the past 7 days Many have pain in the absence of clearly de \201 ned clinical pathology, but distinct disorders (e.g. epicondylitis, carpal tunnel syndrome (CTS)) each affect 1 \200 \2233% of older subjects. Such symptoms are often attributed to work The HSE estimates an incidence of work-attributed upper limb and neck complaints in Britain of 280/100,000 adults/year with 3.6 million lost working days per annum. Clinical features According to NIOSH, some 165 ICD disease codes should be consid- ered und er the umbrella de \201 nition of \200\230Work-related upper limb disorders \200\231 (WRU LD). Classi \201 cation is contentious and complex. The surveillance criteria for 9 of the commoner upper limb disorders (ULDs), as agreed at a UK expert workshop, are listed in the table (see Table 9.1). Clinical assessment and diagnosis \200 Diagnosis is based on history and clinical examina tion \200 Median nerve conduction is used if CTS is suspected \200 Table 9.1 provides a short guide on diagnostic criteria \200 Assessment should cover co-morbid non-occupation al factors, e.g. trauma, diabetes, rheumatoid arthritis, acromegaly, hypothyroidism Medical management \200 For all disorders: non-steroid anti-in \202 ammatory agents (alt hough there is some evidence of non-effectiveness in epicondylitis and possibly other ULDs) , analgesics Shoulder disorders: physical therapy, corticosteroid injection, exercise programs Neck disorders: soft cervical collar, physical therapy (heat pad, exercises, ultrasound/short-wave diathermy, massage, transcutaneous electrical nerve stimul ation (TENS), manipulation, acupuncture) Elbow disorders: corticosteroid injection, pulsed ultrasound, wrist splint (to prevent wrist dorsi \202 exion) Tenosynovitis/peritendinitis: local heat, corticosteroid injection, splinting, surgical decompression of the \201 rst extensor compartment +/ \200\223 tenosynovectomy ( chronic cases) CTS: splinting, local corticosteroid injection, surgical release. Prognosis \200 Acute \202 orid tenosynovitis tends to settle quickly if thoroughly rest ed \200 Frozen shoulder lasts 12 \200\22318mths and is resistant to treatment \200 Epic ondylitis is said to resolve in 8 \200\22312mths, but often lasts longer \200 Symptoms of CTS can improve if the causal factor is removed, but otherwise tend to become chronic 09_Smedley_Chap09.indd 256 12/31/2012 8:56:42 PM WORK-RELATED UPPER LIMB DISORDERS 1 257 Table 9.1 Diagnostic criteria for ULDs proposed by an HSE-convened expert workshop Disorder Diagnostic criteria Rotator cuff tendinitis Pain in deltoid region + pain on resisted active movement (abduction \200\224supraspinatus; external rotation \200\224infraspinatus; internal rotation \200\224subscapularis) Bicipital tendinitis Anterior shoulder pain + pain on resisted active \202 exion or supination of forearm Shoulder capsulitis (frozen shoulder) Pain in deltoid area + equal restriction of active and passive glenohumeral movement with c apsular pattern (external rotation > abduction > internal rotation) Lateral epicondylitis Epicondylar pain + epicondylar tenderness + pain on resisted extension of the wrist Medial epicondylitis Epicondylar pain + epicondylar tenderness + pain on resisted \202 exion of the wrist De Quervain \200\231s disease Pain over radial styloid + tender swelling of \201 rst extensor compartment + either pain reproduced by resisted thumb extension or positive Finkelstein \200\231s test of the wrist Tenosynovitis of wrist Pain on movement localized to the tendon sheaths in the wrist + reproduction of pain by res isted active movement Carpal tunnel syndrome Pain or paraesthesia or sensory loss in the median nerve distribution + one of: Tinel \200 \231s test positive, Phalen \200\231s test positive, nocturnal exacerbation of symptoms, mo tor loss with wasting of abductor pollicis brevis, slowed nerve conduction Non-speci \201 c diffuse forearm pain Pain in the forearm in the absence of a speci \201 c diagnosis or pathology According to one systematic review only a half of new shoulder episodes end in complete recovery within 6mths In general, ULDs tend to persist if causal or aggravating factors remain in place. Persiste nce is more frequent if \200\230yellow \202 ag \200\231 (see Box 9.1) \200\223ve psycho logical factors are also present. 09_Smedley_Chap09.indd 257 12/31/2012 8:56:42 PM CHAPTER 9 Musculoskeletal disorders 258 Work-related upper limb disorders 2 Causal exposures and industries \200 ULDs may be caus ed (or aggravated) by undesirable permutations of force, repetition, duration and posture, with insuf \201 cient recovery time (see Table 9.2) (see also b p. 120, Lifting and handli ng, b p. 124, Posture, b p. 128, Repetitive work) Occupations in which high rates of ULD have been reported include packing, assembly and food processing Psychological risk factors (e.g. low mood, somatizing tendency, job dissatisfaction, negative perceptions about the work environment) are also associated with disease reporting and \200\230yellow \202 ag \200\231 risk factors for persistence. (cid:2) All of the ULDs labeled as \200\230work-related \200\231 also have non-occupationa l risk factors. The clinical pattern may be indistinguishable in occupationally and non-occ upationally related cases, making attribution problematic in the individual case. Prevention Depending on the risk assessment and context, preventive measures at work may in clude: \200 Better design of tools, equipment, and work layout: to make the work easier, the posture better, the forces lower, etc. Advice & training: to promote risk awareness and better working practices An induction period: to allow new employees to start out at a slower pace Job rotation/job enlargement: to provide respite from repetitive monotonous work Rest breaks: to allow recovery time \200 A rehabilitation program: to ease affected worke rs back into productive work Redeployment: as a last resort in recalcitrant cases. Relevant legislation and guidance There are no legal provisions in the UK speci \201 c to the prevention of WRULDs. HSE provides useful advice on good practice and prevention includ ing: \200 Upper limb disorders in the workplace (HSG60) \200 Working with VDUs (INDG36) \200 Aching arms (or RSI) in small businesses (INDG171rev1) \200 The Assessment of Rep etitive Tasks (ART) tool. Available at: M http://www.hse.gov.uk/pubns/indg438.pdf A task rotation worksheet. Available at: M http://www.hse.gov.uk/ msd/uld/art/resources.htm 09_Smedley_Chap09.indd 258 12/31/2012 8:56:42 PM WORK-RELATED UPPER LIMB DISORDERS 2 259 Table 9.2 Associations between mechanical factors and ULDs Anatomic site Strong evidence of effect Some evidence of effect Insuf \201 cient evidence of effect Neck and neck/shoulder Repetition + Force + Posture + Vibration + Shoulder Posture + Force + Repetition + Vibration + Elbow Repetition + Force + Posture + Several of these 3 exposures + Tendonitis of the hand/wrist Repetition + Force + Posture + Several of these exposures + Carpal tunnel syndrome Repetition +/- +/- Force + Posture + Vibration + Several of these exposures + Source: NIOSH Publication No. 97 \200\223141 (1997). 09_Smedley_Chap09.indd 259 12/31/2012 8:56:42 PM CHAPTER 9 Musculoskeletal disorders 260 Osteoarthritis of the hip Epidemiology \200 As with osteoarthritis in other joints, the p revalence of hip osteoarthritis (hip OA) rises steeply with age In Britain, approximately 5% of the elderly population are affected, with slightly higher rates in men than women Hip OA is the main reason for the more than 40,000 total hip replacements that are carried out each year. Clinical features \200 Pain around the hip (in the groin, buttock or lateral to the joint ), with radiation to the knee in some patients Stiffness of the hip after immobility (e.g. on getting up in the morning and after prolonged sitting) Limitation of hip movement, especially internal rotation and \202 exion \200 In severe cases there may be \201 xed \202 exion of the joint. Occupational causes Epidemiological studies have consistently demonstrated an increased inc i- dence in agricultural workers, with relative risks generally in excess of two. There is still some debate about the aspects of agricultural work that are responsible, but the stro ngest evidence is for a role of frequent, heavy lifting. Several studies have indicated an elevated risk also in other occupa- tions that entail heavy lifting. Individual susceptibility A number of non-occupational factors are also associated with an increased risk of hip osteoarthritis, and are likely to make individuals more susceptible t o relevant occupational exposures. These include: \200 Developmental deformities of the h ip (congenital dislocation, Perthes disease, slipped femoral epiphysis) Genetically-determined susceptibility to osteoarthritis in multiple joints \200 Obesity. Clinical assessment and diagnosis \200 History of relevant symptoms and associated disabi lity \200 Clinical examination of the hip, looking particularly for limitation of movement and \201 xed \202 exion deformity Radiology (plain radiograph of the hip), looking for narrowing of the joint space, osteophytes, and subchondral thickening of bone with cyst formation Additional tests may sometimes be appropriate to exclude other types of arthritis. Prognosis Tends to progress, but at a variable rate. Spontaneous improvement in symptoms oc casionally occurs. 09_Smedley_Chap09.indd 260 12/31/2012 8:56:42 PM OSTEOARTHRITIS OF THE HIP 261 Health surveillance This is not currently practiced in the occupational setting. Compensation In Britain, hip osteoarthritis is prescribed for Industrial Injuries Disableme nt Bene \201 t (A13) in people who have worked in agriculture as a farmer or farm worker f or at least 10yrs in total. 09_Smedley_Chap09.indd 261 12/31/2012 8:56:42 PM CHAPTER 9 Musculoskeletal disorders 262 Bursitis The beat conditions are a group of disorders that comprise bursitis or sub- cutane ous cellulitis overlying pressure points in the palm, elbow, or knee. Clinical features \200 Beat hand: bruising or tenderness in the palm \200 Beat elbow/kn ee: painful localized swelling, with in \202 ammation and sometimes effusion in the bursa (olecranon or infrapatellar). Causal exposures/industries Sustained exposure to friction, pressure, or impact \200 Prol onged use of picks or shovels: miners \200 road workers \200 Prolonged kneeling: \200 carpet \201 tters \200 joi ners/carpenters. Treatment and prognosis \200 Usually self-limiting \200 Occasionally require antibiotic s (if infected) or local steroid injection. Prevention The mainstay of prevention is in improving the ergonomics of physical tasks. Sol utions might include attention to working posture, tool redesign, task rotation, frequent r est breaks (see b p. 118, Ergonomics hazards: overview), and appropriate use of personal pr otective equipment (e.g. kneeling pads, padded clothing). Compensation Bursitis or subcutaneous cellulitis is prescribed for Industrial Injuries Disa blement Bene \201 t (A5, A6, A7) in manual workers who sustain severe or prolonged pressur e or friction over the hand, knee, or elbow. Relevant legislation Bursitis or subcutaneous cellulitis of the hand, knee, or elbow that i s attributable to manual work is reportable under RIDDOR. 09_Smedley_Chap09.indd 262 12/31/2012 8:56:42 PM 263 Chapter 10 Gastrointestinal and urinary tract disorders Hepatic angiosarcoma 264 Hepatic cirrhosis 266 Acute hepatotoxicity 268 Gastrointestinal ca ncers 270 Renal failure 272 Bladder cancer 274 10_Smedley_Chap10.indd 263 12/31/2012 8:58:36 PM CHAPTER 10 Gastrointestinal and urinary tract disorders 264 Hepatic angiosarcoma Epidemiology This otherwise very rare hepatic cancer occurs among work ers exposed to VCM and, less frequently, pesticide-exposed agricultural workers. Reactor (a utoclave) cleaners may be highly exposed to VCM, a genoto- xic carcinogen. When this associ ation was \201 rst recognized, VCM produc- tion workers showed 400 \227 expected inciden ce of hepatic angiosarcoma. However, owing to improved exposure control, the disease is now very rare in developed countries. Clinical features \200 Fatigue \200 Abdominal pain \200 Weight loss \200 Pyrexia \200 Jaundice \200 Ascites \200 Hepatosplenomegaly \200 Oesophageal varices. Causal exposure/industries \200 Vinyl chloride monomer production in the plastics industr y \200 Arsenic-containing pesticides used in vineyards. Clinical assessment/diagnosis \200 Thrombocytopenia, anemia, on full blood count \200 A bnormal liver function tests \200 CT/MRI scan: CT scan may show a multifocal tumor with hypo-attenuation; hyper-attenuation to liver suggests hemorrhage into the tumor \200 angiosarcoma is hypo-i ntense to normal liver on T 1 -weighted MRI images Liver biopsy: histology variable within a tumor. Vascular spaces, lined with tumor cells, may or may not be obvious. Prognosis Untreated, death occurs within months from hepatic encephalopathy or intra-abdomi nal bleeding. Health surveillance \200 Long latent interval between exposure and presentation \200 Li ver function tests (alanine aminotransferase (ALT), aspartate aminotransferase (AST)) identify hepatic impairment in VCM exposed workers Hepatic ultrasound has been used to identify pre-symptomatic angiosarcoma. Medical management Hepatic resection and/or chemotherapy may prolong life in those with an operable tumor. 10_Smedley_Chap10.indd 264 12/31/2012 8:58:36 PM HEPATIC ANGIOSARCOMA 265 Prevention Prevent by limiting exposure to VCM. Compensation Angiosarcoma of the liver is a prescribed disease (C24) for Industrial Injurie s Disablement Bene \201 t in those exposed to VCM in the manufacture of PVC. Relevant legislation \200 COSHH Schedule 5: monitor employee breathing zone VCM exposure \200 COSHH Schedule 6: annual health surveillance by HSE appointed doctor EH 40/2005 VCM, WEL 3ppm (8h TWA) \200 RIDDOR Regulations 1995: Angiosarcoma of the liver is a reportable disease among those exposed to VCM. 10_Smedley_Chap10.indd 265 12/31/2012 8:58:36 PM CHAPTER 10 Gastrointestinal and urinary tract disorders 266 Hepatic cirrhosis Epidemiology Common causes of liver cirrhosis worldwide include HBV, HCV, and alco- hol. Most cases of cirrhosis due to these agents are not work-related, but a sma ll proportion may be due to occupational exposure. Other rare causes of cirrhosis include w ork with halogenated hydrocarbons. Clinical features \200 Fatigue \200 Anorexia \200 Nausea \200 Spider naevi \200 J aundice \200 Pruritus \200 Ascites \200 Bleeding/bruising \200 Finger clubbing \200 Portal hypertension \200 Oesophageal varices \200 Hepatocellular cancer \200 He patic encephalopathy. Causal exposures/industries \200 Hepatitis B: \200 HCWs \200 Hepatitis C: \200 HCWs Alcohol: transportation industry \200 publicans and bar staff Organic solvents: carbon tetrachloride \200 1,1,1-trichloroethane. Clinical assessment/diagnosis \200 LFTs \200 Full blood count and clotting studies \200 Hepatitis B surface antigen \200 Hepatitis C antibody \200 Hepatic ultrasound \200 Liver biopsy. Prognosis Depends on the disease stage; once complications such as hepatic enceph- alopathy supervene, the prognosis is generally poor. A small proportion will develop primary carcin oma of the liver as a complication of cirrhosis. 10_Smedley_Chap10.indd 266 12/31/2012 8:58:36 PM HEPATIC CIRRHOSIS 267 Health surveillance \200 Biological monitoring of solvent-exposed workers using urinary metabolites or exhaled breath sampling may be indicated dependent on the risk assessment HCWs and others at risk of hepatitis B should be immunized and their immune status con \201 rmed by measuring hepatitis B surface antibody levels. Medical management \200 See b p. 152, Hepatitis B ; b p. 154, Hepatitis C \200 Abstinen ce from alcohol in alcoholic cirrhosis \200 Liver transplant: employment rates pre-operatively are lower for alcoholic liver disease than other indications for liver transplant. However, return to work rates post-tra nsplant are similar 45 \200\22370% of transplant recipients will return to work \200 poor physical functionin g and fatigue in \202 uence employment status post-transplant some centers employ living donor hepatic lobe transplants. Limited evidence suggests donors have a mean work absence of about 3mths. Prevention Preventing exposure to human blood and body \202 uids \200\224see b p. 104, Hu man tissue and body \202 uids. Compensation Liver \201 brosis is a prescribed disease for Industrial Injuries Disablemen t Bene \201 t in those who have been exposed to VCM in the manufacture of PVC (C24d). Cirr hosis is prescribed in those who have been exposed to chlorinated naphthalenes (C13). 10_Smedley_Chap10.indd 267 12/31/2012 8:58:36 PM CHAPTER 10 Gastrointestinal and urinary tract disorders 268 Acute hepatotoxicity A number of chemicals are recognized as causing acute hepatotoxicity, although some of them are no longer used in the way that once led to workers suffering adve rse effects. Hepatotoxicity due to occupational chemical exposure is now rarely reported in the UK. Epidemiology Common causes of hepatic insult \200 Alcohol \200 Metabolic syndrome \200 Drug reactions. Clinical features \200 Fatigue \200 Weight loss \200 Right upper quadrant abdominal p ain \200 Anorexia \200 Nausea \200 Jaundice \200 Impaired clotting. 2 Mild steatosi s may be asymptomatic Causal exposures/industries \200 Chemical industry including: carbon tetrachloride (CCl 4 ) \200 chlorinated napthalenes \200 dimethylformamide \200 chlordecone (kepone) \200 methylene dianiline \200 polychlorinated biphenyls \200 p hosphorus \200 trinitrotoluene Painting: 2-nitropropane Dry cleaning: perchloroethylene. Mechanism of hepatotoxicity Acute chemical hepatotoxicity may manifest itself in a number o f ways: \200 Steatosis (fatty liver): steatohepatitis if hepatic in \202 ammation present Acute hepatocellular injury (necrosis): direct toxicity \200 idiosyncratic reaction (e.g. halothane) Cholestasis (impaired bile \202 ow). Clinical assessment and diagnosis \200 Clinical examination looking for stigmata of chron ic liver disease or alcohol misuse 10_Smedley_Chap10.indd 268 12/31/2012 8:58:36 PM ACUTE HEPATOTOXICITY 269 Liver enzymes: alkaline phosphatase (AlkPhos) \200 alanine aminotransferase (ALT) \200 gamma glutamyl transpeptidase (GGT)