discharge pneumonia, with pleural effusion and lung abscess \200 septicaemia Chronic infection: with abscess formation in skin, muscle, liver, and spleen. Causal exposures/industries Glanders does not occur in the environment. It can only be acqu ired through prolonged contact with infected animals, although the infectivity of secretion s is extremely low. Realistically, the only occupational cases in the West are likely to be laboratory workers: \200 Laboratory workers handling B. mallei \200 Veterinary practit ioners \200 Horse handlers, grooms, and breeders. Treatment and prognosis Glanders can be treated with antibiotics. Historically, treatment w as with sulphonamides, but newer antibiotics including co-trimoxazole may be effective (the disease disappeared before these could be evaluated). Untreated, it is rapidly fatal in >9 0% of cases (particularly if acquired through the inhalational route). For this reason, it is a potential candidate for bioterrorism (see b p. 830, Biological weapons), although no i nci- dents have occurred to date. Prevention There is currently no vaccine for glanders. Compensation Glanders is a prescribed disease for Industrial Injuries Disablement Bene \201 t in workers who have contact with equine animals or their carcasses. Relevant legislation Glanders that is readily attributable to work would be reportable to H SE under RIDDOR. 06_Smedley_Chap06.indd 178 12/31/2012 8:50:45 PM This page intentionally left blank CHAPTER 6 Occupational infections 180 Leptospirosis Leptospirosis is a zoonotic disease caused by a spirochaete bacterium of the genus Leptospira . There are many different pathogenic varieties that use different animal hosts. Common carriers in the UK are rats ( L. ictohae- mhorrhagica ), cattle ( L. hardjo ) , and pigs. Person to person transfer is rare, if it occurs at all. Epidemiology Leptospirosis is uncommon. Between 28 and 81 cases per year have been noti \201 ed in the UK over the past 10yrs. Some of these are acquired during leisure activities or overseas. In 2010, 42 cases were noti \201 ed in the UK, including 10 of occupational origin. Clinical features \200 Incubation most commonly 7 \200\22314 days (range 2 \200\22330 day s) \200 Biphasic clinical illness. Acute bacteraemic phase Bacteria are disseminated to e very organ system. Characterized by in \202 uenza- like symptoms, headache, chills, and my algia. Most cases are mild and resolve without treatment, but rarely severe illness occurs (Weil \200\231s disease). Immune phase Follows acute phase in some cases. Recurrence of fever, associated with jaundi ce, conjunctivitis, abdominal pain, and rash. Can be complicated by multi-organ failure. Causal exposures/industries Transmission is by direct or indirect contact with infected ani mal urine or contaminated water. This usually occurs through intact mucous mem- branes or n on-intact skin: \200 Farm workers \200 Sewerage workers \200 Dog handlers \200 Abba toir workers \200 Veterinary practitioners. Clinical assessment and diagnosis Serological tests are available through the Leptospira Re ference Unit (LRU). 1 Treatment and prognosis Oral penicillin or doxycycline. IV antibiotics, and intensive suppo rt are required for severe cases. Prognosis is good if the diagnosis is made early and appr o- priate treatment started. Emergency and Intensive Care Units in rural areas should be aw are of the possibility of leptospirosis in febrile icteric illnesses. 1 HPA (2012). Leptospira Reference Unit (LRU). M http://www.hpa.org.uk/ProductsServices/ In fectiousDiseases/LaboratoriesAndReferenceFacilities/LeptospiraReferenceUnit/ 06_Smedley_Chap06.indd 180 12/31/2012 8:50:45 PM LEPTOSPIROSIS 181 Prevention \200 There is no vaccine for humans \200 Prophylactic doxycycline (200mg wee kly) can be given for high-risk occupational tasks Reduce rodent populations by avoiding garbage accumulation and culling Infected farm animals can be immunized and treated \200 PPE (especially waterproof gloves and footwear) for jobs that entail splashing or immersion in rivers, puddles, or sewage Advise workers of risk and symptoms; information cards are often used for this purpose Cover cuts and abrasions with waterproof dressings. Wash new cuts thoroughly if acquired near potentially contaminated water. Compensation Leptospirosis is prescribed (B3) for Industrial Injuries Disablement Bene \201 t for those who work in places which might be infested by rats, \201 eld mice, voles , or other small mammals, in dog kennels or the care or handling of dogs, or in contact wit h bovine animals or their meat products, or pigs or their meat products. Relevant legislation \200 Since 2010, leptospirosis is no longer noti \201 able under pu blic health legislation Leptospirosis that is reliably attributable to work is reportable to HSE under RIDDOR. 06_Smedley_Chap06.indd 181 12/31/2012 8:50:45 PM CHAPTER 6 Occupational infections 182 Streptococcus suis Strep. suis is a zoonotic infection, of which 35 subtypes have been identi- \201 ed. The organism is an important pathogen in pigs, but can occur in cattle and other animals. Epidemiology Transmission to humans is rare, but it is probably under-diagnosed. Only a few hundred human cases have been reported worldwide, and the annual incidence in England and Wales is around two cases. Clinical features Severe febrile illness, with systemic disease: \200 Meningitis \200 S epticaemia \200 Endocarditis \200 Deafness. Causal exposures/industries Transmission is through non-intact skin from infected pig produ cts, although overall the risk of infection is low. There have been no reported cases of tr ansmission through inhalation: \200 Abbatoir workers \200 Butchers \200 Farmers \200 Veterinary practitioners. Individual susceptibility Immunosuppressed (particularly asplenic) individuals are at incre ased risk. Medical management Penicillin is the treatment of choice. Prevention \200 There is no human vaccine \200 The mainstay of prevention is good hygie ne practice in slaughterhouses and butchers. Thorough washing of hands and arms before and after touching pig products is essential Exposed workers must be educated about hygiene, and should report suspicious symptoms (febr ile illness) immediately, declaring their exposure to the treating doctor. Compensation Strep. suis is a prescribed disease (B9) for Industrial Injuries Disablement B ene \201 t among those who are in contact with pigs infected by Strep . suis , or with inf ected carcasses, pig products, or residues. 06_Smedley_Chap06.indd 182 12/31/2012 8:50:45 PM STREPTOCOCCUS SUIS 183 Relevant legislation \200 Strep. suis is not reportable under public health legislation \200 Strep. suis that is readily attributable to work is reportable to HSE under RIDDOR. Further information and guidance HSE (2008). Common zoonoses in agriculture . Agriculture I nformation Sheet No.2 (rev). Available at: M http://www.hse.gov.uk/pubns/ais2.pdf 06_Smedley_Chap06.indd 183 12/31/2012 8:50:45 PM CHAPTER 6 Occupational infections 184 Brucellosis A group of zoonoses caused by the bacterial species Brucella : \200 B. melite nsis : sheep and goats \200 B. abortus : cattle \200 B. suis : pigs. The main source of non-occupational brucellosis is unpasteurized milk products. Epidemiolog y Brucellosis is rare in the UK. The 10 cases per year seen in the UK are almost always acq uired abroad (the disease is still endemic in Africa, the Middle East, Asia, and South Amer ica). There is likely to be under-report- ing of laboratory \200\223acquired occupational infection. Clinical features \200 2 \200\2238wks incubation \200 Non-speci \201 c ILI: fever and malaise \200 arthralgia \200 can affect any organ system. Causal exposures/industries Occupational transmission is through direct contact with non-in tact skin, inhalation, or ingestion. Direct skin exposure occurs in occupations that handle raw meat and unpasteurized dairy products. Respiratory exposure is through washing down fa rm or slaughterhouse buildings. \200 Farm workers \200 Abbatoir workers \200 Meat pac kers (raw products) \200 Veterinary practitioners \200 Animal laboratory workers \200 Laboratory workers handling Brucella species or infected material. Brucella is a potential candidate for bioterrorism in view of its high infec- tivity on inhalation (see b p. 854). Clinical assessment Diagnosis is by serology and culture of blood and body \202 uids in l iaison with the Brucella Reference Unit. 1 Treatment and prognosis \200 Treatment is with antibiotics, usually combination of tetrac ycline-streptomycin or tetracycline-rifampicin Brucellosis is rarely fatal, but it can cause prolonged debilitating illness. 1 HPA (2012). Brucella Reference Unit (BRU) Liverpool . Available at: M http://www.hpa.org. uk/ ProductsServices/InfectiousDiseases/LaboratoriesAndReferenceFacilities/BrucellaReferenc eUnit/ 06_Smedley_Chap06.indd 184 12/31/2012 8:50:45 PM BRUCELLOSIS 185 Prevention \200 There is no human vaccine \200 Prevention is through good hygiene pract ice in slaughterhouses and farms, including handwashing and wearing respiratory protection for aerosol-generating procedures. Compensation Brucellosis is a prescribed disease (B7) for Industrial Injuries Disablement B ene \201 t in those who handle animals infected by Brucella , or their carcasses or their untreated products, or laboratory specimens containing Brucella . Relevant legislation \200 Brucellosis is noti \201 able (to Local Authority Proper Of \201 cers) under the Health Protection (Noti \201 cation) Regulations 2010 Brucellosis that is readily attributable to work is reportable to HSE under RIDDOR. Further information and guidance HSE (2008). Common zoonoses in agriculture . Agriculture I nformation Sheet No.2 (rev). Available at: M http://www.hse.gov.uk/pubns/ais2.pdf 06_Smedley_Chap06.indd 185 12/31/2012 8:50:45 PM CHAPTER 6 Occupational infections 186 Lyme disease Lyme disease is a bacterial infection of birds and mammals caused by the spiro chaete Borrelia burgdorferi . It is spread to humans from the animal reservoir (commonly de er) by a tick vector ( Ixodes species). Epidemiology The reported incidence of Lyme disease has been increasing in the UK over the past 10yrs, reaching a level of 1.79 cases per 100,000 population in 2009. Most cases are n on-occupational. Infections tend to be seasonal, with over half of all cases occurring betw een July and September. Clinical features Erythema migrans, a spreading rash, is the most common manifestation and often the only symptom. However, untreated cases can develop the following complications: \200 Transverse myelitis \200 Cranial nerve palsies \200 Meningitis \200 Arthritis \200 Encephalitis (rare) \200 Post-viral syndrome. Causal exposures/industries \200 Forestry workers \200 Gamekeepers \200 Farmers. Clinical assessment \200 Do not discount the possibility of Lyme disease in the absence o f a history of tick bite as many sufferers cannot recollect a tick bite Diagnosis is by serology, but antibodies are often not detectable within the \201 rst few weeks of appearance of the rash. Treatment and prognosis Treatment is with antibiotics (doxycycline or amoxycillin). The ras h responds promptly, but established neurological symptoms can be slow to improve. Prevention \200 There is no vaccine \200 The mainstay of prevention is tick avoidance: \200 cover skin if working in infested areas \200 use insect repellants \200 daily sk in checks (particularly skin folds, axillae, and groins) and removal of ticks. the risk of transmission is low in the \201 rst 24hrs, and so risk is g reatly reduced by vigilant tick removal education among at-risk groups to report rashes and seek early treatment. 06_Smedley_Chap06.indd 186 12/31/2012 8:50:45 PM LYME DISEASE 187 Compensation Lyme disease is prescribed (B14) for Industrial Injuries Disablement Bene \201 t in those who are exposed to deer or other mammals of a type liable to harbor ticks c arrying Borrelia bacteria. Relevant legislation \200 Lyme disease is NOT reportable by clinicians under public healt h legislation but, since 2010, PHLS microbiology laboratories are required to report all se rologically con \201 rmed cases to the Health Protection Agency Lyme disease that is reliably attributable to work is reportable to HSE under RIDDOR. 06_Smedley_Chap06.indd 187 12/31/2012 8:50:45 PM CHAPTER 6 Occupational infections 188 Chlamydia infections Chlamydiosis is a bacterial zoonosis caused by the organism Chlamydia psittaci . There are two main types: avian chlamydiosis (psittacosis or orni- thosis) and o vine chlamydiosis. Human-to-human spread is rare. Epidemiology Most cases of chlamydiosis are non-occupational, occurring in pet owners. Clinical features Incubation 1 \200\2232wks. Avian chlamydiosis \200 Fever, cough, myalgia \200 Delirium in severe cases \200 Peri carditis, myocarditis, endocarditis \200 Atypical pneumonia \200 Hepatitis. Ovine chlam ydiosis Abortion/stillbirth. Causal exposures Avian chlamydiosis C. psittaci is excreted in the feces and nasal discharg es of infected birds. A range of bird species are susceptible. The most important sources f or occupational transmission are ducks and other poultry, pigeons, and psit- tacines (exoti c birds, e.g. parrots, cockatiels, macaws). The organism is resistant to dessication and ca n remain infectious for months. Transmission to humans is by inhalation of dust containing excreta of infected birds or by direct handling of birds, plumage, and tissues. Ovine chlamydiosis Transmission is through handling infected sheep placentas at lambing. Cl othing soiled with sheep products of conception are also infectious. Industries \200 Pet shop workers \200 Poultry farm workers \200 Feather-processing wo rkers \200 Abbatoir workers \200 Poultry meat inspectors \200 Pigeons nesting in buil dings that are used as workplaces can lead to exposure in a wide range of occupations Sheep farm workers \200 Veterinary practitioners. Individual susceptibility Pregnant women are at risk of ovine chlamydiosis and must avoid c ontact with pregnant sheep. 06_Smedley_Chap06.indd 188 12/31/2012 8:50:46 PM CHLAMYDIA INFECTIONS 189 Clinical assessment and treatment Diagnosis is by serology and treatment is with tetracycli ne. Prevention Avian chlamydiosis The mainstay of prevention is good animal husbandry, and avoi dance of build-up of bird excreta in any area where people are at work. \200 Screen breed ing stock and treat with medicated seed \200 Good \202 ock husbandry (avoidance of over crowding and stress among caged birds) Avoid dry sweeping of bird excreta \200 Good general ventilation where birds are housed \200 Local exhaust ventilation for de-feathering and evisceration tasks \200 PPE: respir ator with protection factor of at least 20 for dust-generating tasks. Ovine chlamydiosis \200 Vaccinate breeding ewes \200 PPE: waterproof overalls and glove s for lambing \200 Segregation and decontamination of soiled PPE: must not be taken home to be washed. Compensation Chlamydiosis is prescribed (B10(a) Avian, B10(b) Ovine) for Industrial Injurie s Disablement Bene \201 t. Relevant legislation \200 Chlamydiosis is NOT reportable under public health legislation \200 Chlamydiosis that is reliably attributable to work is reportable to HSE under RIDDOR. Further information and guidance HSE (2008). Common zoonoses in agriculture . Agriculture I nformation Sheet No.2 (rev). Available at: M http://www.hse.gov.uk/pubns/ais2.pdf 06_Smedley_Chap06.indd 189 12/31/2012 8:50:46 PM CHAPTER 6 Occupational infections 190 Q fever Q fever is a highly infectious zoonosis caused by the bacterium Coxiella burnetii. The organism is widespread in animals, but the most common sources of transmission to human s are cattle, sheep, and goats. Human-to- human spread does not generally occur. Epidemiology It is dif \201 cult to estimate the true incidence of Q fever, as cases are o ften mild and may go unreported. Therefore the 50 \200\223100 cases per year reported in th e UK are probably an underestimate. The peak incidence in the UK is in the spring, associat ed with the lambing season. Clinical features \200 Incubation period 7 \200\22330 days \200 Acute infection: 50% ex perience an acute in \202 uenza-like illness with pneumonia. Symptoms are often mild and o nly 5% need hospital treatment Chronic infection: develops in a small proportion up to 18mths after the acute event. Compl icated by endocarditis. Chronic infection has a high fatality rate if untreated. Causal exposures/industries Transmission is through inhalation of infected dusts or aerosol s compris- ing infected animal products. Direct transmission can occur through non- intact skin. The most common source of infected material is products of conception at lambing: \200 Sheep farmers \200 Abbatoir workers \200 Meat packers (raw) \200 Veterinary pra ctitioners. Individual susceptibility Those with chronic diseases are most at risk (chronic renal disea se, can- cer, prosthetic heart valve, and transplant recipients). Treatment and prognosis Treatment of acute Q fever is with antibiotics (doxycycline or tetr acy- cline) for 7 \200\22314 days. Chronic disease is dif \201 cult to treat, and 50% rela pse despite combination therapy. Therefore, antibiotics for chronic cases must be continued for 3yrs. Prevention \200 There is no vaccine for Q fever \200 Mainstay of prevention is minimizi ng exposure to animal products, including good animal husbandry and hygiene. Use of PPE (gl oves, waterproof overalls) at lambing reduces skin exposure (see b p. 112, Animals and anim al products). 06_Smedley_Chap06.indd 190 12/31/2012 8:50:46 PM Q FEVER 191 Compensation Q fever is a prescribed disease (B11) for Industrial Injuries Disablement Bene \201 t among those who are in contact with infected animals, their remains, or untreated products. Relevant legislation \200 Q fever is NOT reportable under public health legislation \200 Q fever that is readily attributable to work is reportable to HSE under the RIDDOR. 06_Smedley_Chap06.indd 191 12/31/2012 8:50:46 PM CHAPTER 6 Occupational infections 192 Enteric zoonoses A number of organisms colonize the GI tract of farm and domestic ani- mals , and can be transmitted to humans. Causal exposures/industries Infection occurs after contact with animal dung, usually after putting hands or \201 ngers in the mouth without washing: \200 Farm workers \200 Vete rinary practitioners \200 Abbatoir workers \200 Meat packers (raw). Clinical features These are similar for a number of organisms. Escherichia coli 0157 (E.coli 0157) A bacterium that inhabits the gut of cattle, sheep, dee r, goats, pets, and wild birds. It produces a toxin that causes illness in humans ranging f rom diarrhea to renal failure. Can be fatal in humans (but rarely). Few organ- isms are req uired to infect humans. There is no speci \201 c treatment. Salmonella Salmonellosis is caused by Salmonella bacteria, and is characterized by fever, d iarrhea, vomiting, and abdominal pain. As well as the more famil- iar food-borne transmissi on to humans, infection can be acquired directly from farm animals that carry the organism. An important mode of trans- mission is hand-to-hand contact in farm workers. Treatment is with oral cipro \202 oxacin. Cryptosporidium Cryptosporidiosis is caused by the protozoan Cryptosporidium parvum which i s carried by calves, sheep, lambs, deer, and goats. It presents as an in \202 uenza-like i llness with diarrhea and abdominal pain. Prevention Risk controls are outlined in detail on b p.112, Animals and animal prod- ucts. Salmonella is treatable in herds using medicated feed. Relevant legislation Any infection that is readily attributable to work is reportable to HS E under RIDDOR. Further information and guidance HSE Zoonoses . Available at: M http://www.hse.gov.uk/biosa fety/diseases/zoonoses.htm HPA (2012). Escherichia coli . Available at: M http://www.hpa.or g.uk/infections/topics_az/ecoli/ O157/facts.htm 06_Smedley_Chap06.indd 192 12/31/2012 8:50:46 PM This page intentionally left blank CHAPTER 6 Occupational infections 194 Zoonotic skin infections Causal exposures/industries Transmitted by direct skin contact wit h infected animal lesions: \200 Shepherds \200 Farmers \200 Veterinary practitioners \200 Abbatoir workers \200 Meat inspectors. Orf Orf is a viral zoonosis caused by the parapoxvirus. It causes contagious pustular derma titis (ecthyema contagiosum or \200\230scabby mouth \200\231) in sheep (mainly lambs) and goats. Human-to-human transmission has not been recorded. Epidemiology The frequency of orf in the general population is extremely low. Virtually all cases are occupational. Because the disorder is mostly trivial in humans, it is dif \201 cult to obtain accurate incidence data because of under-reporting. Only 8 cases per year on average were reported to the HPA during 1991 \200\223 2006, and just 2 cases per year sinc e 2005. Clinical features, diagnosis, and treatment \200 1-wk incubation period \200 Rapidly de veloping red papule, typically on the \201 nger; usually up to 5cm in diameter, and can ulcerate Can be complicated by fever, lymphadenopathy, erythema multiforme, and (rarely) bullous pemphigoid Diagnosis is by electron microscopy of a lesion biopsy \200 Self-limiting; infection usua lly confers immunity \200 Antibiotics for 2 bacterial infection. Individual susceptibil ity Immunocompromised (particularly hematological malignancy) may develop large fungating g ranuloma or tumor-like lesion. Ringworm Ringworm is a dermatophyte (fungal) infection. Clinical features, diagnosis, and treatment \200 Characteristic annular plaque with raise d edge and central clearing \200 Scaling and pruritis common \200 Diagnosis by microsco py and culture of skin scales \200 Treatment with topical antifungals \200 Oral griseof ulvin only for severe cases \200 Treat secondary bacterial infection with antibiotics. Others \200 Viral warts (papillomavirus) in butchers and \201 shermen \200 Erysipeloi d (erysipelothrix) in \201 sh processors 06_Smedley_Chap06.indd 194 12/31/2012 8:50:46 PM ZOONOTIC SKIN INFECTIONS 195 Cutaneous granulomata ( Mycobacterium marinum ) in tropical \201 sh dealers. Prevention of zoonotic dermatoses \200 Live vaccine for affected \202 ocks \200 Use P PE (gloves) when examining the months of sheep and lambs \200 See b p. 112, Animals and a nimal products, for speci \201 c guidance. Compensation Orf is prescribed (B12) for Industrial Injuries Disablement Bene \201 t in th ose who have contact with sheep or goats, or with the carcasses of sheep or goats. Relevant legislation Orf or ringworm that is reliably attributable to occupation is reporta ble to HSE under RIDDOR. 06_Smedley_Chap06.indd 195 12/31/2012 8:50:46 PM This page intentionally left blank 197 Chapter 7 Respiratory and cardiovascular disorders Occupational asthma and rhinitis 198 Latex allergy 202 Byssinosis 205 Organic dust toxic sy ndrome 205 Hypersensitivity pneumonitis 206 Humidi \201 er fever 208 Metal fume fever 210 Chronic obstructive pulmonary disease 212 Asbestos-related diseases 214 The pneumoconioses 216 Coal worker \200\231s pneumoconiosis 218 Asbestosis 220 Silicosis 222 Berylliosis 224 K aolin pneumoconiosis 225 The \200\230simple \200\231 pneumoconioses 226 Lung cancer 228 Pl eural disorders 230 Nasal disorders 232 Laryngeal cancer 234 Occupational voice loss 236 Co ronary heart disease 238 07_Smedley_Chap07.indd 197 12/31/2012 8:52:22 PM CHAPTER 7 Respiratory and cardiovascular disorders 198 Occupational asthma and rhinitis Occupational asthma and rhinitis are caused by immunologic al sensitiza- tion to agents in the workplace. Once an individual is sensitized, symptoms c an occur after very low level re-exposure. Epidemiology \200 Around 9 \200\22315% of asthma in adults of working age is occupational . \200 The number of new cases of occupational asthma in the UK has been falling over the past 10yrs. The estimated rate of occupational asthma is 45 \200\22375 cases per 100,000 workers per ye ar (based on a European population-based study). Clinical features and etiology \200 Asthma: wheeze, chest tightness, dyspnoea. Classicall y, symptoms are worse at work or soon after work, and better at weekends or during holidays . This pattern can be lost in the later stages of the disease. Late reactions can occur at night or early morning after a day at work \200 Rhinitis and conjunctivitis: rhinorrhea, nasal stuf \201 ness and itching of the eyes/nose, sneezing. These are often associated wi th asthma and may precede chest symptoms When the individual is sensitized, symptoms can be precipitated by non-speci \201 c irritation (e.g. cigarette smoke or cold air). Causal exposures/industries See Table 7.1. Allergens can be divided broadly into: \200 Hi gh molecular weight proteins (e.g. animal and plant proteins) \200 Low molecular weight s ubstances that act as haptens (e.g. isocyanates, acid anhydrides). Individual susceptibility \200 Atopy \200 Cigarette smoking X Atopy is common (30% of t he population); it is not usually appro- priate to screen out atopics from exposure to sens itizing agents at pre-employment. Clinical assessment and diagnosis of occupational asthma \200 Initial investigation with lung function tests (FEV 1 , forced vital capacity (FVC), and peak \202 ow) to explore th e diagnosis of asthma (reversible airways obstruction). Exposure assessment (pattern of exposure and speci \201 c allergens and relationship to sy mptoms, use of respiratory protective equipment): \200 a full history should include curr ent and previous exposures \200 be aware of the possibility of late reactions \200 the lack of a clear temporal relationship to work does not exclude the diagnosis of occupational asthma 07_Smedley_Chap07.indd 198 12/31/2012 8:52:23 PM OCCUPATIONAL ASTHMA AND RHINITIS 199 Table 7.1 Causal exposures/industries Exposure Industry/uses Isocyanates Car body shops Flour, grain dust Bakeries, agriculture Acid anhydrides Manufacturing, use of epoxy resins/varnishes Rosin \202 ux Electronics (soldering) Proteolytic enzymes Manufacture of biological washing powders Animal proteins (urine/dander) Laboratory animal research Platinum salts Platinum industry Antibiotics, cimetidine, ispaghula Pharmaceutical manufacturing Glutaraldehyde, natural rubber latex Health care Wood dust Construction, forestry, carpentry Persulphate salts or henna Hairdressing Fish proteins, soya bean, tea dust Fish preparation, food industry Reactive dyes Cosmetic and rubber manufacture Metal working \202 uids Manufacturing Serial peak \202 ow recording (see b p. 762, Serial peak \202 ow testing) \200 Bronch ial provocation challenge tests: should be carried out in a specialist center (contact your local consultant respiratory physician for advice) individuals can be sensitized to more than one asthmagen Speci \201 c IgE, skin prick testing (if speci \201 c test reagents are available). Prognosis Symptoms usually resolve after removal from exposure, but the practical constrain ts of exposure control can be a real threat to employment. X Where exposure cannot be contr olled completely, individuals are sometimes allowed to continue working whilst wearing PPE. However, they must be informed about risk and have frequent health surveillance. Compensation Occupationally acquired asthma and allergic rhinitis are both prescribed for I ndustrial Injuries Disablement Bene \201 t (D7 and D4, respectively) in those who are expo sed to a known sensitizing agent at work. 07_Smedley_Chap07.indd 199 12/31/2012 8:52:23 PM CHAPTER 7 Respiratory and cardiovascular disorders 200 Health surveillance Individuals who are exposed to respiratory sensitizers must undergo hea lth surveillance (Management of Health and Safety at Work (MHSW) and COSHH Regulations). Th e surveillance program depends on the likelihood of sensitization, and is outlined in speci \201 c guidance from HSE. 1 Relevant legislation and guidance \200 Occupational asthma is reportable under RIDDOR. As thmagen? Critical Assessments of the Evidence for Agents Implicated in Occupational asthma Occupational asthma: a guide for occupational physicians and occupational health physicians. http://www.bohrf.org.uk/downloads/ asthlop.pdf 1 MS 25. Medical Aspects of Occupational Asthma . HSE, Sudbury. 07_Smedley_Chap07.indd 200 12/31/2012 8:52:23 PM This page intentionally left blank CHAPTER 7 Respiratory and cardiovascular disorders 202 Latex allergy Latex allergy may manifest as: \200 A type I immediate hypersensitivity rea ction due to a reaction to natural rubber latex (NRL) proteins More commonly as a type IV delayed hypersensitivity reaction in response to the chemical additives in latex products. Epidemiology During the past 20yrs, latex allergy has become a major occupational haz- ard in the rubber processing and healthcare industries. In the healthcare industry the use of d isposable powdered NRL gloves, many dusted with corn starch to aid donning, increased expon entially after 1987 until the mid-1990s. However, the apparent prevalence of latex allergy has been steadily decreasing since 1998. The prevalence of type I allergy (based on skin-pr ick testing) in HCWs is currently estimated to be up to 12%. Around 1% of the general popul ation are sensitized to NRL, but not all sensitized individuals develop symptoms. Clinical features \200 Type I: urticaria, rhinitis, conjunctivitis, occasionally asthma o r very rarely anaphylaxis. Onset is usually within 20min of exposure. \200 Type IV: derma titis, characterized by a red, itchy, scaly rash often localized to the area of use, i.e. wrists and forearms with glove use, but may spread to ot her areas. Onset is usually >12h after exposure Causal exposures/industries \200 Health care workers \200 Individuals exposed to NRL re gularly, e.g. food handlers, hairdressers and construction workers Latex product manufacturing workers. Individual susceptibility \200 Patients with spina bi \201 da and congenital genitourina ry abnormalities \200 A history of certain food allergies, such as banana, avocado, kiwi and chestnut Individuals with atopic allergic disease may be at increased risk. Clinical assessment and diagnosis \200 The clinical history is essential in establishing the diagnosis of type 1 allergy: \200 supporting tests include a positive skin prick test to latex allergens and a serological test for speci \201 c IgE; not all individuals with a positive skin or serol ogical test manifest allergic disease consider referring the individual for specialist advice and a latex challenge or use test Type IV allergy is diagnosed by a positive patch testing 07_Smedley_Chap07.indd 202 12/31/2012 8:52:23 PM LATEX ALLERGY 203 Prognosis Reducing exposure to latex may lead to a reduction in type 1 allergic symptoms in sensitized individuals. Management Latex policy All health care organizations should have a latex policy outlining the haz- ards of NRL, how to identify and manage individuals with NRL allergy, and how to r educe exposure in the workplace. Organizations should be moving towards a latex free enviro nment. Adjustments to work If NRL allergy is diagnosed, a risk assessment of the individual \200 \231s workplace must be made to ensure a safe working environment. If the individual has a history of severe type I allergy or anaphylaxis, they must work in a latex free environment . Redeployment may be necessary. They should be advised to wear a medic alert bracelet, car ry an epipen, and inform healthcare providers of their NRL allergy. 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