Deaths 1998 2000 2002 2004 1988 1992 1996 } Disablement benefit (MS) cases Fig. 16.2.1 Pneumoconiosis (other than asbestosis). Diagnosis The diagnosis of pneumoconiosis depends on three things: \200 \200 \200 A high quality chest radiograph. A complete occupational history. Clinical examination. The importance of a complete occupational history includ- ing every job since leaving schoo l cannot be over empha- sised, particularly as the relevant dust exposures are likely to ha ve occurred many years ago. Fig. 16.2.2 Progressive massive \201 brosis in a coal miner. Radiology Pneumoconioses give rise to small round or irregular opacities on the CXR. In mor e severe cases of coal work- ers pneumoconiosis and silicosis large opacities can develop b ut these are not seen in asbestosis. Coal workers pneumoconiosis and silicosis give rise to predominantly round opacities situated in the middle and upper zones whereas asbestosis ma nifests with small irregular opacities at the lung bases. Small irregular opacities are designated \200\230s \200\231, \200\230t \200\231 and \200 \230u \200\231. Standard films are available to guide classification for epidemiological pu rposes. Coal workers pneumoconiosis This disease is caused by inhaling coal mine dust and its devel opment is mainly dependent on the mass of respira- ble dust to which the miner has been exp osed. CHAPTER 16.2 Pneumoconiosis 391 Pathology Dust particles arriving in the alveoli are phagocytosed by macrophages and transp orted proximally to the respira- tory bronchioles and the mucociliary escalator. When this system is overwhelmed dust laden macrophages accumu- late near the center of the secondary pulmonary lobule. Reticulin and later collagen are deposited in these macules giving rise t o the discrete \201 brotic lesions which constitute simple pneumoconiosis. In the case of coal workers pneumoconiosis collagen deposition is usually minimal. Complicated pneumoconi osis or progressive massive \201 brosis occurs when large opacities develop. These usuall y occur only in miners with well developed (category 2 or 3) simple pneumoconiosis. These l esions may cavitate. Multiple well de \201 ned round opacities 0.5 \200\2235cm in diameter and distributed throughout the lung \201 elds were observed by Caplan in miners with or who subsequently developed rheumatoid arthritis. The lesions tended to develop rapidly ofte n against a background of minor simple pneumoconio- sis and the lesions could cavitate. Thi s pattern of disease is referred to as Caplan \200\231s syndrome. Silicosis Silicosis is probably the oldest pneumoconiosis to af \202 ict man. Dusty trades have been associated with ill health since antiquity but silicosis should now be a disease of the past. Silica exposure occurs in: \200 \200 \200 \200 Quarrying of slate, granite and sandstone. Hard rock mining. Tunneling. Foundry work where silica was used in molds and cores. Pottery and ceramic industries. Occasional cases of silicosis are still reported often where workers have been exposed to s ilica by new industrial processes where the silica risk had not been appreciated. Pathology Silicosis is caused by inhaling crystalline silica dust. The prevalence and sever ity of disease is largely determined by the intensity of exposure. Silica excites a more \202 orid \201 brotic reaction than coal mine dust. This leads to palpable nodules compos ed of concen- tric layers of \201 brous tissue which may coalesce to produce massive \201 brosis with associated distortion of lung architec- ture and scar emphysema. Signs and symptoms Simple coal workers pneumoconiosis does not give rise to any signs or sy mptoms. The early stages of complicated coal workers pneumoconiosis (Category A) is usually symptomless, but more advanced disease can lead to respi- ratory disability which may be s evere. Melanoptysis, the production of black sputum, can occur if an area of massive \201 brosis cavitates. Coal dust can become incorporated into healing skin abrasions and thereb y give rise to a form of tattooing. This is not particularly associ- ated with pneumoconios is but if observed should serve as a prompt for a full occupational history. Radiology The nodules in silicosis tend to be denser and larger than those in coal workers pneumoconiosis and affect predomi- nantly the upper lobes (see Fig. 16.2.3). Eggshell calci \201 cation of hilar lymph nodes can occur. Lung function testing Simple pneumoconiosis has little effect on lung function. Complicated pneumoconiosis especially categories B and C lead to abnormalities of lung function which are poorly correlated with radiographic appearances. Decline may be found in FEV1, and FVC often with an obstructive pattern. Total lung capacity and gas transfer are usually reduced . Prognosis Simple coal workers pneumoconiosis and Category A complicated pneumoconiosis do n ot shorten life. Complicated coal workers pneumoconiosis of Categories B and C is associate d with increased mortality mainly in association with air \202 ow obstruction. Fig. 16.2.3 Silicosis in a granite quarry worker. Differential diagnosis Simple coal workers pneumoconiosis may be confused with: \200 \200 \200 Sings and symptoms Early disease is usually symptomatic. Cough and breath- lessness occur a s the disease progresses and in severe cases respiratory failure may occur. There are no si gns that are speci \201 c to silicosis. Finger club- bing does not occur. Sarcoidosis. Miliary tuberculosis. Extrinsic allergic alveolitis. Complicated coal workers pneumoconiosis may be confused with: \200 Lung cancer. \200 Pu lmonary metastases. \200 Sarcoidosis. \200 Tuberculosis. \200 Wegener \200\231s granu lomatosis. Lung function Small reductions in vital capacity may occur in simple silicosis. As the dise ase advances there is a decrease in TLC, VC, RV, FRC and there may be evidence of airways o bstruction. I COUTTS 392 Compilications \200 Mixed dust \201 brosis This disease occurs when the effects of silica are modi \201 ed b y accompanying non- \201 brogenic dusts. It has been seen in haematite miners and in found ry workers. It gives rise to an irregular \201 brotic upper lobe disease which radiograph ically resembles \201 brocaseous tuberculosis. The lesions do not calcify nor is eggshell calci \201 cation seen. Tuberculosis \200\223 silicosis predisposes to tuberculosis and in the past silicotubercul osis often lead to death. Environmental mycobacterial infection. Emphysema. Spontaneous pne umothorax. Cancer of the lung. Hard rock miners exposed to silica are often exposed to rado n which is a known lung carcinogen but there is increasing concern that silica itself may b e a lung carcinogen. \200 \200 \200 Kaolinosis Heavy exposure to kaolin (china clay) occurred in certain types of clay drying p rocesses and could lead to a simple pneumoconiosis and very rarely to complicated pneumo- c oniosis. Simple pneumoconiosis cause by kaolin in the UK did not appear to cause symptoms o r shorten life. Prognosis Uncomplicated silicosis does not usually shorten life but may do so if supervenin g tuberculosis is not diagnosed and treated promptly. Complicated silicosis can lead to res piratory failure and thereby shorten life. Talc Talc has been used as a lubricant in the rubber industry and in roof felting. Talc has a precise mineralogical de \201 nition but the term has been used loosely in industry. Co mmercial talc often con- tained impurities including signi \201 cant amounts of quartz and asbestos minerals. It is unclear whether pure talc causes a pneumoconiosis but contaminate d talc has given rise to pneumoconiosis with patterns similar to silicosis, asbestosis or c ombinations of the two diseases. Differential diagnosis \200 \200 \200 \200 Sarcoidosis. Metastases. Lung cancer. Wegener \200\231s granulomatosis. Acute silicosis (alveolar silico-lipoproteinosis) Historically this disease was seen in san dblasters and was often rapidly fatal. Cases are still occasionally seen. Exposure to very high concentrations of \201 nely divided quartz can lead to a rapidly developing disease character- ised by progressive breathlessness, malaise, fatigue and weight loss. Infection with tuberculosis or environmental mycobacteria commonly occurs. The radiographic appearanc es vary from diffuse ground glass opaci \201 cation to a mixture of coarse nodular opaciti es. Further reading International Labor Of \201 ce (ILO) Guidelines for the use of the ILO Int ernational Classi \201 cation of Radiographs of Pneumoconioses, Revised Edition 2000 (Occu pational Safety and Health Series No22) International Labor Of \201 ce: Geneva, 2002. Parkes RW Occupational Lung Disorders 3rd edn. London: Butterworths, 1994. This page intentionally left blank R RUDD & J MOORE-GILLON 394 16.3 Disability assessment Respiratory disability is defined by the World Health Organization (WHO) as a reduction in exercise capacity secondary to impaired lung function. The social and occu- pational disadv antage resulting from disability is designated handicap. Assessment of respiratory disabili ty requires information about lung function impairment and its effect on exercise performan ce. For clinical purposes exercise performance is usually assessed on the basis of the pati ent \200\231s account of symptoms. Various scales have been devised to standardize descript ion of impairment of exercise toler- ance in semi-quantitative terms. In the \201 eld of occupational lung disease disability assessment in quantitative terms is usually required f or the purpose of \201 nancial compensation. The subject may therefore be motivated to ex aggerate his disability. To deal with this problem attempts have been made to assess exerci se capcity more objectively. Table 16.3.2 Coal Miners \200\231 Respiratory Disability Scale Disability Score Symptoms Lung function impairment 0% Not breathless on exercise None 10% Breathless on prolonged or heavy exertion Mild Mild 20% Breathless on walking uphill or climbing stairs or on hurrying on level ground Moderate 40% Breathless on walking 100 yards or climbing one \202 ight of stairs at a normal pace Moderate 50% Breathless on walking 100 yards at a slow pace or climbing one \202 ight of stairs at a s low pace Assessment of symptoms Various questionnaires and scales have been devised for the purpose of systematized semi-quantitative assess- ment of exercise tolerance impairment. A question naire devised by the Medical Research Council (MRC) has been modi \201 ed a number of time s. A currently used version is shown in Table 16.3.1. Severe 60% Breathlessness prevents walking 100 yards at a slow pace without stopping or climbing one \202 ight of stairs without stopping Severe 70% Breathlessness prevents activity outside the home without assistance or supervision Table 16.3.1 Medical Research Council Breathlessness Scale 80% Breathlessness limits activities to within the home Severe 90% Able to walk only a few steps because of breathlessness Severe Grade Description 1 Breathless on strenuous exercise Severe 100% Bed and chair bound, totally dependent on carers because of breathlessness 2 Breathless hurrying on the level or up a slight hill 3 Breathless at a normal pace or has to stop after walking at own pace on the level In the USA a different disability grading system is used which grades disability in four cl asses and then translates those into percentage \200\230impairment of total person \200 \231 of up to 25%, up to 50% and up to 100% using American Medical Association criteria. Th is system has not been widely adopted in the UK. 4 Has to stop after walking 100 yards or after a few minutes on the level 5 Too breathless to leave the home The MRC scale is useful for clinical assessment of breath- lessness and correlates with oth er measures of disability. Problems with using the MRC scale for more formal quanti \201 c ation of disability for the purpose of compensa- tion for occupational lung disease is that it is based only upon subjective description of symptoms and the intervals are wide. A mor e detailed scale was devised by the authors of this chapter for assessing disability from C OPD for the purposes of a compensation scheme for hundreds of thousands of UK coal miners. The scale is shown in Table 16.3.2. This scale integrates information from a description of exercise performance with measures of static lung func- tion. Where there is a discrepancy between the reported breathlessness and the lung function measurements more weight should be accorded to the objective evidence from the lung function tests. If reported breathlessn ess is greater than expected from the lung function measurements pos- sible explanations in clude co-existing cardiac disease or other disorder such as anemia contributing to breathle ss- ness, or deliberate exaggeration. Assessment of lung function The coalminers \200\231 disability rating scale refers to impai rment of lung function as mild, moderate or severe, as shown in Table 16.3.3. Table 16.3.3 Rating of respiratory impairment Grade Criteria FEV1, FVC & DLCO \211 80% , FEV1% \211 75% FEV1 or FVC or TLCO < 80% predicted or FEV1/ FVC < 70% FEV1 or FVC or TLCO < 60% predicted or FEV1/FVC < 60% FEV1or TLCO<40% predicted o r FVC < 50% predicted or FEV1/FVC<50% None Mild Moderate Severe These grades are based on a slight modi \201 cation of criteria formulated by the European Society for Clinical Respiratory CHAPTER 16.3 Disability assessment 395 Exercise tests Various types of exercise test have been devised to assist in assessment of disability. In healthy subjects exercise is limted mainly by the ability of the heart to de liver blood to muscles but in persons with respiratory impairment the ability of the lungs to deliver oxygen to the blood becomes the exercise limiting factor. One of the simplest st andardized exercise tests is the six minute walk. The subject is instructed to walk as far and as fast as he can along a measured route, such as a hospital corridor, in a period of 6 minutes. Additional information may be gained by assessing self-reported breathlessness an d oxygen saturation before and at the end of exercise. Another simple test is the shuttle w alk in which the patient walks back and forth between two markers 10m apart at gradually in creasing speed, paced by an audible signal until unable to keep up when the test is termina ted. Inability to complete 25 shuttles suggested a maximal oxygen uptake (VO2max) of < 10ml /kg/min. Walking tests require motivation to cooperate which may be lacking in the context of assessment of disability for compensation. These simple exercise tests do not provide in formation as to the cause of reduced exercise capacity. More information can be obtained fr om a progressive exercise test performed on a treadmill or cycle ergometer. A treadmill pro vides more familiar and relevant exercise for most patients with respiratory disease but a cycle is more logistically convenient in that the patient is station- ary. Minute ventilati on, oxygen consumption, heart rate, blood pressure and the electrocardiogram are monitored continuously. Results are compared with reference values. In a maximal exercise test the su bject is asked to exercise until he cannot continue. Many patients cannot complete a maxima l exercise test to the point at which their exercise capcity is limited by respiratory capa city because their abil- ity to exercise is limited by non-respiratory factors such as arth ritis, angina or simple fatigue. A sub-maximal test in which the subject exercises up to a pre-determined limit of oxygen consumption, commonly 45mmol min \210\2221, can be completed by more patients. From the measured ventilation at this oxygen uptake an equation can be u sed to estimate VO2max with reasonable precision. A disability rating scale based upon the results of maximal exercise testing has been devised by the SEPCR. Disability was assessed on a linear scale between zero, de \201 ned as a maximal oxygen uptake at or above the low er limit of the normal range, de \201 ned as (reference value \200\223 1.64 residual SD) and 100% disability, de \201 ned as inability to achieve an oxygen uptake more than twice that at rest. Disability thus assessed correlates poorly with breathlessness and in practic e disability is seldom assessed in this way in the UK. In the USA, however, the Social Secu rity Administration requires some measure of exercise capacity in assessing disability for compensation purposes. Physiology (SEPCR) and separately by the American Thoracic Society (ATS). They are arbitrar y with no evidence base to con \201 rm the validity of the boundaries between grades and h ence they should be regarded as guidelines for assessment of disability rather than hard an d fast rules. These grades are appropriate for per- sons with chronic stable lung function impairment. Lung function test results are interpreted in relation to ref- erence values, c ommonly but potentially misleadingly termed \200\230predicted values \200\231. It is impor tant to appreciate that these represent the mean values for persons of the same sex, age an d height without known respiratory dis- ease and are not actually \200\230predictive \200 \231 of an individual \200\231s lung function. The \200\230normal range \200\231, statisti cally should be de \201 ned as the mean +/ \200\223 2 standard deviations (SD) to encompas s 95% of the population. However, the concept of \200\230abnor- mally high \200\231 lung f unction is meaningless and so it is conven- tional to regard the upper 95th centile, de \201 ned by a value above the mean minus 1.64 SD as \200\230normal \200\230. However, for convenience of calculation values \211 80% of the reference value are frequently taken as normal which gives a fair approximation. However the normal range is de \201 ned, a signi \201 cant minority of healthy persons will have lung func- tion \200\230below normal \200\231. Conversely some patients with respi- ratory disease who have lost substantial lun g function may have lung function which is still within the normal range. It is necessary t o interpret the results in the context of clinical and radiological \201 ndings. For exam ple FVC 85% of predicted is probably normal in a well man with normal exercise tolerance an d a normal CXR whereas it is almost certainly abnormal in a man complaining of exertional b reathlessness with interstitial shadowing on CXR. Asthma Since, by de \201 nition, asthma gives rise to respiratory func- tion impairment wh ich is variable over time it is necessary to take into account the pattern of impairment ov er a period in order to assess disability. A disability rating scheme for asthma has been d evised by the ATS. A single set of \200\230normal \200\231 lung function test results does not necessar- ily imply that there is no disability due to asthma. Serial measurement of p eak expiratory \202 ow (PEF) three or more times daily is useful in assessing disability due to asthma. It is reasonable to take into account also treatment required to suppress sy mptoms and maintain lung function. For example, a person with normal PEF readings but who r equires regular inhaled steroids and bronchodilator ther- apy may be regarded as mildly dis abled whereas a person with the same PEF readings without any treatment would not be classe d as disabled. A potential drawback of reliance on self-monitored peak \202 ow readings i s that an individual motivated to exaggerate his disability for the purposes of claiming co mpensation can easily fake low PEF readings unless an electronic recording peak \202 ow m eter which blinds the user to the results is available. A bronchial chal- lenge with histam ine or methacholine to measure bron- chial hyper-reactivity can provide a more objective as sessment of the activity of asthma. If a person complains of asthma symptoms but has normal resting lung function increased a \201 nding of increased bronchial reactivity adds cred ibility to the clinical history. While normal bronchial reactivity does not exclude active asthma, it is rare to have disabling asthma with normal reactivity and normal lung function . Lung function and disability The relation between lung function impairment and conse- quent disability is highly variable. It depends upon the degree of exercise to which the individ ual was accustomed before respiratory impairment developed. There is a sub- stantial reserv e of respiratory function which is called upon only on strenuous physical exertion and peop le who R RUDD & J MOORE-GILLON 396 do not engage in such exertion may lose 10 \200\22320% of their lung function without notic ing breathlessness; they would not have any respiratory disability consequent upon the loss of lung function. The same lung function loss could cause signi \201 cant disability to a person enjoying strenuous sports or in employment involving heavy manual labor. Psychologi cal factors also play an important part in deter- mining disability. Mood affects the perce ption of breath- lessness and attitude towards living with disability itself partly determi nes disability and contributes importantly to variation in reported breathlessness and in e xercise per- formance associated with any given degree of lung function impairment. This ph enomenon is separate from that of exaggeration of symptoms for the purpose of compensa- tio n which also may occur. Co-existing impairments also affect the extent to which lung functi on impairment will cause disability. A person with suf \201 cient lung function impairment to cause 30% dis- ability if he were otherwise well may in fact have no respi- ratory disa bility if he also has a neurological disorder which renders him incapable of walking. Conve rsely, a person who was already breathless on minor exertion as a result of heart disease m ay suffer a signi \201 cant increase in disable- ment from modest loss of lung function wh ich would not have caused disability on its own if he had not had heart disease. Hence, whi le standardized scales relating lung function impairment to disability provide a useful fra mework it is important to take into account individual circumstances in assessing disabilit y. American Thoracic Society. Guidelines for the evaluation of impair- ment/disability in pati ents with asthma. Am Rev Respir Dis 1993; 147: 956 \200\2231061. Bestall JC, Paul EA, Garrod R, et al. Usefulness of the Medical Research Council (MRC) dysp noea scale as a measure of disabil- ity in patients with chronic obstructive pulmonary dise ase. Thorax 1999; 54 581 \200\223586. Butland RJ, Pang J, Gross ER, et al. Two-, six-, and 12-minute walking tests in respiratory disease. Br Med J (Clin Res Ed) 1982; 284: 1607 \200\2238. Cotes JE. Rating respiratory disability: a report on behalf of a work- ing group of the Eur opean Society for Clinical Respiratory Physiolo. Eur Respir J. 1990;3:1074 \200\2237. Cotes JE, Chinn DJ, Reed JW, et al. Experience of a standardized method for assessing respi ratory disability. Eur Respir J 1994; 7: 875-880. De Coster A. Respiratory impairment and disablement. Bull Eur Physiopathol Respir 1983; 19: 1 \200\2233P. Jones NL, Makrides L, Hitchcock C, et al. Normal standards for an incremental progressive c ycle ergometer test. Am Rev Respir Dis 1985; 131: 700 \200\223708. King B, Cotes JE. Relation of lung function and exercise capacity to mood and attitudes to health. Thorax 1989; 44: 402 \200\223409. Revill SM, Morgan MD, Singh SJ, et al. The endurance shuttle walk: a new \201 eld test fo r the assessment of endurance capacity in chronic obstructive pulmonary disease. Thorax 199 9; 54: 213 \200\223222. Weller JJ, el-Gamal FM, Parker L, et al. Indirect estimation of maximal oxygen uptake for s tudy of working populations. Br J Ind Med 1988; 45: 532 \200\223537. World Health Organization. International classi \201 cation of impair- ments, disabilities and handicaps. Geneva: WHO, 1980. Further reading American Medical Association. Guidelines to the Evaluation of Permanent Impairment 5th edn. Chicago 2001. American Thoracic Society, Medical Section of the American Lung Association. Evaluation of impairment/disability secondary to respiratory disease. Am Rev Respir Dis 1986; 133:1205 \200\2231209. This page intentionally left blank S BURGE 398 16.4 Occupational asthma What are the causes of occupational asthma? Occupational asthma is nearly always due to som ething inhaled at work, occupational asthma tends to occur in clusters, it is often easier to start with the job, the most commonly identi \201 ed include: \200 paint sprayers and painters; \200 bakers, pastry makers and food processors; \200 nurses, dental workers and laboratory technicians; \200 chemical, plastic and rubber workers; \200 animal hand lers and farm workers; \200 welders and metal workers; \200 timber and forestry workers ; \200 electrical and electronic production workers; \200 textile workers; \200 stora ge workers; \200 waiters and cleaners. Occupational asthma is now the commonest occupational lung disease in westernized countries , it often affects peo- ple at the height of their working lives and may affect you. There are few diseases where it is so easy to do so much harm. Unsubstantiated diagnoses are as c ommon as missed diagnoses. Advice to leave a job frequently leaves your patient unemployed and similar affected workers unpro- tected. There are now evidenced based guidelines and a BTS endorsed standard of care; they will form the back- bone of this chapter. De \201 nition The de \201 nition of occupational asthma is surprisingly dif \201 - cult and a little controversial. Work-related asthma is asthma which deteriorates following wor k exposures and improves when away. If the worker has pre-existing asthma and the deteriora tion occurs with the \201 rst signi \201 cant exposure the mechanism is likely to be irr itant and the dis- ease called work aggravated asthma. Examples would include asthmatics wo rking in a cold store or in workplaces with signi \201 cant sulfur dioxide exposure. A sin gle large exposure to an irritant can induce asthma for the \201 rst time, which may pers ist for months, or perhaps for ever, without sensitisation. This is usually called acute ir ritant induced (or toxic) asthma. After the acute exposure the worker should be able to wor k with low lev- els of the offending substance in the same way as a pre- existing asthmatic , so a job change is usually not needed. Chlorine exposure is the most commonly recognized cause. Allergic occupational asthma is characterized by a latency period between \201 rst exposure to a respiratory sensitiser at work and the development of symptoms. Once sensiti - sation has occurred levels of exposure below those that were tolerated before cause deter ioration. It can occur de novo or in those with pre-existing asthma, when a new sensitisati on occurs, for instance a doctor with pre-existing asthma may develop latex sensitivity and be unable to tolerate the background latex exposures that are present in hospitals where l atex gloves are used. Allergic occupational asthma is usually divided into high molecular w eight (when speci \201 c IgE is usually found) and low molecular weight, (where an IgE mec hanism is usually not evident). In some of these the precise cause has been hard to pin down, the commonest identi \201 ed agents include: \200 \200 \200 \200 \200 \200 \200 isocyanates; \202 our and grain dust; colophony and \202 uxes; latex; animals; aldehyde s; wood dust. There are however more than 400 documented agents causing occupational asthma, \201 nding the precise cause often needs specialist referral. Diagnosis AUTHOR \200\231S TIPS \200 Every worker with asthma or COPD should be asked whether their symptoms improve on days awa y from work or on holiday. Those who say yes to either should be investigated for occupatio nal asthma. You must decide whether you have the resources and knowledge to investigate and manage your patient yourself, or whether you would be advised to share care with a special ist in occupational lung diseases (as recommended in guidelines). You should start serial P EF measurements as soon as possible, whether you are going to manage the patient alone or a re seeking help from a specialist. How common is occupational asthma? Occupational asthma accounts for about 15% of asthma in adults of working age, the great majority of which is allergic occupational asthma. The pro portion of asthma attributa- ble to work has been increasing over the last 30 years, newer estimates may be greater than this. If you think of the other causes of adult asthma this i s not so surprising, as most asthma is allergic and occurs relatively soon after \201 rst exposure to the sensitizing agent, which usually occurs in childhood. New exposures in adu lthood are usually encountered at work. Other causes would include sali- cylates, drugs suc h as beta blockers, and acute airway insults from infection. The Health and Safety Executiv e (HSE) estimate that 1500 \200\2233000 people develop occupa- tional asthma in the UK each year. This rises to 7000 cases a year if work-aggravated asthma is included. HSE estimates that the costs to society of new cases of occupational asthma are up to 1.1bn over 10 ye ars. The diagnosis of occupational asthma is compounded by pre-conceived beliefs of what is asth ma. Occupational asthma is more commonly identi \201 ed in the older smoking worker, who o ften have an initial label of COPD. Bronchodilator response, diurnal variation in PEF >20% and non-speci \201 c reactivity may all be within normal limits in workers with occupation al asthma. Respiratory symp- toms improving on days away from work or on holiday are the mo st sensitive screening questions, occupational asthma can be con \201 rmed in a little ove r half of positive responders. A clinical history alone is insuf \201 cient to remove a wo rker from exposure. Workers denying respiratory symptoms may sometimes be identi \201 ed f rom accelerated FEV1 decline found during surveillance medicals. CHAPTER 16.4 Occupational asthma 399 The tests available are: 1 Speci \201 c IgE or skin prick tests. 2 Non-speci \201 c respo nsiveness at and away from work. 3 Serial measurements of PEF (or FEV1). 4 Speci \201 c in halation challenge tests. 5 Workplace challenge. daily maximum, mean and minimum with each \200\230day \200\231 starting with the first rea ding at work and finishing with the last reading before work on the next day, as shown in t he Figs. 16.4.1 and 16.4.2. The computer plotter Oasys is a convenient tool for plotting an d analyzing serial PEF meas- urements and has the highest sensitivity and speci \201 city of any diagnostic test for occupational asthma which has external validation. A positive re cord con \201 rms occupa- tional asthma but does not de \201 ne the cause. The production of speci \201 c IgE antibody may be detected by skin prick or serological t ests. Testing is more helpful is de \201 ning the cause than the presence or absence of oc cu- pational asthma. The respective sensitivities and speci \201 ci- ties of the ability o f these tests to detect speci \201 c IgE vary between allergens but in any case are depend ent on the speci \201 c content of the allergen extract and the setting of positive cut-of fs. Blood testing for speci \201 c serum IgE may not be as sensitive as skin prick testing . The presence of speci \201 c IgE con \201 rms sensitisation to an agent at work, but al one does not con \201 rm the presence of occupational asthma. Testing is worthwhile for hi gh molecular weight agents particularly enzymes (food and detergents), latex, rat and mouse urinary antigens, arthropods, \202 our, shell \201 sh and \201 sh. There is a high fa lse-positive rate but few false-negatives. Some of those with positive tests may have occup ational rhinitis, which may precede occupa- tional asthma. Skin prick testing is useful for selected low molecular weight antigens including the ammonium hex- achlorplatinate (platin um re \201 ners), reactive dyes and acid anhydrides. Serial Plot 380 360 340 320 300 280 260 240 220 200 180 160 140 120 100 80 ) n M / L ( i F E P Mon 13/08/2001 Tue 14/08/2001 Wed 15/08/2001 Thu 16/08/2001 Fri 17/08/2001 Sat 18/08/2001 Sun 19/08/2001 Serial Plot 380 360 340 320 300 280 260 240 220 200 180 160 140 120 100 80 ) n M / L ( i F E P Mon 20/08/2001 Tue 21/08/2001 Wed 22/08/2001 Thu 23/08/2001 Fri 24/08/2001 Sat 25/08/2001 Sun 26/08/2001 Serial Plot 380 360 340 320 300 280 260 240 220 200 180 160 140 120 100 80 Sensitivity Speci \201 city Skin prick tests or speci \201 c IgE Variable <100% Often around 30% ) n M / L ( i F E P 3.2 x change in non-speci \201 c reactivity away from work ZPEF >44l/min pre/post shift Se rial PEF \211 4/day and \211 3 weeks 48% 64% 21% 77% Mon 27/08/2001 Tue 28/08/2001 Wed 29/08/2001 Thu 30/08/2001 Fri 31/08/2001 Sat 01/09/2001 Sun 02/09/2001 78% 92% Fig. 16.4.1 A 40-year-old smoking nurse presented with increasing asthma and time off work. She had had quite bad asthma from the age of 6 which had remitted in her teens. She was be tter on days away from work, and better when working night shifts when she would use less l atex gloves than on dayshifts. She was asked to keep 2-hourly measurements of peak \202 o w from waking to sleeping, a sequential plot of the record is shown here \201 gure. Shift s working at night are cross-hatched, periods sleeping are shaded. Her peak \202 ow drops over night shifts and over night when away from work. Serial PEF <4/day or <3 weeks 64% 83% Speci \201 c challenge test Unknown but <100% Unknown but <100% Sensitivity and speci \201 city of diagnostic tests for occupa- tional asthma Non-speci \201 c reactivity as measured with methacholine or histamine is not suf \201 ciently sensi tive on its own to exclude occupational asthma (sensitivity 70-95% in different studies). T he between visit variability in stable asthmatics has a 95% CI of around 3.2-fold. Changes greater than this after 2 weeks away from work have a sensitivity for the diagnosis of occu pational asthma of <50%. Testing is useful but not suf \201 ciently sensitive or speci \201 c on its own. Serial measurements of PEF are the most appropriate \201 rst step in t he physiological con \201 rmation of occupational asthma and should be started at the earl iest opportunity by the \201 rst clinician suspecting occupational asthma. The concept is simple but the precision is in the detail. Usual practice is to ask for approximately 2-ho urly reading from waking to bedtime, with treatment kept constant on work and rest days, an d times of starting and stopping work and waking and sleeping recorded each day. Suitable r ecord forms and instructions can be downloaded from http:// www.occupationalasthma.com/work ers.aspx. The interpretation of the recordings is much easier if plotted as Asthmatics have a diurnal variation in peak \202 ow which is usually lowest at the end of sleeping. As she works at night, the spontaneous diurnal variation might confound the reco rd. Fig. 16.4.3 shows the same data plotted as the mean value from waking, separately for n ightshifts and days away from work. The record shows similar waking values which increase a fter waking, but start to fall 8 hours after working on nightshifts. The bottom panel shows the time, the number of readings from which each datapoint is derived (blue days away from work, red work days, a minimum of 3 readings per datapoint required). The plot con \201 r ms that the night shift deterioration is not due to spontaneous diurnal variation. AUTHOR \200\231S TIP If you suspect occupational asthma start a 2-hourly record of PEF usin g published guidelines S BURGE 400 Average hour from waking for rest and night shift days 220 200 180 160 140 120 100 80 00 \200\22302 12 10 47 Total area between the graphs: 819 02 \200\22304 11 9 65 04 \200\22306 11 7 73 06 \200\22308 11 10 82 08 \200\22310 11 9 104 10 \200\22312 9 11 152 12 \200\22314 11 6 152 14 \200\22316 11 6 144 16 \200\22318 11 4 18 \200\22320 9 2 20 \200\22322 4 0 22 \200\22324 4 0 24 \200\22326 3 0 Hours from waking, number of readings and areas (night shifts) (rest) Fig. 16.4.3 Our nurse whose records are shown in Figs. 16.4.1 \200\22316.4.3 had speci \201 c challeng e tests as her ward used powder-free latex gloves which her employer thought had removed th e risk of latex allergy, also a domestic had developed occupa- tional asthma on the ward fr om a cleaning agent (benzalko- nium chloride) introduced to reduce the risks of cross infec tion. The results are shown in Fig. 16.4.4. The challenge clearly shows an immediate asthma tic reaction induced by donning and removing latex gloves, with no reaction follow- ing the use of nitrile gloves on another day. Her employer then knew what to remove from the work environment. Fig. 16.4.2 Shows the same data as Fig. 16.4.1 plotted as the daily maximum, mean and minim um by the oasys plotter. The upper panel shows the daily diurnal variation in peak \202 o w. The middle panel shows the predicted peak \202 ow (the black dotted line at the top of the record), an assessment of the likelihood of each complex showing occupational asthma ( 4 de \201 nitely yes to 1 de \201 nitely no); below this the daily maximum (blue dotted), mean (black bars) and minimum (red dotted) peak \202 ow. Nightshifts are cross-hatched, days away from work have a clear background. The bottom panel shows the date, the number of readings made per day and the number of hours worked. The deterioration on workdays in muc h more obvious on this plot. 2.20 2.10 2.00 1.90 Latex Blue nitrile 1.80 1.70 1.60 1.50 1.40 1.30 \210\2221 0 1 3 Hours from exposure 2 4 5 6 7 Speci \201 c inhalation tests are the gold standard for diagnos- ing occupational asthma, and are standard practice in some countries with good resources for occupational lung dis- ease (such as Finland, Belgium and Quebec). Occupational type bronchial provocation testing should not be attempted outside specialist centers. Control exposures with moni- toring fo r 24 hours after exposure should always be done \201 rst. Exposures to speci \201 c occu pational agents should start with exposures well below those at work and increase on subseq uent days if no reactions have occurred. Measuring non-speci \201 c reactivity before and after expo- sure may help in the interpretation of borderline reactions. The resources for occupational type provocation testing are very limited in the UK. In practice a patient com ing from a workplace with exposure to a well-identi \201 ed anti- gen and a positive PEF r ecord is suf \201 cient for clinical pur- poses; examples would include a laboratory rat h andler with a positive skin prick test to rat urinary antigen or a polyurethane molder from a workplace with isocyanate exposure where others have previously developed occu- pational asthma. Speci \201 c challenge tests are underused in the UK by international standards a nd are particularly valu- able when a worker is exposed to more than one possible cause, or the workplace has not had previous cases of occupational asthma.