high-risk workplaces, medicolegal statistics and sentinel programmes indicate that y10% of adult-onset asthma is attributable to the workplace. The strategy to identify cases through questionnaires and tools that address functional, immunological and physiopathological issues needs to be improved.Although few in number and limited to a handful of workplaces, cohort studies found that the risk of developing occupational asthma is determined less by individual susceptibility (e.g. atopy, tobacco smoking, human leukocyte antigen phenotype) and more by the level of exposure to its causes; in general, the higher the exposure, the greater the risk, and, by implication, lowering the level of exposure reduces the incidence of disease.Occupational asthma can be used as a satisfactory model for the development of adult-onset asthma. There is a great need to develop intervention strategies through adequate surveillance programmes in high-risk workplaces. Eur Respir J 2003; 22: 551-559. Epidemiology of occupational asthma: general considerations on various study designs and methodological approachesEpidemiology is the study of the distribution, determinants and outcome of disease. In this article, the authors will describe recently acquired knowledge of the epidemiology of occupational asthma, as well as current areas of controversy.BECKLAKE et al.[1] have discussed the features, strengths and weaknesses of several designs used in epidemiological studies. These designs include the randomised control trial, the prospective cohort, the case-referent study, the crosssectional (prevalence) study and the case series. Which design to use in any particular situation is a matter of judgment, determined by a number of factors that may include resources, cost, collaboration of employers and employees, and the question under study. So far, primarily for practical convenience, most epidemiological studies of occupational asthma have been cross-sectional in type. As discussed in several reviews [1,2], this type of study, primarily in the case of occupational asthma (OA), suffers from survivor bias, whose magnitude can be difficult to quantify. Randomised control trials are usually not feasible and are probably unethical in workplace studies, but quasi-experimental studies can provide results of high internal and external validity. Prospective cohort studies are more expensive than cross-sectional studies but are more powerful and less likely to be affected by selection or survivor biases; in particular, it is often possible to track the participants who leave the cohort and determine the possible effect of attrition on the estimates of both the frequency of OA and exposure/effect relationships [3]. This type of study has recently been successfully applied in cohorts of young apprentices [4][5][6][7][8][9][10]. Some case-referent studies have been carried out in the field of OA [11,12]. These studies are valuable in identifying and quantifying risk factors. Finally, there are many case series that mainly describe clinical cases (often si...
Background Allergens from rats, mice, guinea pigs or rabbits cause up to 30% of exposed persons to develop specific immunoglobulin E (IgE) responses. Laboratory animal allergy (LAA) is among the highest occupational risks for asthma in the UK. Elevated levels of nitric oxide (NO) are found in exhaled breath in asthma. In LAA symptoms may progress from conjunctivitis, rhinitis to asthma. Health surveillance aims to detect early sensitization. Objective To assess whether an association exists between LAA and exhaled NO. Methods A cross-sectional study was performed in 39 laboratory workers undergoing LAA health surveillance. Volunteers completed two health questionnaires, had skin-prick tests, spirometry, total IgE and RAST tests. Exhaled and nasal NO was measured by chemiluminescence analyser (LR2000, Logan Research, Rochester, UK). Results There were 23 asymptomatic subjects (mean age 29.53 yearss) and 16 symptomatic subjects (29.63 yearss, P ¼ 0.95); 9 early LAA, seven LAA asthma. Exhaled NO was raised in those with LAA symptoms 17.97 ppb Ϯ 1.24 (mean Ϯ SEM) compared with asymptomatics 6.08 ppb Ϯ 1.15, P < 0.05. A trend of increased NO by allergic status was observed; asymptomatic, to early LAA, to asthma. One-way analysis of variance compared differences between groups (F ratio 13.93, P < 0.001). Symptomatic subjects also had raised nasal NO, vs asymptomatic subjects (mean difference 378 ppb, P < 0.05). A trend was again observed by allergic status (F ratio 5.28, P ¼ 0.01). Conclusion Raised NO levels in LAA increasing with symptom severity suggest NO may prove a useful additional tool in monitoring for LAA, and possibly the response to exposure reduction or allergy due to other respiratory sensitizers.
This c h a p te r is c o n c e rn e d with some o f the transient or p e rm a n e n t pulm onary disorders w hich m ay b e caused by inhalation o f a variety o f dusts, fumes or gases. The num ber o f these w hich cause or, rightly or w rongly, are th o u g h t to cause lung d a m a g e , is very large..." Raym ond Porkes from th e introduction to a c h a p te r on "Miscellaneous Disorders" in "O ccu p a tio n a l Lung Disorders" (1974). "We ore c o n c e rn e d a b o u t th e num ber o f p e o p le w h o h a ve d e v e lo p e d laboratory anim al allergy. There are m ore cases w h o h ove not repo rted their problems". From on internal m em orandum to the m a n a g e m e n t o f a research institution (1977).
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