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Volume 116, Issue 1, Pages 127-132 (July 2005)


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Progression of self-reported symptoms in laboratory animal allergy

Leslie Elliott, PhDaCorresponding Author Informationemail address, Dick Heederik, PhDb, Steve Marshall, PhDa, David Peden, MDc, Dana Loomis, PhDa

Received 2 February 2005; received in revised form 18 March 2005; accepted 29 March 2005. published online 24 May 2005.

Background

Laboratory animal allergy is a common illness among workers exposed to laboratory animals and can progress to symptoms of asthma.

Objectives

This study evaluates the continuum of disease from allergy symptoms to asthma symptoms in a dynamic cohort of workers exposed to animals in a pharmaceutical company.

Methods

Data arose from annual questionnaires administered to workers in a surveillance program established to monitor exposure to animals and the development of allergy. The life-table method was used to compare asthma-free survival between workers with and without symptoms of allergy. A Cox proportional hazards model was used to examine the effects of covariates on the development of asthma.

Results

A total of 603 workers contributed 2527.4 person-years to the study over the 12.3-year period. The probabilities of experiencing asthma symptoms by the 11th year of follow-up were 0.367 for workers with allergy symptoms and 0.052 for those without allergy symptoms. The hazard ratio for asthma symptoms when comparing workers with and without allergy symptoms was 7.39 (95% CI, 3.29-16.60) after adjustment for sex and family history of allergy. Female subjects developed asthma at a rate 3.4 times that of male subjects.

Conclusions

This study supports the hypothesis that laboratory animal allergy symptoms are a major risk factor for the development of asthma. It also suggests a heightened risk of asthma for women who work with laboratory animals, a finding that has not been previously reported.

Chapel Hill, NC, and Utrecht, The Netherlands

a From the Department of Epidemiology, University of North Carolina at Chapel Hill

b Institute of Risk Assessment Sciences, Utrecht University

c Center for Asthma and Lung Biology, Chapel Hill

Corresponding Author InformationReprint requests: Leslie Elliott, PhD, c/o the Department of Epidemiology, CB-7435, University of North Carolina, Chapel Hill, NC 27599-7435.

 Dr Elliott was supported by training grant no. T42/CCT422952 from the National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention. Dr Elliott also worked as a consultant to GlaxoSmithKline, Inc.

Dr Peden was supported by grant no. R01 HL62624, “Endotoxin and bronchial inflammation in asthma.”

Disclosure of potential conflict of interest: L. Elliott worked as a consultant for GlaxoSmithKline from 2000-2003. D. Peden has consultant arrangements with GlaxoSmithKline, Novartis, and Genentech. All other authors—none disclosed.

PII: S0091-6749(05)00699-8

doi:10.1016/j.jaci.2005.03.038


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