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Asthma: A business case for employers and health care purchasers

inhalerThe Lowell Center for Sustainable Production , University of Massachusetts Lowell; and Asthma Regional Council. February 2010.

“The purpose of this report is twofold: to revisit the robust body of evidence demonstrating positive health outcomes and economic benefits of comprehensive asthma programs, and to analyze its implications for employers.”  

The chapter “Promoting Best Practices for Asthma: Strategies and Recommendations” highlights three strategies for reducing the burden of asthma.  Of particular interest for work-related asthma is Strategy #3 Ensuring Healthy Work Environments. The document recommends the following to accomplish Strategy #3:  “Employers should consider two strategies to improve the quality of the work environment for asthma:  a) Good housekeeping practices to minimize exposures to ubiquitous allergens and irritants. b) Workplace-specific measures to minimize exposures to asthmagens and asthma triggers, including adopting safer products and practices.”  The document also encourages making appropriate accommodations for individual employees with asthma.

The wealth of published articles on occupational asthma (OA) can make assessing the state of prevention research challenging. This primer describes and summarizes current literature, and highlights some of the areas where work is still needed.

OA is defined as a reversible, generalized airway narrowing as a result of exposure to airborne dust, gases, vapors, or fumes in the work environment.1 A recent Statement of the American Thoracic Society estimated that approximately 15% of asthma in the adult population is attributable to occupational exposure,2 although other estimates have ranged from 5% to 37%.3,4 A substantial amount of information exists on particular agents or conditions known to cause OA, for which relevant preventive measures have taken place. Recent reviews of OA in the literature have cited hallmark studies that document successful intervention efforts, most notably for health care workers using natural rubber latex (NRL) gloves, laboratory animal handlers, and workers in the detergent industry.5,6 In addition, the recent reviews sound the call for more studies that better evaluate the effectiveness of OA prevention efforts.

Prevention is not a single entity, and it is often divided into three categories: primary, secondary, and tertiary prevention.

“Primary prevention is [the] protection of health by personal and communal efforts, such as enhancing nutritional status, immunizing against communicable diseases, and eliminating environmental risks, such as contaminated water supplies.” 7
Stage: susceptibility8

“Secondary prevention is [the] set of measures available to individuals and communities for the early detection and prompt intervention to control disease and minimize disability, e.g., by the use of screening programs.” 7
Stage: early disease, i.e. pre-clinical and clinical stages 8

“Tertiary prevention consists of measures aimed at softening the impact of long-term disease and disability by eliminating or reducing impairment, disability and handicap; minimizing suffering; and maximizing potential years or useful life” 7
Stage: advanced disease or disability 8

Primary prevention of OA means eliminating or controlling the exposure of interest. For OA, primary prevention may include the use of measures such as pre-employment screening, designed to minimize the proportion of susceptible people among workers.9;10 While elimination of the sensitizing agent is the ideal intervention, reduction of exposure to the agent, use of personal protective equipment (e.g., respirators), and limiting the number of people exposed to the agent should be considered if elimination is not possible.

Secondary prevention aims to reduce disease prevalence by shortening the duration of disease.11 Routine medical screening for the initial symptoms and signs of asthma in workers is one component of secondary prevention used to guide early intervention that effectively slows or stops disease progression. Many workers will react to minute quantities of the offending agent once they become sensitized. It is generally accepted then that early identification of OA and removing the worker from exposure will result in a good outcome, provided that the worker has had symptoms for less than 1 year and has relatively normal pulmonary function values.10 However, other occupational options and economic costs for the worker must also be considered. Finally, tertiary prevention aims at the maximum possible prevention of permanent damage. Pharmaceutical treatment including inhaled corticosteroids and bronchodilators are common measures for tertiary prevention.


We conducted a preliminary literature search for studies published from 1966 up through October 2003 using the Ovid Medline (National Library of Medicine) search engine. We performed a specific keyword search of asthma with each of the following agents: aluminum, anhydride, alpha amylase, colophony, crab, detergent enzyme, enzyme, egg, insect, isocyanate, laboratory animal, latex, meat, platinum, shrimp, solder, and western red cedar..


We selected 94 articles that evaluated primary and/or secondary prevention of OA. Two of the 94 articles evaluated both primary and secondary prevention activities, leading to 96 studies for examination. Twenty-one studies evaluated primary prevention activities, and 75 evaluated secondary prevention activities. Of the studies evaluating primary prevention, 76% (n=16) cited exposure to high-molecular-weight agents and 24% (n=5) to low-molecular-weight agents. Of studies evaluating secondary prevention, 25% (n=19) cited exposure to high-molecular-weight agents, 56% (n=42) to low-molecular-weight agents, and 19% (n=14) cited exposure to both high- and low-molecular-weight agents.

Several occupations, industries, and causative agents were investigated in studies evaluating primary prevention, but the majority of studies were specific to detergent industry workers exposed to enzymes (n=8), laboratory animal handlers exposed to laboratory animal allergen (n=3), and health care workers using NRL gloves (n=3). Intervention strategies for primary prevention included substitution, reduction in exposure, use of personal protective equipment, and pre-employment screening.Methods to reduce exposure included improvement of industrial processes, engineering controls, administrative controls, and education and training of workers. Medical screening was cited as a method for evaluating the effectiveness of primary preventive measures.

Approximately half of the studies evaluating secondary prevention investigated workers exposed to diisocyanates (n=14), anhydrides (n=8), aluminum (n=7), latex (n=5) and western red cedar (n=5). Nearly one-third of the secondary prevention studies evaluated single agent occupational exposures, including baking allergens, chromium, cobalt, colophony, cow dander, crab, detergent enzyme, grain dust, laboratory animal allergen, wheat, persulfates, phytase, platinum, and salmon. The remaining studies documented multiple agent exposures in clinical population settings (n=14). Medical screening, removal of affected workers from exposure, and transfer of affected workers to low-exposure areas were routinely cited as secondary prevention measures. Other preventive measures included agent elimination, reduction in exposure (e.g., engineering controls, improvement of industrial processes, education and training of workforce), and use of personal protective equipment.


Studies examining detergent industry workers, health care workers using NRL gloves, and laboratory animal handlers provide examples of successful interventions for primary prevention of OA. Reduction of exposure was achieved by substitution or elimination of the causative agent, modification of industrial processes, engineering controls, administrative controls, education and training workers, and promoting the use personal protective equipment.13-20 Examples from the detergent and laboratory animal industries illustrate how routine medical screening15-17,19 can be used to document the effectiveness of primary preventive measures and to facilitate secondary prevention by identifying affected workers for whom exposures should be eliminated.
There is also evidence suggesting the role of medical screening in primary prevention of OA. When officials in the province of Ontario in Canada mandated exposure monitoring and medical screening for workers exposed to diisocyanates, the results were earlier diagnosis, less severe disease, and a decline in reported worker compensation claims for diisocyanate-induced asthma.21 It is also possible that more reliable case identification will result in the institution of workplace-specific preventive measures that could prevent incident cases of OA and avert adverse outcomes in existing cases.12

Recent literature reviews on OA indicate greater emphasis on prevention by citing hallmark studies that illustrate successful interventions.7,8 This Web site attempts to summarize information from a large number of published studies that evaluate primary and secondary prevention of OA. In doing so, we provide brief profiles of preventive efforts in many industries, including the limitations for many of these studies. Our observation is similar to the other recent reviews; there are few studies that adequately evaluate the effectiveness of OA prevention. Most of the articles compiled in this review follow a quasi-experimental design, where the investigator lacks control over the assignment (e.g., due to ethics, practicality) and/or timing of intervention to study groups, thereby lacking an adequate comparison group to make causal inferences regarding intervention effectiveness.8,22 Another common occurrence is studies instituting multiple interventions to prevent OA, leading to difficulty linking the measurement of health outcome (e.g., disease incidence) to any specific intervention.

Acknowledgement: A Mehta; P Henneberger; E Lowery. Division of Respiratory Disease Studies, National Institute for Occupational Safety and Health, contributed to this topic page.

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(3) Kogevinas M, Anto JM, Sunyer J, Tobias A, Kromhout H, Burney P. Occupational asthma in Europe and other industrialised areas: a population-based study. European Community Respiratory Health Survey Study Group. Lancet 1999; 353(9166):1750-4.
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(5) Gautrin D, Newman-Taylor AJ, Nordman H, Malo JL. Controversies in epidemiology of occupational asthma. Eur Respir J 2003; 22(3):551-9.
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(7) A Dictionary of Epidemiology. 4 ed. Oxford University Press, 2001.
(8) Mausner JS, Bahn AK. Epidemiology: An Introductory Text. Philadephia: W. B. Saunders Company, 1974.
(9) Saric M, Vuksic M, Marelja J. Can the occurrence of bronchial asthma in potroom workers be prevented? Arh Hig Rada Toksikol 1993; 44(4):317-20.
(10) Sorgdrager B, Pal TM, de Looff AJ, Dubois AE, de Monchy JG. Occupational asthma in aluminium potroom workers related to pre-employment eosinophil count. Eur Respir J 1995; 8(9):1520-4.
(11) A Dictionary of Epidemiology. 4th ed. Oxford University Press, 2001.
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(14) Tarlo SM, Easty A, Eubanks K, Parsons CR, Min F, Juvet S, et al. Outcomes of a natural rubber latex control program in an Ontario teaching hospital. J Allergy Clin Immunol 2001; 108(4):628-33.
(15) Allmers H, Schmengler J, Skudlik C. Primary prevention of natural rubber latex allergy in the German health care system through education and intervention. J Allergy Clin Immunol 2002; 110(2):318-23.
(16) Juniper CP, How MJ, Goodwin BF, Kinshott AK. Bacillus subtilis enzymes: a 7-year clinical, epidemiological and immunological study of an industrial allergen. J Soc Occup Med 1977; 27(1):3-12.
(17) Cathcart M, Nicholson P, Roberts D, Bazley M, Juniper C, Murray P, et al. Enzyme exposure, smoking and lung function in employees in the detergent industry over 20 years. Medical Subcommittee of the UK Soap and Detergent Industry Association. Occup Med (Lond) 1997; 47(8):473-8.
(18) Peters G, MacKenzie DP. Worker Safety: How to establish site enzyme capability. In: van Ee J., Misset O, Baas EJ, editors. Enzymes in Detergency. New York: Marcel Dekker, Inc., 1997: 327-40.
(19) Botham PA, Davies GE, Teasdale EL. Allergy to laboratory animals: a prospective study of its incidence and of the influence of atopy on its development. Br J Ind Med 1987; 44(9):627-32.
(20) Fisher R, Saunders WB, Murray SJ, Stave GM. Prevention of laboratory animal allergy. J Occup Environ Med 1998; 40(7):609-13.
(21) Tarlo SM, Liss GM, Yeung KS. Changes in rates and severity of compensation claims for asthma due to diisocyanates: a possible effect of medical surveillance measures. Occup Environ Med 2002; 59(1):58-62.
(22) Epidemiology of Work-Related Diseases. 2 ed. London: BMJ Books, 2000.
(23) Goldenhar LM, LaMontagne AD, Katz T, Heaney C, Landsbergis P. The intervention research process in occupational safety and health: an overview from the National Occupational Research Agenda Intervention Effectiveness Research Team. J Occup Environ Med 2001; 43(7):616-22.

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