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ASTHMA AND ALLERGIES

Introduction

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: susceptibility (8)

“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.

Methods

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.. These agents were specifically chosen because there is documented risk for OA among exposed workers. (12) We included articles from the resulting Medline search that evaluated primary or secondary prevention of OA, regardless of whether prevention was the principal research topic for the study. Additional articles that were not identified in our preliminary Medline search but were listed as references in the index articles were also included if they evaluated preventive strategies. We then conducted a citation search in Medline for the articles from the preliminary Medline search and additional references. Articles resulting from the citation search were included if they evaluated prevention of OA.

In an effort to unearth articles missed in the preliminary literature search, we conducted an expanded Medline search for studies published from 1966 up through October 2003 using the following combination of Medical Subject Headings (MeSH) and Subheadings: ("Asthma" [MeSH] OR "Status Asthmaticus" [MeSH]) AND ("Occupational Exposure" [MeSH] OR "Occupational Diseases" [MeSH] OR "Occupational Health" [MeSH] OR "Air Pollutants, Occupational" [MeSH] OR "Occupational Medicine" [MeSH]) AND ("Population Surveillance" [MeSH] OR "Epidemiologic Studies" [MeSH] OR "Respiratory Protective Devices" [MeSH] OR "prevention and control" [Subheading] OR "Primary Prevention" [MeSH]). Similar to the preliminary literature search, we only included articles that evaluated prevention of OA.

We indexed selected studies by author, year of publication, high or low molecular weight agent, general category of agent, name of specific agent, and by primary or secondary intervention type. For each study, we produced a brief summary of intervention activity, participation rate, and intervention effectiveness.

Results

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.

Discussion

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 screening (15-17,19) 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.

Several years ago, the National Institute for Occupational Safety Health (NIOSH) and 500 stakeholders from the occupational safety and health community developed the National Occupational Research Agenda (NORA). NORA encompasses 21 priority research areas, of which one is intervention effectiveness research. The NORA Intervention Effectiveness Research team recently proposed a model for evaluating the development, implementation, and effectiveness of interventions.(23)

While there has been substantial progress in recent years in understanding the etiology and epidemiology of OA with respect to a variety of exposures and agents, we only identified 21 papers in the MEDLINE database that evaluated the effectiveness of primary preventive strategies to reduce incidence of OA. This relative lack of intervention effectiveness literature on OA reinforces the call for researchers to integrate evaluation into their plans for primary prevention of OA and to publish results of their findings, thereby enabling policymakers to better understand or judge OA prevention measures.

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

References

(1) Newman Taylor AJ. Occupational asthma. Thorax 1980; 35(4):241-5.

(2) Balmes J, Becklake M, Blanc P, Henneberger P, Kreiss K, Mapp C, et al. American Thoracic Society Statement: Occupational contribution to the burden of airway disease. Am J Respir Crit Care Med 2003; 167(5):787-97.

(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.

(4) Arif AA, Whitehead LW, Delclos GL, Tortolero SR, Lee ES. Prevalence and risk factors of work related asthma by industry among United States workers: data from the third National Health and Nutrition Examination Survey (1988-94). Occup Environ Med 2002; 59(8):505-11.

(5) Gautrin D, Newman-Taylor AJ, Nordman H, Malo JL. Controversies in epidemiology of occupational asthma. Eur Respir J 2003; 22(3):551-9.

(6) Cullinan P, Tarlo S, Nemery B. The prevention of occupational asthma. Eur Respir J 2003; 22(5):853-60.

(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.

(12) Asthma in the Workplace. 2 ed. New York: Marcel Dekker, 1999.

(13) Liss GM, Tarlo SM. Natural rubber latex-related occupational asthma: association with interventions and glove changes over time. Am J Ind Med 2001; 40(4):347-53.

(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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