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ASTHMA 0272-5231/95 $0.00 + .20
OCCUPATIONAL ASTHMA
Diagnosis, Management, and Prevention
Lee S. Newman, MD
Occupational asthma has become the most common work-related respiratory disorder, supplanting such conditions as silicosis, asbestosis, and occupational lung cancer. 105, 125 In the United Kingdom, for example, occupational asthma was estimated to represent 26% of the recognized occupational lung disorde S.12'How common is occupational asthma among asthmatics? Estimates of the proportion of all cases of adult-onset asthma due to occupational exposure range from 2% to 15% .20, 102, 164 'fhese figures do not include the numerous instances in which workplace exposures aggravate preexisting asthma, or in which high-dose, nonsensitizing, irritant exposures induce reactive airways disease. The data suggest ;hat routine clinical consideration of pos~ible work-related causes of asthma will be rewarded with the discovery of tiologic agents in the patient's workplace. Such information can result in better clinical outcomes for the asthmatic patient, and lead to primary prevention of disease in coworkers, as discussed below.
DEFINING OCCUPATIONAL ASTHMA
Occupational asthma has undergone redefinition in recent years in part because of
This work was supported in part by Grant No. R29 ES 06538 and Grant No. SCOR HL 27353 from the National Institutes of Health.
the recognition that both sensitizers and irritants can induce reactive airways disease. Operationally, occupational asthma can be considered "a disease characterized by variable airflow limitation and/or airway hyperresponsiveness due to causes and conditions attributable to a particular occupational envirorunent and not to stimuli encountered outside the workplace."10 The definition embraces two major types of occupational asthma: (1) the "classical" sensitizer-induced forms of occupational asthma, which usually occur following a latent period of exposure to either a high or low molecular weight antigen in the workplace 411; and (2) irritant-induced asthma resulting from exposure to workplace irritants, one form of which has been labeled the reactive airways dysfunction syndrome (RADS) .22-24, 98, 166 Regardless of mechanisms or inciting agent, the final common pathway is a pattern of respiratory embarassment that is clinically indistinguishable from nonoccupational asthma, unless the clinician engages actively in a series of steps that will reveal a link to the work environment.
WHY DIAGNOSE OCCUPATIONAL ASTHMA?
Detection of environmental and specific occupational causes of asthma can change the
From the Occupational and Environmental Medicine Division, National Jewish Center for Immunology and Respiratory Medicine, and Departments of Medicine and Preventive Medicine and Biometrics, Division of Puhnonary and Critical Care Medicine, University of Colorado School of Medicine, Denver, Colorado
CLINICS IN CHEST MEDICINE
VOLUME 16 - NUMBER 4 - DECEMBER 1995
621
622 NEWMAN
clinical outcome for the individual patient. 120 The best treatment of occupational asthma is removal from exposure. Removal of asthmatic patients from inciting occupational allergens can improve or even cure asthma, especially if the disease is diagnosed promptly and the exposure is eliminated early in the course of the disease .49, 91 Persistent exposure to causative agents in the workplace can result in increased need for medication, hospitalization, reduced quality of life, permanent impairment, and death .2, 68, 115, 137, 170 In fact, clinical deterioration is the rule when patients remain exposed after asthma has been diagnosed. More than half of all patients with occupational asthma will have persistent symptoms even years after cessation of exposure, especially when removal from exposure has been delayed. Prognosis is worst for those with the longest duration of exposure before onset of symptoms, longest duration of symptoms before correct diagnosis, and for those with the most severe disease at the time of initial diagnosis (i.e., lowest forced expiratory volume in 1 second [FEV,I, greatest airways hyperresponsiveness).
Detection of occupational causes of asthma can prevent disease from occurring in large numbers of other workers at risk. When a case of occupational asthma is treated by the physician as a "sentinel health event"152 that leads to an investigation of the workplace, other cases of disease will be discovered.170 By consulting with occupational and environmental medicine specialists, the pulmonologists, allergists, and primary care physicians can turn a single case of occupational asthma into a watershed of disease detection and disease prevention for an entire company or industry. 155 Following the diagnosis of even a single case, evaluation of the patient's industry can lead to identification of the causative agent(s), identification of other affected workers, elimination of hazardous substances, improvement in ventilation, and other changes in work practices that reduce the risk of asthma for the entire workforce.
COMMON CAUSES OF
OCCUPATIONAL ASTHMA
Tables I through 3 summarize many of the commonly recognized agents and workplaces associated with occupational asthma. For a more complete listing of presently recognized causes, readers are encouraged to consult one
of several recent references.43, 50, 131 Armed with a general sense of high-risk professions and high-risk exposures, the physician can ask more targeted questions about occupational cause while eliciting the history of present illness.
In collecting the asthmatic patient's occupational history, consider six major categories of agents that can incite asthma:
High Molecular Weight
1. animals, shellfish, fish, arthropods
2. wood, plants, vegetables
3. enzymes and pharmaceuticals
Low Molecular Weight
4. chemicals (including solder fluxes, dyes)
5. metals
Irritants
6. dusts, fumes, gases
Using this simple outline, it is possible to quickly screen any asthmatic patient for potential exposures in the workplace that may be related to the onset of asthma.
DIAGNOSTIC TOOLS
History
The occupational history is the key tool in the assessment of patients with possible work-related asthma. There are three goals in collecting the occupational history: (1) to generate a list of past and present jobs, especially those jobs that coincide with the onset of asthma symptoms; (2) to outline past and present work practices and exposures, including estimates of the extent of exposure; and (3) to assess the likelihood that the asthma condition and the patient's work are linked. Several researchers have published occupational history questionnaire templates. Patients can be asked to complete a simple questionnaire that collects much of the occupational history, offering reliable and valid information without sacrificing physicianpatient contact time.', 60, 73, 109, 151
Particular attention to the occupational history is warranted in examining asthmatics who are welders, electronics assemblers, laboratory technicians, metalworkers, plastics industry workers, bakers, chemical processors, automobile and other spray painters, based on data showing higher incidence of asthma among workers in these trades .125 Knowledge
OCCUPATIONAL ASTHMA 625
Table 3. SELECTED EXAMPLES OF IRRITANT EXPOSURES CAUSING OCCUPATIONAL ASTHMA
Agent Occupation Reference
Chlorine Gas leak; pulp mill workers 64, 166,99
Diesel exhaust Railroad workers 176
Fire smoke Accidental fire 23
Glacial acetic acid Accidental spill 101
Hydrazine Power plant workers 23
Hydrochloric acid Pool cleaners 18, 166
Hydrogen sulfide Argicultural workers 63
Paints Spray painters 24,23, 166
Perchlorethylene Dry cleaners 18
Sulfuric acid House cleaning 18
Toluene diisocyanate Painting 112, 166
Uranium hexafluoride Chemical plant workers 23
Welding fumes Welders 23, 166, 108
periods, he or she may lose the pattern of reversibility that many physicians like to rely on to document work-related asthma. Improvement away from work is usually found at the start of the illness only, if at all. A common mistake made by clinicians is to assume that because the symptoms do not improve away from work, the asthma must not be work-related. This error can have dire consequences for the continually exposed asthmatic worker. Exposure of an asthmatic patient to an agent that is known to cause asthma should be considered sufficient to trigger further investigation of cause, even in the absence of a clear work-related pattern.
A number of clues may improve the predictive value of the occupational history in asthmatics: (1) recognition of high-risk jobs, discussed above; (2) asking the patient about symptomatic coworkers or coworkers who have left the job because of respiratory health; (3) other organ involvement such as rhinitis, conjunctivitis, dermatitis, or urticaria in workers exposed to high-molecular-weight compoundS47, 11; (4) unusual events at the time of onset of symptoms, such as a new job assignment, use of a new chemical, or temporal association with accidental exposures to irritants; and (5) failure of the disease to respond to conventional asthma therapy, suggesting possible ongoing exposure to an environmental or occupational trigger.
What about personal risk factors for occupational asthma? Are there factors of individual susceptibility that help explain why some exposed individuals get asthma while others do not? Because many cases of occupational asthma are mediated at least in part by specific immunoglobulin E (IgE) antibodies, investigators have studied the role of prior
atopy as one risk factor for occupational asthma. The data suggest that atopy is a risk factor only for those who will be exposed to high-molecular-weight antigens and is not a risk factor for development of other forms of occupational asthma. For example, there is a high prevalence of skin-test proven atopy among laboratory handlers who develop occupational asthma '1511, 171 whereas there is no increased prevalence of atopy among asthmatics who respond to the low-molecularweight antigen in Western red cedar .49 In a study of nonsensitizing occupational asthma, irritant-induced asthma patients were less likely to be atopic (20%) than were other asthma controls (58%).166 Even though prior atopy appears to be a risk factor for highmolecular-weight antigen-induced asthma, it should not be used to exclude workers from employment. The positive predictive value of atopy for occupational asthma is far too low to recommend its use in hiring and placement practices at work. 158, 1711, 174AIlergy skin tests should not be used to exclude workers from high-risk occupations. It is better to prevent asthma by controlling the environment rather than excluding "susceptible" workers. It may, however, be helpful to know a person's atopy status to help counsel employees that they may be at a statistically higher risk of developing asthma on the job, to encourage them to use appropriate precautions to minimize their exposure to high-molecular-weight antigens, and to monitor such workers more carefully for early signs of asthma.
Tobacco smoke may act synergistically with atopy to increase the risk of occupational asthma. Tobacco smoke has been shown to increase the chances of developing specific IgE antibody and asthma in the workplace.
626 NEWMAN
In a study of workers exposed to tetrachlorophthalic anhydride, a greater proportion of those with specific IgE antibody to this compound were smokers compared with those who lacked the specific antibody. 173 Similar results were observed in response to ispaghula, green coffee bean, and ammonium hexachloroplatinate.111, 186 In a study of sawmill workers exposed to Western red cedar, however, smoking was not associated with asthma risk .49 Tobacco smoking may contribute to the risk of irritant-induced asthma based on the finding of higher numbers of current smokers in this group compared with other asthmatics .166
Although it may seem logical to expect patients who have preexisting airways hyperreactivity to be at higher risk of developing occupational asthma, two prospective studies suggest that this is not the case. Workers with and without prior nonspecific hyperresponsiveness were equally likely to develop occupational asthma in a study of toluene diisocyanate manufacturing workerS33 and in a study of Western red cedar workers .47
In many circumstances, a good occupational history may be sufficient to reasonably exclude the diagnosis of occupational asthma .122 When the occupational history raises the suspicion of occupational cause, there are two major courses of action that may be taken to lend greater specificity to the diagnosis. These include (1) investigation of the exposure /workplace and (2) assessment of the airways response to the workplace or to putative workplace antigens.
Exposure Assessment
Most pulmonologists are not experienced in the practice of occupational medicine or in the documentation of occupational exposure, and may choose to enlist the aid of an occupational /environmental medicine consultant in examining the relationship of a patient's disease to a specific workplace. Occupational medicine physicians often conduct a "walkthrough" of the patient's workplace. By coordinating efforts with other health and safety professionals, they may collect industrial hygiene data on the nature and extent of exposures and use epidemiologic methods to study the workforce for the presence of similar symptoms.
Short of a visit to the workplace, there are other steps the treating physician can take to
assess the types of exposures encountered by the patient. Material Safety Data Sheets (MSDS) include information such as the names and chemical constituents of products used by the worker. MSDS list many of the recognized health hazards and recommended precautions for handling the product. These information sheets are available to workers in many industries in the United States, as mandated by the Occupational Safety and Health Administration (OSHA). Unfortunately, it is not always possible to find the "smoking gun" among a stack of MSDS because the listing of a toxic compound does not necessarily prove that it is the cause of the illness. It should, however, reinforce the need for further investigation and may provide some reasonable working hypotheses that guide further testing.
Discussing work conditions with the patient's employer, on-site health professionals, health and safety officer, or labor representative can be helpful, but the physician should be certain to obtain patient consent and not jeopardize patient confidentiality. Physicians can contact OSHA or the National Institute for Occupational Safety and Health (NIOSH) for assistance. Under some circumstances, such an inquiry by a physician will prompt these agencies to investigate the potential respiratory hazards in the patient's company.
Temporary work restrictions may help confirm the relationship of the workplace to asthma if performed early in the illness and if adequate objective measures of disease severity are used both before and after removal. Well-documented improvement following a trial removal or restriction may prove that the workplace caused or aggravated the disease. Failure to improve should not be taken as absolution of the workplace. Unless the patient has severe asthma, we generally advise him or her not to quit working until the diagnosis is either excluded or confirmed by additional testing and investigation.
Physiologic Assessment
Pulmonary Function Testing
Although this may sound obvious, the diagnosis of asthma should be confirmed before investigating occupational causes. In our Occupational and Environmental Lung Disease Clinic at National Jewish Center, we fre
OCCUPATIONAL ASTHMA 625
Table 3. SELECTED EXAMPLES OF IRRITANT EXPOSURES CAUSING OCCUPATIONAL ASTHMA
Agent Occupation Reference
Chlorine Gas leak; pulp mill workers 64, 166,99
Diesel exhaust Railroad workers 176
Fire smoke Accidental fire 23
Glacial acetic acid Accidental spill 101
Hydrazine Power plant workers 23
Hydrochloric acid Pool cleaners 18, 166
Hydrogen sulfide Argicultural workers 63
Paints Spray painters 24,23,166
Perchlorethylene Dry cleaners 18
Sulfuric acid House cleaning 18
Toluene diisocyanate Painting 112, 166
Uranium hexafluoride Chemical plant workers 23
Welding fumes Welders 23, 166, 108
periods, he or she may lose the pattern of reversibility that many physicians like to rely on to document work-related asthma. Improvement away from work is usually found at the start of the illness only, if at all. A common mistake made by clinicians is to assume that because the symptoms do not improve away from work, the asthma must not be work-related. This error can have dire consequences for the continually exposed asthmatic worker. Exposure of an asthmatic patient to an agent that is known to cause asthma should be considered sufficient to trigger further investigation of cause, even in the absence of a clear work-related pattern.
A number of clues may improve the predictive value of the occupational history in asthmatics: (1) recognition of high-risk jobs, discussed above; (2) asking the patient about symptomatic coworkers or coworkers who have left the job because of respiratory health; (3) other organ involvement such as rhinitis, conjunctivitis, dermatitis, or urticaria in workers exposed to high-molecular-weight compoundS47, -11; (4) unusual events at the time of onset of symptoms, such as a new job assignment, use of a new chemical, or temporal association with accidental exposures to irritants; and (5) failure of the disease to respond to conventional asthma therapy, suggesting possible ongoing exposure to an environmental or occupational trigger.
What about personal risk factors for occupational asthma? Are there factors of individual susceptibility that help explain why some exposed individuals get asthma while others do not? Because many cases of occupational asthma are mediated at least in part by specific immunoglobulin E (IgE) antibodies, investigators have studied the role of prior
atopy as one risk factor for occupational asthma. The data suggest that atopy is a risk factor only for those who will be exposed to high-molecular-weight antigens and is not a risk factor for development of other forms of occupational asthma. For example, there is a high prevalence of skin-test proven atopy among laboratory handlers who develop occupational asthma,'-58, 171 whereas there is no increased prevalence of atopy among asthmatics who respond to the low-molecularweight antigen in Western red cedar.49 In a study of nonsensitizing occupational asthma, irritant-induced asthma patients were less likely to be atopic (20%) than were other asthma controls (58%).166 Even though prior atopy appears to be a risk factor for highmolecular-weight antigen-induced asthma, it should not be used to exclude workers from employment. The positive predictive value of atopy for occupational asthma is far too low to recommend its use in hiring and placement practices at work. 1,58,170, 174AIlergy skin tests should not be used to exclude workers from high-risk occupations. It is better to prevent asthma by controlling the environment rather than excluding "susceptible" workers. It may, however, be helpful to know a person's atopy status to help counsel employees that they may be at a statistically higher risk of developing asthma on the job, to encourage them to use appropriate precautions to minimize their exposure to high-molecular-weight antigens, and to monitor such workers more carefully for early signs of asthma.
Tobacco smoke may act synergistically with atopy to increase the risk of occupational asthma. Tobacco smoke has been shown to increase the chances of developing specific IgE antibody and asthma in the workplace.
i
OCCUPATIONAL ASTHMA 629
occupational asthma have been successfully pinpointed using serologic assays include Pepys' work with B. subtilis proteolytic enzyme, 14-1 murine urine proteins," grain storage miteS,92 and JOCUStS.1611 Low molecularweight compounds may serve as haptens, combining with endogenous proteins. Examples in which hapten-protein-specific antibodies have been identified include asthma due to the anhydrides90, 114, 185 and to reactive dyes."' The use of assays of antigen-specific cell-mediated immune responses have been studied to only a very limited extent and as yet have no clinical application. The immunologic mechanisms and tests available for diag nosing occupational asthma have been re_ viewed elsewhere. 129
Demonstration of specific antibody indicates sensitization, but this can occur in exposed persons without asthma or other allergic symptoms. In general, the rates of falsenegative results and false-positive results from in vitro immunologic assays in occupational asthma limit their usefulness in clinical practice. Prick skin testing has been used to identify sensitivity to high molecular weight antigens. But a positive response on skin testing only confirms exposure and sensitization. Some individuals can react positively on skin test and not demonstrate antigen-specific asthma. It has been suggested that combining prick testing with measurement of nonspecific airways hyperreactivity is an effective way of documenting antigen-specific occupational asthma, when an allergic mechanism is operative. 121
Skin tests are of lower efficacy in the assessment of the response to low molecular weight antigens because many of these must be conjugated to other proteins, may act as skin irritants, and thus have higher rates of false negativity and of false positivity, if not prepared and applied by experienced personnel.
Given the present state of the art of immunologic testing for occupational asthma, such testing should be reserved for investigative purposes, principally. When used to aid in diagnosis, use a laboratory that specializes in these assays. Close attention must be paid to the laboratory's data concerning the reliability, reproducibility, and validity of their methods. These tests may be helpful in identifying that portion of patients with occupational asthma due to known allergens, especially proteins, but with the caveat that both positive and negative results must be inter-
preted with caution and within a broader clinical context.
MANAGEMENT
Occupational asthma is managed like other forms of asthma, but with one major difference: exposure must cease. Medication use should follow the same guidelines as for other cases of reactive airways diseaseattending to the inflammation and bronchoconstriction. In rare circumstances, immunotherapy may be used as an adjunct in treatment. But paramount in the management of these cases is the removal from exposure. Any patient with immunologically mediated occupational asthma should be advised to avoid further exposure to the causative agent or work environment. In an excellent demonstration of the importance of exposure avoidance, Pisati and colleagues'-"' recently studied the medical outcomes for a group of patients with toluene diisocyanate-induced asthma, some of whom remained in exposure. Despite use of respiratory protection, the 17 workers who remained assigned to jobs that had only an occasional risk of exposure to the chemical showed significant clinical deterioration in FEV, and PC15 for methacholine, compared with 43 workers who were no longer exposed. The workers who had ongoing potential exposures experienced more symptoms, required more medication, and were considered clinically unstable. No worker who had been exposed to isocyanates for more than 10 years or who continued to work for more than 3 years after onset of asthma recovered. This work emphasizes the need to recognize occupational asthma early and to stop all exposure.
Respiratory protection with masks should not be considered an acceptable means of controlling exposure in patients with occupational asthma. Masks may increase the work of breathing, dead space ventilation, and resistance to airflow. Furthermore, none are completely protective, so in the case of a sensitizing exposure, there may still be sufficient exposure to produce symptoms, even when a respirator is worn. With this false sense of security, the patient may be returned to work and continue to be exposed to sensitizers that perpetuate the asthmatic response. When the patient's residual asthma is relatively mild and exposures are irritants not allergens, it may be possible to return to work with respi
NHWMAN
ratory protection, if this is a worker's only "option." This choice is far from optimal when considering the health of both the individual and the larger population of similarly exposed individuals.
Patients require advice from their physicians concerning placement in other areas of the workplace and concerning the hazards of future exposure to the causative dust or fume. The physician has the responsibility to communicate his or her findings to the patient and to the employer with a statement of specific restrictions needed to eliminate ongoing exposure. When doing so, the clinician should state clearly what the restrictions are (e.g., not allowed in the building with the paint booth), and for how long that restriction will be in place (e.g., permanent, or if temporarv, how many weeks on restricted duty). Und~r most circumstances of allergically mediated occupational asthma, the patient should be considered 100% permanently impaired for the specific job that caused the illness or for other jobs with the same exposure .2 Consideration should be given to relocating the worker to a different area of the plant or to a different plant, rehabilitation into a new form of employment, or in some cases, early retirement. Sometimes modification of the job through improved ventilation, change in the industrial process, or substitution of less hazardous substances may enable the patient to continue to perform the job.
When a case of occupational asthma is confirmed, the physician should advise the patient that in the United States this is considered a work-related illness and that they are entitled to file for workers' compensation. In the United States, aggravation of preexisting asthma qualifies the patient for workers' compensation as well. Compensation will help cover medical expenses related to the illness, lost wages, and loss of future wage earning potential due to the occupational condition. Physicians may be called on to assess whether the patient has reached "maximal medical improvement." This is the point in time after which it is unlikely that the patient will improve further. At that juncture, the physician will be asked to assess the level of permanent impairment that has resulted from the occupational asthma. This rating of impairment can range from 0%, if the patient has fully recovered and has no persistent airways hyperreactivity, to 100% impairment for the most severe, debilitating asthma. Guidelines for assessing impairment have been recently pub-
lished by the American Thoracic Society.2 These guides take into account (1) the postbronchodilator FEV,; (2) the degree of airway hyperresponsiveness or reversibility of FEV,; and (3) the minimum medication need of the patient. Most patients with occupational asthma will be left with some degree of permanent impairment based on studies showing that 60% to 90% of subjects fail to recover after leaving exposure.44 Although most do not recover fully, partial recovery can occur for up to 2 years after cessation of exposure. For this reason, it is advisable to wait 2 years before declaring the patient to be maximally medically improved and assigning an impairment rating.118
PREVENTION
Irritant-induced Asthma
Single exposures or multiple exposures to irritants can induce occupational asthma. In its most obvious form-following a high-level irritant exposure-this condition has been called RADS '23 although more recent data suggest that even less severe conditions of exposure can induce airways hyperreactivity.98, 101, 187 Most investigators consider the irritant-induced disease to occur sporadically, following accidents in the workplace, but there are still many unknowns. We do not know how frequently irritants cause asthma. We do not understand the extent to which chronic, lower levels of irritant exposure cause airways hyperreactivity.19, 98 Until more population-based prospective studies are done to examine both exposure and the response of the airways, preventive strategies should focus on encouraging patients and industries to minimize the risk of accidental exposure and reduce chronic exposures to dust, fumes, and gases to the lowest levels reasonably achievable. Alert physicians who identify new cases of irritant-induced asthma should recommend removal of patients from ongoing exposure to irritants and help trigger workplace investigation to (1) identify other affected individuals in need of treatment and (2) rectify hazardous work conditions.
Immunologically Mediated
Occupational Asthma
We have discussed above the secondary preventive strategies in the management of
occupational asthma. But to prevent this dis
ease from ever occurring, it is necessary to
prevent sensitization. Industry has the obliga
tion to reduce exposure to allergens in the
workplace. Appropriate design of new plants,
ventilation controls, safe work practices, sub
stituting nonsensitizing for sensitizing mate
rials, appropriate environmental monitoring,
educating workers about potential hazards
and the early warning signs of asthma are
some of the ways in which workplace aller
gen exposure can be reduced and disease can
be prevented. Occupational medicine and
other health and safety professionals empha
size the need to eliminate exposure, substitute
safer materials, isolate or enclose risky pro
cesses, improve housekeeping practices, and
take other measures to make the workplace
safe. What is the clinician's role? If working
with industry to screen workers, the physi
cian can use routine health surveys, monitor
lung function, and consider the use of immu
nologic markers of exposure. Although po
tentially helpful in identifying disease at early
stages, these medical monitoring tools are less
effective than working toward avoidance of
exposure in the first place. Recognition of
potentially hazardous allergens in a work
place or of a case of occupational asthma
should lead physicians to educate workers
and employers concerning the importance of
eliminating exposure.
We will succeed at stemming the tide of
occupational asthma only through improved
disease surveillance and when physicians rec
ognize occupational asthma when they see it.
Our goal as clinicians should be to work with
industry, labor, governmental agencies, and
specialists in the field of occupational health
to prevent disease through earlier identifica
tion of old and new hazards. Treat each pa
tient with occupational asthma as a "sentinel
event." Seek consultation with those who can
help initiate the cascade of events that will
improve workplace conditions and will take
all patients out of jeopardy.
ACKNOWLEDGMENT
The author thanks Nina Eads for her expert secretarial
assistance.
References
1. American College of Physicians: Occupational and
environmental medicine: The internist's role. Ann 22
Intern Med 113:974-982, 1990
OCCUPATIONAL ASTHMA 631
2. American Thoracic Society: Guidelines for the evaluation of impairment/ disability in patients with asthma. Am Rev Respir Dis 147:1056-1061, 1993
3. Alanko K, Keskinen H, Bjbrkst6n F, et al: Immediate-type hypersensitivity to reactive dyes. Clin Allergy 8:25-31, 1978.
4. Andrasch RH, Bardana Ej, Koster F, et al: Clinical and bronchial provocation studies in patients with meatwrappers' asthma. J Allergy Clin Immunol 58:291-298, 1976
5. Asai A, Shimoda T, Hara K, et al: Occupational asthma caused by isonicotinic acid hydrazide (INH) inhalation. J Allergy Clin Immunol 80:578-582, 1987
6. Bar-Sela S, Teichtahl H, Lutsky 1: Occupational asthma in poultry workers. J Allergy Clin Immunol 73:271-275, 1984
7. Bardy JD, Malo JL, S6guin P, et al: Occupational asthma and IgE sensitization in a pharmaceutical company processing psyllium. Am Rev Respir Dis 135:1033-1038, 1987
8. Baur X, Fruhmann G, Haug B, et al: Role of aspergillus amylase in bakers' asthma. Lancet 1:43, 1986
9. Baur X, Konig G, Bencze K, et al: Clinical symptoms and results of skin test, RAST and bronchial provocation test in thirty-three papain workers: Evidence for strong immunogenic potency and clinically relevant "proteolytic effects of airborne papain." Clin Allergy 12:9-17, 1982
10. Berstein IL, Bernstein DI, Chan-Yeung M, et al: Definition and classification of asthma. In Bernstein IL, Chan-Yeung M, Malo J-L, et al (eds): Asthma in the Workplace. New York, Marcel Dekker, 1993, pp 1-4
11. B6rub6 D, Cartier A, L'Archev6que J, et al: Comparison of peak expiratory flow rate and FEV, in assessing bronchomotor tone after challenges with occupational sensitizers. Chest 99:831-836, 1991
12. Blainey AD, Ollier S, Cundell D, et al: Occupational asthma in a hairdressing salon. Thorax 41:42-50, 1986
13. Blainey AD, Topping MD, Ollier S, et al: Allergic respiratory disease in grain workers: The role of storage mites. J Allergy Clin Immunol 84:296-303, 1989
14. Blanc PD, Trainor WD, Lim DT: Herbal tea asthma. Br J Ind Med 43:137-138, 1986
15. Block G, Chan-Yeung, M: Asthma induced by nickel. JAMA 247:1600-1602,1982
16. Block G, Tse KS, Kijek K, et al: Baker's asthma. Clin Allergy 13:359-370, 1983
17. Bohner CB, Sheldon JM, Trenis JW: Sensitivity to gum acacia, with a report of ten cases of asthma in printers. J Allergy 12:290-294, 1941
18. Boulet LP: Increases in airways responsiveness following acute exposure to respiratory irritants. Chest 94:476-481, 1988
19. Brain JD, Pikus AA, Greaves IA: Asthma and airway reactivity. In Brain JD, Beck BD, Warren Aj, et al (eds): Variations in Susceptibility to Inhaled Pollutants. Baltimore, The Johns Hopkins University Press, 1988, pp 159-181
20. Brooks SM: Bronchial asthma of occupational origin: A review. Scand j Work Environ Health 3:53-72, 1977
1. Brooks SM, Baker DB, Gann PH, et al: Cold air challenge and platinum skin reactivity in platinum refinery workers. Chest 97:1401-1407, 1990
Brooks SM, Bernstein IL: Reactive airways dysfunction syndrome or irritant induced asthma. In Bern
In Reply to: occupational asthma posted by MAI on July 26, 2000 at 01:39:50:
Thanks, MAI.
Walt
In Reply to: Re: occupational asthma (Archive in Multiple Chemical Sensitivity.) posted by Walt Stoll on July 27, 2000 at 11:00:38:
Being one who had an occupational exposure to chemicals I
will have to read this to see if I can learn anything new. I
don't classify my problem as Asthma since it was a one time
exposure that burned my lungs and I believe could have been
more than the copy machine ink in a open trough in my small
unventilated office and the heating/AC system that used to
have too much air flow usually had been adjusted to a more
normal flow Plus it was between seasons so heat and AC
wasn't coming on so fumes built up in the room but an ope
dropped ceiling panel was open because of a roof leak and
though it made breathing easier allowing more air flow it
may have let something else in that caused a much worse
problem. I have wondered if someone mixed bleach and ammonia
accross the hall in that got in but also one previous worker
in the office had violent reactions to stress when visiting
and if a boss complained about something he would throw
whatever was in his hand and i was old when he worked in
there he would holler and curse and kick the tempermental
large copy machine. Another former worker was a heavy
drinker and drank at lunch and after work so possibly the
normal fumes from the ink just made him high.
I fixed the problems that made the machine malfunction
with anything like rubberbands and swapping parts from areas
not needed or critical. The inital MSDS's said the ink was
a 2 part mix with toluene in it and then they came up with a
single sheet saying it had naptha so i think they did a
little slight of hand. I had a sample of the ink and gave it
to my lawyers to have it tested and they Gave it to One of
the Co's they were sueing to test. I hit the roof and requested a
meeting with the judge and he said That was fine or normal
so I figured i was geting screwed. i had not given my lawyer
all the ink but the container must have not sealed and the
rest evaporated so I doubt I could have proved much. I just
hope everyone made money or saved it. I always Liked
challenges and I got a BIG one. Much harder to do what and
like to but Still trying....
VF
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