- Email: [email protected]
The Association Between Occupation and Asthma in General Medical Practice
The Association Between Occupation and Asthma in General Medical Practice* Paul D. Blanc, MD, MSPH, FCCP; Mark D. Eisner, MD; Leslie Israel, DO, MPH; and Edward H. Yelin, PhD
Background: In general practice settings, the proportion of adult asthma attributable to occupational factors is not known. Objective: The goal of this study was to estimate the proportion of adult asthma cases that can be attributed to occupational factors initiating new disease onset and exacerbating preexisting disease. Methods: We performed a cross-sectional analysis of interview data for 150 adults with asthma recruited from a random sample of family practice specialists. We ascertained the asthma and work histories of the subjects and estimated the proportion with likely work-initiated asthma and work-related asthma recrudescence. Results: Seventy-four subjects (49%) reported adult-onset asthma while employed; an additional 25 (17%) reported recrudescence of previously quiescent childhood-onset asthma during employment. Of those with new-onset asthma while employed, 15 (10% of the study group; 95% confidence interval, 5 to 15%) were employed in occupations at increased risk of occupational asthma initiation on the basis of an independent job scoring matrix. Of those with asthma recrudescence in adulthood, seven (5% of the study group; 95% confidence interval, 2 to 8%) were employed in occupations at increased risk of exposures aggravating asthma. Conclusions: Among adults with asthma treated in general practice settings, > 1 in 10 patients has a work history strongly suggestive of a potential relationship between exposure and disease. (CHEST 1999; 115:1259 –1264) Key words: asthma; disability; occupational disease; work-related Abbreviations: CI 5 confidence interval; SF-36 5 Medical Outcomes Study Short-Form Health Survey
general medical practice, many illnesses may be I noccupationally related, but this cause may not be recognized.1 As a result, there have been few reliable estimates of the proportion of work-related conditions encountered in primary care settings. A 1993 survey of 101 consecutive male general medical hospital admissions identified 42 patients with dis*From the Division of Occupational Medicine (Drs. Blanc and Israel), the Arthritis Research Group (Dr. Yelin), Department of Medicine, and the Cardiovascular Research Institute (Dr. Eisner), University of California at San Francisco, San Francisco, CA. Manuscript received October 2, 1998; revision accepted December 15, 1998. Supported in part by National Heart, Lung, and Blood Institute Research Career Development Award K04 HL03225 (Dr. Blanc), National Research Service Award F32 HL10054 (Dr. Eisner), NHLBI R01 HL56348 (Drs. Blanc, Eisher, and Yelin), and National Institute for Occupational Safety and Health (CDC) R01 OH03480 (Drs. Blanc, Israel, and Yelin). Correspondence to: Paul Blanc, MD, MSPH, FCCP, Division of Occupational and Environmental Medicine, UCSF Box 0924, 350 Parnassus Ave, No. 609, San Francisco, CA 94143-0924; e-mail: [email protected]
eases potentially attributable to past occupational exposures.2 Earlier in this century, a 1914 survey of 1,507 male outpatient clinic admissions identified 276 persons “in which industry was either the predominating cause of ill-health or was a very important cause or was very important in treating the patient.”3 Other studies in the 80-year interval between these investigations indicate that existing surveillance mechanisms often fail to identify workrelated illness, even when the link between exposure and disease is strong.4 For example, in studies of acute toxic chemical exposures, most occupational cases are not reported through the workers’ compensation system.5,6 In a recent questionnaire survey of family practice specialists, the reported median proportion of time dealing with occupationally related health problems was 9%.7 The National Institute of Medicine has emphasized the importance of occupational health in general practice and highlighted the critical shortcomings in reliable data in this area.8 Adult asthma is a key sentinel condition for meaCHEST / 115 / 5 / MAY, 1999
1259
suring occupational morbidity.9 A wide number of workplace exposures are known to initiate asthma.10,11 Moreover, other workplace factors can aggravate existing asthma or increase the probability of disability from this condition.12 We studied occupational factors among a patient panel of adults with asthma recruited from a random sample of family practitioners. Our goal was to estimate the proportion of patients at greatest likelihood of adult-onset asthma because of occupation and those with likely work-aggravated asthma, and the associated risk of work disability.
Materials and Methods Physician Recruitment The study recruitment methods have been reported previously.13 In brief, we obtained a list of all certified American Board of Medical Specialty family practice specialists (n 5 2,041) in northern California. We randomly selected 167 physicians (8% of the total group). Of these 167, 42 (25%) did not have sufficient information for contact and an additional 19 (11%) had moved outside the area. Of the remaining 106 family practitioners, 27 (25%) were excluded because they did not work in outpatient civilian settings at least 1 full day per week. We attempted to recruit all 79 eligible family practitioners. Of these, 39 (49%) participated. Most nonparticipants cited lack of time as their reason for not participating. Because some physicians who agreed to participate did not ultimately contribute any participating subjects, the final number of participating family practice specialists was 34 (43% of the eligible pool).
puter-assisted telephone interview lasting approximately 45 min. We used the same structured baseline interview schedule previously administered to 601 subjects recruited from pulmonary and allergy specialists.14 The interview covered asthma history (medical history, symptoms, treatment), employment history, comorbidity, general health, functional status, demographic variables, cigarette smoking, and psychosocial variables. Subjects were informed that the goal of the study was to ascertain the ways in which asthma affects people’s day-to-day lives. The protocol was approved by the University of California San Francisco Committee on Human Research. Asthma History and Severity We ascertained the age of asthma onset with the following question: “How old were you when you first had symptoms or an attack of asthma?” We defined childhood-onset asthma as selfreported occurrence of first symptoms or attack before 18 years of age. We also asked the following question: “Would you say that your asthma ‘went away’ for one year or more or that you ‘outgrew it’ only to have it ‘come back’ later?” We defined recrudescent asthma as childhood disease that “went away” for at least 1 year before returning. We quantified asthma severity using a previously validated disease-specific severity-of-asthma scoring system.13–15 The score has a possible range from 0 to 28 with higher scores reflecting more severe disease. It incorporates respiratory symptoms, systemic corticosteroid use, other asthma medications, and past hospitalizations for asthma. In addition to disease-specific severity, we also quantified asthma-specific quality of life using the “Asthma Quality of Life Questionnaire” of Marks et al.16 General health status was measured with the physical and mental health component summary score measures derived from the Medical Outcomes Study Short-Form Health Survey (SF-36).17 Occupational History
Subject Recruitment Each participating family practice specialist was asked to maintain a registry of persons aged 18 to 50 years with outpatient visits for asthma during a prospective 4-week period, with an additional 4 weeks if subject recruitment numbers were less than five. Participating physicians were asked to register patients with a diagnosis of asthma on clinical grounds. Physicians were asked to exclude patients who also had diagnoses of chronic bronchitis or emphysema. We did not instruct participating physicians to restrict recruitment on the basis of patient follow-up status (new or established patients were eligible) or on the basis of other clinical factors (for example, allergic history). The recruitment methods paralleled those we have used previously to recruit adults with asthma from pulmonary and allergy subspecialty practices.13,14 Each person registered by a participating physician was contacted by mail with a description of the study. Those agreeing to participate were telephoned by the study interviewer to arrange an initial telephone survey. There were 21 persons listed who declined participation or who could not be successfully contacted. We successfully recruited 150 of 171 subjects registered (88%). The median number of subjects contributed per physician was 4 (range, 1 to 10). Interviews and Survey Instrument All subject interviews were performed by a single trained survey worker. The format was a structured, close-ended, com1260
We classified subjects on the basis of their history of ever having had part-time or more salaried employment, by which we defined any labor force participation. We then assessed the temporal relationship between labor force participation and symptomatic asthma. Some subjects gave no history of any labor force participation. The remaining subjects, all of whom had at least some history of labor force participation, fell into one of three groups. The first group comprised subjects whose asthma symptoms occurred before employment. This group includes persons with childhood-onset asthma and no remission before adulthood, as well as adult-onset asthma when the respondent was not a salaried employee at the time, for example a student or housewife. The second group comprised those with full- or part-time salaried employment at the time of their initial onset of asthma. By definition, these would be persons with adult-onset asthma. Finally, the third group comprised those with a recrudescence of previously asymptomatic asthma while employed. By definition, these would be persons with initial asthma onset in childhood followed by a remission. We used several different methods to identify subjects with potentially work-related asthma. First, on the basis of questionnaire responses to a specific list of workplace exposures, we identified those with reported job exposures to known irritants or sensitizers. These exposures included grain or flour dust, animal fur or dander, photographic chemicals, epoxies, polyurethanes, cotton dust, pharmaceuticals, sealants, refrigerants, irritant gases, fire smoke, and metal or other dusts. We have used this approach previously to identify high-risk exposures among a similar group of adults with asthma treated by subspecialists.18 We also elicited Clinical Investigations
subject-reported regular heavy physical exertion on the job (either brief or sustained), as well as subject-reported changes or extremes in temperature at work. As a second method, we used occupation as a surrogate of exposure, with broadly defined categories as surrogates of risk on an a priori basis: technicians, service, and labor (manufacturing, agriculture, and other non– white-collar labor).18 In addition to self-reported specific exposures or broad job category as a surrogate of exposures, we also used a third measure of work-related asthma risk. We did this by assigning exposure probabilities on the basis of a job matrix scheme previously developed by the Occupational Health Surveillance and Evaluation Unit of the California Department of Health Services.19 This scoring system has two matrices: one for likelihood of exposures initiating asthma de novo and the second for the likelihood of exposures worsening preexisting asthma. In each case, scores range from 1 (high likelihood) to 4 (low likelihood). We defined an occupational score of ,2.5 as high likelihood to either initiate or exacerbate asthma, depending on the matrix used. For those with any history of labor force participation, we asked whether the subject had ever changed job or job duties because of asthma symptoms or whether the subject left work entirely and attributed this to asthma. We elicited from respondents whether they had ever received workers’ compensation coverage for treatment of their asthma. We did not ask subjects directly whether they attributed their asthma to occupational factors because we did not wish to potentially affect responses to other work-related questions by raising this issue. We did, however, elicit subject responses broadly measuring self-perceived disease origin. The question was asked as follows: “What do you believe is the underlying cause of your asthma? Please choose the best answer: (1) environment or allergic causes, (2) genetics or vulnerability, (3) psychological or emotional factors, (4) multiple factors, or (5) unknown or mysterious factors.” By ascertaining self-perceived cause in this manner, we could assess potential reporting bias associated with positive responses to the specific job-exposure questions asked elsewhere in the interview. Statistical Analysis Interview data were exported into a compatible format (PCSAS) and analyzed with software (SAS; SAS Institute; Cary, NC). We calculated descriptive frequencies with their 95% confidence intervals (CIs) for labor force and work exposure variables. To calculate these 95% CIs, which give a measure of the observed proportion in terms of sampling variability, we assumed a normal distribution, except when there were # 5 observations, for which we assumed a Poisson distribution. For the former, the 95% CIs were calculated as a function of the observed proportion (p), 1 2 p, the sample size (150), and the two-tailed 0.05 t value of
1.98; for the latter, we used standard table of Poisson-distributed factors given the observed number of subjects yielding the proportion in question.20 We tested the differences in demographic and clinical asthma variables between those with initial onset or recrudescent asthma while employed and all others using the t test, x2, or, for income, the Wilcoxon rank test.
Results Of the 150 subjects studied, 130 (87%) reported at least some history of labor force participation; 106 (71%) were currently employed at the time of interview (Table 1). Two thirds of the entire study group (n 5 99) were at potential risk of work-related asthma, either reporting de novo onset of adult asthma while employed or recrudescence of childhood asthma previously in remission while employed. The ratio of subjects with new to recurrent asthma was 3:1. Table 2 compares the 99 subjects with new or recrudescent asthma temporally associated with employment with the remaining 51 subjects who did not have an association between employment status and asthma onset or recrudescence. There were no statistical differences between the groups in terms of age, sex, race, marital status, or education. Annual family income (per adult) was less in the group whose asthma symptoms preceded employment. By definition, this group includes those with no history of labor force participation and therefore no individual salary income. Although asthma severity and general health status (SF-36) were similar between the two groups, the 51 subjects whose asthma was not associated with employment status reported worse asthma-specific quality of life (higher scores indicate poorer status) (Table 2). The prevalence of potential occupationally associated asthma depended on the surrogate measure of risk used (Table 3). An estimated 10 to 11% of the entire study group were categorized as having a high likelihood of work-related new-onset asthma on the basis of job exposures, defined either by subject report or independently assigned job matrix expo-
Table 1—Labor Force Histories Among 150 Adults With Asthma in Generalist Practice Settings* Work History
n (%)
95% CI
Any labor force participation Symptomatic asthma preceding work entry Asthma symptom onset during employment Recrudescence of asthma asymptomatic since childhood De novo onset of adult asthma Currently employed Previously employed but no longer working No prior labor force participation
130 (87) 31 (21) 99 (66) 25 (17) 74 (49) 106 (71) 24 (16) 20 (13)
81–92 14–27 58–74 11–23 41–57 63–78 12–22 8–19
*All of the percentages are expressed as a proportion of the entire study group (n 5 150). CHEST / 115 / 5 / MAY, 1999
1261
Table 2—Subject Characteristics by Reported Work Status at the Time of Asthma Symptom Onset*
Demographic and Clinical Variables
Asthma Unrelated to Job Status (n 5 51)
Employed, With Recrudescent or New Asthma† (n 5 99)
p Value
Age, yr Female sex White, non-Hispanic Married or cohabitating Years of education Annual income, median Atopic history Asthma severity score SF-36 physical function SF-36 emotional function Quality-of-life score
38 6 9 40 (78) 30 (59) 30 (59) 13 6 2 $15,000 34 (67) 9.0 6 5.9 43 6 14 44 6 9 24 6 18
39 6 8 69 (70) 62 (63) 66 (67) 14 6 2 $25,000 66 (67) 9.5 6 5.3 45 6 11 45 6 8 18 6 13
. 0.5 . 0.3 . 0.7 . 0.4 . 0.2 , 0.01 . 0.9 . 0.5 . 0.3 . 0.3 , 0.05
*Values are expressed as mean 6 SD or No. (%). †Those subjects with asthma linked to employment status (n 5 99) include 74 with new-onset asthma beginning de novo as adults and 25 with past childhood asthma that was asymptomatic and then became recrudescent while employed full- or part-time (see Table 1).
sure score. Defining increased likelihood more liberally, using broadly defined occupational categories, identified 17% of the study group as likely candidates for occupationally related, new-onset asthma. A more narrow definition requiring all of these factors to be present identified 6% (95% CI, 2 to 10%) categorized as having probable new-onset workrelated asthma. Also shown in Table 3, a smaller proportion of those with adult recrudescent asthma had a probable work component: 5% on the basis of reported job exposures and 7% on the basis of job category. Defined by all of the factors studied being present, 3% (95% CI, 1 to 7%) were likely to have had a work-related asthma recrudescence. As a measure of reporting validity, we directly compared job-associated exposures based on a sub-
ject’s report of irritant or sensitizer job exposure (17 among those with new-onset asthma while employed and 8 among those with recrudescence, yielding 25 in total or 17% of the study group) or defined on the basis of an independent job matrix sore (15 among those with new asthma and 7 among those with recrudescence, yielding 22 or 15% of the group) (Table 3). Assigned exposure based on job matrix attribution was strongly associated with a subject’s self-report, both among the 74 with new-onset asthma (p , 0.001) and among the 25 with recrudescent disease (p , 0.001). Of 150 subjects, 69 (46%) attributed the sole cause of their asthma to allergic or environmental factors. This self-attribution was not associated with subjectelicited responses linking the onset or recrudescence of asthma to employment status (n 5 99) as com-
Table 3—Prevalence of Potentially Work-Attributable Asthma Among 150 Adults With Asthma Asthma History New-onset asthma while employed (n 5 74) Reported irritant or sensitizer job exposure Increased risk by job matrix score* Technician, service, labor All of the above risk factors Any of the above risk factors Recrudescence of asthma while employed (n 5 25) Reported irritant or sensitizer job exposure Increased risk by job matrix score* Technician, service, labor Reported physical exertion on job Reported temperature changes on job All of the above risk factors Any of the above risk factors
n (%)
95% CI
17 (11) 15 (10) 25 (17) 9 (6) 31 (21)
6–16 5–15 11–23 2–10 14–27
8 (5) 7 (5) 10 (7) 13 (9) 4 (3) 4 (3) 15 (10)
2–9 2–8 3–11 4–13 1–7 1–7 5–15
*Increased risk by job matrix defined as score , 2.5 over range of 1 to 4. A lower score was defined as the highest likelihood of exposure initiating asthma de novo (job matrix for de novo asthma) or as the highest likelihood of aggravating asthma (job matrix for recrudescent asthma). 1262
Clinical Investigations
pared with all others (n 5 51) (45% vs 47%; p . 0.9). Within the group of 99 subjects with work-associated asthma, there was no association between an allergic or environmental self-attribution and subject-reported irritant or sensitizer job exposures (44% vs 46%; p . 0.9). There were only two subjects who reported leaving work altogether because of their asthma and a third subject who reported an asthma-related change in work activities at the same job. Therefore, of 130 with any history of labor force participation, 3 (2.3%) reported some degree of asthma-related work disability. An additional three subjects, none of whom reported current work disability, reported receiving workers’ compensation coverage for at least some of their asthma care. Of the 99 subjects who reported that their asthma began or recrudesced while employed, 13 (13%) were no longer employed at the time of the baseline interview.
Discussion In a cohort of adults with asthma assembled from a community-based sample of family practice specialists, we observed that a temporal link between employment status and new or recrudescent asthma was frequently reported. We also found that job exposures known to be associated with increased risk of asthma onset or exacerbating preexisting asthma were frequent, whether from subject report or independently assigned on the basis of a risk matrix. Using a job exposure matrix, which may be a conservative measure, 10% of the 150 subjects had adult-onset asthma likely to have been occupational in origin, whereas another 5% had high probability of work-related asthma recrudescence. These data support and amplify our previous estimate of the frequency with which adult asthma morbidity may be attributable to workplace factors. Using a similar analytic strategy, we have previously estimated the attributable fraction of work-related asthma among a cohort of adults recruited from the practices of pulmonary and allergy subspecialists.18 In that cohort, 46% of the subjects had new adultonset asthma while employed, and 13% reported exposure to asthma-associated sensitizers or irritants. These are similar to the estimates we report here for subjects recruited from general as opposed to subspecialty practices. Similar potential limitations would apply to both the current and previous analyses. Although the asthma diagnosis was physician dependent, the data collected on age of asthma onset and its relationship to employment status were subject dependent. Recall bias may have affected ascertainment of expo-
sures, although the proportion of those who believed that their asthma was caused by allergies or the environment did not differ by employment or by job exposure status. Moreover, self-reported exposures were consistent with exposure assigned independently through a job risk matrix. Although our earlier estimates could have been affected by subspecialty referral patterns, the use of subjects treated by physicians in primary care practices strengthens generalization to adults followed in other primary care settings. We cannot exclude, however, the potential for selection bias from the factors that may have been associated with willingness to participate among the physicians who joined the study, if these, in turn, are also linked to a systematically different patient population in terms of occupational risk. Our estimates are consistent with a variety of analyses that have used heterogeneous approaches to estimating etiologic fraction or population-attributable risk percentage for occupationally related asthma among adults with asthma. Although these estimates vary widely, many fall within a 7 to 15% range.21–33 In general, estimates of work attribution have been limited to de novo asthma onset rather than work-related asthma exacerbation or recrudescence. In one relevant community-based study, 5 of 43 cases (12%) of recrudescent adult asthma were identified as likely to be work-related.34 Work as a factor in worsening asthma is particularly relevant to asthma-related work disability. In the current study, only 2 of 130 patients with past labor force participation attributed employment cessation to asthma. This is lower than the 7% disabled proportion we observed among our subspecialist cohort.11 Part of this difference may be consistent with the greater degree of illness severity in the subspecialist group.13 We cannot exclude the possibility that some subjects who ceased employment after the onset or recrudescence of asthma did so in part because of the condition without attributing this change in work status to reasons of health. Although work-associated asthma may be common, there appear to be few obvious demographic or clinical features distinguishing those with a temporal association between their disease and employment status. These findings underscore the critical importance of a targeted occupational history in the evaluation of all adults with asthma. Without such an assessment, the link between exposure and newonset or worsening disease cannot be established.35
References 1 Landrigan PJ, Baker DB. The recognition and control of occupational disease. JAMA 1991; 266:676 – 680 CHEST / 115 / 5 / MAY, 1999
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2 Brancati FL, Hodgson MJ, Karpf M. Occupational exposures and diseases among medical inpatients. J Occup Med 1993; 35:161–165 3 Edsall DL. The relation of industry to general medicine. Boston Med Surg J 1914; 171:659 – 662 4 US Congress, House of Representatives, Committee on Government Operations. Occupational illness data collection: fragmented, unreliable, and seventy years behind communicable disease surveillance. Report 98 –1444. Washington DC: US Congress, 1984 5 Blanc PD, Rempel D, Maizlish N, et al. Occupational illness: case detection by poison control surveillance. Ann Intern Med 1989; 111:238 –244 6 Blanc PD, Maizlish N, Hiatt P, et al. Occupational illness and the poison control center: referral patterns and service needs. West J Med 1990; 152:181–184 7 Goodwin P, Wall EM, Bajorek M. Occupational medicine content of Oregon family physician practices. J Am Board Fam Pract 1995; 8:300 –304 8 Institute of Medicine. Role of the primary care physician in occupational and environmental medicine. Washington, DC: National Academy Press, 1988 9 Rutstein DD, Mullan RJ, Frazier TM, et al. Sentinel health events (occupational): a basis for physician recognition and public health surveillance. Am J Public Health 1983; 73: 1054 –1062 10 Chan-Yeung M, Malo JL. Compendium I: table of the major inducers of occupational asthma. In: Bernstein IL, ChanYeung M, Malo JL, et al, eds. Asthma in the workplace. New York, NY: Marcel Dekker, 1993; 595– 623 11 Venables KM, Chan-Yeung M. Occupational asthma. Lancet 1997; 349:1465–1469 12 Blanc PD. Characterizing the occupational impact of asthma. In: Weiss KB, Buist AS, Sullivan SD, eds. Asthma’s impact on society: the social and economic burden; lung biology in health and disease. New York, NY: Marcel Dekker (in press) 13 Eisner MD, Katz PP, Yelin EH, et al. Assessment of asthma severity in adults with asthma treated by family practitioners, allergists, and pulmonologists. Med Care 1998; 36:1567–1577 14 Blanc PD, Cisternas M, Smith S, et al. Asthma, employment status, and disability among adults treated by pulmonary and allergy specialists. Chest 1996; 109:688 – 696 15 Blanc PD, Jones M, Besson C, et al. Work disability among adults with asthma. Chest 1993; 104:1371–1377 16 Marks GB, Dunn SM, Woolcock AJ. A scale for the measurement of quality of life in adults with asthma. J Clin Epidemiol 1992; 45:461– 472 17 Ware JE, Kosinski M, Keller SD. SF-36 Physical and Mental Summary Scales: a user’s manual. Boston, MA: The Health Institute, New England Medical Center, 1994 18 Blanc PD, Cisternas M, Smith S, et al. Occupational asthma
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34 35
in a community-based survey of adult asthma. Chest 1996; 109(Suppl):56S–57S Harber P, Shimozaki S, Rosenthal E, et. al. Job at onset of asthma. Berkeley, CA: California Department of Health Services, 1989 Lilienfeld AM, Lilienfeld DE. Foundations of epidemiology. 2nd ed. New York, NY: Oxford University Press, 1980; 333–338 Kobayashi S. Different aspects of occupational asthma in Japan. In: Frazier CA, ed. Occupational asthma. New York, NY: Van Nostrand Reinhold, 1980; 229 –244 Blanc P. Occupational asthma in a national disability survey. Chest 1987; 92:613– 617 Syabbalo N. Occupational asthma in a developing country [letter]. Chest 1991; 99:528 Timmer ST, Rosenman K. Occurrence of occupational asthma. Chest 1993; 104:816 – 820 Xu X, Christiani DC. Occupational exposures and physiciandiagnosed asthma. Chest 1993; 104:1364 –1370 Milton D, Christiani D. The risk of asthma attributable to occupational exposures: a population-based study in Spain [letter]. Am J Respir Crit Care Med 1997; 155:382 Ng TP, Hong CY, Goh LG, et al. Risks of asthma associated with occupations in a community-based case-control study. Am J Ind Med 1994; 25:709 –718 Kogevinas M, Anto JM, Soriano JB, et al. The risk of asthma attributable to occupational exposures: a population-based study in Spain. Am J Respir Crit Care Med 1996; 154:137– 143 Blanc PD. Occupation and asthma: through a glass, darkly [editorial]. Chest 1996; 110:3–5 National Center for Health Statistics. National health interview survey 1998 (Occupational health public use data tape). Bethesda, MD: National Center for Health Statistics, 1992 Reijula K, Haahtela T, Klaukka T, et al. Incidence of occupational asthma and persistent asthma in young adults has increased in Finland. Chest 1996; 110:58 – 61 Fishwick D, Pearce N, D’Souza W, et al. Occupational asthma in New Zealanders: a population based survey. Occup Environ Med 1997; 54:301–306 Tarlo S, Leung K, Broder I, et al. Prevalence and characterization of asthmatics symptomatically worse at work among a general asthma clinic population [abstract]. Chest 1997; 112(suppl):133S Milton DK, Solomon G, Rosiello RA, et al. Risk and incidence of asthma attributable to occupational exposure among HMO members. Am J Ind Med 1998; 33:1–10 Blanc PD, Balmes JR. History and physical examination. In: Harber P, Schenker M, Balmes J, eds. Occupational and environmental respiratory diseases. St Louis, MO: Mosby, 1995; 28 –38
Clinical Investigations
Background: In general practice settings, the proportion of adult asthma attributable to occupational factors is not known. Objective: The goal of this study was to estimate the proportion of adult asthma cases that can be attributed to occupational factors initiating new disease onset and exacerbating preexisting disease. Methods: We performed a cross-sectional analysis of interview data for 150 adults with asthma recruited from a random sample of family practice specialists. We ascertained the asthma and work histories of the subjects and estimated the proportion with likely work-initiated asthma and work-related asthma recrudescence. Results: Seventy-four subjects (49%) reported adult-onset asthma while employed; an additional 25 (17%) reported recrudescence of previously quiescent childhood-onset asthma during employment. Of those with new-onset asthma while employed, 15 (10% of the study group; 95% confidence interval, 5 to 15%) were employed in occupations at increased risk of occupational asthma initiation on the basis of an independent job scoring matrix. Of those with asthma recrudescence in adulthood, seven (5% of the study group; 95% confidence interval, 2 to 8%) were employed in occupations at increased risk of exposures aggravating asthma. Conclusions: Among adults with asthma treated in general practice settings, > 1 in 10 patients has a work history strongly suggestive of a potential relationship between exposure and disease. (CHEST 1999; 115:1259 –1264) Key words: asthma; disability; occupational disease; work-related Abbreviations: CI 5 confidence interval; SF-36 5 Medical Outcomes Study Short-Form Health Survey
general medical practice, many illnesses may be I noccupationally related, but this cause may not be recognized.1 As a result, there have been few reliable estimates of the proportion of work-related conditions encountered in primary care settings. A 1993 survey of 101 consecutive male general medical hospital admissions identified 42 patients with dis*From the Division of Occupational Medicine (Drs. Blanc and Israel), the Arthritis Research Group (Dr. Yelin), Department of Medicine, and the Cardiovascular Research Institute (Dr. Eisner), University of California at San Francisco, San Francisco, CA. Manuscript received October 2, 1998; revision accepted December 15, 1998. Supported in part by National Heart, Lung, and Blood Institute Research Career Development Award K04 HL03225 (Dr. Blanc), National Research Service Award F32 HL10054 (Dr. Eisner), NHLBI R01 HL56348 (Drs. Blanc, Eisher, and Yelin), and National Institute for Occupational Safety and Health (CDC) R01 OH03480 (Drs. Blanc, Israel, and Yelin). Correspondence to: Paul Blanc, MD, MSPH, FCCP, Division of Occupational and Environmental Medicine, UCSF Box 0924, 350 Parnassus Ave, No. 609, San Francisco, CA 94143-0924; e-mail: [email protected]
eases potentially attributable to past occupational exposures.2 Earlier in this century, a 1914 survey of 1,507 male outpatient clinic admissions identified 276 persons “in which industry was either the predominating cause of ill-health or was a very important cause or was very important in treating the patient.”3 Other studies in the 80-year interval between these investigations indicate that existing surveillance mechanisms often fail to identify workrelated illness, even when the link between exposure and disease is strong.4 For example, in studies of acute toxic chemical exposures, most occupational cases are not reported through the workers’ compensation system.5,6 In a recent questionnaire survey of family practice specialists, the reported median proportion of time dealing with occupationally related health problems was 9%.7 The National Institute of Medicine has emphasized the importance of occupational health in general practice and highlighted the critical shortcomings in reliable data in this area.8 Adult asthma is a key sentinel condition for meaCHEST / 115 / 5 / MAY, 1999
1259
suring occupational morbidity.9 A wide number of workplace exposures are known to initiate asthma.10,11 Moreover, other workplace factors can aggravate existing asthma or increase the probability of disability from this condition.12 We studied occupational factors among a patient panel of adults with asthma recruited from a random sample of family practitioners. Our goal was to estimate the proportion of patients at greatest likelihood of adult-onset asthma because of occupation and those with likely work-aggravated asthma, and the associated risk of work disability.
Materials and Methods Physician Recruitment The study recruitment methods have been reported previously.13 In brief, we obtained a list of all certified American Board of Medical Specialty family practice specialists (n 5 2,041) in northern California. We randomly selected 167 physicians (8% of the total group). Of these 167, 42 (25%) did not have sufficient information for contact and an additional 19 (11%) had moved outside the area. Of the remaining 106 family practitioners, 27 (25%) were excluded because they did not work in outpatient civilian settings at least 1 full day per week. We attempted to recruit all 79 eligible family practitioners. Of these, 39 (49%) participated. Most nonparticipants cited lack of time as their reason for not participating. Because some physicians who agreed to participate did not ultimately contribute any participating subjects, the final number of participating family practice specialists was 34 (43% of the eligible pool).
puter-assisted telephone interview lasting approximately 45 min. We used the same structured baseline interview schedule previously administered to 601 subjects recruited from pulmonary and allergy specialists.14 The interview covered asthma history (medical history, symptoms, treatment), employment history, comorbidity, general health, functional status, demographic variables, cigarette smoking, and psychosocial variables. Subjects were informed that the goal of the study was to ascertain the ways in which asthma affects people’s day-to-day lives. The protocol was approved by the University of California San Francisco Committee on Human Research. Asthma History and Severity We ascertained the age of asthma onset with the following question: “How old were you when you first had symptoms or an attack of asthma?” We defined childhood-onset asthma as selfreported occurrence of first symptoms or attack before 18 years of age. We also asked the following question: “Would you say that your asthma ‘went away’ for one year or more or that you ‘outgrew it’ only to have it ‘come back’ later?” We defined recrudescent asthma as childhood disease that “went away” for at least 1 year before returning. We quantified asthma severity using a previously validated disease-specific severity-of-asthma scoring system.13–15 The score has a possible range from 0 to 28 with higher scores reflecting more severe disease. It incorporates respiratory symptoms, systemic corticosteroid use, other asthma medications, and past hospitalizations for asthma. In addition to disease-specific severity, we also quantified asthma-specific quality of life using the “Asthma Quality of Life Questionnaire” of Marks et al.16 General health status was measured with the physical and mental health component summary score measures derived from the Medical Outcomes Study Short-Form Health Survey (SF-36).17 Occupational History
Subject Recruitment Each participating family practice specialist was asked to maintain a registry of persons aged 18 to 50 years with outpatient visits for asthma during a prospective 4-week period, with an additional 4 weeks if subject recruitment numbers were less than five. Participating physicians were asked to register patients with a diagnosis of asthma on clinical grounds. Physicians were asked to exclude patients who also had diagnoses of chronic bronchitis or emphysema. We did not instruct participating physicians to restrict recruitment on the basis of patient follow-up status (new or established patients were eligible) or on the basis of other clinical factors (for example, allergic history). The recruitment methods paralleled those we have used previously to recruit adults with asthma from pulmonary and allergy subspecialty practices.13,14 Each person registered by a participating physician was contacted by mail with a description of the study. Those agreeing to participate were telephoned by the study interviewer to arrange an initial telephone survey. There were 21 persons listed who declined participation or who could not be successfully contacted. We successfully recruited 150 of 171 subjects registered (88%). The median number of subjects contributed per physician was 4 (range, 1 to 10). Interviews and Survey Instrument All subject interviews were performed by a single trained survey worker. The format was a structured, close-ended, com1260
We classified subjects on the basis of their history of ever having had part-time or more salaried employment, by which we defined any labor force participation. We then assessed the temporal relationship between labor force participation and symptomatic asthma. Some subjects gave no history of any labor force participation. The remaining subjects, all of whom had at least some history of labor force participation, fell into one of three groups. The first group comprised subjects whose asthma symptoms occurred before employment. This group includes persons with childhood-onset asthma and no remission before adulthood, as well as adult-onset asthma when the respondent was not a salaried employee at the time, for example a student or housewife. The second group comprised those with full- or part-time salaried employment at the time of their initial onset of asthma. By definition, these would be persons with adult-onset asthma. Finally, the third group comprised those with a recrudescence of previously asymptomatic asthma while employed. By definition, these would be persons with initial asthma onset in childhood followed by a remission. We used several different methods to identify subjects with potentially work-related asthma. First, on the basis of questionnaire responses to a specific list of workplace exposures, we identified those with reported job exposures to known irritants or sensitizers. These exposures included grain or flour dust, animal fur or dander, photographic chemicals, epoxies, polyurethanes, cotton dust, pharmaceuticals, sealants, refrigerants, irritant gases, fire smoke, and metal or other dusts. We have used this approach previously to identify high-risk exposures among a similar group of adults with asthma treated by subspecialists.18 We also elicited Clinical Investigations
subject-reported regular heavy physical exertion on the job (either brief or sustained), as well as subject-reported changes or extremes in temperature at work. As a second method, we used occupation as a surrogate of exposure, with broadly defined categories as surrogates of risk on an a priori basis: technicians, service, and labor (manufacturing, agriculture, and other non– white-collar labor).18 In addition to self-reported specific exposures or broad job category as a surrogate of exposures, we also used a third measure of work-related asthma risk. We did this by assigning exposure probabilities on the basis of a job matrix scheme previously developed by the Occupational Health Surveillance and Evaluation Unit of the California Department of Health Services.19 This scoring system has two matrices: one for likelihood of exposures initiating asthma de novo and the second for the likelihood of exposures worsening preexisting asthma. In each case, scores range from 1 (high likelihood) to 4 (low likelihood). We defined an occupational score of ,2.5 as high likelihood to either initiate or exacerbate asthma, depending on the matrix used. For those with any history of labor force participation, we asked whether the subject had ever changed job or job duties because of asthma symptoms or whether the subject left work entirely and attributed this to asthma. We elicited from respondents whether they had ever received workers’ compensation coverage for treatment of their asthma. We did not ask subjects directly whether they attributed their asthma to occupational factors because we did not wish to potentially affect responses to other work-related questions by raising this issue. We did, however, elicit subject responses broadly measuring self-perceived disease origin. The question was asked as follows: “What do you believe is the underlying cause of your asthma? Please choose the best answer: (1) environment or allergic causes, (2) genetics or vulnerability, (3) psychological or emotional factors, (4) multiple factors, or (5) unknown or mysterious factors.” By ascertaining self-perceived cause in this manner, we could assess potential reporting bias associated with positive responses to the specific job-exposure questions asked elsewhere in the interview. Statistical Analysis Interview data were exported into a compatible format (PCSAS) and analyzed with software (SAS; SAS Institute; Cary, NC). We calculated descriptive frequencies with their 95% confidence intervals (CIs) for labor force and work exposure variables. To calculate these 95% CIs, which give a measure of the observed proportion in terms of sampling variability, we assumed a normal distribution, except when there were # 5 observations, for which we assumed a Poisson distribution. For the former, the 95% CIs were calculated as a function of the observed proportion (p), 1 2 p, the sample size (150), and the two-tailed 0.05 t value of
1.98; for the latter, we used standard table of Poisson-distributed factors given the observed number of subjects yielding the proportion in question.20 We tested the differences in demographic and clinical asthma variables between those with initial onset or recrudescent asthma while employed and all others using the t test, x2, or, for income, the Wilcoxon rank test.
Results Of the 150 subjects studied, 130 (87%) reported at least some history of labor force participation; 106 (71%) were currently employed at the time of interview (Table 1). Two thirds of the entire study group (n 5 99) were at potential risk of work-related asthma, either reporting de novo onset of adult asthma while employed or recrudescence of childhood asthma previously in remission while employed. The ratio of subjects with new to recurrent asthma was 3:1. Table 2 compares the 99 subjects with new or recrudescent asthma temporally associated with employment with the remaining 51 subjects who did not have an association between employment status and asthma onset or recrudescence. There were no statistical differences between the groups in terms of age, sex, race, marital status, or education. Annual family income (per adult) was less in the group whose asthma symptoms preceded employment. By definition, this group includes those with no history of labor force participation and therefore no individual salary income. Although asthma severity and general health status (SF-36) were similar between the two groups, the 51 subjects whose asthma was not associated with employment status reported worse asthma-specific quality of life (higher scores indicate poorer status) (Table 2). The prevalence of potential occupationally associated asthma depended on the surrogate measure of risk used (Table 3). An estimated 10 to 11% of the entire study group were categorized as having a high likelihood of work-related new-onset asthma on the basis of job exposures, defined either by subject report or independently assigned job matrix expo-
Table 1—Labor Force Histories Among 150 Adults With Asthma in Generalist Practice Settings* Work History
n (%)
95% CI
Any labor force participation Symptomatic asthma preceding work entry Asthma symptom onset during employment Recrudescence of asthma asymptomatic since childhood De novo onset of adult asthma Currently employed Previously employed but no longer working No prior labor force participation
130 (87) 31 (21) 99 (66) 25 (17) 74 (49) 106 (71) 24 (16) 20 (13)
81–92 14–27 58–74 11–23 41–57 63–78 12–22 8–19
*All of the percentages are expressed as a proportion of the entire study group (n 5 150). CHEST / 115 / 5 / MAY, 1999
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Table 2—Subject Characteristics by Reported Work Status at the Time of Asthma Symptom Onset*
Demographic and Clinical Variables
Asthma Unrelated to Job Status (n 5 51)
Employed, With Recrudescent or New Asthma† (n 5 99)
p Value
Age, yr Female sex White, non-Hispanic Married or cohabitating Years of education Annual income, median Atopic history Asthma severity score SF-36 physical function SF-36 emotional function Quality-of-life score
38 6 9 40 (78) 30 (59) 30 (59) 13 6 2 $15,000 34 (67) 9.0 6 5.9 43 6 14 44 6 9 24 6 18
39 6 8 69 (70) 62 (63) 66 (67) 14 6 2 $25,000 66 (67) 9.5 6 5.3 45 6 11 45 6 8 18 6 13
. 0.5 . 0.3 . 0.7 . 0.4 . 0.2 , 0.01 . 0.9 . 0.5 . 0.3 . 0.3 , 0.05
*Values are expressed as mean 6 SD or No. (%). †Those subjects with asthma linked to employment status (n 5 99) include 74 with new-onset asthma beginning de novo as adults and 25 with past childhood asthma that was asymptomatic and then became recrudescent while employed full- or part-time (see Table 1).
sure score. Defining increased likelihood more liberally, using broadly defined occupational categories, identified 17% of the study group as likely candidates for occupationally related, new-onset asthma. A more narrow definition requiring all of these factors to be present identified 6% (95% CI, 2 to 10%) categorized as having probable new-onset workrelated asthma. Also shown in Table 3, a smaller proportion of those with adult recrudescent asthma had a probable work component: 5% on the basis of reported job exposures and 7% on the basis of job category. Defined by all of the factors studied being present, 3% (95% CI, 1 to 7%) were likely to have had a work-related asthma recrudescence. As a measure of reporting validity, we directly compared job-associated exposures based on a sub-
ject’s report of irritant or sensitizer job exposure (17 among those with new-onset asthma while employed and 8 among those with recrudescence, yielding 25 in total or 17% of the study group) or defined on the basis of an independent job matrix sore (15 among those with new asthma and 7 among those with recrudescence, yielding 22 or 15% of the group) (Table 3). Assigned exposure based on job matrix attribution was strongly associated with a subject’s self-report, both among the 74 with new-onset asthma (p , 0.001) and among the 25 with recrudescent disease (p , 0.001). Of 150 subjects, 69 (46%) attributed the sole cause of their asthma to allergic or environmental factors. This self-attribution was not associated with subjectelicited responses linking the onset or recrudescence of asthma to employment status (n 5 99) as com-
Table 3—Prevalence of Potentially Work-Attributable Asthma Among 150 Adults With Asthma Asthma History New-onset asthma while employed (n 5 74) Reported irritant or sensitizer job exposure Increased risk by job matrix score* Technician, service, labor All of the above risk factors Any of the above risk factors Recrudescence of asthma while employed (n 5 25) Reported irritant or sensitizer job exposure Increased risk by job matrix score* Technician, service, labor Reported physical exertion on job Reported temperature changes on job All of the above risk factors Any of the above risk factors
n (%)
95% CI
17 (11) 15 (10) 25 (17) 9 (6) 31 (21)
6–16 5–15 11–23 2–10 14–27
8 (5) 7 (5) 10 (7) 13 (9) 4 (3) 4 (3) 15 (10)
2–9 2–8 3–11 4–13 1–7 1–7 5–15
*Increased risk by job matrix defined as score , 2.5 over range of 1 to 4. A lower score was defined as the highest likelihood of exposure initiating asthma de novo (job matrix for de novo asthma) or as the highest likelihood of aggravating asthma (job matrix for recrudescent asthma). 1262
Clinical Investigations
pared with all others (n 5 51) (45% vs 47%; p . 0.9). Within the group of 99 subjects with work-associated asthma, there was no association between an allergic or environmental self-attribution and subject-reported irritant or sensitizer job exposures (44% vs 46%; p . 0.9). There were only two subjects who reported leaving work altogether because of their asthma and a third subject who reported an asthma-related change in work activities at the same job. Therefore, of 130 with any history of labor force participation, 3 (2.3%) reported some degree of asthma-related work disability. An additional three subjects, none of whom reported current work disability, reported receiving workers’ compensation coverage for at least some of their asthma care. Of the 99 subjects who reported that their asthma began or recrudesced while employed, 13 (13%) were no longer employed at the time of the baseline interview.
Discussion In a cohort of adults with asthma assembled from a community-based sample of family practice specialists, we observed that a temporal link between employment status and new or recrudescent asthma was frequently reported. We also found that job exposures known to be associated with increased risk of asthma onset or exacerbating preexisting asthma were frequent, whether from subject report or independently assigned on the basis of a risk matrix. Using a job exposure matrix, which may be a conservative measure, 10% of the 150 subjects had adult-onset asthma likely to have been occupational in origin, whereas another 5% had high probability of work-related asthma recrudescence. These data support and amplify our previous estimate of the frequency with which adult asthma morbidity may be attributable to workplace factors. Using a similar analytic strategy, we have previously estimated the attributable fraction of work-related asthma among a cohort of adults recruited from the practices of pulmonary and allergy subspecialists.18 In that cohort, 46% of the subjects had new adultonset asthma while employed, and 13% reported exposure to asthma-associated sensitizers or irritants. These are similar to the estimates we report here for subjects recruited from general as opposed to subspecialty practices. Similar potential limitations would apply to both the current and previous analyses. Although the asthma diagnosis was physician dependent, the data collected on age of asthma onset and its relationship to employment status were subject dependent. Recall bias may have affected ascertainment of expo-
sures, although the proportion of those who believed that their asthma was caused by allergies or the environment did not differ by employment or by job exposure status. Moreover, self-reported exposures were consistent with exposure assigned independently through a job risk matrix. Although our earlier estimates could have been affected by subspecialty referral patterns, the use of subjects treated by physicians in primary care practices strengthens generalization to adults followed in other primary care settings. We cannot exclude, however, the potential for selection bias from the factors that may have been associated with willingness to participate among the physicians who joined the study, if these, in turn, are also linked to a systematically different patient population in terms of occupational risk. Our estimates are consistent with a variety of analyses that have used heterogeneous approaches to estimating etiologic fraction or population-attributable risk percentage for occupationally related asthma among adults with asthma. Although these estimates vary widely, many fall within a 7 to 15% range.21–33 In general, estimates of work attribution have been limited to de novo asthma onset rather than work-related asthma exacerbation or recrudescence. In one relevant community-based study, 5 of 43 cases (12%) of recrudescent adult asthma were identified as likely to be work-related.34 Work as a factor in worsening asthma is particularly relevant to asthma-related work disability. In the current study, only 2 of 130 patients with past labor force participation attributed employment cessation to asthma. This is lower than the 7% disabled proportion we observed among our subspecialist cohort.11 Part of this difference may be consistent with the greater degree of illness severity in the subspecialist group.13 We cannot exclude the possibility that some subjects who ceased employment after the onset or recrudescence of asthma did so in part because of the condition without attributing this change in work status to reasons of health. Although work-associated asthma may be common, there appear to be few obvious demographic or clinical features distinguishing those with a temporal association between their disease and employment status. These findings underscore the critical importance of a targeted occupational history in the evaluation of all adults with asthma. Without such an assessment, the link between exposure and newonset or worsening disease cannot be established.35
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