The Association Between Occupation and Asthma in General Medical Practice

doi:10.1378/chest.115.5.1259

Chest

Volume 115, Issue 5, May 1999, Pages 1259-1264

https://doi.org/10.1378/chest.115.5.1259 Get rights and content

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.

Section snippets

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 = 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

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 = 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 2compares the 99 subjects with

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

References (35)

KM Venables et al.
Occupational asthma
Lancet
(1997)
PD Blanc et al.
Asthma, employment status, and disability among adults treated by pulmonary and allergy specialists
Chest
(1996)
PD Blanc et al.
Work disability among adults with asthma
Chest
(1993)
GB Marks et al.
A scale for the measurement of quality of life in adults with asthma
J Clin Epidemiol
(1992)
PD Blanc et al.
Occupational asthma in a community-based survey of adult asthma
Chest
(1996)
P Blanc
Occupational asthma in a national disability survey
Chest
(1987)
N Syabbalo
Occupational asthma in a developing country [letter]
Chest
(1991)
ST Timmer et al.
Occurrence of occupational asthma
Chest
(1993)
X Xu et al.
Occupational exposures and physician-diagnosed asthma
Chest
(1993)
PD Blanc
Occupation and asthma: through a glass, darkly [editorial]
Chest
(1996)

K Reijula et al.

Incidence of occupational asthma and persistent asthma in young adults has increased in Finland

Chest

(1996)

PJ Landrigan et al.

The recognition and control of occupational disease

JAMA

(1991)

FL Brancati et al.

Occupational exposures and diseases among medical inpatients

J Occup Med

(1993)

DL Edsall

The relation of industry to general medicine

Boston Med Surg J

(1914)

US Congress, House of Representatives et al.

Occupational illness data collection: fragmented, unreliable, and seventy years behind communicable disease surveillance. Report 98–1444

(1984)

PD Blanc et al.

Occupational illness: case detection by poison control surveillance

Ann Intern Med

(1989)

PD Blanc et al.

Occupational illness and the poison control center: referral patterns and service needs

West J Med

(1990)

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The silkworm (Bombyx mori) is an important economic insect that can be used as food in many countries in Asia. However, silkworms and their metabolites are an important source of allergens, which can induce severe allergic reactions. So far, there are no systematic studies on the potential allergens in silkworm and its metabolites. These studies have important guiding significance for the prevention, diagnosis, and treatment of silkworm allergy. The aim of this study was to identify the potential allergens from larva, pupa, moth, silk, slough and feces of silkworm and analyze the sequence homology of silkworm allergens with other allergens identified in the Allergenonline database. We have found 45 potential allergens in silkworm. The results of the homology comparison suggested that silkworm allergens likely cross-react with those of Dermatophagoides farinae, Aedes aegypti, Tyrophagus putrescentiae, Triticum aestivum and Malassezia furfur.
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A working definition of occupational asthma is: ‘variable airways narrowing causally related to exposure in the working environment to airborne dust, gases, vapours or fumes’ (Newman Taylor, 1980). Occupational asthma is now a common, and probably the most common, work-related respiratory disorder in industrialised countries (Blanc et al., 1999; Kogevinas et al., 1999). There is a long history of respiratory diseases associated with the workplace, and some examples were recognised as early as 460BC by Hippocrates as being associated with certain occupations, such as metal working and fishing (Peterson, 1946).
Occupational asthma is an important health problem that can include exacerbation of existing asthma, or induce new asthma either through allergic sensitisation, or non-immunological mechanisms. While allergic sensitisation of the respiratory tract can be acquired to proteins, or to low molecular weight chemicals (chemical respiratory allergens) this article is on the latter exclusively.
Chemical respiratory allergy resulting in occupational asthma is associated with high levels of morbidity and there is a need, therefore, that chemicals which can cause sensitisation of the respiratory tract are identified accurately. However, there are available no validated, or even widely accepted, predictive test methods (in vivo, in vitro or in silico) that have achieved regulatory acceptance for identifying respiratory sensitising hazards. For this reason there is an important reliance on human data for the identification of chemical respiratory allergens, and for distinguishing these from chemicals that cause occupational asthma through non-immunological mechanisms.
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This cohort was first established in 2 successive waves of recruitment (1992-1995). In these waves, adults age 18 to 50 years with asthma whose names were recorded on outpatient clinic visit logs from a random sample of northern California adult pulmonary specialists, allergy immunologists, and family practice physicians were enrolled.14,15 The participation rates of the sampled physicians were as follows: 57 of 92 (62%) pulmonary specialists, 17 of 19 (89%) allergists, and 34 of 74 (46%) family practice physicians.
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FEV₁ % predicted was positively associated with distance from both nearest roadway (P = .01) and nearest major roadway (P = .02). SF-12 PCS and QoL were not significantly associated with either traffic variable. Adjustment for income, smoking, and obesity did not substantively change the associations of the traffic variables with FEV₁ % predicted (P = .04 for nearest roadway and P = .02 for nearest major roadway) and did not cause associations with either SF-12 PCS or QoL to become significant.
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Occupational agents (OA) is a disease characterized by variable airflow limitation and/or airway hyperresponsiveness and/or inflammation due to causes and conditions attributable to a particular occupational environment and not to stimuli encountered outside the workplace. Over 300 agents in the workplace have been implicated in causing asthma. The agents can be divided into two groups according to the pathogenic mechanisms: those that give rise to asthma by immunological mechanisms and those by nonimmunological mechanisms. Agents in the former group can cause asthma by immunoglobulin (Ig)E-dependent or IgE-independent mechanisms. Irritant-induced asthma (IIA) is a type of OA caused by an apparently nonimmunological mechanism. Many patients may have been exposed to multiple sources, and the relative contributions of each may be impossible to disentangle. COPD is the symptomatic and functional consequence of chronic exposure to these polluted air sources. Therefore, it seems appropriate to pose a definition for occupational COPD that allows it to coexist with “smoking-induced COPD” or “urban air pollution-induced COPD.” Asthma is a common respiratory occupational ailment. Whereas improvement in diagnostic tools and pathophysiological mechanisms still need to be considered, emphasis should be put on prevention programs through identification and application of permissible respirable levels and of affected subjects at an early stage of sensitization or disease to prevent long-term sequelae of permanent asthma.
Occupational Agents
2008, Asthma and COPD: Basic Mechanisms and Clinical Management
Occupational agents (OA) is a disease characterized by variable airflow limitation and/or airway hyperresponsiveness and/or inflammation due to causes and conditions attributable to a particular occupational environment and not to stimuli encountered outside the workplace. Over 300 agents in the workplace have been implicated in causing asthma. The agents can be divided into two groups according to the pathogenic mechanisms: those that give rise to asthma by immunological mechanisms and those by nonimmunological mechanisms. Agents in the former group can cause asthma by immunoglobulin (Ig)E-dependent or IgE-independent mechanisms. Irritant-induced asthma (IIA) is a type of OA caused by an apparently nonimmunological mechanism. Many patients may have been exposed to multiple sources, and the relative contributions of each may be impossible to disentangle. COPD is the symptomatic and functional consequence of chronic exposure to these polluted air sources. Therefore, it seems appropriate to pose a definition for occupational COPD that allows it to coexist with “smoking-induced COPD” or “urban air pollution-induced COPD.” Asthma is a common respiratory occupational ailment. Whereas improvement in diagnostic tools and pathophysiological mechanisms still need to be considered, emphasis should be put on prevention programs through identification and application of permissible respirable levels and of affected subjects at an early stage of sensitization or disease to prevent long-term sequelae of permanent asthma.
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We investigated whether perceived neighborhood problems (NP) predicted changes over a 2-year period in asthma-specific quality of life (QOL), physical functioning (PF), and depressive symptomology (DEP) in a longitudinal cohort of 340 adults with asthma. There is a threshold and plateau effect between NP and PF, such that NP do not affect changes in PF until the problems reach the level of Quartile 3. People who had NP scores in Quartile 3 had lower PF compared to people who reported NP in Quartiles 1 or 2 (mean difference −3.09). High NP also predicted over two-fold odds of high DEP (Center for Epidemiological Studies Depression [CES-D] score⩾16) at follow-up (odds ratio=2.34; 95% confidence interval: 1.09–5.00). NP did not predict decline in QOL. Analyses adjusted for demographics, asthma severity, and baseline value of the health outcome.

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: 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).

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Chest

Clinical InvestigationsASTHMAThe Association Between Occupation and Asthma in General Medical Practice

Background

Objective

Methods

Results

Conclusions

Section snippets

Physician Recruitment

Results

Discussion

Lancet

Chest

Chest

J Clin Epidemiol

Chest

Chest

Chest

Chest

Chest

Chest

Chest

The recognition and control of occupational disease

JAMA

Occupational exposures and diseases among medical inpatients

J Occup Med

The relation of industry to general medicine

Boston Med Surg J

Occupational illness data collection: fragmented, unreliable, and seventy years behind communicable disease surveillance. Report 98–1444

Occupational illness: case detection by poison control surveillance

Ann Intern Med

Occupational illness and the poison control center: referral patterns and service needs

West J Med

Clinical Investigations
ASTHMA
The Association Between Occupation and Asthma in General Medical Practice