General Information Chemicals Organic Matter Particulates-Air Pollution
Author(s):
Vandenplas
O ; Malo
JL
Affiliation: Service de Pneumologie, Cliniques de Mont-Godinne,
Université Catholique de Louvain, Yvoir, Belgium.
olivier.vandenplas@pneu.ucl.ac.be
Title: Definitions
and types of work-related asthma: a nosological approach. Source: Eur Respir J (The European respiratory
journal : official journal of the European Society for Clinical Respiratory
Physiology.) 2003 Apr; 21(4): 706-12
Abstract: The workplace can trigger or induce asthma and cause the onset of
different types of work-related asthma. Analysis of previous definitions of
occupational asthma (OA) led to the conclusion that evidence of a direct causal
relationship between workplace exposure and the development of asthma remains
the key element for defining OA. Based on clinical features and
pathophysiological mechanisms, the following conditions should be distinguished
in the spectrum of work-related asthma: 1) immunological OA characterised by a
latency period necessary to acquire immunologically induced sensitisation; 2)
nonimmunological OA characterised by the rapid onset of asthma following single
or multiple exposures to high concentrations of irritant compounds; 3)
work-related asthma defined by exacerbation of symptoms in workers with
pre-existing or coincident asthma; and 4) variant syndromes including
eosinophilic bronchitis, potroom asthma, and asthma-like disorders caused by
organic dusts. The issues and controversies relating to this approach are critically
reviewed in order to stimulate the consensus development of operational
definitions of work-related asthma.
Author(s):
Reinisch
F ; Harrison
RJ ; Cussler
S ; Athanasoulis
M ; Balmes
J ; Blanc
P ; Cone
J
Affiliation: California Department of Health Services, Occupational
Health Branch, Oakland, CA 94612, USA. freinisc@dhs.ca.gov Title: Physician reports of work-related asthma in
California, 1993-1996. Source: Am J Ind Med (American journal of industrial medicine.) 2001 Jan;
39(1): 72-83
Abstract: BACKGROUND: Work-related asthma is a leading cause of occupational
respiratory illness. METHODS: Work-related asthma was studied in California
over a 36-month period, from March 1, 1993 to February 29, 1996. The
surveillance system identified cases from Doctor's First Reports (DFRs), a
mandated physician reporting system. Structured follow-up telephone interviews of
DFR asthma cases were conducted to collect work history, exposure, and medical
information. Statewide employment data was used to calculate disease rates
among industry groups. RESULTS: Based on 945 cases of work-related asthma, the
average annual reporting rate for work-related asthma in California was
25/million workers. We estimate that the actual rate is 78/million, adjusted
for likely underreporting. Janitors and cleaners (625/million) and firefighters
(300/million) had the highest reporting rates of work-related asthma. Half of
all work-related asthma cases were associated with agents not known to be
allergens. CONCLUSIONS: A greater proportion of work-related asthma associated
with irritant exposures was identified than has previously been reported. The
surveillance data provide a very conservative estimate of the incidence of
work-related asthma.
Author(s):
Johnson
AR ; Dimich-Ward
HD ; Manfreda
J ; Becklake
MR ; Ernst
P ; Sears
MR ; Bowie
DM ; Sweet
L ; Chan-Yeung
M
Affiliation: Department of Medicine, University of British Columbia,
Vancouver, British Columbia, Canada. anthonyj@med.usyd.edu.au
Title: Occupational
asthma in adults in six Canadian communities. Source: Am J Respir Crit Care Med (American journal of respiratory
and critical care medicine.) 2000 Dec; 162(6): 2058-62
Abstract: We examined the prevalence, population attributable risk (PAR), and
clinical characteristics of occupational asthma (OA) in a randomly selected
population in six communities in Canada. Our study followed the European
Community Respiratory Health Survey protocol. A randomly selected population of
18,701 (87% response rate) persons from the study communities, ranging in age
from 20 to 44 yr, completed an initial questionnaire, of whom 2,974 (39%
response rate) attended the laboratory and completed supplementary
questionnaires. Of these latter individuals, 383 had asthma. Asthma was defined
as physician-diagnosed asthma, and adult-onset asthma was defined as a first
attack at age 15 yr or older. We used several methods for estimating OA as
follows: (1) reporting of a high-risk job (occupation and industry) for OA at the
time of asthma onset (Probable OA); (2) reporting of exposure to a substance
that may cause OA (Possible OA) while not in a high-risk job at the time of
asthma onset; and (3) combination of the PAR for high-risk jobs and exposures.
The prevalence (95% confidence interval [CI]) of Probable OA and Possible OA
combined was 36.1% (31.3 to 41.0%) among subjects with adult-onset asthma. The
occupations most commonly reported in association with OA were nursing in the
Probable OA group and clerical and food preparation in the Possible OA group.
The clinical characteristics and exposures reported by both groups were
similar. The PAR for adult-onset asthma in high-risk jobs and exposures was
18.2%. The assessment of occupation and industry alone, rather than of exposures,
may underestimate the contribution of occupational exposures to asthma
prevalence.
Author(s):
Mapp
C ; Boschetto
P ; Miotto
D ; De
Rosa E ; Fabbri
LM
Affiliation: Institute of Occupational Medicine, University of Padova,
Italy.
Title: Mechanisms
of occupational asthma. Source: Ann Allergy Asthma Immunol (Annals of allergy, asthma & immunology :
official publication of the American College of Allergy, Asthma, &
Immunology.) 1999 Dec; 83(6) Pt 2: 645-64
Abstract: BACKGROUND: The pathogenesis and the pathologic alterations of
occupational asthma are similar to those of nonoccupational asthma.
Occupational asthma may therefore represent a useful model of "human
asthma" to investigate mechanisms and pathophysiology of asthma in
general. In an occupational setting the cause and onset of asthma may be easily
identified, and the natural history may be examined in follow-up studies. The
mechanisms involved in occupational asthma include genetic predisposition,
immunologically mediated responses, as well as nonspecific airway inflammation.
In particular, high molecular weight (eg, grain dust, flour) and some low
molecular weight sensitizers (eg, acid anhydrides and platinum halide salts)
have been shown to induce occupational asthma through an immunoglobulin E
(IgE)-dependent mechanism, while cell-dependent immunologic mechanisms are
likely to be more relevant for occupational asthma induced by other low
molecular weight sensitizers (eg, toluene diisocyanate and plicatic acid
contained in western red cedar). The pathology of the airway mucosa of
occupational asthma is remarkably similar to the pathology of nonoccupational
asthma, ie, characterized by infiltration and accumulation of eosinophils, mast
cells, and activated lymphocytes along with subepithelial fibrosis. In this
article, the most relevant mechanisms are discussed with particular reference
to the similarities and discrepancies between occupational and nonoccupational
asthma.
Author(s):
Di Stefano F ; Siriruttanapruk S ; McCoach J ; Di Gioacchino M ; Burge PS
Affiliation: Allergy and Clinical Immunology Department, University G.
d'Annunzio, Chieti, Italy.
Title: Occupational
asthma in a highly industrialized region of UK: report from a local
surveillance scheme. Source: Allerg Immunol (Paris) (Allergie et immunologie.) 2004 Feb; 36(2):
56-62
Abstract: Estimates of the incidence of occupational asthma may be derived from surveillance schemes established in several countries. SHIELD is a voluntary surveillance scheme for occupational asthma in the West Midlands, a highly industrialized region of UK. The aim of this study was to estimate the general and specific incidence of occupational asthma in the West Midlands in 1990-97. The annual incidence was 41.2/million. There was a two fold difference in the incidence by sex (male 59.6/million/yr; female 27.4/million/yr). The highest annual incidence (53.2/million) was observed in the age group 45-64 yr (male) and 45-59 yr (female). Spray painters were the occupation at the highest risk of developing occupational asthma, followed by electroplaters, rubber and plastic workers, bakery workers and moulders. Although the percentage of reported cases was low among healthcare workers, there was a raising trend. Isocyanates still remained the most common causative agents with 190 (17.3%) out of the total 1097 cases reported to the surveillance scheme in seven years. There was a decrease in the reported cases due to colophony (9.5% to 4.6%), flour & wheat (8.9% to 4.9%). There was an increase of reported cases due to latex (0.4% to 4.9%) and glutaraldehyde (1.3% to 5.6%). The serial mesurement of peak expiratory flow at and away from work was the most used method of diagnosis to confirm the occupational cause of asthma. Specific bronchial challenge test with the occupational agents were used when the serial measurement of peak expiratory flow was not able to confirm undoubtdely the diagnostic suspicion or when it was difficult to identify the possible causative agent due to multiple exposures in the workplace. Following diagnosis, 24% of the patients were moved away from exposure within the same workplace in 1997, compared to 15.8% in the previous years. Those remaining exposed to the causative agent in the same workplace decreased from 28.3% to 17.7% between 1990-97. The surveillance of occupational asthma trough this voluntary scheme has allowed to monitor the incidence of the disease in the region and to identify clusters of cases, where control measures are a priority.
Author(s):
Jajosky RA ; Harrison R ; Reinisch F ; Flattery J ; Chan J ; Tumpowsky C ; Davis L ; Reilly MJ ; Rosenman KD ; Kalinowski D ; Stanbury M ; Schill DP ; Wood J
Affiliation: National Institute for Occupational Safety and Health, CDC,
USA.
Title: Surveillance
of work-related asthma in selected U.S. states using surveillance guidelines
for state health departments--California, Massachusetts, Michigan, and New
Jersey, 1993-1995. Source: MMWR CDC Surveill Summ (MMWR. CDC surveillance summaries : Morbidity and
mortality weekly report. CDC surveillance summaries / Centers for Disease
Control.) 1999 Jun 25; 48(3): 1-20
Abstract: PROBLEM/CONDITION: Cases of work-related asthma (WRA) are sentinel health
events that indicate the need for preventive intervention. WRA includes
new-onset asthma caused by workplace exposure to sensitizers or irritants and
preexisting asthma exacerbated by workplace exposures. REPORTING PERIOD: This
report reviews cases of WRA identified by state health departments from January
1, 1993, through December 31, 1995, as well as follow-up investigations of
cases and associated workplaces conducted through June 30, 1998. DESCRIPTION OF
THE SYSTEMS: State-based surveillance and intervention programs for WRA are
conducted in California, Massachusetts, Michigan, and New Jersey as part of the
Sentinel Event Notification Systems for Occupational Risks (SENSOR) cooperative
agreement program, initiated by CDC's National Institute for Occupational
Safety and Health (NIOSH). RESULTS: From 1993 through 1995, a total of 1,101
cases of WRA were identified by SENSOR surveillance staff members in
California, Massachusetts, Michigan, and New Jersey. Of these 1,101 cases,
19.1% were classified as work-aggravated asthma, and 80.9% were classified as
new-onset asthma. Objective evidence substantiating asthma work-relatedness was
documented in the medical records of 3.4% of WRA cases identified in the two
states (Michigan and New Jersey) where medical records are routinely reviewed
for this information. Indoor air pollutants, dusts, cleaning materials,
lubricants (e.g., metalworking fluids), and diisocyanates were among the most
frequently reported causes of WRA. In addition, a well-recognized cause of
occupational asthma - natural rubber latex - was identified in a new setting,
the healthcare industry. The most common industries associated with WRA cases
included transportation equipment manufacturing (19.3%), health services
(14.2%), and educational services (8.7%). Air sampling for agents known to
induce occupational asthma was performed in Michigan for comparison with
established federal time-weighted average exposure limits. Sixteen (13.4%) of
119 workplaces tested had airborne concentrations exceeding NIOSH recommended
exposure limits (RELs); 11 (9.1%) of 121 workplaces had concentrations
exceeding permissible exposure limits (PELs) of the Michigan Occupational
Safety and Health Act (MIOSHA) program. INTERPRETATION: The surveillance data
findings confirm well-recognized causes of asthma and have identified new
putative causes (e.g., cleaning materials and metalworking fluids). Because the
surveillance program depends on physicians' recognizing asthma work-relatedness
and reporting diagnosed cases, the data are considered an underestimate of the
magnitude of the WRA problem. The data also indicate that physicians are not
commonly performing objective physiologic tests to substantiate a WRA
diagnosis. Workplace findings suggest a need to evaluate existing exposure
standards for specific agents known to induce occupational asthma (e.g.,
diisocyanates). Case-based surveillance can help improve the recognition,
control, and prevention of WRA. The SENSOR model also provides a mechanism for
workers and physicians to request workplace investigations aimed at primary
prevention for other workers. PUBLIC HEALTH ACTION: NIOSH and state health
department representatives are working to establish a long-term agenda for
state-based surveillance of work-related conditions and hazards. The results
from the SENSOR WRA programs described in this report support inclusion of WRA
as a priority condition warranting surveillance at the state level.
Author(s):
Wintermeyer SF
Affiliation: Division of Pulmonary, Allergy, Critical Care, and
Occupational Medicine, Indiana School of Medicine, Indianapolis, USA.
Title: Occupational
asthma. Source: Lippincotts Prim Care Pract (Lippincott's primary care practice.) 1998 Nov-Dec;
2(6): 614-24
Abstract: Occupational asthma is the most
common occupational lung disease in the world. Occupational asthma comprises
approximately 25-50% of occupational lung diseases and is responsible for up to
15% of all asthma cases. Either immunologic or nonimmunologic causes may be
responsible for occupational asthma. There are approximately 250 compounds known
to cause occupational asthma. Common examples include flour, animal dander,
isocyanates, and latex. The diagnosis of occupational asthma depends on an
accurate history of asthma and documentation that the asthma is caused by
workplace exposure. Peak flow measurements are commonly used to provide data to
define this relationship. Spirometry and bronchial provocation testing are also
helpful. The key management tool in occupational asthma is avoidance of the
causative agent. Avoidance is more important than treatment with medications.
Occupational asthma can have major socioeconomic impacts on an individual, and
the diagnostic work-up and management needs to be performed with this in mind.
Author(s):
Rosenman KD ; Reilly MJ ; Kalinowski DJ
Affiliation: Department of Medicine, Michigan State University, East
Lansing 48824-1316, USA.
Title: A
state-based surveillance system for work-related asthma. Source: J Occup Environ Med (Journal of occupational and
environmental medicine / American College of Occupational and Environmental
Medicine.) 1997 May; 39(5): 415-25
Abstract: The current national surveillance system for occupational illnesses underestimates the incidence of work-related asthma. This article describes a state-based surveillance system for work-related asthma. The Michigan surveillance system enables us to estimate the incidence of work-related asthma, describe the characteristics of affected individuals, and facilitate public health interventions in the form of workplace inspections. The data presented are based on interviews with a case-series of individuals with work-related asthma reported to the Michigan Department of Public Health (MDPH) from 1988 to 1994. We also present cross-sectional data on coworkers of the index cases, who were interviewed during the workplace investigations, and exposure measurements from those investigations. Potential cases were reported by physicians, hospitals, or the Michigan Department of Labor. Case eligibility was based on the criteria for work-related asthma developed by the National Institute for Occupational Safety and Health (NIOSH). Between 1988 and 1994, 725 people who met the NIOSH criteria for work-related asthma were reported to the MDPH. Seventy-six percent of the reports were from physicians, 17.1% were from hospitals, 7.3% were from workers' compensation records, and 3.5% were from other health professionals. Eighty-three percent of the reports were for individuals with the onset of newly diagnosed asthma after a period of symptomless exposure, 7.3% were for aggravation of preexisting asthma, and 9.5% were for reactive airway dysfunction syndrome (RADS). The overall annual average incidence rate of work-related asthma in Michigan was 2.9 cases per 100,000 workers. Rates were 0.8/100,000 in the service industry and 8.5/100,000 in manufacturing. Isocyanates and machining coolants were the two most common causes of asthma among workers reported to the surveillance system. Demographics of the individuals reported are described. During workplace follow-up investigations, 861 fellow workers were identified as having possible work-related asthma. Another 151 coworkers were identified from the company-maintained injury and illness logs as having possible work-related asthma. In addition, the investigations identified two new causes of work-related asthma. The primary limitations of the surveillance system include a lack of objective testing to confirm the diagnosis of work-related asthma and underreporting of cases. Despite these limitations, this state-based surveillance system has proven successful in identifying new cause of asthma and identifying workplaces with a high prevalence of workers with respiratory symptoms who may benefit from public health interventions.
Author(s):
Newman LS
Affiliation: Occupational and Environmental Medicine Division, National
Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado, USA.
Title: Occupational
asthma. Diagnosis, management, and prevention. Source: Clin Chest Med (Clinics in chest medicine.)
1995 Dec; 16(4): 621-36
Abstract: Occupational asthma is the most common work-related respiratory disorder
but frequently goes undetected, leading to poorer clinical outcomes for
asthmatic patients. Inhalational exposures to both allergens and irritants in
the workplace cause asthma. The likelihood of recovery hinges on early
recognition and avoidance of further exposure. This article outlines the
clinical approach to the detection, management, and prevention of occupational
asthma, emphasizing recent advances and practical advice on how to investigate
the causes of reactive airway disease.
Author(s):
Bardana EJ Jr
Affiliation: Department of Medicine, Oregon Health Sciences University,
Portland.
Title: Occupational
asthma and related respiratory disorders. Source: Dis Mon (Disease-a-month : DM.) 1995
Mar; 41(3): 143-99
Abstract: Occupational rhinitis is a common but generally underreported entity. Although
it may occur alone, it is frequently associated with occupational asthma.
Occupational asthma may have one of several presentations that are difficult to
distinguish from non-work conditions. The respiratory tract acts as the final
common pathway for all inhaled environmental pollutants, whether encountered in
the home or at work. More than 200 chemicals have been incriminated as a cause
of work-related asthma. It is said that about 2% of the 10 million Americans
who have asthma acquired it as a result of some chemical irritant or immunogen
in their work environment. A number of predisposing factors facilitate the
development of work-related asthma. These include industrial conditions,
climatic factors, atopic predisposition, smoking, recreational drug use, viral
infection, nonspecific bronchial hyperreactivity, and a variety of
miscellaneous factors. Pathogenetically, occupational asthma may be immunologic
or nonimmunologic in nature. The immunologic variants involve sensitization to
a variety of large-molecular-weight constituents. The major nonimmune variant
is referred to as inflammatory bronchoconstriction or reactive airways
dysfunction syndrome (RADS). There are well-defined criteria for the diagnosis
of immunologic and nonimmunologic asthma. The several clinical variations of
occupational asthma can be difficult to distinguish from nonindustrial
disorders. The most common presentation in practice involves the worker with
preexistent asthma who has been adversely affected by work exposures. Occasionally
these industrial exposures precipitate permanent impairment. It is clear,
however, that occupational asthma is not a single, simple, or homogeneous
entity, even when a single specific causal factor can be identified in the
workplace. Therefore the physician must be aware of the patient's entire
medical history and the precise occupational exposures and must have convincing
physiologic evidence that demonstrates a cause-and-effect relationship before
making a definitive diagnosis of work-related asthma. Once the diagnosis is
established, the worker should be removed from the work-place. If the diagnosis
is made in a timely fashion, the patient should experience a significant
improvement. The major factor in determining a poor prognosis in occupational
asthma is the duration of exposure before the diagnosis is established.
Prevention of the disorder is the best therapeutic intervention.
General Information Chemicals Organic Matter Particulates-Air Pollution
Author(s):
Bernstein
DI
Affiliation: Division of Immunology and Allergy, Department of Internal
Medicine, University of Cincinnati College of Medicine, 231 Albert Sabin Way,
Cincinnati, OH 45267-0563, USA. bernstdd@email.uc.edu
Title: Occupational
asthma caused by exposure to low-molecular-weight chemicals. Source: Immunol Allergy Clin North Am (Immunology and allergy clinics
of North America.) 2003 May; 23(2): 221-34, vi
Abstract: Chemical agents cause approximately 40% of cases of occupational asthma
(OA). Diagnosis of OA caused by chemicals relies on the demonstration of
decrements in lung function at the workplace or during a controlled specific
inhalation challenge to the suspect chemical agent. Evaluation of workers is
accomplished best with a stepwise algorithmic approach and while the worker is
symptomatic and still exposed at work. An early diagnosis followed by cessation
of exposure can result in asthma remission and is likely to prevent progression
to chronic disabling obstructive disease.
Author(s):
Simpson C ; Garabrant D ; Torrey S ; Robins T ; Franzblau A
Affiliation: Department of Environmental and Industrial Health,
University of Michigan, School of Public Health, Ann Arbor 48109-2029, USA.
Title: Hypersensitivity
pneumonitis-like reaction and occupational asthma associated with
1,3-bis(isocyanatomethyl) cyclohexane pre-polymer. Source: Am J Ind Med (American journal of industrial
medicine.) 1996 Jul; 30(1): 48-55
Abstract: Twenty-three of 34 workers who had
worked in the injection molding operation making polyurethane foam parts at an
automobile parts manufacturing plant developed respiratory symptoms and/or
systemic symptoms over a 2-month period following the full production use of a
new diisocyanate paint that contained 1,3-bis(isocyanatomethyl)cyclohexane
pre-polymer (BIC)(CAS #75138-76-0, 38661-72-2). At 3 months, all subjects
underwent an interview, physical examination, pre- and post-shift pulmonary
function tests, and either methacholine challenge test or bronchodilator challenge
at an occupational health clinic. The most frequently cited symptoms were
dyspnea (65%), cough (61%), chest tightness (57%), chills (57%), wheezing
(30%), and myalgias, arthralgias, and nausea (26%). Thirteen subjects had
either a positive methacholine challenge test or a positive response to
bronchodilator challenge, making the overall prevalence of airway
hyperresponsiveness 38%. The overall prevalence of hypersensitivity
pneumonitis-like reactions among line operators in the injection molding process
was 27%. This disease outbreak suggests that
1,3-bis(isocyanatomethyl)cyclohexane pre-polymer may cause asthma and
hypersensitivity pneumonitis-like reactions. The use of BIC was discontinued 6
months after the first workers developed symptoms.
Author(s):
Eisen EA ; Holcroft CA ; Greaves IA ; Wegman DH ; Woskie SR ; Monson RR
Affiliation: Department of Work Environment, University of Massachusetts
Lowell 01854, USA. eisene@wesun.uml.edu
Title: A strategy
to reduce healthy worker effect in a cross-sectional study of asthma and
metalworking fluids. Source: Am J Ind Med (American journal of industrial medicine.) 1997 Jun;
31(6): 671-7
Abstract: This report describes the reanalysis of a cross-sectional study of
asthma in a large cohort of autoworkers with exposure to metalworking fluids
(MWF). There is strong evidence from case reports, clinical studies, and
medical surveillance data that exposure to MWF can cause asthma, yet no
association was found in the original analysis. The central hypothesis of the
reanalysis was that the absence of an association between asthma and MWF
exposure was the result of bias caused by the self-selection of asthmatics out
of exposed jobs. We addressed the potential job transfer bias by redefining
exposure and disease status at the time of asthma onset, rather than at the
time of the health survey. This permitted us to treat the cross-sectional study
as if it were a historical cohort study, despite the fact that the population
was a biased sample of the full cohort. This approach resulted in a significantly
elevated incidence rate ratio of 3.2 (95% CI: 1.2-8.3) for synthetic MWF
estimated in a Cox proportional hazards model. Although the cross-sectional
design makes it impossible to document or control for differential selection
out of the workforce, the approach described here provides a strategy for
reducing the healthy-worker effect due to job transfer bias in cross-sectional
studies.
Author(s):
Bright P ; Burge PS ; O'Hickey SP ; Gannon PF ; Robertson AS ; Boran A
Affiliation: Occupational Lung Disease Unit, Birmingham Heartlands
Hospital, Birmingham, UK.
Title: Occupational
asthma due to chrome and nickel electroplating. Source: Thorax (Thorax.) 1997 Jan; 52(1):
28-32
Abstract: BACKGROUND: Exposure to chromium during electroplating is a recognised
though poorly characterised cause of occupational asthma. The first series of
such patients referred to a specialist occupational lung disease clinic is
reported. METHODS: The diagnosis of occupational asthma was made from a history
of asthma with rest day improvement and confirmed by specific bronchial
provocation testing with potassium dichromate and nickel chloride. RESULTS:
Seven workers had been exposed to chrome and nickel fumes from electroplating
for eight months to six years before asthma developed. One subject, although
exposed for 11 years without symptoms, developed asthma after a single severe
exposure during a ventilation failure. This was the only subject who had never
smoked. The diagnosis was confirmed by specific bronchial challenges. Two
workers had isolated immediate reactions, one a late asthmatic reaction, and
four a dual response following exposure to nebulised potassium dichromate at
1-10 mg/ml. Two of the four subjects were also challenged with nebulised nickel
chloride at 0.1-10 mg/ml. Two showed isolated late asthmatic reactions, in one
at 0.1 mg/ml, where nickel was probably the primary sensitising agent. Four
workers carried out two hourly measurements of peak expiratory flow over days
at and away from work. All were scored as having occupational asthma using
OASYS-2. Breathing zone air monitoring was carried out in 60 workers from four
decorative and two hard chrome plating shops from workers with similar jobs to
those sensitised. No measurement exceeded the current occupational exposure
standard for chromate or nickel, the mean levels of chromate exposure for jobs
similar to those of the affected workers were 9-15 micrograms/m3. CONCLUSION:
Chrome used in electroplating is a potential cause of occupational asthma.
Sensitivity to chrome in electroplaters may occur in situations where exposure
levels are likely to be within the current exposure standards. There may be
cross reactivity with nickel. Inhalation challenge with nebulised potassium
dichromate solution is helpful in making the specific diagnosis where doubt
exists.
Author(s):
Piipari R ; Tuppurainen M ; Tuomi T ; Mäntylä L ; Henriks-Eckerman ML ; Keskinen H ; Nordman H
Affiliation: Finnish Institute of Occupational Health, Helsinki.
Title: Diethanolamine-induced
occupational asthma, a case report. Source: Clin Exp Allergy (Clinical and experimental allergy : journal of
the British Society for Allergy and Clinical Immunology.) 1998 Mar; 28(3):
358-62
Abstract: BACKGROUND: Amino alcohols are low molecular weight chemicals used widely in industrial processes, often as minor constituents. They have been found to cause allergic contact dermatitis. Marked exposure through airways is uncommon in other than occupational settings where chemicals containing amino alcohols may be heated or vaporized, liberating free amino alcohols into the ambient air. A few cases of asthma and allergic rhinitis have been reported, but the amounts inducing the airway reactions have not been defined. OBJECTIVE: To further characterize ethanolamine-induced asthma and define the concentration inducing the asthmatic reaction, a case of diethanolamine-induced occupational asthma in a patient handling diethanolamine containing cutting fluid is reported. METHODS: Suspicion of work related asthma was raised by symptoms and peak expiratory flow monitorings at work and at home. Specific bronchial provocation tests with the cutting fluid containing DEA and with DEA aerosol at two different concentration below the American Conference of Governmental Industrial Hygienists threshold limit value of DEA (2.0 mg/m3) were done. RESULTS: DEA caused asthmatic airway obstruction at two different concentrations below the ACGIH TLV. A slight dose-response relationship was observed. Specific IgE-antibodies against DEA could not be found. CONCLUSIONS: DEA is able to induce occupational asthma by a sensitization mechanism, the exact pathophysiological mechanism of which is not known.
Author(s): Acero S ;
Alvarez MJ ;
García BE ;
Echechipía S ;
Olaguibel JM ;
Tabar AI
Affiliation: Sección Alergología, Hospital Virgen del Camino, Pamplona,
Spain.
Title: Occupational
asthma from natural rubber latex. Specific inhalation challenge test and
evolution. Source: J Investig Allergol Clin Immunol (Journal of investigational allergology & clinical
immunology : official organ of the International Association of Asthmology
(INTERASMA) and Sociedad Latinoamericana de Alergia e Inmunologia.) 2003;
13(3): 155-61
Abstract: BACKGROUND: Natural rubber latex (NRL) is the most frequent cause of
occupational respiratory problems in hospital workers. OBJECTIVE: To describe
the diagnostic methodology, including the specific inhalation challenge (SIC),
used on patients diagnosed as having occupational asthma due to NRL in our
Allergy Department during a 6-year period from 1989 to 1995. METHODS: In 19
patients diagnosed as having occupational asthma due to NRL, clinical severity
was assessed with a combined score for symptoms and medication use. Skin prick
tests with aeroallergens, latex, papain, kiwi and chestnut, total IgE,
serum-specific latex IgE, respiratory function study, methacholine test,
specific conjunctival test, and SIC test with latex were done. RESULTS: All but
three patients worked in hospitals. All presented urticaria and
rhinoconjunctivitis, and six also suffered anaphylaxis, usually preceded by
asthma. Clinical fruit allergy was present in eight patients. The latency
period was variable (0.25-27 years). The intensity of symptoms was low to
moderate. Specific IgE, skin prick, and conjunctival tests to latex were
positive in all cases. SICs were done in 12 patients. All of them presented
isolated immediate reactions. No adverse reactions were observed. Duration of
follow-up ranged from 1 to 7 years. Twenty-six percent of the patients kept
their job, 26% changed jobs but remained in health care, and 48% switched to
jobs unrelated to health care. Only 16% were free of symptoms without
treatment, while 32% needed bronchodilators and 52% needed inhaled steroids.
The specific bronchial challenge test was safe, but it did not predict the
course of the illness. Duration of exposure and intensity of symptoms did
correlate with prognosis, however. CONCLUSIONS: NRL acts as a common
aerollergen. Minor symptoms often precede occupational asthma. The SIC test was
safe in the hands of trained technicians. Occupational asthma due to NRL seems
to have a poor prognosis.
Author(s):
Irsigler GB ; Visser PJ ; Spangenberg PA
Affiliation: Department of Medicine, University of Pretoria, Republic of
South Africa.
Title: Asthma and
chemical bronchitis in vanadium plant workers. Source: Am J Ind Med (American journal of industrial
medicine.) 1999 Apr; 35(4): 366-74
Abstract: BACKGROUND: Whether vanadium induces bronchial hyperresponsiveness and
asthma in previously normal subjects is unresolved: the two reported series
addressing this question both have shortcomings. OBJECTIVE: To determine the
cause of cough and breathlessness in vanadium plant workers after variable
periods of exposure. DESIGN: Case series of employees presenting with
persistent symptoms over a 24-month study period. PATIENTS AND METHODS: Forty
of an estimated 1,440 patients were investigated by 1) blood count and serum
IgE, 2) intracutaneous allergen skin tests, 3) spirometry, and 4)
bronchoprovocation by histamine inhalation or exercise challenge. Exposure was
assessed by measurement of 1) ambient V2O5, NH3 and SO2 over 7 days during the
24-month study period, 2) urine vanadium concentration at time of first
presentation. RESULTS: Twelve of 40 subjects had bronchial hyperreactivity
(BHR), and these were compared to 12 age-matched companion subjects whose BHR was
normal. In 10, BHR was diagnosed by histamine inhalation (PC20 0.25-1.82 mg/ml,
nl > 8.0 mg/ml), and in six of these the abnormality was severe (PC20 <
0.5 mg/ml). A further two had BHR by exercise challenge (FEV1, 600 ml/30% and
770 ml/18% pre/post exercise). After removal from exposure, 9 of the 12
subjects returned for follow-up 5 to 23 months later. BHR was worse in one,
still present although less severe in five, and was no longer found in one
subject. Baseline spirometry measurements were normal in seven subjects and
only mildly impaired in the remaining five of the 12 subjects with BHR.
CONCLUSION: This study provides strong supporting evidence that inhaled V2O5
induces BHR and asthma in subjects previously free of lung disease; the
abnormality may persist for up to 23 months following exposure; routine
spirometry will not detect affected subjects.
Author(s):
Leigh R ; Hargreave FE
Affiliation: Asthma Research Group, Department of Medicine, St Joseph's
Hospital and McMaster University, Hamilton, Ontario, Canada.
Title: Occupational
neutrophilic asthma. Source: Can Respir J (Canadian respiratory journal : journal of the Canadian
Thoracic Society.) 1999 Mar-Apr; 6(2): 194-6
Abstract: Occupational asthma is typically associated with an eosinophilic
bronchitis. The case of a 41-year-old woman who developed symptoms of asthma
after occupational exposure to metal working fluids is reported. The diagnosis
of asthma was confirmed by an forced expiratory volume in 1 s (FEV1) of 1.7
(59% predicted), with 11% reversibility after inhaled bronchodilator and a
provocation concentration of methacholine to cause a fall in FEV1 of 20% (PC20)
of 0.4 mg/mL. Induced sputum examination showed a marked neutrophilia. Over the
next six months, serial sputum analyses confirmed the presence of a marked
sterile neutrophilic bronchitis during periods of occupational exposure to
metal working fluids, which resolved when the patient was away from work and
recurred when she returned to work. The sputum findings were mirrored by
corresponding changes in spirometry and PC20 methacholine. The findings
indicate the occurrence of occupational asthma associated with an intense,
sterile neutrophilic bronchitis after exposure to metal working fluids.
Author(s):
Avila PC ; Shusterman DJ
Affiliation: Department of Medicine, University of California San
Francisco School of Medicine, USA.
Title: Work-related
asthma and latex allergy. Sorting out the types, causes, and consequences.
Source:
Postgrad Med (Postgraduate medicine.)
1999 Jun; 105(7): 39-46
Abstract: Work-related asthma now has clear
definitions based on criteria agreed upon by the American College of Chest
Physicians. The clinician should suspect occupational asthma, irritant-induced
asthma, or work-aggravated asthma in adults with new-onset asthma or asthma
symptoms that worsen during work, after work (late allergic response), or over
the course of workdays. The possible cause should be sought, and a skin test or
immunoassay should be performed, if possible,to he;lp detect sensation. Workup
als o includes objective documentation of worsening of symptoms and airway
obstruction during occupational exposure. If this information is inconclusive,
an inhalation challenge may be considered. Medical management is the same as
for nonoccupational asthma, but cessation of exposure to the specific agent is
necessary to improve long-term diagnosis. Latex allergy and latex-induced
asthma are becoming more common in the workplace, particularly in the
healthcare field. No commercially available standard serum or skin test are
available for diagnosis. The principal treatment is avoidance of latex, which
can be achieved in most cases without extensive changes to the workplace.
Author(s): Wisnewski AV ; Stowe MH ; Cartier A ; Liu Q ; Liu J ; Chen L ; Redlich CA
Affiliation: Department of Internal Medicine, Yale School of Medicine,
333 Cedar Street, LCI-105, New Haven, CT 06520, USA. adam.wisnewski@yale.edu
Title: Isocyanate
vapor-induced antigenicity of human albumin. Source: J Allergy Clin Immunol (The Journal of allergy and
clinical immunology.) 2004 Jun; 113(6): 1178-84
Abstract: BACKGROUND: The bioreactivity of isocyanate, a leading cause of
occupational asthma, has led to uncertainty regarding the chemical's
antigenicity and mechanisms that elicit immunopathology. OBJECTIVE: To
understand better the biologically relevant antigenic forms of hexamethylene
diisocyanate (HDI), commonly used in the auto body industry. METHODS: Human
albumin was exposed to HDI vapors through a novel approach designed to model
the air-liquid interface of the human airway. Vapor HDI-exposed albumin was
characterized by electrophoresis, chemical substitution analysis, mass
spectrometry, and serology studies on auto body shop workers (N=203) and HDI
asthmatics (N=11). RESULTS: HDI vapors caused significant changes in the shape
and/or charge of human albumin, which differed from albumin exposed to liquid
phase HDI, with lower isocyanate substitution ratios and distinct electrophoretic
mobility. Specific sites of vapor HDI conjugation to albumin were identified at
His(247) and Lys(414). Vapor HDI-exposed albumin was specifically recognized by
the humoral arm of the human immune system, with a strong dependence on albumin
as the carrier. Vapor HDI-exposed albumin-specific IgG titers were
significantly associated with HDI exposure (P=.001), and specific IgE was
detectable in 55% (6/11) of isocyanate asthmatics versus 1.5% (3/203) of
exposed healthy workers. Parallel studies using HDI-exposed albumin conjugates
produced by previously published methods showed less significant associations
of HDI-specific IgG and IgE with exposure and disease, respectively.
CONCLUSION: HDI-albumin conjugates produced by novel vapor phase exposure methods
may be more physiologically relevant than those produced by previously
published methods and of greater utility in characterizing the immune responses
associated with HDI exposure and asthma.
Author(s):
Delfino
RJ
Affiliation: Epidemiology Division, Department of Medicine, University
of California, Irvine, California 92697-7550, USA. rdelfino@uci.edu
Title: Epidemiologic
evidence for asthma and exposure to air toxics: linkages between occupational,
indoor, and community air pollution research. Source: Environ Health Perspect (Environmental health
perspectives.) 2002 Aug; 110 Suppl 4: 573-89
Abstract: Outdoor ambient air pollutant exposures in communities are relevant to the acute exacerbation and possibly the onset of asthma. However, the complexity of pollutant mixtures and etiologic heterogeneity of asthma has made it difficult to identify causal components in those mixtures. Occupational exposures associated with asthma may yield clues to causal components in ambient air pollution because such exposures are often identifiable as single-chemical agents (e.g., metal compounds). However, translating occupational to community exposure-response relationships is limited. Of the air toxics found to cause occupational asthma, only formaldehyde has been frequently investigated in epidemiologic studies of allergic respiratory responses to indoor air, where general consistency can be shown despite lower ambient exposures. The specific volatile organic compounds (VOCs) identified in association with occupational asthma are generally not the same as those in studies showing respiratory effects of VOC mixtures on nonoccupational adult and pediatric asthma. In addition, experimental evidence indicates that airborne polycyclic aromatic hydrocarbon (PAH) exposures linked to diesel exhaust particles (DEPs) have proinflammatory effects on airways, but there is insufficient supporting evidence from the occupational literature of effects of DEPs on asthma or lung function. In contrast, nonoccupational epidemiologic studies have frequently shown associations between allergic responses or asthma with exposures to ambient air pollutant mixtures with PAH components, including black smoke, high home or school traffic density (particularly truck traffic), and environmental tobacco smoke. Other particle-phase and gaseous co-pollutants are likely causal in these associations as well. Epidemiologic research on the relationship of both asthma onset and exacerbation to air pollution is needed to disentangle effects of air toxics from monitored criteria air pollutants such as particle mass. Community studies should focus on air toxics expected to have adverse respiratory effects based on biological mechanisms, particularly irritant and immunological pathways to asthma onset and exacerbation.
Author(s): Muñoz X ; Cruz MJ ; Orriols R ; Bravo C ; Espuga M ; Morell F
Affiliation: Servei de Pneumología, Hospital Universitari Vall d'Hebron,
Barcelona, Spain. xmunoz@vhebron.net.es
Title: Occupational
asthma due to persulfate salts: diagnosis and follow-up. Source: Chest (Chest.) 2003 Jun; 123(6):
2124-9
Abstract: BACKGROUND: Persulfate salts have been identified as a cause of
occupational asthma (OA). The aim of the present study was to describe the
clinical characteristics, diagnostic testing results, and follow-up of eight
patients with OA that was triggered by these chemical compounds. METHODS: Eight
patients with OA due to exposure to persulfate salts were studied. Immunologic,
lung function, and specific bronchial challenge tests (SBCTs) were performed in
all patients. Once their condition had been diagnosed, the patients were seen
every 1, 3, and 6 months for a mean duration of 18 months. RESULTS: The mean
time of exposure to persulfate salts up to diagnosis was 15 years (range, 3 to
27 years), and mean time that had elapsed between symptom onset and diagnosis
was 38 months (range, 3 to 120 months). Three patients were smokers, six
patients presented with rhinitis prior to asthma in relation to persulfate
exposure, and three presented with dermatitis. The results of total IgE tests
were positive in six patients, and the results of skin-prick tests for
detection of persulfate salts were positive in five of these patients. The
results of a SBCT was positive in the seven patients in whom it was performed.
Symptoms persisted in all but one patient and required medical treatment.
CONCLUSIONS: The results suggest that the reliable diagnosis of OA due to
persulfate salts must be based on the specific challenge test until further
experience has been acquired. Despite avoiding exposure, patients continued
with symptoms and required treatment for the control of symptoms. Finally, a
dependent IgE mechanism appears to be implicated in the pathogenesis of OA due
to exposure to persulfate salts.
Author(s):
Rosenman
KD ; Reilly
MJ ; Schill
DP ; Valiante
D ; Flattery
J ; Harrison
R ; Reinisch
F ; Pechter
E ; Davis
L ; Tumpowsky
CM ; Filios
M
Affiliation: Michigan State University, 117 West Fee Hall, East Lansing,
MI 48824, USA. Rosenman@msu.edu
Title: Cleaning
products and work-related asthma. Source: J Occup Environ Med (Journal of occupational and environmental
medicine / American College of Occupational and Environmental Medicine.)
2003 May; 45(5): 556-63
Abstract: To describe the characteristics of individuals with work-related asthma
associated with exposure to cleaning products, data from the California-,
Massachusetts-, Michigan-, and New Jersey state-based surveillance systems of
work-related asthma were used to identify cases of asthma associated with
exposure to cleaning products at work. From 1993 to 1997, 236 (12%) of the 1915
confirmed cases of work-related asthma identified by the four states were
associated with exposure to cleaning products. Eighty percent of the reports
were of new-onset asthma and 20% were work-aggravated asthma. Among the
new-onset cases, 22% were consistent with reactive airways dysfunction
syndrome. Individuals identified were generally women (75%), white non-Hispanic
(68%), and 45 years or older (64%). Their most likely exposure had been in
medical settings (39%), schools (13%), or hotels (6%), and they were most
likely to work as janitor/cleaners (22%), nurse/nurses' aides (20%), or
clerical staff (13%). However, cases were reported with exposure to cleaning
products across a wide range of job titles. Cleaning products contain a diverse
group of chemicals that are used in a wide range of industries and occupations
as well as in the home. Their potential to cause or aggravate asthma has
recently been recognized. Further work to characterize the specific agents and
the circumstances of their use associated with asthma is needed. Additional
research to investigate the frequency of adverse respiratory effects among
regular users, such as housekeeping staff, is also needed. In the interim, we
recommend attention to adequate ventilation, improved warning labels and
Material Safety Data Sheets, and workplace training and education.
Author(s):
Draper
A ; Cullinan
P ; Campbell
C ; Jones
M ; Newman
Taylor A
Affiliation: Department of Occupational & Environmental Medicine,
Royal Brompton Hospital & NHLI, 1b Manresa Road, London SW3 6LR, UK.
adrian@adraper.freeserve.co.uk
Title: Occupational
asthma from fungicides fluazinam and chlorothalonil. Source: Occup Environ Med (Occupational and environmental
medicine.) 2003 Jan; 60(1): 76-7
Abstract: We report two cases of occupational asthma caused by sensitisation to
powdered fungicides fluazinam and chlorothalonil, from the same fungicide
formulation plant. Both developed work related lower respiratory symptoms after
a latent interval of asymptomatic exposure. The diagnosis in each case was
confirmed with a serial peak flow record in the workplace followed by specific
inhalation tests. These fungicides are known to cause dermatitis; this report
indicates that these compounds can induce specific immunological reactions in
the airways as well as skin.
Author(s):
Park
HS ; Kim
HY ; Suh
YJ ; Lee
SJ ; Lee
SK ; Kim
SS ; Nahm
DH
Affiliation: Department of Allergy and Clinical Immunology, Ajou
University School of Medicine, Suwon, Korea. hspark@madang.ajou.ac.kr
Title: Alpha
amylase is a major allergenic component in occupational asthma patients caused
by porcine pancreatic extract. Source: J Asthma (The Journal of asthma : official journal of the
Association for the Care of Asthma.) 2002 Sep; 39(6): 511-6
Abstract: Porcine pancreatic extracts (PPE) are composed of alpha-amylase and
lipase, which are common components of digestive enzymes. They have been known
to cause occupational asthma in exposed workers in pharmaceutical and baking
industries, as well as in a laboratory technician, but there has been no report
of PPE-induced occupational asthma in medical personnel and their IgE binding
components to each component. Four asthmatic subjects showing positive results
on PPE-bronchoprovocation testing were enrolled. All of them were nurses
working in a university hospital. Their job included grinding and mixing PPE
powder for admitted patients. Serum-specific IgE antibodies to PPE,
alpha-amylase, and lipase were measured by enzyme linked immunosorbent assay
(ELISA). To confirm specificity of IgE binding and cross-allergenicity among
the three extracts, ELISA inhibition tests were performed. In order to
characterize allergenic components within these three extracts, SDS-PAGE and
IgE immunoblot analysis were done. Specific IgE antibodies to PPE,
alpha-amylase, and lipase were detectable by ELISA in all study subjects. An
alpha-amylase ELISA inhibition test showed significant inhibitions by amylase
and PPE, and minimal inhibition by lipase. However, a lipase ELISA inhibition
test showed significant inhibitions by alpha-amylase and PPE with a lesser
degree of inhibition by lipase. Furthermore, IgE immunoblot analysis showed one
IgE binding component (55 kDa) within PPE, six components (55 kDa, 43 kDa, 41
kDa, 32 kDa, 31 kDa, 29 kDa) within alpha-amylase and two components (31 kDa,
29 kDa) within lipase extracts. Thesefindings suggest that inhalation of PPE
powder can induce IgE-mediated bronchoconstriction in exposed nurses.
Alpha-amylase is a major allergenic component within PPE.
Author(s):
Frazier
LM ; Beasley
BW ; Sharma
GK ; Mohyuddin
AA
Affiliation: Department of Preventive Medicine, and Department of
Internal Medicine, University of Kansas School of Medicine-Wichita, Wichita,
KS, USA. lfrazier@kumc.edu
Title: Health
information in material safety data sheets for a chemical which causes asthma.
Source:
J Gen Intern Med (Journal of general internal
medicine : official journal of the Society for Research and Education in
Primary Care Internal Medicine.) 2001 Feb; 16(2): 89-93
Abstract: OBJECTIVE: To assess the quality of health information on material
safety data sheets (MSDS) for a workplace chemical that is well known to cause
or exacerbate asthma (toluene diisocyanate, TDI). DESIGN: We reviewed a random
sample of 61 MSDSs for TDI products produced by 30 manufacturers. MEASUREMENTS
AND MAIN RESULTS: Two physicians independently abstracted data from each MSDS
onto a standardized audit form. One manufacturer provided no language about any
respiratory effects of TDI exposure. Asthma was listed as a potential health
effect by only 15 of the 30 manufacturers (50%). Listing asthma in the MSDS was
associated with higher toluene diisocyanate concentrations in the product (P
<.042). Allergic or sensitizing respiratory reactions were listed by 21
manufacturers (70%). CONCLUSIONS: Many MSDSs for toluene diisocyanate do not
communicate clearly that exposure can cause or exacerbate asthma. This suggests
that physicians should not rely on the MSDS for information about health
effects of this chemical.
Author(s):
Purohit
A ; Kopferschmitt-Kubler
MC ; Moreau
C ; Popin
E ; Blaumeiser
M ; Pauli
G
Affiliation: Service de Pneumologie, Hôpital Lyautey, Hôpitaux
Universitaires de Strasbourg, France.
Title: Quaternary
ammonium compounds and occupational asthma. Source: Int Arch Occup Environ Health (International archives of
occupational and environmental health.) 2000 Aug; 73(6): 423-7
Abstract: OBJECTIVE: Quaternary ammonium compounds, among which benzalkonium
chloride is one of the best-known, are commonly used as antiseptics,
disinfectants, detergents and preservatives. They can cause occupational
asthma, which however, has been rarely reported so far, despite wide use of
these products. We report three such cases. Possible mechanisms causing asthma
are discussed, taking into account their characteristics. METHODS AND RESULTS:
Our patients, all female nurses, manifested asthma symptoms upon handling
disinfectant solutions containing benzalkonium chloride. Work-related fall in
PEFR was observed in all of them. The diagnosis was confirmed by challenge
tests where the patients were exposed, in a closed chamber, to suspected
disinfectant contained in a tray. All of the women developed early or delayed
symptoms upon exposure. Similar challenge tests to placebo or other
disinfectants devoid of quaternary ammonium compound were negative. CONCLUSION:
These three cases, in addition to others reported in the literature, point out
an as yet poorly known etiology of occupational asthma to quaternary ammonium
compounds in hospital employees. The exact mechanism of the action remains
unexplained.
Author(s):
Daenen
M ; Rogiers
P ; Van
de Walle C ; Rochette
F ; Demedts
M ; Nemery
B
Affiliation: Pneumology, K.U. Leuven, Belgium.
Title: Occupational
asthma caused by palladium. Source: Eur Respir J (The European respiratory journal : official journal of the
European Society for Clinical Respiratory Physiology.) 1999 Jan; 13(1):
213-6
Abstract: Occupational exposure to complex
platinum salts is a well-known cause of occupational asthma. Although there is evidence
that platinum refinery workers may also be sensitized to other precious metals,
such as palladium or rhodium, no instances of occupational asthma due to an
isolated sensitization to palladium have been reported. A case is reported of
occupational rhinoconjunctivitis and asthma in a previously healthy worker
exposed to the fumes of an electroplating bath containing palladium. There was
no exposure to platinum. Sensitization to palladium was documented by
skin-prick tests. The skin-prick test was positive with Pd(NH3)4Cl2, but not
with (NH4)2PdCl4. Corresponding salts of platinum were all negative. A
bronchial provocation test with Pd(NH3)4Cl2 (0.0001% for a total of 315 s,
followed by 0.001% for a total of 210 s) led to an early decrease in forced expiratory
volume in one second (-35%). A similar exposure (0.001% for a total of 16 min)
in an unrelated asthmatic gave no reaction. This case shows that an isolated
sensitization to palladium can occur and that respiratory exposure to palladium
is a novel cause of metal-induced occupational asthma.
Author(s):
Waddell
WJ
Affiliation: Department of Pharmacology and Toxicology, School of
Medicine, University of Louisville, Kentucky, USA.
Title: Toxicologic
considerations in the diagnosis of occupational asthma. Source: Ann Allergy Asthma Immunol (Annals of allergy, asthma &
immunology : official publication of the American College of Allergy, Asthma,
& Immunology.) 1999 Dec; 83(6) Pt 2: 618-23
Abstract: BACKGROUND: The consideration of dose for chemicals inducing occupational asthma is examined from the point of view of a toxicologist. Two widely used chemicals in industry, toluene diisocyanate (TDI) and formaldehyde, are used as examples of agents that are formally recognized by OSHA to cause occupational asthma. The Permissible Exposure Limit (PEL) of OSHA and the Threshold Limit Value (TLV) of ACGIH for TDI are identical and are in the range of values for which occupational asthma has been reported in some workers. The narrow range of exposure values for TDI in studies of workers with and without asthma is discussed and correlated with the background concentration of TDI in the ambient atmosphere. For formaldehyde, the PEL and TLV, in contrast, offer a wide margin of safety for the inducement of occupational asthma. CONCLUSION: From this disparity in exposure limits for TDI and formaldehyde, it is concluded that occupational exposure limits by agencies for specific chemicals do not provide a reliable indication of the concentration of a chemical that is necessary to produce occupational asthma. The need for a better appreciation of dose response, particularly relative to background, ambient levels, in the evaluation of occupational asthma is emphasized.
General Information Chemicals Organic Matter Particulates-Air Pollution
Author(s):
Sherson
D ; Andersen
B ; Hansen
I ; Kjøller
H
Affiliation: Department of Occupational and Environmental Medicine,
Vejle Hospital, Vejle, Denmark. davshe@vs.vejleamt.dk
Title: Occupational
asthma due to freeze-dried raspberry. Source: Ann Allergy Asthma Immunol (Annals of allergy, asthma &
immunology : official publication of the American College of Allergy, Asthma,
& Immunology.) 2003 Jun; 90(6): 660-3
Abstract: OBJECTIVE: To investigate the possibility that inhalation of raspberry
powder at work can cause occupational asthma. METHODS: We report the case of a
35-year-old, nonsmoking woman who complained of hay fever symptoms, wheezing,
and shortness of breath two or three times a month exclusively in association
with coating chewing gum with raspberry powder. Prick test extracts with the five
types of fruit powder were produced. Peak expiratory flow rate monitoring five
times daily was performed for an 8-week period while the patient was at work.
Specific IgE and histamine release tests for raspberry powder were performed.
Breathing zone dust measurements were taken. RESULTS: Baseline lung function
and histamine provocation test results were normal. During the 8-week
monitoring period, 5 episodes of reduced peak expiratory flow rate were
demonstrated. Each period was directly related to working with raspberry
powder. A 9-mm prick test result positive for raspberry powder was seen
(histamine control, 9 mm). In addition, the result of a radioallergosorbent
test for raspberry was positive (0.84 kUA/L). The result of a histamine release
test with raspberry powder from work was negative. Breathing zone total dust
measurement was 5.9 mg/m3. CONCLUSIONS: To our knowledge, this is the first
description of occupational asthma due to the inhalation of raspberry powder.
The symptoms of the patient described herein disappeared after she was moved to
another part of the factory. Hygienic improvements were performed at the
workplace to reduce the sensitization risk of other workers.
Author(s):
De Zotti R ; Gubian F
Affiliation: Institute of Occupational Medicine, University of Trieste,
Italy.
Title: Asthma and
rhinitis in wooding workers. Source: Allergy Asthma Proc (Allergy and asthma proceedings : the official
journal of regional and state allergy societies.) 1996 Jul-Aug; 17(4):
199-203
Abstract: We present some cases of rhinitis and asthma in wooding workers exposed to hard or soft woods. The specific provocation test confirmed the diagnosis of rhinitis in three patients and of asthma in four. Rhinitis was caused by oak, beech, and pine, while asthma was caused by obeche, chestnut, acacia, and iroko. Occupational exposure to the specific wood, before onset of symptoms (symptom latency) was shorter for patients with asthma. All seven patients with respiratory symptoms were nonsmokers; three were atopics and four, all with asthma, had nonspecific bronchial hyperreactivity. Twenty-four hours after the test, PD20FEV1 had decreased in two cases with rhinitis and two with asthma, although the data did not reach statistical significance (Wilcoxon matched-pairs test: NS). After the SBPT, blood eosinophils increased in two cases with rhinitis and three with asthma, and the data were at the limit of statistical significance (P = 0.046). The study confirms that not only hard essences, but also soft woods can cause respiratory symptoms, although the pathogenetic mechanisms are still unclear. A specific provocation test is still the best and sometimes only means of diagnosing wood asthma; standardized protocols with repeated measurements of nonspecific airway responsiveness and of eosinophils in the blood may be helpful for a better understanding of the pathogenetic mechanism and predisposing factors.
Author(s): Añibarro B ;
Fontela JL ;
De La Hoz F
Affiliation: Hospital Virgen de la Luz, Cuenca, Spain.
Title: Occupational
asthma induced by garlic dust. Source: J Allergy Clin Immunol (The Journal of allergy and
clinical immunology.) 1997 Dec; 100(6) Pt 1: 734-8
Abstract: BACKGROUND: Garlic dust has not been a frequently encountered cause of
IgE-mediated disease. OBJECTIVE: We report on 12 patients (all of them garlic
workers) with the clinical criteria for occupational asthma. METHODS: Skin
prick tests and serum-specific IgE determinations were performed with common
inhalants, garlic, and other members of the Liliaceae family (onion, leek, and
asparagus). Bronchial challenge test with garlic powder was performed in all
patients. Garlic and onion extract proteins were separated by sodium
dodecylsulfate-polyacrylamide gel electrophoresis. Immunoblot and IgE
immunoblot inhibition analyses were performed with patients' sera on extracts
of garlic, onion, and pollens of Phleum pratense and Chenopodium album.
RESULTS: Garlic sensitization was demonstrated by bronchial challenge test in
seven patients (group 1) and ruled out in the remaining five (group 2).
Clinical data were similar in both groups. The patients with garlic allergy had
a mean age of 27 years, and all of them had pollen allergy; sensitization to
other members of the Liliaceae family was also common. Electrophoresis of
garlic extract revealed two major protein bands at approximately 12 and 54 kd.
During IgE immunoblotting, the pool of sera reacted with garlic proteins mainly
at 54 kd. Preincubation with onion, Phleum, and Chenopodium partially abolished
the IgE binding to several allergens of garlic. CONCLUSION: We report on seven
patients in whom an occupational garlic allergy was demonstrated. Garlic
allergy is relatively rare but seems to affect young subjects with pollen
allergy, and sensitization to other members of the Liliaceae family is common.
The results of this study confirm the presence of some structurally similar
allergens in garlic, onion, and certain pollens.
Author(s):
Baur X ; Degens PO ; Sander I
Affiliation: Professional Associations' Research Institute for
Occupational Medicine, University of Bochum, Germany.
Title: Baker's
asthma: still among the most frequent occupational respiratory disorders.
Source:
J Allergy Clin Immunol (The Journal of allergy and
clinical immunology.) 1998 Dec; 102(6) Pt 1: 984-97
Abstract: BACKGROUND: Baker's asthma and
rhinitis are among the most frequent occupational respiratory disorders.
OBJECTIVE: The aim of the study was to evaluate the frequency of work-related
symptoms and the clinical relevance of sensitization to allergens in screened
and symptomatic bakers. METHODS: Eighty-nine bakers participating in a
screening study and 104 bakers filing a claim for compensation were examined with
regard to occupational and clinical case history, lung function parameters, and
sensitization to bakery allergens by skin prick tests, specific IgE analyses,
and inhalative challenge tests. RESULTS: A high prevalence of respiratory
disorders, abnormal lung function parameters, and sensitization to bakery
allergens exists. Most frequently, bakers with workplace-related respiratory
symptoms showed sensitization to wheat flour (64%), rye flour (52%), soy bean
flour (25%), and alpha-amylase (21%). The correlation between these
sensitizations and asthma case history and inhalative challenge test responses
was significant. However, approximately 29% of the bakers with respiratory
symptoms showed no sensitization to these bakery allergens, whereas 32% of the
sensitized bakers in the screening group had no workplace-related symptoms.
Atopic status defined by skin prick test sensitization to common allergens or
elevated total IgE levels was found to be a risk factor for the development of
sensitization to bakery allergens and respiratory symptoms. On the other hand,
there is evidence for an increased frequency of elevated total IgE as the
result of occupational allergen exposure because respective findings were
observed in bakers without symptoms. CONCLUSION: Sensitization to bakery
allergens seems to be the main cause of baker's asthma and rhinitis but cannot
explain the asthma case history in each case. Further methods are required to
objectively assume irritative pathomechanisms. Our findings indicate the
necessity for an improved primary prevention of exposure to inhalative noxae in
bakeries.
Author(s):
Suh CH ; Park HS ; Nahm DH ; Kim HY
Affiliation: Department of Allergy and Clinical Immunology, Ajou
University School of Medicine, Suwon, Korea.
Title: Oilseed
rape allergy presented as occupational asthma in the grain industry.
Source:
Clin Exp Allergy (Clinical and experimental allergy
: journal of the British Society for Allergy and Clinical Immunology.) 1998
Sep; 28(9): 1159-63
Abstract: BACKGROUND: There have been several reports on respiratory allergic
symptoms induced by pollen of oilseed rape. To the best of our knowledge, this
is the first report dealing with oilseed rape dust mainly composed of seeds, as
an occupational allergen in the grain industry. In this paper, we present a
case of occupational asthma caused by oilseed rape dust from the Animal Feed
Industry, which proved to be induced by an IgE-mediated reaction. METHODS AND
RESULTS: The patient displayed positive responses to Dermatophagoides farinae
as well as oilseed rape dust extract. The bronchoprovocation test showed an
early asthmatic response to oilseed rape dust extract. Serum specific IgE
antibody to oilseed rape antigen was detected by enzyme-linked immunosorbent
assay (ELISA). ELISA inhibition test showed significant inhibitions with
addition of oilseed rape antigen. In order to further identify the allergenic
components of extract, sodium dodecyl sulphate-polyacrylamide gel
electrophoresis (SDS-PAGE) and immunoblot analysis were performed. Fourteen
IgE-binding components ranging from 10 to 160kDa were detected within the
oilseed rape extract. CONCLUSION: These results suggest that the inhalation of
oilseed rape dust, not pollen, can cause IgE mediated bronchoconstriction in an
exposed worker of the grain industry.
Author(s):
Kronqvist M ; Johansson E ; Pershagen G ; Johansson SG ; van Hage-Hamsten M
Affiliation: Department of Medicine, Danderyd Hospital, Stockholm,
Sweden.
Title: Increasing
prevalence of asthma over 12 years among dairy farmers on Gotland, Sweden:
storage mites remain dominant allergens. Source: Clin Exp Allergy (Clinical and experimental
allergy : journal of the British Society for Allergy and Clinical Immunology.)
1999 Jan; 29(1): 35-41
Abstract: BACKGROUND: Earlier studies from several countries have shown that
IgE-mediated allergy in rural populations is of considerable importance and
that storage mites are dominant allergens. OBJECTIVE: In an epidemiological
follow-up study among farmers on the island of Gotland, Sweden in 1996 we
wished to investigate the prevalence of respiratory allergy and to find out
whether storage mites are still important allergens in a farming environment.
METHODS: A questionnaire concerning airway symptoms, social and working
conditions and smoking habits was distributed to all Gotland farmers aged 15-65
years and was completed by 1577 (86.7%), of whom 1015 were dairy farmers. Based
on the answers, 500 dairy farmers were invited to undergo a medical examination
which included a skin-prick test (SPT) and blood sampling for RAST analyses.
Prevalence figures (symptoms, RAST and SPT) given for the whole population (n =
1015) were based on the investigation of the 461 farmers who took part in the
examination. RESULTS: Immediate onset hypersensitivity was present in 41.7% of
the 1015 farmers studied, which is almost the same figure as in 1984 (40.0%).
The prevalence of asthma had increased significantly during the previous 12
years (5.3% vs 9.8%), as had asthma in combination with rhinoconjunctivitis
(3.7% vs 7.0%). Rhinoconjunctivitis, on the other hand, had not changed
significantly (36.5% vs 33.1%) and remained one of the most common symptoms.
The prevalence of storage mite allergy in the farming population in 1996 was
6.5% and constituted an important cause of allergic symptoms. CONCLUSION: Over
12 years, Gotland dairy farmers have developed significantly more respiratory
symptoms from the lower airways, although the proportion with atopy is
unchanged. Storage mites are still dominant allergens for developing allergic
disease.
Author(s): Lopez-Rubio A ;
Rodriguez J ;
Crespo JF ;
Vives R ;
Daroca P ;
Reaño M
Affiliation: Servicio de Alergia, Hospital Universitario 12 de Octubre,
Madrid, Spain.
Title: Occupational
asthma caused by exposure to asparagus: detection of allergens by
immunoblotting. Source: Allergy (Allergy.)
1998 Dec; 53(12): 1216-20
Abstract: BACKGROUND: Vegetables of the
Liliaceae family, such as garlic or onion, have been reported to cause
occupational asthma. However, there are few data on adverse reactions to
asparagus. We evaluated the role of asparagus as a cause of asthma in a patient
with respiratory symptoms occurring at work (horticulture) and studied relevant
allergens. METHODS: A 28-year-old man complained of rhinoconjunctivitis and
asthma when harvesting asparagus at work. Eating cooked asparagus did not
provoke symptoms. A positive skin test reaction was observed with raw
asparagus, Alternaria alternata, and grass-pollen extracts. The methacholine
test demonstrated mild bronchial hyperresponsiveness. The patient had an
immediate asthmatic response after challenge with raw asparagus extract.
Bronchial provocation tests with boiled asparagus, A. alternata, and control
extracts were negative. Two unexposed subjects with seasonal allergic asthma
did not react to the raw asparagus extract. RESULTS: The double-blind,
placebo-controlled food challenge with raw asparagus was negative. Serum
asparagus-specific IgE was 13.9 kU(A)/l. By SDS-PAGE immunoblot, at least six
IgE-binding components, ranging from 22 to 73 kDa, were detected only in raw
asparagus. CONCLUSIONS: We report a case of occupational asthma caused by
asparagus inhalation, confirmed by specific bronchoprovocation. Immunoblot
analysis showed that asparagus allergens are very labile and quite sensitive to
heat denaturation.
Author(s):
Armentia A ; Lombardero M ; Martinez C ; Barber D ; Vega JM ; Callejo A
Affiliation: Sección de Alergia, Hospital Rio Hortega, Valladolid,
Spain. jmartinsantos@nexo.es
Title: Occupational
asthma due to grain pests Eurygaster and Ephestia. Source: J Asthma (The Journal of asthma :
official journal of the Association for the Care of Asthma.) 2004 Feb;
41(1): 99-107
Abstract:
BACKGROUND: Workers
occupationally exposed to grain dust have a high prevalence of asthma. The
pathogenesis of their respiratory symptoms remains obscure when sensitization
to cereal allergens has not been proved. Given the ubiquity of arthropods in
stored vegetable products, we have studied the allergenic potential of two very
prevalent grain pests, Eurygaster and Ephestia, as a cause of occupational
asthma. We have also studied the allergenic relationship between Anisakis
simplex (AS) and these pests. METHODS: We selected 15 asthmatic workers exposed
to cereal dust, in whom sensitization to cereal allergens was not clear. As
controls, we selected a patient who suffered from anaphylaxis after the
ingestion of cereals, 6 patients sensitized to different arthropods, 1 patient
who suffered from asthma after inhaling fish flour contaminated with AS, and a
pool of 40 asthmatic patients with different ethiologies not due to arthropods
or cereals. We performed prick tests with these pests, AS, and pure and
parasitized flours, bronchial challenges, specific IgE determination, and RAST
inhibition. RESULTS: All of the 15 cereal-exposed workers were sensitized to
Eurygaster and Ephestia. Only 2 had detectable levels of serum IgE to these
pests, but 13 presented a positive prick test result and IgE to AS without
problems after eating fish. Bronchial challenges were positive to Eurygaster in
7 patients and to Ephestia in 2 patients. Twelve patients had positive prick
tests to parasitized flour but not to pure flour. The patient with cereal
anaplylaxis presented sensitization to both flours but not to AS. In the
control group, the patient who suffered from asthma after the inhalation of
AS-parasitized fish flour presented a positive prick test result and high
levels of specific IgE to these pests. The RAST inhibition showed
cross-reactivity between Eurygaster and AS in this patient, but the inhibition
was not as evident with the sera of other workers. The same tests in the group
of 40 asthmatic patients were negative. CONCLUSIONS: The clinical importance of
pests as a cause of baker's asthma should not be underestimated. Sensitization
to Eurygaster and Ephestia could be important in the asthma episodes suffered
by our patients, and the parasitized wheat was found to have a higher
allergenic potential than pure cereal flour.
Author(s): Gomez MI ; Hwang SA ; Lin S ; Stark AD ; May JJ ; Hallman EM
Affiliation: Bureau of Environmental and Occupational Epidemiology, New
York State Department of Health, Troy, New York.
Title: Prevalence
and predictors of respiratory symptoms among New York farmers and farm
residents. Source: Am J Ind Med
(American journal of industrial medicine.) 2004 Jul; 46(1): 42-54
Abstract:
BACKGROUND: Data from
telephone interviews with New York farmers and farm residents were used to
study the prevalence and risk factors of symptoms that could be related to
asthma and allergies. METHODS: Participants were asked if they had wheezing or
whistling in the chest in the past year and about the occurrence of stuffy,
itchy, runny nose or watery, itchy eyes in the past year. RESULTS: The
prevalence of wheeze was 18.2% and of stuffy nose/watery eyes was 57.4% (N =
1,620). Significant risk factors for wheeze were cigarette smoking, a systemic
reaction to allergy skin testing, immunotherapy, or insect sting, reactivity to
a pet, having goats, and more acreage in corn for silage. Significant risk
factors of stuffy nose/watery eyes were younger age, having more than a high
school education, being a worker on the farm, and having done spraying.
CONCLUSIONS: Wheeze may be indicative of existing or latent asthma, a
potentially limiting respiratory illness. Stuffy, itchy, runny nose or watery,
itchy eyes, which may cause irritation and discomfort, may also indicate an
increased sensitivity to respirable dusts and chemicals. This cohort of New
York farmers had significant farm-related risk factors for wheeze and stuffy
nose/watery eyes. Am. J. Ind. Med. 46:42-54, 2004.
Author(s):
Eduard W ; Douwes J ; Omenaas E ; Heederik D
Affiliation: National Institute of Occupational Health, Oslo, Norway. wijnand.eduard@stami.no
Title: Do farming
exposures cause or prevent asthma? Results from a study of adult Norwegian
farmers. Source: Thorax (Thorax.)
2004 May; 59(5): 381-6
Abstract: BACKGROUND: A protective effect of
endotoxin exposure on atopy and asthma in farmers' children has been
postulated. Studies of adult farmers have shown conflicting results but often
lack exposure data. The prevalence of asthma in farmers with different exposure
levels to microbial agents and irritant gases was compared. METHODS: Atopy was
defined as a positive response to multiple radioallergosorbent tests (RAST)
with a panel of 10 common respiratory allergens, and asthma was ascertained by
a questionnaire using a stratified sample (n = 2169) of a farming population
from south-eastern Norway. Exposure of farmers to total dust, fungal spores,
bacteria, endotoxins, and ammonia was assessed by exposure measurements.
RESULTS: The prevalence of asthma was 3.7% for physician diagnosed asthma and
2.7% for current asthma. The prevalence of atopy was 14%, but most asthmatic
subjects were non-atopic (80%). Compared with farmers without livestock, (1)
asthma was significantly higher in cattle farmers (OR(adj) 1.8, 95% CI 1.1 to
2.8) and pig farmers (OR(adj) 1.6, 95% CI 1.0 to 2.5), (2) non-atopic asthma
was significantly higher in pig farmers (OR(adj) 2.0, 95% CI 1.2 to 3.3) and in
farmers with two or more types of livestock (OR(adj) 1.9, 95% CI 1.1 to 3.3),
and (3) atopic asthma was less common in farmers with two or more types of
livestock (OR(adj) 0.32, 95% CI 0.11 to 0.97). Exposure to endotoxins, fungal
spores, and ammonia was positively associated with non-atopic asthma and
negatively associated with atopic asthma. No associations were found with
atopy. CONCLUSIONS: Exposure to endotoxins and fungal spores appears to have a
protective effect on atopic asthma but may induce non-atopic asthma in farmers.
Author(s): Jones MG ; Nielsen J ; Welch J ; Harris J ; Welinder H ; Bensryd I ; Skerfving S ; Welsh K ; Venables KM ; Taylor AN
Affiliation: Department of Occupational and Environmental Medicine,
National Heart and Lung Institute, Faculty of Medicine, Imperial College of
Science, Technology and Medicine, London, UK. meinir.jones@ic.ac.uk
Title: Association
of HLA-DQ5 and HLA-DR1 with sensitization to organic acid anhydrides.
Source:
Clin Exp Allergy (Clinical and experimental allergy:
journal of the British Society for Allergy and Clinical Immunology.) 2004
May; 34(5): 812-6
Abstract: BACKGROUND: Organic acid anhydrides are low molecular weight industrial chemicals, able to cause rhinoconjunctivitis and asthma associated with specific IgE against hapten-carrier protein conjugate. Only a proportion of exposed workers develop IgE-associated allergy to acid anhydrides. OBJECTIVE: We determined whether genetic susceptibility, in particular, HLA Class II alleles may be a risk factor. METHODS: We undertook HLA typing in 52 cases who had confirmed specific IgE and in 73 referents matched on site, age and duration of acid anhydride exposure identified in cross-sectional studies of workers exposed to hexahydrophthalic (HHPA), methylhexahydrophthalic (MHHPA) and methyltetrahydrophthalic (MTHPA) anhydrides. RESULTS: The linked alleles DQ5 (odds ratio [OR]=4.3; 95% confidence interval [95% CI]=1.7, 11) and DR1 (OR 3.0; 95% CI 1.2, 11) were more prevalent in cases than in referents. Within DQ5, DQB1(*)0501 was particularly frequent (OR 3.0; 95% CI 1.2, 7.4). CONCLUSION: DQB1(*)05 gene confers susceptibility to develop specific IgE antibodies against HHPA, MHHPA and a non-significant trend with MTHPA. DQB1(*)0501 is protective for other low molecular chemical sensitizers (isocyanates and plicatic acid) which may indicate varying affinities for the corresponding specific class II molecules.
Author(s):
Koksal
N ; Hasanoglu
HC ; Gokirmak
M ; Yildirim
Z ; Gultek
A
Affiliation: Department of Pulmonary Diseases, Turgut Ozal Medical
Center, Inonu University, Malatya, Turkey.
Title: Apricot
sulfurization: an occupation that induces an asthma-like syndrome in
agricultural environments. Source: Am J Ind Med (American journal of industrial medicine.) 2003 Apr;
43(4): 447-53
Abstract: BACKGROUND: Several cases of bronchial asthma have been presenting with
acute attacks during the seasons of apricot sulfurization. The aim of this
study was to reveal the effects of sulfur dioxide (SO(2)) exposure on the
airways of the workers involved in this process. METHODS: SO(2) levels in air
were measured on 15 apricot farms, while the symptom scores of 69 workers were
recorded before, during, and after SO(2) exposure. Physical examination and
pulmonary function tests (PFT) of the workers were also done prior to and after
exposure periods. RESULTS: The measured SO(2) concentrations ranged between
106.6 and 721.0 ppm. Dyspnea (80%), cough (78%), and eye and nose irritation
(83-70%) were the most commonly observed symptoms. The workers had significant
decreases in pulmonary functions after SO(2) exposure. Decrements in FEV(1),
FEV(1)/FVC%, and FEF(25-75%) showed that the acute effect of SO(2) on pulmonary
functions of the workers was mostly of obstructive pattern. CONCLUSIONS: Acute
exposure to SO(2) induces "asthma-like syndrome" (ALS) in apricot
sulfurization workers. SO(2) which has not been previously reported in
agricultural environments as a cause of ALS may be considered as a new agent.
Copyright 2003 Wiley-Liss, Inc.
Author(s):
Brito
FF ; Mur
P ; Barber
D ; Lombardero
M ; Galindo
PA ; Gómez
E ; Borja
J
Affiliation: Section of Allergy, Hospital Complex, Ronda del Carmen, s/n
13002 Ciudad Real, Madrid, Spain.
Title: Occupational
rhinoconjunctivitis and asthma in a wool worker caused by Dermestidae spp.
Source:
Allergy (Allergy.) 2002 Dec; 57(12):
1191-4
Abstract: BACKGROUND: The family Dermestidae belongs to the order Coleoptera.
Occupational allergy has been described in museum personnel. A 31-year-old male
wool worker presenting rhinoconjunctivitis and asthma episodes probably linked
to exposure to Dermestidae-infected wool was investigated. METHODS: Extracts
prepared either from insect bodies or from dust from parasitized wool were used
for skin prick testing (SPT), conjunctival and bronchial provocation tests and
in vitro determinations. RESULTS: SPT and provocation tests were positive to
both extracts. PEFR measurement demonstrated the association between the
patient's symptoms and occupational exposure to Dermestidae. Specific IgE to
both extracts was detected and immunoblotting revealed several protein bands
from 5 to 200 kDa that were reactive to IgE from the patient's serum.
CONCLUSIONS: Dermestidae exposure in wool workers when handling parasitized
wool can be a cause of IgE-mediated rhinoconjunctivitis and asthma.
Author(s):
Ortega
HG ; Kreiss
K ; Schill
DP ; Weissman
DN
Affiliation: National Institute for Occupational Safety and Health,
Centers for Disease Control and Prevention, HELD/ASB/Mailstop L-4218, 1095
Willowdale Rd., Morgantown, West Virginia 26505, USA.
Title: Fatal
asthma from powdering shark cartilage and review of fatal occupational asthma
literature. Source: Am J Ind Med
(American journal of industrial medicine.) 2002 Jul; 42(1): 50-4
Abstract:
BACKGROUND: Work-related
asthma (WRA) is the most common work-associated respiratory disease in
developed countries. METHOD: We report shark cartilage dust as a new potential
cause of occupational asthma (OA) in the context of other fatal OA case
reports. RESULTS: A 38-year-old white male worked for 8 years in a facility
which primarily granulated and powdered various plastics. Sixteen months prior
to his death, the plant began grinding shark cartilage. After 10 months of
exposure, he reported chest symptoms at work in association with exposure to
shark cartilage dust and a physician diagnosed asthma. Six months later, he
complained of shortness of breath at work and died from autopsy-confirmed
asthma. The latency from onset of exposure to symptoms and from symptom onset
to death was shorter than 10 previously reported OA fatalities. CONCLUSION:
Recognition of occupational causes and triggers of asthma and removal of
affected individuals from these exposures is critical and can prevent
progression to irreversible or even fatal asthma.
Author(s):
Uter
W ; Nöhle
M ; Randerath
B ; Schwanitz
HJ
Affiliation: Deptartment of Medical Informatics, Biometry, and
Epidemiology, University of Erlangen/Nürnberg, Erlangen, Germany.
wolfgang.uter@rzmail.uni-erlangen.de
Title: Occupational
contact urticaria and late-phase bronchial asthma caused by compositae pollen
in a florist. Source: Am J Contact Dermat (American journal of contact dermatitis : official journal of the
American Contact Dermatitis Society.) 2001 Sep; 12(3): 182-4
Abstract: Insect-pollinated members of the plant family Compositae (Asteraceae)
rarely cause immediate-type hypersensitivity disease; however, this may have
quite disabling consequences, which is shown by the case of a 42-year-old
female florist. She developed contact urticaria later accompanied by
rhinoconjunctivitis and bronchial asthma with maximum obstruction occurring
some hours after the end of occupational exposure to the causative Compositae
pollens of, for example, dandelions, blazing star, golden rod, yarrow, Aster
ssp, chrysanthemums, and marguerite. Skin testing revealed immediate-type
hypersensitivity to several members of the above-mentioned plant family
confirmed by demonstration of specific IgE antibodies. Bronchial provocation
testing yielded a positive response with all 4 pollen extracts tested. The
patient had to give up work in a flower shop, because sufficient avoidance of
airborne inhalant exposure was not considered practical.
Copyright 2001 by W.B. Saunders Company
Author(s):
Scala
E ; Giani
M ; Pirrotta
L ; Guerra
EC ; Cadoni
S ; Girardelli
CR ; De
Pità O ; Puddu
P
Affiliation: Dept. of Immunodermatology, Allergy & Clinical
Immunology, Istituto Dermopatico dell'Immacolata, I.D.I.-IRCCS, Rome, Italy.
e.scala@idi.it
Title: Occupational
generalised urticaria and allergic airborne asthma due to anisakis simplex.
Source:
Eur J Dermatol (European journal of dermatology
: EJD.) 2001 May-Jun; 11(3): 249-50
Abstract: Anisakis simplex (AS), a fish and cephalopodes parasite, may cause
allergic reactions in humans on eating and/or handling contaminated fish. We present
a case of occupational hypersensitivity to AS in a woman employed in a
frozen-fish factory. She showed both generalised urticarial rash and asthmatic
symptoms after work place exposure. All these symptoms immediately disappeared
after work place exposure was ceased. The presence of a positive skin prick
test and high specific IgE values confirmed a hypersensitivity to anisakis.
This is the first case reported of both occupational generalised urticaria and
allergic airborne asthma due to AS in the same patient. We suggest that AS
could be an important cause of occupational asthma and/or urticaria in the fish
industry.
Author(s):
O'Connor
TM ; Bourke
JF ; Jones
M ; Brennan
N
Affiliation: Department of Respiratory Medicine, Mercy Hospital, Cork,
Ireland. terryoconnor@eircom.net
Title: Report of occupational
asthma due to phytase and beta-glucanase. Source: Occup Environ Med (Occupational and environmental
medicine.) 2001 Jun; 58(6): 417-9
Abstract: OBJECTIVES: Occupational asthma is the principal cause of respiratory
disease in the workplace. The enzymes phytase and beta-glucanase are used in
the agricultural industry to optimise the nutritional value of animal feeds. A
relation between these enzymes and occupational asthma in a 43 year old man was
suspected. METHODS: Inhalation challenge tests were performed with the enzymes
phytase, beta-glucanase, and amylase. Skin prick tests were performed with the
enzymes diluted to a concentration of 1 mg/ml and 5 mg/ml. Specific IgE to
phytase and beta-glucanase were measured with a radioallergosorbent test.
RESULTS: Baseline spirometry values were normal. A histamine challenge test
showed bronchial hyperreactivity. Exposure to phytase and beta-glucanase led to
significant reductions in forced vital capacity and forced expired volume in 1
second. No significant differences were noted after exposure to amylase. Skin
tests showed a positive reaction to beta-glucanase (5 mm) at a concentration of
1 mg/ml and positive reactions to beta-glucanase (7 mm) and phytase (5 mm) at a
concentration of 5 mg/ml. Similarly specific IgE was present against both
phytase and beta-glucanase, at 2.5% and 9.3% binding respectively (2% binding
is considered positive). CONCLUSIONS: This is the first description of
occupational asthma due to the enzymes phytase and beta-glucanase. Their
addition to the ever increasing list of substances associated with occupational
asthma will have notable implications for those exposed to these enzymes.
Author(s):
Lee
SK ; Cho
HK ; Cho
SH ; Kim
SS ; Nahm
DH ; Park
HS
Affiliation: Department of Allergy and Clinical Immunology, Ajou
University School of Medicine, Suwon, Korea.
Title: Occupational
asthma and rhinitis caused by multiple herbal agents in a pharmacist.
Source:
Ann Allergy Asthma Immunol (Annals of allergy, asthma &
immunology : official publication of the American College of Allergy, Asthma,
& Immunology.) 2001 Apr; 86(4): 469-74
Abstract: BACKGROUND: Herb agents have been widely used for centuries in the
Orient and they have been cultivated throughout Asia. There have been a few
cases of occupational allergy caused by herb materials. We report a case of
occupational asthma and rhinitis caused by six herb materials in a pharmacist
working at a pharmacy. OBJECTIVE: We sought the role of immediate
hypersensitivity in herbal agent-induced asthma in a pharmacist. METHODS AND
RESULTS: The patient had strong positive responses on skin prick test to
extracts of six herb materials: Chunkung (Cnidii rhizoma), Banha (Pinellia
ternata), Sanyak (Dioscorea radix), Kangwhal (Ostericum koreanum), Danggui
(Angelica radix), and Kunkang (Zingiberis rhizoma). Bronchoprovocation tests
showed an early asthmatic response to Danggui extract. Serum specific IgE
antibodies to Chunkung, Banha, and Sanyak were detected by ELISA with no
specific IgE bindings to Kangwhal, Danggui, and Kunkang extracts. Twelve
percent sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE)
and IgE immunoblotting revealed one IgE binding component (60 kD) within
Chunkung extract, two (10, 25 kD) in Banha, and four (33, 34, 65, 98 kD) in
Sanyak. Basophil histamine release test revealed that Danggui extract could
release a greater amount of histamine from basophils in the patient than in a healthy
control. CONCLUSIONS: Chunkung, Banha, and Sanyak may induce IgE-mediated
bronchoconstriction in an exposed worker, and Danggui can cause
bronchoconstriction by direct histamine-releasing effect from mast cells in a
sensitized patient.
Author(s): Alvarez MJ ; Estrada JL ; Gozalo F ; Fernandez-Rojo F ;
Barber D
Affiliation: Sección de Alergología, Hospital de León, Spain.
Title: Oilseed
rape flour: another allergen causing occupational asthma among farmers.
Source:
Allergy (Allergy.) 2001 Feb; 56(2):
185-8
Abstract: BACKGROUND: Farmers are exposed to a wide variety of sensitizers. Since occupational asthma (OA) can lead to permanent disability, exposure discontinuation is the preferred treatment. When this is not possible, the identification of the causative allergen may allow an alternative therapy. METHODS: We present three farmers diagnosed with OA as a consequence of handling fodder. We carried out skin tests with common and occupational allergens and with oilseed rape (OSR) extract. Total and specific serum IgE levels were measured. The patients underwent the OSR-bronchial provocation test (OSR-BPT). The day before and 24 h after the OSR-BPT, the methacholine (M)-BPT and induced sputum were performed. Eosinophil percentages and ECP levels were measured in the sputum samples. RESULTS: OSR sensitization (skin tests and specific serum IgE) was detected in all the patients. The OSR-BPT elicited early responses in two subjects. Methacholine sensitivity, sputum eosinophils, and sputum ECP levels increased 24 h after the OSR-BPT in all the patients. CONCLUSIONS: We have demonstrated that inhalation of OSR flour causes bronchoconstriction, induces an eosinophilic inflammatory bronchial response, and increases bronchial hyperresponsiveness in sensitized asthmatics. OSR flour contained in animal fodder should be considered another potential cause of OA among farmers.
General Information Chemicals Organic Matter Particulates-Air Pollution
Author(s): Khoo GT
Title: Occupational
asthma from welding: a case report. Source: Ann Acad Med Singapore (Annals of the Academy of
Medicine, Singapore.) 1996 Mar; 25(2): 293-5
Abstract: Occupational asthma is one of the commonest occupational lung diseases.
This is a case of asthma related to arc-welding in a shipyard. Serial peak expiratory
flow rate readings were taken with and without exposure to the welding process.
The results showed that the patient had occupational asthma from welding. This
case report serves to remind us of the need to ask every adult with asthma for
their occupational history. It emphasises the need for early diagnosis and
removal from the cause of asthma. A delay in diagnosis may lead to non-specific
bronchial reactivity and persistence of symptoms.
Author(s):
Vandenplas O ; Delwiche JP ; Vanbilsen ML ; Joly J ; Roosels D
Affiliation: Dept of Chest Medicine, Mont-Godinne Hospital, Catholic
University of Louvain, Yvoir, Belgium.
Title: Occupational
asthma caused by aluminium welding. Source: Eur Respir J (The European respiratory journal : official journal of
the European Society for Clinical Respiratory Physiology.) 1998 May; 11(5):
1182-4
Abstract: Work-related asthma has been documented in workers employed in the
primary aluminium industry and in the production of aluminium salts. The role
of aluminium in the development of occupational asthma has, however, never been
convincingly substantiated. We investigated a subject who experienced asthmatic
reactions related to manual metal arc welding on aluminium. Challenge exposure
to aluminium welding with flux-coated electrodes, as well as with electrodes
without flux, elicited marked asthmatic reactions. Manual metal arc welding on
mild steel did not cause significant bronchial response. The results of
inhalation challenges combined with exposure assessments provided evidence that
aluminium can cause asthmatic reactions in the absence of fluorides. Awareness
of this possibility may be relevant to the investigation of asthma in workers
exposed to aluminium.
Author(s):
Di Stefano F ; Siriruttanapruk S ; McCoach JS ; Burge PS
Affiliation: Dept of Respiratory Medicine, Birmingham Heartlands
Hospital, UK.
Title: Occupational
asthma due to glutaraldehyde. Source: Monaldi Arch Chest Dis (Monaldi archives for chest
disease = Archivio Monaldi per le malattie del torace / Fondazione clinica del
lavoro, IRCCS [and] Istituto di clinica tisiologica e malattie apparato
respiratorio, Universita di Napoli, Secondo ateneo.) 1998 Feb; 53(1): 50-5
Abstract: In recent years glutaraldehyde has emerged as the main cause of
occupational asthma among healthcare workers. Presently glutaraldehyde is the
best biocide agent for high-level disinfection and cold sterilization and its
use has become widespread in hospitals. Surveillance schemes in the UK, Finland
and the USA have reported an increasing number of cases of occupational asthma
due to glutaraldehyde. The real magnitude of the problem is not well known as
epidemiological studies carried out on a large scale among healthcare workers
are not yet available. In countries where surveillance schemes are implemented,
reports of occupational asthma cases due to glutaraldehyde should be
circumstantiated by more diagnostic details and the diagnosis confirmed by
objective means, to avoid an overestimation of frequency of disease. The
pathogenetic mechanisms of occupational asthma due to glutaraldehyde are
debatable as with other low molecular weight chemicals. A recent study has
documented the first evidence of immunological sensitization in healthcare
workers exposed to this chemical. Occupational asthma caused by glutaraldehyde
can develop at levels of exposure well below the standards accepted in most
countries. In the UK the Occupational Exposure Standard (OES) of this agent
will be lowered from 0.2 ppm (parts of vapour per million parts of air by
volume) to 0.05 ppm. Substitution of glutaraldehyde with an alternative agent
is not currently feasible. Intervention in the workplace and education of
personnel handling this chemical remain irreplaceable parts of any prevention
strategy. Early detection of disease and prompt removal of personnel from
further exposure are the only ways of avoiding any deterioration of
occupational asthma.
Author(s):
Deschamps F ; Prevost A ; Lavaud F ; Kochman S
Affiliation: Department of Occupational Diseases, Hopital Maison
Blanche, Reims, France.
Title: Mechanisms
of occupational asthma induced by isocyanates. Source: Ann Occup Hyg (The Annals of occupational
hygiene.) 1998 Jan; 42(1): 33-6
Abstract: Isocyanates are some of the most important low molecular weight
chemicals associated with occupational asthma. These compounds are often
volatile and they are highly reactive on mucous membranes, especially the
conjunctivae and respiratory tract. Despite numerous data derived from
experimental and clinical investigations, there is no agreement concerning the
real mechanisms involved in isocyanate-induced occupational asthma. In fact,
the cause of occupational asthma is multifactorial. The aim of this paper is to
review the involved physiological causes of isocyanate-induced asthma; the main
mechanisms are immunological, pharmacological and/or irritative.
Author(s): Monsó E
Affiliation: Servei de Pneumologia, Hospital Germans Trias i Pujol,
Badalona, Catalonia, Spain. emonso@ns.hugtip.scs.es Title: Occupational asthma in greenhouse workers.
Source:
Curr Opin Pulm Med (Current opinion in pulmonary
medicine.) 2004 Mar; 10(2): 147-50
Abstract: PURPOSE OF REVIEW: A prevalence of asthma over 5% has been reported in
flower farmers,and work inside greenhouses has emerged as an additional risk
factor. Workplace determinants behind this high prevalence has been examined,
and a prevalence of sensitization to workplace allergens over 30% has been
reported being pollens, moulds, and Tetranychus urticae allergens the main
sensitizers. Bronchial challenge tests in the workplace have demonstrated
occupational asthma in more than 20% of the sensitized greenhouse growers.
RECENT FINDINGS: Air contamination inside greenhouses is mainly related to
moulds, and is facilitated by the high indoor temperature and humidity.
Cladosporium, Penicillium, Aspergillus, and Alternaria and a wide range of
flower pollens are able to sensitize the greenhouse worker and cause
occupational asthma. Tetranychus urticae have allergens shared with other
mites, but the low prevalence of cross-sensitization between them confirm that
Tetranychus urticae contains species-specific allergens that may cause
respiratory symptoms. Additionally, working inside greenhouses has been related
to an increase in the prevalence of chronic bronchitis in nonsmokers. SUMMARY:
The cultivation of greenhouse crops may cause occupational asthma through
sensitization to workplace pollens, moulds, and Tetranychus urticae allergens.
In greenhouse flower growers, skin testing identifies sensitization to these
allergens in one third of the growers, and more than one fifth of the
sensitized workers will develop occupational asthma. Greenhouse work has also
been related to chronic bronchitis in nonsmokers, suggesting a causal effect of
greenhouse air contaminants on this disease as well.
Author(s): Ong TH ; Tan KL ; Lee HS ; Eng P
Affiliation: Department of Respiratory and Critical Care Medicine,
Singapore General Hospital.
Title: A case report of occupational asthma due to
gluteraldehyde exposure. Source: Ann Acad Med Singapore (Annals of the Academy of Medicine,
Singapore.) 2004 Mar; 33(2): 275-8
Abstract:
INTRODUCTION: We report the
first case of occupational asthma due to gluteraldehyde exposure in Singapore
and also describe the use of a specific inhalational challenge (SIC) test in
confirming the diagnosis. CLINICAL PICTURE: A 32-year-old laboratory technician
presented with adult-onset asthma 2 years after daily exposure to
gluteraldehyde which was used to sterilise the mouthpieces used for lung
function testing. SIC testing showed a 25% drop in FEV1 after exposure to
gluteraldehyde but not after exposure to a control, thus confirming the
diagnosis. TREATMENT: Alternative arrangements were made for sterilisation of
the mouthpieces so that gluteraldehyde could be removed from the workplace.
There was a marked improvement in her asthmatic control thereafter.
CONCLUSIONS: This case illustrates the use of a SIC test in the diagnosis of
occupational asthma. Gluteraldehyde is a known cause of occupational asthma and
should be kept in mind when evaluating asthmatic patients in at-risk
occupations. Effective ventilation and proper storage should be ensured to
minimise exposure to gluteraldehyde where its use is necessary.
Author(s): de Silva HD ; Gardner LM ; Drew AC ; Beezhold DH ; Rolland JM ; O'Hehir RE
Affiliation: Co-operative Research Centre for Asthma, Sydney, Australia.
Title: The hevein
domain of the major latex-glove allergen Hev b 6.01 contains dominant T cell
reactive sites. Source: Clin Exp Allergy (Clinical and experimental allergy : journal of the British Society
for Allergy and Clinical Immunology.) 2004 Apr; 34(4): 611-8
Abstract:
BACKGROUND: Sensitization to
natural rubber latex (Hevea brasiliensis) is a major cause of occupational
asthma and rhinitis affecting frequent latex-glove users. Hev b 6.01, a known
major latex allergen, is cleaved naturally into hevein (4.7 kDa) and a
C-terminal fragment (14 kDa). Hevein is an abundant protein in latex-glove
extracts. As the immune response to allergens is initiated by activation of
allergen-specific CD4(+) T cells, identification of dominant T cell epitopes is
crucial for the development of specific immunotherapy. OBJECTIVE: To identify
dominant T cell epitopes of Hev b 6.01 in latex-allergic glove users. METHODS:
Ten latex-allergic frequent glove users and six non-latex-allergic atopic
control subjects were selected, based on clinical symptoms and positive
latex-specific serum IgE. Serum IgE reactivity to glove extract and recombinant
Hev b 6.01 (rHev b 6.01) were analysed by ELISA. Latex-specific short-term
oligoclonal T cell lines were generated from peripheral blood of latex-allergic
subjects. These lines were tested for proliferative responses to overlapping
20-mer peptides of the Hev b 6.01 molecule. CD4(+) T cell intracellular
cytokines, IL-4 and IFN-gamma were assessed following stimulation with
immobilized anti-CD3 in the presence of IL-2. RESULTS: All ten of the
latex-allergic patients showed serum IgE binding to glove extract while eight of
these also showed IgE binding to rHev b 6.01 by ELISA. Western blotting
confirmed reactivity with rHev b 6.01 at around 20 kDa. T cell proliferation
assays showed that latex-specific T cell lines from all subjects responded to
one or more peptides, with greatest frequency of reactivity to peptides Hev b
6.01 p(10-29) and Hev b 6.01 p(19-38) in the hevein domain. An allergic-type
cytokine profile with considerable IL-4 in addition to IFN-gamma was evident
from intracellular cytokine staining. CONCLUSION: Hevein is an important T cell
as well as B cell immunogen and contains dominant T cell reactive sites.
Author(s):
Tarlo
SM
Affiliation: The University of Toronto, Gage Occupational and
Environmental Health Unit, Toronto, Ontario, Canada.
Title: Workplace
respiratory irritants and asthma. Source: Occup Med (Occupational medicine (Philadelphia, Pa.)) 2000
Apr-Jun; 15(2): 471-84
Abstract: Workplace respiratory irritants can
have a variety of effects in relation to asthma. Very high exposures can cause new-onset
asthma (reactive airways dysfunction syndrome or irritant-induced asthma) with
or without concurrent sensitization, e.g., to diisocyanate. Aggravation of
underlying asthma can result from moderate exposures. Adjuvant or other effects
enhancing the risk of sensitization to high molecular weight allergens have
occurred with chronic low-moderate exposures. Enhancement of airway
responsiveness on a short-term basis can be produced by ozone and biological
irritants such as endotoxin and beta 1-3 glucans. Production of nonasthmatic
responses such as hyperventilation and vocal cord dysfunction can mimic asthma
symptoms. Controversy exists as to whether moderate irritant exposures can
cause asthma or long-term worsening of underlying asthma.
Author(s):
Glindmeyer
HW ; Lefante
JJ ; Freyder
LM ; Friedman
M ; Weill
H ; Jones
RN
Affiliation: Department of Medicine, Tulane University, New Orleans, LA
70112-2699, USA.
Title: Relationship
of asthma to irritant gas exposures in pulp and paper mills. Source: Respir Med (Respiratory medicine.) 2003
May; 97(5): 541-8
Abstract: The potential of chronic or acute irritant gas exposures to cause asthma
or a variant condition, reactive airways dysfunction syndrome (RADS) was
investigated by observing asthma incidence in a large working population, using
person-years at risk (P-YR) to compute relative rates (RR). Health data came
from employee examinations at 62 pulp and paper plants. The 39122 workers who
denied asthma beginning before the observation period included: 19326 denying
irritant exposures, with no gassing exposures; 19349 with self-reported
irritant exposures, and no gassing; and 447 with documented gassings. Asthma
was defined as self-reported asthma beginning after the start of observation.
P-YR accrued from September 29, 1986, for the nonexposed and exposed workers,
and from date of first gassing for gassed workers, and ended with disease onset
in any who developed asthma. RR of asthma with 95% confidence intervals (CI95)
were calculated for the exposed and gassed groups, relative to the nonexposed.
Exposed (nongassed) workers had an elevated asthma rate, RR=1.48,
CI95=1.17-1.86, after adjustment for effects of gender and number of
examinations. The rate in gassed workers was not significantly elevated:
RR=1.95, CI95=0.75-5.08. Of the five asthma cases occurring after gassings,
none conformed to diagnostic criteria for RADS. Chronic exposures were
associated with increased rate of asthma onset, which must be interpreted with
caution because self-reported data defined both exposure category and disease.
Documented gassings were not associated with significantly increased rate, and
none of 447 gassed persons developed RADS.
Author(s):
Sauni
R ; Oksa
P ; Vattulainen
K ; Uitti
J ; Palmroos
P ; Roto
P
Affiliation: Tampere Regional Institute of Occupational Health, Clinic
of Occupational Medicine (Tampere University Hospital), Finland.
Title: The effects
of asthma on the quality of life and employment of construction workers.
Source:
Occup Med (Lond) (Occupational medicine (Oxford,
England)) 2001 May; 51(3): 163-7
Abstract: Relatively little is known about the consequences of asthma for patients' work ability. In particular, the relationship between asthma and construction work has not been studied previously. The aim of this study was to determine how asthma affects construction workers' work ability and quality of life, and the most important conditions that cause respiratory symptoms in construction work. A questionnaire was sent to all construction workers examined in the pulmonary clinic of Tampere University Hospital between 1991 and 1995 who were diagnosed as having 'asthma bronchiale' (n = 104). In addition, 206 non-asthmatic construction workers were recruited from the register of the local trade union. Altogether, 73% of the asthmatic construction workers and 70% of the controls completed the questionnaire. Of the asthmatics, 48% were retired, whereas only 24% of the controls were receiving a pension. The asthmatics evaluated their work ability and general health as significantly worse than did the controls. The asthmatics had more limitations in their work and everyday life than the controls. Asthmatic construction workers had often changed work tasks and also occupation because of their illness. Building renovation, cleaning and insulation with mineral fibre materials were the most common causes of respiratory symptoms in the workplace, among both the asthmatics and the controls. Cold air, physical exercise and all types of dust and smoke caused the asthmatics to experience symptoms. It was concluded that asthma limits the work and everyday life of construction workers. Exposure to dusty, non-sensitizing agents is associated with asthmatic symptoms among construction workers.