occupational and work-aggravated asthma
Post on 25-Feb-2016
38 Views
Preview:
DESCRIPTION
TRANSCRIPT
Occupational and work-aggravated asthma
Institut and Outpatient Clinic for Occupational and Environmental Medicine
Ludwig-Maximilians-Universität Münchendennis.nowak@med.uni-muenchen.de
Dennis Nowak
LMU
Site & intensity of the injury Physico-chemical properties
Particle size…<5u go deeper Concentration… Solubility Density… lighter (as) go deeper Reactivity… higher (NH4) more damage
Duration of exposure Signs of alertness Rate / depth of breathing Host response variability / susceptibility Host defense mechanisms
MechanismsToxic Inflammatory • Irritant : farm dust, chemicals• Allergic : flour (bakers)• Sensitizers : toluene di-isocyanates • Infectious : brucellosisCarcinogenic uranium
Symptoms• Cough• Expectoration• Hemoptysis• Dyspnea at rest and/or on exertion• Wheezing• Chest tightness / pain• Upper airways symptoms• Fever, chills, other
EXPOSURE
AIRWAYS
ALVEOLI
NEUROTOXINSFEVERS
UPPER ITIS BRONCHITIS ASTHMA-LIKE ASTHMABRONCHIOLITIS BOOPPULM. EDEMAPNEUMONITISFIBROSIS
Airways exposure
Acute massive
chemical bronchitis
RADS
Chronic low
Chronic BronchitisAsthma-like disease
Acute low
Allergic asthma
Definition Occupational asthmaA. AsthmaB. Onset after entering workplaceC. Association of symptoms to workplaceD1. Agent known to cause OA orD2. Work-related changes in FEV1 or PEFs +/orD3. “ “ “ “ hyperreactivity +/orD4. Positive specific challenge test +/orD5. Clear sx onset after irritant exposure
OA and BHR: Definition (1)
e.g.,“Occupational asthma is a disease characterized by variable airflow limitation and / or airway hyper-responsiveness due to causes and conditions attributable to a particularoccupational environment and not to stimuli encountered outside the workplace.“Bernstein, I.L., Asthma in the workplace, 1993
OA and BHR: Definition (2)
Generally:Inducers: cause airway inflammation and BHRInciters: trigger airway narrowing in patients with BHR, increase frequency of symptoms in pts. with pre-existing asthma
Thus, only inducers should be considered causal agentsBernstein, I.L., Asthma in the workplace, 1993
Work-aggravated asthma
Pre-existing or concurrent asthma that isaggravated by irritants or physicalstimuli at the workplace
Tarlo S. et al., Chest 118 (2000) 1309: 16 % of asthmaticsSaarinen K. et al., ERJ 22 (2003) 305:
21 % of asthmatics
OA and BHR: Pathogenesis, types of disease
Inducers: common aeroallergens EAR, LARLAR inflammation , BHR Even if no obstruction: inflam. , BHR may require removal from work
Inciters: exercise, cold air, etc.no change in inflammation or BHR may require exposure or therapy
Occupational Asthma
NO LATENCY IRRITANT-INDUCED
LATENCY IgE MEDIATEDSPECIFIC NON-IgE
Etiology Mechanism: InducersImmunologic • IgE mediated
– High molecular wght
– Low molecular haptens
• ? Cell mediated– Low molecular
Nonimmunologic– Irritant-toxic
• Grain, crab, castor beans• Woods, gum acacia• Animal dander, urine• Epoxy resins• Chloramine T• Platinum salts• di-isocyanates• Red Cedar• Cobalt• Ammonia, chlorine
History Exam Lung Function Skin tests Blood:
eosinophils, serology-RAST
Radiology Therapeutic trial
Obstructive pattern FEV1,FVC,FEV1/FVC FEF, PEFR RAW, RV/TLC
Bronchodilators Provocation tests
OA and BHR: Types of disease
Occupational asthma - immunological - non-immunological including RADSWork-aggravated asthmaVariant syndromes - eosinophilic bronchitis - potroom asthma - asthma-like syndrome (e.g., organic dusts)
OA and BHR: Pathogenesis, types of disease - typical agents
• High molecular weight agents flour, latex
• Low molecular weight agentsplatinum salts
• Irritants (RADS)chlorine, phosgen
• Potroom AsthmaHF, SO2, (aluminium chloride? fluoride?)
• Asthma-like Syndromeendotoxin, NH3
Atopic asthma
History, questionnaire, SPT, specific IgE (if possible)
Non-specific provocation challenge (e.g., MCh) if possible at the end of a working week after at least two weeks with relevant exposure
Mostly no asthma(exception: e.g.,
isocyanateasthma)
Specific challenge under laboratory conditions with suspected agent /
extract
Lung function monitoring by the patient
for at least 3 wks with / without
workplace exposure
positive
Probablyoccupational
asthma
Lung function monitoring at the workplace vs. non-exposure
Probably non-occupational asthma
negative suspicious un-suspicious
suspicious un-suspicious
and / or
negative positive
OA and BHR: Diagnostic approach
OA and BHR: Diagnostic approach (1)
Questionnaire: good primary toolwork-relatednessrhinoconjunctivitis?sensitivity good, spec. +/-
Skin prick test: quick, simple, safelimited by lack of available/
standardized extractsSpecific IgE: bit less sensitive,
bit more specificsame limits as SPT
OA and BHR: Diagnostic approach (2)
Spirometry: routine spirometry far less sensitive than questionnaire!
Cross-shift spirometry: sensitivity better, but much better on multiple days!
MCh challenge: if negative, mostly excludes OAChange in BHR: +++, > 2 doubling concentrations
Induced sputum: HMW agents: eosinophils LMW agents: eos. , neutro.
Exhaled NO: usefulness questionable for OA
mechanic
electronic
Mobile, onsite peak flow monitoring / spirometry
4
4
4
4380
360
340
320
300
280
260
240
220
200
180
160
Pea
k E
xpira
tory
Flo
w (P
EF)
Litr
es /
Min
ute
20%
50%
D.V
.By Whole Record Mean
Date
ReadingsWork Hours
Additional
W0304October, 20011011
T0405
1111
F0507
1411
S0708
8
M0809
8
T0910
8
W1011
9
T1111
7
T1112
1011
F1213
1011
S1315
1411
M1516
8
T1617
8
W1718
8
T1818
7
T1819
1011
F1920
1011
S2022
1411
M2223
8
T2324
8
W
cewW
Daily MaxDaily MeanDaily MinOasys 2b score for periodPatient restedPatient worked a day shiftPatient worked an afternoon shiftPatient worked a night shiftPatient workedPatient recorded no dataDay excludedThere are comments for dayDay is marked for exclusionMissing waking reading(s)Waking reading(s) created
P.S. Burge, W. Anees
Workplace provocation challenge
OA and BHR: Exposure-response relationship
- Exposure intensity (dose?)- Isocyanate asthma: peak levels!- No effect level? Flour dust < 0.5 mg/m3
Alpha-amylase 0.25 ng/m3
Rat urin protein 0.7 µg/m3
Latex allergens 0.6 ng/m3
cow allergen 20-30 µg/g dust- Upper end of dose-response curve flattens
- Atopy, atopic rhinitis, atopic asthma
- Smoking: only risk factor for platinum salt asthma
FEV1IMMEDIATE REACTION LATE REACTION
DUAL REACTION PROGRESSIVE-PROLONGED
O
HOME-------------WORK-----HOME—WORK--HOMEWORK
Rx
Reactive Airways DysfunctionSyndrome
Asthma-like syndrome Abrupt onset within 12-24 hrs After high irritant exposure Recurrent and persistant > 3 months No preexisting respiratory complaints Airflow obstruction or Non-specific airways hyperreactivity
PrognosisCan not be predicted by severity, exposure, type,...
Progress
Persistent Recurrent
Resolves
Exposure ceases
RADS
Odor-triggered Irritant-assoc. Panic attacks Vocal Cord Dysfunction
K.B., *13.03.71 Peak flow protocol
E.P., *15.03.1966 (hairdresser) Peak flow record
U.M., *21.08.48 Peak flow record
OA and BHR: Prognosis (1)
Inducer
Red cedarRed cedarColophony
IsocyanatesIsocyanatesIsocyanatesIsocyanates
CrabsCrabsVariaVaria
Subjects(n)
3875201250202231313228
Duration offollow-up (J)
0,5-41-9
1,3-3,81-3>4
0,5-41
0,5-24,8-60,5-44-11
Persistence ofsymptoms (%)
2949906682507761
10093
100
Persistenceof BHR
38/28 (100%)25/33 (76%)7/20 (35%)7/12 (58%)12/19 (63%)9/12 (75%)17/22 (77%)28/31 (91%)26/31 (84%)31/32 (97%)25/2 (96%)
OA and BHR: Prognosis (2)
Cessation of exposure: Persistence of symptoms: 61 %Persistence of BHR: 75 %
Reduction of exposure:Persistence of symptoms: 93 %Persistence of BHR: 95 %
Vandenplas, O., et al., ERJ 22 (2003) 689-697
Cullinan, P., et al., ERJ 22 (2003) 853,from: Cathcart, M., et al., Occup. Med. 47 (1997) 473
OA and BHR: Prevention (1)
Cullinan, P., et al., ERJ 22 (2003) 853,from: Allmers, H., et al., JACI 110 (2002) 318
OA and BHR: Prevention (2)
Work-aggravated asthma: Prevention
Work environment plays an importantrole in the aggravation of symptomsof established asthma.
Tertiary prevention!!!
top related