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Journal of Allergy
Occupational Allergies
Guest Editors: Gordon L. Sussman, Donald H. Beezhold, and Arthur Sussman
Occupational Allergies
Journal of Allergy
Occupational Allergies
Guest Editors: Gordon L. Sussman, Donald H. Beezhold,
and Arthur Sussman
Copyright©2011HindawiPublishingCorporation.Allrightsreserved.
Thisisaspecialissuepublishedinvolume2011of“JournalofAllergy.”AllarticlesareopenaccessarticlesdistributedundertheCreative
CommonsAttributionLicense,whichpermitsunrestricteduse,distribution,andreproductioninanymedium,providedtheoriginal
workisproperlycited.
Journal of Allergy
Editorial Board
P.J.Barnes,UK AlanP.Knutsen,USA H.Renz,Germany
WilliamE.Berger,USA MarekL.Kowalski,Poland NimaRezaei,Iran
K.Blaser,Switzerland TingFanLeung,HongKong RobertP.Schleimer,USA
EugeneR.Bleecker,USA ClareMLloyd,UK RonaldSimon,USA
JandeMonchy,TheNetherlands RedwanMoqbel,Canada MassimoTriggiani,Italy
F.JPHoebers,TheNetherlands D.Passali,Italy HugoVanBever,Singapore
StephenT.Holgate,UK StephenP.Peters,USA A.J.M.vanOosterhout,TheNetherlands
HenkJansen,TheNetherlands DavidG.Proud,Canada GarryWalsh,UK
S.L.Johnston,UK FabienneRance,France RobertA.Wood,USA
YoungJ.Juhn,USA AnuradhaRay,USA
Contents
OccupationalAllergies,DonaldH.BeezholdandGordonL.Sussman
Volume2011,ArticleID519329,2pages
ComparisonbetweenAirwayResponsestoHighversusLowMolecularWeightCompoundsin
OccupationalAsthma,D.Talini,F.Novelli,E.Bacci,F.L.Dente,M.DeSantis,A.DiFranco,L.Melosini,
B.Vagaggini,andP.L.Paggiaro
Volume2011,ArticleID781470,5pages
IndustrialFungalEnzymes:AnOccupationalAllergenPerspective,BrettJ.GreenandDonaldH.Beezhold
Volume2011,ArticleID682574,11pages
ViciafabaHypersensitivityandASAIntoleranceinaFarmer:ACaseReport,ElisabettaDamiani,
AnnaMariaAloia,MariaGiovannaPriore,AngelaPastore,StefaniaNardulli,CristinaLippolis,
LuigiMacchia,andAntonioFerrannini
Volume2011,ArticleID191787,4pages
GumArabicasaCauseofOccupationalAllergy,ArjaViinanen,MaijaSalokannel,andKaijaLammintausta
Volume2011,ArticleID841508,5pages
GeneticVariabilityinSusceptibilitytoOccupationalRespiratorySensitization,BerranYucesoyand
VictorJ.Johnson
Volume2011,ArticleID346719,7pages
Haptenation:ChemicalReactivityandProteinBinding,ItaiChipinda,JustinM.Hettick,andPaulD.Siegel
Volume2011,ArticleID839682,11pages
TheLLNA:ABriefReviewofRecentAdvancesandLimitations,StaceyE.Anderson,PaulD.Siegel,
andB.J.Meade
Volume2011,ArticleID424203,10pages
InhalationofOrtho-PhthalaldehydeVaporCausesRespiratorySensitizationinMice,VictorJ.Johnson,
JeffreyS.Reynolds,WeiWang,KaraFluharty,andBerranYucesoy
Volume2011,ArticleID751052,12pages
AllergicPotentialandImmunotoxicityInducedbyTopicalApplicationof
1-Chloro-4-(Trifluoromethyl)Benzene(PCBTF)inaMurineModel,JenniferFranko,LaurelG.Jackson,
B.JeanMeade,andStaceyE.Anderson
Volume2011,ArticleID238513,8pages
OccupationalAsthmainAntibioticManufacturingWorkers:CaseReportsandSystematicReview,
SaraD´ıazAngulo,JoannaSzram,JennyWelch,JulieCannon,andPaulCullinan
Volume2011,ArticleID365683,9pages
Exercise-InducedBronchoconstrictionandExercise-InducedRespiratorySymptomsinNurses,
JordanMinov,JovankaKaradzinska-Bislimovska,KristinVasilevska,SnezanaRisteska-Kuc,SasoStoleski,
andDraganMijakoski
Volume2011,ArticleID267542,7pages
HindawiPublishingCorporation
JournalofAllergy
Volume2011,ArticleID519329,2pages
doi:10.1155/2011/519329
Editorial
Occupational Allergies
DonaldH.Beezhold1andGordonL.Sussman2
1AllergyandClinicalImmunologyBranch,TheNationalInstituteforOccupationalSafetyandHealth,
1095WillowdaleRoad,Morgantown,WV26505,USA
2DivisionofAllergyandClinicalImmunology,UniversityofToronto,Toronto,ON,CanadaM5S1A1
CorrespondenceshouldbeaddressedtoDonaldH.Beezhold,[email protected]
Received23May2011;Accepted23May2011
Copyright©2011D.H.BeezholdandG.L.Sussman.ThisisanopenaccessarticledistributedundertheCreativeCommons
AttributionLicense,whichpermitsunrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalworkis
properlycited.
Occupational immune diseases are new emerging illnesses implications in developing appropriate intervention and
that affect workers in industrialized societies. Occupational preventionstrategies.
exposures to substances in the workplace environment can Occupational allergy can be stratified into high-molec-
cause inflammation, allergy, or other potentially detrimen- ular-weight-allergenandlow-molecular-weight-allergenme-
tal immune responses. Personal exposure to a variety of diatedresponses.Differentimmunologicmechanismsmedi-
chemicals can exacerbate immune diseases such as contact ateallergicreactivitytotheseoccupationalallergensashigh-
dermatitis as well as respiratory diseases including rhinitis, lighted in this issue by Talini et al. High-molecular-weight
asthma,andhypersensitivitypneumonitis. (HMW) allergens (typically proteins) induce type I hyper-
Next to illnesses due to repeated traumatic injury, sensitivityresponsesortypicalallergiesbyinducingIgEanti-
contact dermatitis is the second most commonly reported bodies which lead to a continuum of symptoms including
occupational illness. It can prevent individuals from per- rhinitis (rhinosinusitis, conjunctivitis), hives, asthma, and
forming job-related tasks or preclude working altogether. life-threatening anaphylaxis. Patients with HMW-allergen-
Occupationally related contact dermatitis is a significant induced asthma show a greater frequency and severity of
public health burden with combined direct annual cost the early-phase response but are less likely to demonstrate
estimates of up to $1 billion in the USA for medical costs, a late-phase response. Occupational outbreaks of reactions
workerscompensation,andlosttimefromwork. to HMW allergens can occur episodically and can be
Respiratory morbidity is also a significant burden to severe and life altering for those affected. These allergies
can affect large numbers of easily identified workers in
public health leading to lost productivity. Prevalence rates
specific industries which can reach epidemic proportions
for occupational rhinitis are significant, varying by occu-
such as latex allergy and Baker’s asthma. It can present
pation between 5% and 65% and costing an estimated
in a less-well-defined population or as local occurrences
$593/year/employeeduetoproductivitylosses.Conservative
estimates made by the American Thoracic Society in 2003 such as agricultural or food processors exposed to soy, sea
estimatethat15%ofchronicobstructivepulmonarydisease foods, pollens, molds, and so forth. Research areas include
andasthmacaseswereworkrelatedandcostapproximately identificationandcharacterizationofhigh-molecular-weight
$7billioninlostproductivityintheUSAWiththechanging occupationalallergens.Usingfungalenzymesasaprototypic
work environment, new occupational hazards continue to HMW occupational allergen, Green et al. describe some of
emerge which require immunologic characterization. In thecharacterizedfungalenzymeallergensanddiscussmon-
ordertoreducethemorbidityandmortalityassociatedwith itoring and avoidance strategies. Characterization of HMW
these illnesses, it is critical that we identify the allergens allergens includes using proteomics, molecular techniques
and understand the immunological mechanism by which andgeneratingrecombinantallergens,andproducingmono-
they exacerbate immune-mediated respiratory and dermal clonalantibodiesforthedevelopmentofimmunoassaysand
diseases. Specific understanding of mechanism has direct improveddetectionoftheallergensintheworkplace.
2 JournalofAllergy
Low-molecular-weight allergens (typically chemicals)
inducetype4hypersensitivityreactionsbyinducingallergen-
specificTlymphocyteswhichcanmediatecontactdermatitis
reactions as well as sensitizations that can lead to severe
asthma such as isocyanates (auto painters) and trimellitic
acid.PatientswithLMW-allergen-inducedasthmaaremore
likely to demonstrate a late-phase airway response. The
reviewbyAndersonetal.describestheidentificationoflow-
molecular-weightallergensinthelaboratoryusingthelocal
lymphnodeassaytodeterminewhethernewchemicalsbeing
introduced can cause workplace sensitizations as well as
testingvariouscomponentstoidentifythespecificsensitizer
andpotentiallynonsensitizingreplacements.Theyexamined
theeffectsofchemicalexposureonimmunefunctionusing
selected assays from a comprehensive tiered approach. This
can be used in detecting toxic effects following chemical
exposure(inrodents)asadoptedbytheNationalToxicology
Program. The utility of analyzing potential replacement
chemicals is highlighted by the study of Johnson et al.
where the chemical ortho-phthalaldehyde (OPA) has been
recommended as a substitute for glutaraldehyde as a ster-
ilant in the healthcare industry. Their laboratory evidence
suggested that the replacement of the chemical OPA is also
a strongsensitizer. Characterization of the biochemicaland
immune mechanisms by which chemicals become allergens
(haptenization) is described in a comprehensive review by
Chipindaetal.Developingnewmethodsforscreeningchem-
icalsforpotentialsensitizershelpstobuildbettermodelsby
whichwepredictwhetherchemicalsareallergens.Yucesoyet
al.describenewstudiesaimedatidentifyingoccupationally
sensitizedindividualsandunderstandingthegeneticprofile
associatedwithsensitizing/anaphylacticagents.
It is important to improve our basic science knowledge
andunderstandingofoccupationalallergiesandtheirpatho-
genesis. If we are able to identify potential allergens, before
clinical symptoms are observed, employers can take neces-
sary precautions to minimize or eliminate their employee’s
exposure.
Acknowledgments
We dedicate this issue to one of our coeditors: Dr. Arthur
Sussman, who passed away April 6 2011, just prior to our
special issues’ publication. Arthur Sussman was a pioneer
in the field of allergy and immunology and witnessed its
emergence first hand during his sixty years of medical
practice. He contributed to this issue of the journal and it
is fitting that this issue would highlight emerging issues in
allergyandImmunology—occupationaldiseases.Hewillbe
sincerelymissed.
DonaldH.Beezhold
GordonL.Sussman
HindawiPublishingCorporation
JournalofAllergy
Volume2011,ArticleID781470,5pages
doi:10.1155/2011/781470
Clinical Study
Comparison between Airway Responses to High versus Low
Molecular Weight Compounds in Occupational Asthma
D.Talini,1F.Novelli,2E.Bacci,2F.L.Dente,2 M.DeSantis,2A.DiFranco,2L.Melosini,2
B.Vagaggini,2andP.L.Paggiaro2
1OccupationalHealthUnit,PreventionDepartment,GalleriaGerace14,56126Pisa,Italy
2Cardio-ThoracicandVascularDepartment,UniversityofPisa,56126Pisa,Italy
CorrespondenceshouldbeaddressedtoD.Talini,[email protected]
Received14February2011;Accepted29March2011
AcademicEditor:DonaldH.Beezhold
Copyright©2011D.Talinietal.ThisisanopenaccessarticledistributedundertheCreativeCommonsAttributionLicense,which
permitsunrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalworkisproperlycited.
Occupationalasthma(OA)isa heterogeneous disease,andthecharacteristics ofthesensitizerresponsibleforOAmayinduce
different clinical, functional, and biological manifestations. We examined the characteristics of 74 patients with OA induced
by lowmolecular weight compounds (LMWC)or by high molecular weight compounds (HMWC)and diagnosedby specific
inhalationchallenge (SIC). Patients with OA induced by LMWChad a longer occupational exposure before the beginning of
symptoms,alowersputumeosinophilia,andahigherprevalenceoflateairwayresponse(LAR),incomparisonwithpatientswith
OAinducedbyHMWC.PulmonaryfunctiontendedtobepoorerandatopytendedtobelessfrequentinLMWC-inducedOA
thaninHMWC-inducedOA.Thesedataconfirmandextendpreviousobservationsshowingthatthecharacteristicsofthespecific
sensitizer inducing OA may determine different clinical, functional, and biological features, probably related to the difference
pathogeneticmechanismsunderlyingthesedifferenttypesofOA.
1.Introduction some studies suggested that patients with asthma induced
by LMWC may have alower sputum eosinophil percentage
Occupational asthma with latency period can be induced
than patients with asthma due to HMWC [4, 5]. Sputum
by sensitization to either a specific allergen (high molecu-
eosinophils increase further after exposure to both HMWC
lar weight compounds, HMWC) or chemical compounds
andLMWC,showing theincreaseinallergicairwayinflam-
(low molecular weight compounds, LMWC) present in the
mationinducedbythesespecificsensitizers[6].Factorsthat
workplace[1].ThegoldstandardforthediagnosisofOAis
influence the type of inflammatory responses are unclear
representedbytheSpecificInhalationChallenge(SIC)which
but may include also the type of asthmatic reaction and
is intended to demonstrate a direct relationship between
theintensityofairwayinflammation. Inparticular, itisnot
exposure to a specific agent present in the workplace and
knownifthetypeand/ortheseverityofairwayinflammation
an asthmatic response [2]. Few studies have analysed the
maycontributetothedeterminationofthepatternofairway
variable patternsofresponse toHMWC and LMWC (early,
responsetothespecificsensitizer.
dual, or late response) in limited numbers of patients, but
how worker’s characteristics may influence the pattern of We compared the clinical characteristics, the airway
response to the sensitising agents remains to be explored. inflammatory pattern, and the model of specific airway
Recent studies [3] have shown that there are significant responseinpatientswithOAinducedbyHMWCorLMWC.
differencesinthetypeofairwaychangesinducedbylowand The aim was to assess, in this specific model of asthma,
highmolecularweightagents. whetherthecharacteristicsofthesensitizerandthedifferent
Sputum eosinophilia has been reported in a variable pathophysiologic mechanisms may be associated with a
percentageofpatientsaffectedbyoccupationalasthma,and differentasthmaphenotype.
2 JournalofAllergy
2.MaterialsandMethods LMWC HMWC
Westudied74subjectswithoccupationalasthmaduetodif-
ferentsensitizers(diisocyanates,latex,hairdresser’sproducts,
wood,andflourdusts)observedconsecutivelyinourasthma
clinic: 48 were exposed to LMWC (isocyanates, persulfate
salts, aziridine, and phenolic resins) agents, and 26 were
exposed to HMWC (flour dusts, wood dusts, latex, deter-
gents,andtobaccodusts).Weselectedonlysubjectsinwhom
thediagnosisofoccupationalasthmahadbeenperformedby
means of positive response to specific inhalation challenge ∗
(SIC). According to the international recommendations [2, P<.05
EAR
7], patients were all exposed to a known occupational
DUAL
sensitizer(Table1)showedasthmadeteriorationatworkand
LAR
nonspecificbronchialhyperresponsivenessduringaworking
period. Figure1:TypeofresponsetoSICinsubjectssensitizedtohighand
Bronchialhyperresponsivenesswasdeterminedbymeth- low molecular weight agents. (EAR: early response, LAR: late
response).
acholinechallengetestperformedaspreviouslyreported[8];
aprovocativedoseofa20%decreaseinFEV1frombaseline
(PD20FEV1)oflessthan1000mcgwasconsideredaspositive
forbronchialhyperresponsiveness.
SIC was performed using different methods (Table1): %)60 ∗ ∗
(
(a) for diisocyanates, subjects were exposed to vapours ne
generated by blowing air on the surface of a small amount aseli
b
oftoluenediisocyanate(TDI)orwarmingasmallamountof m
methylenediphenyl diisocyanate (MDI) at 40◦C, in a chal- fro40
lenge chamber and monitoring isocyanate concentrations ase
e
with a specific TDI/MDI detector (MDA model 7005 iso- cr
e
cyanatedetectionequipment,MDAScientificInc.,Glenview, d
1,20
IL); diluent was used as control exposure; the duration of EV
F
the exposure was 30min in a first test and 120min in a
second test (if the first resulted negative) [9]; (b) for dusts
(flour,wood,persulfate,latex,andtobacco),subjectsinhaled 0
dusts by a mouthpiece connected to a small box where a EAR LAR
suspensionofthedustwasobtainedbyblowingcompressed
air at 5L/min through a bottle containing the dust; lactose
LMWC
powder was used as control test; the concentration of the
HMWC
dusts was measured by blowing air from the box through
a cellulose nitrate filter of 0.8µm porosity by means of Figure2:Magnitudeoftheearly(EAR)andlate(LAR)responses
a vacuum pump [10]; (c) in two cases (one exposed to (expressedaspercentdecreaseinFEV1frombaseline)duringSIC
phenolic resins and the other to detergents), a realistic tolow(LMWC)orhigh(HMWC)molecularweightcompounds,
way was employed in order to simulate in laboratory the ∗P<.05.
exposure of the workplace (spreading the substance on a
small surface); diluent was used as control test, and the
durationof exposure was still 30 minutes. In all SIC, FEV1 and differential counts of inflammatory cells (eosinophils,
was measured immediately before and 5, 15, 30, and 60 macrophages, neutrophils, and lymphocytes) were consid-
minutes after the exposure to the sensitizer, then hourly ered; we chose 2% as the upper limit of normal range for
for 8 hours. A positive response was defined as a decrease sputumeosinophils[12].
in FEV1 from baseline of more than 15% during the first Allpatientsgavetheirinformedconsenttothemanage-
hour (immediate response) or between the second and the mentoftheirpersonaldata.
8th hour (late response), and in absence of a more than Characteristics of subjects (age, sex, smoking habit,
10%decrease inFEV1 during acontrol testperformed ina atopy,durationofsymptomsand exposure, latency,typeof
differentdaywithdiluent(fordiisocyanatesorothersimple response, sputum eosinophilia, and functional data) were
chemicals)orwithlactosedust(forotherdustsensitizers). compared between two groups with asthma induced by
Oneortwoweeksbeforechallenge,othermeasurements HMWCorLMWC.
at diagnosis included skin prick tests to common allergens Descriptive analysis for data collected at diagnosis was
(to check for atopy), and collection of sputum induced by performed, with data expressed as mean (+standard devia-
theinhalationofsaline solution.The methodforinduction tion,SD)ormedian(range)fornormallyandnonnormally
and processing has been previously described [11]. Total distributed data, respectively. PD20FEV1 methacholine was