Bijlage 2 Notulen invitational conference...Bijlage 2 Notulen invitational conference Invitational...

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Bijlage 2 Notulen invitational conference

Transcript of Bijlage 2 Notulen invitational conference...Bijlage 2 Notulen invitational conference Invitational...

Page 1: Bijlage 2 Notulen invitational conference...Bijlage 2 Notulen invitational conference Invitational conference richtlijn Beroepsastma Kennisinstituut van Medisch Specialisten Datum:

Bijlage 2 Notulen invitational conference

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Invitational conference richtlijn Beroepsastma Kennisinstituut van Medisch Specialisten

Datum: 30 juni 2015, 16.00 – 18.00 uur Locatie: Domus Medica, Utrecht Aanwezig: Mischa Niederer (NKAL), Jos Rooijackers (NVALT; voorzitter), Pieter Broos

(Kennisinstituut/NVALT), Hilde Vreeken (Kennisinstituut), Gerda de Groene (NCvB), Remko Houba (NVv Arbeidshygiëne), Lidwien Verweij (VWS), Anna de Boer (aios longarts, NVALT), Emiel Rolink (LAN), Benjamin van Wijngaarden (Longfonds), Taeke Pal (NVAB), Marco Persoons (ZN/CZ)

Afwezig: Petra Jonker (V&VN)

Notulen

1. OPENING EN VOORSTELRONDE Jos Rooijackers heet alle aanwezigen van harte welkom. Iedereen stelt zich even kort voor en vertelt in welke hoedanigheid hij/zij aanwezig is en waarom deelneemt.

Jos Rooijackers geeft een korte toelichting over het doel van de bijeenkomst. Het doel van deze invitational is het horen van de veldpartijen over knelpunten rondom de zorg voor patiënten met beroepsastma. Dit betreft zowel de inhoud als op de organisatie van zorg en de bijeenkomst is dan ook bedoeld om een zo compleet mogelijk beeld te krijgen van de problematiek in de praktijk.

2. PROCES RICHTLIJNONTWIKKELING Hilde Vreeken licht kort het proces van richtlijnontwikkeling toe en vertelt dat de richtlijn beroepsastma onderdeel is van een grote project om te onderzoeken hoe internationale richtlijn gebruikt kunnen worden bij ontwikkeling van Nederlandse richtlijnen. Bij de bespreking van de samenstelling van de werkgroep vraagt Emiel Rolink (LAN) of het mogelijk is de NHG te benaderen voor medewerking aan deze richtlijn. Hij stelt hierbij dat herkenning en signalering van beroepsastma ook veel in de eerste lijn plaatsvindt. Deze richtlijn zou door de medewerking van de NHG de samenwerking tussen de eerste en tweede lijn kunnen verbeteren.

3. INLEIDING BEROEPSASTMA

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Jos Rooijackers geeft een toelichting bij de achtergrond van arbeidsgerelateerd astma (o.a. model arbocuratieve zorg met verschillende stadia van blootstelling tot ziekte) en presenteert een casus om het probleem te illustreren. Beroepsastma wordt gedefinieerd als astma veroorzaakt door een specifieke agens op het werk (ziek door werk). Vermijding van het oorzakelijk agens is de beste oplossing. Bij door het werk verergerend astma is het beleid gericht op afname van de blootstelling. Afbakening van de richtlijn: Beroepsastma, zowel immunologisch als niet-immunologisch beroepsastma. Niet-immunologisch beroepsastma: is moeilijker om te bewijzen, hiervoor is meer informatie over blootstelling (aard en niveau) nodig, maar dit is wel onderdeel van richtlijn. 4. DISCUSSIE Pieter Broos licht kort de achtergrond van de open vragen toe. Knelpunten omtrent de diagnostiek en behandeling van beroepsastma reiken verder dat louter de spreekkamer van de longarts, omdat de organisatie van zorg (o.a. planning longfunctie-onderzoeken) veel verder strekt dan alleen ziekenhuis zorg. De werkgroep van de richtlijn probeert met de algemene vragen in eerste instantie de te ontwikkelen richtlijn duidelijk af te kaderen. De vragen die worden voorgelegd zijn:

Wat verwacht u van de longarts?

Tot hoever reikt de verantwoordelijkheid van de longarts?

Wat verwacht u van de bedrijfsarts?

Tot hoever reikt de verantwoordelijkheid van de bedrijfsarts?

Wat is de rol van medicatie in de behandeling van beroepsastma?

De rode draad door de discussie betreft drie onderwerpen, namelijk signalering/herkenning, behandeling en arbocuratieve samenwerking. Hieronder een korte samenvatting per onderwerp. Van gedachten wordt gewisseld over de vraag in hoeverre de richtlijn –naast een praktisch handvat voor zorgverleners- ook een politiek document is waar bepaalde tekortkomingen (in bijvoorbeeld het stelsel of de samenwerking tussen disciplines of de preventie van beroepsziekten, het ontbreken van bekostigingstitels in de zorgverzekeringswet/basisverzekering) kunnen worden geagendeerd. Er is ruimte voor meer politieke opvattingen, mits het als praktisch handvat bruikbaar blijft voor zorgverleners. Signalering/herkenning Benjamin van Wijngaarden (Longfonds) reageert hierop dat de doelgroep van de ERS-richtlijn wel erg breed is, en begrijpt dat dit specifieker moet om praktische richtlijn te komen, maar jammer dat dan deel van de keten niet wordt meegenomen. Gerda de Groene (NCvB) geeft aan dat reëel afbakenen noodzakelijk is en stelt hierbij dat de richtlijn min of meer moet beschrijven wat de longarts daadwerkelijk doet of wat van hem/haar tenminste wordt verwacht binnen de keten. Eigenlijk komt dit neer op waarvoor de longarts wordt betaald, omdat je realistisch gezien niet kunt verwachten dat er veel meer zorg wordt verleend dan in de DOT is opgenomen. Marco Persoons (ZN/CZ) ziet dit breder, de richtlijn kan ook helpen om nieuwe belangrijke taken te realiseren, anders is er ook geen ruimte voor innovatie. Alle aanwezigen zijn het erover eens dat de richtlijn zich (tenminste) dient te focussen op herkennen/signalering van beroepsastma en handvatten moet bieden welke patiënten wanneer en naar wie dienen te worden (door)verwezen. Knelpunt: een goede arbeidsanamnese kost veel tijd (>10min.) en daarom wordt te vaak niet aan beroepsastma gedacht en wordt geen onderzoek gestart. In praktijk wordt door longartsen vaak naar het beroep van de patiënt gevraagd, maar hierbij gaat lang niet altijd ‘een belletje rinkelen’ dat er

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eventueel sprake is van beroepsastma. Jos Rooijackers vertelt dat NVKA veel verwijzingen krijgt van longartsen, er is ook veel vraag naar kennis, waarvoor de helpdesk wordt gebruikt. Taeke Pal (NVAB) vraagt naar de ervaringen van Jos Rooijackers met binnengekomen verwijzingen. Jos Rooijackers geeft aan dat gedegen diagnostiek van beroepsastma voor een longarts erg veel (regel)werk is en dat ze het daarom vaak uitbesteden. Hierbij wordt problematiek aangekaart waarvoor geen DOT en dus geen vergoeding is. Lidwien Verweij (VWS) vraagt of er wordt doorgestuurd door huisartsen, of alleen door longartsen. Er wordt gesteld dat huisartsen nauwelijks verwijzen. Vooral omdat huisartsen vaak niet bekend zijn met beroepsastma en naar wie ze kunnen verwijzen. Hiervoor is ook weinig plaats in de NHG-standaard. Dit kan komen omdat deze patiënten vaak mildere astmaklachten hebben die met medicatie kunnen worden onderdrukt. Deze patiënten zijn daardoor niet bekend bij de longarts en beroepsastma wordt niet gediagnosticeerd. Emiel Rolink (LAN) merkt dan ook op dat bij iedere schil (huisarts, longarts, etc.) ruis optreedt waardoor veel patiënten worden gemist. Doel van richtlijn zou dan ook moeten zijn om deze ‘ruis’ te verminderen. De discussie wordt kort samengevat dat de awareness m.b.t. beroepsastma onder longartsen (maar ook bij huisartsen en bedrijfsartsen) moeten worden vergroot. Jos Rooijackers merkt op dat er tijdens het traject eigenlijk 2x aan beroepsastma kan worden gedacht: 1) tijdens de anamnese en 2) tijdens de behandeling: ‘ben ik met medicatie alleen wel op de goede weg?’. Eigenlijk is deze medisch specialistische richtlijn dan ook maar een kleine schakel in het geheel en moet worden gezocht naar bredere samenwerking. Onderzoek en behandeling Gesproken wordt over waar het grensvlak van onderzoek door de longarts ligt: bijvoorbeeld WEL piekstroom metingen etc. en vaststellen diagnose beroepsastma, maar NIET uitzoeken welke agens precies de oorzaak is. Dit wordt als taak van de bedrijfsarts en werkgever gezien, omdat zij toegang hebben tot informatie over de werkplek. Benjamin van Wijngaarden (Longfonds) reageert hierop dat medewerking van werkgever dan wel erg belangrijk wordt. Dit is echter geen taak van een algemeen longarts, maar moet wel gedaan kunnen worden door specialistische centra. De richtlijn zou hierop in moeten gaan. Er wordt gediscussieerd over de positie van medicatie bij de behandeling. De beste behandeling bij beroepsastma is het (absoluut) vermijden van blootstelling. Hierover dient met de patiënt te worden overlegd. Niet iedere patiënt zal dit meteen willen of kunnen vanwege de sociaal economische gevolgen, het is een proces dat tijd vraagt. Na een paar jaar met klachten te werken wil een patiënt soms alsnog stoppen met huidig werk. Benjamin van Wijngaarden (Longfonds) merkt op dat de richtlijn de minimale verantwoordelijkheid hieromtrent van de longarts dient te benoemen. Bijvoorbeeld dat een patiënt tenminste moet worden geïnformeerd dat de astmaklachten met werk te maken KAN hebben. Dan kan de patiënt hiermee rekening houden. Patiënt moet in principe zelf de afweging maken, maar de arts dient de procescriteria te benoemen op basis waarvan de patiënt een besluit kan nemen. De keus is uiteindelijk aan de patiënt. Maar let op, dit heeft wel gevolgen voor verantwoordelijkheden van werkgever. Taeke Pal (NVAB) merkt op dat dit ook gevolgen heeft voor de follow-up. Immers, indien een patiënt niet wil of kan stoppen met werken een langere follow-up noodzakelijk zijn.

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Arbocuratieve samenwerking Verschillende aanwezigen merken op dat de moeizame arbocuratieve samenwerking het belangrijkste knelpunt is bij de zorg voor patiënten met beroepsastma. Er wordt opgemerkt dat de samenwerking tussen huisarts, longarts, bedrijfsarts en expertisecentra verbeterd kan worden. Vaak vinden ze elkaar niet. Ook het belang van de rol (en medewerking) van de werkgever wordt aangestipt. Een deel van de zorg (bijv. het onderzoek naar de relatie tussen klachten, aandoening en beroepsmatige blootstelling, na verwijzing naar een expertise centrum) zou door de werkgever moeten worden betaald. Over het algemeen gaat dit goed, maar lang niet altijd. De aanwezigen zijn het erover eens dat het verbeteren van de arbocuratieve samenwerking niet alleen bereikt kan worden met de te ontwikkelen richtlijn en dat hiervoor een gezamenlijk aanpak noodzakelijk is. Tegelijk is deze richtlijn wel een mogelijkheid. Er wordt opgemerkt dat bij de discussie tot nu toe vooral sterk vanuit de klacht is beredeneerd, omdat het over patiënten in de eerste of tweede lijn gaat. Primaire en secundaire preventie zijn nog niet echt aan bod gekomen. Diagnose van beroepsastma bij één patiënt betekent dat collega’s at risk zijn. Besproken wordt dat de richtlijn dus zowel van een “push” als “pull” strategie moet uitgaan. Zodra mensen zich melden met klachten die beroepsastma kunnen zijn, is het eigenlijk al veel te laat.

Bespreking van enkele aanbevelingen uit de richtlijn ‘Work-related asthma’ van de European Respiratory Society Tijdens het tweede deel van de discussie worden de aanbevelingen uit de ERS richtlijn besproken. Hierin zit overleg met de bovenstaande algemene discussie. Alleen aanvullende punten op de eerdere discussie zijn hieronder beschreven. Key questions uit de ERS richtlijn: 1. How are work-related asthma cases diagnosed and how should they be diagnosed? 2. What are the risk factors (host and exposure) for a bad outcome?

o Risicofactoren om in achterhoofd te houden 3. What is the outcome of different management options in subjects who are already affected? 4. What are the benefits of medical screening and surveillance?

o Arbeids-en bedrijfsgeneeskunde waarbij longarts ondersteuning biedt 5. What is the impact of controlling work-related exposure to prevent asthma?

o Primaire preventie

Remko Houba (NVv Arbeidshygiëne) merkt op dat er eigenlijk nog een vraag ontbreekt, namelijk hoe het vermoeden op beroepsastma kan worden gewekt. Jos Rooijackers licht toe dat dit een subvraag is van de eerste key questions van de ERS richtlijn. Aanbeveling key question 1 + 2: awareness en (door)verwijzing Er wordt afgesproken dat er in de richtlijn verwijscriteria worden opgenomen die kortweg handvatten geven t.a.v. wanneer verwijzen naar wie en wat is daarvoor nodig.

Wanneer en wie (door)verwijzen?

Wat verwacht men van de longarts en wanneer verwijzen naar een expertisecentrum?

(longarts verwijst naar specialist)

Wat moet longarts wel/niet zelf doen? (zie bovenstaande discussie)

Er ontstaat discussie over het gebruik van de piekstroommeter. Deze is bij longartsen niet (meer) beschikbaar en/of zij hebben er minder ervaring mee. Dit dient dan ook opnieuw te worden

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geïntroduceerd, maar men twijfelt of dit realiseerbaar is (potentieel implementatieprobleem). Dit is een discussie voor de beroepsgroep. Ook hierbij wordt het ontbreken van een beroepsastma-DOT benoemd als knelpunt. Marco Persoons (ZN/CZ) merkt op dat de beroepsgroep dit kan aankaarten bij zorgverzekeraars om dit wel te bekostigen.

Aanbeveling key question 3: reduceren van blootstelling Dit gaat over het nemen van beheersmaatregelen op het werk als onderdeel van de behandeling (zie bovenstaande discussie). De richtlijn dient in te gaan op het maken van de afweging en hoe de longarts hierbij kan helpen. Absolute vermijding is beste keus bij immunologisch beroepsastma. In andere gevallen het reduceren van blootstelling, maar dan is wel goede monitoring nodig. Aanbevelingen key question 3: medicamenteuze behandeling De aanbevelingen uit de ERS richtlijn zijn:

• ”Beschouw het gebruik van ademhalingsbescherming (maskers etc.) zeker op de lange

termijn en bij patiënten met ernstige astma, niet als een veilige aanpak.”

• “Beschouw anti-astma-medicatie niet als een redelijk alternatief voor het aanpassen van

omgevingsfactoren.”

• “Pas de farmacologische behandeling van werk-gerelateerd astma aan aan het niveau van astma controle, overeenkomstig de algemene aanbevelingen voor astma.”

De aanwezigen zijn hiermee eens. Medicatie is geen oplossing, maar het aanpassen van omgevingsfactoren. Aanbeveling key question 4: secundaire preventie De aanbevelingen uit de ERS richtlijn zijn:

• Identificeer alle werknemers met een risico op het ontwikkelen van werk-gerelateerde astma met vragenlijsten als de basis voor gezondheidsbewaking.

• Identificeer personen met een verhoogd risico op werk-gerelateerde astma vanaf de aanvang van werk waarin zij potentieel worden blootgesteld aan allergenen met een hoog molecuulgewicht door periodiek te testen op sensibilisatie voor specifieke beroepsallergenen.

• Bij klachten of sensibilisatie dient aanvullend onderzoek te worden verricht om werk-gerelateerd astma aan te tonen of uit te sluiten.

Er wordt besproken dat gezondheidsbewaking grotendeels buiten de scope van de te ontwikkelen richtlijn valt en dat secundaire en primaire preventie geen taak van longarts is. Wel kan de longarts betrokken raken bij gezondheidsbewaking, bijvoorbeeld als medewerkers at risk worden verwezen. In een hoofdstuk ‘Organisatie van zorg’ zou dit wel in de richtlijn moeten worden benoemd. Aanbeveling key question 5: primaire preventie De aanbevelingen uit de ERS richtlijn zijn:

• Elimineer blootstelling. Dit is de sterkste preventieve aanpak voor het terugdringen van de ziektelast van immunologisch beroepsastma en heeft als primaire preventie de voorkeur.

Er wordt besproken dat ook primaire preventie, net als secundaire preventie, geen taak van longarts is en daarmee buiten de scope van de te ontwikkelen richtlijn valt, zie opmerking bij key question 4. . Overige algemene opmerkingen Emiel Rolink (LAN) geeft aan dat hij graag zou zien dat deze richtlijn breder wordt aangepakt dan alleen een richtlijn voor longartsen en mist het multidisciplinaire karakter. Pieter Broos onderschrijft

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dit en geeft aan dat het betrekken van de huisartsen in de werkgroep een goede stap is omdat op verschillende plekken in de zorg dezelfde problemen voorkomen. Bijvoorbeeld wat betreft het wanneer verwijzen naar wie, wat is daarvoor nodig, etc. Voor deze richtlijn blijft echter gelden dat deze vooral vanuit perspectief van longarts zal worden opgesteld en wellicht kan worden beschouwd als startpunt voor samenwerking met de update van de richtlijn van bedrijfsartsen. Emiel Rolink geeft aan het antwoord van Pieter Broos te hebben begrepen. Zeker is het van toegevoegde waarde als ook huisartsen worden betrokken. Tegelijk: is en blijft het een gemiste kans. Als we het gebrek aan interactie tussen de bedrijfsgeneeskundige zorg en reguliere zorg als een van de belangrijkste knelpunten zien, dan moeten we juist bij de ontwikkeling van richtlijnen beginnen dit aan te pakken. De NVAB gaat in deze periode ook aan de slag om zijn richtlijn astma / COPD te actualiseren. Emiel Rolink stelt voor dat contact wordt gelegd met de NVAB om beide richtlijnen zoveel mogelijk te combineren. Jos Rooijackers geeft aan dat hij ook lid is van de werkgroep die de NVAB richtlijn gaat actualiseren. Er is een linking pin. Emiel Rolink geeft aan dit goed te vinden. Echter een linking pin is een zwakkere manier van zaken op elkaar aan laten sluiten. Een gezamenlijke richtlijn beroepsastma / COPD voor bedrijfsartsen, longartsen, huisartsen en andere betrokken zorgverleners is sterker. Marco Persoons geeft aan het pleidooi van Emiel Rolink te ondersteunen. Lidwien Verweij (VWS) vraagt zich af of behalve aandacht voor de organisatie van zorg ook aandacht aan de organisatie van de werkplek kan worden besteed in de richtlijn. Bijvoorbeeld, wat moet je op werkplek aanpassen/doen? Dit betreft de arbeidshygiënische strategie, waarbij naar instrumenten kan worden verwezen zoals de leidraad allergenen. Emiel Rolink (LAN) pleit tenslotte voor aansluiting met het KNMG initiatief waarbij een visie wordt ontwikkeld op arbeidsgerichte zorg. De werkgroep zal hier zeker rekening mee houden. Nadrukkelijk wordt aan de orde gesteld (LAN/ZN) dat juist gezien het feit dat er juist knelpunten liggen binnen de arbocuratieve samenwerking (i.c. longartsen/bedrijfsartsen) de ontwikkeling van deze richtlijn juist een kans is om deze richtlijn te combineren met de (komende) update van de richtlijn astma/COPD van de NVAB. Of nog beter: om te komen tot een gezamenlijke richtlijn longartsen, bedrijfsartsen, huisartsen. 5. VERVOLGPROCEDURE Er wordt afgesproken dat het verslag naar de aanwezigen wordt gestuurd zodat zij hier schriftelijk op kunnen reageren. Daarna zal de werkgroep het raamwerk van de richtlijn opstellen en de aanwezigen ter kennisgeving toesturen. Tenslotte krijgen alle veldpartijen de gelegenheid op de conceptrichtlijn te reageren wanneer deze gereed is. 6. RONDVRAAG

Geen. 7. SLUITING Jos Rooijackers bedankt alle aanwezigen voor hun aanwezigheid en goede input.

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Bijlage 3 Patiëntenperspectief

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RAPPORTAGE KWALITATIEF ONDERZOEK RICHTLIJN BEROEPSASTMA MAART 2016 DOOR PEPPERCORN IN OPDRACHT VAN HET LONGFONDS

Achtergrond De Europese richtlijn beroepsastma (astma veroorzaakt of verergerd door werk) wordt uitgewerkt voor Nederland. In het kader hiervan heeft het Longfonds behoefte aan inzicht in de verwachtingen die patiënten hebben van het handelen door de longarts in het geval van beroepsastma. Doel Het Longfonds heeft Peppercorn gevraagd om de ervaringen en verwachtingen bij de doelgroep omtrent de zorg door de longarts bij beroepsastma te inventariseren, zodat input wordt verkregen voor de ontwikkeling van de richtlijn voor Nederland. Opzet: mini-focus group en enkele telefonische interviews met patiënten Peppercorn heeft in februari 2016 een mini-focus group met drie patiënten gehouden en drie telefonische interviews met patiënten. Er zijn in totaal drie mannen en drie vrouwen gesproken in de leeftijd 40+. De respondenten zijn geworven door het Longfonds en ontvingen een vergoeding voor hun deelname. Voorafgaand aan de gesprekken is in overleg met het Longfonds een checklist opgesteld. De gesprekken waren open van aard, waarbij aangesloten is bij het antwoordpatroon van respondenten. Leeswijzer In deze rapportage zijn de belangrijkste bevindingen weergegeven. Het onderzoek is kwalitatief en kleinschalig van aard, dat betekent dat de inzichten en adviezen richtinggevend zijn. Quotes. In het rapport zijn quotes opgenomen om meer gevoel te krijgen bij de resultaten.

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INZICHTEN

LONGARTS - DIAGNOSE 1. Diagnose wordt pas laat gesteld, men loopt er lang mee door

⎯ Men wil dat beroepsastma eerder wordt vastgesteld. Een huisarts, dermatoloog, bedrijfsarts etc. zou eerder aan beroepsastma moeten denken en doorverwijzen naar een specialist. “Ik had het geluk dat mijn huisarts mij doorverwees naar een specialist.” , “Ik liep al jaren bij een dermatoloog. Bij mij viel het kwartje pas tijdens een voorlichtingsavond via mijn werk. Daarop werd duidelijk dat ik de symptomen had die daar werden beschreven.” , “Het duurde een jaar met testjes en afwachten bij de huisarts voordat ik naar de specialist werd doorverwezen.” , “Bedrijfsarts zou in zijn richtlijn moeten hebben staan dat een langdurige rhinitis zonder vorige astma, moet leiden tot het overwegen van beroepsastma.”

⎯ Men geeft ook aan dat men soms van het kastje naar de muur wordt gestuurd. “De longarts verwees naar de KNO-arts en de KNO-arts naar de longarts. Het duurde lang voordat ik uiteindelijk de diagnose beroepsastma kreeg.”

⎯ Soms verwacht men zelf al eerder dat er een relatie is met de werkomgeving. Indien men dit aangeeft bij de zorgverlener wordt dit niet altijd serieus genomen. “Je gaat de patronen herkennen.” , “Je merkt dat de klachten op het werk toenemen en dat je er thuis geen last van hebt.” , “Ik heb het wel gezegd in het begin, maar de huisarts deed er niet veel mee.”

⎯ Men geeft aan dat wanneer men zelf beter voorgelicht zou zijn, dat men dan zelf ook sneller kan herkennen dat er sprake kan zijn van beroepsastma. “Er zou wel wat meer reclame mogen zijn dat je klachten gerelateerd aan werk kunnen zijn.”

2. Voorafgaand aan de diagnose een provocatietest in het ziekenhuis

⎯ Merendeel van de respondenten heeft een provocatietest in het ziekenhuis gehad. Het was in die gevallen blijkbaar niet nodig om verder onderzoek te doen op de werkvloer.

⎯ Men wil voorafgaand aan de provocatietest goed geïnformeerd worden over de gang van zaken en nazorg en medicijnen ontvangen, want na de test heeft men last van astma. “Ik wist al dat het met die schoonmaakdoekjes te maken had, maar dan moet je toch nog een provocatietest doen. Ik begrijp het wel, maar het is niet prettig. Je bent er toch drie dagen niet lekker van.”

3. Werkgever terughoudend ten aanzien van onderzoek op de werkvloer

⎯ Deel geeft aan dat de werkgever niet graag meewerkt aan onderzoek naar de oorzaak van de astma op de werkvloer. “Toen ik eenmaal was overgeplaatst naar een andere afdeling en ik daar geen klachten meer had, toen vond de bedrijfsarts dat verder onderzoek niet langer noodzakelijk was.” , “De werkgever is niet happig op onderzoek.”

⎯ Slechts een enkeling heeft een onderzoek op de werkvloer gehad. Volgens één respondent heeft de werkgever het onderzoek (met succes) gemanipuleerd. Dit geeft opnieuw aan dat dergelijke onderzoeken niet altijd worden verwelkomd door de werkgever.

⎯ Patiënten willen, ook als het probleem zich voor henzelf inmiddels heeft opgelost door bijvoorbeeld overplaatsing naar een andere afdeling, dat het onderzoek op de werkplek alsnog plaatsvindt. Niet alleen om de oorzaak bevestigd te zien, maar ook om anderen te beschermen.

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4. Uitslag = eindelijk weten wat je hebt

⎯ Voor patiënten is de uitslag op zich geen positief bericht, maar na vaak jarenlang zoeken weet men nu eindelijk wat men heeft. Dat biedt een bepaalde mate van opluchting.

⎯ De uitslag kan ook enige verlossing brengen, omdat de uitslag het makkelijker maakt om aan de omgeving uit te leggen wat er aan de hand is. Hoewel men desondanks nog regelmatig op onbegrip kan stuiten (zie later).

5. Tevredenheid over de werkwijze en benadering door de longarts in diagnose fase

⎯ De deelnemers in dit onderzoek zijn tevreden over de werkwijze en benadering door de longarts (en longverpleegkundige). “Na het gesprek met de longarts volgt een gesprek met de longverpleegkundige, die legt alles uit en die kan je alles vragen.”

⎯ Het is voor patiënten een hele verandering dat ze bij de longarts eindelijk serieus genomen worden, dat er iemand is die naar ze luistert en over de juiste expertise beschikt.

⎯ Men waardeert het als de longarts echt op zoek gaat naar de oorzaak en niet alleen medicijnen voorschrijft.

⎯ Men verwacht en ervaart dat de longarts goed uitvraagt wat de klachten zijn en luistert naar hetgeen de patiënt te vertellen heeft. Patiënten willen zich serieus genomen voelen en voldoende aandacht krijgen.

⎯ Men meent zich te herinneren voorafgaand aan het consult bij de longarts een vragenlijst te hebben ingevuld, zodat de longarts vooraf met informatie wordt gevoed. Bovendien stelt het patiënten in staat om zelf een aantal zaken op een rijtje te zetten.

6. Longarts moet duidelijk uitleggen en informeren over de consequenties van de ziekte

⎯ Men vindt het belangrijk dat de longarts duidelijk uitlegt wat de oorzaak van de ziekte is, wat de ziekte inhoudt en wat de consequenties zijn van de ziekte.

⎯ Er moet aan patiënten direct bij de diagnose goed duidelijk worden gemaakt dat men niet mag doorlopen met deze ziekte. “De arts had nog iets meer mogen zeggen over de consequenties van beroepsastma, ik ben er uiteindelijk te lang mee doorgelopen, waardoor mijn astma verergerde. Als ik de blijvende gevolgen beter had begrepen, dan was ik mogelijk eerder gestopt met het werk in de kwekerij.”

7. Deel vindt de acceptatie van de ziekte moeilijk à behoefte aan ondersteuning

⎯ Deel geeft aan moeite te hebben gehad met het accepteren van de ziekte en daar zonder ondersteuning niet of minder goed mee om te kunnen gaan. Zeker wanneer de impact groot is, doordat men bijvoorbeeld niet kan blijven doorwerken. “Medisch maatschappelijk werk heeft mij geleerd om de ziekte te accepteren en geen dingen aan te gaan, die niet meer gaan, zoals het opzetten van een eigen bedrijf.” , “Je wordt geconfronteerd met een permanente beperking. Je gaat met de verwachting dat de een longarts je beter kan maken, dus je moet een teleurstelling verwerken.”

⎯ Anderen hebben minder moeite met de acceptatie van de ziekte. Dit kan liggen aan het type persoon, de ernst van de astma, maar ook bijvoorbeeld aan de impact op de werksituatie: verliest men wel of niet zijn baan, is de werkgever bereidt om de gewenste aanpassingen door te voeren. “Ik heb geen behoefte aan praatgroepjes, het is wat het is.”

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LONGARTS - BEHANDELING 8. De behandeling bestaat vaak uit medicijnen…

⎯ Men krijgt in eerste instantie medicijnen om het leven met de ziekte te verbeteren. ⎯ Men is tevreden over het proces dat hoort bij het afstemmen van de medicijnen (elke drie

maanden controle). ⎯ Men waardeert het wanneer men door de longarts op nieuwe medicijnen wordt gewezen, die

mogelijk goed kunnen werken.

9. …en als de oorzaak bekend is uit het vermijden van de prikkel binnen huidig bedrijf ⎯ De behandeling bestaat ook uit het vermijden van de prikkels die de astma veroorzaken of

verergeren. Bijvoorbeeld door andere werkzaamheden, een overplaatsing naar een andere afdeling binnen hetzelfde bedrijf, minder lange blootstelling. “Na twee uur neemt een collega het van me over.”

⎯ Een enkeling krijgt het advies (niet perse van de longarts) om een hulpmiddel, zoals een mondkapje te dragen. “Daar kreeg ik het alleen maar benauwder van, dat werkt niet voor mij.”

⎯ Indien vermijden onmogelijk is, dan stopt een deel met werken of zoekt men een andere werkomgeving. Dit is een grote stap, die men niet gemakkelijk maakt. Zeker niet als men al wat ouder is en/of parttime werkt. “Vermijden is niet altijd mogelijk. Een laatste optie is om een ander vak te kiezen. Ik ben al in de vijftig, dus ik vind niet zo makkelijk een andere baan.” , “Ik werk nu drie dagen per week, dat vind ik niet makkelijk terug.”

10. Tevredenheid over de werkwijze en benadering in deze fase door de longarts

⎯ De longarts voldoet aan de verwachtingen die men heeft in deze fase: goede uitleg, beslissingen worden in overleg genomen in plaats van opgelegd. “Ik had eerst een oude longarts die nu met pensioen is, maar die zei gewoon wat je moest doen, de huidige longarts vraagt veel meer wat ik voel en hoe ik over dingen denk. Ik vind dat een hele vooruitgang.”

⎯ Tijdens de controles vindt men het prettig dat het gesprek zich niet beperkt tot het medische, maar dat het breder wordt getrokken (welbevinden). Met de longarts kan men zaken bespreken die door de omgeving niet worden begrepen. “Het gaat ook over mijn welbevinden.” , “Je vindt bij de longarts een stukje wederhoor, iemand die ook begrijpt hoe het zit. Dat kan in de privésetting niet altijd.”

⎯ De mogelijkheid van tussentijds contact met de longarts wordt gewaardeerd. “Als ik vragen heb dan kan ik mijn longarts altijd bellen of mailen. Soms duurt het door drukte even voordat ik antwoord krijg, maar ik krijg altijd antwoord. Dat is heel fijn.”

⎯ Daarnaast vindt men het prettig dat men over een telefoonnummer beschikt dat men kan bellen ‘als het fout gaat’.

⎯ Deel van de patiënten geeft aan dat men ook zelf vragen moet stellen en zaken moet overbrengen aan de longarts om tot een goede behandeling te komen. “Je moet ook zelf je mond open doen, van de longarts verwacht ik dat hij de juiste vragen stelt en luistert.”

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WERKOMGEVING 11. Patiënten krijgen op de werkvloer vaak te maken met onbegrip van collega’s

⎯ Collega’s reageren wisselend op de ziekte van de werknemer: de één toont begrip en biedt medewerking, de ander vindt het aanstellerij of vervelend dat men extra wordt belast door de uitval van de collega met beroepsastma. “Het meeste last had ik van het op het werk met de nek te worden aangekeken, dat het aanstellerij was.” , “Het is onzichtbaar en je kunt mensen niet zomaar duidelijk maken wat de ziekte inhoudt, het is alsof je tegen een muur loopt.” , “Mijn leidinggevende dacht dat ik de boel bespeelde, dat ik geen zin meer had om te werken.”

⎯ Als de relatie tussen de werkvloer en astma evident is (bijvoorbeeld bij glasbouw) of als meerdere collega’s hetzelfde probleem hebben, dan heeft men minder last van onbegrip en onvoldoende medewerking door collega’s.

12. Ook bij de werkgever ervaart men regelmatig weerstand ⎯ Een deel loopt er tegenaan dat men onvoldoende medewerking krijgt van de bedrijfsarts en/of

werkgever. Soms probeert men er dan ‘omheen te werken’ door het zelf met de leidinggevende of directe collega’s te regelen. “Er is afgesproken dat ze de schoonmaakdoekjes niet gebruiken als ik dienst heb en men probeert eraan te denken. Maar dat lukt niet altijd. Ik heb liever dat mijn werkgever stopt met het gebruik van de schoonmaakdoekjes. Het is een geldkwestie.” , “De eeuwige strijd met werkgever en bedrijfsarts is vermoeiend.” , “Dan komt het UWV en die zegt dat je kan werken omdat je twee trappen op kunt lopen…” , “Ik heb de bedrijfsarts wel achter me staan, maar er gebeurt nog niks bij de leiding.”

⎯ De officiële diagnose kan het begrip en medewerking vergroten, maar over het algemeen moet men vrij veel druk uitoefenen voordat de werkgever tot actie overgaat. Als belangrijke reden voor de weerstand bij de werkgever ziet men dat de werkgever bang is dat meer mensen gaan klagen en/of dat de benodigde aanpassingen geld gaat kosten. Dit is een belangrijk spanningsveld dat werknemers moeten zien te doorbreken. “De werkgever heeft uiteindelijk gezegd dat ik overspannen was.” , “Ik heb de werkgever aansprakelijk moeten stellen voordat er iets gebeurde.” , “De werkgever doet alsof het allemaal wel meevalt.”

⎯ Enkeling heeft wel voldoende medewerking van de werkgever: “Er wordt door mijn werkgever met alles rekening gehouden en ik kan me terugtrekken als dat nodig is. Dan regel ik wel zelf vervanging. En als het allemaal goed gaat dan ben ik ook bereid om extra uren te maken. Ik ben positief en je hoort mij niet snel klagen.”

13. Uitblijven van erkenning en aanpassing heeft grote consequenties voor werknemer

⎯ Indien de werkgever de oorzaak (uiteindelijk) erkent, betekent dit veel voor de werknemer. “Het is berusting, dat het niet jouw schuld is, dat de oorzaak in de werkomgeving ligt.”

⎯ Bij onvoldoende erkenning van de ziekte en het uitblijven van benodigde aanpassingen is de werknemer de dupe: met minder plezier of angst naar het werk gaan, regelmatig uitvallen of ziekmelden of zelfs het beëindigen van het dienstverband omdat het gewoonweg niet meer gaat. “Ik denk nu elke keer hoe zal het vandaag zijn op het werk, houden ze er rekening mee of niet. Ik zie er steeds meer tegenop om er naartoe te gaan.” , “Uiteindelijk ben ik daar niet meer werkzaam en zit ik nu in de WW.”

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LONGARTS VS. BEDRIJFSARTS 14. Verwachting: longarts = medische kant, bedrijfsarts = consequenties werkomgeving

⎯ Men verwacht van de longarts primair dat deze zich bezighoudt met de medische kant van beroepsastma en dat hij de bedrijfsarts en de huisarts goed informeert. Van de bedrijfsarts verwacht men dat deze formeel richting de werkgever handelt, de longarts spreekt alleen een vermoeden uit. Enkelen hebben het vermoeden dat de bedrijfsarts handelt in het belang van de werkgever. “Het is toch een beetje dat de betaler bepaalt.”

⎯ De samenwerking tussen longarts en bedrijfsarts (en huisarts) kan soms beter. “Mijn ervaring is dat de longarts en de bedrijfsarts dingen niet van elkaar aannemen.”

15. Behoefte aan grotere rol van longarts richting werkgever

⎯ Men wenst dat de longarts meer dan een vermoeden van de componenten die de astma veroorzaken of verergeren vaststelt, zodat men over een krachtiger document richting de werkgever beschikt. “De longarts geeft alleen aan voor welke stoffen je naar alle waarschijnlijkheid overgevoelig bent.” , “Het zou prettig zijn als de longarts echt vaststelt welk component de ziekte veroorzaakt in plaats van alleen een vermoeden uit te spreken.” , “Als er een brief van de longarts zou zijn met welke stoffen ik als werknemer niet kan werken, dan zou ik dat erg fijn vinden. Dan kan ik daarmee naar mijn werkgever en misschien zorgt dat voor de nodige aanpassingen.”

⎯ De rol van de longarts kan ook groter zijn als de bedrijfsarts bijvoorbeeld onvoldoende meewerkt. “Toen de bedrijfsarts niet meewerkte heb ik aan de longarts gevraagd een brief te schrijven aan mijn werkgever.”

INFORMATIEBEHOEFTE 16. Men weet in het begin ‘niets’ over de ziekte, alle informatie is welkom

⎯ Men weet weinig over de ziekte en heeft behoefte aan informatie. Men is tevreden over de informatie die men meekrijgt bij de longarts, zoals informatie over wat hun ziekte inhoudt, welk proces men in het ziekenhuis doorloopt, etc. “Ik vond alles wat ik meekreeg nuttig, want ik wist er helemaal niets over.”

17. Praktische, objectieve informatie over beroepsastma ontbreekt

⎯ Men geeft aan dat, als men daar behoefte aan heeft, het relatief lastig is om goede, objectieve informatie over beroepsastma te vinden of dat de informatie minder toegankelijk is. “Als je wil, kan je het wel vinden op internet, maar je moet goed zoeken.” , “Er zijn heel wat huis-tuin-en-keuken tips te vinden.” , “Veel is in het Engels.”

⎯ Men heeft behoefte aan praktische informatie zoals wat beroepsastma is, hoe je steun kan zoeken (bijvoorbeeld de mogelijkheid van een verwijzing naar een medisch maatschappelijk werker), de consequenties van je aandoening, wat je er zelf aan kan doen, wat je kan doen richting de werkgever, arbodienst en bedrijfsarts, wat veilig werken is, etc.

⎯ Het Longfonds (of vergelijkbare instanties) kunnen hierin volgens patiënten een rol spelen. “Het Longfonds zou inzicht en tips & tricks kunnen geven.”

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18. Men mist informatie over de rechten en plichten van werknemer en werkgever

⎯ Men heeft behoefte aan informatie over de rechten en plichten in relatie tot de werkgever. Zeker wanneer er sprake is van weerstand bij de werkgever.

⎯ Men wil ervan op de hoogte zijn dat de werkgever aansprakelijk kan worden gesteld. “Met name lager opgeleiden moeten goed worden voorgelicht, want zij kunnen makkelijk door de werkgever op een verkeerd spoor worden gezet. En je moet echt je werkgever aansprakelijk stellen anders gebeurt er niks.”

⎯ Men ziet hier niet direct een rol voor de longarts, maar deze kan wel een folder over dit onderwerp meegeven.

19. Behoefte aan grotere rol longarts met betrekking tot preventie en voorlichting ⎯ Enkelen geven aan dat de longarts meer zou kunnen betekenen met betrekking tot preventie

en voorlichting. “De longarts kan bijvoorbeeld risicovolle stoffen aankaarten in (nieuwe) producten.” , “Er zou eigenlijk een soort voorlichting moeten zijn zoals bij roken.”

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ADVIEZEN

De diagnose ‘beroepsastma’ wordt vaak pas laat gesteld. à De mogelijkheid van werkgerelateerde astma moet sneller aan bod komen bij zorgverleners zoals huisarts, dermatoloog en bedrijfsarts. Zorg ervoor dat er bij zorgverleners tijdens de inventariserende schriftelijke vragen en de mondelinge intake ook vragen over beroepsastma aan de orde komen. à Overweeg om werknemers beter voor te lichten dat hun klachten werkgerelateerd kunnen zijn, waardoor zij zelf ook eerder de ziekte kunnen herkennen. à Mogelijk kunnen longartsen een lijst met stoffen opstellen waarvan bekend is dat ze een relatief sterke relatie met beroepsastma hebben. De lijst kan van belang zijn voor zowel preventie als het sneller stellen van een diagnose. Men is tevreden over de werkwijze en benadering door de longarts in de diagnose fase. Het is voor patiënten, die vaak al langer met gezondheidsklachten rondlopen, prettig dat men serieus wordt genomen en de prikkel wordt achterhaald. Men is positief over de vriendelijke benadering, het luisteren en het goed uitvragen van klachten door de longarts. Men ziet enkele aandachtspunten: à Bereid patiënten goed voor op de provocatietest in en zorg voor een goede nazorg. Indien de provocatietest op de werkplek plaatsvindt, zorg ervoor dat de werkgever de zaken niet ophoudt of probeert de uitslag te beïnvloeden. à Leg duidelijk uit wat de consequenties zijn van de ziekte, zodat men er niet alsnog mee blijft doorlopen en hiervan blijvende schade ondervindt. à Bied extra ondersteuning aan patiënten waarvan te verwachten valt dat zij niet goed kunnen omgaan met de uitslag. Bijvoorbeeld in de vorm van een doorverwijzing naar een medisch maatschappelijk werker. De behandeling bestaat uit medicijnen en als de oorzaak eenmaal bekend is uit het vermijden van de prikkel. Men is tevreden over de werkwijze en benadering door de longarts omtrent de behandeling. Patiënten vinden het prettig dat beslissingen in overleg met de patiënt worden genomen, dat de longarts tijdens controles het gesprek breder trekt dan alleen het medische aspect (welbevinden), dat men tussentijds contact kan opnemen met de longarts bij vragen of als het fout gaat. Echter, in de werkomgeving ondervindt men, ook na de diagnose ‘beroepsastma’, regelmatig weerstand bij collega’s, werkgevers en bedrijfsarts. Erkenning van de ziekte door de werkgever is belangrijk voor de patiënt. Hoewel men de primaire rol van de longarts tot het medische beperkt ziet, heeft men behoefte aan meer ondersteuning vanuit de longarts richting de werkgever: à Betere samenwerking tussen longarts en bedrijfsarts. à Document van de longarts waarbij meer dan alleen een vermoeden wordt uitgesproken van de prikkel die beroepsastma veroorzaakt of verergert. à Brief vanuit de longarts richting werkgever wanneer de bedrijfsarts onvoldoende meewerkt. Na de diagnose ‘beroepsastma’ heeft men behoefte aan objectieve, praktische informatie over de ziekte. Men is zeer geïnteresseerd in informatie met betrekking tot de werkgever. à Overweeg om een folder specifiek voor beroepsastma te ontwikkelen, die niet alleen inzicht biedt in zaken als wat de ziekte inhoudt en wat de consequenties zijn, maar ook vertelt wat de rechten en plichten zijn in relatie tot de werkgever. De folder zou ondersteuning moeten bieden bij weerstand in de werkomgeving.

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Bijlage 4 Anamneseformulier

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Vragenlijst over arbeidsgerelateerde luchtwegklachten.

Toelichting bij de vragenlijst

De vragenlijst bevat voornamelijk vragen over longklachten, allergische klachten en klachten tijdens en na het werk.

Veel vragen kunt u met ja of nee beantwoorden. Indien naar getallen wordt gevraagd, wilt u deze dan zo

nauwkeurig mogelijk invullen? U maakt uw keuze door een kruisje binnen het kader van het hokje te plaatsen.

Goed: Indien u zich heeft vergist maak het hokje zwart en kruis dan het andere hokje aan.

Wilt u alleen een zwarte of een donkerblauwe pen of ballpoint gebruiken?

Vragen?

Mocht u nog vragen over deze vragenlijst hebben, dan kunt u deze vragen voorleggen tijdens het bezoek aan

de polikliniek.

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1. Persoonsgegevens

Naam:

Adres:

Postcode en plaats:

Telefoonnummer:

Geboortedatum:

Geslacht:

Burgerlijke staat:

Functie:

Branche

Werkgever:

Adres:

Postcode en plaats:

Telefoonnummer:

Datum in diensttreding:

Arbodienst:

Bedrijfsarts:

Adres:

Postcode en plaats:

Telefoonnummer:

Huisarts:

Adres:

Postcode en plaats:

Telefoonnummer:

Zorgverzekeraar/klantnummer:

Burger Service Nummer:

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2. Functie en werkzaamheden

1 Wilt u in onderstaande tabel aangeven welke functies u in het verleden heeft gehad?

Naam werkgever Adres en plaats

Gewerkt Aantal uren

Beschrijving werkzaamheden

Gezondheids-klachten

Opmerkingen

Van tot Ja Nee

Ruimte voor aantekeningen door arts

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3. Gezondheid

Oogklachten

Ja Nee

3a Heeft u last van jeuk, roodheid of tranende ogen?

3b

Zo ja, sinds wanneer heeft u deze klachten?

Neusklachten

Ja Nee

4a Heeft u last van niezen, loopneus of verstopte neus?

4b

Zo ja, sinds wanneer heeft u deze klachten?

Ja Nee

5a Heeft u last van neusbijholtenontstekingen (sinusitis)?

5b

Zo ja, hoe vaak heeft u deze gehad?

Ja Nee

6 Heeft u last van neuspoliepen?

7 Bent u bekend of onder behandeling (geweest) bij de KNO-arts?

Luchtwegklachten

8 Heeft u last van hoesten, piepen of kortademigheid:

Ja Nee

- In aanvallen

- ’s Nachts

- Na inspanning

- Na blootstelling aan allergenen afkomstig van bijvoorbeeld huisstofmijt

huisdieren, gras, pollen (hooikoorts), invloeden van de seizoenen…

Zo ja, kunt u dit toelichten?

Ja

Nee

- Na blootstelling aan aspecifieke prikkels, bijvoorbeeld temperatuurwisselingen, mist,

chemische geuren…

Ruimte voor aantekeningen door arts

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Zo ja, kunt u dit toelichten?

Sinds wanneer heeft u deze klachten?

Ja

Nee

9 Heeft u gedurende het afgelopen jaar wel drie maanden achtereen vrijwel dagelijks gehoest?

10a Heeft u gedurende het afgelopen jaar wel drie maanden vrijwel dagelijks slijm opgehoest?

Ja Nee

11 Geeft u wel eens bloed op?

Huidaandoeningen

Ja Nee

12a Heeft u last van eczeem?

12b Heeft u last van andere huidproblemen?

12c

Zo ja, sinds wanneer heeft u deze klachten?

Zo ja, kunt u dit toelichten?

Overige klachten

Ja Nee

14 Duurt herstel na een verkoudheid langer dan 10 dagen?

15 Heeft u wel 1 keer per maand of vaker last van koorts of verkoudheid? 16 Snurkt u overmatig?

Ruimte voor aantekeningen door arts

10b

Zo ja, welke kleur heeft het slijm?

Ja Nee

13 Heeft u ooit met een stof gewerkt die huiduitslag of andere huidproblemen veroorzaakte?

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4. Klachten in relatie tot het werk

Wilt u onderstaande vragen beantwoorden en aankruisen op welk gebied uw klachten van toepassing zijn?

Ogen Neus Lucht-wegen

Huid

17a Ontstaan of verergeren uw klachten tijdens uw werk?

Ja

Nee

17b Zijn er collega’s met dezelfde of dergelijke klachten?

Ja

Nee

Indien u bij vraag 17 a en 17 b Nee heeft ingevuld, kunt u doorgaan met vraag 18.

Ogen Neus Lucht-wegen

Huid

17c Verdwijnen uw klachten snel na thuiskomst?

Ja

Nee

17d Blijven uw klachten, na het stoppen met werk, nog lang aanwezig?

Ja

Nee

17e Nemen uw klachten in de loop van de werkweek toe?

Ja

Nee

17f Verbeteren uw klachten in perioden dat u niet werkt, bijvoorbeeld

tijdens weekend of vakanties?

Ja

Nee

17g Keren uw klachten herhaaldelijk terug bij blootstelling?

Ja

Nee

Ja Nee

18 Wordt u op dit moment blootgesteld aan een van de volgende factoren:

- Metalen

- Stof en/of vezels

- Chemicaliën

- Rook, gassen en/of dampen

- Dierlijk en/of plantaardig materiaal

- Straling

- Temperatuurswisselingen

- Biologische agentia

Ruimte voor aantekeningen door arts

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20c

Kunt u aangeven bij welke werkzaamheden deze klachten optreden?

Ja Nee

Ja Nee

23 Heeft er op uw werk onlangs een incident plaatsgevonden?

24 Komt of kwam het materiaal in aanraking met uw huid of kleding?

25 Kunt u of kon u het materiaal of de chemische stof waarmee u werk of heeft gewerkt, ruiken?

Ruimte voor aantekeningen door arts

Ja Nee

19a

19b

Bent u in het verleden aan bovengenoemde factoren blootgesteld?

Zo ja, kunt u dit toelichten?

Ja Nee

20a 20b

Zijn uw klachten ontstaan of veranderd door wijziging in werkomstandigheden of het gebruik van nieuwe producten/ grondstoffen? Zo ja, kunt u dit toelichten?

Ja Nee

21a 21b

Heeft u ooit verzuimd vanwege deze klachten? Zo ja, kunt u dit toelichten?

22a 22b

Bent u ooit vanwege deze klachten van functie veranderd? Zo ja, kunt u dit toelichten?

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Ja Nee

27 Is er voldoende ventilatie op uw werkplek?

28 Wordt of werd uw werkkleding thuis gewassen?

29 Heeft u gedurende uw hele leven meer dan 100 sigaretten / 50 sigaren / 500 g pijptabak gerookt?

Nee, ga verder met vraag 32

Ja, ik heb vroeger gerookt, maar ben nu gestopt met roken ga verder met vraag 30

Ja, ik rook nog steeds ga verder met vraag 31

30 Wilt u aangeven hoeveel sigaretten, sigaren en gram pijptabak u gemiddeld per dag rookte, toen u rookte? (1 pakje shag = 40 sigaretten)

- Sigaretten

per dag

- Sigaren

per dag

- Pijptabak

g per dag

- Hoe oud was u, toen u begon met roken?

jaar

- Hoe oud was u, toen u stopte met roken?

jaar

31 Wilt u aangeven hoeveel sigaretten, sigaren en gram pijptabak u gemiddeld per dag rookt?

(1 pakje shag = 40 sigaretten)

- Sigaretten

per dag

- Sigaren

per dag

- Pijptabak

g per dag

- Hoe oud was u, toen u begon met roken?

jaar

Ruimte voor aantekeningen door arts

Ja Nee

26a

26b

Maakt u gebruik van persoonlijke beschermingsmiddelen (bijvoorbeeld een mondkapje)?

Zo ja, welke persoonlijke beschermingsmiddelen gebruikt u?

5. Roken

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6. Medische voorgeschiedenis en medicatie

Ja Nee

32 Heeft u in uw jeugd de volgende aandoeningen gehad?

- Astma

- Eczeem

33 Heeft u op dit moment een allergie voor:

- Grassen en boompollen (Hooikoorts)

- Huisdieren

- Huisstofmijt

- Overig

34 Heeft u in het verleden bepaalde aandoeningen gehad?

Medische voorgeschiedenis

Jaar

1

2

3

4

5

6

35 Gebruikt u op dit moment geneesmiddelen?

Geneesmiddelen

1

2

3

4

5

6

7. Familie en woonomgeving

Ja Nee

36 Komen de volgende aandoeningen in uw familie voor:

- Astma

- Hooikoorts

- Eczeem

Ruimte voor aantekeningen door arts

Ja Nee

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Zo ja, welke hobby’s?

Zo ja, kunt u dit toelichten?

Zo ja, welke huisdieren?

Ruimte voor aantekeningen door arts

37 Heeft u hobby’s die mogelijk in verband staan met uw klachten?

Ja Nee

38a 38b

Bent u ooit van omgeving veranderd in verband met gezondheidsklachten? Zo ja, kunt u dit toelichten?

Ja Nee

39a 39b

Woont u in de buurt van een industrieterrein, fabriek, stortplaats of snelweg? Zo ja, kunt u dit toelichten?

Ja Nee

40 Heeft u recent nieuwe meubels, vloerbedekking gekocht of uw huis verbouwd?

Ja Nee

41 Heeft u huisdieren of komt u hiermee in aanraking?

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Bijlage 5 Piekstroomkaart

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Bijlage 6 Piekstroomprotocol

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1

Piekstroom-protocol

Wat is de piekstroom?

De piekstroom is de hoogste luchtstroomsnelheid die u bereikt als u met alle kracht uitblaast.

Hoe wijder de luchtwegen des te hoger de piekstroom. De piekstroom verschilt van persoon tot

persoon en is afhankelijk van het geslacht, de leeftijd en de lichaamslengte. Ook het moment

van de dag heeft er invloed op.

Astma en de piekstroom?

Er zijn vele prikkels waarvoor mensen met astma gevoelig zijn. Wanneer uw astma opspeelt,

worden de luchtwegen tijdelijk nauwer. U kunt dan minder gemakkelijk uitademen en de

piekstroom wordt lager. Medicijnen tegen astma maken de luchtwegen weer wijder, zodat u

gemakkelijker kunt uitademen. De piekstroom is dan weer hoger.

Waarom de piekstroom meten?

Dit protocol beschrijft hoe met behulp van piekstroommetingen een relatie gelegd kan worden

tussen werk en luchtwegklachten.

Wanneer de piekstroom meten?

In willekeurige volgorde:

Twee aaneengesloten weken blazen terwijl u niet wordt blootgesteld (bijv.

thuis/vakantie)

Twee aaneengesloten weken blazen terwijl u wel wordt blootgesteld op de werkplek.

Per dag minstens 4 x meten:

’s ochtends direct na het opstaan.

bij aanvang werkzaamheden

o of op het tijdstip dat u normaal zou beginnen met uw werkzaamheden

o of als u niet wordt blootgesteld rond lunchtijd.

direct na het stoppen van de werkzaamheden

o of op het tijdstip dat u normaal uw werkzaamheden zou beëindigen

o of als u niet wordt blootgesteld, rond de avondmaaltijd.

’s avonds voor het slapen.

op het moment dat u klachten heeft.

o Geef op het formulier aan wat u aan het doen was toen u klachten kreeg.

o Als u extra medicijnen wilt gebruiken, blaas dan vooraf uw piekstroom

Per meting blaast u 3 keer waarna u de hoogste waarde noteert.

Het verschil tussen de twee hoogste meetwaarden mag niet meer dan 20 l/min bedragen.

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2

Hoe wordt de piekstroom gemeten?

De piekstroom wordt met een piekstroommeter gemeten. Dit is een apparaat met een

mondstuk om op te blazen. Een metertje geeft de luchtstroomsnelheid (windsnelheid) aan.

Het meten van de piekstroom gaat als volgt:

Tijdens het blazen zit/staat u rechtop, met het hoofd licht achterover. Zitten of staan

geeft geen grote verschillen, maar kies voor één van de twee en houdt dat aan.

Schuif het rode metertje helemaal naar 0.

Houd de piekstroommeter zo vast dat het wijzertje aan de bovenkant zichtbaar is.

Adem diep in, neem het mondstuk tussen de tanden en sluit de lippen om het

mondstuk heen.

Vervolgens ademt u zo krachtig en snel mogelijk uit. Let er op dat u niet met het hoofd

knikt.

Noteer de stand van het wijzertje en herhaal de handeling nog tweemaal. Noteer de

hoogste waarde.

Hoe gaat het verder?

Gedurende de hele periode vragen wij u een dagboek bij te houden. In dit dagboek noteert u

of u werkt, of u klachten heeft en welke medicijnen u gebruikt.

Het medicijngebruik moet, indien mogelijk, stabiel gehouden worden om de invloed van,

veranderd medicijngebruik op de piekstroommetingen te vermijden. Gebruik zonodig alleen

een luchtwegverwijder.

Wij adviseren u direct (in ieder geval binnen 24 uur) contact met ons op te nemen, indien

zich tijdens de metingen de volgende situaties voordoen:

Forse toename van de voor u bekende luchtwegklachten.

Daling van de piekstroom met meer dan 20% van de uitgangswaarde.

Voorbeeld: Stel dat u normaal ± 600 l/min blaast, dan neemt u contact op als de piekstroom

600-(20% X 600) = 480 l/min of lager is.

De telefoonnummers waarop u ons kunt bereiken:

Bij twijfel adviseren wij u eerst met ons te overleggen !!

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Bijlage 7 Zoekstrategie, evidence table en beroepsallergenen

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ONLINE SUPPLEMENTARY MATERIAL

Online supplementary TABLE sO1 Mesh terms and their combinations used for

literature search of individual key questions and ancillary questions

KQ = Key question

Initial

search

date

sub topic search term

initial

hits

(2008)

final hits

(04/2010)

KQ 1: “How are and should WRA cases be diagnosed?"

7/31/2008 KQ1 -

diagnostics

Asthma[Majr] AND "Occupational

Diseases"[Mesh] AND ("Diagnosis"[Majr] OR

"Diagnostic Techniques, Respiratory

System"[Mesh]) AND (("2004/01/01"[PDAT] :

"2099/07/30"[PDAT]) AND "humans"[MeSH

Terms] AND "adult"[MeSH Terms])

88 134

KQ 2: “What are the risk factors – host and exposure – for a bad outcome?”

1/24/2008 KQ2 a -

general risk

factors

(exposure

type)

"Risk factors"[Mesh] AND ("prognosis"[Mesh]

OR "Outcome and Process Assessment (Health

Care)"[Mesh] OR "outcome"[all] OR

"prognosis"[all] OR "prognostic value"[all] OR

"follow-up studies"[Mesh]) AND

"Asthma"[Mesh] AND ("occupational

diseases"[Mesh] OR "occupational

health"[Mesh] OR "occupational

56 64

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exposure"[Mesh] OR "occupational

groups"[Mesh] OR "workplace"[Mesh] OR

"Occupational"[all] OR "work related"[all] OR

"work aggravated"[All] OR "Workplace"[All]

OR "work site"[All] OR "occupational

agent"[all] OR "work related agent"[all] OR

"Job"[All]) AND "humans"[MeSH Terms] NOT

("Child"[Mesh] OR "Parity"[Mesh])

2/25/2008 KQ2 b -

duration

("duration of exposure"[all] OR "exposure

duration"[all] OR "exposure cessation"[all] or

"long-term cessation"[all]) AND

("prognosis"[Mesh] OR "Outcome and Process

Assessment (Health Care)"[Mesh] OR

"outcome"[all] OR "prognosis"[all] OR

"prognostic value"[all] OR "follow-up

studies"[Mesh] OR "Recovery of

Function"[Mesh]) AND "Asthma"[Mesh] AND

("occupational diseases"[Mesh] OR

"occupational health"[Mesh] OR "occupational

exposure"[Mesh] OR "occupational

groups"[Mesh] OR "workplace"[Mesh] OR

"work related"[all] OR "work aggravated"[All])

AND "humans"[MeSH Terms] NOT

("Child"[Mesh] OR "Parity"[Mesh] OR "Risk

factors"[Mesh])

18 18

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2/21/2008 KQ2 e -

atopy

("atopy"[all] OR "atopic status"[all]) AND

("prognosis"[Mesh] OR "Outcome and Process

Assessment (Health Care)"[Mesh] OR

"outcome"[all] OR "prognosis"[all] OR

"prognostic value"[all] OR "follow-up

studies"[Mesh]) AND "Asthma"[Mesh] AND

("occupational diseases"[Mesh] OR

"occupational health"[Mesh] OR "occupational

exposure"[Mesh] OR "occupational

groups"[Mesh] OR "workplace"[Mesh] OR

"work related"[all] OR "work aggravated"[All])

AND "humans"[MeSH Terms] NOT

("Child"[Mesh] OR "Parity"[Mesh] OR "Risk

factors"[Mesh])

15 17

2/21/2008 KQ2 h -

airway

inflammation

"airway inflammation"[all] AND

("prognosis"[Mesh] OR "Outcome and Process

Assessment (Health Care)"[Mesh] OR

"outcome"[all] OR "prognosis"[all] OR

"prognostic value"[all] OR "follow-up

studies"[Mesh]) AND "Asthma"[Mesh] AND

("occupational diseases"[Mesh] OR

"occupational health"[Mesh] OR "occupational

exposure"[Mesh] OR "occupational

groups"[Mesh] OR "workplace"[Mesh] OR

"work related"[all] OR "work aggravated"[All])

17 18

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AND "humans"[MeSH Terms] NOT

("Child"[Mesh] OR "Parity"[Mesh])

2/21/2008 KQ2 d -

smoking

("Smoking"[Mesh] OR "Tobacco Smoke

Pollution"[Mesh] OR "Tobacco Use

Cessation"[Mesh]) AND ("prognosis"[Mesh] OR

"Outcome and Process Assessment (Health

Care)"[Mesh] OR "outcome"[all] OR

"prognosis"[all] OR "prognostic value"[all] OR

"follow-up studies"[Mesh]) AND

"Asthma"[Mesh] AND ("occupational

diseases"[Mesh] OR "occupational

health"[Mesh] OR "occupational

exposure"[Mesh] OR "occupational

groups"[Mesh] OR "workplace"[Mesh] OR

"work related"[all] OR "work aggravated"[All])

AND "humans"[MeSH Terms] NOT

("Child"[Mesh] OR "Parity"[Mesh] OR "Risk

factors"[Mesh])

20 25

2/21/2008 KQ2 f -

impaired

lung function

("Respiratory function tests"[Mesh] AND

("impairment"[all] OR "decrease"[all] OR

"decline"[all] OR "lower"[all])) AND

("prognosis"[Mesh] OR "Outcome and Process

Assessment (Health Care)"[Mesh] OR

"outcome"[all] OR "prognosis"[all] OR

"prognostic value"[all] OR "follow-up

38 39

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studies"[Mesh]) AND "Asthma"[Mesh] AND

("occupational diseases"[Mesh] OR

"occupational health"[Mesh] OR "occupational

exposure"[Mesh] OR "occupational

groups"[Mesh] OR "workplace"[Mesh] OR

"work related"[all] OR "work aggravated"[All])

AND "humans"[MeSH Terms] NOT

("Child"[Mesh] OR "Parity"[Mesh] OR "Risk

factors"[Mesh])

KQ 3: “What is the outcome of different management options in already affected

subjects?”

Ancillary question 1: “What is the effectiveness of complete exposure

avoidance?”- related to Rachiotis et al. and update search from 2004

9/08/2009 KQ3 a -

complete

exposure

avoidance

since 2004

"Asthma"[Mesh] AND "Occupational

Diseases"[Mesh] AND ("Follow-Up

Studies"[Mesh] OR "Prognosis"[Mesh] OR

"Time Factors"[Mesh]) AND

(("2004/01/01"[PDAT] : "2009/09/09"[PDAT])

AND "humans"[MeSH Terms] AND

"adult"[MeSH Terms])

48 50

Ancillary question 2: “What is the effectiveness of reduced exposure?”

2/20/2009 KQ3 b -

exposure

reduction

(generall)

("Asthma"[Mesh] OR "Hypersensitivity"[Mesh])

AND ("Occupational exposure"[Mesh] OR

"Occupational Diseases"[Mesh] OR

"occupational"[all]) AND (("reduction"[all] OR

76 80

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"reduced"[all] OR "reducing"[all] OR

"limitation"[all] OR "limited"[all]) AND

"exposure"[all]) AND ("Prognosis"[Mesh] OR

"Outcome Assessment (Health Care)"[Mesh] OR

"Outcome and Process Assessment (Health

Care)"[Mesh] OR "Follow-Up Studies"[Mesh]

OR "Quality of Life"[Mesh] OR "outcome"[all]

OR "prognosis"[all] OR "prognostic value"[all]

OR "follow-up"[all] OR "time factors"[Mesh])

AND "humans"[MeSH Terms] AND

"adult"[MeSH Terms] NOT "infant"[Mesh]

1/14/2008 KQ3 b 1&2 -

engineering

control or

relocation

("Occupational Exposure"[Mesh] OR

"Occupational Diseases"[Mesh] OR

"Occupational"[all] OR "work related"[all] OR

"work aggravated"[All] OR "Workplace"[All]

OR "work site"[All] OR "occupational

agent"[all] OR "Job"[All]) AND

("prognosis"[Mesh] OR "Outcome and Process

Assessment (Health Care)"[Mesh] OR "Quality

of Life"[Mesh] OR "outcome"[all] OR

"prognosis"[all] OR "prognostic value"[all] OR

"follow-up studies"[Mesh] OR "Controlled

Clinical Trial "[Publication Type]) AND

("Threshold Limit Values"[Mesh] OR "exposure

reduction"[all] OR "reduced exposure"[all] OR

66 70

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"engineering control"[all] OR "relocation"[all]

OR "prevention and control "[Subheading] OR

"exposure avoidance"[all] OR "exposure

cessation"[all] OR "exposure control"[all]) AND

("Asthma"[Mesh] OR "Hypersensitivity"[Mesh]

OR "Hypersensitivity, Immediate"[Mesh]) AND

("humans"[MeSH Terms] AND "adult"[MeSH

Terms])

1/24/2008 KQ3 b 3 -

PPE

("Respiratory Protective Devices"[Mesh] OR

"Head protective devices"[Mesh]) AND

("Asthma"[Mesh] OR "Hypersensitivity"[Mesh]

OR "Hypersensitivity, Immediate"[Mesh]) AND

("Occupational"[all] OR "work related"[all] OR

"work aggravated"[All] OR "Workplace"[All]

OR "work site"[All] OR "occupational

agent"[all] OR "work related agent"[all] OR

"Job"[All])

25 28

Ancillary question 3: “Is it possible to reduce symptoms / improve lung

function by pharmacological treatment in connection with an ongoing

exposure?”

2/21/2008 KQ3 c 1 -

ICS

("Adrenal Cortex Hormones"[Mesh] OR

"Glucocorticoids"[Mesh] OR "Glucocorticoids

"[Pharmacological Action]) AND

("prognosis"[Mesh] OR "Outcome and Process

Assessment (Health Care)"[Mesh] OR "Quality

15 19

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of Life"[Mesh] OR "outcome"[all] OR

"prognosis"[all] OR "prognostic value"[all] OR

"follow-up studies"[Mesh] OR "Controlled

Clinical Trial "[Publication Type]) AND

("Asthma"[Mesh] OR "Hypersensitivity"[Mesh]

OR "Hypersensitivity, Immediate"[Mesh]) AND

("occupational diseases"[Mesh] OR

"occupational health"[Mesh] OR "occupational

exposure"[Mesh] OR "occupational

groups"[Mesh] OR "workplace"[Mesh]) AND

"humans"[MeSH Terms] NOT ("Child"[Mesh]

OR "Parity"[Mesh] OR "Farmer's Lung"[Mesh]

OR "Skin Diseases"[Mesh] OR "Alveolitis,

Extrinsic Allergic"[Mesh] OR "Pulmonary

Fibrosis"[Mesh])

2/14/2008 KQ3 c 2 -

beta agonists

("Adrenergic beta-Agonists"[Mesh] OR

"Sympathomimetics"[Mesh] OR "Bronchodilator

Agents"[Mesh] OR "Adrenergic beta-Agonists

"[Pharmacological Action]) AND

("prognosis"[Mesh] OR "Outcome and Process

Assessment (Health Care)"[Mesh] OR

"outcome"[all] OR "prognosis"[all] OR

"prognostic value"[all] OR "follow-up

studies"[Mesh]) AND ("Asthma"[Mesh] OR

"Hypersensitivity"[Mesh] OR "Hypersensitivity,

16 20

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Immediate"[Mesh]) AND ("occupational

diseases"[Mesh] OR "occupational

health"[Mesh] OR "occupational

exposure"[Mesh] OR "occupational

groups"[Mesh] OR "workplace"[Mesh] OR

"Occupational"[all] OR "work related"[all] OR

"work aggravated"[All] OR "Workplace"[All]

OR "work site"[All] OR "occupational

agent"[all] OR "work related agent"[all] OR

"Job"[All]) AND "humans"[MeSH Terms] NOT

("Child"[Mesh] OR "Parity"[Mesh])

2/21/2008 KQ3 c 3 -

other drugs

("Anti-Asthmatic Agents"[Mesh] OR "Drug

Therapy"[Mesh] OR "Medication Therapy

Management"[Mesh] OR "Administration,

Inhalation"[Mesh]) AND ("prognosis"[Mesh] OR

"Outcome and Process Assessment (Health

Care)"[Mesh] OR "outcome"[all] OR

"prognosis"[all] OR "prognostic value"[all] OR

"follow-up studies"[Mesh]) AND

("Asthma"[Mesh] OR "Hypersensitivity"[Mesh]

OR "Hypersensitivity, Immediate"[Mesh]) AND

("occupational diseases"[Mesh] OR

"occupational health"[Mesh] OR "occupational

exposure"[Mesh] OR "occupational

groups"[Mesh] OR "workplace"[Mesh]) AND

22 39

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"humans"[MeSH Terms] NOT ("Child"[Mesh]

OR "Parity"[Mesh] OR "Adrenergic beta-

Agonists"[Mesh] OR "Adrenal Cortex

Hormones"[Mesh] OR

"Glucocorticoids"[Pharmacological Action] OR

"Adrenergic beta-Agonists"[Pharmacological

Action])

9/09/2009 KQ3 c 4 -

immuno

therapy

"Occupational Diseases"[Mesh] AND

"Asthma"[Mesh] AND "Immunotherapy"[Mesh]

AND ("1984/09/09"[PDAT] :

"2012/09/09"[PDAT]) AND "humans"[MeSH

Terms] AND "adult"[MeSH Terms]

24 24

KQ 4 : “What are the benefits of medical screening and surveillance?”

5/09/2008 KQ4 -

medical

screening

("Mass Screening"[Mesh] OR "screening"[all])

AND "Asthma"[Mesh] AND ("occupational

diseases"[Mesh] OR "occupational

health"[Mesh] OR "occupational

exposure"[Mesh] OR "occupational

groups"[Mesh] OR "workplace"[Mesh] OR

"work related"[all] OR "work aggravated"[All])

AND "humans"[MeSH Terms] NOT

("Child"[Mesh] OR "Parity"[Mesh])

75 79

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8/26/2008 KQ4 -

medical

surveillance

("Safety Management"[Mesh] OR "Population

Surveillance"[Mesh] OR "epidemiology

"[Subheading]) AND "Asthma"[Mesh] AND

("occupational diseases"[Mesh] OR

"occupational health"[Mesh] OR "occupational

exposure"[Mesh] OR "occupational

groups"[Mesh] OR "workplace"[Mesh] OR

"work related"[all] OR "work aggravated"[All])

AND ("prognosis"[Mesh] OR "Outcome and

Process Assessment (Health Care)"[Mesh] OR

"Quality of Life"[Mesh] OR "outcome"[all] OR

"prognosis"[all] OR "prognostic value"[all] OR

"follow-up studies"[Mesh] OR "Controlled

Clinical Trial "[Publication Type]) AND

"humans"[MeSH Terms] NOT ("Child"[Mesh]

OR "Parity"[Mesh]) AND "adult"[MeSH]

18 /

62

73

KQ 5: “What is the impact of controlling work-related exposures to prevent asthma?”

6/16/2008 KQ5 -

outcome and

control

("primary prevention"[Mesh Terms] OR

("prevention and control"[Subheading] AND

"Environmental Exposure"[Mesh])) AND

"Asthma"[Mesh] AND ("occupational

diseases"[Mesh] OR "occupational

health"[Mesh] OR "occupational

exposure"[Mesh] OR "occupational

groups"[Mesh] OR "workplace"[Mesh]) AND

72 78

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"humans"[MeSH Terms] AND "adult"[MeSH

Terms] AND "adult"[MeSH Terms]

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Online supplementary TABLE sO2 Supplemental search strategy for literature search

for each key question and ancillary question

Supplemental literature searches by the individual expert groups

search

date /

period

sub topic search term / key words additional

findings

(date)

KQ 1: „How are and should WRA cases be diagnosed?“

07/2008

2004-2010

Diagnostics

ancillary

questions

Asthma[Majr] AND ("occupational diseases"[Mesh] OR

"occupational health"[Mesh] OR "occupational

exposure"[Mesh] OR "occupational groups"[Mesh] OR

"workplace"[Mesh] OR "work related"[all] OR "work

aggravated"[All]) AND ("Diagnosis"[Majr] OR

"Diagnostic Techniques, Respiratory System"[Mesh])

AND (("2004/01/01"[PDAT] : "2099/07/30"[PDAT])

AND "humans"[MeSH Terms] AND "adult"[MeSH

Terms]) Limits: Publication Date to 2010/04.

203

KQ 2: „What are the risk factors – host and exposure – for a bad outcome?”

2008 -

2010

General risk

factors

Risk factors"[Mesh] AND ("prognosis"[Mesh] OR

"Outcome and Process Assessment (Health Care)"[Mesh]

OR "outcome"[all] OR "prognosis"[all] OR "prognostic

value"[all] OR "follow-up studies"[Mesh]) AND

"Asthma"[Mesh] AND ("occupational diseases"[Mesh]

OR "occupational health"[Mesh] OR "occupational

0

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exposure"[Mesh] OR "occupational groups"[Mesh] OR

"workplace"[Mesh] OR "work related"[all] OR "work

aggravated"[All]) AND "humans"[MeSH Terms] NOT

("Child"[Mesh] OR "Parity"[Mesh]

2008 -

2010

Smoking: ("Smoking"[Mesh] OR "Tobacco Smoke

Pollution"[Mesh] OR "Tobacco Use Cessation"[Mesh])

AND ("prognosis"[Mesh] OR "Outcome and Process

Assessment (Health Care)"[Mesh] OR "outcome"[all]

OR "prognosis"[all] OR "prognostic value"[all] OR

"follow-up studies"[Mesh]) AND "Asthma"[Mesh] AND

("occupational diseases"[Mesh] OR "occupational

health"[Mesh] OR "occupational exposure"[Mesh] OR

"occupational groups"[Mesh] OR "workplace"[Mesh]

OR "work related"[all] OR "work aggravated"[All])

AND "humans"[MeSH Terms] NOT ("Child"[Mesh] OR

"Parity"[Mesh] OR "Risk factors"[Mesh]) AND

"Asthma"[Mesh] AND ("occupational diseases"[Mesh]

OR "occupational health"[Mesh] OR "occupational

exposure"[Mesh] OR "occupational groups"[Mesh] OR

"workplace"[Mesh] OR "work related"[all] OR "work

aggravated"[All]) AND "humans"[MeSH Terms] NOT

("Child"[Mesh] OR "Parity"[Mesh] OR "Risk

factors"[Mesh])

0

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2008 -

2010

Atopy: ("atopy"[all] OR "atopic status"[all]) AND

("prognosis"[Mesh] OR "Outcome and Process

Assessment (Health Care)"[Mesh] OR "outcome"[all]

OR "prognosis"[all] OR "prognostic value"[all] OR

"follow-up studies"[Mesh]) AND "Asthma"[Mesh] AND

("occupational diseases"[Mesh] OR "occupational

health"[Mesh] OR "occupational exposure"[Mesh] OR

"occupational groups"[Mesh] OR "workplace"[Mesh]

OR "work related"[all] OR "work aggravated"[All])

AND "humans"[MeSH Terms] NOT ("Child"[Mesh] OR

"Parity"[Mesh] OR "Risk factors"[Mesh]) AND

"Asthma"[Mesh] AND ("occupational diseases"[Mesh]

OR "occupational health"[Mesh] OR "occupational

exposure"[Mesh] OR "occupational groups"[Mesh] OR

"workplace"[Mesh] OR "work related"[all] OR "work

aggravated"[All]) AND "humans"[MeSH Terms] NOT

("Child"[Mesh] OR "Parity"[Mesh] OR "Risk

factors"[Mesh])

0

2008 -

2010

Duration

and

cessation:

("duration of exposure"[all] OR "exposure duration"[all]

OR "exposure cessation"[all] or "long-term

cessation"[all]) AND ("prognosis"[Mesh] OR "Outcome

and Process Assessment (Health Care)"[Mesh] OR

"outcome"[all] OR "prognosis"[all] OR "prognostic

value"[all] OR "follow-up studies"[Mesh] OR "Recovery

of Function"[Mesh]) "Asthma"[Mesh] AND

0

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("occupational diseases"[Mesh] OR "occupational

health"[Mesh] OR "occupational exposure"[Mesh] OR

"occupational groups"[Mesh] OR "workplace"[Mesh]

OR "work related"[all] OR "work aggravated"[All])

AND "humans"[MeSH Terms] NOT ("Child"[Mesh] OR

"Parity"[Mesh] OR "Risk factors"[Mesh]) AND

"Asthma"[Mesh] AND ("occupational diseases"[Mesh]

OR "occupational health"[Mesh] OR "occupational

exposure"[Mesh] OR "occupational groups"[Mesh] OR

"workplace"[Mesh] OR "work related"[all] OR "work

aggravated"[All]) AND "humans"[MeSH Terms] NOT

("Child"[Mesh] OR "Parity"[Mesh] OR "Risk

factors"[Mesh])

KQ 3: „What is the outcome of different management options in already affected

subjects?“

- Management

of WAR

no supplemental search performed

KQ 4: „What are the benefits of medical screening and surveillance?“

- medical

screening

no supplemental search performed -

KQ 4: „What are the benefits of medical screening and surveillance?“

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5/07/2009 medical

surveillance

"Occupational Exposure"[Mesh] OR "Occupational

Diseases"[Mesh] OR "Occupational"[all] OR "work

related"[all] OR "work aggravated"[All] OR

"Workplace"[All] OR "work site"[All] OR "occupational

agent"[all] OR "Job"[All] AND "prognosis"[Mesh] OR

"Outcome and Process Assessment (Health Care)"[Mesh]

OR "Quality of Life"[Mesh] OR "outcome"[all] OR

"prognosis"[all] OR "prognostic value"[all] OR "follow-

up studies"[Mesh] OR "Controlled Clinical Trial

"[Publication Type] AND "Asthma"[Mesh] OR

"Hypersensitivity"[Mesh] OR "Hypersensitivity,

Immediate"[Mesh] AND "Occupational"[all] OR "work

related"[all] OR "work aggravated"[All] OR

"Workplace"[All] OR "work site"[All] OR "occupational

agent"[all] OR "work related agent"[all] OR "Job"[All]

AND "Population Surveillance"[Mesh] OR "Sentinel

Surveillance"[Mesh] OR "Safety Management"[Mesh])

23

5/07/2009 medical

surveillance

Search own archive 17

KQ 5: „What is the impact of controlling work-related exposures to prevent asthma?”

03/2010 Respirators

in primary

prevention

"Air Pollutants, Occupational"[Mesh] AND "Respiratory

Protective Devices"[Mesh] AND ("Asthma"[Mesh] OR

"Occupational Exposure/prevention and control"[Mesh])

AND "humans"[MeSH Terms] Respirators

in primary

77

(13

selected)

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03/2010 Skin

exposure

and

prevention

(“skin” [all] OR “dermal”[all]) AND (“occupational

diseases”[all] OR “occupational exposures”[all] OR

“isocyanates”[all] OR “diisocyanates”[all]) AND

“asthma”[all] AND “human”[all]

44 (15

selected)

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Online supplementary TABLE sO3 Evidence Tables for KQ 2 – 5

Author / year Authors main conclusion SIGN grade Study type Exposure /occupation

Subjects (n)

Chapter 1: Contribution of host factors and workplace exposure to the outcome of occupational asthma (for more details including elaboration of references see [1] Allard 1989 [2] Duration of exposure after onset of

symptoms was negatively correlated to PC20 at second follow-up. Total duration of exposure was negatively correlated to changes in PC20 between baseline and second follow-up. There was not significant correlation between duration of exposure and baseline lung function or lung function at follow-up. In general no improvement was seen among OA patients after several years of exposure cessation.

2- Longitudinal Various HMW and LMW agents

28

Anees 2006 [3]

FEV1 declines rapidly (101 ml/year) in OA subjects still exposed compared to OA subjects not exposed anymore (27 ml/year). Baseline age, sex, baseline FEV1, current smoking, and use of steroids was not associated to decline in FEV1. Mean step-up of FEV1 (during 1 year after removal from exposure) is not related to age, atopic status, smoking, latent interval between first exposure and first symptoms, duration of symptomatic exposuree, initial FEV1% predicted. There's not influence of therapy with steroids. Mean decline of FEV1 after removal from exposure is not related to duration of symptomatic exposure or latent interval between first

2+ Longitudinal Various HMW and LMW agents

156

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exposure and first symptoms, nor with smoking status.

Chang-Yeung 1977 [4] Most patients with occupational asthma due to Thuja Plicata recover after leaving the industry and above all nonsmokers, but BHR, irrespective of symptoms, persist after cessation of exposure.

2- Longitudinal Western red cedar

38

Chang-Yeung 1982 [5] Symptoms after a follow up of 3.5 yrs are worse when continuing exposure. Among no longer exposed there’s a worse outcome when there are: older age, longer duration of exposure before the onset of symptoms, longer duration of symptoms before diagnosis, worse lung function and higher BHR at diagnosis.

2- Longitudinal Western red cedar

125

Cote 1990 [6] Subjects who deteriorated had stronger early and late asthmatic reactions to SIC with plicatic acid. They also had no different symptoms, medications, FEV1, FVC, PC20 vs subjects who didn’t deteriorated. Atopy and smoking were not risk factors for a bad outcome at follow up.

2+ Longitudinal Plicatic acid (Western red cedar)

48

Descatha 2007 [7] Outcome is worse when there’s a longer latency period. Not significant to outcome are: smoking habits, atopy and molecular weight of causal agent.

2+ Case series various HMW and LMW agents

227

Gassert 1998 [8] Women and industrial sector workers were at increase risk of severe asthma at follow up. Smoking at baseline was not associated to severity of asthma at follow-up.

2- Longitudinal Various 55

Hudson 1985 [9] Patients with crab OA had significantly improved PC20 at follow-up, this was not the case for patients with OA due to various agents. Duration of exposure after onset of symptoms is significantly longer and FEV1 is significantly lower (at initial and follow-up evaluation) in patients with

2- Longitudinal Crab; various HMW and LMW agents

63

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poorer prognosis of both groups (respectively in symptomatic subjects among patients with asthma due to crab, and in subjects requiring medication among patients with asthma due to various agents).

Labrecque 2006 [10] A lower BHR and a worse FEV1 at diagnosis are related to a worse outcome. A longer exposure relates to a poorer prognosis.

2- Longitudinal Isocyanates 79

Lemière 1996 [11] To the outcome are not relevant: clinical improvement, molecular weight of causing agent, specific Abs, duration of exposure, type of asthmatic reaction.

3 Longitudinal various HMW and LMW agents

15

Lozewicz 1987 [12] Patients with poorer outcome (treatment once per week or more often) had increased BHR and decreased FEV1 at baseline compared with patients with better outcome (treatment less than once per week). No association between outcome and duration of exposure, atopy, smoking, and if the patients were relocated at work or left the factory.

2+ Longitudinal Isocyanates (TDI, MDI)

56

Maghni 2004 [13] PC20 at follow-up is significantly associated with baseline PC20 and with time lapse since diagnosis. Patients considered 'cured'(with normal PC20 at follow-up) have significantly longer time laps since diagnosis and higer PC20 at time of diagnosis than 'not improved' and 'improved' patients. 32.1% with no improvement vs.10.7% subjects with improvement had increased sputum eosinophils. 39.3% with no improvement vs. 19.6% with improvement showed increased sputum neutrophils Levels of interleukin-8 and of the neutrophil-derived myeloperoxidase were significantly more elevated in sputum of subjects with no

2+ Longitudinal various HMW and LMW agents

133

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improvement.

Malo 2004 [14] Factors significantly related with rapid recovery of bronchial responsiveness to methacholine in the first 2,5 y after cessation of exposure are: sex (the process results more rapid in females), PC20 and FEV1 at diagnosis. Recovery was not related to duration of exposure, molecular weight for asthmatogen, smoking habits or use of steorids at baseline.

2+ Longitudinal various HMW and LMW agents

80

Mapp 1988 [15] No significant differences between subjects who recover and those who don't with regard to age, smoking, atopy, duration of symptoms, baseline FEV1 and PD20 methacholine. Late asthmatic response (at diagnosis) is significantly higher in subjects who fail to recover. Severity of dual reaction (at diagnosis) in subjects who don't recover is significantly higher compared to subjects with dual reaction who recover.

2- Longitudinal TDI 35

Marabini 1993 [16] Persistence of exposure significantly correlates with symptoms as weezing and shortness of breath, with medication score and severity of asthma at follow-up: persistence of exposure results in a deterioration in the asthma despite the use of more medications.

2- Longitudinal Plicatic acid (Western red cedar)

128

Marabini 1994 [17] No significant differences have been found in symptoms prevalence or in lung function between exposed and not exposed subjects at follow-up. Persistence of exposure at follow-up is correlated (in both exposed and not exposed subjects) with significant reduction of FVC. Subjects with late response to SBPT present at follow-up a significative reduction of FVC and FEV1.

2+ Longitudinal TDI 40

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Merget 1994 [18] Smoking, time from onset of symptoms to removal, positive skin test for environmental allergens did not influence the change in BHR between baseline and follow up.

2- Longitudinal Platinum salts 24

Merget 1999 [19] Subjects still employed in production had more symptoms and more sensitization compared to subjects with less or no exposure, but no difference between low exposed and no exposed. There is a positive association between exposure and FEV1 and between duration of symptoms in high exposure areas and bronchial hyperresponsiveness to methacholine.

3 Longitudinal Platinium salts 83

Merget 2000 [20] A new positive skin prick test to platinum in the follow-up period was seen in the highest exposure group. Among high exposed, smoking was a risk factor for sensitization, but atopy or BHR was not.

2- Cohort Platinum salts 275

Moscato 1993 [21] A lower duration of a total exposure relates to a better outcome. Also younger age, longer avoidance, better baseline FEV1 are related to a better outcome.

2+ Longitudinal Various 29

Orriols 1999 [22] Longer exposure relates to worse outcome. Cessation of exposure improves the outcome and lung function.

3 Longitudinal Isocyanates 21

Padoan 2003 [23] There is a better outcome (and higher PD20 at follow up) when: there are better lung function and lower degree of airway responsiveness to methacholine at diagnosis; there’s a longer interval from cessation of exposure.

2++ Longitudinal TDI 87

Park 1997 [24] A better outcome (remission or improvement) is related to: shorter duration of symptoms before diagnosis, a short time lag between diagnosis and removal from exposure, milder degree of BHR at diagnosis, maybe specific IgE due to TDI-

2- Longitudinal TDI 35

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HAS and duration of exposure before symptoms (p < 0.1). Smoking and atopic status are not related to the outcome.

Park 2002 [25] Favourable outcome is related to shorter duration of exposure after onset of symptoms and a higher initial PC20. Age, sex, atopy, duration of exposure and type of asthmatic response during TDI-BPT not appear to be important factors for remission of disease. Significant difference of level of IgE in group with improvement of symptoms compared to no improvement group - high level of IgE at diagnosis as marker of better prognosis. Significant difference of level of IgG in group with improvement of symptoms compared to no improvement group - high level of IgG at diagnosis as marker of worse prognosis.

2- Longitudinal TDI 41

Perfetti 1998 [26] A better BHR at follow-up was found in case of: higher BHR at diagnosis, shorter exposure, longer removal from exposure and better baseline FEV1. A worse PC20 at follow-up was related negatively to HMW agents and longer duration of exposure.

2- Longitudinal various HMW and LMW agents

99

Pisati 1993 [27] Complete removal from exposure and early diagnosis relate to a better outcome of asthma due to isocyanate. In no longer exposed group type of reaction, duration of exposure and duration of symptomatic period aren’t relevant.

2+ Longitudinal TDI 60

Pisati 2007 [28] A longer symptomatic exposure relates to a worse outcome. The following determinants are not relevant to a worse outcome: duration of exposure before the onset o symptoms, PD20, VC and FEV1 at baseline.

2- Longitudinal TDI 25

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Rachiotis 2007 [29] Symptom outcome worsens with increasing age at diagnosis and longer duration of symptomatic exposure. Persistent BHR was found in asthma related to High molecular weight agents and in Canada more than in Europe.

1- Systematic review

Various 2376

Saric 1991 [30] Severity of symptoms and BHR is not related to duration of exposure.

3 Longitudinal Fluoride/SO2 30

Sorgdrager 2001 [31] A worse FEV1 at follow-up was related to: worse baseline FEV1, longer exposure time (more than 1 yr) and smoking.

2- Longitudinal Fluorides 122

Soyseth 1995 [32] BHR is lower at the follow up visit if: there’s an higher initial BHR; patients take anti asthmatic treatment; patients are removed from exposure. Smoking, FEV1 and duration of exposure are not relevant to the outcome.

2+ Longitudinal Fluorides 38

Tarlo 1997 [33] A better outcome was found when there were: shorter symptomatic period, shorter total exposure, higher PC20 at diagnosis, better baseline spirometry. A worse outcome was related to continuing exposure. The type of isocyanate and of reaction were not relevant to the outcome.

3 Descriptive study of disease register

Isocyanates 235

Valentino 2002 [34] Removal from exposure relates to a better outcome. In removed workers, the following topics are not relevant to the outcome: type of asthmatic reaction, duration of exposure, duration of symptomatic period, smoking and atopy.

2+ Longitudinal TDI 50

Chapter 2: What is the optimal management option in occupational asthma? (for more details including elaboration of references see [35]) Ancillary question 1. “What are the consequences of persistent exposure to the causal agent?”

Anees 2006 [3] FEV1 measurements for at least 1 year before removal from exposure. FEV1 declines rapidly in exposed workers with occupational asthma with a mean (SE) rate of decline in FEV1 was 100.9 (17.7)

2- Longitudinal follow-up

Occupational asthma due to various agents

90

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ml/year.

Chan-Yeung 1987 [36] All patients with continued exposure had respiratory symptoms and required medication while 40% recovered completely among those who avoided exposure.

2- Longitudinal follow-up

Red cedar Avoidance of exposure (136); persistence of exposure (54); reduced exposure (42)

Gannon 1993 [37] Workers who remained exposed had more symptoms, took more often inhaled corticosteroids, and showed a greater fall in FEV1.

2- Longitudinal follow-up

Various agents Avoidance of exposure (78); persistence of exposure (34)

Lin 1996 [38] Patients who remained exposed showed a greater decline in FEV1 than sawmill workers.

2- Longitudinal follow-up (comparison with a control population of sawmill workers)

Red cedar Avoidance of exposure (109); persistence of exposure (92; sawmill workers (399))

Merget 1999 [19] Workers who remained exposed experienced asthma symptoms.

2- Cross-sectional retrospective survey

Platinum salts Avoidance of exposure (58); persistence of exposure (9); reduction of exposure (16)

Moscato 1993 [21] All patients who remained exposed were still symptomatic and required pharmacologic treatment.

2- Longitudinal follow-up

Various agents Avoidance of exposure (18); persistence of exposure (4); reduction of exposure (7)

Orriols 1999 [22] Workers who remained exposed became clinically and functionally worse.

2- Longitudinal follow-up

Isocyanates (various occupations)

Avoidance of exposure (17); persistence of exposure (4)

Padoan 2003 [23] A more favourable prognosis was associated with a better lung function and a lower degree of airway hyperresponsiveness to methacholine at diagnosis

2- Longitudinal follow-up

Isocyanates (TDI)-(various occupations)

Avoidance of exposure (74); persistence of exposure (13) but no distinction between complete persistence and reduction of exposure

Rosenberg 1987 [39] Patients who remained exposed to the same work conditions experienced unchanged or worse respiratory symptoms. Patients who became asymptomatic after cessation or reduction of exposure were

2- Longitudinal follow-up

Isocyanates (various occupations)

Avoidance of exposure (20); persistence of exposure (4)

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younger and had a shorter duration of symptomatic exposure.

Tarlo 1997 [33] None of the subjects who stayed at the same work recovered and 4/10 worsened.

2- Retrospective review

Isocyanates (compensated cases with various occupations)

Avoidance of exposure (126); persistence of exposure (10)

Valentino 2002 [34] The condition of subjects with persistent

exposure deteriorated significantly during the follow-up period in terms of symptoms, pulmonary function parameters, PD20 and use of medications

2- Longitudinal follow-up

Isocyanates (various occupations)

Avoidance of exposure (37); persistence of exposure (13) but no distinction between complete persistence and reduction of exposure

Ancillary question 2. “Is it possible to improve symptoms and lung function by pharmacological treatment in affected workers with persistent exposure?”

Anees 2006 [3] The decline in FEV1 before removal from exposure was not significantly affected by the use of inhaled corticosteroids.

2+ Retrospective cohort

Various agents 90

Marabini 2003 [40] Observational study of 10 subjects with OA who remained exposed and were treated with beclomethasone dipropionate (500 mcg bid) and salmeterol (50 mcg bid) over 3 years Treatment with inhaled corticosteroids and long-acting bronchodilators seems to prevent respiratory deterioration over a 3-year period.

2- Uncontrolled, non-randomized intervention

Various agents 10

Ancillary question 3. “What is the effectiveness of complete avoidance of exposure?”

Beach 2005 [41] Most of the studies (23 of 30) documented an improvement in asthma symptoms, but only few (3 of 30) reported complete resolution of symptoms in the majority of the subjects. An improvement in non-specific bronchial hyper-responsiveness was reported in 14 of 15 studies and an increase in the mean FEV1 in 8 of 17 studies. However, a substantial proportion of the subjects, ranging from 17% to 100%, still required medications to control their

1- Systematic review

Various agents 41 cohort studies

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symptoms

Brant 2006 [42] Most patients continue to be troubled by, albeit improved, symptoms and experience difficulty in re-employment 2 yars after avoidance of exposure.

2+ Workforce-based follow-up

Enzymes (detergent industry)

35

Klusackova 2006 [43] Symptoms of asthma and histamine hyperresponsiveness persisted in 86% and 61% of the patients, respectively, after avoidance of exposure.

3 Longitudinal follow-up

Various agents 37

Labrecque 2006 [10] Nonspecific bronchial hyperresponsiveness was normalized in 11% of the patients and clinical remission occurred in 5%. No statistical difference for spirometry data and antiasthmatic medication use.

2- Retrospective cohort

Isocyanates (compensated cases with various occupations)

79

Munoz 2008 [44] Nonspecific bronchial hyperresponsiveness improved in 3 of those 7 patients who avoided exposure.

2- Longitudinal follow-up

Persulfate salts (hairdressers)

7

Park 2006 [45] Nonspecific bronchial hyperresponsiveness and lung function of patients can sometimes recover slowly through avoidance measures.

2- Longitudinal follow-up

Reactive dyes 26

Park 2007 [46] Not improvement in lung function, asthma severity (as determined by symptom and medication scores) and non-specific airway hyper-responsiveness to methacholine.

2- Longitudinal follow-up

Reactive dyes 11

Pisati 2007 [28] Airway sensitization to TDI and symptoms and functional airway abnormalities can persist for years after cessation of exposure.

2- Longitudinal follow-up

Isocyanates (TDI) spray painters

25

Rachiotis 2007 [29] The pooled rate of symptomatic recovery was 32% (95% CI: 26% to 38%). The pooled prevalence of persistent bronchial hyperresponsiveness was 73% (95% CI: 66% to 79%).

1- Systematic review

Various agents Assessment of symptomatic recovery in 39 studies; 1,681 patients and improvement in NSBHR in 28 studies; 695 patients.

Yacoub 2007 [47] There was a significant improvement in airway responsiveness and inflammation 2

2- Longitudinal follow-up

Various agents 40

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years after cessation of exposure.

Ancillary question 4. “What is the effectiveness of reducing exposure through engineering control or relocation of affected workers”

Beach 2005 [41] Lack of data prevented conclusions about the effectiveness of reducing exposure

1- Systematic review

Various agents 41 cohort studies

Bernstein 2003 [48] No specific conclusion on reduction of exposure.

2- Retrospective cohort

Latex Reduction of exposure (20); avoidance of exposure (4)

Burge 1982 [49] Nonspecific bronchial hyperresponsiveness returned to normal in only 1/8 workers with reduced exposure as compared with half of those who avoided exposure.

Longitudinal follow-up

Colophony (electronic solderers)

Reduction of exposure (8); avoidance of exposure (20)

Chan-Yeung 1987 [36] All patients with continued exposure had respiratory symptoms and required medication while 40% recovered completely among those who avoided exposure.

2- Longitudinal follow-up

Red cedar Reduction of exposure (42); avoidance of exposure (136); persistence of exposure (54);

Merget 1999 [19] For the majority of subjects with OA due to Pt salts transfer to low exposure areas as defined in this study may not be associated with a more unfavorable outcome as compared with complete removal from exposure sources.

2- Cross-sectional retrospective survey

Platinum salts Reduction of exposure (16); avoidance of exposure (58); persistence of exposure (9);

Moscato 1993 [21] All patients who remained exposed were still symptomatic and required pharmacologic treatment.

2- Longitudinal follow-up

Various agents reduction of exposure (7); avoidance of exposure (18); persistence of exposure (n=4)

Munoz 2008 [44] No improvement was observed in patients who continued to be exposed.

2- Longitudinal follow-up

Persulfate salts (hairdressers)

Reduction of exposure (3); avoidance of exposure (7)

Paggiaro 1993 [50] In most subjects, nonspecific bronchial hyperresponsiveness did not change. No specific conclusion pertaining to reduction of exposure.

2- Longitudinal follow-up

Isocyanates (various occupations)

Reduction of exposure (7); avoidance of exposure (7)

Pisati 1993 [27] Complete removal from exposure is the only effective way of preventing deterioration of asthma.

2- Longitudinal follow-up

Isocyanates (TDI) with various occupations

Reduction of exposure (17); avoidance of exposure (43)

Rosenberg 1987 [39] Patients who remained exposed to the 2- Longitudinal Isocyanates Reduction of exposure

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same work conditions experienced unchanged or worse respiratory symptoms

follow-up (various occupations)

(7); avoidance of exposure (20); persistence of exposure (4)

Vandenplas 2002 [51] Reduction of exposure to latex should be considered a reasonably safe alternative that is associated with fewer socioeconomic consequences than removal from exposure.

2- Longitudinal follow-up

Latex Reduction of exposure (20); avoidance of exposure (16)

Ancillary question 5. “What is the effectiveness of reducing exposure through personal protective equipment?”

Côté 1990 [6] Indirect evidence supporting a beneficial effect of some personal respiratory devices. The proportion of subjects who used a twin-cartridge respirator was higher among the group with stable asthma (30%) than among the group with a deterioration of asthma (0%).

2- Retrospective cohort

Red cedar dust 48

Kongerud 1991 [52] Assessment: AH60 Airsteam helmet. Findings: Non significant reduction of symptom score in 10/17 subjects.; iimprovement in the mean peak expiratory flow values.

1- Workplace exposure for 2 weeks; randomized controlled study but only workers with non severe disease.

Aluminium potroom work

19

Laoprasert 1998 [53] Assessment: Laminar flow HEPA–filtered helmet. Findings: Decrease of symptom score and reduction of the decline in FEV1.

1+ Laboratory challenge study, randomize with placebo

Latex allergens (quantified exposure)

9

Muller-Wening 1998 [54] Assessment: "Dustmaster" P2 filter (n=21), "Airstream helmet" P2 filter (n=4), "Airlite" P2 filter (n=1). Findings: Suppression of respiratory symptoms in 11/26 subjects, reduction in 15/26, but 4 required inhaled bronchodilator; reduction of the increase in airway resistance.

2+ Laboratory challenge study, non-randomized

Organic farm allergens

26

Slovak 1985 [55] Assessment: Racal Airstream helmet respirator.

3 Workplace exposure for 6

Laboratory animal 10

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Findings: Suppression of respiratory symptoms and changes in peak expiratory flows in 6 of 8 asthmatic patients

weeks; uncontrolled intervention study.

Taivainen 1998 [56] Assessment: Powered dust respirator helmet with P2 filter. Findings. No effect on respiratory symptoms with the exception of sputum, rhinitis symptoms, corticosteroid treatment, and number of sick leaves; increase in morning peak expiratory flow values and reduced daily peak flow variability; no effect in subjects with severe asthma or irregular use of protective devices.

2+ Workplace exposure for 10 months; non-randomized, non-controlled trial.

Farming 24

Chapter 3: “What are the benefits of medical screening and surveillance?” (for more details including elaboration of references see [57]) Agrup 1986 [58] The prevalence of allergy to laboratory

animals (LAA); On clinical investigation 30 were found to have symptoms and signs related to contact with animals, and allergy was confirmed by radioallergosorbent tests (RAST) and skin tests in 19.

2+ Cross sectional Laboratory technicians and animal keepers

101

Agrup 1986 [58] Out of 19 people with laboratory animal allergy symptoms & positive SPT for animals, 13 (68%) had a history of atopic dermatitis, rhinitis or asthma before they started work at the laboratory or reacted to one or more allergens in the standard battery, or both and were regarded as atopics. Of these 13 individuals 6 had a history of atopy and 12 had at least one positive SPT to the standard battery (animal test excluded). Atopic features were present in 3/11 (27%) people with animal related symptoms but with negative animal RAST & skin tests.

2- Cross-sectional Laboratory animals

124

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Of the 30 with no animal related symptoms, 6 (20%) had a history of atopic disease and / or a positive reaction to a standard test. Atopy (history of atopic diseases or positive SPT results with common allergens, or both) was more common among those with positive tests to laboratory animal allergens (p<0,001). Smoking habits did not differ significantly. (The first symptoms appeared after a mean latent period of 2.3 years).

Amital 2004 [59] A total of 151 cases of sudden and unexpected death occurred among enlisted military personnel during the period. Cardiac disorders caused 47% of deaths, followed by pulmonary causes (11%). Asthma was the most common risk factor having been previously recognized in 10 cases (6.7%). Eight of the 13 subjects with asthma died following an acute asthmatic attack. The frequency of subjects with asthma was found to be higher than that in the general age-adjusted population.

3 Case studies, retrospective

Military 151

Armentia 1990 [60] One hundred thirty-nine bakers and pastry cooks were included in a prevalence study of IgE-mediated hypersensitivity to wheat flour demonstrated by skin tests, specific IgE to wheat flour (RAST), and inhalation challenge. From the sensitized workers, 30 asthmatic patients were selected. Twenty patients were treated with a standardized wheat flour extract, and ten with a placebo in a double-blind clinical trial. Before and after immunotherapy we performed tests in vivo (skin tests with wheat flour and methacholine tests), and in vitro (total IgE and specific IgE to wheat flour). Substantial

2- Contr. clin. trial Wheat/ baker

139

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prevalence of wheat flour allergy (25.17% of workers) were found, and a significant decrease (P less than .001) in hyperresponsiveness to methacholine, skin sensitivity (P = .002), and specific IgE (P less than .005) to wheat flour after 20 months of immunotherapy. There was also significant subjective improvement (P less than 0.001). The placebo group showed no changes in these variables.

Auger 2002 [61] Asthma from exposure to inhalation of

isocyanates is an affection recognised

under the title of workplace diseases

within table no 62 in the General

Regulations and no 43 in the Agricultural

Regulations. If workplace induced asthma

is the most frequent of the workplace

respiratory illnesses with a frequency of 2

to 15% of the asthmatic population, 1

patient in 2 will only be the object of a

declaration and 1 in 3 the objective of a

survey by the administrative authorities.

The frequency of isocyanate asthma is on

average 16.4% amongst workplace

asthmas (19.6% in the industrial

environment and 1.5% in an agricultural

environment); if this prevalence is dose-

dependent according to Baur, 30% of

patients exposed to weak doses of

isocyanate (0.3% ppb according to White)

develop asthmatic disease whilst

Bernstein estimates as 5 to 10% the

frequency of asthmatic disease per

100,000 persons who are exposed to

isocyanates.

3 Nonanalytical study

Isocyanates

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Baur 2001 [62] Methods In the present study we described five cases with workplace-related asthma and one case with extrinsic allergic alveolitis associated with pulmonary hemorrhage after NDI exposure.

3 Case studies NDI, diisocyanate/ synthetic resin plant

6

Baur 2005 [63] The literature review shows that airborne enzymes occurring in the general environment and in purified form in industrial production have a high allergenic potential to the airways, causing rhinitis, conjunctivitis and asthma. Cross-sectional studies demonstrate exposure-response relations for IgE-mediated sensitisation and airway disorders. Atopic individuals are more susceptible to enzyme allergy than non-atopic individuals. Skin prick testing and measurement of specific IgE antibodies have been shown to be useful diagnostic tools. There is also evidence for non-allergic airway inflammation by proteases.

2+ Cross-sectional Enzymes

Baur 1998 [64] Study aimed to evaluate the frequency of work-related symptoms & the clinical relevance of sensitisation to allergens in 89 bakers participating in a screening study & 104 bakers filing a claim for compensation for bakers asthma. The correlation between the sensitisations to work-related allergens & present asthma case history & inhalative challenge test responses was significant. However, approximately 29% of the bakers with respiratory symptoms showed no sensitisation 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 sensitisation to common allergens or elevated total IgE levels was

2- Cross sectional Flour & baking enzymes

193

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found to be a risk factor for the development of sensitisation to bakery allergens & respiratory symptoms. However, 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. Further methods are required to objectively assume irritative patho-mechanisms. Authors conclude that findings indicate the necessity for an improved primary prevention of exposure to inhalative noxae in bakeries.

Baur 1982 [65] Seventeen out of thirty-three workers who have been exposed to airborne papain at their place of work regularly developed asthmatic symptoms; Clinical symptoms and results of skin test, RAST and bronchial provocation test in thirty-three papain workers: evidence for strong immunogenic potency and clinically relevant 'proteolytic effects of airborne papain'. Only one case with pre-existing atopic diseases (allergic rhinitis). So it is not likely that that an atopic diathesis is a prerequisite for papain induced allergic reactions. As six subjects developed clinically relevant hypersensitivity to common allergens during the time of papain exposure, it is thought that airborne papain may constitute a triggering effect to further sensitisation. (Blood-stained nasal

secretion, itching and flare reaction appearing on uncovered skin areas in heavily exposed subjects of whom three had negative and one weak positive SPT and RAST results, suggest a direct irritative effect and damage human tissue by high concentration of active proteinase papain.)

3 Case studies Papain 33

Brant 2005 [66] A cross-sectional survey was undertaken 2- Cross-sectional Flour, α-amylase, 239

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involving 239 (71%) employees from 20 different supermarket bakerles. The geometric mean dust exposure for bakers was 1.2 mg/m

3, a total of 37 (15%)

employees also reported work-related chest symptoms. Serum IgE to flour was present in 24 (11%) employees and to fungal α-amylase in ine (4%) employees. The combination of work-related chest symptoms and specific IgE was found in six (9%) bakers, one (4%) manager and two (3%) assistants. Conclusions: This population of bakery workers has important levels of sensitisation and work-related respiratory symptoms, despite low levels of dust exposure.

supermarket

Bryant 1995 [67]

Allergy to laboratory animals is an occupational hazard among laboratory animal handlers, especially for those who are atopic and sensitised to domestic animals, and may lead to the development of asthma. 228 Subjects were surveyed. Atopic subjects (positive SPT results with at least one common allergen) exposed to laboratory animals (particularly those sensitized to domestic animals) and animal attendants (with a high intensity of exposure to laboratory animals) had significantly higher frequencies of skin reactivity to laboratory animals and asthma than other subjects (77% and 30% respectively, among exposed atopic subjects and 84% and 33% respectively among animal attendants). LAA is an occupational hazard among laboratory animal handlers especially for those who are atopic and sensitised to domestic animals and may lead to the development of asthma. Screening for atopy and skin

2- Cross-sectional study

Laboratory animals

228

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reactivity to lab animals before and during employment would enable those at risk to take precaution.

Cockcroft 1981 [68]

An association significant at the 2% level was found between skin test atopic status & asthma from animal contact. Subjects with a previous history of asthma were not significantly more likely to develop symptoms from animal contact but were more likely to develop animal-related asthma. But nearly half of the subjects with animal-related asthma were non-atopic, two-thirds of the subjects with animal related-asthma had no previous history of asthma. The authors conclude that excluding atopic individuals will not solve the problem, & screening new entrants is unlikely to be successful in view of the long average exposure period before symptoms develop & the fact that skin reactivity to animal extracts is rarely present without symptoms.

2- Cross-sectional Laboratory animals

179

Codina 2000 [69] 56 (15.3%) out of 365 asthmatic/allergic rhinitis subjects showed positive SPT to soybean hulls but none out of 50 controls. There was a significant dose-response relationship in the first group (occupational > indirect > urban exposures). Monosensitization to soybean hulls was absent in all subjects. Asthmatic patients with a positive SPT to soybean hulls compared with those exclusively sensitized to mites, had a higher frequency of daily or weekly symptoms and a higher percent of glucocorticoid dependence.

2- Cross-sectional Soybean hulls 365

Cullinan 1994 [70] 344 employees exposed to flour in bakeries or mills in 7 sites were assessed by self completed questionnaire, & sensitisation measured by the response to skin prick

2+ Cross-sectional Flour / bakers 344

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tests, were related to intensity of exposure both to total dust & to flour aeroallergen. Among 264 previously unexposed subjects, work-related symptoms (which started after first employment at site) were related to exposure intensity, especially when exposure was expressed in terms of flour aeroallergen. The relations with eye/nose & skin symptoms were independent of atopic status & cigarette smoking. Positive skin test responses to mixed flour & to α-amylase were also more frequent with increasing exposure intensity, although this was confounded by atopic status. There was only a weak association between symptoms & specific sensitisation.

De Zotti 2000 [71] Work-related respiratory symptoms are significantly associated with personal history of allergic disease (OR 5,8 95%CI 1,8-18,2). and skin sensitisation to wheat flour or a-amxlase (OR 4,3 95%CI 1,2-14,9). Atopy based on SPT was not related to respiratory symptoms over time (OR 1,1 95%CI 0,3-3,8). Similarly family atopy, atopy based on IgE concentration and positive RAST results for wheat flour were not associated with work-related respiratory symptoms. Authors conclude that personal history of allergic disease is a predisposing factor for the development of symptoms caused by exposure to wheat flour & may be a criterion of unsuitability for starting a career as a baker. Atopy based on the skin prick test is useful for identifying subjects with allergic disease, but should not be used to exclude nonsymptomatic atopic people from bakery work.

2+ Cohort Flour / bakers 125

Gautrin 2001 [72] 28/417 apprentices satisfied the definition 2+ Prospective Laboratory 417

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for ‘probable occupational asthma’, i.e., onset of immediate skin reactivity to > 1 occupational inhalant & > 3.2-fold decrease of PC20. The incidence of ‘probable occupational asthma’ was 2.7%. Baseline immediate skin reactivity to pets (rate ratio [RR] 4.1, 95% CI=1,6-10,8) & bronchial responsiveness (PC20 ≤ 32 versus PC20 > 32 mg/ ml) (RR = 2.5) were associated with an increased risk of probable occupational asthma; a lower FEV1 had an apparent, protective effect (RR = 0.58, 95%CI= 0,43 – 0,78). Authors conclude that apprentices in animal health show a high incidence of probable occupational asthma, & that preexposure airway calibre & responsiveness as well as sensitisation to pets are associated with an increased risk. After multivariant analysis, atopy increases not significantly the likehood of developing OA. This study adds some evidence that asthma is not a risk factor for the incidence of ‘probable occupational asthma, & also suggests that having a high FEV1 does not preclude the development of ‘probable occupational asthma’.

cohort study animals

Gautrin 2000 [73] Prospetive cohort study including 769 apprentices (animal health technology: 417, pastry-making: 230, dental hygiene: 122). Atopy (> positive SPT results with common inhalants), nasal and respiratory symptoms in the pollen season (and duration of exposure to rodents) were the most significant predictors for sensitisation in the animal health program. Rhinitis symptoms on the contact pets before starting apprenticeship were also associated with incidence of sensitisation in the case of animal health apprentices. Hay fever on

2+ Prospetive cohort

Laboratory animals

169

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entry into program was strongly associated with the risk of sensitisation to flour in the pastry-making program. Reporting asthma on the entry in the dental-hygiene program is related to the probability of developing specific sensitisation. The apprenticeship in the animal health technology carries a greater risk of developing specific sensitisation than do apprenticeships in pastry-making and dental hygiene. A non-negligible number of new cases of sensitization ton non-WR occupational antigens was found in all three programmes.

Gautrin 2001 [74] Study describes the time-course of the incidence of work-related symptoms, skin reactivity and occupational rhino-conjunctivitis (RC), and occupational asthma; & assesses the predictive value of skin testing & RC symptoms in apprentices exposed to laboratory animals. The positive predictive values (PPVs) of skin reactivity to work-related allergens for the development of work-related RC & respiratory symptoms were 30% & 9.0%, respectively, while the PPV of work-related RC for the development of occupational asthma was 11.4%. The PPV of WR respiratory symptoms for the development of OA was 25%. Skin reactivity to work-related allergens & rhino-conjunctivitis symptoms have low positive predictive values. The data suggest that assessment of skin reactivity and RC symptoms should still be considered in the context of screening programmes. Sensitization, symptoms and diseases occur maximally in the first 2–3 yrs after starting exposure to laboratory animals.

2+ Prospective cohort (same collective as Gautrin 2001 [72]

Laboratory animals, pastry making, dental hygiene technology

417

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Gautrin 2008 [75] Sensitization to mites and NSBHR at baseline are significantly associated to new sensitization to work-related allergens. Physician diagnosed asthma and NSBHR at start are significantly associated with the incidence of chest symptoms. Sensitisation to pets at baseline and respiratory symptoms at the end at apprenticeship are significantly associated with an increase in BHR. The changes in frequency (incidence and remission) of sensitisation and diseases are unlikely to be due to frequently incriminated host factors such as atopy or smoking.

2+ Cohort Laboratory animals

408

Gordon 1997 [76] A questionnaire was issued to 362 flour-exposed workers in a large bakery. The respiratory screening questionnaire identified 68 workers with respiratory symptoms. Of these, 21 proceeded to full assessment. A diagnosis of asthma was made in 5 cases, one of which was bakers' asthma. In addition, 11 workers not reporting any symptoms by questionnaire were referred to clinic & five were diagnosed as having asthma. Authors conclude that screening questionnaires may lead to an underestimate of the prevalence of asthmatic symptoms & as such should not be used alone in workplace screening. In terms of sensitivity the questionnaire used in this study missed as least as many cases as it detected.

2- Cross-sectional Flour / bakers 362

Grammer 1993 [77] The objective of the study was to determine the clinical and immunologic status of trimellitic anhydride (TMA) workers who have had immunologic lung diseases and who have been moved to lower exposure jobs. Twenty-nine consecutive workers with TMA-induced immunologic lung diseases

2- cohort, retrospective

TMA 29

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who had been moved to low exposure jobs for more than 1 yr were studied retrospectively. Pulmonary symptoms were obtained by physician-administered questionnaire. Immunologic studies were performed using radioimmunoassay. Spirometry and chest film were obtained. Workers with late asthma (LA) (n=3), late respiratory systemic syndrome (LRSS) (n=8), or both LRSS and asthma rhinitis (A/R) (n=6) had improved symptoms, improved pulmonary functions, and lower total antibody against TM-HSA

Houba 1996 [78] In this cross-sectional study, sensitization to occupational allergens and work-related symptoms were studied in 178 bakery workers and related to allergen exposure. α-amylase allergen concentrations were measured in personal dust samples. Of all workers 25% had one or more work-related symptoms. As much as 9 %of the bakery workers showed a positive skin prick test reaction to fungal amylase, and in 8% amylase-specific IgE was demonstrated. Alpha-amylase exposure and atopy appeared to be the most important determinants of skin sensitization, with prevalence ratios for atopy of 20.8 and for medium and high α-amylase exposure groups of 8.6 and 15.9 respectively. Furthermore, a positive association was found between positive skin prick tests to α-amylase and work-related respiratory symptoms. There is a strong and positive relationship between α-amylase allergen exposure levels in bakeries and specific sensitization in bakery workers.

2+ Cross-sectional α-amylase (bakers)

178

Juniper 1984 [79] Atopics were significantly more likely to suffer from enzyme asthma than non-

2- Cohort Alcalase (enzyme)

55

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atopics. The authors conclude that subjects with previous chest disease should not be exposed to Alcalase or similar occupational allergens, but that exclusion of asymptomatic atopics from this type of work is probably not justified. 62/1642 subjects experienced enzyme asthma with higher incidence in atopics.

Kim 1999 [80] The prevalence of asthma was higher in subjects with positive SPT results or high serum specific IgE antibodys to citrus red mite than in those without skin response or serum specific IgE (p<0,05, respectively). In this study, sensitization to citrus red mite (CRM) and the prevalence of CRM-sensitive asthma and rhinitis were significantly higher in farmers with positive SPT results to other inhalant allergens than in those without. This finding suggests 1. that atopy may be a risk factor for sensitization to CRM and for the development of asthma and rhinitis caused by CRM. 2. a +SPT to house dust mites may reflect cross-reactivity.

2- Cross-sectional Citrus red mite 181

Kongerud 1991 [81]

The influence of occupational work exposure and host factors on the incidence of dyspnea and wheezing as reported in questionnaires was examined in 1301 new employees in aluminium electrolytic potrooms. Childhood allergy was not significantly associated to these outcomes. A family history of asthma was associated with the reporting of work related asthmatic symptoms (RR=1.58) although the estimate did not reach the level of statistical significance, but was found to be significant in a previous study (OR=1.64). Exposure to dust or gases in previous jobs was significantly related to appearance of

3+ Cohort Aluminium potroom workers

1301

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symptoms. Increased risk with increasing amount of tobacco smoking and total fluoride exposure was found. A dose response gradient was seen for both variables. No significant differences in FEV1 and FVC were observed between symptomatic and asymptomatic subjects. In this study the increased risk from allergy to develop asthmatic symptoms was small (OR=1.35), unsignificant and in accordance with a previous study of the same group (OR=1.38). Exclusion of allergic people from potroom work would probably have no effect on the incidence of asthmatic symptoms. (CAVE: Diagnosis only base on self-reported symptoms.) Flouride exposure and smoking are the major risk factors for the development of dyspnea and wheezing.

Kongerud 1990 [82] 1. Family history of asthma is sign. related to dyspnea (OR 1,53 95%CI 1,14 - 2,06) and work-related asthmatic symtoms (OR 1,64 95%CI 1,08 - 2,49) 2. Allergy (history of hayfever or atopic eczema) provided no sign. risk for resp symptoms and was neg. correlated with airflow limitation.

2+ Cross-sectional Aluminium potroom workers

1679

Kronqvist 1999 [83] 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

2++

Epidemiological follow-up

Storage mite/ Dairy farmers

1015

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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

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unchanged. Storage mites are still

dominant allergens for developing allergic

disease.

Kruize 1997 [84] Aimed to study the role of exposure, atopy & smoking in the development of LAA. Study showed that both non-atopic & atopic people seemed to have an increased risk related to exposure intensity when exposed to laboratory animal allergens. Atopic people developed LAA earlier & in more severe forms (asthma) than non-atopics (13% v 6%). An increased RR was found for atopic people to develop LAA (RR=4,2 (1,5 – 11,3), p<0,05). Authors conclude that exposure & atopy are significant predictors of LAA & that the risk of developing LAA remained present for a much longer period (>3 years) than considered before. Sex, smoking and age were no risk factors.

2+ Cohort Laboratory animals

99

Larbanois 2002 [85] Subjects (n=157) who were being investigated for work-related asthma, were surveyed. Of these 86 had OA, ascertained by a positive specific inhalation challenge (SIC), and 71 subjects had a negative SIC response. After a median interval of 43 months (range 12–85 months), the subjects were interviewed to collect information on employment status, income changes, and asthma-related work disability. Rates of work disruption and income loss at follow-up were similar in subjects with negative SIC (46% and 59%, respectively) and in those with OA (38% and 62%). The median loss as a percentage of initial income was 23% in subjects with negative SIC and 22% in subjects with OA. Asthma-related work disability, defined as any job change or

2- Cohort Various 157

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work loss due to asthma, was slightly more common in subjects with OA (72%) than in those with negative SIC (54%). This study shows that, even in the absence of demonstrable occupational asthma, work-related asthma symptoms are associated with considerable socioeconomic consequences.

Mackie 2008 [86] To assess the efficacy of a UK-wide health surveillance programme provided to the motor vehicle repair industry. Analysis of respiratory questionnaire and spirometry results during the period 1995–2000 and more detailed assessment of the outcome of cases suggestive of OA between 1998 and 2000. Approximately 3,700 employees underwent health surveillance each year. As a result, a number (27%) required further assessment; information on 92 employees who were referred to their general practitioner (GP) for further assessment was examined. Half of these employees subsequently failed to see their GP and of those referred to a specialist only 63% attended that appointment. Of the 20 employees who did see a specialist, nine (45%) were subsequently diagnosed as having OA due to isocyanates, indicating a mean annual incidence rate of 0.79 per 1,000 workers identified by surveillance. A year after identification, five of the diagnosed employees were still working in the same job.

2- Cohort, retrospective

Diisocyanates / vehicle repair industry

92

Mapp 1986 [87] Six workers with TDI induced OA were studied. Methacholin challenge was within normal limits before TDI-Inhalation, but went into asthmatic range after TDI challenge. Isolated neg. Methacholin test

3 Case series Isocyanates / TDI 6

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cannot be used to exclude sensitization. Since variable airflow obstruction and BHR are the main characteristics of asthma, serial measurements of BHR and PEF may be helpful in providing data on sensitized workers and in following workers with OA. BHR may be a helpful screening test in the pre-employment visit.

Meadway 1980 [88] Seven workers using an epoxy adhesive cured with pyromellitic dianhydride were studied. There is no clear relationship between smoking habits, atopic status or skin rashes with resin and a fall in FEV1. There is no simple way to identify those at risk of developing wheeze. Where sensitization occurs a simple questionnaire would provide a screening method.

3 Case series Epoxy adhesives 7

Meijer 2002 [89] High and low risk categories for work related sensitisation can be distinguished from simple questionnaire data and SPT results. The method can easily be applied in occupational medical practice and may markedly increase the efficiency of occupational health surveillance in laboratory animal workers as well as other workers exposed to HMW allergens.

2+(+) Cohort Laboratory animal workers

551

Meijer 2010 [90]

Performance of the model was evaluated in 674 randomly selected bakers who participated in the medical surveillance program and in the validation study. Clinical investigations were evaluated in the firstly referred 73 bakers. This prediction based stratification procedure appeared effective in detecting work-related allergy among bakers and can accurately be used for periodic examination, especially in small enterprises where delivery of adequate care is difficult. The approach may contribute to cost

2- Cross sectional survey

Wheat / bakers 5325

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reduction.

Meijer 2004 [91] Diagnostic and prognostic prediction models to detect and predict occupational allergic diseases; The risk of (future) sensitisation and the severity of laboratory animal allergy can be predicted accurately with diagnostic and prognostic prediction models based on questionnaire items. Workers with an increased risk of future sensitisation also showed serious allergic symptoms at follow up. Workers with a low risk have a low risk of becoming diseased in the future.

2+ Model/cohort Lab animal workers

351

Meijer 2002 [91] Prediction models based on questionnaires can be used effectively. The diagnostic model derived from questionnaire items included gender, wheeze, allergic symptoms during work, allergic symptoms during last year, and work for more than 20h / week with rats as independent predictors for outcome (sensitisation). Splitting a population of laboratory animal workers into a group with high and a low probability of sensitisation, offers an appropriate and practical first diagnostic step (sensitivity 71%, specificity 69%, accuracy 69%) and increases the efficiency of medical investigations by occupational professionals. Accuracy can be improved by additional test (specific IgE or SPT for common allergens). Additional testing recommended in the high risk group. Prediction models based on standardised questionnaire extended with work related questions can be used to detect and predict accurately the risk of sensitisation to HMW workplace allergens and the severity of allergic diseases. A strategy to initially divide the population into

2+ Review-like study with data derived model

Laboratory animals

586

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a group with high and low sensitisation probability by applying a diagnostic model can markly The developed strategy has been shown to be reliable by identifying relatively sever allergic diseases absenteeism, and doctor’s visit in workers with high sensitisation probability. Workers with a high risk of future sensitisation presented serious allergic symptoms at follow up. Workers with a low risk of future sensitisation have a low risk of becoming diseased in the future.

Merget 1988 [92] Anamnestic & immunological data of platinum refinery workers were compared (group A: workers with work-related symptoms (8); group B: workers with symptoms not clearly work-related (9); group C: asymptomatic workers (13) & controls (group D: atopics (10); group E: non-atopics (16)). Exposure to platinum salt was higher in group A than in groups B or C. All subjects of group A & 3 workers of group B, but none of the workers of the other groups, showed a positive cutaneous reaction to platinum salts. Total serum IgE was higher in groups A & D than other groups, however platinum salt-specific IgE was higher in group A. Histamine release with platinum salts was found in all groups & was highest in atopic controls. History of pre-exposure allergic diseases was more frequently in a group with work related symptoms (n.s.). It is not possible to predict weather a subject will acquire platinum salt allergy by means of anamnestic data. Authors conclude that neither histamine release from basophils with platinum salts, nor RAST for the detection of platinum salt-specific IgE are helpful in the diagnosis of

2- Cross-sectional Platinum salts 27

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platinum salt allergy.

Merget 2001 [93] Objective: We sought to assess the effectiveness of a medical surveillance program in workers with exposure to platinum salts. Methods: A nested case-control study was performed in 14 workers of a catalyst production plant whose skin prick test (SPT) responses to platinum salt converted from negative to positive during a 5-year prospective cohort study with yearly medical examinations and 42 matched control subjects from the plant who did not experience SPT response conversion. With the exception of 2 subjects, the workers showing SPT response conversion were removed completely from exposure sources and followed for up to 42 months. Results: Work-related new symptoms were reported by 9 of the 14 subjects, and new symptoms without relation to work were reported by 3 subjects at the time of SPT response conversion. Symptoms were not accompanied by a change in FEV1 or bronchial responsiveness to histamine. Symptoms resolved after transferral, but occasional shortness of breath or wheeze persisted in 4 subjects. SPT reactions decreased or became negative in all workers after complete removal but remained unchanged in a craftsman with ongoing occasional exposure to contaminated materials. Conclusion: Although no randomized intervention was performed, this study proves the effectiveness of a medical surveillance program for the prevention of occupational asthma caused by platinum salts.

2++ Nested case-control, prospective

Platinum salts/catalyst production plant

56

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Monsó 2004 [94] A sample of participants in the European farmers’ study was selected for a cross-sectional study assessing lung function and air contaminants. COPD was found in 18 of 105 farmers. Dust and endotoxin showed a dose-response relationship with COPD, with the highest prevalence of COPD in subjects with high dust and endotoxin exposure. This association was statistically significant for dust in the multivariate analysis.

2- Cross-sectional Farming dust, endotoxin

105

Newill 1986 [95]

The use of screening criteria as determinants for hiring persons to work with laboratory animals is unwarranted because of the dearth of reliable estimates of the strength of association between the screening criteria and LAA.

2- Data analysis Laboratory animals

Nielsen 2001 [96] 154 exposed workers and 57 referents where studied. Air levels where low and associated with the concentrations of metabolites in urine. Furthermore, for the exposed workers, there were high prevalences of sensitization which correlated with the exposure. Neither atopy nor smoking increased this risk significantly. Furthermore, work-related symptoms were more prevalent among the exposed workers than among the referents and they were related to the exposure in the highest group and the specific IgE levels.

2- Cross-sectional (heavy exposure was excluded)

Anhydrides 154

Park 2001 [97] Study aimed to evaluate the clinical validation of skin prick tests (SPT) & measurement of specific IgE to vinyl sulphone reactive dyes by ELISA. 42 patients with occupational asthma from reactive dyes, 93 asymptomatic factory workers & 16 unexposed controls were enrolled. None of the unexposed controls

2- Case-control Vinyl sulphone active dyes

42

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had a positive response to SPTs. The sensitivity (76.2% v 53.7%), specificity (91.4% v 86.0%), positive predictive value (80.0% v 62.9%), & negative predictive value (89.5% v 80.8%) of SPTs were higher than those of ELISAs. Sensitivity (83,3%) and NPV (91,7%) of combined test are even higher. In 4 patients with occupational asthma from reactive dyes & 8 control subjects exposed to reactive dye, IgE specific to reactive dye conjugated to human serum albumin was detected with ELISA even though they showed negative skin reactivity. 6 patients completely avoided the reactive dye for a mean (SD) 27.8 (10.3) months, IgE specific to reactive dyes decreased in all six patients during this time. Authors conclude that both SPTs & detection of IgE specific to reactive dye in serum samples could be valuable for screening, diagnosis, & monitoring occupational asthma resulting from exposure to reactive dyes. These two tests would complement each other. Atopy (pos. SPT for common allergens) higher in OA group (52,4% vs. 32,3% p<0,05).

Peretz 2005 [98] About 270 Dutch wheat flour exposed bakers, millers and bakery-ingredient goodproducers were investigated for sensitization to wheat and common allergens. Further, 520 inhalable dust and wheat-allergen measurements were done. The relation for the whole study population was best described as quadratic, and the probability of sensitization increased with exposure up to c. 2.7 mg/m

3 for inhalable

dust and c 25.7 μg EQ/m3 for wheat

allergens. The risk decreased at higher exposures. Atopy and sector of industry

2+ Cross-sectional Flour

270

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modified the sensitization risk significantly in all the analyses. Conclusions: Exposure-response relationships for allergens may be nonlinear and differ between industries. A threshold is not indicated.

Portengen 2005 [99] 162 pig farmers underwent a cross-sectional case-control study. Data on endotoxin exposure and serum-IgE levels were available. IgE to one or more common allergens was detected in sera from 28 (17%) farmers. A strong inverse relationship was found between endotoxin and sensitization to common allergens for exposures of 75 ng/m

3 or less, with an odds

ratio of 0.03 (95% CI, 0.0-0.34) for a 2-fold increase in endotoxin. For endotoxin exposure of greater than 75 ng/m

3 , the

association was weak. No association was found between endotoxin exposure and total IgE levels. Endotoxin was associated with increased airway responsiveness to histamine and lower lung function in sensitized farmers, without evidence of a nonlinear relationship. Conclusions: Endotoxin or related exposures might protect from sensitization, even in an adult working population, but is a risk factor for increased airway responsiveness and low lung function.

2+ Cross-sectional Pig farmers 162

Redlich 2001 [100, 101] Objectives We have initiated a cross-sectional field epidemiologic study, Survey of Painters and Repairers of Auto bodies by Yale (SPRAY), to characterize the effects of diisocyanate exposures on actively employed auto body shop workers. Methods and Results We present here questionnaire, physiologic, immunologic, and exposure data on 75 subjects enrolled in the study. No overt cases of clinically

2+ Cross-sectional field epidemiologic study

Autorepair/ HDI isoc

75

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apparent diisocyanate asthma were identifed based on spirometry, methacholine challenge, peak flows, and symptoms.

Redlich 2002 [101] Objectives A 1-year follow-up was undertaken as an adjunct to the cross-sectional SPRAY study (Survey of Painters & Repairers of Auto bodies by Yale) to investigate the effects of HDI on auto body shop workers over time and whether or not the healthy worker effect may exist in this industry. Conclusions The differences in workers who stayed at their shop compared to those who left, combined with the low asthma prevalence and high job turnover rate, all suggest that a healthy worker effect may exist in the auto body industry, and may in part account for the low prevalence of asthma noted in SPRAY and other cross-sectional studies of diisocyante workers.

2+ Cross-sectional, follow-up

LMW/isoc HDI/ Autorepair

48

Renstrom 1994 [102] In a prospective study of laboratory technicians, selected indicators of allergy & atopy were studied in an attempt to determine predictors of laboratory animal allergy (LAA). Total IgE was sign. higher before exposure in subjects who developed symptoms [and sensitisation] than in non symptomatic subjects, total IgE > 100 kU/l PPV=0.44 [PPV =0.33]. Nasal symptoms before exposure more frequent in sensitised subjects (PPV = 0.44). PPV of family allergy was 0.17. From results it does not seem likely that refusing to employ atopic subjects in animal work will prevent the development of LAA. Preventing atopic subjects from animal work would only have reduced the 9

2+ Cohort Laboratory animals

225

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sensitised and/or symptomatic subjects to 7. Preventing subjects with total IgE levels >100 kU/l from working with animals would have reduced the number of subjects developing LAA to 2 instead of 9. On the other hand, 8 non-reactive subjects (after this study) would also have been excluded from such work.

Roberts 2004 [103] The prevalence of asthma among working adults continues to rise each year. The California Department of Health Services conducts surveillance of work related asthma (WRA) to classify each work related exposure using Doctor's First Reports of Occupational Illness and Injury (DFRs). Using a cross-sectional, descriptive, comparative design, additional interviews were conducted and medical records were reviewed to explore workers' and providers' perceptions of follow up care. Two cohorts were compared: workers with WRA who belonged to a large, single HMO (n = 79) and workers with WRA who underwent follow up outside this HMO (n = 76). The interview asked about providers seen, tests ordered, and the impact of asthma on work. The HMO clients were significantly more likely than the non-HMO clients to see occupational medicine specialists (p = .004) and have pulmonary function testing (p = .049) during initial treatment. Twenty-four percent of clients currently working reported missed workdays caused by asthma in the past 6 months. The findings indicate management of WRA varies by health care system in California.

Cross-sectional 155

Robertson 2007 [104] Investigation of an outbreak (12 workers) of EAA in the UK between 12/2003 and

2+ Cross-sectional Metal working fluid / car

808

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05/204. Half of the asthma cases (74, defined by serial peak flow records) had asthma before 2003. Exposure related diagnosis (OA, EAA): 3,5 fold greater risk at largest common sump.

engineers

Schumacher 1981 [105] 121 exposed and 50 unexposed subjects were studied by questionnaire and SPT with 7 common aeroallergens and allergens from mice. In subjects with seasonal allergic rhinitis or positive SPT results with common aeroallergens, work-related nasal symptoms and mouse-specific positive SPT and IgE were more prevalent. This suggests a predisposition to mouse allergy was related to the coexistence of atopic diathesis. Work-related eye or chest symptoms are not significantly associated with seasonal rhinitis. WR Symptoms from mice or +SPT to mouse AGs did not correlate sign. with a family history of allergic rhinitis, asthma or eczema A negative association between the incidence of HLA-DRW6 and SPT+ to mice antigens suggests a possibility of genetic influence on susceptibility to mouse allergy. Screening of prospective employees in mouse laboratories by questionnaires could be improved by use of pollen SPT in the pre-employment assessment to minimize need for compensation for occupational disability. But many pollen SPT+ subjects did not develop symptoms, indicating that pollen SPT for screening purpose could preclude employment of a person who could work among mice without becoming sensitized.

2- Cross-sectional Laboratory animals

171

Sjostedt 1989 [106] LAA asthmatics have an increased frequency of family history of allergy

2+ Cohort Laboratory animals

101

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(RR=3,8; PPV=0,27) and a positive SPT results with common non-animal allergens (RR=15; PPV 0,60). All persons with marked positive SPT to environmental allergens have developed animal positive LAA asthma. 56% LAA asthama cases IgE > 100 kU/L Pre-employment screening: family history of allergy and pos SPT.

Skjold 2008 [107] 114 baker apprentices were surveyed over 20 month period. An increased risk of asthma like symptoms was found in atopics and females. In subjects with new onset respiratory symptoms an increase of BHR from baseline was observed. FEV1 and FVC did not change during follow up period. No relationship between new sensitisation and new symptoms. The mechanism by which symptoms arose was perceived to reflect the development of an inflammation rather than the production of a specific IgE pathway, as sensitization to WR allergens was rarely observed. Hence respiratory symptoms and allergy may also develop through separate pathways.

2+ Cohort Bakers 114

Slovak 1987 [108] Helmet respirator would appear to be a valuable adjunct in the management of occupational asthma in those that opt to remain in exposure. However, they should be monitored carefully & regularly to ensure that their respiratory function has not deteriorated. Objective evidence of good protection was obtained in 6/8 asthmatics.

2- Case series Laboratory animals

146

Smit 2008 [109] Occupational endotoxin exposure in adulthood is associated with asthma-like symptoms (wheezing, shortness of breath, daily cough) but reduced prevalence of hay fever

2- Cross-sectional Endotoxine 877

Smith 1999 [110] The objective of this study was to describe 2+ Cross-sectional, Wheat, amylase/ 3,450

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the incidence of allergic respiratory disease and its outcome in terms of symptoms and jobs,.across different flour-using industries. It uses the findings of a health surveillance programme in a large food organization over a five-year period. The population under surveillance consisted of 3,450 employees with exposure to ingredient dusts, of whom 400 were in flour milling, 1,650 in bread baking, 550 in cake baking and 850 in other flour-using operations. A total of 66 employees with either asthma or rhinitis symptoms attributable to sensitization to allergens in the workplace were identified. The majority of these (48/66) had become symptomatic prior to the commencement of the hearth surveillance programme in 1993. The incidence rates (per million employees per year) for those who developed symptoms between 1993 and 1997 were 550 for flour milling, 1,940 for bread baking, 0 for cake baking and 235 for other flour-using operations. The agent believed to be responsible for symptoms was most commonly grain dust in flour millers and fungal amytase in bread bakers. Wheat flour appeared to have a weaker sensitizing potential than these other two substances. In terms of outcome, at follow-up 18% of symptomatically sensitized employees had left the company. Two of the ex-employees retired through ill health due to occupational asthma. Of those still in employment, 63% described an improvement in symptoms, 32% were unchanged and 4% were worse than when first diagnosed. Over half the cases still in employment were continuing to work in the

follow-up; health surveillance programme

millers and bakers

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same job as at the time of diagnosis.

Suarthana 2005 [111]

Dutch laboratory animal (LA) workers and bakers using logistic regression analysis. Validity was assessed internally by bootstrapping procedure, and externally in British LA workers. It is possible to develop a generic model for sensitization to occupational HMW allergens. However, the weighing of predictors differs across specific work environments

(2+) Modeling Bakers, laboratory animals workers,

427, 936

Suarthana 2008 [112] The baseline value of a questionnaire used alone or in combination with SPT to common allergens and/or BHR testing with Methacholin in predicting the occurrence of sensitization to laboratory animal (LA) allergens and respiratory symptoms was assessed. Questionnaire is a good tool to predict the incidence of occupational sensitization and symptoms. Additional test improve the specificity of the prediction for LA sensitization.

? Cross-sectional Laboratory animals

314

Taiwo 2006 [113] Asthma occurs excessively among potroom workers and if so, delineate dose–response relationships for possible causal risk factors. The prevalence of asthma in our study population at baseline was 6.9%. The annual incidence of asthma observed in potroom workers in this study population was 1.17%. Potroom asthma appears to occur at the studied U.S. aluminum smelters at doses within regulatory guidelines.

2+ Cross-sectional Potroom / fluoride

14,002

Tarlo 1997 [114] Within this database, levels of isocyanate concentrations measured were compared at 20 case companies with 203 non-case companies, based on air samples collected during the 4-year period during which occupational asthma claims arose. The

2- Database and case statistic analyses

Isocyanates 6,308

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proportion of case companies that were ever recorded as having a measured ambient isocyanate concentration of ≥ 0.005 ppm was greater than that for noncase companies, for TDI users (43% vs 22%), and for MDI users (40% vs 27%). This reached conventional significance when combined across companies and isocyanate types.

Tarlo 1997 [115] 203 students and staff members completed the questionnaire. 5 percent reported asthma symptoms on exposure to rubber products, 13% reported symptoms of rhinitis or conjunctivitis and 17% reported pruritus or urticaria within minutes of exposure to rubber. Among the students tested, there were increasing percentages of positive skin test responses to latex with increasing years of study. Positive responses were seen as early as year 3 in students. Positive skin prick test responses to latex were related to a personal history of atopy (p = 0.005), positive skin prick test responses to common allergens (p < 0.005), latex-attributed immediate pruritus or urticaria (p < 0.05), rhinoconjunctivitis (p < 0.001), and asthma symptoms (p < 0.001). Conclusion: Dental school students and faculty are at high risk for latex sensitization…

2- Cross-sectional Latex (dental students)

203

Tarlo 2001 [116] This study assesses the effects of intervention to reduce NRL allergy in an Ontario teaching hospital with approximately 8,000 employees. A retrospective review assessed annual numbers of employees visiting the occupational health clinic, allergy clinic, or both for manifestations of NRL allergy compared with the timing of introduction of

2+ Cohort, retrospective

Latex / health care workers

8,000

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intervention strategies, such as worker education, voluntary medical surveillance, and hospital conversion to low-protein, powder-free NRL gloves. The number of workers identified with NRL allergy rose annually, from 1 in 1988 to 6 in 1993. When worker education and voluntary medical surveillance were introduced in 1994, a further 25 workers were identified. Nonsterile gloves were changed to low–protein, powder-free NRL gloves in 1995: Diagnoses fell to 8 workers that year, and 2 of the 3 nurses who had been off work because of asthma-anaphylaxis were able to return to work with personal avoidance of NRL products. With a change to lower protein, powder-free NRL sterile gloves in 1997, allergy diagnoses fell to 3, and only 1 new case was identified subsequently up to May 1999. No increased glove costs were incurred as a result of consolidated glove purchases. This program to reduce NRL allergy in employees was effectively achieved without additional glove costs while reducing expenses from time off work and workers’ compensation claims.

Tarlo 2002 [117] The introduction of a medical surveillance program (in Ontario, Canada) in 1983 was followed by retrospective assessments to determine benefits. Between 1980 and 1993, the proportion of all accepted compensation claims for OA that were attributed to diisocyanates, classified by year of symptom onset in the province with the program, rose to 64 percent by 1988, then fell significantly down to 29 percent in 1992 and 35 percent in 1993. Among those with diisocyanate-induced OA, an earlier diagnosis and a trend to

2+ Case series, retrospective

Isocyanates 136

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better outcome was found in workers from companies that were identified to be in compliance with surveillance measures.

Venables 1985 An outbreak of occupational asthma, of unknown cause and extent, was detected in a steel coating plant. In 1979 a cross-sectional study which defined occupational asthma in terms of respiratory symptoms detected 21 people with suggestive symptoms among the 221 studied.

2- Cross-sectional Steel coating / isocyanates

221

Venables 1988 [118] The correlation of symptoms suggestive of occupational asthma, symptoms suggestive of any occupational allergy, skin wheals to animal urine extracts, & serum RAST tests with urine extracts with atopy or smoking was investigated. Pooled data showed an association between smoking & all indices except RAST; the association was significant for symptoms of occupational asthma. One of the three surveys consistently showed a stronger association of allergy indices with smoking than with atopy (positive SPT results with non-animal aeroallergens). The ratio of prevalence in atopics compared with the group of non-atopics was 2,6 (p=0,023) for LAA chest symptoms, 2,1 (p<0,001) for skin weal to animal urine extract and 2,2 (p<0,001) for RAST+ to animal urine extract. No significant association was found between atopy and any LAA symtomy (ratio=1,3; p=0,332).

2+ Survey of 3 cross-sectional studies

Laboratory animals

296

Venables 1988 [118] Survey was carried out on 138 workers exposed to laboratory animals. 44% had symptoms in a self-completed questionnaire that were consistent with laboratory animal allergy (LAA) of whom 11% had chest symptoms. LAA chest symptoms were almost 5 times more

3 Cross-sectional Laboratory animals

158

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common in atopic (positive SPT result with non-animal aeroallergens) than non-atopic subjects. Positive SPT results with animal urine extracts was associated with LAA chest symtoms and atopy. Atopy was not associated with LAA eye, nose or skin symptoms when present without chest symptoms and only weakly associated with positive RAST results when present without a positive SPT results. As atopy is common in the general population it is difficult to justify excluding atopic subjects from employment with animals, but atopic subjects who develop positive skin tests to animal allergens may be at particular risk of chest symptoms & could be identified during employment & advised on risk. Regular screening at least provides useful information on the scale of the LAA within an organisation & in conjunction with occupational histories may point to particular working areas or practices that should be modified.

Wild 2005 [120] The authors used a mathematical simulation model of isocyanate asthma to compare annual surveillance to passive case finding. Outcome measures included symptom free days (SFD), quality adjusted life years (QALY), direct costs, productivity losses, and incremental cost effectiveness ratio (CER), measured from the employer and the societal perspectives. Input data were obtained from a variety of published sources. For 100,000 exposed workers, surveillance resulted in 683 fewer cases of disability over 10 years. Surveillance conferred benefits at an incremental cost of $24,000/QALY (employer perspective;

2++ Mathematical simulation model

Isocyanates 100,000

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$13.33/SFD) and was cost saving from the societal perspective. Results were sensitive to assumptions about sensitisation rate, removal rates, and time to diagnosis, but not to assumptions about therapy costs and disability rates.

Zuskin 1997 [121] A follow-up investigation was performed on 49 female workers studied 2 years earlier in a vegetable-pickling plant. Acute and chronic respiratory symptoms and ventilatory capacity measurements were recorded during the original and the follow-up studies.

Cohort Vegetable-pickling plant

49

Chapter 4: Primary prevention of occupational asthma: exposure reduction, skin exposure, respiratory protection (for more details including elaboration of references see [122]

Ancillary question 1: “Evidence for prevention of asthma due to natural rubber latex (NRL)”

Allmers 2002 [123] Decreased use of powdered gloves and increased use of powder-free gloves correlated with decline in suspected NRL OA and skin allergy cases, 1997-2001. CONCLUSION: Primary prevention of occupational NRL allergies is possible with properly implemented practical interventions.

From LaMontagne 2006

Case series, reported number of suspected NRL allergy cases from German health care system

NRL exposure from gloves

3 million insured health care workers in Germany

Heilman 1996 [124] Latex aeroallergen levels (ng/m3) and extractable latex glove allergen contents in an operating room measured on 52 consecutive days, including 19 non-surgery days, with 12 exposure crossovers. On 33 surgery days, all personnel wore either high allergen gloves (n = 18 days) or low allergen gloves (n = 15 days). Internal comparison (cross-over). CONCLUSION: Substitution of low-allergen-NRL gloves for high-allergen NRL gloves can reduce latex aeroallergen levels by more than 10-fold in an OR environment.

From LaMontagne 2006

Prospective evaluation of an intervention

Operating room (OR) personnel exposed to NRL

Measurements on 52 days

Jones 2004 [125] Studied dental students from 1st to last year

in training. Students used only powder-free From LaMontagne 2006

Prospective evaluation of

NRL exposure in dental students

63 dental students at baseline, 34 at final

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NRL gloves and were tested annually. Students were 65% atopic, but none developed latex sensitivity in 5 years of study. CONCLUSION: Exposure to powder-free NRL gloves was not associated with sensitization over 5 years in a highly atopic population.

intervention year (loss to follow-up)

LaMontagne 2006 [126] Substitution of powdered latex gloves with low protein powder-free NRL gloves or latex-free gloves greatly reduces NRL aeroallergens, NRL sensitisation, and NRL-asthma in healthcare workers.

Lit. search Systematic review

Natural rubber latex (NRL) exposure

8 studies ranging from exposure studies and observational data from cohort studies

Lee 2001 [127] Education to reduce NRL glove use in food handlers. Use was reduced from 10 stalls to 1. CONCLUSION: Educate food handlers to prevent NRL allergy in workers and customers.

From LaMontagne 2006

Intervention among food handlers in Australia

NRL glove use in food handlers

30 food stalls at market

Levy 1999 [128] Last-year dental students in Paris, France, and London, England completed a questionnaire and skin prick testing with NRL extract. The odds ratio for latex sensitivity was 11.3 (95 % CI 2.4-53.0) for using protein-rich gloves. CONCLUSION: Use of powder-free protein poor NRL gloves may reduce latex sensitization.

From LaMontagne 2006

Cross-sectional: Some students had used protein-rich gloves and others had not

Use of protein-rich vs, protein poor NRL gloves in dental clinic

189 5th year

(graduating) dental students working in clinics

Liss 2001 [129] In 1996, Ontario government recommended change to powder-free, low-protein or non-NRL gloves in health care, and hospitals changed related policies about the same time. Researchers documented a decline in worker comp claims for NRL OA, from highs of 7-11/yr in 1991-94 to 1-2/yr in 1997-99. CONCLUSION: Use of low-protein or non-NRL gloves is associated with a decrease in number of NRL OA cases.

From LaMontagne 2006

Case series based on worker comp claims in Ontario province, Canada

Use of powdered NRL gloves and change to low-powder NRL and non-NRL gloves in health care facilities.

66 WC claims for NRL through 1999

Saary 2002 [130] Dental school in Ontario province, Canada, changed from high protein/ powdered to low protein/ non-powdered NRL gloves. A

From LaMontagne 2006

Intervention for students and staff in dental

NRL gloves in dental school

131 in 1995 and 97 in 2000

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positive NRL skin prick test in students decreased from 10% in 1995 to 3% in 2000 (p=0.03). There was a decline in % with urticaria, immediate pruritis, and rhino-conjunctivitis, but not asthma or eczema. CONCLUSION: Suggestive preventive effect by change to low-protein/powder-free NRL gloves in dental school.

school, between cross-sectional surveys in 1995 and 2000 (two different study cohorts).

Tarlo 2001 [116] Study conducted in teaching hospital in Ontario, Canada. Intervention was education and medical surveillance, and change to powder-free NRL gloves. Decline in symptom onsets and clinic visits after change in non-sterile gloves in 1995 and sterile gloves in 1997, to final year of study in 1999. CONCLUSION: NRL allergy reduced.

From LaMontagne 2006

Intervention & retrospective record review to detect NRL allergy cases in occupational health and allergy clinics

NRL in gloves in hospital

8000 employees, 52 staff with positive skin test responses and clinical NRL allergy.

Ancillary question 2: “Evidence for prevention of asthma due to a variety of agents”

Anhydrides

Grammer 2002 [131]

Before introduction of respirators, annual incidence for asthma was 10%. During 7 years of follow-up after introduction of respirators, highest annual incidence was 2%. CONCLUSION: Respirators can reduce incidence of occupational immunologic respiratory disease, including OA, in workers exposed to hexahydrophthalic anhydride (HHPA)

2+ Prospective cohort study following intervention (introduction of respirators)

HHPA 66 new workers who made HHPA

Diisocyanates

Tarlo 2002 [117] In 1983, Ontario province in Canada mandated medical surveillance program for workers exposed to diisocyanates. This was followed by retrospective assessments to determine benefits. Frequency of diisocyanate asthma worker comp claims (both in number and % of all OA claims) rose to peak in 1988, and then declined significantly to 1993. CONCLUSION: Medical surveillance program contributed to

3 for surveillance and 2+ for case

control study within case series.

Registry based ecologic study. Case series from worker comp claims for OA attributed to diisocyanates in province of Ontario, Canada.

Diisocyanate exposure (study had exposure above TLV as readout parameter.)

Number of claims varied by year, from high of 55-58 claims/yr in 1988-1990, to low of 19-20 claims by 1992-1993

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the positive change, but cannot rule out that reduced diisocyanate exposures and increased awareness of problem by workers and physicians may have also contributed to decline.

Flour And Other Bakery Exposures

Meijster 2009 [132] Changes in exposure over time varied substantially between sectors and jobs. For bakeries: modest downward trend of -2%/yr for flour dust and -8%/yr for amylase. For flour mills: -12%/yr for flour dust and significant trend for amylase. For ingredient producers: results generally non-significant, but indicated a reduction in flour dust and increase in fungal alpha-amylase. Modest increase in use of control measures and proper work practices reported in most sectors, especially the use of local exhaust ventilation and decreased use of compressed air. CONCLUSION: The magnitude of the observed reductions in exposure levels indicates that the sector-wide intervention strategy implemented during the covenant period had a limited overall effect.

2+ Sector-wide intervention program, with education on good work practices, and non-randomised pre-post evaluation of exposure to wheat and fungal

α-amylase

Bakery workers, flour millers, bakery ingredient workers

1770 personal exposure measurements generally including data

on flour dust and

fungal α-amylase levels, taken in 4 surveys (1993, 2001, 2005, 2007).

Smith 2004 [133] Intervention was reducing bread improver levels by better exhaust ventilation, respiratory protection when handling bread improver, and education; respiratory health surveillance; and dust sampling. There was an overall reduction in the incidence of new cases of symptomatic sensitization, from 2085 per million employees per year in the first 5 years of the surveillance programme, to 405 per million employees per year in the subsequent 5 years. Symptomatic sensitization incidence was not related to total inhalable dust levels. CONCLUSION: The strategy of targeting

2- Prospective intervention in UK food company. Based on surveillance data in combination with a triage approach which was not validated

Bakery workers, flour millers exposed to flour and enzymes, especially fungal amylase

>3000 workers per year under surveillance

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bread improver exposure is an effective approach for preventing new cases of symptomatic sensitization in bread bakeries.

Detergent Enzymes

Cathcart 1997 [134] At five production facilities in the UK: studied dust and enzymes levels 1969-1993; lung function of workers 1972-1991, and cases of OA 1968-1992. Exposure groups were defined by job history. Enzyme levels declined over study period. Rates of fall in FEV1 and FVC showed no consistent trends in relationship to enzyme exposure. The annual number of cases of enzyme allergy and asthma declined.

2- Registry based study, case series, ecological

Detergent enzyme exposure in production facilities

731 male workers

Schweigert 2000 [135] Variety of controls introduced across detergent enzyme manufacturing industry. Decrease in number of OA cases in Latin American and North American detergent enzyme manufacturing sites 1969 – 1998, but no denominators indicated.

4 Review article with minimal data and documentation.

Detergent enzyme manufacturing industry

Unclear

Laboratory Animal Allergy and Asthma

Botham 1987 [136] Prospective studied incidence of allergy to laboratory animals (ALA) in 383 workers exposed to rodents and to rabbits. Intervention was introduction of a site order and code of practice for working with animals and an education programme. Concurrent with the intervention, incidence of allergy after 1 year of exposure to animals fell from 37% in 1980-81 to 20% in 1982, 10% in 1983, and 12% in 1984. Atopy increased risk of allergy in first year of exposure but not in 2

nd or 3

rd years of

exposure.

2- Intervention study with longitudinal, repeated measurements

Laboratory animal workers with exposure to rodents and rabbits

383 workers

Fisher 1998 [137] Intervention program included education, engineering controls, administrative controls, use of personal protective equipment, and medical surveillance. They

2- Comprehensive intervention program with longitudinal,

Laboratory animal workers

159 employees

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conducted a prospective survey of 5 years of data to determine effect program (1991-1995). At start of program, prevalence of laboratory animal allergy (LAA) was 12%-22% at first, and then 0% in last 2 years of the 5-year observation period. CONCLUSION: LAA is preventable through the implementation of a comprehensive effort to reduce exposure to allergens.

repeated measurements

Ancillary question 3: “Selected References on occupational skin exposure to isocyanates”

Bello 2008 [138]

Quantitative skin wipe sampling method developed. 92% of samples under PPE had detectable NCO levels, mostly pHDI. Highest total NCO concentrations associated with spraying and mixing.

Cross-sectional HDI, auto body repair workers

185 samples from 81 auto body shop painters and techs during different tasks. 43 samples under PPE

Fent 2008 [139]

Log-transformed concentrations of HDI (r-0.79, p<0.001) in skin of workers correlated with log-transformed product of air concentration and painting time. Other polyisocyanates detected on skin for less than 25% of paint tasks.

Cross-sectional HDI, auto body spray painters

13 auto body spray painters – air and skin concentrations

Fent 2009 [140]

Isocyanurate predominant isocyanate. Dermal HDI concentrations higher in those not wearing gloves/coveralls. NCO detected on skin during 23% of paint tasks. Linear mixed modeling identified breathing-zone concentration and paint time significant predictors skin concentration.

Cross-sectional HDI, auto body spray painters

47 spray painters dermal and inhalational exposure assessment 15 painters no gloves

Flack 2009 [141]

- HDA detected in 76% plasma samples. - Correlation between plasma HDA and same day dermal exposures low but significant, correlation between HDA and 20-60 day dermal exposure higher (r=0.36)

Cohort HDI, auto body shop painters

46 spray painters -blood, inhalation and dermal exposures measured. 288 tasks.

Liljelind 2010 [142]

Average personal air concentrations below Swedish exposure limit. Tape tripping used measure MDI skin exposure. Decreasing levels of MDI in consecutive tape strips per site indicate dermal penetration.

Cross-sectional MDI, iron-foundry workers

19 workers in different areas of foundry – tape strip dermal sampling repeated on five exposed skin areas

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and air sampling

Liu 2009 [143]

Skin exposure algorithm using diaries, task based skin sampling, PPE. Median daily SEI (skin exposure index) estimated for each worker. Was associated with job category. Weakly correlated with daily airborne exposure.

Cross-sectional Workers in auto body shops

232 workers in 33 shops. 893 exposure person-days skin exposure, work diary

Pronk 2006 [144]

- Inhalation HDI exposure associated with tasks involving aerosolisation. Dermal exposure assessed by extraction HDI from nitrile gloves; associated with paint-handling tasks, glove use. - HDA detected in 36% of repair shop workers, 10% of industrial workers. - HDA significantly elevated at end of workday. HDI oligomers main exposure.

Cross-sectional Pre-post shift sampling

HDI (mostly oligomers), auto body repair workers

A) 68 task-based paired inhalation and dermal samples from 6 auto repair shops. 239 urine samples from 45 workers B) 27 paired inhalation and dermal samples fm 5 industrial paint co. 52 urine samples from 10 painters.

Robert 2007 [145]

- MDA detectable in 73% of post-shift urine samples. These levels significantly higher than pre-shift levels. - Highest MDA levels associated with spraying or hot processes. Skin exposure associated with significant MDA levels in urine.

Cross-sectional MDI, polyurethane workers

169 workers of 19 French factories and 120 controls

Todd 2008 [146] - 8-21% of workers exposed to mixtures of chemicals (solvents, HDI) > OELs; 39-69% of surface samples positive for un-reacted isocyanates using qualitative CLI SWYPES

TM.

- PPE, IH controls not adequate.

Cross-sectional Workers at footwear and equipment factories

286 personal air samples, 64 surface, tool, or hand samples from 4 factories in Thailand

Ancillary question 4: “References which address the association between skin exposure and asthma”

Bernstein 1993 [48, 147] Based on questionnaire-derived diagnoses of 243 workers: 4% workers occupational asthma (OA), 36% occupational rhinitis, 11% irritant lower respiratory symptoms. 2 / 243 (0.4%) MDI-specific IgG – both worked in finishing area where they had direct MDI skin contact. Plant designed to minimize

3 Cross-sectional / case series isocyanate asthma

MDI, urethane mold plant

243 workers exposed to MDI – questionnaire and serum antibody tests. 147 workers on urethane mold lines. 3 cases isocyanate

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exposures MDI. 24-hr / day air monitoring area samples. All air levels < 0.005 ppm over 3 yrs. Selected workers further medical evaluation: 3 cases OA from MDI (1.2%) and 1 case MDI-induced cutaneous anaphylaxis (positive MDI-HSA skin test and MDI-IgE). These 4 workers worked in areas with potential MDI skin contact – maintenance and finish area. 1 case MDI asthma onset of symptoms after MDI spill. Conclusions: Low prevalence of sensitization (MDI-IgG) and OA. Recommend avoid MDI skin contact.

asthma

Dernehl 1966 [148] Mentions personal experience isocyanate skin exposure increases risk asthma.

3 Personal experience

MDI Workers with respirator protection and repeated skin contact

Donnelly 2004 [149] Nurse with MDI asthma. Case confirmed by specific inhalation challenge with MDI cast material (39% decreased FEV1).

3 Case study MDI, hospital – synthetic plaster casts

1 nurse working with MDI-containing plaster casts for 4 years

Lenaerts-Langanke 1992 [150]

Population 1) Half reported skin exposure. 6.5% (14/216 pressure grouters) MDI-related respiratory symptoms. 4/216 pressure grouters isocyanate hyper-responsiveness, 2 positive MDI-specific inhalation challenge. Air exposures very low (<1 ppb) Population 3 – 6/8 pressure grouters with heavy skin exposure MDI metabolites in urine. Skin irritation MDI rare – only 1 in all workers. MDI skin exposure common, “typical phenomenon”. MDI sensitization through skin contact possible. Important prevent skin exposure.

3 Cross-sectional MDI, coal miners 3 populations: 1) 284 total: 216 pressure grouters – inject MDI polyurethane (PU) foam; 55 control miners 2) 245 exposed miners 3) 8 pressure grouters with heavy PU skin exposure

Nemery 1993 [151] Surface worker who handled half-empty MDI drums at the mine without safety precautions developed probable isocyanate

3 Case study MDI, coal miners Surface worker from coal mine

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asthma. Risk of isocyanate exposure with polyurethane rock consolidation. Cite Lenaerts – skin most likely sensitization.

Petsonk 2000 [152] 27% of workers in areas with high potential for liquid MDI exposure reported new-onset asthma-like symptoms, versus 0% in low-potential areas. Skin staining and MDI on clothes, working around and cleaning up MDI was associated with new asthma-like symptoms. Follow-up asthma symptoms were associated with variable airflow limitation and MDI-specific IgE, not allergy skin prick testing. Air monitoring data (6 personal breathing zone samples) no detectable MDI. A single glove wipe sample was taken and had 0.078 mg MDI. Conclusions: Skin may be site for potential immunologic sensitization and subsequent risk for development of respiratory symptoms.

2+ Cohort (1 year follow-up)

MDI, wood manufacturing plant

214 plant employees, 83% participated in follow-up survey. Questionnaires prior to use of MDI and every 6 months afterwards. Serial peak flows, spirometry, methacholine challenge, MDI-IgE, skin prick testing performed certain times, selected workers

Shahzad 2006 [153]

Asthma prevalence 10.8% (69/641). Multivariate analysis –asthma associated with educational status, ethnicity, smoking, glove use (never use OR=3.28; 95% CI: 1.72-6.26), perceived allergy, duration of work. Protective effect glove use may be due to protection skin from sensitizing chemicals.

2- Cross-sectional Leather tannery workers in Pakistan

641 workers in 95 tanneries, all workers enrolled working with tanning process. Questionnaire. No exposure information.

Ancillary question 5: “Evidence for effectiveness of respirators to prevent onset of occupational asthma” Grammer 2002 [154]

Before introduction of respirators, annual incidence for asthma was 10%. During 7 years after respirators introduced, highest annua20l incidence was 2%. Authors concluded respirators can reduce incidence of occupational immunologic respiratory disease, including OA, in workers exposed to hexahydrophthalic anhydride (HHPA)

2+ Prospective cohort; following intervention (introduce respirators)

Acid anhydride 66 new workers who made HHPA

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Online supplementary TABLE sO4 Major causative agents for work-related asthma

(see also following references with lists of agents and corresponding reviews) [155-161] http://www.uke.de/institute/arbeitsmedizin/downloads/universitaetsprofessur-arbeitsmedizin/R42_und_R37A-EU09.pdf; http://www.uke.de/institute/arbeitsmedizin/downloads/universitaetsprofessur-arbeitsmedizin/Table_2_Irritants.pdf; http://www.worldallergy.org/professional/allergic_diseases_center/occupational_allergens/; www.asmanet.com; www.asthme.csst.qc.ca; http://www.occupationalasthma.com Flour/grain dust Isocyanates Paints Laboratory animals and insects Enzymes Wood dust Bioaerosols containing moulds and bacteria Latex Seafood (crab, prawn, shellfish) Persulfates, bleaches Cutting oils and coolants Anhydrides Solder/colophony/welding fumes Acrylates and acrylics Cleaning products Formaldehyde, glutaraldehyde Platinum salts Cobalt Nickel sulphate, chromium Spills of irritants such as chlorine, acetic acid, smoke from fires

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Online supplementary text sO5

Clinical outcome of work-related asthma

In total, our literature search identified 88 papers which had evaluated the outcome of WRA

[2, 4, 5, 8-19, 21, 37, 38, 43, 48, 53, 54, 75, 77, 85, 162-186] [36, 42, 187] [22-28, 33, 34, 39,

46, 50, 51, 55, 56, 110, 119, 188-205]. Sixty-one of the 88 papers focused on specific

exposures in cohort studies or case series. Of those, isocyanates (24), anhydrides (7), latex (6),

and red cedar (5) were the most frequently studied exposures. Seventy-one of 88 studies (81

%) were published in 2000 or earlier. In addition to symptoms and lung function, the variables

used to evaluate the outcome of asthma have included both NSBHR [9-11, 13, 14, 38, 42, 43,

75, 85, 163, 164, 171, 175, 179-182, 187] [18, 19, 21-28, 46, 50, 54, 183, 185, 189-195, 197,

198, 200-203, 205], and specific immunogical responses (specific IgE [25, 42, 77, 164, 172-

174, 177, 178, 199, 205], specific IgG [25, 77, 172, 173, 178], and specific bronchial

responsiveness) [11, 18, 28, 53, 54, 179, 187, 188, 200, 202, 203]. Fewer studies were

available concerning measurements of inflammatory activity, which included those that used

induced sputum [13, 38, 43, 46], BAL [167, 190, 193] or fractional exhaled nitric oxide

(FeNO) [38]. Bronchial biopsy studies were uncommon [50, 193, 197, 198]. In addition, other

outcomes researchers investigated were employment [15, 16, 33, 37, 39, 42, 85, 110, 162,

166, 168, 175, 182, 185] and income [37, 85, 162, 166, 182, 185], assessment of asthma

severity [8, 185] and QoL [180, 181, 187].

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104. Robertson W, Robertson AS, Burge CB, Moore VC, Jaakkola MS, Dawkins PA, Burd M, Rawbone R, Gardner I, Kinoulty M, Crook B, Evans GS, Harris-Roberts J, Rice S, Burge PS. Clinical investigation of an outbreak of alveolitis and asthma in a car engine manufacturing plant. Thorax 2007: 62(11): 981-990. 105. Schumacher MJ, Tait BD, Holmes MC. Allergy to murine antigens in a biological research institute. The Journal of allergy and clinical immunology 1981: 68(4): 310-318. 106. Sjostedt L, Willers S. Predisposing factors in laboratory animal allergy: a study of atopy and environmental factors. Am J Ind Med 1989: 16(2): 199-208. 107. Skjold T, Dahl R, Juhl B, Sigsgaard T. The incidence of respiratory symptoms and sensitisation in baker apprentices. Eur Respir J 2008: 32(2): 452-459. 108. Slovak AJ, Hill RN. Does atopy have any predictive value for laboratory animal allergy? A comparison of different concepts of atopy. Br J Ind Med 1987: 44(2): 129-132. 109. Smit LA, Heederik D, Doekes G, Blom C, van Zweden I, Wouters IM. Exposure-response analysis of allergy and respiratory symptoms in endotoxin-exposed adults. Eur Respir J 2008: 31(6): 1241-1248. 110. Smith TA, Patton J. Health surveillance in milling, baking and other food manufacturing operations--five years' experience. Occup Med (Lond) 1999: 49(3): 147-153. 111. Suarthana E, Vergouwe Y, Nieuwenhuijsen M, Heederik D, Grobbee DE, Meijer E. Diagnostic model for sensitization in workers exposed to occupational high molecular weight allergens. Am J Ind Med 2005: 48(3): 168-174. 112. Suarthana E. Predicting occupational lung diseases. Utrecht University, Utrecht, 2008; p. 127. 113. Taiwo OA, Sircar KD, Slade MD, Cantley LF, Vegso SJ, Rabinowitz PM, Fiellin MG, Cullen MR. Incidence of asthma among aluminum workers. J Occup Environ Med 2006: 48(3): 275-282. 114. Tarlo SM, Liss GM, Dias C, Banks DE. Assessment of the relationship between isocyanate exposure levels and occupational asthma. Am J Ind Med 1997: 32(5): 517-521. 115. Tarlo SM, Sussman GL, Holness DL. Latex sensitivity in dental students and staff: a cross-sectional study. The Journal of allergy and clinical immunology 1997: 99(3): 396-401. 116. Tarlo SM, Easty A, Eubanks K, Parsons CR, Min F, Juvet S, Liss GM. Outcomes of a natural rubber latex control program in an Ontario teaching hospital. The Journal of allergy and clinical immunology 2001: 108(4): 628-633. 117. Tarlo SM, Liss GM, Yeung KS. Changes in rates and severity of compensation claims for asthma due to diisocyanates: a possible effect of medical surveillance measures. Occup Environ Med 2002: 59(1): 58-62. 118. Venables KM, Tee RD, Hawkins ER, Gordon DJ, Wale CJ, Farrer NM, Lam TH, Baxter PJ, Newman Taylor AJ. Laboratory animal allergy in a pharmaceutical company. Br J Ind Med 1988: 45(10): 660-666. 119. Venables KM, Dally MB, Burge PS, Pickering CA, Newman Taylor AJ. Occupational asthma in a steel coating plant. Br J Ind Med 1985: 42(8): 517-524. 120. Wild DM, Redlich CA, Paltiel AD. Surveillance for isocyanate asthma: a model based cost effectiveness analysis. Occup Environ Med 2005: 62(11): 743-749. 121. Zuskin E, Mustajbegovic J, Schachter EN, Pavicic D, Budak A. A follow-up study of respiratory function in workers exposed to acid aerosols in a food-processing industry. Int Arch Occup Environ Health 1997: 70(6): 413-418. 122. Heederik D, Henneberger P, Redlich C. Chapter 4 of ERS guidelines "Management of work-related asthma": Primary prevention of occupational asthma: Exposure reduction, skin exposure, and respiratory protection. Eur Respir Rev submitted. 123. Allmers H, Schmengler J, Skudlik C. Primary prevention of natural rubber latex allergy in the German health care system through education and intervention. The Journal of allergy and clinical immunology 2002: 110(2): 318-323.

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124. Heilman DK, Jones RT, Swanson MC, Yunginger JW. A prospective, controlled study showing that rubber gloves are the major contributor to latex aeroallergen levels in the operating room. The Journal of allergy and clinical immunology 1996: 98(2): 325-330. 125. Jones KP, Rolf S, Stingl C, Edmunds D, Davies BH. Longitudinal study of sensitization to natural rubber latex among dental school students using powder-free gloves. Ann Occup Hyg 2004: 48(5): 455-457. 126. LaMontagne AD, Radi S, Elder DS, Abramson MJ, Sim M. Primary prevention of latex related sensitisation and occupational asthma: a systematic review. Occup Environ Med 2006: 63(5): 359-364. 127. Lee A, Nixon R, Frowen K. Reduction of use of latex gloves in food handlers: an intervention study. Contact Dermatitis 2001: 44(2): 75-79. 128. Levy D, Allouache S, Chabane MH, Leynadier F, Burney P. Powder-free protein-poor natural rubber latex gloves and latex sensitization. Jama 1999: 281(11): 988. 129. Liss GM, Tarlo SM. Natural rubber latex-related occupational asthma: association with interventions and glove changes over time. Am J Ind Med 2001: 40(4): 347-353. 130. Saary MJ, Kanani A, Alghadeer H, Holness DL, Tarlo SM. Changes in rates of natural rubber latex sensitivity among dental school students and staff members after changes in latex gloves. The Journal of allergy and clinical immunology 2002: 109(1): 131-135. 131. Grammer LC, Ditto AM, Tripathi A, Harris KE. Prevalence and onset of rhinitis and conjunctivitis in subjects with occupational asthma caused by trimellitic anhydride (TMA). J Occup Environ Med 2002: 44(12): 1179-1181. 132. Meijster T, Tielemans E, Heederik D. Effect of an intervention aimed at reducing the risk of allergic respiratory disease in bakers: change in flour dust and fungal alpha-amylase levels. Occup Environ Med 2009: 66(8): 543-549. 133. Smith TA. Preventing baker's asthma: an alternative strategy. Occup Med (Lond) 2004: 54(1): 21-27. 134. Cathcart M, Nicholson P, Roberts D, Bazley M, Juniper C, Murray P, Randell M. Enzyme exposure, smoking and lung function in employees in the detergent industry over 20 years. Medical Subcommittee of the UK Soap and Detergent Industry Association. Occup Med (Lond) 1997: 47(8): 473-478. 135. Schweigert MK, Mackenzie DP, Sarlo K. Occupational asthma and allergy associated with the use of enzymes in the detergent industry--a review of the epidemiology, toxicology and methods of prevention. Clin Exp Allergy 2000: 30(11): 1511-1518. 136. Botham PA, Davies GE, Teasdale EL. Allergy to laboratory animals: a prospective study of its incidence and of the influence of atopy on its development. Br J Ind Med 1987: 44(9): 627-632. 137. Fisher R, Saunders WB, Murray SJ, Stave GM. Prevention of laboratory animal allergy. J Occup Environ Med 1998: 40: 609-613. 138. Bello D, Redlich CA, Stowe MH, Sparer J, Woskie SR, Streicher RP, Hosgood HD, Liu Y. Skin exposure to aliphatic polyisocyanates in the auto body repair and refinishing industry: II. A quantitative assessment. Ann Occup Hyg 2008: 52(2): 117-124. 139. Fent KW, Jayaraj K, Ball LM, Nylander-French LA. Quantitative monitoring of dermal and inhalation exposure to 1,6-hexamethylene diisocyanate monomer and oligomers. J Environ Monit 2008: 10(4): 500-507. 140. Fent KW, Trelles Gaines LG, Thomasen JM, Flack SL, Ding K, Herring AH, Whittaker SG, Nylander-French LA. Quantification and statistical modeling--part II: dermal concentrations of monomeric and polymeric 1,6-hexamethylene diisocyanate. Ann Occup Hyg 2009: 53(7): 691-702. 141. Flack SL, Fent KW, Trelles Gaines LG, Thomasen JM, Whittaker S, Ball LM, Nylander-French LA. Quantitative plasma biomarker analysis in HDI exposure assessment. Ann Occup Hyg 2010: 54(1): 41-54.

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142. Liljelind I, Norberg C, Egelrud L, Westberg H, Eriksson K, Nylander-French LA. Dermal and inhalation exposure to methylene bisphenyl isocyanate (MDI) in iron foundry workers. Ann Occup Hyg 2010: 54(1): 31-40. 143. Liu Y, Stowe MH, Bello D, Sparer J, Gore RJ, Cullen MR, Redlich CA, Woskie SR. Skin exposure to aliphatic polyisocyanates in the auto body repair and refinishing industry: III. A personal exposure algorithm. Ann Occup Hyg 2009: 53(1): 33-40. 144. Pronk A, Yu F, Vlaanderen J, Tielemans E, Preller L, Bobeldijk I, Deddens JA, Latza U, Baur X, Heederik D. Dermal, inhalation, and internal exposure to 1,6-HDI and its oligomers in car body repair shop workers and industrial spray painters. Occup Environ Med 2006: 63(9): 624-631. 145. Robert A, Ducos P, Francin JM, Marsan P. Biological monitoring of workers exposed to 4,4'-methylenediphenyl diisocyanate (MDI) in 19 French polyurethane industries. Int Arch Occup Environ Health 2007: 80(5): 412-422. 146. Todd LA, Mottus K, Mihlan GJ. A survey of airborne and skin exposures to chemicals in footwear and equipment factories in Thailand. J Occup Environ Hyg 2008: 5(3): 169-181. 147. Bernstein DI, Korbee L, Stauder T, Bernstein JA, Scinto J, Herd ZL, Bernstein IL. The low prevalence of occupational asthma and antibody-dependent sensitization to diphenylmethane diisocyanate in a plant engineered for minimal exposure to diisocyanates. The Journal of allergy and clinical immunology 1993: 92(3): 387-396. 148. Dernehl CU. Health hazards associated with polyurethane foams. J Occup Med 1966: 8: 59-62. 149. Donnelly R, Buick JB, Macmahon J. Occupational asthma after exposure to plaster casts containing methylene diphenyl diisocyanate. Occup Med (Lond) 2004: 54(6): 432-434. 150. Lenaerts-Langanke H. Isocyanate-induced respiratory disease in coal miners. Zbl Arbeitsmedizin 1992: 42: 2-25. 151. Nemery B, Lenaerts L. Exposure to methylene diphenyl diisocyanate in coal mines. Lancet 1993: 341(8840): 318. 152. Petsonk EL, Wang ML, Lewis DM, Siegel PD, Husberg BJ. Asthma-like symptoms in wood product plant workers exposed to methylene diphenyl diisocyanate. Chest 2000: 118(4): 1183-1193. 153. Shahzad K, Akhtar S, Mahmud S. Prevalence and determinants of asthma in adult male leather tannery workers in Karachi, Pakistan: a cross sectional study. BMC Public Health 2006: 6: 292. 154. Grammer LC, Harris KE, Yarnold PR. Effect of respiratory protective devices on development of antibody and occupational asthma to an acid anhydride. Chest 2002: 121(4): 1317-1322. 155. Malo JL, Chan-Yeung M. Agents causing occupational asthma with key references. In: IBernstein IL, Chan-Yeung M, Malo JL, Bernstein DI, eds. Asthma in the workplace. 3rd ed. Taylor & Francis Group, New York, London, 2006. 156. Baur X. Airborne allergens and irritants in the workplace. In: Kay AB, Kaplan AP, Bousquet J, Holt PG, eds. Allergy and allergic diseases. Blackwell Publishing, 2008; pp. 1017-1122. 157. Brooks SM, Weiss MA, Bernstein IL. Reactive airways dysfunction syndrome (RADS). Persistent asthma syndrome after high level irritant exposures. Chest 1985: 88(3): 376-384. 158. van Kampen V, Merget R, Baur X. Occupational airway sensitizers: an overview on the respective literature. Am J Ind Med 2000: 38(2): 164-218. 159. Gautrin D, Bernstein IL, Brooks SM, Henneberger PK. Reactive airways dysfunction syndrome and irritant-induced asthma. In: Bernstein IL, Chan-Yeung M, Malo JL, Bernstein DI, eds. Asthma in the workplace. Taylor & Francis Group, New York, London, 2006; pp. 581-629.

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160. Alberts WM, do Pico GA. Reactive airways dysfunction syndrome. Chest 1996: 109(6): 1618-1626. 161. Sastre J, Vandenplas O, Park HS. Pathogenesis of occupational asthma. Eur Respir J 2003: 22(2): 364-373. 162. Ameille J, Pairon JC, Bayeux MC, Brochard P, Choudat D, Conso F, Devienne A, Garnier R, Iwatsubo Y. Consequences of occupational asthma on employment and financial status: a follow-up study. Eur Respir J 1997: 10(1): 55-58. 163. Banks DE, Rando RJ, Barkman HW, Jr. Persistence of toluene diisocyanate-induced asthma despite negligible workplace exposures. Chest 1990: 97(1): 121-125. 164. Barker RD, Harris JM, Welch JA, Venables KM, Newman Taylor AJ. Occupational asthma caused by tetrachlorophthalic anhydride: a 12-year follow-up. The Journal of allergy and clinical immunology 1998: 101(6 Pt 1): 717-719. 165. Burge PS. Occupational asthma in electronics workers caused by colophony fumes: follow-up of affected workers. Thorax 1982: 37(5): 348-353. 166. Cannon J, Cullinan P, Newman Taylor A. Consequences of occupational asthma. BMJ (Clinical research ed 1995: 311(7005): 602-603. 167. Chan-Yeung M, Leriche J, Maclean L, Lam S. Comparison of cellular and protein changes in bronchial lavage fluid of symptomatic and asymptomatic patients with red cedar asthma on follow-up examination. Clin Allergy 1988: 18(4): 359-365. 168. Douglas JD, McSharry C, Blaikie L, Morrow T, Miles S, Franklin D. Occupational asthma caused by automated salmon processing. Lancet 1995: 346(8977): 737-740. 169. Drexler H, Schaller KH, Nielsen J, Weber A, Weihrauch M, Welinder H, Skerfving S. Efficacy of measures of hygiene in workers sensitised to acid anhydrides and the influence of selection bias on the results. Occup Environ Med 1999: 56(3): 202-205. 170. Flood DF, Blofeld RE, Bruce CF, Hewitt JI, Juniper CP, Roberts DM. Lung function, atopy, specific hypersensitivity, and smoking of workers in the enzyme detergent industry over 11 years. Br J Ind Med 1985: 42(1): 43-50. 171. Gorski P, Kolacinska B, Wittczak T. Analysis of the clinical state of patients with occupational asthma following cessation of exposure to allergens. Occup Med (Lond) 1999: 49(5): 285-289. 172. Grammer LC, Shaughnessy MA. Study of employees with anhydride-induced respiratory disease after removal from exposure. J Occup Environ Med 1996: 38(8): 771-774. 173. Grammer LC, Shaughnessy MA, Hogan MB, Lowenthal M, Yarnold PR, Watkins DM, Berggruen SM. Study of employees with anhydride-induced respiratory disease after removal from exposure. J Occup Environ Med 1995: 37(7): 820-825. 174. Grammer LC, Shaughnessy MA, Kenamore BD. Clinical and immunologic outcome of 42 individuals with trimellitic anhydride-induced immunologic lung disease after transfer to low exposure. Allergy Asthma Proc 2000: 21(6): 355-359. 175. Hannu T, Piipari R, Tuppurainen M, Nordman H, Tuomi T. Occupational asthma caused by stainless steel welding fumes: a clinical study. Eur Respir J 2007: 29(1): 85-90. 176. Harries MG, Burge PS, Samson M, Taylor AJ, Pepys J. Isocyanate asthma: respiratory symptoms due to 1,5-naphthylene di-isocyanate. Thorax 1979: 34(6): 762-766. 177. Juniper CP, How MJ, Goodwin BF, Kinshott AK. Bacillus subtilis enzymes: a 7-year clinical, epidemiological and immunological study of an industrial allergen. J Soc Occup Med 1977: 27(1): 3-12. 178. Jyo T, Kodomari Y, Kodomari N, Kuwabara W, Katsutani T, Otsuka T, Tsuboi S, Oka S, Shigeta S, Ono K. Therapeutic effect and titers of the specific IgE and IgG antibodies in patients with sea squirt allergy (Hoya asthma) under a long-term hyposensitization with three sea squirt antigens. The Journal of allergy and clinical immunology 1989: 83(2 Pt 1): 386-393.

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179. Lemiere C, Cartier A, Malo JL, Lehrer SB. Persistent specific bronchial reactivity to occupational agents in workers with normal nonspecific bronchial reactivity. Am J Respir Crit Care Med 2000: 162(3 Pt 1): 976-980. 180. Malo JL, Cartier A, Boulet LP, L'Archeveque J, Saint-Denis F, Bherer L, Courteau JP. Bronchial hyperresponsiveness can improve while spirometry plateaus two to three years after repeated exposure to chlorine causing respiratory symptoms. Am J Respir Crit Care Med 1994: 150(4): 1142-1145. 181. Malo JL, Cartier A, Cote J, Milot J, Leblanc C, Paquette L, Ghezzo H, Boulet LP. Influence of inhaled steroids on recovery from occupational asthma after cessation of exposure: an 18-month double-blind crossover study. Am J Respir Crit Care Med 1996: 153(3): 953-960. 182. Malo JL, Cartier A, Ghezzo H, Lafrance M, McCants M, Lehrer SB. Patterns of improvement in spirometry, bronchial hyperresponsiveness, and specific IgE antibody levels after cessation of exposure in occupational asthma caused by snow-crab processing. Am Rev Respir Dis 1988: 138(4): 807-812. 183. Meyer WC. [Prognosis of occupational bronchial asthma after change of occupation and elimination of antigen (author's transl)]. MMW Munch Med Wochenschr 1977: 119(11): 363-366. 184. Moller DR, Brooks SM, McKay RT, Cassedy K, Kopp S, Bernstein IL. Chronic asthma due to toluene diisocyanate. Chest 1986: 90(4): 494-499. 185. Moscato G, Dellabianca A, Perfetti L, Brame B, Galdi E, Niniano R, Paggiaro P. Occupational asthma: a longitudinal study on the clinical and socioeconomic outcome after diagnosis. Chest 1999: 115(1): 249-256. 186. Munoz X, Cruz MJ, Orriols R, Bravo C, Espuga M, Morell F. Occupational asthma due to persulfate salts: diagnosis and follow-up. Chest 2003: 123(6): 2124-2129. 187. Malo JL, Dewitte JD, Cartier A, Ghezzo H, L'Archeveque J, Boulet LP, Cote J, Bedard G, Boucher S, Champagne F. Le système québécois d'indemnisation pour asthme professionel. Rev Mal Respir 1993: 10: 313-323. 188. Obase Y, Shimoda T, Mitsuta K, Matsuse H, Kohno S. Two patients with occupational asthma who returned to work with dust respirators. Occup Environ Med 2000: 57(1): 62-64. 189. O'Donnell TV, Welford B, Coleman ED. Potroom asthma: New Zealand experience and follow-up. Am J Ind Med 1989: 15(1): 43-49. 190. Paggiaro P, Bacci E, Paoletti P, Bernard P, Dente FL, Marchetti G, Talini D, Menconi GF, Giuntini C. Bronchoalveolar lavage and morphology of the airways after cessation of exposure in asthmatic subjects sensitized to toluene diisocyanate. Chest 1990: 98(3): 536-542. 191. Paggiaro PL, Loi AM, Rossi O, Ferrante B, Pardi F, Roselli MG, Baschieri L. Follow-up study of patients with respiratory disease due to toluene diisocyanate (TDI). Clin Allergy 1984: 14(5): 463-469. 192. Park HS, Yu HJ, Jung KS. Occupational asthma caused by chromium. Clin Exp Allergy 1994: 24(7): 676-681. 193. Piirila PL, Meuronen A, Majuri ML, Luukkonen R, Mantyla T, Wolff HJ, Nordman H, Alenius H, Laitinen A. Inflammation and functional outcome in diisocyanate-induced asthma after cessation of exposure. Allergy 2008: 63(5): 583-591. 194. Piirila PL, Nordman H, Keskinen HM, Luukkonen R, Salo SP, Tuomi TO, Tuppurainen M. Long-term follow-up of hexamethylene diisocyanate-, diphenylmethane diisocyanate-, and toluene diisocyanate-induced asthma. Am J Respir Crit Care Med 2000: 162(2 Pt 1): 516-522. 195. Pisati G, Zedda S. Outcome of occupational asthma due to cobalt hypersensitivity. Sci Total Environ 1994: 150(1-3): 167-171. 196. Ross DJ, McDonald JC. Health and employment after a diagnosis of occupational asthma: a descriptive study. Occup Med (Lond) 1998: 48(4): 219-225.

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197. Saetta M, Maestrelli P, Di Stefano A, De Marzo N, Milani GF, Pivirotto F, Mapp CE, Fabbri LM. Effect of cessation of exposure to toluene diisocyanate (TDI) on bronchial mucosa of subjects with TDI-induced asthma. Am Rev Respir Dis 1992: 145(1): 169-174. 198. Saetta M, Maestrelli P, Turato G, Mapp CE, Milani G, Pivirotto F, Fabbri LM, Di Stefano A. Airway wall remodeling after cessation of exposure to isocyanates in sensitized asthmatic subjects. Am J Respir Crit Care Med 1995: 151(2 Pt 1): 489-494. 199. Sen D, Wiley K, Williams JG. Occupational asthma in fruit salad processing. Clin Exp Allergy 1998: 28(3): 363-367. 200. Simonsson BG, Sjoberg A, Rolf C, Haeger-Aronsen B. Acute and long-term airway hyperreactivity in aluminium-salt exposed workers with nocturnal asthma. Eur J Respir Dis 1985: 66(2): 105-118. 201. Soyseth V, Kongerud J, Boe J, Fonneland T. Bronchial responsiveness and work-related asthma in aluminium potroom workers: effect of removal from exposure. Eur Respir J 1992: 5(7): 829-833. 202. Valentino M, Pizzichini MA, Monaco F, Governa M. Latex-induced asthma in four healthcare workers in a regional hospital. Occup Med (Lond) 1994: 44(3): 161-164. 203. Vandenplas O, Delwiche JP, Depelchin S, Sibille Y, Vande Weyer R, Delaunois L. Latex gloves with a lower protein content reduce bronchial reactions in subjects with occupational asthma caused by latex. Am J Respir Crit Care Med 1995: 151(3 Pt 1): 887-891. 204. Venables KM, Davison AG, Newman Taylor AJ. Consequences of occupational asthma. Respir Med 1989: 83(5): 437-440. 205. Venables KM, Topping MD, Nunn AJ, Howe W, Newman Taylor AJ. Immunologic and functional consequences of chemical (tetrachlorophthalic anhydride)-induced asthma after four years of avoidance of exposure. The Journal of allergy and clinical immunology 1987: 80(2): 212-218.

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Bijlage 8 Implementatieplan

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Inleiding Dit implementatieplan is opgesteld ter bevordering van de implementatie van de richtlijn werkgerelateerd astma. Voor het opstellen van dit plan zijn de bevorderende en belemmerende factoren voor het toepassen van de aanbevelingen geïnventariseerd. Daarbij heeft de richtlijnwerkgroep een advies uitgebracht over het tijdspad voor implementatie, de daarvoor benodigde randvoorwaarden en de acties die door verschillende partijen ondernomen dienen te worden. Werkwijze De werkgroep heeft per aanbeveling geïnventariseerd: ­ per wanneer de aanbeveling overal geïmplementeerd moet kunnen zijn; ­ de verwachte impact van implementatie van de aanbeveling op de zorgkosten; ­ randvoorwaarden om de aanbeveling te kunnen implementeren; ­ mogelijk barrières om de aanbeveling te kunnen implementeren; ­ mogelijke acties om de implementatie van de aanbeveling te bevorderen; ­ verantwoordelijke partij voor de te ondernemen acties. Voor iedere aanbevelingen is nagedacht over de hierboven genoemde punten. Echter niet voor iedere aanbeveling kon ieder punt worden beantwoord. Er kan een onderscheid worden gemaakt tussen sterk geformuleerde aanbevelingen en zwak geformuleerde aanbevelingen. In het eerste geval doet de richtlijncommissie een duidelijke uitspraak over iets dat zeker wel of zeker niet gedaan moet worden. In het tweede geval wordt de aanbeveling minder zeker gesteld (bijvoorbeeld Overweeg om…) en wordt dus meer ruimte gelaten voor alternatieve opties. Voor sterk geformuleerde aanbevelingen zijn bovengenoemde punten in principe meer uitgewerkt dan voor de zwak geformuleerde aanbevelingen. Implementatietermijnen Voor sterk geformuleerde aanbevelingen geldt dat zij zo spoedig mogelijk geïmplementeerd dienen te worden. Voor de meeste sterk geformuleerde aanbevelingen betekent dat dat zij komend jaar direct geïmplementeerd moeten worden en dat per november 2017 dus iedereen aan deze aanbevelingen dient te voldoen. Voordat onderstaande aanbevelingen kunnen worden geïmplementeerd zal eerst aan een aantal randvoorwaarden moeten worden voldaan, die betrekking hebben op de inrichting van ons zorgstelsel. Daarom is de implementatietermijn onzeker. Rekening moet worden gehouden met een termijn van ten minste drie tot vijf jaar. Er kan niet van worden uitgegaan dat iedereen vóór 2021 aan de aanbevelingen kan voldoen: Hoofdstuk 3

Objectiveer werkgerelateerd astma door sequentieel longfunctieonderzoek en bevestig een immunologisch beroepsastma indien mogelijk door allergologisch onderzoek door het testen van sensibilisatie voor het vermoedelijke allergeen.

Overweeg bij niet-immunologisch astma beroepsmatige blootstelling aan mogelijk hoge concentraties irriterende stoffen als relevante factor in de pathogenese.

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Spreek follow up metingen af als na uitgebreid onderzoek twijfel blijft bestaan over een werkgerelateerd astma, die gericht zijn op monitoring van de longfunctie, piekstroomregistratie, aspecifieke bronchiale hyperreactiviteit en sensibilisatie.

Een specifieke bronchiale provocatietest kan alleen in een centrum met ervaring worden uitgevoerd in gevallen waarbij de diagnose beroepsastma niet op voorhand vaststaat, als sprake is van een mogelijk nieuw oorzakelijk agens, of als de uitslag van belang is voor re-integratie van de individuele medewerker.

Voer een provocatie op de werkplek uit onder medische begeleiding als een specifieke bronchiale provocatietest niet mogelijk is of geen duidelijke uitslag oplevert.

Hoofdstuk 4

Streef naar vroegtijdige herkenning en diagnose van werkgerelateerd astma, in het bijzonder immunologisch beroepsastma, omdat een kortere periode van klachten als gevolg van beroepsmatige blootstelling is geassocieerd met een gunstiger beloop en prognose.

Hoofdstuk 5

Adviseer patiënten met immunologisch beroepsastma absolute vermijding van de blootstelling aan het oorzakelijk agens. Indien dit vanwege ongunstige sociaaleconomische gevolgen niet mogelijk is en wordt gekozen voor het reduceren van de blootstelling aan het oorzakelijk agens, voer dan zorgvuldige medische monitoring uit om verslechtering van astma vroegtijdig op te sporen.

Adviseer patiënten met niet-immunologisch beroepsastma of door het werk verergerend astma het zoveel mogelijk reduceren van de blootstelling aan aspecifieke prikkels. Indien dit niet mogelijk is, voer dan zorgvuldige medische monitoring uit om verslechtering van astma vroegtijdig op te sporen.

Informeer patiënten over de rol van de longarts en over de mogelijke sociaaleconomische gevolgen van werkgerelateerd astma. Verwijs naar de bedrijfsarts of naar een centrum en maak afspraken omtrent verdere ondersteuning en begeleiding.

Hoofdstuk 6

Na het identificeren van klachten of sensibilisatie tijdens gezondheidsbewaking is aanvullende diagnostiek aangewezen voor het aantonen of uitsluiten van werkgerelateerd astma, rhinitis of COPD. Dit geldt ook voor werkgerelateerde luchtwegklachten die ontstaan in de perioden tussen de periodieke onderzoeken.

Informeer de patiënt mondeling en schriftelijk over de mogelijke oorzaken van werkgerelateerd astma en over de behandeling. Benadruk dat aandacht nodig is voor onderzoek en interventie op de werkplek, voor de mogelijke gevolgen voor werk en inkomen, voor de relaties op het werk met collega’s en de werkgever en bespreek de rol van de bedrijfsarts.

Verwijs altijd naar de bedrijfsarts voor het beleid ten aanzien van verzuim, arbeidsongeschiktheid en re-integratie.

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Behalve schriftelijke informatie voor de patiënt wordt het ontwikkelen van een brochure voor werkgevers aanbevolen. Deze zou door longartsen en bedrijfsartsen gezamenlijk kunnen worden ontwikkeld.

Randvoorwaarden Alleen als arbeidsgerelateerde zorg onderdeel uitmaakt van het zorgstelsel kan deze zorg worden opgenomen in het basispakket. Dit opent de weg tot het ontwikkelen van een DBC of zorgproduct of een regeling voor de vergoeding van de diagnostiek (anamnese, evaluatie van de blootstelling, het longfunctieonderzoek en allergologisch onderzoek), advisering en follow up metingen in het kader van monitoring. Een tweede randvoorwaarde is volwaardige deelname van de bedrijfsarts aan de reguliere zorg, waarbij de beschikbaarheid, de kwaliteit van de geleverde zorg en de onafhankelijkheid zijn geborgd. Dit is van belang om samenwerking tussen longartsen, bedrijfsartsen en huisartsen tot stand te brengen. Deze samenwerking is essentieel voor deze vorm van zorg en van belang voor het ontwikkelen van gezamenlijke producten zoals brochures. Voor een uitgebreide bespreking van de knelpunten in de arbocuratieve zorg wordt verwezen naar Hoofdstuk 6 en de literatuur (Advies Beter zorg voor werkenden, 2014). Barrières op het gebied van de professionals en het ziekenhuis worden bepaald door de beperkte kennis over en de beschikbaarheid van specifiek allergologisch onderzoek. Gezien de gewenste expertise en de kosten van dit onderzoek in relatie tot de beperkte behoefte geniet concentratie in een aantal centra hier wellicht de voorkeur. De overige diagnostiek is niet complex en vergt geen bijzonder faciliteiten, investeringen of taakherschikking. Longartsen zijn zich bewust van het voorkomen van beroepsziekten. Het onderwerp werkgerelateerde allergie is opgenomen in het landelijk cursorisch onderwijs voor AIOS. Werkgerelateerde longaandoeningen worden behandeld tijdens het regionaal onderwijs en komen regelmatig aan bod tijdens nascholing voor longartsen (Bronkhorst colloquium, Longartsenweek/dagen). Zonder dat aan de randvoorwaarden is voldaan, zal aandacht voor het toepassen van de richtlijn een aanzienlijk risico opleveren op demotivatie door teleurstelling en frustratie. Impact op zorgkosten Omdat werkgerelateerde zorg geen onderdeel uitmaakt van het zorgstelsel zal toepassing van bijna alle aanbevelingen op korte termijn gevolgen hebben voor de directe medische zorgkosten. Voor zover werkgerelateerde zorg op dit moment wordt geleverd, worden de meeste kosten gedragen door de werkgever of de inkomensverzekeraar. Op macroniveau zal toepassing van de aanbevelingen daarom geen toename maar een verschuiving van deze kosten betekenen. Op de lange termijn mag worden verwacht dat zowel de maatschappelijke kosten door verzuim en arbeidsongeschiktheid als de medische zorgkosten zullen afnemen. Immers, bij werkgerelateerd astma wordt interventie op de werkplek als meest effectief beschouwd, terwijl juist deze interventie nog geen vaste plaats heeft in de behandeling van patiënten met werkgerelateerd astma. Welke partijen daarbij het meest profiteren van de opbrengsten laat zich moeilijk inschatten. Te ondernemen acties per partij

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Hieronder wordt per partij toegelicht welke acties zij kunnen ondernemen om de implementatie van de richtlijn te bevorderen.

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Alle direct betrokken wetenschappelijk verenigingen/beroepsorganisaties (NVALT, NVAB, Longfonds) ­ bekend maken van de richtlijn onder de leden; ­ publiciteit voor de richtlijn maken door over de richtlijn te publiceren in tijdschriften en te

vertellen op congressen; ­ ontwikkelen van gerichte bijscholing over werkgerelateerd astma; ­ ontwikkelen en aanpassen van patiënteninformatie/keuzehulpen; ­ controleren van de toepassing van de aanbevelingen middels audits en de

kwaliteitsvisitatie; ­ gezamenlijk afspraken maken over en opstarten van continu modulair onderhoud van de

richtlijn. De lokale vakgroepen/individuele medisch professionals ­ het bespreken van de aanbevelingen in de vakgroepsvergadering en lokale werkgroepen; ­ het volgen van bijscholing die bij deze richtlijn ontwikkeld gaat worden; ­ aanpassen lokale patiënteninformatie op grond van de materialen die door de verenigingen

beschikbaar gesteld zullen worden; ­ afstemmen en afspraken maken met andere betrokken disciplines om de toepassing van de

aanbevelingen in de praktijk te borgen. De systeemstakeholders (onder andere zorgverzekeraars, (koepelorganisaties van) ziekenhuisbestuurders, IGZ) Ten aanzien van de financiering van de zorg voor patiënten met werkgerelateerd astma van het bestuur van de ziekenhuizen verwacht dat zij bereid zijn om de aanbevelingen in deze richtlijn te kunnen implementeren. Daarnaast wordt van de bestuurders verwacht dat zij bij de betrokken medisch professionals nagaan op welke wijze zij kennis hebben genomen van de nieuwe richtlijn en deze toepassen in de praktijk. Van zorgverleners wordt verwacht dat zij de zorg die in deze richtlijn wordt voorgeschreven zullen vergoeden. De sterk geformuleerde aanbevelingen in deze richtlijn kunnen, na verloop van de aangegeven implementatietermijnen door zorgverzekeraars worden gebruikt voor de inkoop van zorg. Het Kennisinstituut van Medisch Specialisten Het Kennisinstituut zal de richtlijn toevoegen aan richtlijnendatabase. Daarbij zal dit implementatieplan worden opgenomen op een voor alle partijen goed te vinden plaats. Literatuurlijst Advies Betere zorg voor werkenden: Een visie op de toekomst van de arbeidsgerelateerde zorg. SER, nr 7, september 2014:

http://www.ser.nl/nl/publicaties/adviezen/2010-2019/2014/toekomst-arbeidsgerelateerde-zorg.aspx.