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Harmfuleffectsofammoniaonbirds
Oct25,2010 views:21206 comments:5
Ammoniagasinpoultryhousesseriouslyaffectsthehealthconditionofthebirds.
Goodlittermanagementandventilationwillminimisethelevelofammonia,improve
productivity,reducethelikelihoodofrespiratorydiseases,improvethebirds'welfare
andprovideapleasant,safeenvironmentforworkers.
ByDr.TahseenAziz,RollinsAnimalDiseaseDiagnostic
Laboratory,NorthCarolinaDepartmentofAgricultureand
ConsumerServices,andDr.H.JohnBarnes,Collegeof
VeterinaryMedicine,NCStateUniversity,Raleigh,NC,USA

Ammoniaisagaspresentintheatmosphereofeverypoultryhouse.Itresultsfromthe
chemicaldecompositionofuricacidindroppingsbycertainbacteriainthelitter.Itis
particularlyhighinhouseswherethesamelitterisusedforsuccessiveflocks.The
mainfactorsaffectingatmosphericammoniaconcentrationinpoultryhousesarelitter
conditionsandairmovement(ventilation).Moisturecontent,pHandthetemperatureof
thelitter,influencethedegradationofuricacidbybacteria.Poorventilation,loose
droppingsandfaulty,overfilledorlowpositioneddrinkers,arecommoncausesofwet
litterinpoultryhouses.

Generaleffectofammoniagas
Ammoniagashasacharacteristicpungentodour.Athighconcentrationsitisirritating
tomucousmembranesoftherespiratorytractandtheconjunctivaeandcorneasofthe
eyes.Damagetothemucousmembranesoftherespiratorysystemincreasesthe
susceptibilityofbirdstobacterialrespiratoryinfection,especiallyE.coliinfection.High
levelsalsohaveanegativeimpactonoveralllivability,weightgain,feedconversion,
condemnationrateatprocessingandtheimmunesystemofthebirds.Experimentally,
broilerchickenskeptinanenvironmentwithammoniaconcentrationsof50ppmand
75ppmwereshowntohavereductionsinbodyweightof17%and20%,respectively,
at7weeksofagecomparedtobroilerchickenskeptinanenvironmentwithnear0
ammoniaconcentration.IntheUS,maximumlevelsofammoniainpoultryhouses
havebeensetat25ppmbytheNationalInstituteofOccupationalSafetyandHealth
(NIOSH)and50ppmbytheOccupationalSafetyandHealthAdministration(OSHA).
Theselevelshavebeenestablishedbasedonhumansafetyandrepresentthelimits
for8hoursofexposure.OSHAconsiders50ppmtobethelowestleveltocause
irritationtotheeyes,noseandthroatofthemostsensitiveindividuals.Peoplecan
generallysmellammoniaatconcentrationsbetween20and30ppm.

Damagetotherespiratorysystem
Theeffectofammoniagasonthemucosalsurfaceofthetrachearangesfrom
paralysisofcilia,todeciliation(lossofcilia)ofepithelialcells,toinjury(necrosis)ofthe

mucosalepitheliumitself.Attenuationofthemucosalepithelium,withlossofciliaand
increasednumbersofgobletcells,arecommonlesionsofaerialammoniatoxicityseen
inthetracheasofaffectedbirds.Thetypeanddegreeofdamagedependsonthe
concentrationofammoniaintheairandthelengthoftimeofexposure.Ciliaaretiny,
hairlikeprojectionsonthesurfaceofrespiratoryepithelialcellsthatlinethetrachea.
Theyformpartofthemucociliaryapparatus(alsocalledmucociliaryblanketor
mucociliaryescalator),whichconsistsoftheciliaandsecretionofmucus.The
mucociliaryapparatusisresponsibleforentrappingandcleaningparticlesinhaledfrom
theenvironment.Dustparticleshavelargenumbersofbacteriaattachedtotheir
surface.PoultryhousedusthasbeenshowntobeareservoirforE.coliinparticular.
Inhaledparticlesareentrappedinmucussecretedbymucousglandsandgobletcells.
Propulsiveactionsofciliacontinuouslymovethemucuswithentrappedparticlesup
thetracheatowardthepharynx,thuspreventingtheparticlesfromreachingthelower
respiratorytract(lungsandairsacs).Clearanceofparticlesfromtherespiratorytractof
birdsisapproximately30timesfasterthanthatofmammals.Whenciliabecome
paralyzedorarelostduetohighammonialevelsinthepoultryhouse,mucusonthe
mucosalsurfaceofthetracheacannotbecleared,andthusentrappedbacteriaondust
particlesmayreachthelungsandairsacsandcauseinfection.Devitalisationofthe
trachealmucosamayexplaininpartthehighincidenceofairsacculitis,pneumoniaand
septicemiacausedbyE.coliinpoultryflocksthathavebeenexposedtohigh
atmosphericammonialevels.Prolongedexposuretoatmosphericammoniamayalso
inciteproliferationoftheepithelialcellsthatlinetheatrialspacesinthelung.The
proliferativelesioncausesthickeningofparabronchialwalls.Inseverecases,total
obliterationofatrialspaces,withsubsequentreductioninpulmonarygasexchangecan
occur.

Damagetotheeyes
Atmosphericammoniaathighconcentrationscausesconjunctivitis(inflammationof
conjunctivae)anddamagesthecorneaoftheeyes.Asintherespiratorysystem,the
severityofdamagedependsontheconcentrationofammoniaintheenvironmentand
durationofexposure.Swellingandreddeningoftheeyelids,reddeningofthe
conjunctiveandnictitatingmembrane(thirdeyelid),andpartialorcompleteclosureof
theeyesarecommonclinicalsigns.Inseverecases,theeyelidsareoftenclosedshut.
Eyescanbecomealmondshapedafterlongtermexposuretohighammonialevels
becauseofscarringandretractionoftheeyelids.Conjunctivitiscausedbyammonia
alsoincreasestheriskandseverityofswollenheadsyndromeinrespiratoryviral
infections.Histopathologiclesionsinconjunctivaeincludehyperemia(congestionof
bloodvesselswithblood),variabledegreesofdisorganisationandhyperplasiaof
conjunctivalepithelium,andmildtomoderateinfiltrationofheterophils.Intheeyelids,
theremaybeedema,withsubepithelialinfiltrationofheterophils.

Lesionsinthecornea
Thetermammoniaburnisusedbysometorefertoammoniainducedcorneal
erosion,butthistermisinaccurate,asammoniadoesnotdirectlyinjurethecorneal
epithelium.Damagetothebasementmembraneonwhichtheepitheliumrestsis
responsiblefordetachmentoftheepitheliallayer,whichisthecharacteristiceyelesion
thatresultsfromexcessammoniaexposure.Thelesionisanalmostcircular,grey
white,opaque,roughlookingareainthecentreofthecornea.Closeexaminationof
theeyeusingobliquelightmaybenecessarytoseeearlylesionsthatareslightly
depressedwithanirregularmargin.Theperipheryofthecorneaisunaffected,
presumablybecauseitispartiallycoveredbytheeyelidandreceiveslessexposure
thanthecentralcornea.Botheyesaresimilarlyaffected,whichhelpstodifferentiate
ammoniatoxicityfromothereyediseases.Thesebirdsarepartiallytocompletelyblind.

Histologically,thecorneallesionisanerosioninwhichthereisseparationandlossof
thecornealepitheliumfromtheunderlyingbasementmembraneinthecentralcornea.
Alongthemarginsoftheerosion,thecornealepitheliumisliftedfromthebasement
membrane.Insomecases,whichprobablyrepresentearlylesions,thecorneal
epitheliumisstillpresent,butitisseparatedfromthebasementmembrane.The
denudedbasementmembraneisthickenedandbasophilicbecauseofthedeposition
ofcalciumsalts.Theresultingbandofmineralizedbasementmembraneisknownas
calcifycbandkeratopathy.Itischaracteristicofammoniatoxicityinpoultry.How
ammoniainducesbandkeratopathy,whichsubsequentlyresultsindetachmentofthe
epitheliumfromthebasementmembrane,isunknown.Inpeopleandsomeother
animals,calcificbandkeratopathyoccursasacomplicationofuveitis(inflammationof
themiddletunicoftheeyecomposedofthechoroid,irisandciliarybody).

Thecorneausuallyremainsintactanddoesnotperforate.Inchroniclesions,thereis
fibroplasiainthecornealstromaunderandaroundtheerodedarea,andbloodvessels
extendintothecornea(normallytherearenobloodvesselsinthecornea).
Regeneratingepitheliumusuallycoversthefibroplasticareaindicativeofahealing
process.Anotherlesioncommonlyseeninaffectedeyesisvaryingdegreesofiritis
(inflammationoftheiris)characterizedbyinfiltrationbylymphocytes,plasmacells,and
somegranulocyticleukocytes.Mild,mixedinflammatorycellinfiltratemayalsopresent
intheciliarybody.Bandkeratopathyandcornealerosionmaybesecondarytothese
inflammatorychangesintheuvea.

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