Toxicity of Ambient Air PM10. A critical review of potentially causative PM properties and mechanisms associated with health effects
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Series / Report no.
Open Access
Type
Report
Language
en
Date
2000-08-31
Research Projects
Organizational Units
Journal Issue
Title
Toxicity of Ambient Air PM10. A critical review of
potentially causative PM properties and mechanisms associated with health
effects
Translated Title
Toxiciteit van PM10 in de buitenlucht. Een
kritische beoordeling van potentieel verantwoordelijke PM-eigenschappen en
mechanismen geassocieerd met gezondheidseffecten
Published in
Abstract
Dit rapport bevat een evaluatie van studies gericht op
buitenlucht fijn stof (PM) toxiciteit, deeltjeshypotheses en mechanismen,
teneinde causaliteit en plausibiliteit van acute gezondheidseffecten beter
te begrijpen. Mechanistische studies met hoge doses wijzen uit dat PM 1)
oxidatieve ontstekingsreacties induceert en 2) cardiorespiratoire funkties
vermindert, hetgeen biologisch plausibel lijkt met verergering van
aandoeningen als mechanisme. PM oppervlakte-reactiviteit wordt belangrijker
gevonden dan PM massa, hetgeen suggereert dat de antropogene (roethoudende)
fijne PM fractie belangrijk is. De zeer beperkte gegevens uit inhalatie
studies met lage PM doses ondersteunen dit vermoeden. De grovere ("coarse")
PM fractie zou ook nog belangrijk kunnen zijn, met name daar waar het
effecten in de hogere luchtwegen betreft, zoals verergering van astma. Een
rol voor secundaire PM componenten (sulfaat, nitraat) of ultrafijn PM, op de
niveaus zoals ze in de buitenlucht voorkomen, is nog niet duidelijk
aangetoond. Studies suggereren ook dat mengsels van PM en gassen zoals ozon
tot meer toxiciteit leidt dan op grond van de afzonderlijke componenten
verwacht kan worden. De huidige dosimetrie modellen voorspellen dat
(oudere) mensen met cardiorespiratoire aandoeningen een grotere dosis kunnen
binnenkrijgen. De laatste jaren zijn studies naar de toxiciteit van PM
toegenomen. De huidige gegevens hebben echter nog niet geresulteerd in
voldoende bewijs om overtuigende aanwijzingen te kunnen geven over 1) een
specifiek belangrijke en causale rol voor een bepaalde PM fractie of
samenstelling en 2) mechanismen die PM gezondheidseffecten in personen die
tot risicogroepen worden gerekend plausibel kunnen
verklaren.
In this critical review studies focus on ambient particulate air pollution (PM) toxicity and particle hypotheses. Mechanisms were also evaluated to investigate causality and plausibility of acute health effects associated with ambient exposure. High-dose studies indicate that PM: 1) induces oxidative pulmonary inflammation and cardio-respiratory malfunctioning, which could contribute to a disease exacerbation mechanism. PM surface reactivity seems more important than PM mass, thereby prudently suggesting an important role for the anthropogenic (carbonaceous) fine fraction. The limited number of low-dose PM inhalation studies supports this suggestion. Coarse PM may still be important in health effects related to upper airways (like worsening of asthma); however, a role for secondary components (sulfates, nitrates) or ultrafine PM at levels occurring in ambient air have not yet been established. Evidence that (diesel) exhaust particles play a role in PM health effects is still marginal. Studies have indicated that mixtures of particles and gases like ozone may result in more toxicity than the components separately. Current dosimetry models predict that (older) people with cardio-respiratory diseases may receive increased PM doses upon exposure. Ambient PM toxicity studies have been intensified in recent years. The current limited data, however, have not yet resulted in sufficient evidence to be convincing in indicating: 1) a specifically important and causal role for one form of PM fraction or composition and 2) mechanisms explaining PM health effects in people considered to be at increased risk.
In this critical review studies focus on ambient particulate air pollution (PM) toxicity and particle hypotheses. Mechanisms were also evaluated to investigate causality and plausibility of acute health effects associated with ambient exposure. High-dose studies indicate that PM: 1) induces oxidative pulmonary inflammation and cardio-respiratory malfunctioning, which could contribute to a disease exacerbation mechanism. PM surface reactivity seems more important than PM mass, thereby prudently suggesting an important role for the anthropogenic (carbonaceous) fine fraction. The limited number of low-dose PM inhalation studies supports this suggestion. Coarse PM may still be important in health effects related to upper airways (like worsening of asthma); however, a role for secondary components (sulfates, nitrates) or ultrafine PM at levels occurring in ambient air have not yet been established. Evidence that (diesel) exhaust particles play a role in PM health effects is still marginal. Studies have indicated that mixtures of particles and gases like ozone may result in more toxicity than the components separately. Current dosimetry models predict that (older) people with cardio-respiratory diseases may receive increased PM doses upon exposure. Ambient PM toxicity studies have been intensified in recent years. The current limited data, however, have not yet resulted in sufficient evidence to be convincing in indicating: 1) a specifically important and causal role for one form of PM fraction or composition and 2) mechanisms explaining PM health effects in people considered to be at increased risk.
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