Association of Particulate Air Pollution and Acute Mortality: Involvement of Ultrafine Particles?

Abstract Recent epidemiological studies show an association between particulate air pollution and acute mortality and morbidity down to ambient particle concentrations below 100 μml/m3. Whether this association also implies a causality between acute health effects and particle exposure at these low...

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Veröffentlicht in:Inhalation toxicology 1995, Vol.7 (1), p.111-124
Hauptverfasser: Oberdörster, Günter, Celein, Robert M., Ferin, Juraj, Weiss, Bernard
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container_title Inhalation toxicology
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creator Oberdörster, Günter
Celein, Robert M.
Ferin, Juraj
Weiss, Bernard
description Abstract Recent epidemiological studies show an association between particulate air pollution and acute mortality and morbidity down to ambient particle concentrations below 100 μml/m3. Whether this association also implies a causality between acute health effects and particle exposure at these low levels is unclear at this time; no mechanism is known that would explain such dramatic effects of low ambient particle concentrations. Based on results of our past and most recent inhalation studies with utlrafine particles in rats, we propose that such particles, that is, particles below ∼50 nm in diameter, may contribute to the observed increased mortality and morbidity. In the past we demonstrated that inhalation of highly insoluble particles of low intrinsic toxicity, such as TiO2, results in significantly increased pulmonary inflammatory responses when their size is in the ultrafine particle range, ∼20 nm in diameter. However, these effects were not of an acute nature and occurred only after prolonged inhalation exposure of the aggregated ultrafine particles at concentrations in the milligrams per cubic meter range. In contrast, in the course of our most recent studies with thermodegradation products of polytetrafluoroethylene IPTFE) we found that freshly generated PTFE fumes containing singlet ultrafine particles (median diameter 26 nm) were highly toxic to rats at inhaled concentrations of 0.7-1.0 × 706 particles/cm3, resulting in acute hemorrhagic pulmonary inflammation and death after 70-30 min of exposure. We also found that work performance of the rats in a running wheel was severely affected by PTFE fume exposure. These results confirm reports from other laboratories of the highly toxic nature of PJFE fumes, which cannot be attributed to gas-phase components of these fumes such as HF, carbonylfluoride, or perfluoroisobutylene, or to reactive radicals. The calculated mass concentration of the inhaled ultrafine PTFE particles in our studies was less than 60 yg/m3, a very low value to cause mortality in healthy rats. Aging of the fumes with concomitant aggregation of the ultrafine particles significantly decreases their toxicity. Since ultrafine particles are always present in the urban atmosphere, we suggest that they play a role in causing acute lung injury in sensitive parts of the population.
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Whether this association also implies a causality between acute health effects and particle exposure at these low levels is unclear at this time; no mechanism is known that would explain such dramatic effects of low ambient particle concentrations. Based on results of our past and most recent inhalation studies with utlrafine particles in rats, we propose that such particles, that is, particles below ∼50 nm in diameter, may contribute to the observed increased mortality and morbidity. In the past we demonstrated that inhalation of highly insoluble particles of low intrinsic toxicity, such as TiO2, results in significantly increased pulmonary inflammatory responses when their size is in the ultrafine particle range, ∼20 nm in diameter. However, these effects were not of an acute nature and occurred only after prolonged inhalation exposure of the aggregated ultrafine particles at concentrations in the milligrams per cubic meter range. In contrast, in the course of our most recent studies with thermodegradation products of polytetrafluoroethylene IPTFE) we found that freshly generated PTFE fumes containing singlet ultrafine particles (median diameter 26 nm) were highly toxic to rats at inhaled concentrations of 0.7-1.0 × 706 particles/cm3, resulting in acute hemorrhagic pulmonary inflammation and death after 70-30 min of exposure. We also found that work performance of the rats in a running wheel was severely affected by PTFE fume exposure. These results confirm reports from other laboratories of the highly toxic nature of PJFE fumes, which cannot be attributed to gas-phase components of these fumes such as HF, carbonylfluoride, or perfluoroisobutylene, or to reactive radicals. The calculated mass concentration of the inhaled ultrafine PTFE particles in our studies was less than 60 yg/m3, a very low value to cause mortality in healthy rats. 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Whether this association also implies a causality between acute health effects and particle exposure at these low levels is unclear at this time; no mechanism is known that would explain such dramatic effects of low ambient particle concentrations. Based on results of our past and most recent inhalation studies with utlrafine particles in rats, we propose that such particles, that is, particles below ∼50 nm in diameter, may contribute to the observed increased mortality and morbidity. In the past we demonstrated that inhalation of highly insoluble particles of low intrinsic toxicity, such as TiO2, results in significantly increased pulmonary inflammatory responses when their size is in the ultrafine particle range, ∼20 nm in diameter. However, these effects were not of an acute nature and occurred only after prolonged inhalation exposure of the aggregated ultrafine particles at concentrations in the milligrams per cubic meter range. In contrast, in the course of our most recent studies with thermodegradation products of polytetrafluoroethylene IPTFE) we found that freshly generated PTFE fumes containing singlet ultrafine particles (median diameter 26 nm) were highly toxic to rats at inhaled concentrations of 0.7-1.0 × 706 particles/cm3, resulting in acute hemorrhagic pulmonary inflammation and death after 70-30 min of exposure. We also found that work performance of the rats in a running wheel was severely affected by PTFE fume exposure. These results confirm reports from other laboratories of the highly toxic nature of PJFE fumes, which cannot be attributed to gas-phase components of these fumes such as HF, carbonylfluoride, or perfluoroisobutylene, or to reactive radicals. The calculated mass concentration of the inhaled ultrafine PTFE particles in our studies was less than 60 yg/m3, a very low value to cause mortality in healthy rats. 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source MEDLINE; Taylor & Francis:Master (3349 titles); Taylor & Francis Medical Library - CRKN; NASA Technical Reports Server
subjects Aerosols
Air Pollutants - adverse effects
Air Pollutants - toxicity
Air Pollution - adverse effects
Air Pollution - analysis
Air Pollution - statistics & numerical data
Animals
Disease Models, Animal
Dose-Response Relationship, Drug
Environment Pollution
Hot Temperature
Humans
Inhalation Exposure - adverse effects
Lung Diseases - chemically induced
Lung Diseases - epidemiology
Lung Diseases - mortality
Male
Mortality
Motor Activity
Particle Size
Polytetrafluoroethylene - administration & dosage
Polytetrafluoroethylene - adverse effects
Polytetrafluoroethylene - toxicity
Rats
Rats, Inbred F344
title Association of Particulate Air Pollution and Acute Mortality: Involvement of Ultrafine Particles?
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