Toxic potency and effects of diffuse air pollution

T.H.M. Hamers

Research output: Thesisinternal PhD, WUAcademic

Abstract

<p>Diffuse air pollution consists of an omnipresent complex mixture of pollutants that is emitted from many widely dispersed sources as traffic, industries, households, energy plants, waste incinerators, and agriculture. It can be deposited in relatively remote areas as a result of (long-range) airborne transport. It has a heterogeneous composition in time and space and consists of many known and unknown compounds. Given the unknown chemical identity and toxicity of many constituents of this mixture, it is virtually impossible to make a toxicological characterization of diffuse air pollution based on evaluations of the individual compounds. Alternatively, in the present thesis the integrated toxic potency and the subsequent effects have been studied of the air polluting mixture as a whole. Three objectives were defined:</p><OL><p><LI>to determine the overall exposure to diffuse air pollution by measuring biomarker responses to relevant environmental samples;</LI></p><p><LI>to determine possible (early-warning) effects of diffuse air pollution by analyzing biomarkers in ecologically relevant exposed organisms;</LI></p><p><LI>to develop a strategic research concept for a toxicological risk characterization of diffuse air pollution based on overall exposure and effect assessments.</LI></p></OL><p>To meet these objectives, the integrated toxic potency has been qualified and quantified in small-scale <em>in vitro</em> bio-assays (exposure assessment) and the possible changes in biochemical and physiological endpoints have been quantified by measuring biomarkers in organisms exposed to airborne pollution in the field (effect assessment). Biomarkers were selected based on their specific response to toxicants with a specific mode of action. Selected toxicants were [1] genotoxic compounds, including PAHs, [2] arylhydrocarbon receptor (AhR) agonists including dioxin-like compounds, [3] estrogenic compounds, and [4] esterase inhibitors. Most of these toxicants were known to be relevant airborne pollutants, except for the estrogenic compounds, of which the atmospheric presence had hardly been studied yet. Exposure and effects of diffuse air pollution have been compared between background locations and locations with notoriously exposure to traffic or to pesticide emissions.</p><p> Genotoxic and AhR-activating potency was demonstrated for almost any of the of airborne particulate matter (APM) samples studied. APM collected at a relatively ghway, but differences were amply within one order of magnitude. In general, genotoxic potency could mainly be attributed to direct genotoxicants, rather than to compounds that first need to be metabolized to become genotoxic. However, during easterly wind conditions some APM samples contained relatively high indirect genotoxic potency with little differences between a highway and a background location. Trajectory analysis suggested that the different composition of pollutants in these samples is due to industrial pollutants that have been transported over long distances through the atmosphere. The AhR activating potency of APM was completely attributed to readily biodegradable compounds such as polycyclic aromatic hydrocarbons (PAHs), and not to stable congeners as dioxins or polychlorinated biphenyls (PCBs).</p><p> Differences among toxic potencies of APM collected next to a highway and in a background location were too small to be reflected in biomarker responses in small mammals. Actually, relatively high levels of aromatic DNA adduct in heart, lung, and liver and relatively low hepatic retinyl-palmitate levels were found in herbivorous bank voles ( <em>Clethrionomys glareolus</em> ) from the background location compared to the sampling locations closer to the highway. As these differences were not found in carnivorous common shrews ( <em>Sorex araneus</em> ), they were attributed to oral exposure to an actual deposition of airborne pollutants on the vegetation.</p><p> Esterase inhibiting potency was demonstrated in rainwater using a specially adapted bio-assay. Esterase inhibition correlated with analyzed concentrations of organophosphate and carbamate insecticides in rainwater and significantly depended on sampling location, with highest potency in an area with intense horticultural practice (greenhouses). Maximum concentrations of individually analyzed pesticides and maximum esterase inhibiting potencies (expressed as dichlorvos equivalent concentrations) incidentally exceeded EC <sub>50</sub> -values for Daphnia and maximum permissible concentrations (MPCs) set for surface water in The Netherlands. Estrogenic potency was observed in all rainwater samples tested and differed significantly with sampling season. Highest estrogenic potency was found in spring, and correlated significantly with the presence of organochlorine compounds in the rainwater, although it could not be explained by the analyzed concentrations of these compounds. Incidentally, estrogenic potency (expressed as estradiol equivalent concentrations ) exceeded lowest observed effect concentrations reported in literature for vitellogenesis in male rainbow trout. In conclusion, rainwater was frequently polluted with estrogenic and esterase inhibiting compounds at concentrations above MPCs for surface water and incidentally at effect levels for aquatic organisms, also in relatively remote and seemingly unpolluted areas. Because rainwater pollutants are diluted by surface water and adsorbed by particles after deposition, aquatic ecosystems will be exposed to lower concentrations and are probably not directly at risk. Possibly, shallow and mainly rainwater-fed water pools are an exception, and further studies should focus on such pools, especially in remote areas.</p><font size="3"><p> B</font>ased on the experiences gained in the present study<font size="3">,</font>a strategic research concept is proposed for the risk characterization of diffuse air pollution. The strategy includes several steps: [1] Relevant environmental samples are collected and adequately processed and their toxic potency is tested in bio-assays. [2] Bio-assay responses are compared to threshold levels for toxic effects. [3] For active environmental samples, a Toxicity Identity and Evaluation (TIE) procedure is proposed to identify the compounds that contribute most to its toxic potency. [4] <em>In vivo</em> responses should be studied in indicative organisms that are exposed via relevant routes of exposure to those compounds or groups of pollutants that exceeded thresholds levels in the bio-assays. [5] A risk assessment of diffuse air pollution can be made, based on the outcome of the exposure and effect assessments.
LanguageEnglish
QualificationDoctor of Philosophy
Awarding Institution
  • Wageningen University
Supervisors/Advisors
  • Koeman, J.H., Promotor
  • Murk, Tinka, Promotor
Award date4 Oct 2002
Place of PublicationS.l.
Publisher
Print ISBNs9789058087096
Publication statusPublished - 2002

Fingerprint

rainwater
atmospheric pollution
biomarker
bioassay
particulate matter
pollutant
estrogenic compound
road
surface water
dioxin
PAH
sampling
pesticide
toxicity
household energy
carbamate (ester)
effect
exposure
organophosphate
small mammal

Keywords

  • air pollution
  • air pollutants
  • toxicity
  • genotoxicity
  • mutagenicity
  • xenobiotics

Cite this

Hamers, T. H. M. (2002). Toxic potency and effects of diffuse air pollution. S.l.: S.n.
Hamers, T.H.M.. / Toxic potency and effects of diffuse air pollution. S.l. : S.n., 2002. 176 p.
@phdthesis{02f4ec27e9be4f3e88b221fa0b8953b5,
title = "Toxic potency and effects of diffuse air pollution",
abstract = "Diffuse air pollution consists of an omnipresent complex mixture of pollutants that is emitted from many widely dispersed sources as traffic, industries, households, energy plants, waste incinerators, and agriculture. It can be deposited in relatively remote areas as a result of (long-range) airborne transport. It has a heterogeneous composition in time and space and consists of many known and unknown compounds. Given the unknown chemical identity and toxicity of many constituents of this mixture, it is virtually impossible to make a toxicological characterization of diffuse air pollution based on evaluations of the individual compounds. Alternatively, in the present thesis the integrated toxic potency and the subsequent effects have been studied of the air polluting mixture as a whole. Three objectives were defined:<OL><LI>to determine the overall exposure to diffuse air pollution by measuring biomarker responses to relevant environmental samples;<LI>to determine possible (early-warning) effects of diffuse air pollution by analyzing biomarkers in ecologically relevant exposed organisms;<LI>to develop a strategic research concept for a toxicological risk characterization of diffuse air pollution based on overall exposure and effect assessments.To meet these objectives, the integrated toxic potency has been qualified and quantified in small-scale in vitro bio-assays (exposure assessment) and the possible changes in biochemical and physiological endpoints have been quantified by measuring biomarkers in organisms exposed to airborne pollution in the field (effect assessment). Biomarkers were selected based on their specific response to toxicants with a specific mode of action. Selected toxicants were [1] genotoxic compounds, including PAHs, [2] arylhydrocarbon receptor (AhR) agonists including dioxin-like compounds, [3] estrogenic compounds, and [4] esterase inhibitors. Most of these toxicants were known to be relevant airborne pollutants, except for the estrogenic compounds, of which the atmospheric presence had hardly been studied yet. Exposure and effects of diffuse air pollution have been compared between background locations and locations with notoriously exposure to traffic or to pesticide emissions. Genotoxic and AhR-activating potency was demonstrated for almost any of the of airborne particulate matter (APM) samples studied. APM collected at a relatively ghway, but differences were amply within one order of magnitude. In general, genotoxic potency could mainly be attributed to direct genotoxicants, rather than to compounds that first need to be metabolized to become genotoxic. However, during easterly wind conditions some APM samples contained relatively high indirect genotoxic potency with little differences between a highway and a background location. Trajectory analysis suggested that the different composition of pollutants in these samples is due to industrial pollutants that have been transported over long distances through the atmosphere. The AhR activating potency of APM was completely attributed to readily biodegradable compounds such as polycyclic aromatic hydrocarbons (PAHs), and not to stable congeners as dioxins or polychlorinated biphenyls (PCBs). Differences among toxic potencies of APM collected next to a highway and in a background location were too small to be reflected in biomarker responses in small mammals. Actually, relatively high levels of aromatic DNA adduct in heart, lung, and liver and relatively low hepatic retinyl-palmitate levels were found in herbivorous bank voles ( Clethrionomys glareolus ) from the background location compared to the sampling locations closer to the highway. As these differences were not found in carnivorous common shrews ( Sorex araneus ), they were attributed to oral exposure to an actual deposition of airborne pollutants on the vegetation. Esterase inhibiting potency was demonstrated in rainwater using a specially adapted bio-assay. Esterase inhibition correlated with analyzed concentrations of organophosphate and carbamate insecticides in rainwater and significantly depended on sampling location, with highest potency in an area with intense horticultural practice (greenhouses). Maximum concentrations of individually analyzed pesticides and maximum esterase inhibiting potencies (expressed as dichlorvos equivalent concentrations) incidentally exceeded EC 50 -values for Daphnia and maximum permissible concentrations (MPCs) set for surface water in The Netherlands. Estrogenic potency was observed in all rainwater samples tested and differed significantly with sampling season. Highest estrogenic potency was found in spring, and correlated significantly with the presence of organochlorine compounds in the rainwater, although it could not be explained by the analyzed concentrations of these compounds. Incidentally, estrogenic potency (expressed as estradiol equivalent concentrations ) exceeded lowest observed effect concentrations reported in literature for vitellogenesis in male rainbow trout. In conclusion, rainwater was frequently polluted with estrogenic and esterase inhibiting compounds at concentrations above MPCs for surface water and incidentally at effect levels for aquatic organisms, also in relatively remote and seemingly unpolluted areas. Because rainwater pollutants are diluted by surface water and adsorbed by particles after deposition, aquatic ecosystems will be exposed to lower concentrations and are probably not directly at risk. Possibly, shallow and mainly rainwater-fed water pools are an exception, and further studies should focus on such pools, especially in remote areas. Based on the experiences gained in the present study,a strategic research concept is proposed for the risk characterization of diffuse air pollution. The strategy includes several steps: [1] Relevant environmental samples are collected and adequately processed and their toxic potency is tested in bio-assays. [2] Bio-assay responses are compared to threshold levels for toxic effects. [3] For active environmental samples, a Toxicity Identity and Evaluation (TIE) procedure is proposed to identify the compounds that contribute most to its toxic potency. [4] In vivo responses should be studied in indicative organisms that are exposed via relevant routes of exposure to those compounds or groups of pollutants that exceeded thresholds levels in the bio-assays. [5] A risk assessment of diffuse air pollution can be made, based on the outcome of the exposure and effect assessments.",
keywords = "luchtverontreiniging, luchtverontreinigende stoffen, toxiciteit, genotoxiciteit, mutageniciteit, xenobiotica, air pollution, air pollutants, toxicity, genotoxicity, mutagenicity, xenobiotics",
author = "T.H.M. Hamers",
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Hamers, THM 2002, 'Toxic potency and effects of diffuse air pollution', Doctor of Philosophy, Wageningen University, S.l..

Toxic potency and effects of diffuse air pollution. / Hamers, T.H.M.

S.l. : S.n., 2002. 176 p.

Research output: Thesisinternal PhD, WUAcademic

TY - THES

T1 - Toxic potency and effects of diffuse air pollution

AU - Hamers, T.H.M.

N1 - WU thesis 3272 Auteursvermelding op de omslag: Timo Hamers Met lit.opg. - Met samenvatting in het Engels en het Nederlands Proefschrift Wageningen

PY - 2002

Y1 - 2002

N2 - Diffuse air pollution consists of an omnipresent complex mixture of pollutants that is emitted from many widely dispersed sources as traffic, industries, households, energy plants, waste incinerators, and agriculture. It can be deposited in relatively remote areas as a result of (long-range) airborne transport. It has a heterogeneous composition in time and space and consists of many known and unknown compounds. Given the unknown chemical identity and toxicity of many constituents of this mixture, it is virtually impossible to make a toxicological characterization of diffuse air pollution based on evaluations of the individual compounds. Alternatively, in the present thesis the integrated toxic potency and the subsequent effects have been studied of the air polluting mixture as a whole. Three objectives were defined:<OL><LI>to determine the overall exposure to diffuse air pollution by measuring biomarker responses to relevant environmental samples;<LI>to determine possible (early-warning) effects of diffuse air pollution by analyzing biomarkers in ecologically relevant exposed organisms;<LI>to develop a strategic research concept for a toxicological risk characterization of diffuse air pollution based on overall exposure and effect assessments.To meet these objectives, the integrated toxic potency has been qualified and quantified in small-scale in vitro bio-assays (exposure assessment) and the possible changes in biochemical and physiological endpoints have been quantified by measuring biomarkers in organisms exposed to airborne pollution in the field (effect assessment). Biomarkers were selected based on their specific response to toxicants with a specific mode of action. Selected toxicants were [1] genotoxic compounds, including PAHs, [2] arylhydrocarbon receptor (AhR) agonists including dioxin-like compounds, [3] estrogenic compounds, and [4] esterase inhibitors. Most of these toxicants were known to be relevant airborne pollutants, except for the estrogenic compounds, of which the atmospheric presence had hardly been studied yet. Exposure and effects of diffuse air pollution have been compared between background locations and locations with notoriously exposure to traffic or to pesticide emissions. Genotoxic and AhR-activating potency was demonstrated for almost any of the of airborne particulate matter (APM) samples studied. APM collected at a relatively ghway, but differences were amply within one order of magnitude. In general, genotoxic potency could mainly be attributed to direct genotoxicants, rather than to compounds that first need to be metabolized to become genotoxic. However, during easterly wind conditions some APM samples contained relatively high indirect genotoxic potency with little differences between a highway and a background location. Trajectory analysis suggested that the different composition of pollutants in these samples is due to industrial pollutants that have been transported over long distances through the atmosphere. The AhR activating potency of APM was completely attributed to readily biodegradable compounds such as polycyclic aromatic hydrocarbons (PAHs), and not to stable congeners as dioxins or polychlorinated biphenyls (PCBs). Differences among toxic potencies of APM collected next to a highway and in a background location were too small to be reflected in biomarker responses in small mammals. Actually, relatively high levels of aromatic DNA adduct in heart, lung, and liver and relatively low hepatic retinyl-palmitate levels were found in herbivorous bank voles ( Clethrionomys glareolus ) from the background location compared to the sampling locations closer to the highway. As these differences were not found in carnivorous common shrews ( Sorex araneus ), they were attributed to oral exposure to an actual deposition of airborne pollutants on the vegetation. Esterase inhibiting potency was demonstrated in rainwater using a specially adapted bio-assay. Esterase inhibition correlated with analyzed concentrations of organophosphate and carbamate insecticides in rainwater and significantly depended on sampling location, with highest potency in an area with intense horticultural practice (greenhouses). Maximum concentrations of individually analyzed pesticides and maximum esterase inhibiting potencies (expressed as dichlorvos equivalent concentrations) incidentally exceeded EC 50 -values for Daphnia and maximum permissible concentrations (MPCs) set for surface water in The Netherlands. Estrogenic potency was observed in all rainwater samples tested and differed significantly with sampling season. Highest estrogenic potency was found in spring, and correlated significantly with the presence of organochlorine compounds in the rainwater, although it could not be explained by the analyzed concentrations of these compounds. Incidentally, estrogenic potency (expressed as estradiol equivalent concentrations ) exceeded lowest observed effect concentrations reported in literature for vitellogenesis in male rainbow trout. In conclusion, rainwater was frequently polluted with estrogenic and esterase inhibiting compounds at concentrations above MPCs for surface water and incidentally at effect levels for aquatic organisms, also in relatively remote and seemingly unpolluted areas. Because rainwater pollutants are diluted by surface water and adsorbed by particles after deposition, aquatic ecosystems will be exposed to lower concentrations and are probably not directly at risk. Possibly, shallow and mainly rainwater-fed water pools are an exception, and further studies should focus on such pools, especially in remote areas. Based on the experiences gained in the present study,a strategic research concept is proposed for the risk characterization of diffuse air pollution. The strategy includes several steps: [1] Relevant environmental samples are collected and adequately processed and their toxic potency is tested in bio-assays. [2] Bio-assay responses are compared to threshold levels for toxic effects. [3] For active environmental samples, a Toxicity Identity and Evaluation (TIE) procedure is proposed to identify the compounds that contribute most to its toxic potency. [4] In vivo responses should be studied in indicative organisms that are exposed via relevant routes of exposure to those compounds or groups of pollutants that exceeded thresholds levels in the bio-assays. [5] A risk assessment of diffuse air pollution can be made, based on the outcome of the exposure and effect assessments.

AB - Diffuse air pollution consists of an omnipresent complex mixture of pollutants that is emitted from many widely dispersed sources as traffic, industries, households, energy plants, waste incinerators, and agriculture. It can be deposited in relatively remote areas as a result of (long-range) airborne transport. It has a heterogeneous composition in time and space and consists of many known and unknown compounds. Given the unknown chemical identity and toxicity of many constituents of this mixture, it is virtually impossible to make a toxicological characterization of diffuse air pollution based on evaluations of the individual compounds. Alternatively, in the present thesis the integrated toxic potency and the subsequent effects have been studied of the air polluting mixture as a whole. Three objectives were defined:<OL><LI>to determine the overall exposure to diffuse air pollution by measuring biomarker responses to relevant environmental samples;<LI>to determine possible (early-warning) effects of diffuse air pollution by analyzing biomarkers in ecologically relevant exposed organisms;<LI>to develop a strategic research concept for a toxicological risk characterization of diffuse air pollution based on overall exposure and effect assessments.To meet these objectives, the integrated toxic potency has been qualified and quantified in small-scale in vitro bio-assays (exposure assessment) and the possible changes in biochemical and physiological endpoints have been quantified by measuring biomarkers in organisms exposed to airborne pollution in the field (effect assessment). Biomarkers were selected based on their specific response to toxicants with a specific mode of action. Selected toxicants were [1] genotoxic compounds, including PAHs, [2] arylhydrocarbon receptor (AhR) agonists including dioxin-like compounds, [3] estrogenic compounds, and [4] esterase inhibitors. Most of these toxicants were known to be relevant airborne pollutants, except for the estrogenic compounds, of which the atmospheric presence had hardly been studied yet. Exposure and effects of diffuse air pollution have been compared between background locations and locations with notoriously exposure to traffic or to pesticide emissions. Genotoxic and AhR-activating potency was demonstrated for almost any of the of airborne particulate matter (APM) samples studied. APM collected at a relatively ghway, but differences were amply within one order of magnitude. In general, genotoxic potency could mainly be attributed to direct genotoxicants, rather than to compounds that first need to be metabolized to become genotoxic. However, during easterly wind conditions some APM samples contained relatively high indirect genotoxic potency with little differences between a highway and a background location. Trajectory analysis suggested that the different composition of pollutants in these samples is due to industrial pollutants that have been transported over long distances through the atmosphere. The AhR activating potency of APM was completely attributed to readily biodegradable compounds such as polycyclic aromatic hydrocarbons (PAHs), and not to stable congeners as dioxins or polychlorinated biphenyls (PCBs). Differences among toxic potencies of APM collected next to a highway and in a background location were too small to be reflected in biomarker responses in small mammals. Actually, relatively high levels of aromatic DNA adduct in heart, lung, and liver and relatively low hepatic retinyl-palmitate levels were found in herbivorous bank voles ( Clethrionomys glareolus ) from the background location compared to the sampling locations closer to the highway. As these differences were not found in carnivorous common shrews ( Sorex araneus ), they were attributed to oral exposure to an actual deposition of airborne pollutants on the vegetation. Esterase inhibiting potency was demonstrated in rainwater using a specially adapted bio-assay. Esterase inhibition correlated with analyzed concentrations of organophosphate and carbamate insecticides in rainwater and significantly depended on sampling location, with highest potency in an area with intense horticultural practice (greenhouses). Maximum concentrations of individually analyzed pesticides and maximum esterase inhibiting potencies (expressed as dichlorvos equivalent concentrations) incidentally exceeded EC 50 -values for Daphnia and maximum permissible concentrations (MPCs) set for surface water in The Netherlands. Estrogenic potency was observed in all rainwater samples tested and differed significantly with sampling season. Highest estrogenic potency was found in spring, and correlated significantly with the presence of organochlorine compounds in the rainwater, although it could not be explained by the analyzed concentrations of these compounds. Incidentally, estrogenic potency (expressed as estradiol equivalent concentrations ) exceeded lowest observed effect concentrations reported in literature for vitellogenesis in male rainbow trout. In conclusion, rainwater was frequently polluted with estrogenic and esterase inhibiting compounds at concentrations above MPCs for surface water and incidentally at effect levels for aquatic organisms, also in relatively remote and seemingly unpolluted areas. Because rainwater pollutants are diluted by surface water and adsorbed by particles after deposition, aquatic ecosystems will be exposed to lower concentrations and are probably not directly at risk. Possibly, shallow and mainly rainwater-fed water pools are an exception, and further studies should focus on such pools, especially in remote areas. Based on the experiences gained in the present study,a strategic research concept is proposed for the risk characterization of diffuse air pollution. The strategy includes several steps: [1] Relevant environmental samples are collected and adequately processed and their toxic potency is tested in bio-assays. [2] Bio-assay responses are compared to threshold levels for toxic effects. [3] For active environmental samples, a Toxicity Identity and Evaluation (TIE) procedure is proposed to identify the compounds that contribute most to its toxic potency. [4] In vivo responses should be studied in indicative organisms that are exposed via relevant routes of exposure to those compounds or groups of pollutants that exceeded thresholds levels in the bio-assays. [5] A risk assessment of diffuse air pollution can be made, based on the outcome of the exposure and effect assessments.

KW - luchtverontreiniging

KW - luchtverontreinigende stoffen

KW - toxiciteit

KW - genotoxiciteit

KW - mutageniciteit

KW - xenobiotica

KW - air pollution

KW - air pollutants

KW - toxicity

KW - genotoxicity

KW - mutagenicity

KW - xenobiotics

M3 - internal PhD, WU

SN - 9789058087096

PB - S.n.

CY - S.l.

ER -

Hamers THM. Toxic potency and effects of diffuse air pollution. S.l.: S.n., 2002. 176 p.